Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss

jan_miezda

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Hopefuel. When will this be available on grey market ? Some say 3 to 5 years before end of phase 2 in page 7. I don't know how it works in Asia.

Edit: before market launch, not end of phase 2.
This provides general info for chinas drug approval

 

poopfeast420

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Says we aren't stuck waiting for scams then says we're waiting for Samumed lol

I agree with your point though, things like Bayer, Tsuji, Surrozen, Tissuse, Stemson, Olix, KY, are all more impressive than previous disappointments. Most are more than 5 years away though.
I agree that the way the CEO is overhyping it is pretty close to scam territory.

Still, I'm excited for it. The study had 20%+ growth in 4 months for nw4 and under, if it could just do a quarter of that long term while maintaining it's a huge win. Don't need a cure, just need something to maintain until kintor comes out, then BAY, then tsuji, etc etc.
 

pegasus2

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Hlbgone

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As usual I'm trying to remain grounded and not get my hopes up to avoid shattered expectations. It's difficult since this seems to hold so much potential. I find it surprising that no one on the YouTube vlogs has covered it. Also I haven't seen anything mentioned on tressless.

A new efficacious treatment is long overdue.
 

eeyore

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As usual I'm trying to remain grounded and not get my hopes up to avoid shattered expectations. It's difficult since this seems to hold so much potential. I find it surprising that no one on the YouTube vlogs has covered it. Also I haven't seen anything mentioned on tressless.

A new efficacious treatment is long overdue.
I'm in the same boat as you. For once a company actually has actually shown efficacy in primates and not mice.
 

Charger

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Did some quick reading on the negative effects of very low prolactin as I wasn't very informed, and it apparently such a state can induce a low 5AR type state by reducing the output of adrenal androgens (DHEA for example), and can result in low DHT, which I'm guessing is where a majority of the effectiveness of this treatment comes from.

So, again, another promising treatment is going to come down to being highly anti-androgenic and whether or not you can tolerate it. I'm just going to assume that the more effective a treatment is, the more intense the side effects are likely to be. If you're comfortable with a low androgen state, I'm not sure whats keeping someone from stacking finasteride/dutasteride with ru58841, which I can't imagine wouldn't provide some results for most.

 

Throwaway94

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Did some quick reading on the negative effects of very low prolactin as I wasn't very informed, and it apparently such a state can induce a low 5AR type state by reducing the output of adrenal androgens (DHEA for example), and can result in low DHT, which I'm guessing is where a majority of the effectiveness of this treatment comes from.

So, again, another promising treatment is going to come down to being highly anti-androgenic and whether or not you can tolerate it. I'm just going to assume that the more effective a treatment is, the more intense the side effects are likely to be. If you're comfortable with a low androgen state, I'm not sure whats keeping someone from stacking finasteride/dutasteride with ru58841, which I can't imagine wouldn't provide some results for most.

But the purpose of the PRL receptor antagonist is to prevent transcription locally in the follicle just like a local antiandrogen, just a different angle. The hair follicle produces a very small amount of prolactin just as it does DHT, systemically it's quite an insignificant amount but it's responsible for the majority of prolactin related damage to hair.
 

RagnarLothbrok

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I think the Kintor AR degradation angle is going to end better than this because of side effect profile, unless they make the miracle molleculle that only acts locally, which usually doesnt happen for hairloss.
 

SausageDawg

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4709B808-411B-4DB5-86AA-100D573BF44B.jpeg
 

pegasus2

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Did some quick reading on the negative effects of very low prolactin as I wasn't very informed, and it apparently such a state can induce a low 5AR type state by reducing the output of adrenal androgens (DHEA for example), and can result in low DHT, which I'm guessing is where a majority of the effectiveness of this treatment comes from.
Castration doesn't reverse hair loss so that's not how this works. A drug that targets the AR can prevent hair loss, but will never be able to give the regrowth that this does. Also, there's no point in combining finasteride with dutasteride, they do the same thing. Combing dutasteride with RU can't do more than castration, which isn't much.

