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PunkassDerm
Posted on: Yesterday, 09:29 PM


Group: Member
Posts: 509

ANTI-INFLAMMATORY
ANTI-MICROBIAL
ANTI-FUNGAL
NON-TOXIC

PSORIASIS POTENTIAL



https://www.hindawi.com/journals/bmri/2014/874610/


Alpha-Melanocyte Stimulating Hormone: An Emerging Anti-Inflammatory Antimicrobial Peptide
Madhuri Singh1,2 and Kasturi Mukhopadhyay1
BioMed Research International
Volume 2014, Article ID 874610, 10 pages
2014


Conclusions

In this postantibiotic era, AMPs have already created huge hopes for their host defense mechanism and several of these peptides find ways into medical practice although the numbers are less than expected. The development of AMPs as therapeutic alternatives to combat the resistant pathogenic microbes is facing problems, majorly due to the enhanced inflammatory reactions associated with them and their potential for toxicity. -MSH overcomes both of these issues being anti-inflammatory and nontoxic. This endogenous neuropeptide was initially characterized as a pigment producing peptide and later received serious attention due to its potent protective and anti-inflammatory activity. -MSH performs these actions by binding to centrally expressed melanocortin receptors, which subsequently coordinate numerous anti-inflammatory pathways leading to shutting down all the downstream effector proinflammatory mechanisms. Besides anti-inflammation, it also exhibited immunosuppression in case of skin-inflammatory diseases like psoriasis. The striking resemblance of this anti-inflammatory neuropeptide with cationic AMPs compelled the scientists to further explore its antimicrobial efficacy. Indeed, -MSH appeared to possess potent antimicrobial activity against pathogens from different classes like C. albicans, S. aureus, E. coli, and more. It also adopts variable approaches to kill different microbes. For instance, it kills fungal cells through the induction of cAMP and bacterial cells by damaging the membrane [14, 18]. The C-terminal region (KPV) of -MSH demands special attention for several reasons. It exhibits in vitro and in vivo anti-inflammatory activity similar to that of parent peptide without melanotropic effect. This observation removes the main obstacle in developing -MSH based peptides as therapeutics, which is nothing, but its pigmentary effects and KPV are devoid of that. Moreover, this essential anti-inflammatory sequence, that is, C-terminal tripeptide (KPV) of -MSH, is also essential for its direct antimicrobial efficacy. Therefore, this short molecule KPV appears to have tremendous potential to be developed as therapeutic agent as it is more suitable for clinical use and demands further research. The dimer of this short peptide, that is, (CKPV)2 being both anti-inflammatory and antimicrobial, is already in clinical trial and will definitely make its way to enter into medical practice in near future.

The pleiotropic effects of -MSH and its C-terminal peptides, including their anti-inflammatory, immunosuppressive, antipyretic, and antimicrobial activities, are unique. These endogenous properties make them the most promising antimicrobial host defense peptides. More work is however needed to bring these peptides from the lab to clinic. First, a deeper corelation is required to be established between its anti-inflammatory and anti-infective reactions through the in vivo models of infections. Second, further biophysical studies are required to design a potent -MSH based AMP with enhanced killing and immunomodulatory activities. Third, the possibility of resistance developing against this peptide needs to be ruled out. Fourth, overall safety profile of these peptides particularly with -MSH fragments requires to be vigorously examined.

In conclusion, -MSH, its analogues, and related C-terminal tripeptide with broad-spectrum antimicrobial activity combined with immunomodulating effects and no cytotoxicity could emerge as excellent therapeutic agents against resistant pathogens.
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PunkassDerm
Posted on: Sep 14 2019, 10:05 PM


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More readable article, Scientific America. Maybe the Dermatology powerhouse couple should read this. Less wordy for them.
P53 activation from MSH activation

And yes, the tan (pigment) protects against UVR oxidative damage, plus MSH/P53 DNA repair mechanisms.


https://www.scientificamerican.com/article/...omotes-tanning/


A Protein Twofer That Triggers Tanning and Protects against Skin Cancer
Researchers find that a protein activated to repair DNA damage also activates tanning, which can protect against melanoma


A powerful protein known as p53 has long been considered the master regulator of the genome because of its amazing ability to repair damaged DNA. Now scientists at Harvard's Dana-Farber Cancer Institute have discovered that p53 not only mends genetic material but also kicks off the chemical cascade that results in tanning.

The researchers report in Cell that when p53 is activated (in response to DNA damage caused by the sun's ultraviolet (UV) rays and other factors), it triggers production of alpha-MSH, a hormone that then prompts production of melanin, or pigment. Recognizing that p53 is the linchpin of this chain of events could result in a way to "give people tans without needing the sun" (or creams or sprays to artificially color their skin), says senior study author David Fisher, director of Dana-Farber's Cutaneous Oncology and Melanoma Program.

In many types of cancer, p53 is disabled and cannot fulfill its role as a tumor suppressor. Deprived of their ability to fix new DNA damage, defective cells often become tumor cells and proliferate unchecked. In the case of skin cancer—which Fisher notes is "the most common and most preventable" form of the disease—the ability to tan is an extremely strong predictor of cancer susceptibility: Fair-skinned people who are more likely to burn than tan in the sun are at higher risk of developing skin cancer than individuals who tan easily.

In work published last year, the Dana-Farber group found that alpha-MSH, needed to induce melanin production, does not come from melanocytes (melanin-producing cells in the skin). They believe the hormone, instead, is produced in keratinocytes, the most common type of skin cells. The reason: they found broken alpha-MSH receptors on the surface of melanocytes in subjects with an inability to tan.

Other lab work had shown that p53 activates during tanning. And, sure enough, when the Dana-Farber team probed the protein pro-opiomelanocortin (POMC)—which splits to make several hormones including alpha-MSH—it discovered "a perfect p53 binding element there," Fisher says. When testing both mouse and human keratinocytes in vitro, the team observed that after six hours of exposure to UV radiation, p53, POMC and alpha-MSH levels had all jumped dramatically, with the latter's rising 30 times higher than normal. The finding was confirmed in knockout mice missing the gene that codes for p53: Without the protein, POMC was never activated, the mice did not tan (on their hairless ears and tails), and eventually they all developed melanomas.

"What we were stumbling into here was actually a role for p53 in absolutely normal cells," Fisher says, "and it's a normal physiologic response that happens anytime any of us walks out of the house in the morning." He adds that people have a "love-hate relationship" with UV rays, which stimulate vitamin D production needed to keep bones strong and healthy, but also cause potentially deadly skin cancer and premature wrinkling.

Barbara Gilchrest, chair of the Department of Dermatology at Boston University School of Medicine, says that the new findings demonstrate that the p53 system is a broad-response mechanism that has both reparative and preventative properties for DNA damage. "When you damage DNA in cells, they not only work very hard to fix that DNA, but they also work hard to prepare the cell and tissue to be resistant to future DNA damage," she says. "Once you have that tan, your DNA is better protected for the next time that you're out in the sun, because of that melanin cover over the nucleus shielding it from UV rays that would damage [the] DNA inside."
Fisher says that, in theory, the p53 pathway could be a "druggable" one. "In fact, one of the directions that we're taking to use this information is to try to identify small molecules that could potentially be delivered topically," he reveals, "to either increase or decrease pigmentation through interfering [with] or mimicking this pathway."
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PunkassDerm
Posted on: Sep 14 2019, 09:55 PM


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Agreed, these concepts are beyond myself as well. But there are pathways to repair. Some are more likely specific to certain tissues and tumors.

https://www.cell.com/trends/genetics/pdf/S0...(14)00096-1.pdf


Cancer-specific defects in DNA repair pathways as targets for personalized therapeutic approaches
Felix Dietlein1,2, Lisa Thelen1, and H. Christian Reinhardt1,2


Defects in DNA repair pathways enable cancer cells to accumulate genomic alterations that contribute to their aggressive phenotype. However, tumors rely on residual DNA repair capacities to survive the damage induced by genotoxic stress. This dichotomy might explain why only isolated DNA repair pathways are inactivated in cancer cells. Accordingly, synergism has been observed between DNA-damaging drugs and targeted inhibitors of DNA repair. DNA repair pathways are generally thought of as mutually exclusive mechanistic units han- dling different types of lesions in distinct cell cycle phases. Recent preclinical studies, however, provide strong evidence that multifunctional DNA repair hubs, which are involved in multiple conventional DNA repair pathways, are frequently altered in cancer. We therefore propose that targeted anticancer therapies should not only exploit synthetic lethal interactions between two single genes but also consider alterations in DNA repair hubs. Such a network-based approach considerably increases the opportunities for targeting DNA repair- defective tumors.

During the cell cycle, cells progress through a series of cell cycle checkpoints before mitotic cell division and distribu- tion of the genomic material to the daughter cells [1]. In response to genotoxic stress, cells activate these check- points to prevent further progression through the cell cycle and initiate DNA repair [2]. If the extent of DNA damage is beyond repair capacity, additional signaling pathways leading to the induction of apoptosis are activated, elimi- nating potentially dangerous mutated cells [3]. This sig- naling network, which is commonly referred to as the DNA damage response (DDR), is tightly controlled and involves regulation at the transcriptional, post-transcriptional, and post-translational levels [1,4,5].
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PunkassDerm
Posted on: Sep 14 2019, 05:16 AM


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Multiple mechanisms and pathways.
Discussion of lung adenocarcioma.
Answer is probably..in some cases yes.
Cells with MC1R receptors? Specific transcription mistakes?

OMNIPOTENT p53 gene

https://cancerres.aacrjournals.org/content/70/9/3547


Discussion

α-MSH is a propigmentation hormone, which is produced and secreted by both keratinocytes and melanocytes in the skin following UV irradiation (10, 32, 33). Normal synthesis of α-MSH and ACTH is crucial for constitutive human pigmentation and the cutaneous response to UV irradiation (10, 34, 35). In addition to being the key factor in UV-induced melanogenesis, α-MSH also has crucial antiinflammatory effects in response to UV irradiation (36, 37). These data indicate that POMC/α-MSH functions as a “protective factor” against the harmful effects of UV irradiation to maintain epidermal homeostasis and genomic stability. We have further shown that the downstream target of p53 in keratinocytes (POMC/α-MSH) is also an activator of DNA repair in these cells after UV irradiation, independent of its previously known role in inducing pigmentation.

It has been previously shown by Abdel-Malek's and Schwarz's groups that α-MSH protects HPMs from UV-induced apoptosis and DNA damage (photoproducts production and oxidative stress; refs. 1, 6–8). Specifically, the antiapoptotic effects of α-MSH were mediated by the activation of the inositol triphosphate kinase–Akt pathway and microphthalmia-associated transcription factor (8). The Abdel-Malek group has also developed melanocortin analogues, which, in addition to stimulating pigmentation, effectively reduced and repaired DNA damage resulting from exposure to solar UV radiation (1, 3). Together, these studies suggest the existence of alternative mechanisms for pigmentation induction through which α-MSH protects skin from UV irradiation.

Interestingly, Abdel-Malek, Schwarz, and their colleagues have found that α-MSH does not induce the cell cycle arrest nor the activation of apoptosis-related proteins (6–8). One recent report showed that α-MSH prevented the UVB-induced suppression of a pathway functioning in protection against oxidative stress (38). In particular, it showed that UVB failed to inhibit Nrf2, a transcription factor critical to antioxidant induction, and Nrf-dependent genes upon α-MSH treatment in both keratinocytes and melanocytes (38). Complementary to these results, we showed that α-MSH is involved in the protection against UV-induced DNA damage through the activation of DNA repair machinery, including XAB1 and XPA DNA repair factors.

Several independent groups have characterized the expression of MC1R in keratinocytes (39, 40). However, the role of MC1R in keratinocytes is still unclear. Here, we showed that MC1R is required in the α-MSH–mediated UV-induced DNA repair in keratinocytes. Usually, following the binding of hormones to the membrane receptors, the receptors undergo conformational changes, which will permit the receptor to augment the exchange of GTP for GDP on a subunit of the trimeric G protein. The GTP-bound and activated G-protein subunits finally interact with their respective effectors to generate the appropriate signals (41). Here, we determined that the protective effect of α-MSH against DNA damage works in a MC1R-, XAB1-, and XPA-dependent manner. Thus, we postulated the signaling pathway of α-MSH–mediated DNA repair as shown in Supplementary Fig. S7. Following the binding of α-MSH, MC1R, which couples with a specific G protein, is activated and acts as a guanine nucleotide exchange factor for its respective G proteins. The α-MSH binding elicits a conformational change on MC1R, permitting it to augment the exchange of GTP for GDP on a subunit of the trimeric G protein. The XAB1 GTPase activity is then activated after the binding of GTP and eventually induces the nuclear translocation of the XPA protein to accelerate the clearance of photoproducts.

cAMP, a pivotal second messenger, regulates a diverse range of key cellular behaviors, including cell metabolism, cell growth and differentiation, apoptosis, and inflammatory responses. It is produced by an enzymatic reaction catalyzed by adenylyl cyclase. In eukaryotic cells, the effects of cAMP are mediated by two intracellular cAMP receptors, cAMP-dependent kinase (PKA), and Epac (42). Previous reports have shown that Epac proteins bind to cAMP with high affinity and activate the Ras superfamily small GTPase Rap1 and Rap2 (43). We showed that adenylyl cyclase is required in the activation of XAB1 GTPase activity needed for α-MSH–mediated DNA repair after UV irradiation. Our results also show that Epac, not PKA, is required for α-MSH–mediated DNA repair.

Cells use the NER system to eliminate DNA photoproducts. XPA is part of the core incision complex of the NER system (44). Here, we showed that α-MSH induces/augments XPA nuclear import and then activates the core incision complex in the NER system. We also found that the α-MSH–mediated translocation of XPA is modulated by XAB1. One group has shown that endogenous XPA protein is phosphorylated after UV irradiation in a lung adenocarcinoma cell line (45). However, we did not detect the phosphorylated XPA protein after UVB irradiation in keratinocytes nor any effect of α-MSH in the regulation of XPA phosphorylation. It is possible that the phosphorylated XPA is not as abundant in keratinocytes and therefore was below the detection threshold in our assay. It is also possible that XPA activity is modulated via different mechanisms in different cell types.

After UV-induced and p53-transactivated POMC/α-MSH is secreted from keratinocytes, it then binds to MC1R in both melanocytes and keratinocytes. Interestingly, distinct pathways downstream of MSH/MC1R become activated in these two cell types to reduce UV-induced DNA damages. In melanocytes, the α-MSH/MC1R complex activates the cAMP pathway and then induces melanin production. Melanin (eumelanin) functions as a physical barrier that scatters incident UV light, serving as a filter to reduce the penetration of UV light through the epidermis (46). In keratinocytes, the α-MSH/MC1R complex upregulates adenylyl cyclase activity and XAB1 GTPase activity inducing the nuclear translocation of XPA to repair the damaged DNA. In both the pigmentation induction and DNA repair activation processes, POMC/α-MSH functions as the crucial downstream target of the “guardian of genome” protein p53 (47).
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PunkassDerm
Posted on: Sep 12 2019, 12:23 PM


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Posts: 509

Drafted and sent, based on response to the "expert" in the UK.
My frustration is as palpable as a metastatic lymph node...from the control group.


Drs. Zirwas and Fichtel

Re: Melanin Injections Are the Dangerous Way Some People Are Trying to Tan

I am a PA in Dermatology near Worcester, MA. In 2004 I was introduced to afamelanotide when Clinuvel was still Epitan. Now approved by the EMA, waiting for FDA approval for EPP October 6 of this year. There is potential for this drug or another MSH analog to accomplish free radical scavenging, anti-inflammatory properties and DNA repair. So a possible melanoma preventative. Melanocortins will be disruptive to medicine, so many potential applications. Vitiligo, HHD, XP probably next. Should have made note in your article for future potential to reduce melanoma incidence. Absolutely agree regarding black market MSH injections, but there is a HUGE difference and ought not to be bundled in conversation for the layperson.

See below abstract, there are many others like it. Your only experience it appears is with rogue lab product, not afamelanotide or any melanocortin drug candidate. Suggest some more research before commenting, "dark moles bad." Your comments are uneducated and careless...for a Dermatology Powerhouse and literally the best there are at what they do (that passage is awkward). Just Wow, lots of superlatives on your page!

In the afamelanotide trials there was one melanoma, in the CONTROL (placebo) group. Also in below link.

Thanks for your time.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5161401/

Concern has been raised regarding the potential for it to promote the development of melanoma.34,36 Several in vivo and in vitro studies have not shown a correlation between afamelanotide use and malignancy, and, in fact, have shown that melanoma cell proliferation is inhibited.36 The primary risk factor for melanoma is ultraviolet B (UVB) radiation, which can induce DNA damage leading to a pro-proliferative state.36 α-MSH increases eumelanin production and provides protection against melanoma by reducing exposure to UVB irradiation, scavenging oxygen free radicals produced after exposure to UVB radiation, and by stimulating DNA repair via MC1R signaling in response to α-MSH.34,36 Additionally, melanoma stem cells do not express the MC1R, and it is important to note that the elevated levels of melanin seen with melanoma are not the cause of melanoma.36 Thus, it seems likely that afamelanotide will decrease the risk of development of malignant melanoma.
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PunkassDerm
Posted on: Sep 11 2019, 08:36 PM


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Still uneducated MDs commenting on MSH. Speaking only to blackmarket peptides and not afamelanotide.
No mention of DNA repair, contrary to ignorant statements.
Attention Wolgen/Hay, MAYBE you should be reaching out to these publications to correct misperceptions? Including a medical community, that appears clueless.

Dermatologist Matthew Zirwas, MD is a tool for his uneducated assumptions and lack of scientific protocol.


Melanin Injections Are the Dangerous Way Some People Are Trying to Tan
By Emily Taylor, Editorial Assistant | August 19, 2019


Where Did Melanin Injections Come From?

Created by faculty at the University of Arizona Cancer Center in the 1980s, synthetic melanotan, also known as the molecule afamelanotide, is not actually melanin at all; it's an artificial peptide (it mimics the naturally-occurring alpha-melanocyte stimulating hormone, or alpha-MSH) that signals our melanocytes (pigment-producing cells) to make more melanin, giving skin a richer, darker color.

The initial goal of this compound—which included two iterations called melanotan types I and II—was the treatment of skin pigmentation disorders like vitiligo, and of sun-sensitivity disorders like erythropoietic protoporphyria (EPP). Boosting melanin levels was thought to protect against that photosensitivity, since melanin absorbs light and can dissipate UV radiation.

Melanotan-I was licensed to an Australian company in 2000 as a potential EPP treatment (that firm developed it into a drug called Scenesse that's now under FDA review for approval). A New Jersey-based pharmaceutical company bought Melanotan-II for its promise in relieving sexual dysfunction; a variation (swap a hydroxyl group for an amide and you’re there) eventually became Vylessi, which the FDA approved in June 2019 to treat abnormally low sex drive in premenopausal women (that’s right, a relative of melanotan can ignite libido and sexual response).


Can Melanotan Trigger Skin Cancer?

Because there's been so little research, we don't know if injecting melanotan could have negative heath impact down the road. “Even if the shot has what it is supposed to have, we have no idea what the long-term effects are,” Dr. Fichtel explains. “You can’t even claim that because the injections are just stimulating your body to do more of something it already does naturally, they are safe. We know that isn't true for other things. If you take shots to stimulate muscle cells (i.e. anabolic steroids), it has lots of other major side effects.”

And there's one particularly troubling potential risk: skin cancer. “Injections definitely can cause moles to darken and look bad," Dr. Fichtel notes. "I haven’t found any proof that they increase the risk of melanoma, but there aren't any long-term studies and I could totally imagine there being a significant lag between the shots and any increase in melanoma risk.”

In fact, Dr. Fichtel’s husband, dermatologist Matthew Zirwas, MD, is currently studying how moles can darken after starting melanotan injections, which happened to one of his own patients. “I had a patient who noticed all moles get darker after beginning the injections, and on exam, the two moles looked particularly worrisome and dark to me,” he says. “They both were moderately abnormal moles that needed to be completely removed to prevent the risk of turning into severely abnormal moles or even melanoma. I did not do an exam prior to him starting the injections, so it’s hard to tell if they were abnormal prior to that, but it is definitely possible that the melanocyte-stimulating hormone could have led to the abnormal change in his moles.”
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PunkassDerm
Posted on: Sep 5 2019, 10:56 PM


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Attached Image
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PunkassDerm
Posted on: Sep 5 2019, 10:11 AM


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Yes Yes...I used to tally my 40million USD before the reverse split. Helicopter skiing with Wolgen.
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PunkassDerm
Posted on: Aug 31 2019, 02:52 AM


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Sounds great...but said frugality incongruent with delays and missteps coupled with performance rights.
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PunkassDerm
Posted on: Aug 30 2019, 08:31 PM


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https://www.fool.com.au/2019/08/29/3-asx-re...woods-clinuvel/


3 ASX results you might have missed: Australian Ethical, Cedar Woods, & CLINUVEL


CLINUVEL Pharmaceuticals Limited (ASX: CUV)

The shares of this skin disorder-focused biopharmaceutical company pushed higher yesterday after it released its full year results. CLINUVEL revealed a 21.8% increase in revenue to $31.05 million and a 40% lift in net profit before tax to $18.1 million in FY 2019. Strong demand for its SCENESSE product was the driver of this strong growth. Management advised: “The posting of our third consecutive and record annual net profit before tax is a milestone for the CLINUVEL Group and underpins our determination to continue self-distribution of our lead treatment, SCENESSE to patients with erythropoietic protoporphyria in Europe.” If the product is approved by the U.S. FDA then FY 2020 could prove to be just as successful.
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PunkassDerm
Posted on: Aug 29 2019, 10:51 AM


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Wish I could vote my shares.
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PunkassDerm
Posted on: Aug 26 2019, 11:43 PM


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No it's not, sustained tapered release is the key. Also goes on to say more likely with daily use, akin to using MTII regularly.
How can they reject Scenesse?
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PunkassDerm
Posted on: Aug 26 2019, 11:09 PM


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Vyleesi available....

COME ON WOLGEN et al!


https://www.vyleesi.com/?gclsrc=aw.ds


Attached Image


Side effects include: ohmy.gif

Darkening of the skin on certain parts of the body (focal hyperpigmentation) including the face, gums (gingiva) and breast. The chance of darkening of the skin is increased in people with darker skin color. The chance of darkening of the skin is higher if VYLEESI is used every day. Darkening of the skin may not go away, even after you stop using VYLEESI.
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PunkassDerm
Posted on: Aug 9 2019, 10:23 AM


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Kinda need the cash I used. Finishing a house that I've held off waiting for the big boom. No matter what, gotta pull some back out in a few weeks.

And...bought a bunch of PTN, that's going to be awhile for returns.

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PunkassDerm
Posted on: Aug 9 2019, 04:56 AM


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Posts: 509

Same here 5k shares at 18.50.
Kinda need it, hopefully sell high 20s in 3-4 weeks?
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PunkassDerm
Posted on: Aug 6 2019, 12:57 AM


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Posts: 509

Trying to learn myself, I hope ramp up is soon and wish I had feee cash to buy.
Could it be more difficult to predict as Clinuvel is currently not listed NASDAQ?


Analysis of stock market reactions to FDA and EMEA announcements


https://lib.ugent.be/fulltxt/RUG01/002/062/...013_0001_AC.pdf


2.2.1. STOCK PRICE ANTICIPATION

Knowledge of non-public clinical trial results or regulatory decisions before they are made public can offer a ‘free lunch’ opportunity for investors having access to this non-public information. However, when many people have access to this non-public information, a buying frenzy can affect the price of a drug company’s stock in the runup to the actual announcement. Several scientific studies have tried to systematically investigate the role of insider trading in pharmaceutical and biotechnology companies.
Rothenstein and colleagues investigated the public announcements from 23 positive clinical trials, 41 positive FDA regulatory decisions (“winners”), 36 negative clinical trials, and 9 negative FDA regulatory decisions (“losers”) between 2000 and 2009. All the trial results and regulatory decisions were regarding experimental anticancer drugs developed by the companies. The average stock price change from 60 days before the announcement to the actual announcement day was positive for the winners and negative for the losers. After the decision, the stock price increased on average for the winners and decreased for the losers (Rothenstein, Tomlinson et al. 2011). Overgaard and colleagues analysed the stock price anticipation of biotechnology stocks to 98 phase III trial decisions and 49 FDA regulatory decisions between 1990 and 1998. The average stock price change from 120 to 3 days before public announcement was significantly higher for the winners compared to the losers (Overgaard, van den Broek et al. 2000).
Both studies concluded that insider trading is the most likely explanation for the observed stock price anticipation prior to the announcement. Recently, researchers from academia have raised their concern about hedge funds and expert network firms which are constantly probing doctors, researchs and other academics for non-public information related to the clinical research (Ledford 2013). However, a recent study contradicts the idea that insider trading is responsible for the observed stock price anticipation.


Attached Image





4.3. CONCLUDING REMARKS

Over a 60 trading days window prior to an FDA or EMEA announcement, NASDAQ listed companies outperform both a broad market index and a more specific life science index. NYSE listed companies outperform a broad market index and a more specific life science index in case of positive FDA announcements. Both NYSE and NASDAQ listed companies do not systematically outperform different reference indexes in anticipation of EMEA announcements.
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PunkassDerm
Posted on: Aug 5 2019, 12:09 AM


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Maybe by cardiac catheterization.

But my thought is if this really affects outcomes positively...
Everyone who presents in the Emergency Department and has elevated cardiac enzymes, gets an implant.
Prevent cardiac muscle (and brain neuron) necrosis and protective against nosocomial infection.
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PunkassDerm
Posted on: Aug 4 2019, 10:12 PM


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Add cardio-protective against ischemia in acute MI (heart attack)
AND modulation of JAK pathway without messy immunosuppression/side effects?


Modulation of the JAK/ERK/STAT signaling in melanocortin-induced inhibition of local and systemic responses to myocardial ischemia/reperfusion
Alessandra Ottania,Maria Galantuccia, Ettore Ardimentoa, Laura Neria, FabrizioCanalinia, Anita Calevroa, Davide Zaffeb, Ettore Novellinoc, Paolo Grieco, Daniela Giuliania, Salvatore Guarinia


https://www.sciencedirect.com/science/artic...043661813000546


Blockade of JAK and ERK pathways with AG490 and U0126, respectively, abrogated the myocardial infarct size reduction by NDP-α-MSH. These results indicate that melanocortins inhibit local and systemic inflammatory and apoptotic cascades triggered by prolonged myocardial ischemia/reperfusion, with consequent reduction in myocardium infarct size, seemingly via activation of the JAK/STAT signaling and with modulation of an ERK (STAT unrelated) signaling pathway.


Attached Image

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PunkassDerm
Posted on: Aug 4 2019, 10:43 AM


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Yes melanin is the pigment and that does sound non-informed.

AND afamelanotide is approved in GB, just blocked by NICE for reimbursement.
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PunkassDerm
Posted on: Aug 3 2019, 11:33 PM


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Article by a UK Dermatologist regarding fake tanning product, Melanotan.
DR Catherine Borysiewicz

https://www.netdoctor.co.uk/conditions/skin...186/how-to-tan/


QUOTE
Do tanning injections work?

Tanning injections are very dangerous! Melanin injections are illegal to sell in the UK as they are unlicensed - this is because they have not been tested for safety, quality and effectiveness and there are serious concerns about potentially dangerous side effects. The MHRA is clear that these products are unlicensed and therefore it is illegal to advertise or sell these products in the UK. Similar warnings have been issued in the US and several other countries.

Melanin injections are illegal to sell in the UK as they are unlicensed and have not been tested for safety.
Two forms of melanin injections exist, Melanotan I or afamelanotide which is an alpha-melanocyte-stimulating hormone (alpha MSH) analogue which stimulates the production of eumelanin (tanning pigment) in the skin.

