Efficacy Of Topical Tofacitinib In Promoting Hair Growth In Non-scarring Alopecia

[Min0]

Arch Dermatol Res. 2017 Sep 7.
Efficacy of topical tofacitinib in promoting hair growth in non-scarring alopecia: possible mechanism via VEGF induction.
https://www.ncbi.nlm.nih.gov/pubmed/28884378
Abstract
Tofacitinib is a Janus kinase 3 (JAK3) inhibitor that promotes hair growth; however, the efficacy and mechanism of this effect are not yet understood. This study aimed to evaluate the efficacy and mechanism of topical tofacitinib on hair growth in mice. Eight-week-old male C57BL/6 mice were divided equally into four groups and treated topically with tofacitinib, minoxidil, or vehicle once daily for 21 days. Weekly photographs were taken to determine the area and rate of hair growth, and tissue samples were collected for histopathological evaluation. mRNA and protein expression of anagen-maintaining growth factors, including vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1), were determined via RT-PCR and ELISA, respectively. Tofacitinib-treated mice exhibited more hair regrowth than either minoxidil-treated or control mice did between day 7 and 21 (P < 0.05). Topical tofacitinib also promoted more rapid hair growth rate than topical minoxidil or control did (P < 0.001). Histopathology showed a distinct increase in the number of hair follicles, mostly in the anagen phase, in the tofacitinib-treated group. Hair follicles in the minoxidil- and vehicle-treated groups were more often classified as catagen and anagen. VEGF mRNA and protein expression in the tofacitinib-treated group was significantly greater than those in the other groups (P < 0.05). IGF-1 mRNA expression was not upregulated in tofacitinib-treated mice. Topical tofacitinib is effective in promoting hair growth, and the possible mechanism involves increased VEGF levels and lowered inflammation. This study will help develop a new therapeutic option for non-scarring alopecia.
KEYWORDS:
Hair growth; IGF-1; JAK3 inhibitor; Non-scarring alopecia; VEGF


My comment :
MICE ! that means it will work for human beard or bodyhair better because androgens can't hurt it.
also, confirms that growth factors (here they are talking in particular about vascular endothelial growth factor) grow hair.

DHT on human scalp is known to not promote growth factors. unlike what it does on beard hair for example.
we still don't know why DHT doesn't create growth factors on the scalp dermal papilla cells. this study is useless for Androgenetic Alopecia, but still relevant. maybe it can negate the DHT action for a while like minoxidil does.


quoting my lasy post about why mice studies don't mean much :

[112]
Androgen-dependent beard dermal papilla cells secrete autocrine growth factor(s) in response to testosterone unlike scalp cells.
https://www.ncbi.nlm.nih.gov/pubmed/9804329
[114] Hibberts NA, Randall VA. Testosterone inhibits the capacity of cultured cells from human balding scalp dermal
papilla cells to produce keratinocyte mitogenic factors.
In: Van Neste DV, Randall VA, eds. Hair research for the
next millennium. Amsterdam: Elsevier, 1996: 303–306

[117] Obana N, Chang C, Uno H. Inhibition of hair growth by
testosterone in the presence of dermal papilla cells from
the frontal bald scalp of the post-pubertal stump-tailed
macaque. Endocrinol 1997: 138: 356–361


so, what makes animal bodyhair grow doesn't necessarily grow head hair for humans and some primates.
because our head hair is designed to be fucked by androgens at a certain age. yes even doner area and non balding people hair is getting nuked by androgens as we speak, but they either have less androgen receptors or less 5aR or have a mechanism that negates the effect of androgens.

if you take dermal papilla cells from the head of a non balding guy or a woman, and apply enough DHT, it will die.

THEY TYPE OF HAIR in question is the most important thing in hairloss research. for example if you want to study what estrogens effect on hair you must specify the type of hair you're talking about, because estrogens are good for head hair but are bad for body hair. the inverse is correct for androgens.

 

[c_super2]

This is actually a great study. It gives good insight.

 

[NewUser]

Tofacitinib-treated mice exhibited more hair regrowth than either minoxidil-treated or control mice did between day 7 and 21 (P < 0.05 or statistically significant). Topical tofacitinib also promoted more rapid hair growth rate than topical minoxidil or control did (P < 0.001 or less than one in a thousand chance of being wrong). Histopathology showed a distinct increase in the number of hair follicles, mostly in the anagen phase, in the tofacitinib-treated group.

Apparently mice respond better to tofa than minoxidil.

 

[AnxiousAndy]

Ok i did not read all that because im drunk and depressed. Does it work for androgenic alopecia?

 

[Min0]

Ok i did not read all that because im drunk and depressed. Does it work for androgenic alopecia?

think of it as a superior minoxidil.

 

[rupture]

so since I'm on CPA , Duta and estro this should be all I need to grow my hair

 

[NewUser]

And in case anyone is wondering about Christiano's discovery for JAK-inhibition versus UCLA's findings for Jak-STAT activation producing lactate causing hair to grow, I'm not sure, either. Christiano did state that the Jak-STAT signalling pathway is an interesting area of hair cell biology that needs further investigation to determine if something can be done for androgenetic and other kinds of hair loss.


In an issue of Journal of Investigative Dermatology, Columbia University’s Drs. Angela Christiano, Etienne Wang and Sivan Harel published a paper entitled Jak-STAT signaling jump starts the hair cycle. That paper is an analysis by Christiano's Columbia U. team of a study that was published in early 2016 by Dr. Julien Legrand et al of the The University of Queensland. Legrand's study is titled, STAT5 activation in the dermal papilla Is important for hair follicle growth phase Induction. The conclusion of that paper was that "STAT5 activation acts as a mesenchymal switch to trigger anagen entry in post-developmental hair follicle cycling“.

Christiano's analysis of Legrand’s research states that JAK/STAT5 signaling in the dermal papilla is required for anagen onset in the mice hair cycle. Meanwhile, other researchers have shown that JAK-inhibition is able to affect the transition of telogen to anagen in the HFs of lab mice. This shows that the JAK-STAT signaling pathway still requires some research to be fully understood.

And then in 2017, UCLA researchers state that Jak-STAT activation leads to the increased production of lactate and this in turn drives hair follicle stem cell activation and quicker hair growth. It is obvious by now that Christiano, Legrand and others believe further study of Jak-STAT signalling may lead to drug therapies that will grow hair for various kinds of hair loss.