- Reaction score
- 29
I've been researching this chemical for some time now and I think it has its place within a hair loss regimen.
"Pirfenidone(AMR69) is an inhibitor for TGF-β production and TGF-β stimulated collagen production, reduces production of TNF-α and IL-1β, and also has anti-fibrotic and anti-inflammatory properties."
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Pirfenidone (< 300 μg/mL) suppresses the proinflammatory cytokine tumor necrosis factor-α (TNF-α) by a translational mechanism in RAW264.7 cells, which is independent of activation of the mitogen-activated protain kinase (MAPK) 2, p38 MAP kinase, and c-Jun N-terminal kinase (JNK). Pirfenidone (250 mg/kg) potently inhibits the production of the proinflammatory cytokines, TNF-alpha, interferon-gamma, and interleukin-6, but enhances the production of the anti-inflammatory cytokine, interleukin-10, in mice [1]. Pirfenidone (< 10 mM) leads to reduced glioma cell density in concentration-dependent manner in LN-18, T98G, LNT-229 and LN-308 cell lines. Pirfenidone (< 5 mM) reduces TGF-β bioactivity by affecting TGF-β2 mRNA expression and processing of pro-TGF-β in CCL-64 cells. Pirfenidone (< 8.3 mM) inhibits the activity of recombinant furin and downregulates the expression of MMP-11 in a dose-dependent manner in LN-308 cells [2].
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TGF is blocked, therefore hypercollagenses within the hair follicle is also blocked.
IL-6 is blocked, therefore it cannot activate AR transcription machinery in the absence of an androgen (see picture 2).
Block the androgen receptor with RU or CB.
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AS you can see in the attached photo, IL-6 has the ability to cause activation of androgen receptor genes even when DHT is absent from the actual receptor site. This could explain why some people still experience hair loss even while on finasteride/dutasteride.
"Pirfenidone(AMR69) is an inhibitor for TGF-β production and TGF-β stimulated collagen production, reduces production of TNF-α and IL-1β, and also has anti-fibrotic and anti-inflammatory properties."
- - - Updated - - -
Pirfenidone (< 300 μg/mL) suppresses the proinflammatory cytokine tumor necrosis factor-α (TNF-α) by a translational mechanism in RAW264.7 cells, which is independent of activation of the mitogen-activated protain kinase (MAPK) 2, p38 MAP kinase, and c-Jun N-terminal kinase (JNK). Pirfenidone (250 mg/kg) potently inhibits the production of the proinflammatory cytokines, TNF-alpha, interferon-gamma, and interleukin-6, but enhances the production of the anti-inflammatory cytokine, interleukin-10, in mice [1]. Pirfenidone (< 10 mM) leads to reduced glioma cell density in concentration-dependent manner in LN-18, T98G, LNT-229 and LN-308 cell lines. Pirfenidone (< 5 mM) reduces TGF-β bioactivity by affecting TGF-β2 mRNA expression and processing of pro-TGF-β in CCL-64 cells. Pirfenidone (< 8.3 mM) inhibits the activity of recombinant furin and downregulates the expression of MMP-11 in a dose-dependent manner in LN-308 cells [2].
- - - Updated - - -
TGF is blocked, therefore hypercollagenses within the hair follicle is also blocked.
IL-6 is blocked, therefore it cannot activate AR transcription machinery in the absence of an androgen (see picture 2).
Block the androgen receptor with RU or CB.
- - - Updated - - -
AS you can see in the attached photo, IL-6 has the ability to cause activation of androgen receptor genes even when DHT is absent from the actual receptor site. This could explain why some people still experience hair loss even while on finasteride/dutasteride.
