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The "brass tacks" on how Follica might work.....via Harold


#1

Im going to cut-and-paste a post from the RSG (Real Smart Guy) Harold from over at hlt. He’s very bright and well-read. These are his thoughts on how Follica might work theoretically:

Maybe I should have put this in the follica thread but oh well.
EGF inhibitors can cause slower scalp hair growth and longer eyelash growth… But EGF overexpression seems to mess with hair cycling. Slows it down.
J Invest Dermatol. 2008 May;128(5):1256-65. Epub 2007 Oct 25.Click here to read Links

Betacellulin regulates hair follicle development and hair cycle induction and enhances angiogenesis in wounded skin.
Schneider MR, Antsiferova M, Feldmeyer L, Dahlhoff M, Bugnon P, Hasse S, Paus R, Wolf E, Werner S.

Institute of Molecular Animal Breeding and Biotechnology, Gene Center, University of Munich, Munich, Germany. schnder@lmb.uni-muenchen.de

Betacellulin (BTC) belongs to the EGF family, whose members play important roles in skin morphogenesis, homeostasis, and repair. However, the role of BTC in skin biology is still unknown. We employed transgenic mice overexpressing BTC ubiquitously to study its role in skin physiology. Immunohistochemistry revealed increased levels of BTC especially in the hair follicles and in the epidermis of transgenic animals. Expression of key markers of epithelial differentiation was unaltered, but keratinocyte proliferation was significantly increased. At post-natal day 1 (P1), transgenic mice displayed a significant retardation of hair follicle morphogenesis. At P17, when most follicles in control mice had initiated hair follicle cycling and had already entered into their first late catagen or telogen phase, all follicles of transgenic mice were still at the mid- to late catagen phases, indicating retarded initiation of hair follicle cycling. Healing of full-thickness excisional wounds and bursting strength of incisional wounds were similar in control and transgenic mice. However, an increase in the area covered by blood vessels at the wound site was detected in transgenic animals. These results provide evidence for a role of BTC in the regulation of epidermal homeostasis, hair follicle morphogenesis and cycling, and wound angiogenesis.

I’m not gonna pretend to be on top of everything that this abstract mentions but a lot of those targets of EGF interact very strongly with wnt/BMP signalling pathways indicating some kind of convergence.

Mol Cell Biol. 2006 Aug;26(16):6283-98.Click here to read Click here to read Links
Selective modulation of Hedgehog/GLI target gene expression by epidermal growth factor signaling in human keratinocytes.
Kasper M, Schnidar H, Neill GW, Hanneder M, Klingler S, Blaas L, Schmid C, Hauser-Kronberger C, Regl G, Philpott MP, Aberger F.

Department of Molecular Biology, University of Salzburg, Hellbrunnerstrasse 34, A-5020 Salzburg, Austria.

Hedgehog (HH)/GLI signaling plays a critical role in epidermal development and basal cell carcinoma. Here, we provide evidence that epidermal growth factor receptor (EGFR) signaling modulates the target gene expression profile of GLI transcription factors in epidermal cells. Using expression profiling and quantitative reverse transcriptase PCR, we identified a set of 19 genes whose transcription is synergistically induced by GLI1 and parallel EGF treatment. Promoter studies of a subset of GLI/EGF-regulated genes, including the genes encoding interleukin-1 antagonist IL1R2, Jagged 2, cyclin D1, S100A7, and S100A9, suggest convergence of EGFR and HH/GLI signaling at the level of promoters of selected direct GLI target genes. Inhibition of EGFR and MEK/ERK but not of phosphatidylinositol 3-kinase/AKT abrogated synergistic activation of GLI/EGF target genes, showing that EGFR can signal via RAF/MEK/ERK to cooperate with GLI proteins in selective target gene regulation. Coexpression of the GLI/EGF target IL1R2, EGFR, and activated ERK1/2 in human anagen hair follicles argues for a cooperative role of EGFR and HH/GLI signaling in specifying the fate of outer root sheath (ORS) cells. We also show that EGF treatment neutralizes GLI-mediated induction of epidermal stem cell marker expression and provide evidence that EGFR signaling is essential for GLI-induced cell cycle progression in epidermal cells. The results suggest that EGFR signaling modulates GLI target gene profiles which may play an important regulatory role in ORS specification, hair growth, and possibly cancer.

