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#1

Ive read through some of the patent, and paid attention to the experimental details section. It seems to me that they are dermabrating the skin with a felt wheel (both human skin grafted onto mice, and mouse skin), and SUPPRESSING WNT EXPRESSION FOR NINE DAYS EXACTLY, and then just watching the new PIGMENTEDfollicles grow in.

If wnt epression is not blocked (they used DKK-1, which inhibits wnt) for the first nine days, the hairs will lack pigment during this “epilithealization” period.

Maybe Im reading it wrong, but I dont’ see where wnt is ever specifically applied or a analogue or wnt-mimicing subtance thereof. Apparently the wounding gets the body to make it enough on its own. If someone reads the patent and sees where something is being used to induce wnt-pathways after the first nine days, please let me know.

The expiremental details are below:

EXPERIMENTAL DETAILS SECTION

EXAMPLE 1

DEPILATION AND EPIDERMAL ABRASION CAUSES DE NOVO HAIR FOLLICLE

FORMATION

MATERIALS AND EXPERIMENTAL METHODS

Depilation and epidermal abrasion

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[000187] Mice were anesthetized with an injection of sodium pentobarbital before the hair on the back was clipped and depilated withNair (Carter-Wallace, New York, NY), then epidermis was removed using a rotating felt wheel as described by Argyris T, J Invest Dermatol, 75: 360-362, 1980). After scrubbing with 70% ethanol and drying under an incandescent lamp, the basal and supra-basal layers in an area of (1.5 cm)2 cm of the inter-folHcular epidermis were removed by careful abrasion with a felt wheel mounted on a Dremel Moto-tool (Racine, WI). After abrasion, the skin was shiny and smooth, and there was no blood. One day later, the abraded area was covered by a fibrin crust, which fell off after 3-7 days, exposing the newly regenerated epidermis. A group of control mice was sacrificed immediately after abrasion to confirm microscopically the complete removal of the interfollicular epidermis.

Immunohistochemistry

[000188] Skin samples were fixed in PBS-buffered 10% formalin. Six-micron thick paraffin sections were cut and stained, where applicable, with antibodies.

BrdU labeling [000189] The protocol described by Bickenbach and colleagues (Bickenbach et al, Cell Tiss Kinet 19: 325-333, 1986; Bickenbach et al, Exp Cell Res 244. 184-195, 1998) was used. Mice were injected with 50 milligrams per kilogram (mg/kg) bodyweight 5-bromo-2’-deoxyuridine (BrdU) every 12 hours for a total of four injections.

RESULTS

[000190] An area of the backs of 50-day old mice was subjected to depilation and removal of the epidermis using a rotating felt wheel. Fifteen days later, HF placodes, hair germs and other signs of follicle neogenesis were present (Figure 1 ; arrow indicates a hair germ). Morphology of the follicles was similar to embryonic follicle development. To further characterize proliferation in the new follicles, the skin was labeled with BrdU 60 minutes before sacrifice. As depicted in Figure 2, the proliferation pattern was similar to developing follicles in the embryo.

[000191] These findings demonstrate that (a) disruption of the epidermis causes generation of new

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HF, and that this generation of new HF can occur (b) in adult subjects and © during telogen (50- day-old mice are in the second telogen stage of the hair cycle).

EXAMPLE 2

INDUCTION OF A LARGE EXCISIONAL WOUND, BUT NOT A SMALL PUNCH WOUND, CAUSES DE NOVO HAIR FOLLICLE FORMATION

MATERIALS AND EXPERIMENTAL METHODS

Punch wound and excisional wound induction

[000192] The backs of 21 -day-old mice were depilated as described for Example 1 and sterilized with alcohol, followed by 1% iodine solution. Punch wounds, 4 mm in diameter, were induced using a dermal biopsy punch, down to, but not through, the muscle fascia. Excisional wounds were full thickness and 1 cm in diameter; skin and panniculus carnosus was excised using fine surgical scissors.

RESULTS

[000193] To test whether wounding could induce HF formation, punch wounds or excisional wounds were induced in mice. Both types of wounds exhibited contraction and re-epithelialization following wound induction; however, unlike the mice receiving punch wounds, the mice receiving excisional wounds also exhibited scar formation within 10 days of wound induction (Figure 3, left panel). No follicles were evident at this time point (Figure 3, right panel). 12 days after wound induction, hair germs, with similar morphology to fetal hair germs, were observed in the wound site, following BrdU pulse labeling (Figure 4). Several markers were used to verify that the observed structures were HF. The structures exhibited staining with anti-keratin 17 (K 17), an HF marker (Figure 5), and staining with anti-alkaline phosphatase at the 12 day time point verified that the structures had dermal papilli containing fibroblasts, as expected for HF (Figure 6; HF at earlier and later stages are depicted in the left and right panels, respectively).