Normally this pigment is stimulated by exposure to UV radiation in sunlight. It was developed and registered for the treatment of a condition called erythropoietic protopophyria- this is a rare inherited condition that causes sufferers to develop prolonged burning pain, swelling and redness after 1-20min of sun exposure.

Melanotan II is an unlicensed and untested form of alpha MSH which is not approved for the treatment of any medical conditions.




I did reach out to her on FB to clarify afamelanotide and new drugs with the ability to prevent or treat Melanoma. Hopefully she amends her article.

QUOTE
I am a PA(physician assistant) in Dermatology in Worcester, MA USA. About 15 years ago I was turned onto afamelanotide when Clinuvel was still Epitan. Now approved in the EMA, waiting for FDA approval for EPP October 6 of this year. There is potential for this drug or another MSH analog to accomplish free radical scavenging, anti-inflammatory properties and DNA repair. So a possible melanoma preventative. Melanocortins will be disruptive to medicine, so many potential applications. Vitiligo, HHD, XP probably next. Should have made note in your article for future potential. Absolutely agree regarding black market MSH injections, but there is a difference. Thanks for your time.


https://www.fasebj.org/doi/abs/10.1096/fase...pplement.1268.6
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PunkassDerm
Posted on: Jul 18 2019, 11:32 AM


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THE PRIZE!!!

Development of α-Melanocortin Analogs for Melanoma Prevention and Targeting


https://link.springer.com/chapter/10.1007/9...-4419-6354-3_10


Melanocortins, particularly α-Melanocortin (α-Melanocyte stimulating hormone, α-MSH), were first identified as the physiological regulators of pigmentation in many vertebrate species. Their role in regulating human pigmentation was unequivocally demonstrated in the 1990s, with the cloning of the human melanocortin 1 receptor (MC1R) gene from human melanocytes and the demonstration that functional MC1R is expressed by these cells. α-Melanocyte stimulating hormone is a tridecapeptide, with the core sequence His6-Phe7-Arg8-Trp9 shared with β- and γ-MSH and identified as essential for receptor activation and stimulation of pigmentation. The small size of α-MSH makes it an attractive molecule for drug design. There has been longstanding interest in the development of melanocortin analogs that target the MC1R expressed on normal melanocytes and melanoma cells. The aim has been to develop MC1R agonists that stimulate melanogenesis and confer photoprotection to human melanocytes and thus prevent skin cancer formation. Recent findings that the physiological α-MSH not only stimulates melanogenesis, but also reduces the extent of DNA damage caused by exposure to solar ultraviolet radiation have further rejuvenated the interest in developing synthetic MC1R agonists for skin cancer prevention. α-Melanocortin analogs have also been developed for imaging of melanoma tumors, localization of residual metastasis and specific delivery of radionuclides to eradicate melanoma tumors, sparing normal tissues. The main challenge is to develop specific MC1R agonists that will target melanocytes for skin cancer prevention, or for localization and treatment of metastatic melanoma.
  Forum: By Share Code

PunkassDerm
Posted on: Jul 13 2019, 11:43 PM


Group: Member
Posts: 509

Great timeline KRD!

Anyone know if ADR holders are forced to take a dividend? We can't vote, would we even have the option to re-invest?

Love to see 45+, that's about my target price to take out funds to build my natural looking pool/spa/waterfall feature! Time to enjoy after 15+ years.
  Forum: By Share Code

PunkassDerm
Posted on: Jul 9 2019, 07:23 AM


Group: Member
Posts: 509

Off label vs new indication not far behind. Sales may be higher for bremelanotide if shared by couples? If out of pocket, see no reason it won't happen.


https://www.nature.com/articles/ijir200817....raft=collection

Preclinical effects of melanocortins in male sexual dysfunction
AM Shadiack and S Altho


The neurobiology of sexual behavior involves the interrelationships between sex steroids and neurotransmitters that result in both central nervous system (CNS) effects and effects in the genitalia. Tools such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) scanning can help determine what areas of the brain are activated under sexual stimulation. Our understanding of the role of various neurotransmitters, neurosteroids and other CNS-acting compounds is improving. The role of CNS-acting compounds such as dopamine agonists in the treatment of male sexual dysfunction is under active investigation. Melanocortins have CNS and peripheral roles in a wide variety of bodily functions. The melanocortin agonist bremelanotide appears to act in the CNS to promote erections in preclinical models, and may also stimulate behaviors that facilitate sexual activity beyond their erectogenic effects.
International Journal of Impotence Research (2008) 20, S11–S16; doi:10.1038/ijir.2008.17

....

Melanocortins
Melanocortins are a group of small protein mole- cules that share the same precursor molecule, POMC (proopiomelanocortin).25 These peptides include ACTH (adrenocorticotropic hormone), the melano- cyte-stimulating hormones (a-MSH, b-MSH and g-MSH), b- and g-lipotropin, and b-endorphin. In the CNS, melanocortins may act as neurohormones or neurotransmitters, regulating numerous functions within the neuronal systems in which they are synthesized and secreted.26 It has been proposed that melanocortins, oxytocin and dopamine use a common pathway in the CNS that involves activa- tion of NO to control erection.27
Five melanocortin receptors have been identified that are associated with such diverse biological functions as skin pigmentation, food intake, the sleep–wake cycle and sexual response. Investiga- tions into the role of the melanocortin system on sexual response has focused on the melanocortin 3 (MC3R) and melanocortin 4 (MC4R) receptors in the CNS. There is abundant expression of both MC3R and MC4R in the brain and in peripheral genital sensory outputs (Figure 2).27 However, MC4R has been shown to modulate erectile function and sexual behavior, whereas MC3R has not been shown to have a pro-erectile effect.28 MC4R is expressed in the rat and human penis, as well as in rat spinal cord, hypothalamus, brainstem and pelvic ganglion, but not in rat corpus cavernosal smooth muscle cells. In mice, administration of an MC4R agonist increased copulation, whereas knockout mice lack- ing the gene encoding for the receptor showed decreased copulatory behavior.


Bremelanotide preclinical investigations
Bremelanotide (formerly known as PT-141) is a synthetic analogue of a-MSH, which is an agonist of the MC4R.33 Bremelanotide shows about double the affinity for the MC4R as for the MC3R in cells containing cloned human melanocortin receptors.
In preclinical experiments, central doses of bre- melanotide delivered into the right lateral ventricle show consistent initiation of spontaneous penile erections in adult male rats (Figure 3).34 In addition, administration of bremelanotide either intrave- nously or intranasally also resulted in spontaneous erections. The frequency of erections increased in a dose-dependent manner (Figure 4). In addition, with repeat doses of bremelanotide, spontaneous erec- tions continue to be produced without evidence of tachyphylaxis. Repeat dosing also results in a reduction in the time to first erection (latency). Administering L-NAME (an inhibitor of NOS) blocked the pro-erectile effects of bremelanotide, suggesting that NO is involved in this mechanism (Figure 5).
To assess the degree of the extent and distribution of neuronal activation, a c-Fos immunoreactivity assay was used.33 Immunoreactivity after systemic administration of efficacious doses of bremelanotide was seen in the PVN and the supraoptic nucleus of the hypothalamus. In addition, an experiment using pseudorabies virus injected into the corpora caver- nosa was used to determine associations between the hypothalamus and nerve endings in the penis associated with the erectogenic activity of bremela- notide. Pseudorabies virus was detected in the PVN after a 4- or 5-day wait for retrograde trans-synaptic transport of the virus to the spinal cord and then the brain. The neuronal activation studies and the pseudorabies experiment suggest that bremelanotide acts in the hypothalamus by activating MC3R and/or MC4R.
Preclinical experiments in female rats suggest that bremelanotide may not merely be pro-erectile as in male rats, but may also facilitate behavioral changes that support sexual activity.35 Female rats who were given bremelanotide exhibited behaviors associated with increased proceptivity or motivation to copula- tion compared with those given a placebo. In this experiment, the rats were placed in specially designed cages where the female rat was allowed to set the pace of sexual activity. It was up to the female rats to initiate sexual contact with the male rats. The increase in proceptive or solicitation behaviors was not due to any general stimulatory effect of bremelanotide or accompanied by an effect on receptive behaviors such as lordosis.


Acknowledgments
This work was supported by a grant from Palatin Technologies, Inc. Editorial support for the development of this paper was provided by Kevin Keres.
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PunkassDerm
Posted on: Jul 9 2019, 01:41 AM


Group: Member
Posts: 509

Delay is the norm for Clinuvel. Progress for Vitiligo? Study results? What exactly prevents updates on Vitiligo? Slippery as Voldemort.
5 patient trial!
Waiting for acquisition after FDA approval?

Has Clinuvel ever tallied countries offering Scenesse for EPP? Where is the map?

It is not the EMA or FDA solely, Clinuvel is not transparent about missteps and learning on the fly.
Potential Vitiligo approval in 2016? Bahahahahahahahahahah
Maybe why there are no further updates or coverage from Normura?

The silver lining, look at the old target price, AUD 3.19 (2013)

I'm critical b/c I'm part owner, and my employees (management) do provide [meaningful] updates on my investment.


https://www.clinuvel.com/wp-content/uploads...05NomuraWeb.pdf


Delay for EMA EPP decision

Clinuvel filed its MAA for afamelanotide 16mg implant on 6 February 2012 for the preventative treatment of the orphan light intolerance disorder erythropoietic protoporphyria (EPP). CUV announced that the European Medicines Agency (EMA) has allowed more time to complete the review of CUV’s Marketing Authorisation Application (MAA) under the Centralised Procedure. The EMA procedure, led by the CHMP, has had at least a 10-week extension.

We believe the delay is likely to be due to the EMA’s need to better understand this treatment for a rare patient population, and this delay is reasonably common in the cases of potential orphan drug approvals for rare diseases. We note that the EMA generally looks at: 1) manufacturing – CUV management previously reported that it had clearing its manufacturing audit in February 2013; and then 2) clinical and other – the clinical discussion is usually through the discussion of the disease treatment with medical Key Opinion Leaders and patient groups. We believe discussions from the EMA may occur in this case to demonstrate the potential importance of this drug to the relevant patient population.

Approval would allow CUV to market afamelanotide in all 27 European Union member states as well as Norway, Iceland and Lichtenstein. To date, four trials in EPP have been completed by the company.


Fig. 1: CUV’s EPP clinical trial program
Trial Phase
Patients enrolled 5
101 77 74 257
Study design (months duration)
Provocation of symptoms by artifical light source (4)
Cross over study (12) 2 Parallel arms placebo-active (9) 2 Parallel arms placebo-active (6)
CUV010
CUV017 CUV029 CUV030
II (EU)
III (EU/AU) III (EU) II (US) Total


Source: Company data, Nomura research Should not delay Vitiligo clinical trials

At 31 December 2012, CUV had AUD9.9mn in cash and marketable securities. We forecast 2HFY13 cash burn of AUD6mn (in part due to ongoing Vitiligo trials, which we expect to continue).
That said, should 2HFY13 cash burn be greater than we expect, this delay in potential earnings from afamelanotide could impact near-term liquidity. We continue to forecast a positive EMA EPP decision, which should lead to strong revenue growth for CUV in FY14F, and this has not changed as a result of this delay.
Background on Phase IIa Vitiligo trial: primary endpoint reached

The primary endpoint was the extent of repigmentation between Day 0 and Day 168 as measured by the VASI and VETF scores (standard scoring methods for Vitiligo). The extent of repigmentation in the
See Appendix A-1 for analyst certification, important disclosures and the status of non-US analysts.

Research analysts
Australia Health Care & Pharmaceuticals
Dr David Stanton - NAL
Zara Lyons - NAL

Nomura | Clinuvel Pharmaceuticals
April 5, 2013

afamelanotide/NB‐UVB group was significantly greater than observed in the NB‐UVB‐alone group (VASI, p=0.025; VETF p=0.023; 95% CI).
What are the VASI and VETF?

The Vitiligo Area Scoring Index (VASI) recording system is a quantitative clinical tool that is used to evaluate Vitiligo and responses to treatment. Basically, the body is divided into five separate and mutually exclusive regions: hands, upper extremities (excluding hands), trunk, lower extremities (excluding the feet), and feet. At each follow-up assessment, any macular repigmentation is noted, and the extent of residual depigmentation within each affected patch that had been present at baseline is estimated to the nearest of one of the following percentages: 0, 10%, 25%, 50%, 75%, 90%, or 100%. The total body VASI is calculated by considering the contributions of all body regions.

The Vitiligo European Task Force (VETF) recording system is a quantitative clinical tool that is used to evaluate Vitiligo and responses to treatment. Staging is based on cutaneous and hair pigmentation, and the disease is staged 0–4 on the largest macule in each body region, except hands and feet, which are assessed separately and globally as one unique area. Assessment of spreading is based on Wood’s lamp examination of the same largest macule in each body area.

Apart from achieving its primary endpoint, here were a number of other interesting points to note from the trial result:
Treatment completion: Forty‐one (75.9%, n=41) patients completed the treatment. Thirteen patients withdrew due to their inability to comply with the demanding treatment protocol, or, in the case of five patients, due to the intensity of pigmentation experienced. Overall, the combined treatment was well tolerated and no serious drug‐related adverse events were reported;

May work better in those with darkest skin (i.e. those most affected by the cosmetic aspects of the disease): As a subset analysis reflected by the VASI scores, significantly better, more complete and deeper repigmentation was observed for those patients with the darkest skin complexion (phototype IV‐VI, n=24) who had received the combination therapy compared to those on monotherapy (p=0.046; 95% CI).
What does it mean for CUV?

From here, CUV will undertake a Phase IIb trial likely to be conducted first in Europe and Asia. Starting from potential approval in 2016F, we believe that if an eventual 10% of US and EU patients were to use afamelanotide, the total CUV NSV opportunity is worth AUD7.73/share. At the current clinical stage, this translates to a risk-weighted NPV of AUD1.65/share from Vitiligo.
  Forum: By Share Code

PunkassDerm
Posted on: Jul 2 2019, 03:23 AM


Group: Member
Posts: 509

Saw this and almost posted this AM myself. PTN is hungry, organized and open to communication (and cooperation). That is attractive to me the fool.
  Forum: By Share Code

PunkassDerm
Posted on: Jul 1 2019, 09:56 PM


Group: Member
Posts: 509

Only a matter of time before catches on fire for cosmetic/anti-aging.
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PunkassDerm
Posted on: Jun 29 2019, 09:52 AM


Group: Member
Posts: 509

Botox by its very nature is an IM medication. It aims to block acetylcholine from crossing the neuromuscular junction (aka weaken or paralyze target muscles)
In the case of hyperhidrosis it is injected intradermally where the targets are smooth muscle of sweat glands
I've used it successfully IL (intralesional) for painful Cutaneous Leiomyomas of the face.
Injected SQ, wouldn't serve any purpose (diffuse from target site), and possibly predispose to migration and side effects (say to diaphragm and affect breathing)

Agree the implant is a bit more than an SQ injection, but not by much. I could watch a video and be certified. Make a tiny incision, place implant, tape closed (doubtful stitched).



See article below, can be debated and unique to medications (pharmacokinetics). Has a great table:


The optimal choice of medication administration route regarding intravenous, intramuscular, and subcutaneous injection

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4494621/


SQ (sub-cutaneous):

Most biologic medications, Afamelanotide, bremelanotide
insulin
anti-emetics
some vaccines
fluids (vs IV)

IM (intramuscular):

Typically:
Botox
epinephrine
Antipsychotics (depo)
Anxiolytics
Narcotics
Methotrextate
many antibiotics (depo)
Sex hormones
Ketamine
Narcan
B12
Steroids (depo)
Many vaccines but not all
  Forum: By Share Code

PunkassDerm
Posted on: Jun 29 2019, 03:04 AM


Group: Member
Posts: 509

Is this criminal of AF?? Criminal AF!

And maybe the article had little to do with SP changes. Multiple issues: Shorters and dilution, sell the news and last effort for management to grab shares?

FDA HAS TO APPROVE SCENESSE NOW!


Bearish Vyleesi Article Omits Key Information. Skeptics Overlooking Clinical Data


https://seekingalpha.com/article/4272670-be...g-clinical-data


Summary
Vyleesi's safety and efficacy is well supported by multiple phase 3 clinical data.

The number of patients affected by HSDD is several magnitudes larger than what investors anticipate.

Adverse events with respect to the drug have minimal impact on the drug's risk-reward profile.

Clinical data involving Bremelanotide directl contradicts Adam Feuerstein's critique of the drug, but no such information exists regarding the Vyleesi's potential negative synergistic effects with alcohol.


There Is No Evidence Female Patients Fear An Intravenous Injection

The comparable precedent as to whether or not female patients are satisfied with intravenous injections is Allergan's (AGN)'s Botox. Despite a painful injection and various adverse events, this drug remains the primary standard of care in women's cosmetics and even long after patent expiry, continues to generate over $2.5 Billion in sales as of FY2018 (as it is a trade secret). Furthermore, the drug is still generating double digit % revenue growth Y/Y. Hence, the author finds female patients "fearing" intravenous deliveries of gynecological drugs to be a myth, and sees no reason why such claim could be applied to Bremelanotide's method of delivery.


Final Thoughts:
After an analysis of Bremelanotide's clinical date and economics, the author concludes Vyleesi to be a safe and efficacious drug which addresses a huge patient size with unmet medical needs regarding HSDD. In regards to Adam Feurestein's article, the author finds the biotech journalist has done an amazing job of outlining the potential FDA oversight of Bremelanotide's synergistic effects when taken with alcohol, yet presented a string of estimates that I disagree with in regards to the drug's efficacy and other safety metrics. In my assessment, 4 out the 5 claims raised by Adam are demonstrably false based on the assessment of clinical and financial evidence, while the last claim actually raises a potential risk shareholders may have overlooked amid the approval hype. Investors therefore should be both celebratory in regards to AMAG and PTN's approval and be aware of additional R&D expenses in regards to potential FDA post-marketing clinical trial requests.
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PunkassDerm
Posted on: Jun 28 2019, 05:19 AM


Group: Member
Posts: 509

Wasn't planning to re-invest that much, but cost averaging my new position. I can't say that I have a big plan, I've been winging it and been very lucky. Some flops over the years, but Clinuvel was always the dream play. PTN for me was a way to play all the melanocortin opportunities early on. I figure it will pay out huge, or I lost a little clinuvel gain. Right now it feels like monopoly money. Don't put it in if you're not willing to lose it. And the only way to win big is to buy a crapload of shares.

Not technical, gut only. I am not a model to follow.
  Forum: By Share Code

PunkassDerm
Posted on: Jun 27 2019, 10:55 PM


Group: Member
Posts: 509

I've always kicked myself for not buying more CLVLY at a buck. So pre-market I grabbed more PTN. Over 135K shares now. Built on CLVLY profit.

Hoping there is some crazy posturing for a buyout of PTN + AMAG, they are cheap for big pharma.
Label extension for ED can't be far behind, shit how many guys will be shooting their girls Vyleesi if it works?

Independence or bust!

Pfizer, who brought Viagra to market? Good sense.
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PunkassDerm
Posted on: Jun 25 2019, 11:13 PM


Group: Member
Posts: 509

If you're talking about John Harris from UMASS? I think the nexus is this: His peer in the Dermatology Dept, Dori Golberg, is doing melanocyte transplants. Maybe external motivation. Seems odd his was hot on afamelanotide before, only to go to procedures and I believe more dangerous immunosuppressives (JAK).

Abbvie research is literally across the street from UMASS, and they are heavily into JAK research. Yes.

AND...Beechwood hotel / Sonoma restaurant is owned by a rheumatologist that has done countless RA studies, including for Humira (Abbvie). Dr Charles Birbara


Attached Image

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PunkassDerm
Posted on: Jun 25 2019, 11:03 PM


Group: Member
Posts: 509

I'm strongly guessing the dance is already on, probably already decided. Just pending on October 6. Let this SP rip please.
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PunkassDerm
Posted on: Jun 25 2019, 10:25 PM


Group: Member
Posts: 509

Agree...remember how smooth last rollout was. So little news on new products despite plans to share. Can only mean acquisition. Allergan/Abbvie please!
  Forum: By Share Code

PunkassDerm
Posted on: Jun 25 2019, 10:20 PM


Group: Member
Posts: 509

OM-freaking-G

This is a skin and inflammatory powerhouse in the works, they NEED TO ACQUIRE PTN AND CUV!!!
I have a boner sans medicine.


AbbVie to Acquire Allergan in Transformative Move for Both Companies


https://news.abbvie.com/news/press-releases...h-companies.htm


"This is a transformational transaction for both companies and achieves unique and complementary strategic objectives," said Richard A. Gonzalez, chairman and chief executive officer, AbbVie. "The combination of AbbVie and Allergan increases our ability to continue to deliver on our mission to patients and shareholders. With our enhanced growth platform to fuel industry-leading growth, this strategy allows us to diversify AbbVie's business while sustaining our focus on innovative science and the advancement of our industry-leading pipeline well into the future."

"This acquisition creates compelling value for Allergan's stakeholders, including our customers, patients and shareholders. With 2019 annual combined revenue of approximately $48 billion, scale in more than 175 countries, an industry-leading R&D pipeline and robust cash flows, our combined company will have the opportunity to make even bigger contributions to global health than either can alone," said Brent Saunders, chairman and chief executive officer, Allergan. "Our fast-growing therapeutic areas, including our world class medical aesthetics, eye care, CNS and gastrointestinal businesses, will enhance AbbVie's strong growth platform and create substantial value for shareholders of both companies."

Strategic Rationale

New growth platforms and leadership positions to diversify and expand revenue base: The combined company will consist of several attractive franchises with leadership positions across immunology, hematologic oncology, medical aesthetics, neuroscience, women's health, eye care and virology. Allergan's product portfolio will be enhanced by AbbVie's commercial strength, expertise and international infrastructure.
Immediate scale and enhanced profitability for AbbVie's growth platform: AbbVie's enhanced growth platform, comprised of growing and durable franchises across highly-attractive therapeutic areas, is expected to grow at a high-single digit annual growth rate well into the next decade, from more than $30 billion in 2020.
Financially attractive with immediate EPS accretion: This transaction is expected to be 10% accretive to adjusted earnings per share over the first full year following the close of the transaction, with peak accretion of greater than 20%.1 ROIC is expected to exceed AbbVie's cost of capital within the first full year.
Significant cash flow generation: The success and scale of the combined commercial business ensures funding capacity and flexibility for simultaneous robust pipeline investment, debt reduction and capital return to shareholders. The combined companies generated $19 billion in operating cash flow in 2018.
  Forum: By Share Code

PunkassDerm
Posted on: Jun 25 2019, 08:10 AM


Group: Member
Posts: 509

I'd shoot her twice and myself thrice, then shoot her again so to speak.
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PunkassDerm
Posted on: Jun 25 2019, 02:50 AM


Group: Member
Posts: 509

Can one bear move a stock like this?
Isn't heroin an indictable? Doesn't seem a deterrent to many.


https://seekingalpha.com/news/3473312-palat...-vyleesi-parade


Palatin and AMAG give up gains after Feuerstein rains on Vyleesi parade

Jun. 24, 2019 12:31 PM ET|
About: AMAG Pharmaceuticals, ... (AMAG)|By: Douglas W. House, SA News Editor
STAT's Adam Feuerstein has thrown a bucket of cold water on investors in Palatin Technologies (PTN -6.7%) and AMAG Pharmaceuticals (AMAG -5.4%) after the FDA nod for female hypoactive sexual desire disorder med Vyleesi (bremelanotide injection) on Friday. Shares were up 39% and 12%, respectively, since then before retracing.

Mr. Feuerstein has been a long-term bear on the drug, questioning its efficacy and the fact that it is an injectable rather than a pill which may constrain demand.
  Forum: By Share Code

PunkassDerm
Posted on: Jun 25 2019, 02:37 AM


Group: Member
Posts: 509

No access, but I like the sound of this:

Palatin Technologies (PTN) PT Raised to $7.50 at H.C. Wainwright After Vyleesi Approval

H.C. Wainwright analyst Joseph Pantginis raised the price target on Palatin Technologies (NYSE: PTN) to $7.50 (from $6.00) after the ...


The age of melanocortins and regenerative medicine (stem cells and exosomes)
  Forum: By Share Code

PunkassDerm
Posted on: Jun 25 2019, 02:13 AM


Group: Member
Posts: 509

Read on another board, 1.5million shorts as well. So I added 25K shares. I'll be nuts or lucky.
  Forum: By Share Code

PunkassDerm
Posted on: Jun 25 2019, 01:09 AM


Group: Member
Posts: 509

INHIBITION OF PRO-INFLAMMATORY CYTOKINES:
AKA INTERLEUKINS AND TNF (TARGETS OF MOST RA, IBD, PSORIASIS, PSORIATIC ARTHRITIS, HS AND AS DRUGS)

1. The melanocortins play important roles in both maintaining immune homeostasis and suppressing inflammation
2. Melanocortin receptors have been detected recently on adipocytes, keratinocytes, endothelial cells, fibroblasts, immunocompetent cells, and inflammatory cells
3. A central mediator of the anti-inflammatory activity is the non-steroidogenic melanocortin peptide alpha-melanocyte stimulating hormone (α-MSH)
4. α-MSH could exert various immune-modulating effects to regulate the T and B cell functions and prevent sensitization with potent contact allergens
5. α-MSH also directly downregulates the mRNA expression of IL-1 and TNF-α in human mast cells (Luger et al., 2000).

All the above-mentioned findings suggest that α-MSH may exert protective effects in the development of knee OA.



Synovial Fluid Alpha-Melanocyte-stimulating Hormone May Act as a Protective Biomarker for Primary Knee Osteoarthritis
Published on January 24, 2019


http://www.discoverymedicine.com/Jian-Guan...osteoarthritis/


Introduction

Osteoarthritis (OA) is characterized by cartilage destruction, subchondral bone sclerosis or cyst, and osteophyte formation (McAlindon and Bannuru, 2018). Although the etiology of OA is complex and involves many cellular and biochemical processes, genetic predisposition, obesity, and aging are generally identified as the main factors leading to OA (Knapik et al., 2018). OA mainly affects the weight-bearing joints, including knee, hip, and ankle, and the knee joint is the most involved (Roos and Arden, 2016). The prevalence of knee OA is increasing worldwide and this burden will continue to increase due to aging of the general population. According to the statistics, the global prevalence of radiographically confirmed symptomatic knee OA in 2010 was estimated to be 3.8% (Cross et al., 2014). One large-scale population-based survey performed in China, from 2011 to 2012, demonstrated that the morbidity of symptomatic knee OA was 8.1% (Tang et al., 2016), suggesting a large number of individuals suffering from knee OA all over the world.

Currently, the knee OA is mainly identified by symptoms of pain, functional disability, and radiographic changes in the knee joint. However, radiographic images including plain X-ray, MRI, and those generated by other methodologies were not able to detect and monitor the biochemical alternations in the inner joint tissue which can occur long before symptoms are present (Hafezi-Nejad et al., 2018). Therefore, alternative diagnostic methods for knee OA are in urgent need.

Since OA needs to take years and even decades to develop, characterizing potential biochemical markers associated with OA is an alternative method for early diagnosis. As they could be used to diagnose and predict prognosis in patients in ways that radiography is not capable of, they can, therefore, be early indicators of patients at risk of developing the disease as well as predictors for prognosis (Mobasheri et al., 2017). In recent years, intense research has investigated mainly two major candidate biomarker groups. The first is products of bone and cartilage degradation such as cartilage oligomeric matrix protein (COMP) and a number of matrix metalloproteinases (MMPs) (Hunter, 2014). The second group of possible candidates has come to light with the increased understanding that inflammation plays a key role in OA, including interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) (Daghestani and Kraus, 2015). These two categories of biomarkers could reflect disease severity of OA. However, compared with the number of disease severity biomarkers, the work made to seek protective biomarkers is scarce. The protective biomarkers seem to be more important than disease severity markers as they can directly be used to treat knee OA. Hence, uncovering potential and novel protective biomarkers makes great differences and helps understand better the pathophysiological process of knee OA.