OK I think a big action of androgens in the skin is that they promote sebaceous gland growth more or less everywhere and retard hair follicle formation on the scalp. Epidermal stem cells are in a state (roughly) where they can become sebaceous glands, hair follicles or skin cells. Wnt signalling is one of the things that biases a stem cell to become a ahir follicle rather than a sebaceous gland or skin cell. Wnt and DKK1 are 2 molecules that seem to determine hair follicle spacing in the scalp according to a reaction diffusion principle - this forms a natural pattern much like spots on a leopard, stripes on a zebra - not too random, not too regular. One of the notes from the first Cotsarelis wounding patent was constantly talking about a method to induce hair growth by bringing a hair follicle or portion thereof or an inductive cell close to the uncomitted epidermal cell to convince it to become a hair follicle. I think this is because as animals are furry all over when you wound them they have more of a tendency to grow fur back. The same would be true of a hairy persons scalp. But i think if you tried wounding your palm you wouldnt grow any hairs back partly because there would be alot of DKK1 floating around and partly because these stem cells seem to take cues from their neighbours as to what they should differentiate into. I think this is why its easier to regrow on a thinning vertex than temples. Less interference from the neighbours. But EGF inhibition probably overcomes that inhibition.

Mucking with BMP/Wnt signalling seems to promote sebaceous gland enlargement at the same time as inhibiting hair follicle growth . I think this is very important. This is one of the key things that separates MPB from alopecia areata and other hair loss conditions. Its practically synonymous with androgenic effects in the scalp.
There are many mouse models of alopecia that dont apply to MPB that well. However when mice overexprssed COX-2 in the skin they developed sparse coats of thinning hair. That hair was also greasy due to sebaceous gland enlargement. Importantly the hair loss could be prevented by using a COX inhibitor but seemingly could not be reversed. Much like MPB hair loss and antiandrogens.
When Cotsarelis found the elevation in prostaglandin D2 in bald scalp someone was canny enough to remember this model and make the connection between increased prostaglandin production in mouse skin. Looking at it they saw that PGD2 was through the roof in the skin of these mice. Inhibiting prostaglandin d2 could reverse the sebaceous gland growth and prevent the loss of hair. Though this is very suggestive it is not an airtight case yet by any means. One would have to show cause and effect in humans between PGD2 and hair loss. Not just correlation. That would take a trial. And trials take at least about 6 months let alone writing up etc.
At any rate I think it suggests that PGD2 messes with the balance of wnt/bmp/dkk1 in the skin and what would have become hair follicles start to thin while sebaceous glands become fat…
anyway I have digressed. I may have even written this before but it was in my head and i had to get it out
hh


