Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss

RolfLeeBuckler

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They have a partnership with PAREXEL to do clinical trials in Europe.
PAREXEL has Clinics in London and Berlin so they should Start Trial in Berlin as they Said they will do trials in Europe and Asia.

So why they only Start trials in US now ?!
 

lostandfind

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What quesitions do you refer to? According to my life experience in China it's almost impossible for a stranger like me to get the personal contact info of Professor Xiao and have her answer some undisclosed questions regarding a breakthrough drug for comercialization.
I just found a Chinese wechat blogger wrote to Professor Xiao Ruiping through email and got a courtesy reply to his questions. Here's the link:
https://mp.weixin.qq.com/s/nJ97CFClMs1vB9DyaEZ-IQ
 

pegasus2

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Thank you for your attention to my research. The results of the red-faced monkey are exciting and are currently being tested in the applicant's[volunteer's?] body. Hope to have good news to share with you in the near future.good luck,Xiao Ruiping

Does this mean they started phase 2 in China already?

It's funny that this blogger got attacked for calling this the best treatment because Chinese herbal medicine treatments have better pictures lol. Different country same story.
 

lostandfind

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Does this mean they started phase 2 in China already?

It's funny that this blogger got attacked for calling this the best treatment because Chinese herbal medicine treatments have better pictures lol. Different country same story.
Let me correct that part “and are currently being tested in the applicant's[volunteer's?] body”. The original Chinese means "the application for human experiment is underway".
 

pegasus2

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Although it's been documented that Zinc won't have any cosmetic results, if we take into account that our GH levels already naturally decrease as we age and that this downregulation may be locally exponentiated during hairloss, it could be a reasonable approach to implement in order to control extra pituitary prolactin (ePRL the one produced locally by hair and skin) activity.

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Leaving some of the studies and information I read today in case someone considers it useful.

"Regulation of extra pituitary prolactin

The 2 key hormones, estrogen and TRH, that control pPRL secretion also regulate ePRL and PRL-R expression in human scalp skin and hair follicles in vitro. Estrogen increases the expression of ePRL and PRL-R proteins in the epidermis, eccrine sweat glands and hair follicle ORS, corresponding to increased ePRL and PRL-R mRNA expression in ORS keratinocytes (87). The effect of TRH is more complex. In cultured human hair follicles, TRH increases ePRL mRNA and protein expression similar to estrogen. However, PRL-R expression at the protein level is decreased whereas PRL-R mRNA at the gene level is increased (87)... Recently, both PRL and its receptor have been located in inner root sheath and outer root sheath (ORS) keratinocytes of anagen and catagen hair follicles of mice".


"Oestrogen treatment significantly upregulated PRL and PRLR immunoreactivity in selected skin and hair follicle compartments, at the gene and protein level (P < 0.05). TRH significantly increased PRL immunoreactivity and transcription in hair follicles (P < 0.05); however, while it also increased PRLR transcription in hair follicles, it downregulated PRLR immunoreactivity in the hair follicle ORS"



"Estradiol activates the hPrl promoter in extra pituitary sites such as skin and human hair follicles. This study, we show that E2 acts through ERα to activate the hPrl promoter through a degenerate estrogen response element (ERE) sequence found at −1189 bp relative to the transcription start site."





I will note a couple things about this before people freak out. As highlighted above, estrogen receptor alpha is the one that promotes prolactin production. Estrogen receptor alpha is also shown to initiate the catagen phase. Estrogen grows hair because the predominant estrogen receptor in human hair follicles is beta. ERb silences the actions of ERa, so estrogen does not promote prolactin production in human scalp hair follicles.
 

JaneyElizabeth

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Although it's been documented that Zinc won't have any cosmetic results, if we take into account that our GH levels already naturally decrease as we age and that this downregulation may be locally exponentiated during hairloss, it could be a reasonable approach to implement in order to control extra pituitary prolactin (ePRL the one produced locally by hair and skin) activity.

------ - - - -

Leaving some of the studies and information I read today in case someone considers it useful.

"Regulation of extra pituitary prolactin

The 2 key hormones, estrogen and TRH, that control pPRL secretion also regulate ePRL and PRL-R expression in human scalp skin and hair follicles in vitro. Estrogen increases the expression of ePRL and PRL-R proteins in the epidermis, eccrine sweat glands and hair follicle ORS, corresponding to increased ePRL and PRL-R mRNA expression in ORS keratinocytes (87). The effect of TRH is more complex. In cultured human hair follicles, TRH increases ePRL mRNA and protein expression similar to estrogen. However, PRL-R expression at the protein level is decreased whereas PRL-R mRNA at the gene level is increased (87)... Recently, both PRL and its receptor have been located in inner root sheath and outer root sheath (ORS) keratinocytes of anagen and catagen hair follicles of mice".


