Prolactin "minitherapy" with SMI-1 (novel protocol for lowering prolactin locally)

[1919]

Holy sh*t if Pegasus2 is boarding the hype train then I will buy my ticket too

To be fair, sometimes peg can go overboard. Like the Tsuji speculations that they had some secret human trials. Nevertheless, ill be sitting across from you on this train.

 

[TurboFixer]

To be fair, sometimes peg can go overboard. Like the Tsuji speculations that they had some secret human trials. Nevertheless, ill be sitting across from you on this train.

Safe travels my friend

 

[FollicleGuardian]

Safe travels my friend

View attachment 158522

Lmao

 

[Will Be an Egg in 5 years]

I Wonder If the results are the same in the sides and back of the Head.

 

[hairDespair]

Yes it really does look like it comes down to AR/PRLR. Neutralize them both and throw in a potent Wnt agonist, and this could get really good. I can't wait for SMI and KY to get here. I feel like a kid waiting for Christmas lol

What is this SMI and KY? Sorry, haven't had time to read all of this thread. Is it something coming out this year?

 

[1919]

I never speculated they had some secret trials. I speculated they did a phase 0 in a human, and according to their Twitter they did. Phase 0 never gets reported, it's just a toxicology test, but in this case that's enough to show them that it works

Fair enough. Though, it is my opinion that some things you speculated had unrealistic allusions.

 

[Gegen]

What is this SMI and KY? Sorry, haven't had time to read all of this thread. Is it something coming out this year?

No, both are experimental compounds. SMI is a PRLR antagonist and is thought to have similar effects to BAY ( bayer's prlr antagonist ) and KY is a promising Wnt agonist ( inhibits CXXC5 and GSK3 ).

We are the phase 1 trial.

 

[trialAcc]

No, both are experimental compounds. SMI is a PRLR antagonist and is thought to have similar effects to BAY ( bayer's prlr antagonist ) and KY is a promising Wnt agonist ( inhibits CXXC5 and GSK3 ).

We are the phase 1 trial.

That's not true. BAY has a phase 1, just hasn't released the data, that's why HOPE is saying they will initiate phase 2 this year. I'm sure if they initiate a phase 2 this year it would be released.

 

[Gegen]

That's not true. BAY has a phase 1, just hasn't released the data, that's why HOPE is saying they will initiate phase 2 this year. I'm sure if they initiate a phase 2 this year it would be released.

I talked about SMI and KY. But yes BAY has done a phase 1 and are currently doing a phase 2 if I remember correctly.

 

[1919]

That's not true. BAY has a phase 1, just hasn't released the data, that's why HOPE is saying they will initiate phase 2 this year. I'm sure if they initiate a phase 2 this year it would be released.

How are we speculating that BAY works very well. From the theorized mechanisms? or is there a similar compound that was studied?

 

[trialAcc]

How are we speculating that BAY works very well. From the theorized mechanisms? or is there a similar compound that was studied?

It was actually tested for male pattern baldness on primates, similar to how minodoxil/RU was.

The patent data says it grew/restored hair on completely bald stump tailed macaque scalp (the monkey that also have a form of male pattern baldness so are ideal for testing), continued to grow after the treatment ended and lasted over 4+ years. I think something of significance was also that it worked on the oldest monkeys as well, which would indicate they lost their hair awhile back yet still saw growth once the stem cells were able to proliferate again.

 

[trialAcc]

It was the youngest macaques which had the best response, the only males that didn't respond to treatment was the senile ones iirc.

Right, makes sense age and time of loss is a significant factor for regrowth.

 

[1919]

It was actually tested for male pattern baldness on primates, similar to how minodoxil/RU was.

The patent data says it grew/restored hair on completely bald stump tailed macaque scalp (the monkey that also have a form of male pattern baldness so are ideal for testing), continued to grow after the treatment ended and lasted over 4+ years. I think something of significance was also that it worked on the oldest monkeys as well, which would indicate they lost their hair awhile back yet still saw growth once the stem cells were able to proliferate again.

woah, I hope this translates onto humans well. Crazy how it lasted 4+ years as well. Thanks for the explanation.

 

[binuga]

Eagerly awaiting our phase 3 tests for launch on the black market.

From what I've read about AA results like these are unprecedented. Right?

I've been reading BAY's patents...
Why is it not possible to synthesize mat3? Is any information missing?

 

[Superman H_M]

That's awesome. I wonder why @FollicleGuardian you didn't launch that 1 year ago when we were discussing that on the Choi discord or when @Ollie brought itn you maybe missed it.

I'm impatient to see their Phase 1/2 results.

 

[Zon Ama]

I remember some guy in this section (not sure which thread exactly) once posted something like "f*** this haircloning stuff, itll prolly be some cheap small molecule that will save us"
Well, I hope he is right

 

[FollicleGuardian]

That's awesome. I wonder why @FollicleGuardian you didn't launch that 1 year ago when we were discussing that on the Choi discord or when @Ollie brought itn you maybe missed it.

I'm impatient to see their Phase 1/2 results.

My account was created October 2020

 

[poopfeast420]

Eagerly awaiting our phase 3 tests for launch on the black market.

From what I've read about AA results like these are unprecedented. Right?

I've been reading BAY's patents...
Why is it not possible to synthesize mat3? Is any information missing?

I did a bit of research and it seems like antibody medications are really freaking expensive to manufacture. Monoclonal antibody treatments are the most expensive treatments in the world right now IIRC

 

[Armando Jose]

Reconciled is the key word there. The conflicting effects of prolactin support the pattern of hair loss found in Androgenetic Alopecia. Of course there's the question of which came first, as they point out in the gene expression study, but it's obvious given castration experiments that the AR has the primary causal role in Androgenetic Alopecia. It also seems a pretty good bet when putting this study together with the macaque study, which produced amazing regrowth from a PRLR antagonist, that the PRLR is another highly important causal factor.

"If confirmed" can be the key word there.
And it´s obvious that castration Hamilton`s experiments where AR has a primary casual role in Androgenic Alopecia were made more 80 years ago when each sex had its own hormones and its concentration test was measured in crest of chickens. No more paper regarding this issue, strange....

 

[DogoDiLaurentiis]

Hi everyone. Lot of talk about prolactin these days. But it is just so freaking promising. Prolactin might be responsible for keeping stem cells in a dormant state (credit to @pegasus2 and @ElToso for this find about dormancy). Which might be the reason why it is so hard to get regrowth even with a really potent WNT-agonist.

So let me introduce what I call "Prolactin Minitherapy". This is a novel way to potently inhibit prolactin locally in the hair follicle. This minitherapy protocol suggests using a really high concentrated topical with a prolactin antagonist. But use a low volume of it. In other words a strong solution of PRL inhibitor, on a small area. Treatment in the area continously for 3 months. To "wake up" the dormant stem cells, and then switch to another small area. Working through the whole scalp eventually.

By keeping the % high, but total volume low we minimize the risk for side effects if it goes systemic. The effects of BAY were lasting, so in theory it will be with this protocol as well. The high % of PRL inhibitor will absolutely flood the cells in the treated area with these antagonists, the intracellular level will be high. This concentration will be needed in order to compete with prolactin for the PL receptor. This is the same mechanism as CB uses, they leverage the sheer volume, and don't focus on pure binding affinity. Not that CB is an amazing treatment, but to be so weak in terms of binding affinity, it tells us this method work.

There is two small molecule antagonist of the prolactin receptor called SMI-1 and SMI-6. Minitherapy is an option with these.

PS! This is not medical advice. This is purely a hypotethical/theoretical discussions of treatment options.

What substance do you have in mind to act as the prolactin antagonist?