#2

» Im going to cut-and-paste a post from the RSG (Real Smart Guy)
» Harold from over at hlt. He’s very bright and well-read. These are his
» thoughts on how Follica might work theoretically:
»
»
»
» Maybe I should have put this in the follica thread but oh
» well.
» EGF inhibitors can cause slower scalp hair growth and longer eyelash
» growth… But EGF overexpression seems to mess with hair cycling. Slows it
» down.
» J Invest Dermatol. 2008 May;128(5):1256-65. Epub 2007 Oct 25.Click here to
» read Links
»
» Betacellulin regulates hair follicle development and hair cycle induction
» and enhances angiogenesis in wounded skin.
» Schneider MR, Antsiferova M, Feldmeyer L, Dahlhoff M, Bugnon P, Hasse S,
» Paus R, Wolf E, Werner S.
»
» Institute of Molecular Animal Breeding and Biotechnology, Gene Center,
» University of Munich, Munich, Germany. schnder@lmb.uni-muenchen.de
»
» Betacellulin (BTC) belongs to the EGF family, whose members play important
» roles in skin morphogenesis, homeostasis, and repair. However, the role of
» BTC in skin biology is still unknown. We employed transgenic mice
» overexpressing BTC ubiquitously to study its role in skin physiology.
» Immunohistochemistry revealed increased levels of BTC especially in the
» hair follicles and in the epidermis of transgenic animals. Expression of
» key markers of epithelial differentiation was unaltered, but keratinocyte
» proliferation was significantly increased. At post-natal day 1 (P1),
» transgenic mice displayed a significant retardation of hair follicle
» morphogenesis. At P17, when most follicles in control mice had initiated
» hair follicle cycling and had already entered into their first late catagen
» or telogen phase, all follicles of transgenic mice were still at the mid-
» to late catagen phases, indicating retarded initiation of hair follicle
» cycling. Healing of full-thickness excisional wounds and bursting strength
» of incisional wounds were similar in control and transgenic mice. However,
» an increase in the area covered by blood vessels at the wound site was
» detected in transgenic animals. These results provide evidence for a role
» of BTC in the regulation of epidermal homeostasis, hair follicle
» morphogenesis and cycling, and wound angiogenesis.
»
» I’m not gonna pretend to be on top of everything that this
» abstract mentions but a lot of those targets of EGF interact very strongly
» with wnt/BMP signalling pathways indicating some kind of convergence.
»
» Mol Cell Biol. 2006 Aug;26(16):6283-98.Click here to read Click here to
» read Links
» Selective modulation of Hedgehog/GLI target gene expression by epidermal
» growth factor signaling in human keratinocytes.
» Kasper M, Schnidar H, Neill GW, Hanneder M, Klingler S, Blaas L, Schmid C,
» Hauser-Kronberger C, Regl G, Philpott MP, Aberger F.
»
» Department of Molecular Biology, University of Salzburg,
» Hellbrunnerstrasse 34, A-5020 Salzburg, Austria.
»
» Hedgehog (HH)/GLI signaling plays a critical role in epidermal development
» and basal cell carcinoma. Here, we provide evidence that epidermal growth
» factor receptor (EGFR) signaling modulates the target gene expression
» profile of GLI transcription factors in epidermal cells. Using expression
» profiling and quantitative reverse transcriptase PCR, we identified a set
» of 19 genes whose transcription is synergistically induced by GLI1 and
» parallel EGF treatment. Promoter studies of a subset of GLI/EGF-regulated
» genes, including the genes encoding interleukin-1 antagonist IL1R2, Jagged
» 2, cyclin D1, S100A7, and S100A9, suggest convergence of EGFR and HH/GLI
» signaling at the level of promoters of selected direct GLI target genes.
» Inhibition of EGFR and MEK/ERK but not of phosphatidylinositol 3-kinase/AKT
» abrogated synergistic activation of GLI/EGF target genes, showing that EGFR
» can signal via RAF/MEK/ERK to cooperate with GLI proteins in selective
» target gene regulation. Coexpression of the GLI/EGF target IL1R2, EGFR, and
» activated ERK1/2 in human anagen hair follicles argues for a cooperative
» role of EGFR and HH/GLI signaling in specifying the fate of outer root
» sheath (ORS) cells. We also show that EGF treatment neutralizes
» GLI-mediated induction of epidermal stem cell marker expression and provide
» evidence that EGFR signaling is essential for GLI-induced cell cycle
» progression in epidermal cells. The results suggest that EGFR signaling
» modulates GLI target gene profiles which may play an important regulatory
» role in ORS specification, hair growth, and possibly cancer.
»
» OK I think a big action of androgens in the skin is that they promote
» sebaceous gland growth more or less everywhere and retard hair follicle
» formation on the scalp. Epidermal stem cells are in a state (roughly) where
» they can become sebaceous glands, hair follicles or skin cells.
Wnt
» signalling is one of the things that biases a stem cell to become a ahir
» follicle rather than a sebaceous gland or skin cell. Wnt and DKK1 are 2
» molecules that seem to determine hair follicle spacing in the scalp
» according to a reaction diffusion principle - this forms a natural pattern
» much like spots on a leopard, stripes on a zebra - not too random, not too
» regular
. One of the notes from the first Cotsarelis wounding patent
» was constantly talking about a method to induce hair growth by bringing a
» hair follicle or portion thereof or an inductive cell close to the
» uncomitted epidermal cell to convince it to become a hair follicle. I think
» this is because as animals are furry all over when you wound them they have
» more of a tendency to grow fur back. The same would be true of a hairy
» persons scalp. But i think if you tried wounding your palm you wouldnt grow
» any hairs back partly because there would be alot of DKK1 floating around
» and partly because these stem cells seem to take cues from their neighbours
» as to what they should differentiate into. I think this is why its easier
» to regrow on a thinning vertex than temples. Less interference from the
» neighbours. But EGF inhibition probably overcomes that inhibition.

