Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss

badnewsbearer

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What do you guys think about Hairclone? Its supposed to be out in 2022 I think and it's an upgrade over replicel? Any hope?
i have read a lot of literature on every angle ans i have very little hope. i think there is a very good chance that in 2030 there will be no alternative to RU and finasteride (in terms of safety and efficacy) sure maybe CB will be around or other AA but there is very little evidence to this day that they will be either free of side effects or effective. as someone who gets severe sides on 5ARi i am not hopeful for the future, hairclone is not even tested in any trial, i think it will be another scam
 

John Difool

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This is not at all what happened.

How can you say that it's not what happened? Even the wikipedia puts the emphasis on smaller prostate in the development of the drug.

In 1975, copies of Imperato-McGinley's presentation were seen by P. Roy Vagelos, who was then serving as Merck's basic-research chief. He was intrigued by the notion that decreased levels of DHT led to the development of smaller prostates. Dr. Vagelos then sought to create a drug which could mimic the condition found in these children to treat older men who were suffering from benign prostatic hyperplasia.[85]

Finasteride was developed by Merck under the code name MK-906.[61] A team led by chemist Gary Rasmusson and biologist Jerry Brooks developed potential 5α-reductase inhibitors based on transition state inhibitors, using an iterative process of molecular design, testing, and redesign.[86] In 1992, finasteride (5 mg) was approved by the U.S. Food and Drug Administration (FDA) for treatment of BPH, which Merck marketed under the brand name Proscar

In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1 mg) for treatment of male pattern hair loss, which was marketed under the brand name Propecia.[88] It was the first 5α-reductase inhibitor to be introduced and was followed by dutasteride in 2001.[89] The first study of finasteride in the treatment of hirsutism in women was published in 1994.[90]

5 years apart. Even hisutism was 2 years later. You are such a moron.

PS: I can't wait to read your next uneducated post to flame you down again. Please don't make me wait too long.
 
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badnewsbearer

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How can you say that it's not what happened? Even the wikipedia puts the emphasis on smaller prostate in the development of the drug.

In 1975, copies of Imperato-McGinley's presentation were seen by P. Roy Vagelos, who was then serving as Merck's basic-research chief. He was intrigued by the notion that decreased levels of DHT led to the development of smaller prostates. Dr. Vagelos then sought to create a drug which could mimic the condition found in these children to treat older men who were suffering from benign prostatic hyperplasia.[85]

Finasteride was developed by Merck under the code name MK-906.[61] A team led by chemist Gary Rasmusson and biologist Jerry Brooks developed potential 5α-reductase inhibitors based on transition state inhibitors, using an iterative process of molecular design, testing, and redesign.[86] In 1992, finasteride (5 mg) was approved by the U.S. Food and Drug Administration (FDA) for treatment of BPH, which Merck marketed under the brand name Proscar

In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1 mg) for treatment of male pattern hair loss, which was marketed under the brand name Propecia.[88] It was the first 5α-reductase inhibitor to be introduced and was followed by dutasteride in 2001.[89] The first study of finasteride in the treatment of hirsutism in women was published in 1994.[90]

5 years apart. Even hisutism was 2 years later. You are such a moron.
the traveling imperators presentation caused the interest thag is a fact and nothing else has been said
 

John Difool

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The causation is clear. I think it's a fact that if scientists would put the emphasis on hair loss vs curing cancer, the facts could have been reverted, but this is not the case. Most hair loss treatments will come out of a result of benefiting other more important deceases.
 

badnewsbearer

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The causation is clear. I think it's a fact that if scientists would put the emphasis on hair loss vs curing cancer, the facts could have been reverted, but this is not the case. Most hair loss treatments will come out of a result of benefiting other more important deceases.
pf course same with hair cloning which was only investigated by tsuji etc becausw it is an easy model to start with for tissue generation in general, not for financial reasons or because they see it as cure worthy
 

Armando Jose

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Hola Armando,
You are true veteran here. I still remember you even from threads about seti etc. Btw. Since you have seen a lot of hypes here. What are you thoughts on Kintor and HMI?
Honestly I have given up hope in a process that recovers long lost hair. The only thing could be the cloning of the hair, but due to its complexity, other organs and tissues can be created before a simple hair.
On the other hand, I think that the focus on prolactin and DHT are not very real because they are effects and consequences of another previous event. Prevention is possible if the initial and triggering factor is found, prevention better than cure.
 