[000194] The HF generated by wound induction were further characterized by morphological

P-7628-PC comparison to embryonic HF9 following BrdU staining; a clear correspondence in morphology was observed at various stages (Figure 7). In addition., several markers of embryonic HF development, namely Left, wingless/ int (Wnt) 10b, and sonic hedgehog (Shh), were also induced in the epidermal disruption-induced HF neogenesis (EDIHN) (Figure 8). Additional BrdU staining (Figure 9) and staining for HF markers S 100A3 and S 100A6 (Figure 10; left panel: tissue section parallel to HF axis; right panel: cross-sectional view of follicle) provided further verification that the development of the EDIHN follicles closely paralleled embryonic HF development.

[000195] These findings provide further evidence that disruption of the epidermis causes generation of new HF, and that this generation of new HF can occur (b) in adult subjects and © during telogen (21 -day-old mice are in the first telogen stage of the hair cycle).

EXAMPLE 3

EDIHN-INDUCED HAIR FOLLICLES GENERATE HAIRS

[000196] At 25 and 45 days after wound induction, wound sites contained new hairs (Figure 11 „ left and right panels, respectively). New hairs appeared to lack pigmentation, except when the wnt pathway was inhibited, using Dkk-1 (Dickkopf-1) during the first nine days after wounding (see Example 10).

[000197] These findings indicate that EDIHN-induced HF function normally; Le. are capable of generating hairs.

EXAMPLE 4

EDIHN HAIR FOLLICLES RETAIN THE ABILITY TO ENTER INTO CYCLICAL

HAHl GROWTH

MATERIALS AND EXPERIMENTAL METHODS

BrdU labeling

[000198] 50 mg/kg bodyweight BrdU (Sigma) was injected twice per day for 3 days beginning 20

P-7628-PC days after wounding. BrdU was detected 40 days after wounding (17 day chase).

Whole mounting and immunofluorescence

[000199] HF whole mounts were obtained by incubating fresh skin with EDTA (2OmM in PBS) at 37

0C overnight, then separating the epidermis and dermis. Epidermis was then fixed in 10% formalin for 10 min, room temperature (RT). Dermis was fixed in acetone overnight, RT. After rinsing with

PBS, whole mounts were stained with antibodies for immunohistochemistry (schematically depicted in Figure 12) and were imaged using a Leica confocal microscope.

RESULTS

[000200] To determine whether EDIHN-induced HF contain normal levels of HF stem cells, mouse skin was examined for the presence of label-retaining cells at 21 days after wound induction.

Retention of BrdU during a long chase period is, under these conditions, one of the hallmarks of HF stem cells. Normal numbers and placement of label-retaining cells (in the bulge of the HF) were observed (Figure 13). To verify that the label-retaining cells were HF stem cells, K15-eGFP mice were utilized. In these mice, eGFP (enhanced green fluorescent protein) is expressed from the Kl 5 promoter; thus, expression of eGFP identifies HF stem cells. As depicted in Figure 14A5 eGFP- expressing cells were observed in in tissue sections (right side) of newly formed hair follicles 35 days following wound induction. eGFP-expressing cells were also seen in the epidermis whole mounts (bottom, far left panel) indicating the conversion of epidermal cells into cells with hair follicle stem cell characteristics, ([bottom, second from left] panel is same as [bottom, far left] panel but viewed under white light) This finding shows that the observed label-retaining cells exhibited

HF stem cell properties.

[00020I] To determine whether EDIHN-induced HF cycle normally, mounts were prepared from additional mice at 35, 38 and 45 days after wounding. As depicted in Figure 14B, the EDIHN- induced HF entered the resting phase, telogen, and then re-entered a new anagen stage.