»
» Mucking with BMP/Wnt signalling seems to promote sebaceous gland
» enlargement at the same time as inhibiting hair follicle growth
. I
» think this is very important. This is one of the key things that separates
» MPB from alopecia areata and other hair loss conditions. Its practically
» synonymous with androgenic effects in the scalp.
» There are many mouse models of alopecia that dont apply to MPB that well.
» However when mice overexprssed COX-2 in the skin they developed sparse
» coats of thinning hair. That hair was also greasy due to sebaceous gland
» enlargement. Importantly the hair loss could be prevented by using a COX
» inhibitor but seemingly could not be reversed. Much like MPB hair loss and
» antiandrogens.
» When Cotsarelis found the elevation in prostaglandin D2 in bald scalp
» someone was canny enough to remember this model and make the connection
» between increased prostaglandin production in mouse skin. Looking at it
» they saw that PGD2 was through the roof in the skin of these mice.
» Inhibiting prostaglandin d2 could reverse the sebaceous gland growth and
» prevent the loss of hair. Though this is very suggestive it is not an
» airtight case yet by any means. One would have to show cause and effect in
» humans between PGD2 and hair loss. Not just correlation. That would take a
» trial. And trials take at least about 6 months let alone writing up etc.
» At any rate I think it suggests that PGD2 messes with the balance of
» wnt/bmp/dkk1 in the skin and what would have become hair follicles start to
» thin while sebaceous glands become fat…
» anyway I have digressed. I may have even written this before but it was in
» my head and i had to get it out
» hh

Good stuff, Benji. So do you think they have any data that goes beyond correlation with regards to the PGD2?


#3

»
» Good stuff, Benji. So do you think they have any data that goes beyond
» correlation with regards to the PGD2?

PGD2 might be an initiator of events that lead to sebacous hyperplasia (or not), but what is known is that when Cotsarialis et al added PGD2 to mice after their first shed (something like 28 days in life for them usually), they could keep them from having a second anagen phase by applying this substance to their coats daily. They noted sebaceous gland enlargement when they did this. Its noted also by them that PGD2 is upregulated a good deal in balding scalp over hirsute scalp by a good bit (four or five times if I remember right).

HOWEVER, this may be a “downstream” event and not causitive.

I agree with Bryan Shelton that the real solution to the dilemma (without some kind of hair multiplication or being able to make “new” hair) long term would be to find what genes are being activated downstream of androgen uptake by the dermal papilla via the androgen receptors and why are they different than body hair’s genetic response. The solution may be as elegant as upping or downing one thing there that isn’t androgenic at all…and voilia’—the hair begins to like androgen or at least be ambivalent to it. That is of course, probably several years away.

Until then…its anti-androgens and growth stimulants.

The “alphabet soup” of negative growth factors (like tgf beta 1 and 2, Protien Kinease C, thrombospondin, TNF-alpha, DKK-1, Fiberblast growth factor five) and positive growth factors (there are several…IL-this and that, BMP, and a few others) are apparently fairly many. It looks like there are five or more catagen-inducers and at least as many anagen inducers. So applying topicals that block or upreg this or that ONE might only be beneficial for a while unless one hits upon the one that induces an immunological response. But, then again, the immune response might be induced by dying keratinocyte cells, cellular DNA damage downstream of oxides, just too many antigens present at any one time, etc. We dont know…

But PGD2 sure as hell aint good for hair. We can deduce that. Cotsarialis obviously found a correlation and went ahead and filed a patent so he could research it in detail later, but I have a feeling his hands are pretty full now (as well as the rest of the dermatology department at Penn) with Follica.

Little by little they are learning more and more about AGA and what makes it tick. Someday, hopefully, they will know every little event that typcially goes on and why…

Follica’s “discovery” (I put that in parenthesis because George Cotsarialis almost certainly knew based on animal experiments fifty years ago/Kligman’s observation of de noveau hairgrowth in dermabrasion/acne patients in the seventies exactly what he was going to find when he wounded those mice) WILL GIVE RESEARCHERS THE ABILITY TO WATCH HAIR DEVELOP IN HUMAN SKIN GRAFTED ONTO MICE UP CLOSE OUTSIDE THE WOMB, SO THAT THEY CAN NOTE EVERY TINY CHEMICAL THAT IS BEING BROUGHT INTO PLAY, AND WHAT GENES DO WHAT ETC…so they can learn PRECISELY how hair is formed and what genes make it prone to loss in later life in response to testosterone. Maybe, just maybe…they will someday be able to block these genes in their wounding protocol or even give your mamma something to take when she is pregnant in the first trimbester that blocks them. All of that is of course decades out there, but wouldn’t it be nice to see androgen-related dermal disorders like acne and baldness and roseacea defeated for all humaninty permanently. I think it would anyway.


