Tofa (0.1), sulfa, lithium chloride, alfatradiol..
All useless mate, complete bunk. At best you'll get minimal sh*t growth lol.
What I'm interested in though... What happened with your smoothened agonist experiment?
After further research, it's been shown that activation of smoothened is not sufficient enough to grow hair by itself, albeit still essential to stimulate anagen (Kishimoto, Burgeson, & Morgan, 2000; Fu & Hsu, 2013) (see attached)
(photo from Kishimoto et al., 2000)
It appears that hair follicle differentiation involves the participation and control of a multitude of signalling factors, each step dependent on the last. The photo above shows a control mouse (No Shh or Wnt-3a activity), a mouse with only Shh (and not Wnt3a activity), and a mouse that only demonstrates Wnt3a activity (absent of Shh). Wnt3A-only mice experienced
100% hair follicle induction, in comparison to Shh-only mice who demonstrated only 2% induction.
What can we deduce from this data ?
WNTs play a more influential influential role on HF differentiation compared to Shh-only mice.
I think a combination of a Dkk-1 (Prevents Wnt inactivation stimulating subsequent activation) + GSK-3B inhibitor (Prevents phosphorylation of B-Catenin) would positively stimulate the formation of Hair follicles. (Aside: Phosphorylation of B-Catenin renders it inactive, which we don't want.})
High levels B-Catenin is what want.
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My theory
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If androgens upregulate Dkk-1, Wnt becomes down-regulated. If Wnt is down-regulated, GSK-3B will remain bound to B-catenin which will cause subsequent down-regulation (of B-cat). If B-cat is down regulated, hair growth begins to cease and miniaturization occurs. This miniaturization continues until it begins to stop producing active hair follicles entirely.
I hypothesize that the Wnt pathway and prostaglandin pathways have a synergetic crosstalk, that is primarily dependent on Wnt. Wnt up-regulation (good) inhibits the bad prostaglandins (PGD) and up-regulates the good ones (PGF2a, PGE). This could be why some people don't see much success using one or the other, but swisstemples was able to achieve new growth with combination therapy.
I dont think that WNT and Prostaglandins, are going to become the magic cure. Though, I am confident that they both play an integral role in HF formation, and the subsequent growth of actual hair.
Obviously preventing androgen receptor activation would be necessary to PREVENT further hair loss, but WNT/Prostag has to be necessary for further growth.
Maybe Anti-androgens or AR antagonists might even be able to be avoided all together if my research is correct.
Hang in there boys, I'll pull through for ALL of us.
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They may appear ineffective if used on their own, but I believe multi-targeted therapy will prove much more beneficial. Let the science speak for itself.