Melanocortins comprised of a highly conserved family of peptides and receptors that include multiple proopiomelanocortin-derived peptides and melanocortin receptors (Leone et al., 2015). The melanocortins play important roles in both maintaining immune homeostasis and suppressing inflammation (Giuliani et al., 2010). Melanocortins exert their activities via a group of five melanocortin receptors belonging to the family of G-protein-coupled receptors with seven transmembrane domains (Rouault et al., 2017). In addition to the central nervous system and melanocytes, melanocortin receptors have been detected recently on adipocytes, keratinocytes, endothelial cells, fibroblasts, immunocompetent cells, and inflammatory cells (Yang and Harmon, 2017) A central mediator of the anti-inflammatory activity is the non-steroidogenic melanocortin peptide alpha-melanocyte stimulating hormone (α-MSH) (Anderson et al., 2016). α-MSH could exert various immune-modulating effects to regulate the T and B cell functions and prevent sensitization with potent contact allergens (Luger et al., 2003). α-MSH also directly downregulates the mRNA expression of IL-1 and TNF-α in human mast cells (Luger et al., 2000).

Recently, the role that α-MSH performed in bone and cartilage has been investigated. In a study by Kaneva et al. (2014), α-MSH pre-treatment prevented chondrocyte death following mechanical impact to cartilage and led to a marked reduction of pro-inflammatory cytokines. Yoon et al. (2008) found that α-MSH could inhibit TNF-α-guided MMP-13 expression by reducing p38 kinase phosphorylation and, thereby, preventing subsequent activation of the NF-κB pathway. This finding is consistent with another study in which α-MSH reduced the secretion of pro-MMP-13 and pro-MMP-2 in addition to suppressing mRNA levels of IL-1β and TNF in articular OA chondrocytes (Grassel et al., 2009). In addition, α-MSH induced significant inhibition of MMP-3 gene expression and secretion from IL-1β or TNF-α-stimulated chondrocytes (Capsoni et al., 2015). Besides, Bohm et al. (2016) showed that α-MSH stimulation of primary, mixed synoviocytes inhibited IL-6 and TNF-α production.

All the above-mentioned findings suggest that α-MSH may exert protective effects in the development of knee OA. However, there have been no previous studies available investigating α-MSH levels in serum and SF of patients with different phases of knee OA. We speculated that reduced α-MSH expression may be associated with knee OA progression. Hence, this study was carried out to investigate α-MSH expression in the serum and SF of knee OA patients and uncover the potential relationships with the disease progression of knee OA, which may be used as a meaningful tool for indicating the disease severity and monitoring progression of knee OA.
  Forum: By Share Code

PunkassDerm
Posted on: Jun 24 2019, 12:34 AM


Group: Member
Posts: 509

Totally agree, Scenesse has it for photoprotection. If they ever get a melanocortin cream out there, we are a 100+/share stock (USD).

In my mind the companies portfolios/targets are complementary not competitive. That's why I added PTN without the caution I chose with Clinuvel back in the day.

That said, I'd love to see Allergan buy them both and bring MELANOCORTINS to the masses. Or partner.

ANTI-INFLAMMATORY
ANTI-OXIDANT
DNA REPAIR
HOMEOSTATIS
PHOTOPROTECTION

SKIN - Porphyrias, Vitiligo, Psoriasis, ?Eczema, XP, HHD, HS, ?AK ?PMLE... COSMETIC and PROTECTION
BRAIN - MS, Stroke, Parkinson's, Dementia
GI - IBD, IBS
GU - Boners, sexual dysfunction
KIDNEYS - Renal failure
ORTHO - OA, RA
IMMUNE FUNCTION - ?Melanoma, infection
EYES - Uveitis


JUST WOW!

AND FRILLY-WALLY SAFE YES!

I've said it before, this is the prednisone of our time. But like the biologics, more targeted instead of shotgun approach to inflammation. Minus immunosuppression.
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PunkassDerm
Posted on: Jun 23 2019, 09:49 AM


Group: Member
Posts: 509

Good question San Diego....bremelanotide is a metabolite of MTII (I think boner drug without tan)
Can't be far behind for guys.


https://www.vice.com/en_us/article/xygkpj/m...erful-erections



Melanotan II first captured the public's imagination when the mainstream media briefly touted it as a Viagra-like panacea for middle-aged men. Norman Levine, a dermatologist who led the team that developed the drug, had first conducted experiments in which he darkened the pigments of frogs by injecting them with a hormone called Alpha MSH. After Melanotan II was modified for human use and put through clinical trials, Levine reported that "one very astute observer who took this drug told us that he was developing spontaneous erections."

During the 2000s, the Melanotan II peptide and the metabolite derived from it, the erectile dysfunction-focused Bremelanotide (also known as PT-141), were patented and then licensed to biotechnology companies hoping to develop them into profitable prescription drugs. However, these companies also offer the peptides for direct sale to researchers. These transactions occupy a legal gray area, since the peptides are banned for human use outside clinical trials. While they can be purchased from various websites specializing in research chemicals, the purchaser usually has to affirm prior to final sale that the peptide "will not be used for human consumption" and is being acquired for "research purposes only."
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PunkassDerm
Posted on: Jun 23 2019, 05:04 AM


Group: Member
Posts: 509

Will a dude study be needed, approved to market? But yes, same bremelanotide.

https://metallicman.com/laoban4site/bremelanotide-pt-141/


Enter PT-141 (Bremelanotide)

Instead of being a PDE5 inhibitor like Viagra and Cialis, consider a melanocyte stimulating hormone (MSH). MSH induces lordosis in animal subjects. Or in other words, lordosis is a sign of physical preparation for copulation. It is a hormone that tells the body “get ready, we are going to have sex”.

It is a hormone that puts an animal in “heat”.

It is hardwired in our brains. In animals such as dogs and cats, it tells the female to rise up their butts, and tells males to start thrusting. Now, as man has evolved this hormone has been repressed. We have replaced it with other cultural triggers. Or, in other words, what we visually see that has value has replaced this hormone. The natural lordosis behavior has atrophied in humans.

Not so when you take this drug. This drug reactivates it.


PT-141 Bremelanotide is easily available outside of the United States. You can buy it in many English speaking countries such as Australia and the UK, as well as communist countries such as Communist China and Russia. However, Americans are FORBIDDEN to have access to this medicine.
This drug was being developed by Palatin Technologies. It showed great promise as it works equally well on both the male and the female sexes. (Though who knows about the other 55 genders that somehow mysteriously popped into existence under the Obama administration.)

It’s not only that men can get a nice sold and hard erection. It is more than that. People who take this also feel differently. People who take it feel young and horny like a sex-crazed 16 year old.
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PunkassDerm
Posted on: Jun 22 2019, 09:09 AM


Group: Member
Posts: 509

It's all good and SCENESSE benefits, now on the coat tails of PTN/AMAG!

Secondly, if Clinuvel didn't trip all over their novice selves (and took a partner like AMAG) then they would be THE FIRST APPROVED MELANOCORTIN. No diggity no doubt.

PTN has a great pipeline, and dude version Vyleesi is probably close behind. I'm rooting for all melanocortins.

No matter:

200K Clinuvel
75K PTN
100K Avita

I have to say 2019 is looking great bee-yach-as! I just wish I grabbed some more PTN this morning on that dip.
And thank you Sharesceners who bring these great stocks up, I feel blessed.



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PunkassDerm
Posted on: Jun 20 2019, 02:53 PM


Group: Member
Posts: 509

Let’s pray for swift approval of Vyleesi (bremelanotide) as well in the days ahead. Class-mate approval bodes well for Scenesse.
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PunkassDerm
Posted on: Jun 16 2019, 12:27 PM


Group: Member
Posts: 509

Sorry a little long, great vitiligo pipeline article. Nice summary of Clinuvel.

Also odd they didn't mention the other excimer company, Ra. With the Pharos excimer laser. They have a better financial model for providers, I've used both units: XTRAC and Pharos
https://www.ramed.com/dermatology/#products


What I'd like to see?

A Vitiligo protocol that goes something like this:

1. Microneedling plus RECELL
2. Excimer laser (focused UVB) plus SCENESSE, second phase until therapeutic response
3. Clinuvel topical for maintenance


With potential for clearance and remission, why take the risk of JAK inhibitors?

Severe side effects of JAK Inhibitors include liver damage, neutropenia and lymphopenia (dangerously low white cell counts and immune system suppression). Additionally, JAK inhibitors may interact with DMARDs (disease modifying anti-rheumatic drugs) or with other immunosuppressants.



SCIENTIFIC BREAKTHROUGH SEEKS TO END THE SUFFERING OF PEOPLE WITH VITILIGO


http://www.aviseanalytics.com/scientific-b...-with-vitiligo/


Americans across all age groups according to a Burden of Skin Disease report commissioned by the American Academy of Dermatology in 2013. The total healthcare costs of Vitiligo were estimated at $49 million, with a lost productivity of $6 million and an average cost per patient of $328. The latest reports however suggest that the number of people affected may be between 2 to 5 million in the U.S alone.

There is currently no cure available for this disorder; however, treatment options such as steroid based creams, UVA and UVB light treatments, skin grafting and depigmentation creams help alleviate the condition. A research report by Zion Market Research projects the global Pigmentation Disorders Treatment Market which was worth USD 5,283.82 million in 2017 is expected to reach USD 8,479.08 Million by 2024 growing at a CAGR of 7.02%.

The rise in incidences of skin disorders, increased lifestyle spending on beauty and self-grooming, higher disposable incomes, advancements in research and development and rising global warming will help in the growth of the market. However, the cost of treatment and a major lack of awareness will impede the growth in the market.

The current treatment options for vitiligo consist of Corticosteroids, Depigmentation therapy, Immunomodulators and Calcium modulators which offer limited respite and come with many side effects. However, there are a few companies that are working on creating solutions that could end the suffering and social stigma attached to this disease. We take a look at some of them below:



Aclaris Therapeutics (NASDAQ: ACRS)

Aclaris is a biotechnology company with focus on creating solutions for areas of dermatology that is lacking in FDA-approved therapies especially in skin and hair related disorders. The company’s pipeline consists of drug candidates for treatment of Common warts, Alopcia Areta, Vitiligo, Atopic Dermatitis, Rheumatoid Arthritis, Psoriasis, etc. that seek to unlock the potential of Kinome, a subset of human genome, to control dysregulation and/or mutations of cells.

Its proprietary KINect™ platform can identify drug candidates with the help of its chemical library of kinase inhibitors, a structure based drug design and a custom kinase assay. The companies lead drug candidate for Vitiligo is ATI-502, a JAK1/JAK3 Inhibitor and ATI-1777, a JAK1/JAK3 Inhibitor that are currently in Phase II clinical trial and IND enabling studies respectively.



Clinuvel Pharmaceuticals (OTCPK: CLVLY)

This biopharmaceutical company is committed to finding cures for skin and genetic disorders with its lead product candidate SCENESSE® (afamelanotide 16mg), a novel photoprotective drug for the treatment of erythropoietic protoporphyria (EPP) and prevention of phototoxicity in adult patients. It is currently engaged in Phase II and phase III trials in the US and Europe. The drug has already been granted marketing authorization under exceptional circumstances in Europe, and has submitted a new drug application to the FDA in the U.S and is awaiting marketing approvals. It is also conducting clinical trials for Vitiligo.

SCENESSE® is based on the company’s path breaking work on synthesising human hormones using the properties of alpha-MSH (melanocyte stimulating hormone) to protect the human skin with the development of a first-in class dissolvable implant that could mimic the benefits of the sun minus the damage for treatment of disorders such as erythropoietic proto- and congenital porphyria [EPP, CEP], Solar Urticaria and other light-induced diseases. SCENESSE® is a chemical analogue of α-MSH and is a linear peptide with 13 amino acids.

It combines its expertise and understating of electromagnetic spectrum, skin physiology and the interaction between light and environment to come up with innovations in fields of erythropoietic porphyria, Variegate porphyria (VP), Xeroderma Pigmentosum (XP) to name a few.

It has successfully completed clinical trials for studying the efficacy of re-pigmentation therapy in Vitiligo. As per the company, its SCENESSE® is being evaluated for its ability to activate melanocytes within the vitiliginous lesions and achieve repigmentation in combination with NB-UVB in patients with vitiligo.

Its product pipeline consists of CUV9900, an alpha-Melanocyte Stimulating Hormone (alpha-MSH) analogue with skin protection capabilities, VLRX001, a melanocortin analogue that can improve and prolong cellular activity and is intended for topical administration for patients suffering from Vitiligo that is being developed through CLINUVEL’s Singaporean subsidiary.

As per its financial results, the revenues as on December, 2018 stood at $8.98 million, while the net profits were reported to be at $4.08 million.



Strata Skin Sciences (NASDAQ: SSKN)

The company’s proprietary XTRAC and VTRAC excimer laser device use UVB light to treat Psoriasis, Vitiligo Eczema, Leukoderma and Atopic Dermatitis with minimal peripheral tissue damage overcoming limitations of conventional treatment options such as biologics, drug therapies, application of topical lotions and UV treatment. XTRAC produces a monochromatic wavelength (308nm) of UV light that has shown to reduce psoriasis lesions by 95 percent in 10-12 treatments offering long-lasting relief.



AVITA Medical (OTCQX: AVMXY)

A pioneer in regenerative medicine, Avita’s proprietary RECELL system is an autologous cell harvesting device that can produce a suspension of Spray-On Skin™ Cells using a patient’s own skin cells to regenerate the outer layer of skin all under 30 minutes. The company growth strategy is focused on creating solutions for areas with unmet medical needs such as Vitiligo, Trauma and chronic wounds, aesthetic cell and gene therapy.

Avita Medical has entered into collaboration with the Japan-based COSMOTEC for marketing and distribution of RECELL® Autologous Cell Harvesting Device (RECELL® System), the company has submitted a Japan’s Pharmaceuticals and Medical Devices Act (“JPMDA”) application for marketing approvals in Japan for treatment of Vitiligo that affects over two million people in Japan, in addition to being considered as a treatment for severe burns chronic wounds and decubitus ulcers.



Arrien Pharmaceuticals (Private)

A biopharmaceutical company with a diverse pipeline of drug candidates under development, Arrien’s ARN-4079 is an orally available Janus Kinase 3 (JAK3) inhibitor that is irreversible, durable and has the potential to treat inflammatory and autoimmune diseases such as Vitiligo, Rheumatoid Arthritis, atopic dermatitis and other skin disorders. The company plans to file for an Investigation New Drug Status for ARN-4079 with the FDA and is seeking partnerships that will enable it to fulfill IND enabling studies and Phase I clinical trials.
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PunkassDerm
Posted on: Jun 15 2019, 06:05 AM


Group: Member
Posts: 509

Would love to see a $5 (AUD) 15% bump in a week!

$5 USD even better!
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PunkassDerm
Posted on: Jun 14 2019, 01:11 PM


Group: Member
Posts: 509

List of Australian exchange-traded funds

https://en.m.wikipedia.org/wiki/List_of_Aus...ge-traded_funds
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PunkassDerm
Posted on: Jun 13 2019, 10:21 AM


Group: Member
Posts: 509

14th
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PunkassDerm
Posted on: Jun 12 2019, 12:05 AM


Group: Member
Posts: 509

Palatin pushing forward. Maybe Clinuvel is active but on the QT, but its time to start disclosing. Take a que from your (drug)classmate.

https://finance.yahoo.com/news/palatin-tech...-113000440.html


Palatin Technologies Granted FDA Orphan Drug Designation - PL-8177 for the Treatment of Non-Infectious Uveitis

PL-8177 is a Melanocortin Receptor 1 Agonist

CRANBURY, N.J., June 6, 2019 /PRNewswire/ -- Palatin Technologies, Inc. (NYSE American: PTN), a biopharmaceutical company developing targeted, receptor-specific peptide therapeutics for the treatment of diseases with significant unmet medical need and commercial potential, today announced that the U.S. Food and Drug Administration (FDA) granted orphan drug designation for PL-8177 for the treatment of non-infectious intermediate, posterior, pan and chronic anterior uveitis. Non-infectious uveitis is a group of inflammatory diseases that produces swelling and destroys eye tissue and can result in vision loss.

"We are very pleased to receive our first orphan drug designation for a melanocortin agonist peptide from the FDA," said Dr. Carl Spana, President and Chief Executive Officer of Palatin Technologies. "Unlike corticosteroids, immunosuppressive agents, and biological therapies targeting specific cytokines or receptors, melanocortin receptor 1 peptides work to resolve chronic inflammations and restore normal immune function. We look forward to initiating clinical trials with PL-8177 for non-infectious uveitis, a high medical need disease with limited treatment options."

Palatin has conducted a single and multiple ascending-dose Phase 1 study with PL-8177 under an investigational new drug (IND) application for ulcerative colitis. Palatin plans to file an IND application for non-infectious uveitis with the FDA in the third quarter of calendar year 2019, and initiate a Phase 2 clinical study in the first half of calendar year 2020. In both animal studies and Phase 1 subcutaneous studies with PL-8177 no safety or tolerability concerns were reported.

PL-8177 has been evaluated in animal models of experimental autoimmune uveitis, a model presenting certain clinical features of human uveitis. In these studies, PL-8177 showed reduction of inflammation and restoration of normal retinal structure. Spana C, Taylor AW, Yee DG, Makhlina M, Yang W and Dodd J (2019) Probing the Role of Melanocortin Type 1 Receptor Agonists in Diverse Immunological Diseases. Front. Pharmacol. 9:1535. doi: 10.3389/fphar.2018.01535.

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PunkassDerm
Posted on: Jun 11 2019, 05:03 AM


Group: Member
Posts: 509

OK...one more shot, trying to include everyone's likes/ideas. This last will probably be closest and most inclusive. I like this best. And don't want to keep inundating board with T shirt ideas.

This is not a business endeavor of mine (don't want to profit) I wanted something cool for the group. We've (I've) been checking this board daily for YEARS now.
Sometimes spirited, sometimes contentious, sometimes sigh...but always learning.

AND AS ALWAYS, AN OMAGE TO FRILLY!

Received a reply from the printer, they can do a group order but I'd really love to find someone who can ship to EVERYONE GLOBALLY.

I'm also thinking to offer link to the APF, and find a printer that will donate a portion of proceeds to them (I'll pay a buck or 2 more for a shirt). Do some good same time.


QUOTE
Once you have created your design you are definitely welcome to set up a group order. This will provide you with a link you can share with everyone you would like to have the opportunity to join. When they click on the link they can enter their own selections and payment.

The order automatically is set up to bulk ship (bulk shipping is free of charge). If you would like I can manually set up your order to individually ship. This costs an additional $5.95 for the first shirt + $2.00 for each additional shirt shipping to the same person. This service is only available for U.S. locations. Unfortunately, we can't ship to Australia at this time. Please let me know if you end up wanting to individually ship your order and I can update your order accordingly.



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PunkassDerm
Posted on: Jun 9 2019, 12:35 AM


Group: Member
Posts: 509

While I'm waiting to hear on details about orders, I tried a front and back design and dropped frilly text. Really like a link to order, where you can pick your shirt and have shipped worldwide... since we are an international rag tag team.

Hopefully not a problem Farma, if not sold for profit. We're like a church group, the Clinuvologists. Tax exempt too?

front
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back
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PunkassDerm
Posted on: Jun 8 2019, 03:07 PM


Group: Member
Posts: 509

on the back
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PunkassDerm
Posted on: Jun 8 2019, 02:55 PM


Group: Member
Posts: 509

With AKAs

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PunkassDerm
Posted on: Jun 8 2019, 02:34 PM


Group: Member
Posts: 509

If I can create a link for group order, anyone interested? Have a request pending, including possible shipments to AU and US.
Design changes?

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PunkassDerm
Posted on: Jun 7 2019, 08:21 AM


Group: Member
Posts: 509

Love to see CLVLY hit 75 USD and PTN hit 25 USD, a beautiful imbalance indeed.
And it's not one three month delay...it's delay after delay after delay after countdown clock. Wash rinse repeat.
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PunkassDerm
Posted on: Jun 7 2019, 07:59 AM


Group: Member
Posts: 509

I don't see them as competitors but complementary drugs for a new class at this time. PTN wins, CUV does too. Just wanted to be first horse.


3 Drug Stocks That Could Win From Key FDA Approvals in June
Two hope to pick up additional indications for existing blockbuster drugs, while another could score a big victory for a new drug.

Keith Speights (TMFFishBiz)
Jun 4, 2019 at 7:15AM


https://www.fool.com/investing/2019/06/04/3...a-approval.aspx


2. AMAG Pharmaceuticals
AMAG Pharmaceuticals awaits an FDA decision that's more critical to the company than the approval decisions on Keytruda are for Merck. The FDA should hand down its verdict on Vyleesi in treating hypoactive sexual desire disorder (HSDD) in premenopausal women by June 23.

If approved, Vyleesi won't be the first drug on the market for treating HSDD. Sprout Pharmaceuticals' Addyi gained FDA approval in 2015. But it hasn't been as big a hit as some expected because of safety-related hurdles. Vyleesi shouldn't have the same issues, though. AMAG thinks its drug could have blockbuster potential. Analysts project that sales for Vyleesi could top $800 million by 2024 if it wins approval.

It should be noted that an FDA approval for Vyleesi would also be great news for Palatin Technologies (NYSEMKT:PTN). Palatin licensed North American rights to the drug to AMAG in 2017 and stands to receive a significant milestone payment if Vyleesi wins approval.
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PunkassDerm
Posted on: Jun 6 2019, 08:27 PM


Group: Member
Posts: 509

now...not in the coming weeks
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PunkassDerm
Posted on: Jun 6 2019, 08:10 PM


Group: Member
Posts: 509

You addressing me?

1. I still have north of 200K shares. sold 15K up to 22 USD, bought back 5K at 16.21
2. See 1, I'd like to see my investment handled with deftness and skill, not the keystone cops.

Always been a fan of the molecule, the management is meh. It is ok to question, ESPECIALLY when Wolgen is scant on truth about what is going on.

Don't be a blind Kool-Aid drinkin' lemming.

I'll toast the world when we have a long overdue FDA approval. Until then I'll be critical of management, got the farm on it and this farmer ain't getting younger.

And I would smile big if Allergan swoops in and brings this bitch home.
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PunkassDerm
Posted on: Jun 6 2019, 12:12 PM


Group: Member
Posts: 509

Integrity, transparency, honesty, efficiency. More than SP

(Probably) lost a chance at first in class melanocortin after a HUGE headstart.
Losing market exclusivity with each passing month.

Much more at stake.

Yes greed, but its all perspective where that greed is coming from. Recruiting the right right help to navigate the approval process for an inexperience company.

And yes I think I'm due for my payday too.
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PunkassDerm
Posted on: Jun 6 2019, 11:11 AM


Group: Member
Posts: 509

Wholeheartedly and disappointingly agree, we've probably been pushed back to second in class melanocortin. Takes the wind out of my sails after 15 years of waiting/hoping.
And yes, if Clinuvel at least partnered like PTN to AMAG I think we'd have had approval 3 or more years ago.
Glad I bought some PTN just in case.

sigh...in it for the long haul but so so tired. And aging
  Forum: By Share Code

PunkassDerm
Posted on: Jun 1 2019, 06:55 AM


Group: Member
Posts: 509

https://www.cnbc.com/2019/05/31/pharma-bro-...rom-prison.html


Pharma bro’ Martin Shkreli sues Retrophin directors, ex-general counsel for more than $30 million from prison in Pennsylvania



Notorious ‘pharma bro’ Martin Shkreli on Friday sued two directors and the ex-general counsel of his former biopharmaceutical company Retrophin, accusing them of using fraud to oust him as head of the firm in 2014.

Shkreli’s lawsuit, which was filed in federal court in Manhattan, is seeking damages of more than $30 million.

It was lodged within days of the 36-year-old Shkreli being transferred to a new prison in Pennsylvania, where he will continue serving a seven-year sentence for securities fraud related to his two defunct hedge funds and to Retrophin, which he founded after the funds financially collapsed.

The named defendants in the case are Retrophin’s chairman of the board of directors, Gary Lyons, former company CEO Stephen Aselage, who currently is a director, and the firm’s former top lawyer Margaret Valeur-Jensen.

“After starting a biopharmaceutical company from scratch and turning it into a successful enterprise worth hundreds of millions of dollars, Mr. Shkreli was unceremoniously and illegally ousted from the company at the hands of Defendants,” the suit claims.

“Defendants, who had little to do with the success of the company but were instead driven by their egos, jealousy, and greed, were successful in only one thing: creating and carrying out a scheme to oust Mr. Shkreli from the company for their selfish benefit,” the suit says.

“Indeed, the only people who benefitted from Mr. Shkreli’s ouster were the three Defendants and a few other people they recruited.”

Shkreli’s lawyer in the case Edward Kang of Philadelphia, declined to comment when contacted by CNBC.

A spokesman for Retrophin declined to comment.

Valeur-Jensen did not immediately return a request for comment sent to her via her LinkedIn account.

Shkreli gained national infamy in 2015 after the company he founded after his ouster from Retrophin – Turing Pharmaceuticals — hiked the price of its drug Daraprim by more than 5,000%.

The medication is used to treat a parasitic infection found in pregnant women, babies and HIV patients. Turing is now known as Phoenixus AG.

In August 2017, a jury convicted Shkreli of three of eight criminal counts related to his hedge funds and to Retrophin. His $5 million release bond was revoked a month later after his trial judge ruled him to be a danger because of his offer, to his Facebook followers, of a $5,000 bounty for samples of Hillary Clinton’s hair.

Since last year, he had been serving his criminal sentence in the low-security prison in Fort Dix, NJ.

But two months ago he was transferred to a federal jail in Brooklyn, New York, after The Wall Street Journal reported in March that he was still helping to “call the shots” at Phoenixus with the help of a contraband cell phone at Fort Dix.

This week, Shkreli was transferred to another low-security prison, in Allenwood, Pennsylvania, according to the Bureau of Prisons website.
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PunkassDerm
Posted on: May 15 2019, 08:00 PM


Group: Member
Posts: 509

Avita has spilled over into CUV a couple of times now. You really thinking possible synergies with MSH (afamelanotide or new topical) for vitiligo? I also see regenerative medicine as the future, interested in this.
Though already had a big jump, just added 50K shares to my holdings.
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PunkassDerm
Posted on: May 8 2019, 01:24 AM


Group: Member
Posts: 509

I love all of this, and hope to see and benefit from it in my lifetime. I think this also means partnership or acquisition to avoid glacial progress and rookie mis-steps.

Allergan - botulinum toxin type A model
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PunkassDerm
Posted on: May 3 2019, 12:08 AM


Group: Member
Posts: 509

Agreed that Wolgen has been cautious, more so tight lipped. So why even comment on CRL at this point, even for him this is purely conjecture? Why deviate now?

What purpose does this serve other than for cover in case of delay, the modus operandi for the team? Or as seeva states, allow some last minute buys for friends?
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PunkassDerm
Posted on: Apr 29 2019, 10:27 PM


Group: Member
Posts: 509

One more, posted directly on FDA.gov
It appears focus on orphan diseases


https://www.fda.gov/news-events/fda-voices-...american-public



2018: A Year of Innovation, Efficiency, and New Advances in Drug Therapy for the American Public
By: Janet Woodcock, M.D.