Dimitri001

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Right, but the primary effect being sought here appears to be threshold based, whereas blocking ARs has a very obvious dose-response via well-understood mechanism.

So working backwards from the hypothesis that a sufficient PRLR antagonism/PRL reduction for enough time might be able to replicate the effects of HMI of regrowing hair in bald areas - what's a good protocol/experiment that lets you conclude if that's even possible?

I'd argue it looks pretty much nothing like what was attempted.

The group buys are really good at buying the compounds, but fall over instantly when evaluating them.
How can you conclude that the effect is threshold based when all that's been studied scientifically is a complete shutdown of the PRLR?
I agree with most of what you said, and not implying that you thought SMI would work or anything. Surely nobody will admit to that now

Just want to clarify my point re:

the prolactin angle merits research, but: changing species + changing compounds + poorly understood model = near certain failure

ie the further you deviate from the original HMI conditions, the less likely the effect is to be preserved


because the current hair loss model was not able to predict/understand the effect in the first place, and there's still no real actionable information available...

it'd be one thing to try out the actual antibody, but to find a compound that had very little chance of working and not record any meaningful observations...what was the point?
It is perfectly reasonable to believe SMI MIGHT work. It is definitely not guaranteed, far from it, but it isn't guaranteed failure either.

Changing species - AFAIK minoxidil and RU work on monkeys, too, so that's some indication that what works for them might work for us.

Changing compounds - It's the same mechanism. It doesn't matter what you stop the effect of the PRLR activation with. Of course, it's an antagonist, not an antibody, but so are CB and RU and a million other antagonists used in medicine and they all work.

Poorly understood model - What difference does this make??? If something works it doesn't stop working because you don't know why it works.

People shouldn't be discouraged from experimenting with SMI. Yes, results are very uncertain and definitely not guaranteed and anyone getting into SMI should do so soberly aware of that, but there's definitely reason to believe it might work. HMI is a long way off and if you want a chance to POTENTIALLY get those kind of results right now, we have to experiment with SMI.
 

Otrebor

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other interesting studies on the role of hif 1-a. In the next few days I will do a further study on possible links with prolactin.
In addition to the study that binds hif1a to the shh path (I remember that when I was not yet registered someone tried some agonists of that path).




The most interesting study in my view is this here:

There is an analysis of how minoxidil works and a possible reason why it sooner or later loses its effectiveness, it is possible that at some point the hif will disappear almost completely.


I make it short hif1a is basically positive for hair growth, its inhibition starting from phd can be negative and I venture to say that it can be the basis of the path of miniaturization, baldness can be a way of "freezing" the situation. in action by the organism (possibly alarmed by cell proliferation in hypoxia, which is related to cancer, in which the immune system may be important).

Targeting phd is doable if you live in japan (lol)

Otherwise, other possible drugs are listed here https://en.wikipedia.org/wiki/HIF_prolyl-hydroxylase_inhibitor. it might be useful to create lotions to apply topically and observe the results, I don't think that's already been done
 

John Difool

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Thank you, we absolutely needed your insight on this. I don't think we would be anywhere near where we are today within the scientific research field, without your amazing advices and your dedication to rehash the same things over and over for us.
 
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fashy

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When are we having the annual awards for worst user on this site cause I already have my pick cemented. Seldom can anyone else make visiting this forum an actual mental chore.
 

pegasus2

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Rhesus macaques have denser hair than the stumptailed macaques used in the study. The pictures speak for themselves, those are some very thick terminal hairs they grew.
 

pegasus2

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But they seem to have done whatever it takes to get Series B funding and a fileable patent...maybe the effect is real but I'll wait for phase II
Bayer owned the drug when the macaque test was conducted by a third party at the IMM in China. The IMM had no incentive to inflate the results. If they wanted to buy the drug from bayer they had every incentive to downplay the results.

Since you keep rehashing the same points which have already been addressed, I will make an faq on the science behind prolactin and hair loss. Then when you post your inane babbling people only have to link to that thread where it will all be laid out clearly.
 

John Difool

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@hmmmmmmmm is on a full spin with his conspiracy theories. Maybe should we contribute to volunteer liking some of his posts just as a christmas present?
 

John Difool

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Lol why do you feel the need to reply to each of my comments with such bitterness? Focus on your grandma natural cope you put on your head.

Also learn how to form intelligent sentences you idiot.
 

John Difool

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Why would I be mad when the Chinese powders I bought have helped me save my hair so I could remain a nw1 all these years? But since you have minoxidil and microneedling to help you with, you should be happy too, right?
 
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