"Oestrogen treatment significantly upregulated PRL and PRLR immunoreactivity in selected skin and hair follicle compartments, at the gene and protein level (P < 0.05). TRH significantly increased PRL immunoreactivity and transcription in hair follicles (P < 0.05); however, while it also increased PRLR transcription in hair follicles, it downregulated PRLR immunoreactivity in the hair follicle ORS"



"Estradiol activates the hPrl promoter in extra pituitary sites such as skin and human hair follicles. This study, we show that E2 acts through ERα to activate the hPrl promoter through a degenerate estrogen response element (ERE) sequence found at −1189 bp relative to the transcription start site."





Impressive. Mr. Dog.
 

RolfLeeBuckler

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Here you Can Read about the partnership of Hope Medicine and PAREXEL in developping HMI-115 with clinical trials planned in Europe:

I Hope they will Start the clinical study in Berlin as soon as possible
 

LouisSarkozy

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I will note a couple things about this before people freak out. As highlighted above, estrogen receptor alpha is the one that promotes prolactin production. Estrogen receptor alpha is also shown to initiate the catagen phase. Estrogen grows hair because the predominant estrogen receptor in human hair follicles is beta. ERb silences the actions of ERa, so estrogen does not promote prolactin production in human scalp hair follicles.
maybe i'm totally out of context and no talking about the right type of oestrogen but if ERa are bad why does product like pantostin conaining 17a oestradiol are recommended for hairloss? https://pubmed.ncbi.nlm.nih.gov/7398983/ thanks
 

pegasus2

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maybe i'm totally out of context and no talking about the right type of oestrogen but if ERa are bad why does product like pantostin conaining 17a oestradiol are recommended for hairloss? https://pubmed.ncbi.nlm.nih.gov/7398983/ thanks
It binds to both main estrogen receptors, alpha and beta same as 17b estradiol. The a and b in estradiol have nothing to do with the receptor it binds to.
 

pegasus2

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"In vivo inhibition of macrophage function was sufficient to induce HFSC proliferation and hair cycle induction. Together these results clarify how JAK-STAT signaling actively inhibits hair growth"



"PRL synergized with the TH1 cytokine IFN-gamma, a known activator of macrophages..."


"macrophages have been reported to produce PRL and express high levels of prolactin receptor (PRLR)"



"PRL synergized with the TH1 cytokine IFN-gamma, a known activator of macrophages"

This is why I have concerns about topical SMI, I worry that PRLR must be blocked systemically to prevent macrophages from outside invading the HF.
 

pegasus2

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sh*t this is bad news. Hope you re wrong..

Maybe cabergoline + topical smi combo will do the trick ?
I don't think it's a problem, just a small potential that it could be. If it was then adding cabergoline wouldn't help. Macrophages produce their own prolactin and have their own PRLRs
 

Dimitri001

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"In vivo inhibition of macrophage function was sufficient to induce HFSC proliferation and hair cycle induction. Together these results clarify how JAK-STAT signaling actively inhibits hair growth"



"PRL synergized with the TH1 cytokine IFN-gamma, a known activator of macrophages..."


"macrophages have been reported to produce PRL and express high levels of prolactin receptor (PRLR)"



"PRL synergized with the TH1 cytokine IFN-gamma, a known activator of macrophages"


Our observations further suggest that PRL alone and in synergy with IFN-gamma, released through induction of IL-12, may generate tumoricidal macrophages and thus regulate the antitumor immune response of tumor hosts.

That's got me worried a bit. If PRL generates macrophages which are needed to fight tumors, are we putting ourselves at risk with no antitumor immune response? On the other hand, they say PRL, not PRLR, so IDK if it's that you just need PRL for this function, rather than PRL activation of the PRLR, in which case we'd be fine, since we're just blocking the receptor, rather than lowering PRL.
 

charlie76761

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https://europepmc.org/article/pmc/1606541

Not sure if the above has been shared already, but seems to be further research showing lower PRL can be good for hair when elevated

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 hyper-prolactinemia
 

Letitgrow

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I haven't been on this forum for a while now, in short when did Prolactin became a culprit for hair loss?
 
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