The beginning of a new year is a good opportunity to look back over the past year and see how all the valuable work done at FDA's Center for Drug Evaluation and Research (CDER) results in bringing important new drug therapies to patients in need. It is particularly clear that our work is about people—and advancing patient care and public health.

In 2018, we approved many new drugs never before marketed in the United States, known as "novel" drugs, along with a wide variety of approvals of drugs already on the market to put to new and innovative uses. Many of these new approvals will have a significant impact on improving—and indeed, saving—countless patients' lives.

This past year was important for meeting the critical needs of people suffering from rare diseases who will benefit from these advances. Among many new orphan therapies, in 2018 CDER approved the first drug to treat patients with a rare, inherited form of rickets, a condition that leads to impaired bone growth and development. Also, CDER approved the first orally-administered drug to treat Fabry disease, a rare and serious disorder that can cause many adverse symptoms, including pain and burning in the hands and feet, and damage to the kidneys and heart. We also approved a new drug to treat patients with phenylketonuria, a rare dietary condition in which patients are born with an inability to break down protein-containing foods and certain sweeteners, and which can lead to brain and nerve damage.

Many of CDER's other 2018 approvals will provide hope, relief, and enhanced quality of life for patients in need:

CDER approved the first drug ever to treat smallpox, the first of a new class of drugs to treat patients with HIV-1 infection who have failed other therapies, and a new single dose treatment for influenza (flu).
CDER approved a new drug to treat seizures in patients with the rare and severe forms of epilepsy Lennox-Gastaut syndrome and Dravet syndrome, and a second drug to treat seizures in patients with Dravet syndrome. Previously there had been no FDA-approved therapy for Dravet syndrome. We approved three new drugs—all in a new drug class—to treat patients with migraines. Additionally, CDER approved the first therapy to treat multiple sclerosis in children.
We approved new advances for certain patients with breast cancer, prostate cancer, lung cancer, and thyroid cancer. We also approved a variety of new drug therapies to treat blood cancers and other blood disorders such as acute myeloid leukemia (a type of blood cancer), and classical Hodgkin lymphoma (a type of cancer of a part of the immune system called the lymphatic system); and thrombocytopenia (a deficiency of platelets in the blood) in patients with chronic liver disease scheduled to undergo a medical or dental procedure.
We also approved seven new biosimilars, which will further help to create competition, increase patient access, and potentially reduce the cost of important biological drug therapies.
Of course, even the best drug therapies are of no use to patients if they are stuck in the approval process. I want to recognize the importance of the efficiencies with which we brought these new therapies to approval.

Under the Prescription Drug User Fee Act (PDUFA), drug developers are assessed user fees that provide FDA with the additional resources needed to maintain an efficient and effective review process. PDUFA includes goal dates for application review agreed to with the pharmaceutical industry and approved by Congress. In 2018, CDER met its PDUFA goal dates for 100 percent of the novel drugs approved (59 of 59).
We use four specific regulatory tools to ensure prompt and efficient expedited review for approval decisions: Fast Track, Breakthrough, Accelerated Approval, and Priority Review. Each serves a purpose in helping to speed a drug’s development or review. In 2018, 73 percent of CDER’s novel drug approvals (43 of 59) were designated in one or more of these expedited review categories. These innovative approval methods can bring a therapy to patients months or even years sooner than if their application went through the standard review process.

In 2018, CDER approved 95 percent of its novel drug approvals (56 of 59) on the first cycle. A "cycle" is the time from when CDER accepts an application for a new drug until we decide about whether or not to approve it. A typical cycle generally takes somewhere between six months to a year, but sometimes things can go wrong. For instance, miscommunication, omissions of important data, and other issues in these complex applications, can lengthen the time it takes to complete a review and may also result in the need for a second cycle, further delaying access to the drug for patients in need. From 2011 through 2017, CDER approved 250 novel drugs, of which 205 (82 percent) were approved on the first cycle. Our consistently high first cycle approval rate reflects CDER’s commitment to working closely with applicants as they design their studies and build their application data. It also reflects our efficiency in getting new therapies to patients as quickly as possible.

Although regulatory processes differ widely between FDA and those of regulatory agencies in other countries, 42 of the 59 novel drugs approved in 2018 (71 percent) were approved in the United States before receiving approval in any other country.


More details about CDER’s new drug therapy approvals—including many specific examples of notable new approvals for the year—are available in our annual New Drug Therapy Approvals report.

I am proud to be part of a team of dedicated professionals who work tirelessly to find innovative, efficient, and, most importantly, safe ways to bring new therapies to patients as quickly as possible.
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PunkassDerm
Posted on: Apr 29 2019, 01:07 PM


Group: Member
Posts: 509

Some stats on 2018...any day now????


http://eyeonfda.com/2018/03/pdufa-dates-ad...ls-2018-so-far/


PDUFA Dates, AdComms and Approvals – 2018 So Far
Posted on March 14, 2018 by Mark Senak


There would seem to be a momentum for new approvals brought on by a number of circumstances, not the least of which is the fact that last year saw a record number (47) of approvals for new molecular entities (NMEs), but also for generic approvals (1027). And among those approvals, there were a number of “firsts” – such as first gene therapy and the first CAR-T therapies. In addition there were a significant number of approvals in oncology. A lot happened last year. That means a lot of eyes turn to this year to see what kind of year it is going to be in 2018.

So how are we doing? There are a few places to look when you are making that assessment that are kind of surrogate markers to tell us how things are going. First, of course, there would be the NME approvals. By the end of February this year, FDA had approved only 4 NMEs, which might sound discouraging, but in fact, it is only one less than was approved by the same time last year. There is still a lot of time for a lot to happen in 2018.

Another place to look is at PDUFA dates, and in doing so there is perhaps reason for cheer. During January and February there were 15 PDUFA dates, 3 of which resulted in Complete Response Letters and 12 of which were approvals, some of which not only occurred early, but very early. At least three of these were approved in December 2017, two months before the PDUFA date. Of the approvals during the first two months, 9 of them were NDAs and 6 were sNDAs.

And finally, if we take into consideration the activity among advisory committees – last year there was only 1 advisory committee meeting held during the January/February period to consider an NDA for a new drug. During the entire year by my count there were 23 such meetings. By contrast, during the January/February time period this year there were 5 advisory committee meetings held to consider NDAs and there have been 10 meetings scheduled so far this year, with more surely to come, particularly with the increase of drugs that have priority review.

Back to PDUFA, for the future, right now by my count, I am currently counting 60 more decision dates for 2018, 41 of which are for NDAs and the balance are sNDAs, and of course, there are more to come. Five of these involve product NDAs in oncology, two of which FDA have already acted upon away before their actual PDUFA dates. There are also five in cardiovascular, two in antimicrobial and six in pain.

In short, at this early juncture, judging by a look at these “surrogate endpoints” it would seem that there is a good chance this year will not be a slacker in terms of progress in approvals overall or in advances in major disease areas.
  Forum: By Share Code

PunkassDerm
Posted on: Apr 23 2019, 01:02 PM


Group: Member
Posts: 509

Is it finally time for the countdown clock? T-minus 76 days...or sooner?

https://days.to/until/8-july
  Forum: By Share Code

PunkassDerm
Posted on: Apr 23 2019, 01:27 AM


Group: Member
Posts: 509

Had to do it...

Just bought back 5k shares @16.21
  Forum: By Share Code

PunkassDerm
Posted on: Apr 22 2019, 10:19 PM


Group: Member
Posts: 509

Clearly established, these skin conditions are not merely cosmetic.
Take note NICE and cost cutters, at the peril of individuals.
What is the true cost of dismissing these diseases?


https://www.medpagetoday.com/dermatology/ge...rmatology/79331


Vitiligo, Alopecia Merely Cosmetic? Think Again
Studies show links with depression, quality of life -- and early death

by Ashley Lyles, Staff Writer, MedPage Today
April 18, 2019


Skin health is closely associated with overall quality of life, mental health, and risk of death, three studies appearing in the Journal of the American Academy of Dermatology showed:

In a population-based cohort study, researchers found a bidirectional relationship between major depression and vitiligo, such that having either one increased the risk for developing the other. For example, those with major depressive disorder (MDD) were at 64% greater risk for vitiligo (P<0.0001) when compared to the general population, reported Isabelle Vallerand, PhD, of the University of Calgary in Alberta, Canada, and colleagues.

A prospective cross-sectional study found impaired quality of life among parents of children with alopecia, especially for older children and those with more severe disease.

And a systematic review indicated that psoriasis is related to a greater risk of death.


Depression, Vitiligo Intertwined
  Forum: By Share Code

PunkassDerm
Posted on: Apr 12 2019, 01:04 PM


Group: Member
Posts: 509

I think....when your account cross a certain threshold you become an apex client. They want to "help" you invest those gains. I had a conversation with my TDA rep too. She's very receptive now.
  Forum: By Share Code

PunkassDerm
Posted on: Apr 7 2019, 10:36 PM


Group: Member
Posts: 509

Too expensive for a spec buy for me.

Looking at this, why aren't we 50USD by now??? No one knows but our group? And the selling instos!
It does show that melanocortins are about to explode!


Setmelanotide: An Investigational, First-in-Class MC4R Agonist
Our lead product candidate, setmelanotide, is an investigational, first-in-class melanocortin-4 receptor (MC4R) agonist in development for the treatment of rare genetic disorders of obesity. Setmelanotide is thought to activate the MC4R, part of a key biological pathway in humans that regulates weight by increasing energy expenditure and reducing appetite. Variants in genes within the MC4 pathway are associated with unrelenting hunger, known as hyperphagia, and severe, early-onset obesity.

We believe setmelanotide is a potential replacement therapy that may restore lost activity in the MC4 pathway, reestablishing weight and appetite control in patients with these rare genetic disorders.


RYTM (Common Stock)
$27.99
  Forum: By Share Code

PunkassDerm
Posted on: Apr 7 2019, 10:13 AM


Group: Member
Posts: 509

I know the rhythm method???

I jumped on PTN because of pending FDA decision, not another 15 years mehopes. What is the status of Rhythm? Indication? How far along? Interesting!

Frilly Frilly
  Forum: By Share Code

PunkassDerm
Posted on: Apr 5 2019, 08:37 PM


Group: Member
Posts: 509

Not my perspective at all. I'm not actually favoring either stock but I am ALL IN MELOCORTINS. I've realized why not take advantage of the first 2 in class drugs hopefully slated to gain FDA approval just weeks apart. PTN WITH PARTNER AMAG seems to be more efficiently run and stock volumes look very good. But all my stock pick are emotional.

These companies for now are targeting different indications, in THE PLATFORM OF THE FUTURE.

As for same period, also perspective:

I've held CLVLY for 15+ years now and watched cash burn for many many years, finally enjoying hopefully a meteoric rise. Only in the past 3 years in positive territory for me.
600 percent plus gain for me, and I've cashed out 20K shares from 16.50-20 bucks. I still have 200K to play with.
I took 40K and purchased 50K shares of PTN on a whim. That investment in a mere couple of months has produced a 20% gain. Zero return is not my experience.
It may tank, but I doubt it and no biggie. But I may have another multi-bagger on my hands fueled with pure profit on my other blockbuster.

I say let it ride, I welcome all melanocortins equally for medicine and for investment.

Smile emoji PTN
Smile happy ending emoji CUV
Smile with hot chick in my GT3 (I don't need a soccer club)

Frilly Frilly

D
  Forum: By Share Code

PunkassDerm
Posted on: Apr 4 2019, 10:39 PM


Group: Member
Posts: 509

Here's for a great summer! IBD indication, melanocortins are disruptive!!!


https://seekingalpha.com/news/3448345-palat...minus-8177-data


Palatin up 16% premarket on positive PL-8177 data
Apr. 4, 2019 7:52 AM ET|About: Palatin Technologies, ... (PTN)|By: Douglas W. House, SA News Editor
Palatin Technologies (NYSEMKT:PTN) announces successful results from a micro-dose study evaluating an oral, delayed-release polymer formulation of radiolabeled PL-8177, a candidate for the potential treatment of ulcerative colitis and other inflammatory bowel diseases.

Topline data showed that PL-8177, a melanocortin receptor 1 agonist, was released in the lower GI tract while avoiding systemic absorption. It was well-tolerated with no adverse events reported.

Development is ongoing.

Shares are up 16% premarket on light volume.
  Forum: By Share Code

PunkassDerm
Posted on: Apr 4 2019, 08:02 PM


Group: Member
Posts: 509

AK would be a great indication for a new topical formulation, along with vitiligo maintenance (acne rosacea too).
  Forum: By Share Code

PunkassDerm
Posted on: Apr 4 2019, 07:48 PM


Group: Member
Posts: 509


See below key players in AK market??? Interesting, I thought this indication was lost. Maybe nothing but...I treat these all day long


https://www.marketwatch.com/press-release/g...d=mw_quote_news


Global Actinic Keratosis Treatment Market - Prognosticated To Perceive a Thriving Growth CAGR of 5% by 2022 - An Exorbitant Study Report by the Expert of Market Research Future

Published: May 11, 2018 7:07 p.m. ET


May 11, 2018 (AB Digital via COMTEX) -- Global Actinic Keratosis Treatment Market Information, by Surgical Procedures (Photodynamic therapy, Cryotherapy, Curettage and Desiccation, Laser surgery, Combination therapy and others), by Prescription Products (Fluorouracil cream, Imiquimod cream, Ingenol&nbsp;mebutate&nbsp;gel, Diclofenac gel and others), by end user (Hospitals, Clinics, Oncology Centers, Dermatology Service Centers and others) - Forecast till 2022

The global market for actinic keratosis treatment market is expected to reach around USD 9 billion by the end of the forecast period and is expected to grow at a striking CAGR of ~5% during the forecast period of 2016-2022.

KEY PLAYERS FOR ACTINIC KERATOSIS TREATMENT MARKET

LEO Pharma Inc., Clinuvel Pharmaceuticals Ltd, Biofrontera AG, DUSA Pharmaceuticals, Inc., TOLMAR Pharmaceuticals, Inc., Valeant, Galderma S.A., Perrigo Company plc. and others.

Get Sample Report @&nbsp;https://www.marketresearchfuture.com/sample_request/2366&nbsp;.



MARKET SCENARIO FOR ACTINIC KERATOSIS TREATMENT MARKET

An actinic keratosis is a type of skin cancer in which the skin gets rough, there&nbsp;are&nbsp;scaly&nbsp;patch on skin that develops from years of exposure to the sun. Its most commonly found on&nbsp;face, lips, ears, back of hands, forearms, scalp or neck. It is also known as a solar keratosis. An actinic keratosis enlarges slowly and usually causes no signs or symptoms other than a patch or small spot on&nbsp;skin. These patches&nbsp;appears&nbsp;in people over the age of 40. The market for actinic keratosis treatment is growing at a reasonably good rate. Growing new cases for skin cancers around the globe and increasing exposure&nbsp;of&nbsp;UV rays due to the depletion of ozone layers are some factors which&nbsp;has&nbsp;fueled the growth of actinic keratosis treatment market.

SEGMENTS FOR ACTINIC KERATOSIS TREATMENT MARKET

Global Actinic Keratosis treatment market has been segmented on the basis of surgical procedures which comprises photodynamic therapy, cryotherapy, curettage and desiccation, laser surgery, combination therapy and others. On the basis of prescription products;&nbsp;market&nbsp;is segmented into fluorouracil cream, imiquimod cream,&nbsp;ingenol&nbsp;mebutate&nbsp;gel, diclofenac gel and others. On the basis of end users;&nbsp;market&nbsp;is segmented into hospitals, clinics, oncology centers, dermatology service centers and others.

REGIONAL ANALYSIS FOR ACTINIC KERATOSIS TREATMENT MARKET

Globally, Americas is the largest market for actinic keratosis treatment. The Americas market for actinic keratosis treatment market is expected to reach around USD 3.8 billion by the end of the forecast period of 2016-2022. Europe is the second-largest market for actinic keratosis treatment. Asia&nbsp;pacific&nbsp;region is expected to be&nbsp;fastest&nbsp;growing region in actinic keratosis treatment market.

Get Discount @&nbsp;https://www.marketresearchfuture.com/check-discount/2366&nbsp;.

MAJOR TOC FOR ACTINIC KERATOSIS TREATMENT MARKET

CHAPTER 1. INTRODUCTION

1.1 Definition

1.2 Scope Of Study

1.3 Research Objective

1.4 Assumptions & Limitations

1.5 Market Structure:

CHAPTER 2. RESEARCH METHODOLOGY

2.1 Research Process

2.2 Primary Research

2.3 Secondary Research

CHAPTER 3. MARKET DYNAMICS

3.1 Drivers

3.2 Restraints

3.3 Opportunities

3.4 Challenges

3.5 Macroeconomic Indicators

CHAPTER 4. MARKET FACTOR ANALYSIS

4.1 Porter&rsquo;s Five Forces Model

4.1.1 Bargaining Power of Suppliers

4.1.2 Bargaining Power of Customer

4.1.3 Intensity Of Competitor&rsquo;s

4.1.4 Threat of New Entrants

CHAPTER 5. GLOBAL ACTINIC KERATOSIS TREATMENT MARKET, BY SURGICAL PROCEDURE

5.1 Introduction

5.1.1 Photodynamic Therapy

5.1.2 Cryotherapy

5.1.3 Curettage And Desiccation

5.1.4 Laser Surgery

5.1.5 Combination Therapy

5.1.6 Others

TOC Continued&hellip;

Ask to Expert Inquire @&nbsp;https://www.marketresearchfuture.com/enquiry/2366&nbsp;.

About Us:
  Forum: By Share Code

PunkassDerm
Posted on: Apr 4 2019, 02:05 PM


Group: Member
Posts: 509

DNA Repair? Wonder if they would ever consider revisiting AKs? I couldn't even imagine, mind blown.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921754/



Nonsurgical Innovations in the Treatment of Nonmelanoma Skin Cancer
Sadegh Amini, MD, Martha H. Viera, MD, Whitney Valins, BS, and Brian Berman, MD, PhDcorresponding author


Abstract

Basal cell carcinoma and squamous cell carcinoma are the most frequent types of cancer in the United States and represent 75 percent and 20 percent, respectively, of all nonmelanoma skin cancers. Since ultraviolet radiation is implicated in their development, photoprotection is fundamental in their prevention. Additional preventive measures include identifying high-risk individuals for early detection along with using agents, such as retinoids, that are effective in decreasing the risk of premalignant cells further developing into carcinomas. Newer agents achieving this goal include perillyl alcohol, T4 endonuclease 5, DL-α-tocopherol, and α-difluoromethylornithine. Procedural modalities are currently the standard of treatment, but recent evidence has consistently shown that newer (nonsurgical) therapies, such as interferon, imiquimod, retinoids, and 5-fluorouracil, can be used effectively either as monotherapies or as adjuvants to those surgical modalities for the treatment of superficial nonmelanoma skin cancers and premalignant lesions. These newer therapies have achieved significant reductions in morbidity and mortality. Procedural modalities that have been evolving into important tools for the treatment of actinic keratosis and nonmelanoma skin cancers include photodynamic therapy and lasers. Nonsurgical therapies currently proving to be effective in clinical trials include ingenol mebutate and cyclooxygenase-2 inhibitors. Agents that are showing promising results in early phases of clinical trials include betulinic acid; hedgehog signaling pathway inhibitors, such as cyclopamine and GDC-0449; α-melanocyte–stimulating hormone analogs, such as afamelanotide; epidermal growth factor receptor inhibitors, such as gefitinib and erlotinib; anti-epidermal growth factor receptor monoclonal antibodies, such as cetuximab and panitumumab; and the 5-fluorouracil prodrug capecitabine.



Afamelanotide (CUV1647)

UVB induces the synthesis of melanin in melanocytes through the release of a-melanocyte stimulating hormone (a-MSH) from cutaneous melanocytes and keratinocytes. This effect is produced after UVB has already caused substantial damage to keratinocytes.228 The increase in melanin may have protective effects against UVB. Afamelanotide (CUV1647) is an analogue of a-MSH with higher potency and longer action than the naturally occurring hormone.229 It is currently being studied to evaluate its efficacy in reducing the number of AKs and SCCs in organ transplant recipients on chronic immunosuppressive therapy.230
  Forum: By Share Code

PunkassDerm
Posted on: Mar 31 2019, 12:25 AM


Group: Member
Posts: 509

The introduction says it all...Savannah Fulkerson I presume.


Please see below: Savannah and her EPP story, XP and afamelanotide also featured. Soon Savannah, they need to accelerate pediatric indication!


https://www.youtube.com/watch?v=KYyOai2R7q8


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  Forum: By Share Code

PunkassDerm
Posted on: Mar 28 2019, 01:29 PM


Group: Member
Posts: 509

Way back to the beginning...What a road it has been!

Nightly news with Tom Brokaw, 1991. My HS graduation, wow. Early approval would be quite a gift given time passed.

Frilly Frilly


https://www.youtube.com/watch?v=1JvytU6KMLY


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  Forum: By Share Code

PunkassDerm
Posted on: Mar 27 2019, 02:59 AM


Group: Member
Posts: 509

Not even SPDRs?

https://www.investopedia.com/articles/etfs/top-etfs-nasdaq/


Fidelity Nasdaq Composite Index ETF (ONEQ)
Issuer: Fidelity
AUM: $1.86 billion
2018 YTD Performance: 17.14%
Expense Ratio: 0.20%
Since its inception in 2003, this Fidelity ETF has attempted to replicate the Nasdaq Composite Index. Almost 93% of its holdings are common stock included in the index, and more than 97% of the assets represent domestic companies.

The fund is weighted toward information technology, healthcare and consumer discretionary sectors, and you'll see lots of familiar names -- Apple Inc. (AAPL), Amazon.com, Inc. (AMZN) and Microsoft Corporation (MSFT) are the top three holdings. Its one-year, three-year and five-year annualized returns are 24.81%, 21.58% and 17.62%, respectively.
  Forum: By Share Code

PunkassDerm
Posted on: Mar 18 2019, 01:44 PM


Group: Member
Posts: 509

Anyone take notice, Clinuvel passed 1B USD?

Sláinte is táinte!


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  Forum: By Share Code

PunkassDerm
Posted on: Mar 7 2019, 01:33 PM


Group: Member
Posts: 509

FDA approves Special K for depression...but they express concern about a tan as a side effect. uh huh? July 8 FDA, July 8


https://www.vox.com/2019/3/6/18253041/ketam...ohnson-spravato


A ketamine-like drug is the first new antidepressant to get FDA approval in decades
But it’s also controversial.
By Julia Belluz@juliaoftorontojulia.belluz@voxmedia.com Mar 6, 2019, 11:30am EST


Building on years of preliminary research about ketamine’s potential benefits for treating depression, Johnson & Johnson developed a drug called esketamine, sold under the brand name Spravato. Courtesy of Janssen Pharmaceutica
The Food and Drug Administration just approved a big pharma variant on the hallucinogenic club drug Special K for the treatment of depression.

Yes, you read that right.
  Forum: By Share Code

PunkassDerm
Posted on: Mar 6 2019, 01:15 PM


Group: Member
Posts: 509

And followup to that...voting shares.

  Forum: By Share Code

PunkassDerm
Posted on: Mar 5 2019, 11:41 PM


Group: Member
Posts: 509

Awesome! ...as long as it "pays off in the end," for all

Rich Bosses 2019: Meet Australia's 10 wealthiest executives
James Thomson
Mar 5, 2019 — 11.00pm

Canny investors have long believed that backing executives with skin in the game is a winning strategy. The 2019 Rich Bosses list is more proof of that strategy.
The list ranks managers and executive directors from companies in the ASX 300 according to value of the business they work in.
The full list, which was last year topped by Seven Group executive chairman Kerry Stokes, will be published in Boss magazine in Friday's edition of The Australian Financial Review.

.........

Clinuvel Pharmaceutical

Another strong performer was Clinuvel Pharmaceuticals, which produced a total shareholder return of 151 per cent in the year in question.
The biotechnology firm focused on developing treatments for a range of severe genetic and skin disorders; it's flagship drug Scenesse is in trials in the United States and Europe.
The company's chief executive, Philippe Wolgen, is a former life sciences equity analyst with deep experience in European financial markets; he has a stake worth $72 million and had total remuneration of $2.3 million in the 2018 financial year.
  Forum: By Share Code

PunkassDerm
Posted on: Mar 5 2019, 04:11 AM


Group: Member
Posts: 509

I agreed wholeheartedly. The free radial protection alone is anti-aging/anti-cancer.

I think shareholders of note should have access to 4x yearly implants, sign me up.

Frilly Frilly
  Forum: By Share Code

PunkassDerm
Posted on: Mar 2 2019, 09:52 AM


Group: Member
Posts: 509

Best guess...

Going to connect ions of oxygen in the atmosphere supercharged by solar winds, losing energy and giving off beautiful light shows;
to Reactive Oxygen Species - ROS AKA free radicals, like super oxide. Implications to disease and DNA damage, Scenesse as a free radical scavenger and repairer of DNA.

Encompassing OXIDATIVE STRESS.

Artemis shield so to speak for ionizing radiation, UVR. And for free radical damage to body as part of disease and aging.
LOOK AT POTENTIAL THERAPEUTIC TARGETS BELOW!!!

At least better be their angle or WTF???



https://earthsky.org/earth/what-causes-the-...northern-lights


What causes the aurora borealis?
By Eleanor Imster in EARTH | February 15, 2017

The aurora borealis, or northern lights, are an ethereal display of colored lights shimmering across the night sky. What causes them?

Those who live at or visit high latitudes might at times experience colored lights shimmering across the night sky. Some Inuit believed that the spirits of their ancestors could be seen dancing in the flickering aurora. In Norse mythology, the aurora was a fire bridge to the sky built by the gods. This ethereal display – the aurora borealis or aurora australis, the northern or southern lights – is beautiful. What causes these lights to appear?

Our sun is 93 million miles away. But its effects extend far beyond its visible surface. Great storms on the sun send gusts of charged solar particles hurtling across space. If Earth is in the path of the particle stream, our planet’s magnetic field and atmosphere react.

When the charged particles from the sun strike atoms and molecules in Earth’s atmosphere, they excite those atoms, causing them to light up.

What does it mean for an atom to be excited? Atoms consist of a central nucleus and a surrounding cloud of electrons encircling the nucleus in an orbit. When charged particles from the sun strike atoms in Earth’s atmosphere, electrons move to higher-energy orbits, further away from the nucleus. Then when an electron moves back to a lower-energy orbit, it releases a particle of light or photon.

What happens in an aurora is similar to what happens in the neon lights we see on many business signs. Electricity is used to excite the atoms in the neon gas within the glass tubes of a neon sign. That’s why these signs give off their brilliant colors. The aurora works on the same principle – but at a far more vast scale.


When charged particles from the sun strike air molecules in Earth's magnetic field, they cause those molecules' atoms to become excited. The molecules give off light as they calm down. Image via NASA

The aurora often appears as curtains of lights, but they can also be arcs or spirals, often following lines of force in Earth’s magnetic field. Most are green in color but sometimes you’ll see a hint of pink, and strong displays might also have red, violet and white colors. The lights typically are seen in the far north – the nations bordering the Arctic Ocean – Canada and Alaska, Scandinavian countries, Iceland, Greenland and Russia. But strong displays of the lights can extend down into more southerly latitudes in the United States. And of course, the lights have a counterpart at Earth’s south polar regions.