We still have stem cells in bald scalp, they just don't proliferate anymore. Prolactin apparently is the brake that keeps HF stem cells in a quiescent state. It's my hope that if you shut down prolactin along with a Wnt agonist you'll wake up every follicle that isn't completely destroyed. That is, it's the best treatment that we could possibly have without creating new follicles.
At the cellular level, PRL has been shown to regulate a wide variety of critical cell responses, including proliferation, differentiation, survival, and migration, to cite only a few. Intriguingly, PRL can in some instances regulate these responses in opposite ways depending on the context...

such functional diversity is also observed at the level of stem/progenitor cell regulation. For example, in the hair follicle, PRL contributes to maintain the stem cell pool in quiescence

 

Armando Jose

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It is complex,..., results in vitro can be different than in vivo. I´ll bet that PRL concentration can vary depending stage oh hair cycle
PRL receptors, expressed in HFs, are functional and that human skin and human scalp HFs are both direct targets and sources of PRL. Our data suggest that PRL acts as an autocrine hair growth modulator with catagen-promoting functions and that the hair growth-inhibitory effects of PRL demonstrated here may underlie the as yet ill-understood hair loss in patients with hyperprolactinemia.
 

fearofthereaper

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Castration doesn't reverse hair loss so that's not how this works. A drug that targets the AR can prevent hair loss, but will never be able to give the regrowth that this does. Also, there's no point in combining finasteride with dutasteride, they do the same thing. Combing dutasteride with RU can't do more than castration, which isn't much.

We still have stem cells in bald scalp, they just don't proliferate anymore. Prolactin apparently is the brake that keeps HF stem cells in a quiescent state. It's my hope that if you shut down prolactin along with a Wnt agonist you'll wake up every follicle that isn't completely destroyed. That is, it's the best treatment that we could possibly have without creating new follicles.


Do we have an exact guess how many follicles get destroyed, and how long it takes? If someone is NW7 at say 25, would he still have a sufficient portion of his follicles to get back to NW1 once he'd take those drugs?
 

pegasus2

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Do we have an exact guess how many follicles get destroyed, and how long it takes? If someone is NW7 at say 25, would he still have a sufficient portion of his follicles to get back to NW1 once he'd take those drugs?
I don't know. Fibrosis can set in after a few years according to some sources. How much fibrosis is needed to destroy the follicle, maybe it takes 5 years in one person, 30 years in another. Even at 25 if you're slick bald I wouldn't get your hopes up. In the macaques, only senile monkeys failed to regrow hair. The younger they were the more hair they grew back.
 

Gegen

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Do we have an exact guess how many follicles get destroyed, and how long it takes? If someone is NW7 at say 25, would he still have a sufficient portion of his follicles to get back to NW1 once he'd take those drugs?
Interesting question that I share. I thought follicles never died but only miniaturized heavily.
 

Charger

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Castration doesn't reverse hair loss so that's not how this works. A drug that targets the AR can prevent hair loss, but will never be able to give the regrowth that this does. Also, there's no point in combining finasteride with dutasteride, they do the same thing. Combing dutasteride with RU can't do more than castration, which isn't much.
Finasteride/dutasteride was meant to imply picking either/or, not combining.

Still interested to see how this plays out, but I'll have to let others more brave than me be the guinea pigs, hopefully you guys can get your hands on it.
 

pegasus2

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Interesting question that I share. I thought follicles never died but only miniaturized heavily.
All depends on the amount of fibrosis. Keep treating your hair even if it's not working to prevent further damage so that when something like BAY does come out you can benefit from it.

"However, FAPD is often diagnosed with delay and well established before introduction of treatment, and destruction of hair follicles in the scarred area is irreversible"
 

Selb

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All depends on the amount of fibrosis. Keep treating your hair even if it's not working to prevent further damage so that when something like BAY does come out you can benefit from it.

"However, FAPD is often diagnosed with delay and well established before introduction of treatment, and destruction of hair follicles in the scarred area is irreversible"
Would the destruction by way of fibrosis be reversed through wounding and a wnt agonist?
 
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