[000202] In summary, the findings of this Example show that EDIHN-induced HF contain HF stem cells, as do embryonically generated HF. The presence of the HF stem cells shows that EDIHN-

P-7628-PC induced HF retain the ability to enter into cyclical hair growth in the same manner as embryonically generated HF. The findings also show that wounding induces epidermal cells to assume a hair follicle stem cell state (expressing Kl 5-eGFP). This model is shown schematically in Figure 15. The findings of Examples 2, 3, and 4 showthat EDIHN-induced HF are fully functional and thus able to restore hair growth to a subject in need.

EXAMPLE 5

EPIHN-INDUCES NEW HAIR FOLLICLES IN MICE AT THE TELOGEN STAGE OF

THE HAIR CYCLE

[000203] To determine whether EDIHN was induced new hair follicles in mice wounded at the telogen stage of the hair cycle, 21 -day-old mice were subj ected to ED3ΗN using a 1 -cm excisional wound, as described in Example 2, Sldn was then examined by whole-mount assay for indications of new HF. As depicted in Figure 16, after 11 days, new HF were not evident by macroscopic examination (top panel), AP staining of the dermis (bottom left panel), or KI 7 staining of the epidermis (bottom right panel). After 14 days, as depicted in Figure 17, dermal papilla cells were detected in the dermis (left panel) and HF stem cells in the epidermis (right panel), demonstrating that new follicles were being formed. After 17 days, the new follicles were more developed, as shown by examination of the dermis and epidermis (Figure 18, left and right panels, respectively). This method induced formation of an average of 49 new follicles in the wound, a number that was consistent over three separate experiments, as depicted in Table 1.

[000204] Table 1. Results of three separate experiments performed on 21 -day-old mice.

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[000205] The findings of this Example demonstrate that EDIHN is capable of inducing formation of new HF in mice at the telogen stage of the hair cycle, despite that fact that these mice do not contain HF at the anagen stage during wounding.

EXAMPLE 6

IN ADULT MICE. INDUCTION OF ANAGEN INCREASES THE EFFICIENCY OF

EDIHN

[000206] The experiment described in Example 5 was repeated with mice of different ages, and therefore at different stages of the hair cycle. To ensure that wound scarring occurred, larger wounds were in induced in the older mice. As depicted in Table 2, adult mice at telogen, such as 8-week-old mice, exhibited lower efficiencies of HF formation by EDIHN.

[000207] Table 2. Efficiency of HF formation by EDIHN in adult mice at various stages of the hair cycle.

  • The second telogen lasts approximately 40 days in mice. Thus, 14-week-old and 20- week-old mice contained a mixture of telogen and anagen HF.

[000208] To determine whether experimental induction of anagen increased the efficiency of EDIHN,

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8-week-old mice were depilated several days prior to wound induction. As depicted in Figure 19, the wounds closed similarly whether or not they were preceded by depilation. As depicted in Figure 20A-B, the depilated mice exhibited enhanced EDIHN relative to the non-depilated mice depicted in the previous Example by a factor of 11 -fold.

[000209] The findings of this Example demonstrate that anagen induction enhances EDIHN. In addition, these findings show that EDIHN is capable of not only forming new HF, but also of activating anagen in pre-existing HF in the telogen stage.

EXAMPLE 7

EDIHN-INDUCES NEW HAIR FOLLICLES IN HUMAN SKIN

MATERIALS AND EXPERIMENTAL METHODS

Grafting

[000210] Discarded human, adult scalp from the preauricular area obtained from plastic surgery was grafted onto immunodeficient (scid) mice. The graft was bandaged and allowed to heal, then was used in the wound healing study 3 months after grafting.

RESULTS

[000211 ] To determine whether human skin responded to EDIHN as did mouse skin, human skin was grafted onto SCID (immuno-deficient) mice and subjected to depilation by plucking and wound induction three days later. Seven days following wound induction, formation of new HF was observed in the human skin (Figure 2 IA; arrows indicate new HF) by hematoxylin and eosin staining of paraffin embedded tissue sections.

[000212] In additional experiments, adult human skin was grafted onto mice., abraded, and examined at 7 days post-abrasion. New HF were generated in the human skkx, which mimicked normal hair follicle formation during fetal development, as evidenced by staining for SlOO A6 or S100A4 (Figure 21B).

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[000213] The results of this Example show that EDIHN can be used to generate hair growth inhuman skin as for mouse skin.