The colors in the aurora were also a source of mystery throughout human history. But science says that different gases in Earth’s atmosphere give off different colors when they are excited. Oxygen gives off the green color of the aurora, for example. Nitrogen causes blue or red colors.



https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310837/


Free Radicals: Properties, Sources, Targets, and Their Implication in Various Diseases
Alugoju Phaniendra, Dinesh Babu Jestadi, and Latha Periyasamycorresponding author

Abstract
Free radicals and other oxidants have gained importance in the field of biology due to their central role in various physiological conditions as well as their implication in a diverse range of diseases. The free radicals, both the reactive oxygen species (ROS) and reactive nitrogen species (RNS), are derived from both endogenous sources (mitochondria, peroxisomes, endoplasmic reticulum, phagocytic cells etc.) and exogenous sources (pollution, alcohol, tobacco smoke, heavy metals, transition metals, industrial solvents, pesticides, certain drugs like halothane, paracetamol, and radiation). Free radicals can adversely affect various important classes of biological molecules such as nucleic acids, lipids, and proteins, thereby altering the normal redox status leading to increased oxidative stress. The free radicals induced oxidative stress has been reported to be involved in several diseased conditions such as diabetes mellitus, neurodegenerative disorders (Parkinson’s disease-PD, Alzheimer’s disease-AD and Multiple sclerosis-MS), cardiovascular diseases (atherosclerosis and hypertension), respiratory diseases (asthma), cataract development, rheumatoid arthritis and in various cancers (colorectal, prostate, breast, lung, bladder cancers). This review deals with chemistry, formation and sources, and molecular targets of free radicals and it provides a brief overview on the pathogenesis of various diseased conditions caused by ROS/RNS.

Keywords: Free radicals, Reactive oxygen species (ROS), Reactive nitrogen species (RNS), Oxidative stress
  Forum: By Share Code

PunkassDerm
Posted on: Feb 27 2019, 12:24 AM


Group: Member
Posts: 509

Drop in unit price...I think would lead to wider acceptance by insurances. Would also allow 6 implants a year for EPP sufferers. Long run better for patients and stockholders.

Imagine the PR announcement..we want the people who need this drug to receive it, therefore we will capitulate to the evil insurers.
  Forum: By Share Code

PunkassDerm
Posted on: Feb 25 2019, 02:33 PM


Group: Member
Posts: 509

I don’t know any of this, simply asking why it’s crickets right now. Or has been at least.

Free Frilly
  Forum: By Share Code

PunkassDerm
Posted on: Feb 25 2019, 12:17 PM


Group: Member
Posts: 509

When CLVLY was a buck, it didn't seem to have crazy volume either. Except for a couple of occasions. But yes higher price less shares, in general.
  Forum: By Share Code

PunkassDerm
Posted on: Feb 25 2019, 06:09 AM


Group: Member
Posts: 509

Why is the volume for PTN so much higher than CLVLY while both poised for approval, both of new Melanocortin class? Still an exposure issue, PR issue? ASX vs US?
  Forum: By Share Code

PunkassDerm
Posted on: Feb 20 2019, 09:47 AM


Group: Member
Posts: 509

Last drop I believe was for the long delay and uncertainty. This time we have July 8 FDA decision date on the books. ASX 200 would be a nice prelude, early catalyst.

I get to to smirk as I drive off in a big smokey GT3 burnout, at the bozos who laughed at my 15 years sacrificed and invested.

Next to my smart smiling friends in their respective supercars!
  Forum: By Share Code

PunkassDerm
Posted on: Feb 19 2019, 06:51 AM


Group: Member
Posts: 509

If you shuffle the letters of Giles Delaney...does it spell Lord Voldemort?
  Forum: By Share Code

PunkassDerm
Posted on: Feb 16 2019, 01:43 PM


Group: Member
Posts: 509

Maybe announcement 1 week before inclusion? Its darn close either way! Like dividend record vs payment date.

....and you said that!
  Forum: By Share Code

PunkassDerm
Posted on: Feb 16 2019, 01:25 PM


Group: Member
Posts: 509

Last year March 18...it's the 8th this year?

EDIT:

https://www.marketindex.com.au/asx200

Could it be March 15? see link

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  Forum: By Share Code

PunkassDerm
Posted on: Feb 13 2019, 08:39 PM


Group: Member
Posts: 509

Nostalgic for a naturally aspirated combustion engine and manual transmission. I suppose I'll have to invest in algae biofuel next to stave off electric cars. Carbon sequestration in process, cleaner than batteries in the long run. Kinda carbon neutral.

If I must go electric (hybrid) I'd suffer with a 918 Spyder.
  Forum: By Share Code

PunkassDerm
Posted on: Feb 13 2019, 02:22 PM


Group: Member
Posts: 509

Who knows what tomorrow brings...and I have 200k+ shares to play with. Don't wanna be Smaug.
Grateful for an extremely long, finally rewarding run. Toys.
  Forum: By Share Code

PunkassDerm
Posted on: Feb 13 2019, 02:12 PM


Group: Member
Posts: 509

I'd say stem cell injections plus Scenesse or new topical formulation, there might be something there.
  Forum: By Share Code

PunkassDerm
Posted on: Feb 13 2019, 02:01 PM


Group: Member
Posts: 509

Little diversion:


I sold my first 5K shares today (CLVLY), right at opening for 16.50. First purchase in 2004, time to take some profit and have a little fun.
I hope everyone with skin in the game has a little guilty pleasure coming, especially those who have endured and sacrificed. Mine arrived on Saturday and oh she purrs. Wish I could post a video of the exhaust note.

Cheers,

PAD

PS And she's a 3 pedal, the only way to go!



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  Forum: By Share Code

PunkassDerm
Posted on: Feb 11 2019, 10:16 PM


Group: Member
Posts: 509

I dunno...maybe attempts to manipulate on message boards because lack of communication from corporate?

My guess still undervalued. What is the most recent research (reliable) target price? Makes me feel another breakout imminent.
Again, I am not a sophisticated investor but sounds like shorter speak?
  Forum: By Share Code

PunkassDerm
Posted on: Feb 4 2019, 01:59 PM


Group: Member
Posts: 509

Not sure if there was any more than a pilot study for acne, 3 patients. Acne Rosacea is a variant of acne. As an anti-inflammatory should help. But there are so many effective treatments out there. Isotretinoin can be curative in a 6 month course. There is no superior treatment for hidradenitis suppurativa (HS) though, maybe a more severe under-treated disease to focus on.

https://www.ncbi.nlm.nih.gov/pubmed/22845050

Beneficial effects of the melanocortin analogue Nle4-D-Phe7-α-MSH in acne vulgaris.
J Eur Acad Dermatol Venereol. 2014 Jan;28(1):108-11. doi: 10.1111/j.1468-3083.2012.04658.x. Epub 2012 Jul 27.


Böhm M1, Ehrchen J, Luger TA.

Abstract

BACKGROUND:
α-Melanocyte-stimulating hormone (α-MSH) is a melanocortin peptide that increases skin pigmentation during ultraviolet light-mediated tanning. As α-MSH has been shown to possess anti-inflammatory effects, we assessed the clinical potential of a superpotent α-MSH analogue, afamelanotide (Nle(4)-D-Phe(7)-α-MSH), in patients with acne vulgaris, the most common inflammatory skin disorder.

METHODS:
Afamelanotide (16 mg) was given in a phase II open-label pilot study subcutaneously as a sustained-release resorbable implant formulation to 3 patients with mild-to-moderate facial acne vulgaris. Evaluation included lesion count, adverse effects and patient-reported outcome. Monitoring of laboratory parameters included differential blood counts, electrolytes, urine analysis, and liver and kidney function tests. Skin melanin density was measured by reflectance spectrophotometry.

RESULTS:
The total number as well as the number of inflammatory acne lesions declined in all patients 56 days after the first injection of afamelanotide. Life quality as measured by Dermatology Life Quality Index likewise improved in all 3 patients 56 days after the first injection of afamelanotide. There were no adverse effects except mild and short-term fatigue in one patient. All patients experienced increased pigmentation especially on the face. Clinically relevant changes in laboratory parameters were not detected.

CONCLUSIONS:
Afamelanotide appears to have anti-inflammatory effects in patients with mild-to-moderate acne vulgaris. Future trials are needed to confirm the anti-inflammatory action of this melanocortin analogue in patients with acne vulgaris.
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PunkassDerm
Posted on: Feb 2 2019, 05:26 AM


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Just added some shares of PTN for shits n giggles, in case there is some major blockbuster there. I think i just started my own melanocortin SPDR/Hedge.
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PunkassDerm
Posted on: Feb 1 2019, 03:40 AM


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bremelanotide gets a focus page (5), afamelanotide gets another footnote.


https://www1.magellanrx.com/media/839400/mr...rx1119_0119.pdf


afamelanotide Clinuvel Erythropoietic porphyria Intradermal Submitted - NDA;
Fast Track; Orphan
Drug; Priority
Review
07/08/2019


bremelanotide AMAG Hypoactive sexual desire
disorder (premenopausal
women)
SC Submitted - NDA 06/21/2019




Women's Health
bremelanotide SC
AMAG


PROPOSED INDICATIONS
Hypoactive sexual desire disorder (HSDD) in premenopausal women

CLINICAL OVERVIEW
Bremelanotide is a melanocortin 4 receptor agonist that acts on the MC1 and MC4 receptors, which regulate
sexual behavior. Its proposed mechanism of action balances inhibitory and excitatory neural pathways in the
brain to restore sexual desire. Bremelanotide is intended to be used in anticipation of a sexual encounter.
Two pivotal, randomized, double-blind, placebo-controlled RECONNECT trials enrolled a total of 1,202
premenopausal women (≥ 18 years old; mean age 39 years) with HSDD and no psychological, gynecological,
or urological conditions suspected to contribute to the sexual dysfunction. In both trials, after 24 weeks of
treatment, bremelanotide demonstrated statistically significant improvement in desire, as measured by the
Female Sexual Function Index – Desire (FSFI-D) domain, and decrease in associated distress, as measured
by the Female Sexual Distress Scale – Desire/Arousal/Orgasm (FSDS-DAO) Desire score. While many
secondary endpoints were met and both studies reported improvement in the number of satisfying sexual
events (SSEs), the difference between bremelanotide and placebo in number of SSEs was not statistically
significant (64.4% versus 50.9% in Study 301 and 64.8% versus 47.3% in Study 302, respectively). The
most common adverse effects were transient mild nausea, flushing, and headache.
Bremelanotide was studied at a dose of 1.75 mg taken as-desired prior to a sexual encounter; no more
than 1 dose was taken every 24 hours. Bremelanotide was self-administered SC via an auto-injector.

PLACE IN THERAPY
HSDD is one facet of female sexual disorder. It occurs in approximately 5% to 13% of women, with a
peak incidence at around 40 to 60 years of age. In younger women, HSDD is frequently associated with
patient factors, such as dysfunctional relationships, chronic disease, depression, gynecologic disorders,
and use of certain medications (e.g., SSRIs). Diagnosis is usually made when symptoms cause distress or
negatively impact relationships.
Treatment of female sexual dysfunction should be individualized to address underlying physical,
psychological, and relational factors. It can include psychotherapy and pharmacotherapy (estrogen, shortterm testosterone, antidepressants [e.g., bupropion, SSRI]). However, currently available pharmacologic
therapies for female sexual dysfunction have limited efficacy and are associated with side effects and
potential risks. The only FDA-approved medication for HSDD in premenopausal women is the oral oncedaily serotonin agonist/antagonist, flibanserin (Addyi®). Flibanserin is taken at bedtime due to its sedative
affects and carries boxed warnings for alcohol consumption, hypotension, and syncope.
If approved, bremelanotide, a first-in-class melanocortin agonist, will provide a new mechanism and route
of administration to treat HSDD in premenopausal women. Unlike flibanserin, it is administered on an asdesired basis and can be safely used concurrently with alcohol.

FDA APPROVAL TIMELINE
June 21, 2019
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PunkassDerm
Posted on: Jan 28 2019, 10:35 AM


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Posts: 509

I guess it can...and Scenesse can provide sufferers the independence to stay off of disability benefits (be productive members of society, dignity).

https://www.disabilitybenefitshome.com/disa...ility-benefits/


Winning SSDI or SSI for Porphyrias

Regardless of your health condition, the SSA will first determine whether a claimant meets the nonmedical requirements of SSI or SSDI. For SSDI this means the claimant will need to have sufficient work credits to be considered insured, and their condition must be expected to last for 12 continuous months. For SSI the claimant must be aged, blind or disabled and not be able to work for at least 12 continuous months. Additionally, they must meet the income and resource limitations of the SSI program.

Determining disability status for SSDI and SSI for Porphyrias

The Social Security Administration has two methods of determining whether a claimant is disabled: is there condition and corresponding symptoms listed in the SSA Listing of Impairments (or does it “meet or exceed” a listing) or do they have the residual capacity to work (this consideration is made through a medical vocational allowance).

There are several listings for porphyrias, and the listing which is used to evaluate your condition will depend on the type of porphyria. For instance, familial porphyria or erythropoietic protoporphyria are considered photosensitive disorders and can be evaluated under 8.0 Skin Disorders, Section 8.07 Genetic Photosensitive Disorders.

Under this listing the SSA will determine if your condition has caused “extensive skin lesions that have lasted or can be expected to last for a continuous period of at least 12 months or you do not have the ability to function outside of a “highly protective environment for a continuous period of at least 12 months.”

Other acute porphyrias which cause seizures or paralysis can be evaluated under separate listings which correspond to your symptoms. For instance, if you are experiencing seizures you may meet or exceed a listing under 11.00 Neurological.

Winning SSDI or SSI through a medical vocational allowance

If your condition does not meet or exceed a listing you will need sufficient evidence to prove you do not have the residual capacity to work. Through the medical vocational allowance process, the SSA will review your medical records and work history and determine whether you can continue to work your current job, previous job or retrain for new work given your age, education, work history, and health condition.
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PunkassDerm
Posted on: Jan 20 2019, 01:32 PM


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Posts: 509

Maybe transition to cosmetics / regenerative medicine. Stem cells and MSH.

Cure HPV (warts), non-melanoma skin cancer and acne....we would be twiddling thumbs in derm.
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PunkassDerm
Posted on: Jan 20 2019, 12:38 PM


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Still in infancy, how many GI absorption peptides are currently on market? How far off?

I'm still waiting for my safe tan anti-inflammatory drug.

Totally ready to retire at 200/share. But I'll take 300.
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PunkassDerm
Posted on: Jan 20 2019, 11:23 AM


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Posts: 509

Seems purposefully vague. The intention to monopolize an entire class without actually have a drug? Would this sort of patent have any teeth legally? I nothing of drug patents.

Claiming a patent for every variant of a structure.
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PunkassDerm
Posted on: Jan 20 2019, 07:54 AM


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Posts: 509

That's why I saw a study co-administered with a PPI. Already an issue. Thanks! Gotta take a second med just for absorption?

Oh wait...they could use cimetidine.
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PunkassDerm
Posted on: Jan 20 2019, 05:47 AM


Group: Member
Posts: 509

See disclosures at the end...This is race, and they better speed it up.


https://www.medpagetoday.com/dermatology/ge...rmatology/52419


Novel Drug Works for Photosensitivity
Side effect profile acceptable


by Kay Jackson, Contributing Writer, MedPage Today
July 02, 2015

Action Points
The alpha-melanocyte-stimulating hormone analogue, afamelanotide, appears to be safe and efficacious in the treatment of erythropoietic protoporphyria -- the rare condition whose sufferers become people of the night.
Afamelanotide had an acceptable side-effect and adverse-event profile and improved the quality of life for patients with this severe photodermatitis, allowing them to tolerate more sun exposure without pain due to phototoxicity, Robert J. Desnick, PhD, MD, of the department of genetics and genomic sciences, Icahn School of Medicine at Mount Sinai, New York, NY, and colleagues reported in two studies published in the New England Journal of Medicine. "The main results, which were concordant and consistent across the two trials, indicated that afamelanotide was safe and effective," said the researchers.

Prior to this, there was no effective treatment for erythropoietic protoporphyria, noted Desnick. "Although several treatments, including beta carotene, N-acetyl-L-cysteine, and vitamin C, have been described in the literature, a systematic review of more than 20 studies showed little to no benefit," he said.
"For the first time, there is a treatment (afamelanotide) that results in improvement of quality of life of patients with erythropoietic protoporphyria," Henry W. Lim, MD, Chairman, department of dermatology at Henry Ford Hospital, Detroit, MI, told MedPage Today. Lim was also a co-investigator in the study.


The study was funded by Clinuvel Pharmaceuticals; ClinicalTrials.gov numbers, NCT01605136 and NCT00979745, a grant from the National Institutes of Health (NIH) (R15 HL 117199), and an NIH Career Development Award (K23 DK095946).

Desnick reported consulting fees from Alnylam and Recordati Rare Diseases and grant support and stock options from Alnylam and a pending patent related to the treatment of acute hepatic porphyrias (13/835,613).

Lim has received consulting fees from Ferndale Laboratories, Uriage, Sanofi, and Johnson & Johnson, and grant support from Ferndale Laboratories and Estee Lauder.

Co-investigators also reported relationships with Mitsubishi Tanabe, Allergan, Orphan Europe and Orion Pharma.
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PunkassDerm
Posted on: Jan 20 2019, 05:42 AM


Group: Member
Posts: 509

Was going to say same thing. Like insulin, a peptide cannot be delivered PO (per os) or by oral route.

1. Peptides are fragile, need to be injectable or transdermal, also good call.
2. I think it's now well known side effects profile better with the tapered intermittent dose, depo. SAFETY!!!
3. See above, plus ensures patient compliance to regimen.
4. In office administration, measure of control and compliance. Ensures all metric monitored to receive dose.
5. There are many injected drugs:
insulin
all biologics by nature are monoclonal antibodies and are injected
birth control
oncology, nearly all new immunotherapies are injectables or infusions (PO peptides it appears will be far off and not available for every sequence)
6. MT-7117 still makes you tan, and efficacy is unknown
7. Higher potential for cosmetic "abuse" with a self administered pill.


I cannot find information on pharmacokinetics or mechanism of action (or even confirm a melanocortin), but Mitsubishi has had its fingers in Clinuvel trials through investigators.
Also not against oral medications, but it seems FDA liked the idea of control by SQ administration.


Lastly I would not feed the animals (or Iggiots). Keloids from large bore needle? Infection? Unless Iggy was personally administering the drug I would not worry.
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PunkassDerm
Posted on: Jan 17 2019, 09:27 AM


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Posts: 509

First step to auto-photoprotection and DNA repair...

What happens if Key West bans some sunscreens? Depends on where you stand
BY GWEN FILOSA
JANUARY 14, 2019 12:47 PM

https://www.miamiherald.com/news/local/comm...e224135955.html


Key West city leaders on Tuesday will consider a proposal to ban the sale of certain sunscreens that contain two ingredients some scientists and activists say are harming the coral reef.

But the sunscreen industry and some doctors are fighting back, saying those two ingredients at issue, oxybenzone and octinoxate, prevent skin cancer and that without them skin cancer rates will rise dramatically. Banning them won’t save the reef, they say.

“Coral reefs have been disappearing for 50 years; these sunscreens have been around 25 years,” said Dr. Andy Weinstein, president of the Florida Society of Dermatology and Dermatologic Surgeons.

Weinstein, who sees about 8,000 cases of skin cancer at his small office in Boynton Beach, notes that those two ingredients are what make it possible to produce sunscreens with SPF percentages of 40 to 60.


“There’s no question that the skin cancer rates would increase in those who don’t have access to these sunscreens,” Weinstein said. “There will be fewer people using sunscreen in Key West. You’re going to have some finite increase in the rate of skin cancer.”

The Key West City Commission will take a first look and vote on the issue Tuesday during its 6 p.m. meeting at City Hall. A second vote at a future meeting is required to make it a law, punishable by a $100 fine.

If approved, the law wouldn’t go into effect for a year, giving retailers time to phase out the targeted sunscreens. After that, it will cost them $100 a sale if they deviate from the ordinance.


The issue could turn into an emotional fight Tuesday evening.

Reef Relief, a Keys environmental protection nonprofit group, has been rallying local people to show up in support of the sunscreen ban.

They believe Craig Downs, a scientist whose peer-reviewed study published in 2015 in the Archives of Environmental Contamination and Toxicology, showed oxybenzone was harmful to the reef. He helped inspire a similar ban by Hawaii, passed earlier this year.

Downs told the City Commission during a first discussion last month, “We’re not seeing new coral. Ninety-nine percent of Florida Keys coral coverage has disappeared in the last 50 years. You lose that last one percent, you’ve got nothing.”

One Florida dermatologist, who is also a Ph.D scientist, says he supports the ban on sunscreen containing the two ingredients. He said that sunscreen is only one layer of protection from the sun, along with clothing and sun shades.

“This proposed ordinance will not prevent people from being able to protect themselves,” said Dr. John Strasswimmer, a research professor of biochemistry and a clinical professor of dermatology at Florida Atlantic University in Boca Raton. “If the ordinance goes into effect, people will still have a very good choice of environmentally friendly sunscreen available.”

Strasswimmer believes the chemical-based sunscreens with oxybenzone are harmful to the reef. As a scuba diver, he is concerned about the effects of sunscreen chemicals on the reef.

He prefers a mineral-based sunscreen, ones with zinc or titanium. The problem is, he sometimes travels to places where he doesn’t have an option.

“I always reach for a mineral sunscreen, that’s my personal preference,” Strasswimmer said. But often, when he takes flights, he can’t bring his own and sometimes has to settle for chemical-based sunscreens. “I use that when need be,” he said.

The pro-ban science is like going out on a limb, Weinstein said.


“Other researchers aren’t necessarily aligned with his perspective,” Weinstein said. “The last thing we want is a public health crisis being caused by bad environmental research. “
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PunkassDerm
Posted on: Jan 16 2019, 09:51 AM


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Posts: 509

I think the cost per implant will prevent off label use, unless good research supports otherwise (and insurance allows). Like HHD, XP other porphyrias. Maybe vitiligo ahead of approval.
Other question...will the instos jump back in until next plateau?
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PunkassDerm
Posted on: Jan 10 2019, 10:51 AM


Group: Member
Posts: 509

Thank God, I'm ready to take some profit no matter what.

I caved and bought my GT3 this week, get busy living or get busy dying Andy Dufresne.
Nice metal roof for the house forever in renovation.

And some relief for the shadow jumpers.
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PunkassDerm
Posted on: Jan 2 2019, 10:07 AM


Group: Member
Posts: 509

Unless that's a puka shell necklace and not a vitiligo patch. Hard to tell, quite linear.
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PunkassDerm
Posted on: Jan 2 2019, 08:35 AM


Group: Member
Posts: 509

Face responds best to treatment, that may be why.
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PunkassDerm
Posted on: Dec 20 2018, 03:30 AM


Group: Member
Posts: 509

https://seekingalpha.com/news/3418194-clinu...arkening-effect


Clinuvel Pharma's afamelanotide shows positive effect in vitiligo study but skin darkening effect dampens recruitment
Dec. 19, 2018 10:42 AM ET|


A Phase 2 clinical trial evaluating Aussie drugmaker Clinuvel Pharmaceuticals' (OTCPK:CLVLY) SCENESSE (afamelanotide) plus ultraviolet B therapy in Asian patients with a skin discoloration disorder called vitiligo showed a positive effect in restoring pigmentation.

Skin darkening during treatment prompted the withdrawal of three participants (out of 21) and has hampered recruitment since this population considers it undesirable.

The company is assessing its options for future labeling, possibly refining suitable patients to those with a loss of pigmentation of at least 10% of their body surface area. Patients with more modest disease, less than 2% of their body surface area, may prefer topical therapy.

Clinical trials in North America are being planned.
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PunkassDerm
Posted on: Dec 3 2018, 01:26 AM


Group: Member
Posts: 509

Boards tomorrow and taking a break from cramming, thinking of Parkinson's, a horrible disease for the individual and family. No good treatment, hopes to slow with dopamine agonists and control symptoms. The dopamine centers in the substantial nigra are subject to degradation in this disease, dark structures pigment originally termed neuromelanin (by appearance) but turns out structurally composed of true melanin compounds. Just look at the loss of pigment in the substantial nigra below, that occurs with the progression of PD. THEN the link between PD and Melanoma. MSH may again serve as a free radial scavenger to protect these dopamine producing cells, protecting from degradation. This blows my mind.

I am increasingly frustrated with Clinuvel, but hope to bloody hell there is a larger plan to explore/treat/capitalize on these neurodegenerative diseases. Give me something, do your #^%#$% jobs.



Attached Image




Substantia nigra neuromelanin: structure, synthesis, and molecular behaviour
L Zecca, D Tampellini, M Gerlach, P Riederer, R G Fariello, and D Sulzer
Mol Pathol. 2001 Dec; 54(6): 414–418.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1187132/


Abstract

The pigmented neurones of the substantia nigra are typically lost in Parkinson's disease; however, the possible relation between neuronal vulnerability and the presence of neuromelanin has not been elucidated. Early histological studies revealed the presence of increasing amounts of neuromelanin in the substantia nigra with aging in higher mammals, showed that the neuromelanin granules are surrounded by a membrane, and comparatively evaluated the pigmentation of the substantia nigra in different animal species. Histochemical studies showed the association of neuromelanin with lipofuscins. However, systematic investigations of the structure, synthesis, and molecular interactions of neuromelanin have been undertaken only during the past decade. In these later studies, neuromelanin was identified as a genuine melanin with a strong chelating ability for iron and an affinity for compounds such as lipids, pesticides, and MPP+. The affinity of neuromelanin for a variety of inorganic and organic toxins is consistent with a postulated protective function for neuromelanin. Moreover, the neuronal accumulation of neuromelanin during aging and the link between its synthesis and a high cytosolic concentration of catechols suggest a protective role. However, its putative neuroprotective effects could be quenched in conditions of toxin overload.
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PunkassDerm
Posted on: Dec 3 2018, 12:51 AM


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The melanoma‐linked “redhead” MC1R influences dopaminergic neuron survival

Xiqun Chen MD, PhD Hongxiang Chen MD, PhD Waijiao Cai MD, PhD Michael Maguire MS Bailiu Ya MD, PhD Fuxing Zuo MD, PhD Robert Logan MS Hui Li MD, PhD Katey Robinson PhD Charles R. Vanderburg PhD Yang Yu PhD Yinsheng Wang PhD David E. Fisher MD, PhD Michael A. Schwarzschild MD, PhD
First published: 26 December 2016 https://doi.org/10.1002/ana.24852


https://onlinelibrary.wiley.com/doi/full/10.1002/ana.24852


Abstract

Objective

Individuals with Parkinson disease are more likely to develop melanoma, and melanoma patients are reciprocally at higher risk of developing Parkinson disease. Melanoma is strongly tied to red hair/fair skin, a phenotype of loss‐of‐function polymorphisms in the MC1R (melanocortin 1 receptor) gene. Loss‐of‐function variants of MC1R have also been linked to increased risk of Parkinson disease. The present study is to investigate the role of MC1R in dopaminergic neurons in vivo.

Methods

Genetic and pharmacological approaches were employed to manipulate MC1R, and nigrostriatal dopaminergic integrity was determined by comprehensive behavioral, neurochemical, and neuropathological measures.

Results

MC1Re/e mice, which carry an inactivating mutation of MC1R and mimic the human redhead phenotype, have compromised nigrostriatal dopaminergic neuronal integrity, and they are more susceptible to dopaminergic neuron toxins 6‐hydroxydopamine and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP). Furthermore, a selective MC1R agonist protects against MPTP‐induced dopaminergic neurotoxicity.