#4

They’ve been doing gene replacement therapy for a rare form of blindness. Researchers say it’s a shot in the arm for gene therapy in general.

» Maybe, just maybe…they will someday be able to block these genes
» in their wounding protocol or even give your mamma something to take when
» she is pregnant in the first trimbester that blocks them. All of that is of
» course decades out there, but wouldn’t it be nice to see androgen-related
» dermal disorders like acne and baldness and roseacea defeated for all
» humaninty permanently. I think it would anyway.


#5

so is it the increased WNT signalling or EGF inhibition that is primarily responsible for new hair follicles?

Also benji & haraldo, do you guys think that there is a good possibility of Follica procedure actually rejuvenating old follicles? i’m asking this because even though I’m NW6, I can see dense vellus hair all along my NW1 area - if only I could revive those, all my troubles be over!

EDIT: Found this article http://www-hsc.usc.edu/~widelitz/2007_chuong_nature.pdf

Read the last paragraph on first page, it says that increased WNT signaling is responsible for normal hair cycling…does that also mean that increased WNT signaling will cause minitaurized hair follciles to return to their normal cycle (i.e. get thicker and darker)?


#6

goata ,

Why dont you do like me ? I’m rubbing olive oil on my sclap (sometimes Aloe vera juice too) and curcumin/ginger orally each day hoping to stop apopstosis (even for vellus hair) might that save me if follica or any other reawakening treatment starts to work .


#7

» goata ,
»
» Why dont you do like me ? I’m rubbing olive oil on my sclap (sometimes
» Aloe vera juice too) and curcumin/ginger orally each day hoping to stop
» apopstosis (even for vellus hair) might that save me if follica or any
» other reawakening treatment starts to work .

I started using (somewhat regularly) that herbal receipe that I mentiond a while ago. It’s olive oil mixed with garlic (lithium) and clove (anti-androgen) and then cooked. It does have a really bad odour, actually I feel it less now - maybe i’ve gotten used to it. The herbal doctor said to massage it every night before bed and in about 6-months I should see growth. So that’s what I’m doing for now.

What i’m really interested in is seeing if I can get regrowth sooner. That’s why I was asking benji/haraldo what they think about that article i.e. WNT is responsible for normal hair cycling.

Btw, whats the reasoning behind taking curcumin/ginger?


#8

Ginger/curcumin is supposed to have one of the strongest natural agents ,available ,capable of breaking the inflammatory cascade that leads to hair loss and death of cells (apopstosis) in general.

This was preached by Waseda years ago as he was a believer that Hair loss is primarly an auto-immune problem …In other words it’s our immunity that kills our hair follicules in the end beacuse of some reasons : adrogens or whatever tag our hair cells or do something to them that make them look like hostile to our immunity .

I do believe in this theory to a certain extent…Unfortunately and for some reason curcumin is not the silver bullet :frowning:

P.S : some studies claim that it’s a potent androgen inhibitor too.


#9

The entire male population has a strong inflammatory response to foreign invaders, and only half the male population gets MPB problems. Just like the entire male population has major amounts of DHT, and only half of us lose major hair over it.

We can fight MPB with inflammatory stuff but I don’t think we’re chasing the real problem with that. We’re just chasing the symptom.

The difference between us and the guys w/o MPB is our follicles’ stronger androgen sensitivity.


#10

» The entire male population has a strong inflammatory response to foreign
» invaders, and only half the male population gets MPB problems. Just like
» the entire male population has major amounts of DHT, and only half of us
» lose major hair over it.
»
»
» We can fight MPB with inflammatory stuff but I don’t think we’re chasing
» the real problem with that. We’re just chasing the symptom.
»
» The difference between us and the guys w/o MPB is our follicles’ stronger
» androgen sensitivity.

What you said goes too for Finasteride , Dutasteride and any other drug available at this time in the market…They go all after the symptoms ,not the sensitivity of our follicules.


#11

» so is it the increased WNT signalling or EGF inhibition that is primarily
» responsible for new hair follicles?

Both. In the patent there is a stage where he gives a brief overview of results with certain things that help the formation of new hair follicles. Amongst these are beta-catenin activators (wnt stuff), minoxidil, FGF Fibroglast growth Factor, EDAR ligands. If you want to stop the development of hair follicles then EGF is good stuff.

