Fk506

Stimulation of hair growth by topical application of FK506, a potent immunosuppressive agent

S Yamamoto 1 , H Jiang, R Kato

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Abstract

FK506, a macrolide antibiotic produced by Streptomyces tsukubaensis, is known as a potent T cell-specific immunosuppressant, and is effective against graft rejection after organ transplantation. Topical application of FK506 (0.03-1 mumol) to dorsal skin of CD-1 mice stimulated hair growth in a dose-dependent manner. Unlike topical application, oral administration of 30 mg/kg of FK506, a dose that induces marked immunosuppression, did not stimulate significant hair growth. Topical application of FK506 also stimulated hair growth of rats and Syrian golden hamsters. FK506 stimulated hair growth even in SCID mice that lack both B- and T-cell immunity. Therefore, it is unlikely that the hair growth-stimulatory effect of FK506 results from its immunosuppressive effect. FK506 (0.01-1 microM) stimulated both [3H]thymidine and [3H]glycine uptakes to cultured mouse vibrissae follicles in a concentration-dependent manner. Moreover, when the follicles were treated with FK506 (1 microM) for 16 d, the size of the follicles (length of hair plus follicle) increased slightly but significantly. On the other hand, the size of the non-treated follicles did not increase significantly. These results indicate that FK506 directly stimulates hair follicles. Long-term treatment of mice with FK506, i.e., topical application of 1 mumol FK506 twice a week for 6 months, did not affect body weight gain of mice, and the FK506-treated mice looked healthy. FK506 may be useful as a stimulant of hair growth.


Effects of immunosuppressive peptidyl-prolyl cis-trans isomerase (PPIase) inhibitors, cyclosporin A, FK506, ascomycin and rapamycin, on hair growth initiation in mouse: immunosuppression is not required for new hair growth

T Iwabuchi 1 , T Maruyama, Y Sei, K Adachi

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Abstract

The effects of immunosuppressive peptidyl-prolyl cis-trans isomerase (PPIase) inhibitors, cyclosporin A, FK506, ascomycin and rapamycin, on hair growth initiation (anagen hair induction) in mouse were studied by topical application on the dorsal skin surface during the telogen phase of the hair cycle. Single applications of cyclosporin A and FK506 (10 to 100 nmol in 5 microliters of ethanol) induced new hair growth in 12 days within the restricted area where the compounds were applied. On the other hand, ascomycin and rapamycin did not initiate new anagen hairs even at higher doses (1 mumol in 5 to 10 microliters of ethanol). The effects of simultaneous application of the immunosuppressants were also tested by a single topical application. Ascomycin did not inhibit the anagen hair induction by cyclosporin A, but inhibited hair induction by FK506. Rapamycin inhibited new hair growth induced by cyclosporin A and FK506. These results suggest that the inhibition of PPIase is not required for the initiation of a new hair cycle in mice, and that anagen hair induction caused by cyclosporin A and FK506 is not a result of immunosuppression. The present results also indicate that a single application of an adequate quantity of cyclosporin A and FK506 is sufficient to initiate new hair growth.


Its nothing new for me that Cyclosporin may trigger hair growth and never thought about trying it since it is a HEAVY IMMUNO SUPRESSANT for surgeries but the fact that a SINGLE application is enough to revert back to a growth-awake phase is completely a new data for me.


Since I have achieved significant entertaining-regrowth of baby hair shafts even terminal, correct-angles* and pigmented I would seriously consider the FK506 anti-biotic. Any insights ?

We dont have it in Tunisia possibly.


I am also searching for scientific papers that studied cases of ancedotic full head of hair re-growth. I think I have seen at least 2 papers addressing this topic. One of them states sunburn as the cause of this full head of hair growth. While the papers may identify alopecia as Areata or arithithis or Totalis, I am still very interested in such papers and DONT buy too much this story of Alopecia androgene as not the diagnosis for this kind of data.

Any links please ? I dont know what s wrong with search engines.
Also they have took out hairlosshelp dot com for the best interest of the ***hit Hair transplant market -sorry- but you have to know the truth.

Thanks.

  • The Angles issue is a no-issue from my experience.

I read in Wikipedia about Thymidine:

Thymidine (other names deoxythymidine , deoxyribosylthymine , thymine deoxyriboside ) is a pyrimidine deoxynucleoside. Deoxythymidine is the DNA nucleoside T, which pairs with deoxyadenosine (A) in double-stranded DNA. In cell biology it is used to synchronize the cells in G1/early S phase. The prefix deoxy- is often left out since there are no precursors of thymine nucleotides involved in RNA synthesis.

Source: Thymidine - Wikipedia

------> If some of you have been reading me, I was exploring a possibility of resolving the so-called Demal Papillas issue through migration in small circles with half of each circle, at maximum, is related to a last-in-time balding spot and the remaining area is healthy.
Thus, the frontier or the separation line should cross the circles in 2 points. Now, I developed the theory such a Gaps Analysis approach wherein I aim to decrease the gap/difference of behaviour, in a consistent manner, between the healthy spot and the bald spot. This, should resolve multiple issues-complications including the so-called Dermal Papilla issue, the hair induction problem, the shrinkage problem, the fall problem, the allergy, the immune-reaction, the skin-dermis toughness for an adult (typically). For instance, an in-increase of consumption of such a factor-element, i.e., Thymidine or derivative, related to this concept of Synchronization in Genomic phases and/or process looks for me as a possible tool for such a migration of the correct behaviour from stable hair spots to bald spots.
It is the first time I come across such terminology. It could be that consortiums decided to darken the terminology afterwards (The two papers have been published in and around 1995).
The therapy would mean a consistent reduction of the differential/gap in behaviour towards the benchmark of the healthy behaviour of the hair stable spots.
I think this makes sense once the PB reached convergence-stability.

Read for the so called G1 phase:

https://www.nature.com/articles/s41586-019-1778-y

For the S phase:

https://www.nature.com/scitable/topicpage/dna-replication-and-checkpoint-control-in-s-14202419/
https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/s-phase

Regards.
Mahdi.