Interpretation

Our findings reveal a protective role of MC1R in the nigrostriatal dopaminergic system, and they provide a rationale for MC1R as a potential therapeutic target for Parkinson disease. Together with its established role in melanoma, MC1R may represent a common pathogenic pathway for melanoma and Parkinson disease. Ann Neurol 2017;81:395–406
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PunkassDerm
Posted on: Dec 3 2018, 12:48 AM


Group: Member
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Parkinson’s Disease and Melanoma: Co-Occurrence and Mechanisms
Journal of Parkinson's Disease, vol. 8, no. 3, pp. 385-398, 2018
Authors: Bose, Aninditaa; * | Petsko, Gregory A.a | Eliezer, Davidb


https://content.iospress.com/articles/journ...sease/jpd171263

Abstract

Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by loss of dopaminergic neurons in the substantia nigra pars compacta, depletion of dopamine in the striatum and the presence of Lewy bodies. Cancer is uncontrolled growth of cells in the body and migration of these cells from their site of origin to other parts of the body. PD and cancer are two opposite diseases, one arising from cell proliferation and the other from cell degeneration. This fundamental difference is consistent with inverse comorbidity between most cancers and neurodegenerative diseases. However, a positive association of PD and melanoma has been reported which has recently become of significant interest. A link between PD and cancer has been supported by many epidemiological studies, most of which show that PD patients have a lower risk of developing most cancers than the general population. However, the mechanisms underlying this epidemiological observation are not known. In this review we focus on epidemiological studies correlating PD and melanoma and the possible mechanisms underlying the co-occurrence of the two diseases. We explore possible explanations for the important observations that more PD patients develop melanoma that would otherwise be expected and vice-versa.
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PunkassDerm
Posted on: Oct 31 2018, 05:22 AM


Group: Member
Posts: 509

Or convert shares at a premium fee.
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PunkassDerm
Posted on: Oct 30 2018, 10:44 PM


Group: Member
Posts: 509

Could you get in with 1 share? International platform like Scottrade, purchase 1 CUV? For them to exclude shows devious intent.
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PunkassDerm
Posted on: Oct 30 2018, 06:51 AM


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Posts: 509

Needs a 😂 button!
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PunkassDerm
Posted on: Oct 30 2018, 03:49 AM


Group: Member
Posts: 509

1. Donate to APF, check.

2. Write to my congressman/women, now check.
Just made request for civil discourse and bipartisan cooperation. That healthcare is difficult mostly to providers.
And to look into FDA obfuscation/obstruction of the afamelanotide application.

US holders may request the same of their representatives.
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PunkassDerm
Posted on: Oct 30 2018, 12:13 AM


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Posts: 509

Where is FDA status update? Even a definite delay would go further to stop the bleeding than nothing. Or this BS lab expansion.

Also very comical Lachlan Hay email is listed. Does anyone receive a reply from Clinuvel?
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PunkassDerm
Posted on: Oct 29 2018, 10:17 AM


Group: Member
Posts: 509

What makes me upset is the reality...

delay delay delay, no news and delay some more. Wolgen pays himself. Rinse and repeat.

Is that announcement actual news?
Whats happening with FDA application?
Cosmetic line?
How about Vitiligo results/direction?
New indication identified?

Equally as fatigued after almost a decade and a half. I said before SP heals all wounds, well direct relationship up and down.
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PunkassDerm
Posted on: Oct 28 2018, 08:15 AM


Group: Member
Posts: 509

Reading for my recertification exam and came across ACTH as a treatment for gout.
Along with RA and PsA, melanocortin class as tx for inflammatory arthritis is solid.
It appears they are the keys to the cytokines, master-regulators up and down.


Now who is blocking the first FDA approval of a Melanocortin? Or who is pulling the marionette strings of FDA bozos?
Or inept Wolgen?

Just wanted to break the deafening silence.
Watch Haunting of Hill house. Ghosts come in many forms.



https://www.ncbi.nlm.nih.gov/m/pubmed/19814819/

Melanocortin peptides inhibit urate crystal-induced activation of phagocytic cells.

Abstract

INTRODUCTION: The melanocortin peptides have marked anti-inflammatory potential, primarily through inhibition of proinflammatory cytokine production and action on phagocytic cell functions. Gout is an acute form of arthritis caused by the deposition of urate crystals, in which phagocytic cells and cytokines play a major pathogenic role. We examined whether alpha-melanocyte-stimulating hormone (alpha-MSH) and its synthetic derivative (CKPV)2 influence urate crystal-induced monocyte (Mo) activation and neutrophil responses in vitro.

METHODS: Purified Mos were stimulated with monosodium urate (MSU) crystals in the presence or absence of melanocortin peptides. The supernatants were tested for their ability to induce neutrophil activation in terms of chemotaxis, production of reactive oxygen intermediates (ROIs), and membrane expression of CD11b, Toll-like receptor-2 (TLR2) and TLR4. The proinflammatory cytokines interleukin (IL)-1beta, IL-8, and tumor necrosis factor-alpha (TNF-alpha) and caspase-1 were determined in the cell-free supernatants. In parallel experiments, purified neutrophils were preincubated overnight with or without melanocortin peptides before the functional assays.

RESULTS: The supernatants from MSU crystal-stimulated Mos exerted chemoattractant and priming activity on neutrophils, estimated as ROI production and CD11b membrane expression. The supernatants of Mos stimulated with MSU in the presence of melanocortin peptides had less chemoattractant activity for neutrophils and less ability to prime neutrophils for CD11b membrane expression and oxidative burst. MSU crystal-stimulated Mos produced significant levels of IL-1beta, IL-8, TNF-alpha, and caspase-1. The concentrations of proinflammatory cytokines, but not of caspase-1, were reduced in the supernatants from Mos stimulated by MSU crystals in the presence of melanocortin peptides. Overnight incubation of neutrophils with the peptides significantly inhibited their ability to migrate toward chemotactic supernatants and their capacity to be primed in terms of ROI production.

CONCLUSIONS: Alpha-MSH and (CKPV)2 have a dual effect on MSU crystal-induced inflammation, inhibiting the Mos' ability to produce neutrophil chemoattractants and activating compounds and preventing the neutrophil responses to these proinflammatory substances. These findings reinforce previous observations on the potential role of alpha-MSH and related peptides as a new class of drugs for treatment of inflammatory arthritis.

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PunkassDerm
Posted on: Oct 22 2018, 01:07 AM


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Posts: 509

OUTRAGE or JUST PLAIN RAGE
...Wolgen, Desiree and everyone involved should be breaking down the doors of the FDA. How is this balanced?
This is big pharma lobby at it pinnacle, corruption


https://www.rollingstone.com/culture/cultur...-opioid-744475/


FDA Could Approve Opioid 10 Times Stronger Than Fentanyl

This week, an FDA panel voted 10-3 to recommend approval for a new fast-acting form of an opioid drug that’s 10 times more potent than fentanyl.
Opioid overdose is the leading cause of death for Americans under the age of 50, with the sharpest increase in overdose deaths in 2017 connected to fentanyl and other synthetic opioids. Fentanyl — a highly regulated prescription drug that has been extensively counterfeited in recent years — is extremely dangerous because it’s much stronger than heroin, so drug users who either don’t realize the substance they’re using is cut with fentanyl, or don’t anticipate such a strong effect, can easily overdose.
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PunkassDerm
Posted on: Oct 20 2018, 08:29 AM


Group: Member
Posts: 509

Not quite...

But I do have the farm bet on it, also “all in” club. Adding since April 2004.

Id like my own Wolgen Tan someday, with a slight green glow
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PunkassDerm
Posted on: Oct 20 2018, 07:58 AM


Group: Member
Posts: 509

I've also seen in practice, 5-10 cases of both Darier's and HHD. Never XP. Japan is that market no?
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PunkassDerm
Posted on: Oct 20 2018, 07:52 AM


Group: Member
Posts: 509

CLVLY dividend breakdown... 0.01412/share with fees and taxes withheld


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PunkassDerm
Posted on: Oct 20 2018, 07:42 AM


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Novel idea to pursue simultaneously...walk AND chew gum

...instead of a .02 dividend
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PunkassDerm
Posted on: Oct 20 2018, 07:40 AM


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After a couple of indications, hopefully will simply be approved by insurances off indication with some good study evidence. No need to gain approval over and over?

or label extension/new indication to be much faster with safety data established?


https://www.sciencedirect.com/science/artic...149291813001768


Conclusions

Development of and regulatory approval for new uses of already-approved drugs and biologics is an important source of innovation by biopharmaceutical firms. Despite rising development costs, the output of new-use approvals has remained stable in recent years, driven largely by the pursuit of new pediatric indications. FDA approval-phase times have generally declined substantially for all types of applications since the mid-1990s following legislation that provided a new source of income for the agency. However, while the resources needed to review supplemental applications are likely lower in general than for original-use approvals, the approval-phase times for important new uses are no lower than for important original-use applications.
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PunkassDerm
Posted on: Oct 20 2018, 03:38 AM


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Isn’t HHD already in phase II, with known excellent response? I’d love to see both, but HHD seems further along.

Everything with Clinuvel is conjecture, maybe strategically important in this case to keep quiet until well underway.
We are the ginger bastard stepchildren of Dr Wolgen. IMHO BTW, who is either on Senesse himself or is not working hard enough to have a tan like his. What bets you say he is also a client/patient?
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PunkassDerm
Posted on: Oct 20 2018, 02:11 AM


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I’m hoping HHD, appears to control an uncontrollable disease. Genetic condition. Money on dat


http://www.orphan-drugs.org/2014/02/10/pha...ease-commences/

Hailey-Hailey Disease

Hailey-Hailey Disease (HHD, also known as familial benign chronic pemphigus) is a rare, lifelong, inherited disorder where epidermal skin cells (keratinocytes) cannot properly adhere. This causes periodic eruption of plaque-like lesions, blisters and ulcerations on areas where skin folds (flexural), often on the neck, armpits or groin. Most patients have permanent lesions. HHD usually appears in the third or fourth decade of life.

HHD is passed on as a dominant trait (autosomal dominant). In approximately 70% of all patients a positive family history can be traced. Mutations in the ATP2C1 gene (localised on chromosome 3q21-q24), encoding the Golgi secretory pathway calcium pump (Ca2+-dependent ATPase), impair epidermal keratinocyte adhesion.

....In 2012, the first proof of concept open-label pilot study of afamelanotide in HHD was carried out in two female patients (age 53 and 61). At the time of the start of the study, the patients both had existing skin lesions and ulcerations which had been present since their adolescent years.

Following afamelanotide treatment, the lesions began to visibly decrease in size and totally disappeared by day 60. The clinical remission was also reflected by an improved QOL measured by the Medical Outcome Survey Short-Form 36 (SF-36). No adverse reactions were reported. Both patients experienced moderate skin tanning, as expected on the basis of the secondary pharmacology of SCENESSE®. Disease recurrence was only seen in the patients eight months after completion of the treatment (Biolcati et al., 2013). By comparison, only few complete or partial remissions are reported in the literature.

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PunkassDerm
Posted on: Oct 16 2018, 02:40 AM


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Personal note from Desiree and from her staff. If you want know what she thinks about afamelanotide, please donate yourself.
She is amazing and such an advocate, works so hard for EPP.
When we hit it big time, I pledge to increase that donation. Selfish feel good.

I think she is by far, a stronger influence on FDA than Wolgen could ever be.
...altruistically and in practice
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PunkassDerm
Posted on: Oct 14 2018, 03:39 AM


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C/O ShareScene PAD

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PunkassDerm
Posted on: Oct 14 2018, 03:19 AM


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totally odd. has exchange rate changed drastically?
Mine was on TD Ameritrade, my broker. Seems like a heavy hit for a fee.
Fixed at record date or fluid until payout?

Still pennies, I'm waiting for SP30USD
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PunkassDerm
Posted on: Oct 14 2018, 03:07 AM


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Looks same to me: 0.0141
simple exchange

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PunkassDerm
Posted on: Oct 10 2018, 01:24 PM


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Dramatic

The other cream is Efudex-Carac-5FU or 5-fluorouracil.

It works great and its cheap.
You can titrate dosing and use in smaller quadrants to control downtime.
You can dilute with moisturizer.
See below, lower micronized version with less irritation.
You can take off the panties and take your medicine. Jest of course.

BTW, I've seen the worst inflammatory responses with imiquimod (Aldara/Zyclara) resulting in scarring hypopigmentation.
It's all about using with common sense. Which also means a few extra minutes counseling patients, and showing them the raw hamburger picks so they don't go there.


There are bigger fish to fry, 5FU is an effective treatment for AK, doubtful will ever get the indication. Plus AKs are acquired, you earned them!
Same with PMLE, wasted resources exploring.

In all seriousness Efudex works awesome, I put that shit on everything.


I also truly believe in cost/efficacy. If there is something effective and cheap, I prefer it. EPP, Vitiligo, HHD are all needy indications and worthy of afamelanotide.
Photoprotection some day...when the price goes down. That will be golden.


Cutis. 2002 Aug;70(2 Suppl):22-9.
Effective treatment of actinic keratosis with 0.5% fluorouracil cream for 1, 2, or 4 weeks.

Weiss J1, Menter A, Hevia O, Jones T, Ling M, Rist T, Roberts J, Shavin JS, Sklar J, Webster G, Connolly M, Furst K, Levy S.

Abstract
New therapeutic options would benefit patients with actinic keratosis (AK), a precancerous condition that is a significant health concern. The efficacy and safety of a microsphere-based formulation of 0.5% fluorouracil cream were evaluated in a randomized, double-blind, multicenter, parallel-group study. Patients (N= 177) were randomized to receive 0.5% fluorouracil or vehicle once daily for 1, 2, or 4 weeks. Efficacy was assessed by lesion counts and clearance. Safety was evaluated by monitoring adverse events, including facial irritation. Significant improvements were seen from baseline to posttreatment follow-up in all efficacy variables for all fluorouracil regimens compared with vehicle. Patients treated for one week experienced significant improvements compared with vehicle, although efficacy increased with increasing treatment duration. Most patients experienced mild to moderate facial irritation of predictable onset and duration. Once-daily administration of 0.5% fluorouracil cream for 1, 2, or 4 weeks is safe and effective for the treatment of AKs.
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PunkassDerm
Posted on: Oct 9 2018, 01:17 AM


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CLVLY holders:

Ex-dividend date - September 20, 2018
Amount - $0.0143
Record date - September 21, 2018
Pay date - October 18, 2018

I forgot about the exchange rate, my enthusiasm wanes.
Above from my on-line broker account.
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PunkassDerm
Posted on: Oct 8 2018, 11:48 PM


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I bet its multifactorial:

FDA dragging feet
Worried about tan as side effect, agree duh its a benefit
Lobby from large pharma, money corrupts the poor regulators
Clinuvel mis-management. Though they may have a great big picture, it is a company learning on the fly. Ego-driven CEO
See above, study design and inability the multitask FDA/EMA/marketing/roll-out

Recruit good help to navigate
Or Partner with big Pharma
Or be acquired by Allergan



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PunkassDerm
Posted on: Oct 8 2018, 11:41 PM


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I also think ambulance chasing lawyers jump on every freaking medication/implant/procedure. Sick of the commercials for EVERYTHING MEDICAL.

Every medication has side effects, finasteride clearly lists impotence as a side effect. BPH itself can cause ED.

I was also on Finasteride for both BPH and to help maintain an early receding hairline. I took 1.25mg every other day for 2 years. Didn't seem to help my GU symptoms too much and I stopped. Mostly noticed an increase in energy within 2-3 weeks, so it was bogging me down. I think slamming finasteride is a bit much though, works for many although not me. Karma is a bitch, the lawyers and greedy people looking for a payday will go after every medication. People choose to take these meds and side effects are inevitable, as long as they are disclosed it is the choice of the patient and provider to make together.

Safety profile for afamelanotide appears stellar, I would stick to that instead. Life is a series of choices. Patients should also take some responsibility for outcomes.


Soft finasteride suffers should pop a little blue pill and move on. General health and lifestyle isn't figured into these things either.
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PunkassDerm
Posted on: Oct 8 2018, 10:31 PM


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Before male pattern alopecia, finasteride approved for BPH (swelling of prostate).


Hopefully we follow suit:


MEDICINES EVOLVED TO MAKE YOU BEAUTIFUL, LABEL EXTENSIONS/NEW INDICATIONS

Minoxidil: Hypertension > Pattern Alopecia (Rogaine)

Botox: Blepharospasm > rhytides, migraines, bladder spasticity, hyperhidrosi, upper and lower limb spasticity

Bimatoprost (latisse): Glaucoma > Hypotrichosis eyelashes, soon pattern alopecia and testing for vitiligo

HA (hyaluronic acid): Eye surgery adjuvant (1970's) > atopic dermatitis, osteoarthritis, artificial tears, dermal fillers (Restylane, Juvederm etc)

Tretinoin: Acne > Rhytides and anti-aging (Retin-A)

Stem cell Therapies: Leukemia (1950s) > 1997 sheep Dolly cloned, joint repair, tendon repair, regenerative medicine (anti-aging) still evolving, possibly dementia and autism, ?cure for diabetes


personal note: I just had umbilical cord mesenchymal cells injected into my achilles and IV push, to extend my running life. Outcome pending.


And finally...

AFAMELANOTIDE: EPP > All porphyrias, HHD, XP, vitiligo, solar urticaria, photoprotection, premature graying, tan, lupus, dementia, MS, antibiotic synergist, arthritis, psoriasis, HS, acne, rosacea, atherosclerosis, stroke, RA, stroke, IBS, vasculitis, ARS, ischemia/shock, organ transplantation, ?melanoma through DNA repair...

and the beat goes on, the beat goes on
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PunkassDerm
Posted on: Oct 7 2018, 08:27 AM


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Looks like Uhoh has already chimed in on this molecule:


https://groups.google.com/forum/#!msg/c...H4/R8vmiusQCQAJ

My thought is there is a niche to fill, not that it is an absolute competitor. What happened to cosmetic product line announcement?
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PunkassDerm
Posted on: Oct 7 2018, 02:14 AM


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http://lucasmeyercosmetics.com/en/products...5&from=name


Melitaneâ„¢
Healthy Glow

Origin

α-MSH biomimetic peptide

INCI Name

Glycerin (and) Water (and) Dextran (and) Acetyl Hexapeptide-1

Mode of Action

Agonist of α-MSH
Stimulates melanin synthesis
Properties

Strengthens the natural skin photoprotection
Reduces skin erythema and soothes sun-ravaged skin
Limits photoaging and premature aging
Enhance skin pigmentation
Dosage

0.5-5%

In vitro
Ex vivo
Clinical
Applications

Hair Care
Soothing / Sensitive Skin
Sunless Tanning / Tan Accelerator / Sun Care
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PunkassDerm
Posted on: Oct 7 2018, 02:02 AM


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Another obvious target I have not seen a lot about, but on my mind. Worrying and aging while waiting for Clinuvel has grayed me prematurely. Turn back the Wolgen clock.

For implant or lotion or shampoo?

Canities - Graying

Allergan competitor or acquisition, either fantastic with me.


https://www.ncbi.nlm.nih.gov/pubmed/30222197


Efficacy of an agonist of α-MSH, the palmitoyl tetrapeptide-20, in hair pigmentation.
Int J Cosmet Sci. 2018 Sep 17. doi: 10.1111/ics.12494.

Almeida Scalvino S1, Chapelle A2, Hajem N3, Lati E1, Gasser P1, Choulot JC3, Michel L4, Hocquaux M5, Loing E6, Attia J5, Wdzieczak-Bakala J2.


OBJECTIVE:
Hair greying (i.e., canities) is a component of chronological aging and occurs regardless of gender or ethnicity. Canities is directly linked to the loss of melanin and increase in oxidative stress in the hair follicle and shaft. To promote hair pigmentation and reduce the hair greying process, an agonist of α-melanocyte-stimulating hormone (α-MSH), a biomimetic peptide (palmitoyl tetrapeptide-20; PTP20) was developed. The aim of this study was to describe the effects of the designed peptide on hair greying.

METHODS:
Effect of the PTP20 on the enzymatic activity of catalase and the production of H2 O2 by Human Follicle Dermal Papilla Cells (HFDPC) was evaluated. Influence of PTP20 on the expression of melanocortin receptor-1 (MC1-R) and the production of melanin were investigated. Enzymatic activity of sirtuin 1 (SIRT1) after treatment with PTP20 was also determined. Ex vivo studies using human micro-dissected hairs allowed to visualise the effect of PTP20 on the expression in hair follicle of catalase, TRP-1, TRP-2, Melan-A, ASIP and MC1-R. These investigations were completed by a clinical study on 15 human male volunteers suffering from premature canities.

RESULTS:
The in vitro and ex vivo studies revealed the capacity of the examined PTP20 peptide to enhance the expression of catalase and to decrease (30%) the intracellular level of H2 O2 . Moreover, PTP20 was shown to activate in vitro and ex vivo the melanogenesis process. In fact, an increase in the production of melanin was shown to be correlated with elevated expression of MC1-R, TRP-1 and Melan-A, and with the reduction in ASIP expression. A modulation on TRP-2 was also observed. The pivotal role of MC1-R was confirmed on protein expression analyzed on volunteer's plucked hairs after 3 months of the daily application of lotion containing 10 ppm of PTP20 peptide.

CONCLUSION:
The current findings demonstrate the ability of the biomimetic PTP20 peptide to preserve the function of follicular melanocytes. The present results suggest potential cosmetic application of this newly designed agonist of α-MSH to promote hair pigmentation and thus, reduce the hair greying process. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
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PunkassDerm
Posted on: Oct 7 2018, 12:20 AM


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Don't forget HHD. Miracle for these patients. Great label extension or off label use after approval. It initiates long lasting remission in a disease that has no effective treatment.
Add to your numbers.

NOTE: NO SIDE EFFECTS. MODERATE TANNING. NO LAB ABNORMALITIES. SAFE! #whatdoyouknowaboutthat?

Affected Populations

Hailey-Hailey disease affects males and females in equal numbers. According to one estimate, the disorder affects 1 in 50,000 people in the general population. Hailey-Hailey disease often goes misdiagnosed or undiagnosed, making it difficult to determine its true frequency in the general population.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255790/


Clin Exp Dermatol. 2014 Mar; 39(2): 168–175.
Published online 2013 Oct 25. doi: 10.1111/ced.12203

Efficacy of the melanocortin analogue Nle4-D-Phe7-α-melanocyte-stimulating hormone in the treatment of patients with Hailey–Hailey disease
G Biolcati,1 C Aurizi,1 L Barbieri,1 S Cialfi,2 I Screpanti,2 and C Talora2


Snippets from Article:


Background

Hailey–Hailey disease (HHD) is a rare, chronic and recurrent blistering disorder, which is characterized clinically by erosions occurring primarily in intertriginous regions, and histologically by suprabasal acantholysis. Oxidative stress plays a specific role in the pathogenesis of HHD, by regulating the expression of factors playing an important role in keratinocyte proliferation and differentiation.


Conclusions

Afamelanotide is effective for the treatment of skin lesions in HHD.



Introduction

Familial benign chronic pemphigus or Hailey–Hailey disease (HHD; OMIM 169600) is a rare, autosomal dominant genodermatosis. The prevalence of HHD is unknown. HHD is characterized by development of relapsing and recurrent blisters, erosions and crusts in the intertriginous areas. Although lesions generally first appear after adolescence, with peak onset around the age of 30–40 years, they can develop at any age. Lesions can be complicated by heat, rubbing or superinfection, and they can have a substantial negative effect on patients' quality of life (QOL).1

...There is no known cure for HHD, and existing treatments do not provide a long-lasting positive therapeutic result. Therapies for HHD often attempt to control the underlying inflammatory immune response associated with the disease to induce symptomatic remission. The most commonly used therapies include steroids, antifungals and antibiotics, administered either topically or systemically. α-MSH is a peptide hormone member of a family of peptides known as the melanocortins, and can bind to five known melanocortin receptors: MC1R, MC2R, MC3R, MC4R and MC5R.5–7 Many studies have provided evidence that α-MSH has potent protective and antioxidative effects.8–13 At the molecular level, α-MSH affects various pathways implicated in the regulation of inflammation and protection. In particular, in primary keratinocytes, α-MSH increased expression of Nrf2 [Nuclear factor (erythroid-derived 2)-like 2], a key transcription factor involved in orchestrating the expression of antioxidative enzymes.10 Nrf2 has emerged as a master regulator of an intracellular antioxidant response operating through transcriptional activation of an array of genes, including phase II detoxifying enzymes, antioxidants and transporters, which protect cells from toxic and carcinogenic chemicals.14–16 Additionally, reports have shown that α-MSH is capable of inducing expression of both Nrf2 and Nrf-dependent phase II detoxifying enzymes in keratinocytes, suggesting the potential role of α-MSH not only as a pigment inducer but also as a guardian of epidermal homeostasis and oxidative stress balance.10

Nle4-D-Phe7-α-melanocyte-stimulating hormone (afamelanotide) is an α-MSH analogue.17 Deficiency of ATP2C1 in HHD-derived keratinocytes is associated with alterations in proliferation and differentiation, and increased oxidative stress.3,4 In the current study, we aimed to find evidence to support a strategy for the use of afamelanotide as a therapeutic approach for HHD.


Results:

...During the initial 30-day treatment period with afamelanotide, the lesions began to reduce in size, and during the following 30-day period, they reduced further, until by day 60, the lesions had disappeared completely, restoring the skin's natural appearance (Fig.​(Fig.2).2). The clinical remission was reflected in the improved QOL as measured by the SF-36.

There were no side-effects noted. Both patients experienced moderate skin tanning, but no clinically important laboratory abnormalities were detected. After afamelanotide withdrawal, there was no recurrence of clinical disease for 8 months, but signs of recurrence were seen after this point.


Discussion

α-MSH is known to have protective and antioxidative effects, thus in this study, we aimed to assess the clinical potential of an α-MSH analogue, afamelanotide in patients with HHD. Our previously published results had implicated oxidative stress and the response to it as contributing factors to the presentation of HHD.3,4 We hypothesized that afamelanotide might be an effective treatment for HHD by decreasing the level of oxidative stress. Our hypothesis was based on previous observations suggesting that α-MSH defends cells against the detrimental effects of oxidative stress, and may also abate the consequences of this stress.8–13

...The precise mechanism of how afamelanotide affects the course of HHD lesions remains to be determined. Our findings suggest that afamelanotide acts directly on keratinocytes to increase Nrf2 expression, and this may be relevant to its mechanism of action in HHD. However, we cannot exclude the possibility that the anti-inflammatory property of afamelanotide may be the mechanism of action that produces the in vivo effect of afamelanotide in our treated patients. Thus, it will be interesting to measure in future studies if afamelanotide affects the level of inflammatory mediators, e.g. cytokines and regulatory T cells, in patients with HHD.


Conclusion

In summary, this pilot study suggests that afamelanotide has a therapeutic efficacy in patients with chronic and treatment-resistant HHD. Despite the fact that HHD is a rare disease and it is therefore difficult to enrol sufficient patients in a placebo-controlled trial, a much larger number of patients with HHD receiving afamelanotide will be needed to confirm the preliminary data of this small pilot study. An interesting possibility would be use of a therapeutic protocol in which patients are scheduled for treatment with afamelanotide suspension every 6–7 months. Based on the responses of our two patients with HHD to a sustained resorbable implant formulation of afamelanotide in an open-label pilot study, afamelanotide treatment may be able to induce long-term disease remission.

Go to:

Acknowledgments
We would like to thank Clinuvel Pharmaceuticals for providing afamelanotide. The financial support of Telethon – Italy (grant no. GGP12264) is gratefully acknowledged.
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PunkassDerm
Posted on: Oct 5 2018, 02:30 AM


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I used the Pharos excimer by Ra.
It has an adjustable aperature that made following a lesion easier by adjusting treatment size on the fly instead of masking good skin.

https://www.ramed.com/patients/dermatology/
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PunkassDerm
Posted on: Oct 4 2018, 01:17 PM


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A good reminder for clinical efficacy. AS FAST AS 2 DAYS???!!!