EXAMPLE 8

MOLECULAR PATHWAYS ACTIVATED DURING HF STEM CELL ACTIVATION

MATERIALS AND EXPERIMENTAL METHODS

Isolation and activation of HF stem cells

[000214] Kl 5~eGFP mice were depliated in order to induce formation of new HF. Activated hair follicle stem cells were isolated from K15-eGFP mice using fluorescence-activated cell sorting (FACS) two days after depilation and 5 μg (micrograms) total RNA from the cell population was isolated, reverse-transcribed and hybridized to an Affymetπx (Santa Clara, California) array MG_U74v2 chip. Scanned chip images were analyzed using Affymetrix Microarray Suite 5.0 and GeneSpring software (Silicon Genetics) to detect fold-change differences between activated HF stem cells (HFSCs) and non-activated (telogen) HFSCs. Values were normalized before computing fold-changes and differences between non-activated “bs-line” and activated (“expt”) samples.

RESULTS

[000215] To identify molecular pathways up-regulated during HF stem cell activation, activated HF stem cells were isolated, and the gene expression patterns of the cells were analyzed to detect up- regulated transcripts. The transcripts depicted in Table 3 were up-regulated at least 2~fold in the activated HF stem cells relative to the cells prior to activation. In some cases, the sequence in Table 3 is a genomic sequence that contains the sequence of the transcript. Data pertaining to the up- regulation of the transcripts and further information about them is provided in Figure 22.

Me again…
here is the patent page, http://www.wipo.int/pctdb/en/wo.jsp?wo=2006105109&IA=WO2006105109&DISPLAY=DESC ,

I dont see where anything external (other than delipidation done with conventional NAIR, which was admittedly not really necessary for effect) was done other than the blockage of wnt for nine days. The description would seem to indicate that they are prepared for ORAL administration of the wnt-‘blocker’ by the verbiage below
000181] The pharmaceutical compositions containing the HF stem cell-inducing or -activating compound can, in another embodiment, be administered to a subject by any method known to a person skilled in the art, such as topically, parenterally, paracancerally, transmucosally, transdermally. intramuscularly, intravenously, intradermally, subcutaneously, intraperitonealy, intraventricularly, intracranially, intravaginally or intratumorally. Each possibility represents a separate embodiment of the present invention.

[000182] In another embodiment, the pharmaceutical compositions are administered orally, and are thus formulated in a form suitable for oral administration, i.e. as a solid or a liquid preparation. Suitable solid oral formulations include tablets, capsules, pills, granules, pellets and the like. Suitable liquid oral formulations include solutions, suspensions, dispersions, emulsions, oils and the like. In one embodiment of the present invention;, the HF stem cell-inducing or -activating compounds are formulated in a capsule, hi another embodiment, the compositions of the present invention comprise, in addition to the HF stem cell-inducing or -activating compound active compound and the inert carrier or diluent, a hard gelating capsule.

Green tea catechin ECGC and curcumoids both inhibit wnt expression. I keep looking into the patent to see where something that activates wnt comes in, but haven’t noted it yet. If anyone does, let me know. It appears at this point they are merely dermabrating skin over five millimeters in width and just deep enough to remove its top layer (but the experimtal subjects did NOT bleed), and blocking wnt for 9 days, and voila’…new DARK hair.
Surely it can’t be that easy.

I’d like to note that they had the same success in human skin on mousebacks as they did with mere mouseskin.


#2

A little more on their approach from NATURE:

Nature 447, 316-320 (17 May 2007) | doi:10.1038/nature05766; Received 30 August 2006; Accepted 20 March 2007

Wnt-dependent de novo hair follicle regeneration in adult mouse skin after wounding
Mayumi Ito1, Zaixin Yang1, Thomas Andl1, Chunhua Cui1, Noori Kim1, Sarah E. Millar1 & George Cotsarelis1

Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
Correspondence to: George Cotsarelis1 Correspondence and requests for materials should be addressed to G.C. (Email: cotsarel@mail.med.upenn.edu).

