Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss

JohnDoe5

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Oh, that's right. So then they CAN produce it, I guess the question then becomes can they produce it at some reasonable price. I mean we've come to terms now with the likelihood that it's gonna cost a lot of money, 10s of 1000s of $, so could the labs produce it at something like that kinda price is the question now.
I would think the blackmarket price would be cheaper because a lot of the blackmarket chemicals come from countries where labor is less expensive, such as India and China.
 

coolio

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IMO the difficulty of producing monoclonals is the main thing standing in the way of black market HMI-115.

If it was easy enough to do, then somebody would be willing to rip off somebody and sell it. If it's not one Chinese company ripping off another then it would be an Indian lab ripping off the Chinese or something. One way or anther it would happen.
 

pegasus2

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86 pages… Can someone summarize for me; is high prolactin good or bad? What is Bayern trying to achieve with this antibody?
If you wanted to know that all you had to do is look up the definition of antibody.
 

coolio

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86 pages… Can someone summarize for me; is high prolactin good or bad? What is Bayern trying to achieve with this antibody?

Stump Macaques regrew a lot of hair for months, still increasing at the end of the studied period, after one set of injections. Any questions?
 

Ralph Wiggum

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Virtually all humans regrow hair with oral minoxidil. Many don't regrow hair with topical minoxidil because they lack the enzyme in the skin which converts minoxidil into its active form. Taking it orally converts it in the liver where the enzyme is present in all humans, so that's why all of them respond to oral minoxidil even though they don't respond to topical. Apparently all macaques have the sulfotransferase enzyme in their skin.
Is this definite? Dr. Rassman said this yesterday:

Do you prefer to prescribe oral or topical minoxidil?​

Jun 6, 2022/by William Rassman, M.D./Hair Loss Causes
I have no preference. Only about 40% of men are minoxidil responders and when they do respond, they respond to both the topical and the oral. The topical keeps it local
 

pegasus2

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Is this definite? Dr. Rassman said this yesterday:

Do you prefer to prescribe oral or topical minoxidil?​

Jun 6, 2022/by William Rassman, M.D./Hair Loss Causes
I have no preference. Only about 40% of men are minoxidil responders and when they do respond, they respond to both the topical and the oral. The topical keeps it local
Response rate is around that for topical, but studies have found a response rate near 100 for oral minoxidil
 

RagnarLothbrok

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Yeah although there still seems to be a link with SULT1A genes and higher Oral Minoxidil response which is interesting. I guess follicles having more SULT1A could enhance OM effects further
 

EndlessPossibilities

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Acetylation modulates prolactin receptor dimerization







HDAC4/9 are present in healthy hair follicles and this study reveals they are strongly associated with Androgenetic Alopecia. It was always assumed that this association was due to them being corepressors of the AR, but they are also corepressors of the PRLR.





I think the balance of HDACs and HATs is skewed in Androgenetic Alopecia creating upregulation of AR and PRLR, which ultimately represses canonical Wnt signaling, causing a progressively shorter anagen phase. From the top SNPs in this study there is the AR of course, then genes that regulate AR and PRLR transactivation, PAX1 and TWIST which are involved in Wnt signaling and upregulated by PRLR. It certainly seems like Androgenetic Alopecia is driven by coactivation of the AR and PRLR. AR activation itself recruits histone acetyltransferases, which upregulate PRLR. Crosstalk between the two then takes place.






ASC-J9 may be an ideal AR antagonist to use with HMI-115, as curcumin inhibits HATs.


HAT inhibitors have shown success in prostate cancer.

"A limited number of HAT inhibitors are in preclinical or clinical trials, with p300/CBP and P/CAF-specific inhibitors showing the most promising effects"



Estradiol promotes prolactin transactivation by inducing histone acetylation through ERα, but the predominant estrogen receptor in the scalp is ERβ and it silences ERα. So estradiol does not upregulate prolactin signaling in the hair follicle, despite upregulating it in other tissues.


HDAC inhibitors also work for prostate cancer, through inhibiting HSP90.




Prolactin actually upregulates HSP90



It is theorized that in castration resistant prostate cancer AR activation is continued in part by "mechanisms including activation of kinase pathways that can both stabilize AR and enhance its transcriptional activity and upregulations of AR coactivators that increase AR mediated transcription. These sensitize AR to lower levels of ligand."




Prolactin upregulates all of these pathways that hypersensitize the AR.

Also of importance, HSP90 promotes transcription of Twist1. Twist1 ablation results in perpetual anagen phase in mice.


You can see from all this that the AR and PRLR are very interconnected. It's not hard to imagine that silencing the PRLR would stop the positive feedback loop between the two receptors and reverse male pattern baldness in a more potent and lasting way than current treatments, which is what was observed in stump-tailed macaques. Returning AR sensitivity to normal and restoring homeostasis could give lasting results that simple DHT inhibition does not.


Ultimate hair loss stack?: HMI-115, ASC-J9, Estriol. Nothing else needed for full reversal?
This is great stuff. But here’s what doesn’t make any sense. Hdac4 apparently inhibits runx2. From my understanding runx2 is needed for hair growth.
 

GotHair?

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Phase 1 will be over in 2024. Until then we just have to wait. Still can't believe they need 2 years to recruit 20 individuals and treat them over 24-Week period. I think they are being very cautious about safety.
 

RagnarLothbrok

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Yeah it sucks, usually Phase 1s are pretty fast, and thats literally all we need to know if HMI works similar to monkeys or not. But it is an injected antibody, so I guess the Phase 1 is much more delicate than usual.
 

RolfLeeBuckler

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Phase 1 will be over in 2024. Until then we just have to wait. Still can't believe they need 2 years to recruit 20 individuals and treat them over 24-Week period. I think they are being very cautious about safety.

Safety cant be their concern. They Are doing an endometriosis Trial with 152 participants with the same product (https://clinicaltrials.gov/ct2/show/NCT05101317)

i think they Are Glad about the 56m$ they got from the Investors. They Arent motivated enough to bring HMI-115 to Market fast. They Are just scientist No Business man.
-They got the license of Bayer in 2019 and they need 3 Years (!!!!!) to start a Phase 1 trial
- the Phase 1 Trial is much to Long
- they started a Phase 1 trial in Australia despite the fact that they got FDA permissions For doing a multicenter study in US

it is an obvious situation that it was a terrible mistake that Pharma Giant Bayer gave their Technology to a Little Company called Hope Medicine who isnt able to bring HMI-115 to Market as this brilliant product deserves it.
 

pegasus2

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Phase 1 will be over in 2024. Until then we just have to wait. Still can't believe they need 2 years to recruit 20 individuals and treat them over 24-Week period. I think they are being very cautious about safety.
Stop saying this. Those estimated completion dates are meaningless. They are just placeholders. The study will be done next year. We should have the results by March
 

GotHair?

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Stop saying this. Those estimated completion dates are meaningless. They are just placeholders. The study will be done next year. We should have the results by March
I hope so. If true it will be very interesting to get them.
 

Redgate

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neglecting probability got you the wrong answer (to a really easy question)

HMI not only doesn't have phase II results, it's literally not even done the treatment stage of the tiny phase I
They were going to do a global phase 2 directly in the US, EU, Australia and China because the drug has already passed phase 1 for endometriosis. Australian regulators didn't like that so they're doing a phase 1 in Australia.
This has been mentioned multiple times in this thread so how about you read it instead of being retarded and cherry-picking older posts before this information was known?
 
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