January 2013

The Efficacy of Afamelanotide and Narrowband UV-B Phototherapy for Repigmentation of Vitiligo
Pearl E. Grimes, MD; Iltefat Hamzavi, MD; Mark Lebwohl, MD; et al Jean Paul Ortonne, MD; Henry W. Lim, MD

JAMA Dermatol. 2013;149(1):68-73. doi:10.1001/2013.jamadermatol.386

Background
Vitiligo is characterized by depigmented patches of skin due to loss of cutaneous melanocytes. Many recent studies have demonstrated defects in the melanocortin system in patients with vitiligo, including decreased circulating and lesional skin levels of α–melanocyte-stimulating hormone (α-MSH). Afamelanotide is a potent and longer-lasting synthetic analogue of naturally occurring α-MSH.

Observations
We describe the preliminary results of 4 patients with generalized vitiligo who developed repigmentation using afamelanotide in combination with narrowband UV-B (NB–UV-B) phototherapy. Patients were treated 3 times weekly with NB–UV-B and starting in the second month received a series of 4 monthly implants containing 16 mg of afamelanotide. Afamelanotide induced faster and deeper repigmentation in each case. All patients experienced follicular and confluent areas of repigmentation within 2 days to 4 weeks after the initial implant, which progressed significantly throughout treatment. All patients experienced diffuse hyperpigmentation.


https://jamanetwork.com/journals/jamadermat...article/1377949


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PunkassDerm
Posted on: Oct 4 2018, 12:58 PM


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This can be completely overcome by focused NB-UVB in the form of the Excimer laser. 308nm

Focused - Only the affected skin is treated
Higher energy in short time, more effective
Excimer penetrates deeper to recruit surviving melanocytes

Afamelanotide reduced free radial damage and DNA repair, stimulated re-pigmnetation


I used the Pharos Excimer laser at my last clinic. Usually combined with topical steroids alternating with Protopic. Occasional bust of prednisone or IL-Kenalog (steroid injection)

The UVB booth more for extensive Eczema or Psoriasis
PUVA more dangerous never liked and did not start any patients on this, NB-UVB has become the standard




http://www.dermatologytimes.com/ophthalmol...-treatment-time


Excimer laser slashes vitiligo treatment time
Sep 1, 2004


In the treatment of vitiligo, the 308-nm excimer laser (PhotoMedex) achieves results as favorable as those of other phototherapy modalities in one-third the time, according to James M. Spencer, M.D.

The skin disorder is present in 1percent to 2 percent of the world's population and has no predilection for race.

"Vitiligo is characterized by localized loss of pigmentation, which is cosmetically distressing for patients," Dr. Spencer says. "The affected area is very sensitive to sunburn, and treatment with topical steroids and immune response modifiers (e.g., tacrolimus) alone is rarely successful. And the traditional psoralen with ultraviolet-A (PUVA) requires twice-weekly treatments for a year or longer, which is a major commitment (for the patient)."

Dr. Spencer is vice chairman of the department of dermatology at Mt. Sinai School of Medicine in New York.


Other modalities

PUVA has an overall success rate of 50 percent, but that rate can be misleading because it represents an average of all skin types and all parts of the body, according to Dr. Spencer.

"Results vary with skin type and location of the disease," he says. "People with dark skin do better than people with fair skin. The face tends to do well, the hands tend to fail, and the rest of the body is in the middle." Narrow-band UV-B given twice a week for up to a year has a slightly higher reported success rate (53 percent) and a higher safety profile than PUVA, which is associated with the development of skin cancer on normal skin, he adds.

Physicians can almost promise African Americans with facial vitiligo that they will get their color back permanently, Dr. Spencer says.

"As for fair-skinned patients with vitiligo on the hands, the laser and other phototherapies will probably fail, and there is no plan B. Surgical procedures, though effective, can lead to scarring and textural changes," he says.


Excimer has advantages

At Mt. Sinai, Dr. Spencer and his colleagues have been using the 308-nm excimer laser to treat patients with vitiligo.

"The excimer laser penetrates deeply enough to stimulate surviving melanocytes to migrate up hair follicles to the vitiligo patches on the skin," Dr. Spencer says.

The laser has practical and theoretical advantages over non-laser light treatments, according to Dr. Spencer.

"You shine the UV-B light onto only diseased skin and normal skin is spared exposure," he says. "The laser also has high energy, so treatment is more rapid. Theoretically, lasers may also penetrate more deeply, and a given dose is delivered more rapidly. For example, 100 joules given quickly may be more effective than 100 joules given slowly."

Although lasers deliver large doses quickly, they are limited by their small 2 cm-by-2 cm spot size, according to Dr. Spencer.

"Fortunately, most vitiligo is limited," he says.


Time slashed

In a study published in the July issue of Dermatologic Surgery, Dr. Spencer and colleagues reported a 53 percent success rate in patients treated with the excimer laser twice weekly for 15 weeks, one-third of the time required for other phototherapy treatments. Success was defined as 75 percent or greater repigmentation, and patients were of all skin types and had vitiligo at all body locations.

"Just as with PUVA, dark-skinned people do better than light-skinned people," Dr. Spencer says. "The face responds well, the hands respond poorly, and the body's response is in the middle. But the excimer laser is as good as PUVA or narrow-band UV — in a fraction of the time — and normal skin is spared exposure." Dr. Spencer has also found that tacrolimus (Protopic, Fujisawa Healthcare) enhances the effects of the excimer laser.

A temporary "sunburn" is the only adverse effect of treatment, he says.
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PunkassDerm
Posted on: Sep 27 2018, 09:20 AM


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Isn’t by definition a hedge fund about risk/reward, hedging the market?
Isn’t Lagoda a hedge fund? A substantial holder in Clinuvel.

Plus there’s EMA approval and sales.
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PunkassDerm
Posted on: Sep 26 2018, 03:53 AM


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Add cosmetic approval/photoprotection en masse...$200 after 2 splits! Always the holy grail.

How long will that take? How many years of safety and proven protection/repair. Against lobby from other forces.
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PunkassDerm
Posted on: Sep 25 2018, 04:53 PM


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Posts: 509

What a year does!

Management is almost forgiven for their sins, SP heals all wounds.
I held off my sell order for now, maybe some profit at 20USD, a little.
All these years, I did everything wrong.
Strong diversfied portfolio with dividends,
Funneled into one crazy obscure molecule.

I can almost smell it...
Independence.

And for medicine, a gem.
Disruptive.
Hopefully the melanocortins live up to my dreams of protection and repair.
And the FDA conducts swiftly with integrity.

Thanks everyone for sharing, contributing.
I hope even Iggy and RC have some shares on the line.

EDIT: 3AM in MA USA and can’t sleep

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PunkassDerm
Posted on: Sep 20 2018, 01:04 PM


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TURNING JAPANESE I REALLY THINK SO
I didn't realize the prevalence so high. I think necessitates a price drop, just add that to vitiligo. Fair and equitable.

Xeroderma pigmentosum (XP) is a rare disorder of defective UV-radiation induced damage repair that is characterized by photosensitivity with easy skin burning following minimal sun exposure, early freckling and development of lentiginous pigmentation along with other features of poikiloderma and a propensity for developing skin cancer at an early age. In this short review, the clinical, pathological, genetic and molecular aspects of XP are reviewed in the current literature. XP encompasses a spectrum of disease that overlaps with other diseases of DNA repair systems. In addition to cutaneous complications, patients are susceptible to eye conditions, neurodegenerative processes, central nervous system tumors and other tumors as a result of UV radiation exposure and its byproducts. Patients with XP frequently experience a shorter life span due to skin cancer and neurodegenerative sequelae, but aggressive preventative measures to minimize UV radiation exposure and damage can improve the course of disease and prolong life. The disease has served as a model for photoaging and UV radiation-induced cancer and has led to a better understanding of cell processes that prevent development of these disease features in normal individuals.


Xeroderma pigmentosum (XP) is a rare autosomal recessive disorder that has been reported around the world with variable prevalence, affecting 1 per million in the United States, 2.3 per million in Western Europe, and 45 per million in Japan [1]. Affected populations have also been described in North Africa and the Middle East, with less well-understood frequency [1–4].


There is currently no cure for xeroderma pigmentosum, but there is profound benefit in consistent UV-radiation protection, which can substantially decrease the number of skin cancers, and consists of layered clothing along with sunscreen and eye protection [21]. Decreasing UV radiation exposure may not decrease neurodegenerative effects. Patients often require Vitamin D supplementation to offset sun avoidance [21]. Systemic treatment with retinoids has been attempted and shows some benefit in reducing the number of skin cancers [29], though side effects prohibit use in children. Early resection of premalignant and malignant lesions is important for long term survival. Investigative therapies using gene therapy and antioxidants to reduce oxidative damage may result in future treatment options [30].


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4838978/
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PunkassDerm
Posted on: Sep 20 2018, 12:06 PM


Group: Member
Posts: 509

I love the new focus on photo-protection / DNA repair.

Fits much better with XP, using as a segway to ubiquitous photo-protection. If anti-skin cancer benefits can be highlighted, we are there.


excerpt:
The sensitivity to UV radiation results in increased freckling, as well as areas of lighter skin pigmentation. They may also have very dry skin. There is a high risk of squamous cell and basal cell skin cancers and melanoma. People with XP also have eye problems, especially with their eyelids.


https://www.cancer.net/cancer-types/xeroderma-pigmentosum
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PunkassDerm
Posted on: Sep 16 2018, 01:06 AM


Group: Member
Posts: 509

Soon will will be getting ETF SPDR INDEX exposure? Looks like more traction once access to the ASX200, but even now should we see new instos obligated to add CUV?
Broad market and Healthcare? Not my expertise but this will add to organic (hopefully exponential) growth? That list of insto holders should grow now.

Then add NASDAQ

any expert thoughts?

https://www.stockspot.com.au/what-are-etfs/etfs-compared/


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PunkassDerm
Posted on: Sep 15 2018, 02:17 PM


Group: Member
Posts: 509

Followup on Investek post...

http://www.sachsforum.com/18bef-presenters.html


18TH ANNUAL BIOTECH IN EUROPE FORUM
4TH-5TH OCTOBER 2018 @ CONGRESS CENTER BASEL, SWITZERLAND

CLINUVEL AG

CLINUVEL PHARMACEUTICALS LTD is a global biopharmaceutical company focused on developing and delivering treatments for patients with a range of severe genetic and skin disorders. As pioneers in photomedicine and understanding the interaction of light and human biology, CLINUVEL’s research and development has led to innovative treatments for patient populations with a clinical need for photoprotection and regimentation. These patient groups range in size from 5,000 to 45 million worldwide.

CLINUVEL’s lead compound, SCENESSE® (afamelanotide 16mg), was approved by the European Commission in 2014 for the prevention of phototoxicity (anaphylactoid reactions and burns) in adult patients with the rare genetic disorder erythropoietic protoporphyria (EPP).

As the first ever photoprotective drug, SCENESSE® activates eumelanin, the dark pigment in skin. Eumelanin is capable of selective light absorption, including at the wavelengths of light which excite protoporphyrin IX, the compound which causes phototoxic reactions in patients diagnosed with EPP, a disorder which causes absolute intolerance to light (blue and green spectrum).
​
Headquartered in Melbourne, Australia, CLINUVEL has operations in Europe, Switzerland, the US and Singapore.

http://www.clinuvel.com/
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PunkassDerm
Posted on: Sep 15 2018, 01:43 PM


Group: Member
Posts: 509

Love to see that in email or letter, go public! FDA promotes a drug for US citizens, shouldn't it be FLASH tracked? Like instant approval!
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PunkassDerm
Posted on: Sep 12 2018, 01:06 PM


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Posts: 509

Bahaha...not quite there. And my holdings unlikely to make a dent in SP.
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PunkassDerm
Posted on: Sep 11 2018, 12:47 AM


Group: Member
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If I could think of one acquisition for Clinuvel, it would be surmodics, their manufacturing partner. Stock price around 80 and a market cap at 1 billion. Even-Steven but don't know what debt they have. Climb is similar to our baby.


Attached Image

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PunkassDerm
Posted on: Sep 10 2018, 09:55 PM


Group: Member
Posts: 509

I give myself grief and stress from the same thing, funneled my diversified holdings into one stock. With continued safety this melanocortin platform will be disruptive to medicine, and I can't wait. Almost time for me to take a little profit for the first time, little de-risking. Average 2.50/share now USD.

EPP patients, HHD, Vitiligo, XP, and TBD indications...so many will benefit
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PunkassDerm
Posted on: Sep 10 2018, 01:47 PM


Group: Member
Posts: 509

Mkt cap 859.88M

Exponential growth or takeover, OK!
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PunkassDerm
Posted on: Sep 10 2018, 12:07 PM


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25K implant price will keep off-label use down. Even 5K won't bring out cosmetic/photoprotection for the masses.
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PunkassDerm
Posted on: Sep 10 2018, 02:07 AM


Group: Member
Posts: 509

Regulation of p53 by MC1R signaling

p53, also known as TP53 or tumor protein (EC :2.7.1.37) is a gene that codes for a protein that regulates the cell cycle and hence functions as a tumor suppression. It is very important for cells in multicellular organisms to suppress cancer.

ergo - Aids in melanoma prevention. And in the absence of ionizing radiation, SUN. It's the sun not the tan that causes DNA damage. This is lost on many including EXPERTS that assume tan increases risk of melanoma, without reading all these studies.


http://mcr.aacrjournals.org/content/molcan.../6/778.full.pdf


Alpha-Melanocyte–Stimulating Hormone Suppresses Oxidative Stress through a p53-Mediated Signaling Pathway in Human Melanocytes
Ana Luisa Kadekaro1, Juping Chen1,2, Jennifer Yang1, Shuna Chen1, Joshua Jameson1, Viki B. Swope1, Tan Cheng1,3, Madhavi Kadakia4, and Zalfa Abdel-Malek1

Abstract

Epidermal melanocytes are skin cells specialized in melanin production. Activation of the melanocortin 1 receptor (MC1R) on melanocytes by a-melanocyte–stimulating hormone (a-MSH) induces synthesis of the brown/black pigment eumelanin that confers photoprotection from solar UV radiation (UVR). Contrary to keratinocytes, melanocytes are slow proliferating cells that persist in the skin for decades, in an environment with high levels of UVR-induced reactive oxygen species (ROS). We previously reported that in addition to its role in pigmentation, a-MSH also reduces oxidative stress and enhances the repair of DNA photoproducts in melanocytes, independent of melanin synthesis. Given the significance of ROS in carcinogenesis, here we investigated the mechanisms by which a-MSH exerts antioxidant effects in melanocytes. We show that activation of the MC1R by a-MSH contributes to phosphorylation of p53 on serine 15, a known requirement for stabilization and activation of p53, a major sensor of DNA damage. This effect is mediated by the cAMP/PKA pathway and by the activation of phosphoinositide 3-kinase (PI3K) ATR and DNA protein kinase (DNA-PK). a-MSH increases the levels of 8-oxoguanine DNA glycosylase (OGG1) and apurinic apyrimidinic endonuclease 1 (APE-1/Ref-1), enzymes essential for base excision repair. Nutlin-3, an HDM2 inhibitor, mimicked the effects of a-MSH resulting in reduced phosphorylation of H2AX (g -H2AX), a marker of DNA damage. Conversely, the p53 inhibitor pifithrin-a or silencing of p53 abolished the effects of a-MSH and augmented oxidative stress. These results show that p53 is an important target of the downstream MC1R signaling that reduces oxidative stress and possibly malignant transformation of melanocytes. Mol Cancer Res; 10(6); 778–86. !2012 AACR.
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PunkassDerm
Posted on: Sep 10 2018, 02:01 AM


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Reduced but not absent function in loss of function MC1R individuals is how I read it. Simplistically, if given proper stimulation can be (partially) corrected. Maybe the sort sequence afamelanotide more effective binder? Definitely not a biochemist but I think this is what we're looking for.


Your quote seems to support this (in vivo):
"Two trials in human volunteers showed that neither MC1R variants nor fair skin reduced the afamelanotide-induced increase in skin pigmentation."

translation, it still works

And as we clearly see stated over and over, it is not only the eumelanin tan but DNA repair and free radical scavenging that augments the anti-cancer potential.



https://academic.oup.com/hmg/article/10/21/2397/2901534


Functional variation of MC1R alleles from red-haired individuals

Eugene Healy Siobhán A. Jordan Peter S. Budd Ruth Suffolk Jonathan L. Rees Ian J. Jackson
Human Molecular Genetics, Volume 10, Issue 21, 2 October 2001, Pages 2397–2402, https://doi.org/10.1093/hmg/10.21.2397
Published: 02 October 2001

Red hair in humans is associated with variant alleles of the αMSH receptor gene, MC1R. Loss of MC1R function in other mammals results in red or yellow hair pigmentation. We show that a mouse bacterial artificial chromosome (BAC) which contains Mc1r will efficiently rescue loss of Mc1r in transgenic mice, and that overexpression of the receptor suppresses the effect of the endogenous antagonist, agouti protein. We engineered the BAC to replace the mouse coding region with the human MC1R sequence and used this in the transgenic assay. The human receptor also efficiently rescued Mc1r deficiency, and in addition, appeared to be completely resistant to the effects of agouti, suggesting agouti protein may not play a role in human pigmentary variation. Three human variant alleles account for 60% of all cases of red hair. We engineered each of these in turn into the BAC and find that they have reduced, but not completely absent, function in transgenic mice. Comparison of the phenotypes of αMSH-deficient mice and humans in conjunction with this data suggests that red hair may not be the null phenotype of MC1R.


DISCUSSION

We have demonstrated that Mc1r-containing BAC transgenes are able to very efficiently rescue the yellow, loss-of-function phenotype of Mc1re homozygous mice. Furthermore, the transgenic mice show a strong dosage-sensitive phenotype. Addition of only one or two copies in excess of the normal diploid complement darkens the coat by reduction of the yellow, agouti-induced band on the hair. A total Mc1r complement of approximately six copies almost completely suppresses the effect of agouti. We do not know whether the suppression of agouti is due to the increase in MC1R on the melanocyte surface saturating out a limited amount of agouti protein or whether there is normally a low level of signalling from the receptors even in the presence of agouti, which has an additive effect with increased receptor number and overcomes the antagonism.

Transgenic mice expressing human MC1R show a much greater suppression of agouti. Indeed, mice expressing only the normal diploid complement of human MC1R have no detectable phaemelanin and are completely black. This is not due to a lack of activity of mouse agouti protein on the human receptor, as others have demonstrated that in cells in culture the human MC1R is 10-fold more sensitive to mouse agouti than to the human protein (14). There is evidence to suggest that human MC1R is more sensitive to stimulation by hormone than the mouse receptor and this may be sufficient to overcome the antagonsim by agouti. It also appears that the density of MC1R on human melanocytes is considerably lower than the receptor density on mouse melanocytes (24). The transgenic system we describe here, in which the human receptor is expressed from the mouse promoter, may result in MC1R being present at non-physiological, high levels. The variant human MC1R receptors in transgenic mice do respond to agouti protein, as shown by the phaeomelanic patterning on their hairs. These receptors have attenuated signalling (demonstrated by the pale eumelanin synthesized on a non-agouti background) which appears to allow agouti to act.

Our data indicate that although the variant MC1R proteins are clearly defective, in accordance with population and family data associating them with red hair, none has complete loss of function when assayed in transgenic mice. Rare patients mutated in the POMC gene and thus lacking αMSH, have red hair that is apparently the same as the MC1R-associated red hair (20). However, POMC-deficient mice do not have the same phenotype as loss of Mc1r (15). Our finding that red-hair associated variant human receptors still allow significant eumelanin synthesis, may indicate that red hair is not the null phenotype. Although a few MC1R frameshift alleles that clearly do not produce functional protein have been described (17,26,27), they are rare and no homozygotes have been found. Whether MC1R-null individuals have different or additional phenotypes which means they have not been included in case control or population studies is unclear at this stage. MC1R has been suggested to have a role in melanocyte proliferation and in various non-melanocytic functions such as inflammation. There is no evidence that MC1R-associated red-haired individuals have any additional phenotype. However, identification and study of individuals homozygous for MC1R loss of function might reveal further roles for MC1R in humans.
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PunkassDerm
Posted on: Sep 5 2018, 01:37 PM


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Posts: 509

Maybe they should have invested that brilliant and exhorbitant dividend into a team of regulatory experts.

So this doesn’t freaking happen.

Again

That’s my 2cents...literally
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PunkassDerm
Posted on: Sep 5 2018, 12:34 PM


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Where is this guy BTW? In the corner with baby and the poor dude from Blair Witch no doubt.


Attached Image


Nobody puts Wolgy in the corner!
It's Karma for killing Frilly
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PunkassDerm
Posted on: Sep 5 2018, 10:56 AM


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Posts: 509

ALLERGAN
COMPETENCE
TAKEOVER


edit: unless tweak ensures PR

edit: sigh

edit: How many mulligans do you get and still receive performance rights as if on point?
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PunkassDerm
Posted on: Sep 4 2018, 12:35 AM


Group: Member
Posts: 509

Yes, cautious optimism. Botox was around a long time before cosmetic applications arose. FDA since seems to have clamped down on similar paths. Hence Melanotan to Scenesse and the long road for Clinuvel and our ragtag bunch of investors. Still Allergen is the model in my opinion, and the perfect company to get this accomplished. If it took this long to see EPP, and Vitiligo appears to have no urgency...it will be awhile before we see photoprotection. Hopefully that all changes with new class melanocortin status with FDA. I pray your optimism for speed is founded Wally.

If in the meantime: If the SP shoots up nicely and I can take some profits to live comfortably, I'll be happy to leave a big chunk to ride on a lifestyle drug. Get my photo-medicine boutique clinic up and running.

Queue the Wolgen clock.



A HISTORY OF BOTOX INJECTION THERAPY

By Dr. Scott W. Mosser

Botox® is a highly purified form of botulinum toxin Type A, which is produced by the bacteria clostridium botulinum. It was developed in the 1970’s by a San Francisco doctor searching for ways to correct strabismus, or crossed eyes. He discovered that a purified form of this potentially lethal poison (a toxin once commonly produced by bacteria in improperly processed food) when injected in the appropriate overactive muscles caused a temporary relaxation or paralysis which allowed other eye muscles to take over normal eye function.

Allergan, Inc., small drug company specializing in products for use in the fields of ophthalmology and dermatology, purchased the rights to the discovery in 1987, and the toxin was marketed for use in correcting eye muscle disorders such as blepharospasm (uncontrollable blinking) and strabismus (crossed eyes). This form of botulinum toxin A was licensed by Allergan, Inc. in 1989.

Over the following decade, doctors found additional uses for botulinum toxin Type A, including the treatment of cervical dystonia, a disorder that causes severe neck and shoulder contractions, as well as reducing the stiffness and tremors that often follow a stroke.

“FOUNTAIN OF YOUTH” TREATMENT CAUSES A MEDIA BLITZ
In the mid 1990’s, word of mouth among ophthalmologists and dermatologists in the U.S. and Canada spread the fame of the exciting cosmetic side effects observed after injecting the purified toxin – reduction of forehead wrinkles, facial creases and crow’s feet, resulting in a fresher, more youthful facial contour.

When the FDA approved the use of Botox® for cosmetic purposes in 2002, it triggered wide media coverage and catapulted the demand for Botox® injections specifically for cosmetic effect onto the world stage.

This huge demand led to a period of misuse of Botox® injections by non-medically trained cosmeticians, or in back-door treatments under non-medical condition, which resulted in reports of ineffectiveness or unpleasant side effects. It was only as the public became more informed and Board-Certified Plastic Surgeons and dermatologists began adding Botox® injection procedures to their non-surgical facial cosmetic programs that the full benefits became apparent and the safety and efficacy of Botox® injection therapy became mainstream.

The use of Botox® treatments to relax or eradicate wrinkles and frown lines on the forehead and around the eyes is currently the most popular non-cosmetic procedure in the United States, Europe and many other countries. When injected directly into overactive facial muscles, Botox® inhibits the release of acetylcholine, a neurotransmitter that causes muscles to contract. The result is inhibition, or relaxation, of the muscles, an effect that can last up to several months.

According to Allergan, almost 3.3 billion Botox® Cosmetic procedures were performed in 2005 alone.

A CONTINUING POPULARITY
The huge popularity of Botox® injections is likely due to its non-surgical nature (leaving no scars), little or no recovery time, its effectiveness, and its relatively low cost compared to surgical face lifts or other procedures. Its safety is also an important factor. Botox® has been widely used for more than a dozen years and there have been no documented systemic complications associated with Botox® injections when administered by qualified medical personnel in accordance with the recommended dosage and guidelines.

The United States Food and Drug Administration (US FDA) cautions that Botox® is a prescription drug that should be administered by a qualified physician in an appropriate medical setting. Any other venue runs the risks of improper technique, inappropriate dosages and unsanitary conditions. The FDA also recommends that Botox® Cosmetic be injected no more frequently than once every three months, and that the lowest effective dose should be used.

The continuing popularity of Botox® cosmetic treatments among men and women in every walk of life (from the glamour industry to the housewife to executives) and the familiarity with which the term is used, has perhaps somewhat obscured the history of the toxin and its original uses. However, physicians and medical researcher have not forgotten and recent developments of new medical uses for Botox are causing renewed excitement.

A NEW WRINKLE FOR AN ANTI-WRINKLE TREATMENT
This unusual substance, which started life as a life-threatening toxin, was later purified for use in treating eye disorders, and then met fame and fortune as an anti-wrinkle treatment, has in the past few years been found to have exciting new health applications: most notably, in the treatment of migraine headaches.

Again, plastic surgeons using Botox® injections on patients who were incidentally migraine headache sufferers began to notice that in addition to a smoother, more youthful facial contour, patients were reporting a lessening in the strength and frequency of migraine attacks.
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PunkassDerm
Posted on: Sep 3 2018, 12:04 AM


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Then pricing:

Vitiligo approval: 5000USD per implant

Fastforward 10-15 years....

Photo protection/antioxidant/DNA repair "supplement" : 500USD

let her rip
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PunkassDerm
Posted on: Sep 2 2018, 11:50 PM


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I emailed Mr Hay in 2004 asking why Vitiligo is not in their sights, always the prize and agree with recent posts. See below prevalence stats that I pulled, trying to find average values.
Vitiligo market potentially much lager than I had ever hoped, yet psoriasis gets all of the attention. Inevitably through pharma marketing and awareness. Yet Vitiligo carries same emotional disability about self image. This is huge. See prevalence number below and the worldwide psoriasis market of about 11.5 billion and growing.

Then understand the psoriasis biologic market alone saturated with new products. I count at least 13 injectables.

Translate that to a wide open and underserved vitiligo market with no adequate clinically efficacious treatment. There is room for multiple drugs, JAK and melanocortins. Maybe great synergies and so much opportunity for Scenesse and new topical formulations. First in class, with EMA and FDA approval.

Also, new indication for approved drug should be smoother/faster with existing safety and pharmacokinetics data in place.

Eyes wide open.

Punk



New indications for already-approved drugs: an analysis of regulatory review times.

DiMasi JA1, Kaitin KI, Fernandez-Carol C, Lasagna L.

A survey of the U.S. pharmaceutical industry was conducted to obtain data on the length of the review process for supplemental indications of already-approved new chemical entities (NCEs). Responses were received from 51 firms and covered supplemental indications of 348 NCEs that were approved during 1963 to 1988. Since extensive toxicity and safety evaluation would generally not be required for supplemental indication reviews, one would expect supplemental indications, on average, to be reviewed more quickly than applications for the associated original indications. The mean +/- standard deviation review time for the 172 supplemental indications in the sample is 21.5 +/- 18 months; the average review time for the associated 94 original indications is 23.5 +/- 18 months. The difference in average review times is not statistically significant. Analysis of review times for indications grouped by Food and Drug Administration (FDA) reviewing division showed a statistically significant difference between supplemental and associated original indication review times only in the cardio-renal division. In that division, average review times were longer for supplemental indications (25.6 vs. 19.3 mo; P less than .05). Analysis of time trends showed a significant increase in average supplemental indication review time for 1985 to 1988 approvals relative to the average associated original indication review time (P less than .01) and to average supplemental indication review time for earlier time periods (P less than .01). These results suggest the need for a close examination of the supplemental indication review policy of the FDA.