» Also benji & haraldo, do you guys think that there is a good possibility
» of Follica procedure actually rejuvenating old follicles? i’m asking this
» because even though I’m NW6, I can see dense vellus hair all along my NW1
» area - if only I could revive those, all my troubles be over!
»
» EDIT: Found this article
» http://www-hsc.usc.edu/~widelitz/2007_chuong_nature.pdf
»
» Read the last paragraph on first page, it says that increased WNT
» signaling is responsible for normal hair cycling…does that also mean that
» increased WNT signaling will cause minitaurized hair follciles to return to
» their normal cycle (i.e. get thicker and darker)?

wnt is vey much involved in both follicle morphogenesis and hair cycling. MPB does seem to involve some antagonism of wnt signalling but it is unclear how important this is. The Foliicaprocess does help put telogen follicles back into anagen though so thats some good news.
hh


#12

» wnt is vey much involved in both follicle morphogenesis and hair cycling.
» MPB does seem to involve some antagonism of wnt signalling but it is
» unclear how important this is. The Foliicaprocess does help put telogen
» follicles back into anagen though so thats some good news.
» hh

so if Follica fine tunes the process, they can actually rejuvenate pretty much all hair on the head? Can you point me the patent page that specifically talks about this…i’m really excited now :slight_smile:


#13

» so if Follica fine tunes the process, they can actually rejuvenate pretty
» much all hair on the head? Can you point me the patent page that
» specifically talks about this…i’m really excited now :slight_smile:

I don’t know the page number, but this is from my notes on the patent:

  • Procedure creates new follicles and induces anagen in existing resting follicles.

Also, depilating existing hair (done 3 days prior to the abrasion) increases follicular neogenesis 11-fold, which is pretty huge. This is a very interesting effect, BTW.


#14

» I don’t know the page number, but this is from my notes on the patent:
»
» - Procedure creates new follicles and induces anagen in existing resting
» follicles.
»
» Also, depilating existing hair (done 3 days prior to the abrasion)
» increases follicular neogenesis 11-fold, which is pretty huge. This is a
» very interesting effect, BTW.

Inducing anagen in existing follicles is the holy grail of treating hair loss. But it seems Follica is pushing more of a neogenesis aspect of their treatment, maybe because the inducing anagen is somewhat harder than neogensis? Btw, did the patent mention anything specifically about what induces anagen as opposed to neogensis (the last part of your post)?


#15

Inducing anagen in existing follicles is the holy grail of treating hair
loss.

Well, for existing follicles, it would have to both induce anagen and enlarge the follices. Even those tiny, balding, vellus follicles cycle and go into anagen every once in a while (if you look really close at bald guy’s scalp, you can see some very fine peach fuzz growing). It’s just that the miniaturized follicles spend most of their time in telogen, and only a brief period in anagen.

Btw, did the patent mention anything specifically about what induces
anagen as opposed to neogensis (the last part of your post)?

No…


#16

» » wnt is vey much involved in both follicle morphogenesis and hair
» cycling.
» » MPB does seem to involve some antagonism of wnt signalling but it is
» » unclear how important this is. The Foliicaprocess does help put telogen
» » follicles back into anagen though so thats some good news.
» » hh
»
» so if Follica fine tunes the process, they can actually rejuvenate pretty
» much all hair on the head? Can you point me the patent page that
» specifically talks about this…i’m really excited now :slight_smile:

Page 54.
hh


#17

Lordy, lordy . . . let’s just hope all this stuff works.

Let’s just pray that the hair regrowth on the Folica mice isn’t a product of the immunosupression alone. Let’s pray that they’re really ONTO something.


#18

.


#19

Those prayers are in the 3 monotheistic faiths :smiley:


#20

You know looking at that part of the patent I am not sure if and how those results show that “EDIHN is capable of not only forming new hair follicles, but also of activating anagen in pre-existing hair follicles in the telogen stage”. The experimnt basically showed that depilation or induced anagen enhanced new hair follicle formation by about 10 times the ammount of hairs. Maybe they left something out.
However I do have some old, old studies from the 60s where a guy showed that hairs surrounding a wound were stimulated to come out of the resting/telogen stage early. Futhermore he showed that hairs surrounding the wound that were in an anagen state when the wound was made stayed in telogen for a shorter period of time before producing new hairs. So good news on that front it seems.
hh