Bayer Prolactin Receptor Antibody For Male And Female Pattern Hair Loss

coolio

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Prolactin receptor expression is also closely tied to serum GH. This study shows for group B (20-40 years old) as GH receptor expression declines PRLC expression increases. This can be why younger kids dont experience hair loss. As we age IGF - receptor reactivity in hair follicles declines in balding people.

Definitely interesting.
 

RolfLeeBuckler

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Who is able to translate the timelinie of HMI-115? It looks like they do Phase II/ Phase II in one round

1616518732493.png


 

trialAcc

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Who is able to translate the timelinie of HMI-115? It looks like they do Phase II/ Phase II in one round

View attachment 160022

Lots of companies do this, it just means the trial will probably have an extension set of phase 3 outcomes if the primary phase 2 outcomes measurements are met during the trial. Similarly a phase 1/2 trial will have phase 1 end points that are usually largely based on safety with some phase 2 end points of effectiveness.
 

Tom4362

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Kagaho

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The macaque study evidence is promising, undoubtely. But with human Androgenetic Alopecia fucked up stem cells (premature scenescence) play a big role. Its going to be a new powerful weapon, but to think this thing its going to reverse balding mmm.
 

pegasus2

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The macaque study evidence is promising, undoubtely. But with human Androgenetic Alopecia fucked up stem cells (premature scenescence) play a big role. Its going to be a new powerful weapon, but to think this thing its going to reverse balding mmm.
PRL keeps hair follicle stem cells in a quiescent state, so hmmmm
 

Norwood-null-by-2021

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RolfLeeBuckler

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what is your conlusion out of this article?
 

pegasus2

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It's not even a good attempt to dismiss HMI. He's just hoping no one will even read the study he posted, and it proves he's just trolling.


"no change in the stability of prolactin receptor mRNA was observed during 12 h of retinoic acid treatment"
 

pegasus2

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Pax1 and RUNX2 are possible downstream targets of prolactin. Antagonizing the PRLR downregulates Pax1 and upregulates RUNX2. There should be a good synergistic effect with Wnt agonists like KY19382 or VPA.

Pax1 and other Pax genes are strongly upregulated by prolactin. Pax1 is the gene with the greatest association with Androgenetic Alopecia after the androgen receptor. You can check your Androgenetic Alopecia risk on three of the Pax1 SNPs here. This is a tumor suppressor gene(anti-proliferative). It likely acts to shut down cell proliferation in the HF as if it were a tumor.

Primary SNP:

PAX1
rs2180439 [R, R]

  • ‘C’ = Higher odds of male-pattern baldness, relative to ‘T’
  • ‘T’ = Lower odds of male-pattern baldness, relative to ‘C’
Other Important SNPs:

PAX1
rs1160312 [R]

  • ‘A’ = Higher odds of male-pattern baldness, relative to ‘G’
  • ‘G’ = Lower odds of male-pattern baldness, relative to ‘A’
PAX1 rs6047844 [R]

  • ‘T’ = Higher odds of male-pattern baldness, relative to ‘C’
  • ‘C’ = Lower odds of male-pattern baldness, relative to ‘T’
Cobb found the second strongest association with male pattern baldness from the 20p11 region between PAX1 encoding paired box protein 1 and FOXA2 encoding forkhead box protein A2

The results showed that PAX1 was expressed at very high levels in the scalp skin. Although the PAX1 gene is more than 100 kb away from the 20p11–associated LD block, the expression data might suggest that PAX1 confers the Androgenetic Alopecia-relevant effect at this locus and that a regulatory variant within the associated LD block may modulate its expression through long-range control.


On the other side of the coin prolactin has been shown to downregulate RUNX2, a protein that is important for stem cell differentiation and has a synergistic relationship with Wnt signaling. The RUNX family of genes is also closely associated with A.G.A.

Osteoblasts exposed for 48 h to 1000 ng/mL PRL, but not to 10 or 100 ng/mL PRL, showed decreases in the mRNA expression of Runx2, osteoprotegerin (OPG), and receptor activator of nuclear factor kappaBeta ligand (RANKL) by 60.49%, 72.74%, and 87.51%
 
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Dimitri001

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Pax1 and RUNX2 are possible downstream effectors of prolactin's regulation of hair growth. Antagonizing the PRLR downregulates Pax1 and upregulates RUNX2. There should be a good synergistic effect with Wnt agonists like KY19382 or VPA.

Pax1 and other Pax genes are strongly upregulated by prolactin. Pax1 is the gene with the greatest association with Androgenetic Alopecia after the androgen receptor. You can check your Androgenetic Alopecia risk on three of the Pax1 SNPs here. This is a tumor suppressor gene(anti-proliferative). It likely acts to shut down cell proliferation in the HF as if it were a tumor.

Primary SNP:

PAX1
rs2180439 [R, R]

  • ‘C’ = Higher odds of male-pattern baldness, relative to ‘T’
  • ‘T’ = Lower odds of male-pattern baldness, relative to ‘C’
Other Important SNPs:

PAX1
rs1160312 [R]

  • ‘A’ = Higher odds of male-pattern baldness, relative to ‘G’
  • ‘G’ = Lower odds of male-pattern baldness, relative to ‘A’
PAX1 rs6047844 [R]

  • ‘T’ = Higher odds of male-pattern baldness, relative to ‘C’
  • ‘C’ = Lower odds of male-pattern baldness, relative to ‘T’





On the other side of the coin prolactin has been shown to downregulate RUNX2, a protein that is important for stem cell differentiation and has a synergistic relationship with Wnt signaling. The RUNX family of genes is also closely associated with A.G.A.



If we downregulate a tumor suppressing gene systemically, is that a concern?
 

pegasus2

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If we downregulate a tumor suppressing gene systemically, is that a concern?
I don't think so because BAY doesn't directly antagonize it, it only antagonizes one thing that is theoretically upregulating it in the hair follicle. It can still be activated by other processes. Also prolactin is normally proliferative and Pax1 is probably upregulated as a negative feedback regulator. Inhibiting prolactin is a treatment for brain tumors, prostate cancer, and best cancer. It would theoretically reduce your risk of cancer
 
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pegasus2

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This image shows the expression of several hair growth genes in mesenchymal cells of RUNX2- mice. GLI1, FGFR2, TCF7, and Wnt10b are virtually eliminated when RUNX2 is downregulated.
runxko.JPG


Here is a review on prolactin's regulation of stem/progenitor cells, with a little bit about prolactin in the hair follicle.
 

Redgate

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Interesting. I looked around a bit and found that that RUNX2 is upregulated by PGE2 in some studies & Cotsarelis patent.
Perhaps using HMI/SMI & PGE2 could have a greater synergistic effect.
 

Dimitri001

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Interesting. I looked around a bit and found that that RUNX2 is upregulated by PGE2 in some studies & Cotsarelis patent.
Perhaps using HMI/SMI & PGE2 could have a greater synergistic effect.

If HMI restores things to normal (with regards to RUNX2) and is sufficient for regrowth (as with the monkeys), then maybe we should leave it at that and not push it past normal levels, because maybe like with wnt it can have bad effects. But I'm just speculating, I don't know that that's the case.
 
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