PREVALENCE:

Psoriasis Worldwide: up to 2 - 3%
As many as 7.5 million Americans— 125 million people worldwide

Vitiligo Worldwide: 0.5 - 2%
Reports show 65-95 million people affected



Vitiligo is an acquired skin disorder characterized by patchy depigmentation of the skin [1]. Vitiligo affects approximately 0.5% to 2% of the population worldwide, and the prevalence appears to be equal between men and women [2,3]. The pathogenesis of vitiligo is still not fully understood and mounting evidences have suggested that it might be related to autoimmunity and oxidative stress [4]. Although neither life-threatening nor symptomatic, the effect of vitiligo can be cosmetically and psychologically devastating, resulting in low selfesteem, poor body image and other negative effects [5-7].


Prevalence of vitiligo

Although vitiligo occurs worldwide, it is known that its prevalence varies between races and regions. Recent studies have revealed the prevalence from 0.06-2.28% [8-28]. Howitz et al. [8] reported that the prevalence of vitiligo in Denmark was 0.38%. Mehta et al. [9] reported that the prevalence was 0.49% in rural areas of Indian and 1.78% in urban areas. Abdel-Hafez et al. [10] performed a survey in Upper Egypt and found the prevalence of vitiligo to be 1.2%. In USA, the prevalence of vitiligo was 0.74% [11]. Other studies have shown a prevalence of 0.17% in Italy [12], 0.5-1% in the French West Indies [13], and 0.28% in France [14]. In China, several studies have been performed and the prevalence of vitiligo ranged from 0.10 to 0.3% [15-19]. Lu et al. [15] conducted a survey in Shaanxi province, northwest China and found that the prevalence of vitiligo was 0.10%.


CONTRAST PSORIASIS BIOLOGIC MARKET ALONE

The global psoriasis therapeutics market size was valued at USD 11.5 billion in 2016 and is estimated to grow at a CAGR of 9.3% during the forecast period. Increasing awareness about treatment and rising demand for improved healthcare infrastructure are major factors expected to drive the psoriasis market.

The changing lifestyle of people leading to increased alcohol consumption and smoking, unhealthy diet and a sedentary living makes more people prone to this condition. Psoriasis is a genetic condition that may not be present at birth. The condition may be triggered by certain environmental and genetic factors.

According to the International Federation of Psoriasis Association, approximately 5.0% people suffer from one or more forms of psoriasis, globally. In the U.S. alone, the condition affects nearly 7.5 million people, which is roughly 2.0% of the population. Moreover, approximately 100,000 new cases are registered and reported every year.

Plaque psoriasis is spearheading the segment with more than 80.0% patients suffering at a global level. Guttate psoriasis is the second most common type, affecting about 10.0% of the patients. Erythrodermic psoriasis is the rarest but the most dangerous type. This condition demands a medical emergency, often leading to hospitalization of patients.

The market space can be divided into various therapeutic classes such as Tumor Necrosis Factor (TNF)-inhibitors, Interleukin inhibitors and Vitamin D Analogues. TNF inhibitors have dominated the therapeutic space. However, they are likely to lose shares over the forecast. The marketed TNF-inhibitors used for psoriasis are Humira (adalimumab), Enbrel (etanercept) and Remicade (infliximab).

Interleukin (IL) inhibitors are expected to witness the fastest growth over the forecast period due to their improved safety and efficacy profiles and rising adoption among end users. Marketed interleukin inhibitors include Stelara (ustekinumab), Cosentyx (secukinumab), Taltz (ixekizumab), Siliq (brodalumab) and Tremfya (guselkumab).

Just the biologics are numerous:

Tumor necrosis factor-alpha (TNF-alpha) inhibitors

Cimzia (certolizumab pegol), Enbrel (etanercept), Humira (adalimumab), Remicade (infliximab), Simponi (golimumab) and Simponi Aria (golimumab) are drugs that block TNF-alpha. TNF-alpha is a cytokine, or a protein, that prompts the body to create inflammation. In psoriasis and psoriatic arthritis, there is excess production of TNF-alpha in the skin or joints. That leads to the rapid growth of skin cells and/or damage to joint tissue. Blocking TNF-alpha production helps stop the inflammatory cycle of psoriatic disease.

Interleukin 12 and 23 (IL-12/23) inhibitors

Stelara (ustekinumab) works by selectively targeting the proteins, or cytokines, interleukin-12 (IL-12) and interleukin 23 (IL-23). Interleukins-12/23 are associated with psoriatic inflammation.

Interleukin 17 (IL-17) inhibitors

Cosentyx (secukinumab), and Taltz (ixekizumab) block a cytokine, or protein, called interleukin-17 (IL-17), which is involved in inflammatory and immune responses. Siliq (brodalumab) blocks the receptor of this cytokine, IL-17 receptor A (IL-17 RA) through which IL-17 mediates the inflammatory and immune responses. There are elevated levels of IL-17 in psoriatic plaques. By interfering with IL-17 signaling, Cosentyx, Siliq and Taltz interrupt the inflammatory cycle of psoriasis. This can lead to improvement in symptoms for many people who take it.

T cell inhibitors

Orencia (abatacept) targets T cells in the immune system. T cells are a type of white blood cell that is involved in the inflammation in psoriasis and psoriatic disease. Orencia inhibits T cells from becoming activated to reduce inflammation.

Interleukin 23 (IL-23) inhibitors

Tremfya (guselkumab) and Ilumya (tildrakizumab-asmn) work by targeting interleukin 23 (IL-23). This cytokine is linked with inflammation in psoriasis and psoriatic arthritis. Tremfya and Ilumya work to reduce psoriatic symptoms and slow disease progression.
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PunkassDerm
Posted on: Sep 2 2018, 01:45 AM


Group: Member
Posts: 509

FDA's Expedited Approval Mechanisms for New Drug Products
Erin E. Kepplinger


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4326266/


Modern medicine and science have made incredible strides in improving and extending lives. Nonetheless, many diseases and conditions still lack adequate therapies. According to a report issued by the President's Council of Advisors on Science and Technology (PCAST) in September 2012 on Propelling Innovation in Drug Discovery, Development, and Evaluation, roughly 30 million Americans suffer from 7,000 rare diseases, but only 350 therapies are approved as treatments.1 Indeed, “[96] percent of orphan diseases, including rare cancers, lack effective therapies.”2 Other conditions demand improved therapies as well. For example, “[h]eart disease and stroke remain leading causes of mortality.”3 The public health need for continued research and development of new drug and biologic products for significant diseases is clear and compelling.

But beyond these important health reasons for stimulating research and development of new compounds, there are ancillary and supportive economic considerations for propelling innovative research and development. According to the Pharmaceutical Research and Manufacturers of America (PhRMA),4 the United States' biopharmaceutical industry contributes substantially to the U.S. economy. PhRMA reports that the industry directly employs over 800,000 workers in well-paid jobs and diverse fields, and supports an additional 2.5 million jobs across the country.5 Moreover, PhRMA asserts that it supports over $789 billion in total economic output.6 For several years, though, the increased time and money necessary to develop a new compound, the failure rate of prospective products, and a decrease in venture capital investments, among other strains on the industry, have propelled concerns that innovative research in the U.S. might wither, stop, or move to other nations or regions, decreasing the potential short term access for U.S. patients to some new products, potentially leaving others unexplored entirely, and hurting a significant segment of the U.S. economy.

As a result, Congress, the Food and Drug Administration (FDA), and the pharmaceutical industry have sought to nurture an “ecosystem” conducive to the development of innovative, safe, and effective new compounds in the U.S. Among the mechanisms developed are four expedited approval mechanisms, the most recent of which—the Breakthrough Therapy designation—Congress created in 2012 through the Food and Drug Administration Safety and Innovation Act (FDASIA). Sponsors of new drug and biologic products (sponsors) have embraced the new Breakthrough Therapy designation: as of roughly December 2014, FDA reported having received 260 requests for Breakthrough Therapy designation, of which it granted 74 and denied 139.7 Of the 41 designated compounds, four have been approved for marketing.
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PunkassDerm
Posted on: Aug 30 2018, 09:46 AM


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Posts: 509

My beef with Lachlan Gay started with this very issue. Said he'd get back to me about voting shares and never did. Now no replies to anything. Great Investor relations.
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PunkassDerm
Posted on: Aug 30 2018, 09:09 AM


Group: Member
Posts: 509

Maybe I'm wrong and not an investment guru, but I don't think anything has to change for Clinuvel to trade on the NASDAQ. It simply goes from the OTC to NASDAQ exchange. Not super complicated and no tax implications.

For example I held and traded BP for years. BP is an ADR on the NYSE (6:1 ADR to common stock).

I think I was able to vote my shares too. Clinuvel chooses to deny this right, in their purview to allow or not.
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PunkassDerm
Posted on: Aug 29 2018, 11:20 AM


Group: Member
Posts: 509

We pool together and build a compound off Greece. I hear Mykonos is great!
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PunkassDerm
Posted on: Aug 29 2018, 10:44 AM


Group: Member
Posts: 509

If this girl is good to me and goes 30+ I'm willing to take the penalty. Cash out my 600K+ investment to do some things I've been waiting for, way too long. Majority long term holdings as well. Assuming Taxachusetts not unlike Cali. No plans for shelters, happy to come out on top with money for play and re-invest.

Hold onto 150K shares for photo protection approval.
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PunkassDerm
Posted on: Aug 29 2018, 02:41 AM


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Posts: 509

My portfolio jumped 200K just now! Announcement known to Clinuvel and a select few? Instos?
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PunkassDerm
Posted on: Aug 22 2018, 08:31 PM


Group: Member
Posts: 509

Vitiligo studies, test doses? States Scenesse doses to date? Not just EPP?
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PunkassDerm
Posted on: Aug 14 2018, 11:27 PM


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But who's the black sheep? to quote my old rap friends...
It would change the product (wool) in this case.

Attached Image
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PunkassDerm
Posted on: Aug 7 2018, 10:40 PM


Group: Member
Posts: 509

Instead of becoming dangerously over-leveraged and bloated for a small company. Why don't they utilize a portion of those funds and hire the right staff/scientists/regulatory experts to fund an expert vitiligo trial and application. Or merger, or partnership...or be acquired.

...and Free Frilly
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PunkassDerm
Posted on: Aug 6 2018, 12:33 PM


Group: Member
Posts: 509

Approaching recent high...

Next milestone @21AUD to reach 1 billion valuation. correct?
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PunkassDerm
Posted on: Aug 4 2018, 03:48 AM


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Posts: 509

read on....I understand as the latter

In 1998, the first year of Fast Track, the FDA received 27 requests, of which 21 were granted (78%). The number has increased steadily year over year, with 187 requests received in 2016, of which 131 were granted (70%).

Ultimately, the Fast Track program has been deemed a success, with approximately two thirds of all 770 Fast Track requests approved by the FDA from 2007 to 2015, according to the Government Accountability Office (GAO).
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PunkassDerm
Posted on: Aug 4 2018, 02:43 AM


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Posts: 509

770 Fast Track 2005-2017
approximately 2/3 approved
see below


https://www.centerwatch.com/news-online/201...ch-20th-year-2/


FDA Fast Track designations reach 20th year
SUNDAY, OCTOBER 1, 2017


Twenty years after its inception, the FDA’s Fast Track designation program is going strong, with many signs that it has achieved its goal of bringing novel drugs to the market faster. Now, even with a new FDA Commissioner at the helm, the Fast Track program is unlikely to change substantially, although it may adjust to more explicitly address current areas of high-unmet medical need such as antibiotic resistance and cardiovascular disease.


Introduced in 1997 as part of the Food and Drug Administration Modernization Act (FDAMA), the Fast Track designation became the FDA’s third expedited review program after Priority Review and Accelerated Approval.

Launched in the wake of the AIDS crisis, these expedited review programs were designed to speed up drug development for life threatening illnesses. “Given that one of the primary goals of the Fast Track program was to be more inclusive and to apply to a wider swath of products, the qualifying criteria for the program were intentionally set quite low,” said Mark Mathieu, director, Publications, Parexel. “FDA guidance notes that a Fast Track designation can be obtained quite early in development, based on nonclinical evidence or even a mechanistic rationale,” Mathieu continued.

In 1998, the first year of Fast Track, the FDA received 27 requests, of which 21 were granted (78%). The number has increased steadily year over year, with 187 requests received in 2016, of which 131 were granted (70%).

If granted, Fast Track can bolster a company’s stock valuation by 18%, making it attractive to smaller biotechs. According to a 2009 review of the program, Fast Track was the most significant factor among variables affecting the chances of first-cycle approval, with 78% of Fast Track applications accomplishing this milestone.

The barriers to entry have risen over time. “Although many experts today would argue that a bit more is typically needed to gain Fast Track status (e.g., early biological response data in humans), it’s clear that the evidentiary hurdle remains reasonably low,” Mathieu said. “The success rates for Fast Track applications submitted to FDA’s Center for Drug Evaluation and Research (CDER) have ranged between 70% and 80% over the last three years.”

Once Fast Track is granted, there are significant benefits to a sponsor company, including the ability to “put in parts of your application piecemeal” and less risk of an “action by the FDA that would slow things down,” said Christopher-Paul Milne, director of Research, Tufts Center for the Study of Drug Development (CSDD).

“Basically, that’s what Fast Track is designed to do—head off problems while you’re in your normal development cycle,” Milne said. In addition, the program may trim the cost of drug development by shorting research timelines, opening up the opportunity of early approval.

Ultimately, the Fast Track program has been deemed a success, with approximately two thirds of all 770 Fast Track requests approved by the FDA from 2007 to 2015, according to the Government Accountability Office (GAO). The Fast Track program has “withstood the test of time” and is unlikely to be curtailed under the new FDA Commissioner Scott Gottlieb, said Milne.AO). The Fast Track program has “withstood the test of time” and is unlikely to be curtailed under the new FDA Commissioner Scott Gottlieb, said Milne.
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PunkassDerm
Posted on: Aug 1 2018, 11:44 AM


Group: Member
Posts: 509

Still like to paddle my own, GT3 Manual.
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PunkassDerm
Posted on: Aug 1 2018, 10:57 AM


Group: Member
Posts: 509

I originally had dreams of 200-300/share in 2007. Today, just happy to see her hold ground. Should it be organically higher? Is some unknown entity holding the stock back as part of a plan? $30 would just be a nice endpoint for me to justify these last 14 years. I can live with that now. Timeline unknown, deadlines and goals are disappointing.

How about, before a competing melanocortin is approved?

Goals: Finish the home that diverted funds went to CLVLY, add a nice pool, put a Porsche in the garage bay.
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PunkassDerm
Posted on: Aug 1 2018, 01:23 AM


Group: Member
Posts: 509

I think Wolgen won't give up until he maxes out all his performance rights. Then maybe buyout/merger. I'd love to see 30AUD, a fair evaluation and be forced to be done. How many hours do we all spend watching these boards, researching and fretting? A good positive run and out, back to living. I for one fret much!
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PunkassDerm
Posted on: Jul 25 2018, 09:23 AM


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Posts: 509

Begs the question...what's next. Is beef cultured from a cell line still beef?
Biosimilar meat for PETA, here it comes. They hate monsanto GMO, but this I bet they approve.

http://www.fdalawblog.net/2018/04/what-is-beef-round-two/

What is Beef? Round Two

April 20, 2018
By Riëtte van Laack —

As we previously reported, the United States Cattlemen’s Association (USCA) filed a Petition with the Food Safety and Inspection Service (FSIS), asking that FSIS establish formal definitions of “meat” and “beef” that exclude what petitioners call lab grown meat and products prepared from plant or insect protein. Until April 17, the majority of comments submitted have been in support of the petition.

The National Cattlemen’s Beef Association, (NCBA), however, does not support the Petition. As described in its comment to the Petition, the NCBA does not believe that the action requested by USCA “will adequately provide meaningful protection for beef nomenclature.” In contrast to the USCA, the NCBA wants FSIS to assert jurisdiction over foods produced from cell or tissue culture that are derived from livestock and poultry animals or their parts, so as to ensure a level playing field. NCBA takes the position that, since cell-cultured or lab-grown meat products are derived from parts of a carcass, in this case stem cells, these products fall squarely within the definition of meat food product. Even if this were not the case, NCBA believes that “FSIS should assert jurisdiction as a means of ensuring regulatory equity.”

As to the labeling of the product, NCBA seems of two minds. It asserts that the cultured meat should not be permitted to be marketed as beef. Yet, it argues that, if the producers of lab-grown or cultured meat products wish to call these products meat, they must adhere to the same food safety inspection standards and comply with the same labeling standards as traditional meat food products; only in that way can “arbitrary marketing claims,” such as “clean meat,” be avoided.
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PunkassDerm
Posted on: Jul 25 2018, 09:06 AM


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Posts: 509

Biosimilar is actually the "generic" form of a biologic drug. These days often a monoclonal antibody. Whereas traditional drugs are made with a recipe and chemical reactants (can be exactly reproduced) a biosimilar can never be exactly the same. As I understand (hopefully correctly) there are often made from bacteria or cell lines. A rip-off biosimilar can have as similar structure and therapeutic effect, but is never ever identical, hence bio-SIMILAR. I think Harris was referring to biologics in general and likely JAK inhibitors.

The FDA discussing biosimilars has nothing to do with traditional drugs, i.e. afamelanotide; but to making cheap versions of established biologic drugs like Humira, Stelara and cancer drugs like Zelboraf and Yervoy... etc


Understanding biologics: How they differ from drugs and why they cost more

https://www.everydayhealth.com/columns/zimn...they-cost-more/


Because second-generation biologics are complex proteins they can't yet be made by following a chemical recipe. We just don't know how to do that. But since all living cells know how to make proteins, that's basically what they do for a living, so to speak, second-generation biologics are made by exploiting this fact. We "trick" certain cells to make the proteins for us using biotechnology. A variety of cells have been used to make biologics, but the key is that they have to be alive and fully functioning. We've used yeast and bacteria (E coli), and even cells that come from mammals. One of the most widely used mammalian cells is called CHO because it originally came from the Chinese hamster (the "O" signifies that the specific cell used came from the ovary).

There are two fundamental requirements for making a biologic. One is that the cells in which the product will be made have to be grown in extremely large quantities. You need huge vats of yeast, bacteria or CHO cells, and they have to be maintained under conditions that allow them to live and to function normally. But if you think that's complicated, it's the second requirement that's the real mind blower. Since the cellular instructions for making all proteins are carried by the DNA in the genes, if you could either isolate or create the right gene you'd have the blueprint that would tell the cell how to make the protein you want.



What is a biosimilar, from the FDA

https://www.fda.gov/downloads/Drugs/Develop...s/UCM585738.pdf
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PunkassDerm
Posted on: Jul 25 2018, 02:14 AM


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Posts: 509

https://www.umassmed.edu/vitiligo/about/dir...-harris-md-phd/


Director: John E. Harris, MD, PhD

John Harris: Dr. Harris is a tenure-track Assistant Professor in the Dermatology Division, Department of Medicine at the University of Massachusetts Medical School (UMMS) in Worcester, MA. Dr. Harris directs the Vitiligo Clinic and Research Center at UMMS, which incorporates a specialty clinic for the diagnosis and treatment of patients with vitiligo, as well as a vitiligo research laboratory. He uses basic, translational, and clinical research approaches to better understand autoimmunity in vitiligo, with a particular focus on developing more effective treatments.

He earned his MD and PhD degrees at UMMS, and his PhD thesis was focused on the loss of autoimmune tolerance in juvenile diabetes. He entered a combined research/residency program in dermatology at the University of Pennsylvania in Philadelphia, PA, and his postdoctoral research focused on the development of a mouse model of vitiligo with epidermal depigmentation. He now advises multiple graduate students, MD/PhD students, and postdoctoral fellows in his research laboratory at UMMS, and teaches medical students and residents in his vitiligo clinic.

He has authored multiple research publications and textbook chapters on vitiligo and other topics, and serves on a number of advisory boards and committees, including the Dermatology Foundation, Skin of Color Society, Vitiligo Working Group, Vitiligo Research Foundation, National Alopecia Areata Foundation, American Academy of Dermatology and the New England Dermatology Society, among others. He is an advisor and collaborator with multiple pharmaceutical companies, including AbbVie, Combe Inc, Genzyme/Sanofi, and Pfizer.

Dr. Harris is an ad hoc reviewer on grant applications for the National Institutes of Health (NIH), Dermatology Foundation, and National Alopecia Areata Foundation, as well as multiple research journals, including Science Translational Medicine, the Journal of Clinical Investigation, the Journal of Investigative Dermatology, Pigment Cell & Melanoma Research, Experimental Dermatology, the Journal of the American Academy of Dermatology, JAMA Dermatology, and others. He receives generous grant support from the NIH, Dermatology Foundation, Kawaja Vitiligo Initiative, and the Vitiligo Research Foundation. He has lectured on vitiligo and other topics to local, regional, national, and international audiences.
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PunkassDerm
Posted on: Jul 25 2018, 12:27 AM


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Vitiligo pathogenesis and emerging treatments
Mehdi Rashighi, MD and John E. Harris, MD, PhD


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5362109/


Afamelaotide mentioned, and may compliment JAK inhibitors...as a multi-therapeutic approach. Same John Harris from UMASS.
Another little fact, Abbvie has a research facility literally across the street from UMASS main campus.



Attached Image




see below proximity Abbvie bio-research to UMASS medical school. Abbvie highly active in JAK inhibitors.

Attached Image

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PunkassDerm
Posted on: Jul 24 2018, 11:51 PM


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Posts: 509

Interesting!

I've also noticed afamelanotide has disappeared from Dr Harris' vernacular, giving way to memory-T research and melanocyte transplantation (performed in house BTW by Dr Dorie Goldberg). Has has group turned their backs in order to monetize a different avenue? Why did he not even mention afamelanotide as a promising alternative given he was involved in studies?
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PunkassDerm
Posted on: Jul 24 2018, 01:59 PM


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Posts: 509

MagellanRx Pipeline - July 2018
p24


ETA of Feb 25, 2019


https://www1.magellanrx.com/media/773130/mr...y-2018_0718.pdf


Attached Image

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PunkassDerm
Posted on: Jun 25 2018, 10:48 PM


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Posts: 509

https://www.nasdaq.com/press-release/fda-to...-20180625-00168

FDA to Review Australian Drug for Genetic Disorder of Absolute Light Intolerance
By GlobeNewswire, June 25, 2018, 06:00:00 AM EDT



Historic treatment proposed for rare disease causing burns, ulcerations and lifelong isolation of patients forced to live in the dark
MELBOURNE, Australia, June 25, 2018 (GLOBE NEWSWIRE) -- In a landmark case, the US Food and Drug Administration (FDA) has begun a review of an innovative drug developed for patients who carry a rare genetic blood disorder known as erythropoietic protoporphyria (EPP). EPP patients suffer extreme biochemical reactions when they expose their skin to any light source, particularly the spectrum of visible light, restricting their ability to function properly and forcing them to lead an isolated life in the dark.


The pharmaceutical innovation - known as SCENESSE® or afamelanotide 16mg - was developed for EPP over the past 14 years by the Australian pharmaceutical company CLINUVEL.

Due to a genetic defect, EPP patients carry a deficiency in one of their key enzymes to produce heme, and consequently accumulate a chemical substance in their blood which immediately reacts when patients are exposed to light, including sun, ambient and artificial sources. Patients incur physical burns and ulcers, and are in a state of crisis following light exposure, summarized as phototoxicity. This usually occurs within minutes of exposure to bright lights, especially sunlight. Phototoxic reactions last from days to weeks, and are unresponsive to any other medications.

SCENESSE®, which is already authorized in Europe for adult EPP patients, uses the body's own defensive systems to protect EPP patients from light.1 The drug, administered as a subcutaneous dose every two months, activates melanin (pigment) in skin, which acts as a physical protective barrier to shield the chemicals in the blood from light. CLINUVEL has now submitted a new drug application to the FDA requesting SCENESSE® be authorized for distribution in the US, and expects the review to be completed in 2019.

"The innovation developed as SCENESSE® activates an umbrella of melanin which shields patients' skin cells from light sources," CLINUVEL's Chief Scientific Officer Dr Dennis Wright said.

Professor Elisabeth Minder, head of Biochemical Laboratory Analytics at Triemli Hospital in Zurich, was involved in the first clinical trials of the product in EPP and continues to treat EPP patients.

"My patients tell me, since 2006, that this treatment facilitates a life which was unthinkable for them and their immediate families," Prof Minder said. "Therefore, I am delighted that this treatment finally nears the point of becoming available to all American EPP patients."

Over 800 patients have received SCENESSE®, including 350 EPP patients in clinical trials. Results from these trials showed the drug is able to reduce the number and severity of phototoxic reactions, and allows a life which patients could never lead before. Two Phase III trials, from the US and Europe, were published in the New England Journal of Medicine, noting good tolerance to the drug.2 CLINUVEL continues to monitor the drug's ongoing use in Europe, and will establish a similar program in the US, if approved.

"We are proud to have worked so hard to be in a position where SCENESSE® may become available to US EPP patients as early as next year," Dr Wright said. "EPP is a significantly neglected disease, one which our team have focused on since 2005. It is fantastic news for US patients and their families that there is finally hope of receiving a treatment that will allow them to come out of the dark. The US EPP patients have proven to be very motivated during the clinical trials and deserve adequate medical care."

1 SCENESSE® (afamelanotide 16mg) is approved in Europe as an orphan medicinal product for the prevention of phototoxicity in adult patients with EPP. Information on the product can be found on CLINUVEL's website at www.clinuvel.com.
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PunkassDerm
Posted on: Jun 25 2018, 10:20 AM


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Posts: 509

15 today for CUV? More? bets?

I could cry
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PunkassDerm
Posted on: Jun 23 2018, 11:42 PM


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Posts: 509

that logo...
is painful
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PunkassDerm
Posted on: Jun 22 2018, 01:33 PM


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Posts: 509

Refocused? Shopping for a GT3!
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PunkassDerm
Posted on: Jun 21 2018, 01:00 PM


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Posts: 509

we got marketing team, new blood.
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PunkassDerm
Posted on: Jun 21 2018, 12:53 PM


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Posts: 509

I propose rebranding in a new direction:

CLINUSNAIL

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PunkassDerm
Posted on: Jun 21 2018, 12:28 PM


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Posts: 509

What I really have a difficult time grasping...

Palatin in a short amount of time gets their FDA-NDA accepted for a FEMALE BONER DRUG

Yet Clinuvel's keystone cops can't get their shit together for an efficacious drug geared towards an ULTRA-ORPHAN DISEASE with no effective treatment.

EVERY FREAKING DELAY, AND THIS GOES BACK...SHOULD RESULT IN PERFORMANCE RIGHTS PENALTIES FOR CORPORATE SILLY NANNIES!
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PunkassDerm
Posted on: Jun 20 2018, 04:55 AM


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Posts: 509

I know this is medicine and all...

But no news IS NOT good news.

tick tock I can't stand it
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PunkassDerm
Posted on: Jun 16 2018, 06:13 AM


Group: Member
Posts: 509

With many prayers, YES. If I'm right and if it shoots up to 15, happy to give to an EPP sufferer either way!


A step further, I'll donate to the APF:

http://www.porphyriafoundation.com/content...yria-foundation



Then the American Vitiligo Foundation:

http://www.avrf.org/
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