Top of pageThe mammalian hair follicle is a complex ‘mini-organ’ thought to form only during development1; loss of an adult follicle is considered permanent. However, the possibility that hair follicles develop de novo following wounding was raised in studies on rabbits2, 3, mice4 and even humans fifty years ago5. Subsequently, these observations were generally discounted because definitive evidence for follicular neogenesis was not presented6. Here we show that, after wounding, hair follicles form de novo in genetically normal adult mice. The regenerated hair follicles establish a stem cell population, express known molecular markers of follicle differentiation, produce a hair shaft and progress through all stages of the hair follicle cycle. Lineage analysis demonstrated that the nascent follicles arise from epithelial cells outside of the hair follicle stem cell niche, suggesting that epidermal cells in the wound assume a hair follicle stem cell phenotype. Inhibition of Wnt signalling after re-epithelialization completely abrogates this wounding-induced folliculogenesis, whereas overexpression of Wnt ligand in the epidermis increases the number of regenerated hair follicles. These remarkable regenerative capabilities of the adult support the notion that wounding induces an embryonic phenotype in skin, and that this provides a window for manipulation of hair follicle neogenesis by Wnt proteins. . These findings suggest treatments for wounds, hair loss and other degenerative skin disorders.

Im guessing that for nine days…inhibit Wnt, and thereafter increase the hell out of it as much as you can?


#3

"EXAMPLE 3

EDIHN-INDUCED HAIR FOLLICLES GENERATE HAIRS

[000196] At 25 and 45 days after wound induction, wound sites contained new hairs (Figure 11 „ left and right panels, respectively). New hairs appeared to lack pigmentation, except when the wnt pathway was inhibited, using Dkk-1 (Dickkopf-1) during the first nine days after wounding (see Example 10).

[000197] These findings indicate that EDIHN-induced HF function normally; Le. are capable of generating hairs."

I think this sums up what they are doing succinctly. Nine days of no WNT signalling, and every day thereafter as much of it as you can get until the hairs are growing out of the scalp proper which should be about 45 days down the line


#4

Hi all,
Benji,

First, Thanks for the insights…You gave me a pretty good idea about the patent even before I start reading it.
Second,and I’m not sure here since I did not yet come across all sections of the patent, That the skin wound is a start point for Wnt signaling and the 9 days inhibition is designed to stop the skin from doing it…When the inhibition is stopped…the Wnt signaling comes naturally.


#5

I’ll soon be more informed about the procedure…


#6

» I’ll soon be more informed about the procedure…

There was a link posted to an article about Follica in the previous thread. One of their people (David Steinberg) posted a reply in the comments, when questioned about whether the new hair will be DHT resistant he wrote:

“David Steinberg 1/4/08 2:12 pm
I am with the company. While we have not tested this in humans yet we fully expect that hair will persist. There are multiple reasons for this. First of all, consider hair transplants - while they have other flaws, the hair does indeed persist despite the presence of circulating DHT. In a distinct, but similar way, the Follica treatment changes the microenvironment of the follicles. Further, a single hair cycle lasts several years, and at the very least the new hair should last one full cycle (because of the underlying physiology of the condition). Also, circulating levels of DHT actually drop over a man’s life. We have seen numerous clinical reports of patients showing sustained hair cycling when exposed to conditions similar to the treatment Follica is pursuing (in a carefully directed and controlled way).”


#7

Good find cockneyninja !


#8

Do you mind givine the link cockneyninja ?


#9

» Do you mind givine the link cockneyninja ?

Sure.

http://www.xconomy.com/2008/01/04/gone-today-hair-tomorrow-follica-raises-funds-to-begin-human-trial-of-baldness-treatment/

Just scroll down to the comments.

Does anyone know what kind of devlopment period will they have? Do they still have to do the 3 Phase trials?


#10

» I think this sums up what they are doing succinctly. Nine
» days of no WNT signalling, and every day thereafter as much of it as you
» can get until the hairs are growing out of the scalp proper which should
» be about 45 days down the line

Come on all other smart people, help benji with the patent! What exactly does it say?
You know, if they are using drugs already available on the market people could go and have a scalp dermabrasion, use the drugs and let the body create a full head of hair. But then we need to know exactly what the patent says.

JB? JTR? Break the silence!


#11

The study was done in mice. You can ignore that.


#12

» The study was done in mice. You can ignore that.

can I? :wink: but also in human skin grafts on mice.


#13

» Does anyone know what kind of devlopment period will they have? Do they
» still have to do the 3 Phase trials?

To quote myself from the other thread on the subject:

Relevant paragraphs from various articles related to the original May 2007 journal article.

"The scientists are optimistic that the finding could lead to a salve or other product to combat human hair loss—and, perhaps, even to regenerate hair where the sun now shines by performing dermabrasion to the bald scalp and slathering ointment on the wounds.
“For this to become therapeutic, you’d probably have to find ways to activate the Wnt pathways with a topical agent,” Cotsarelis says. He notes that he and his colleagues have founded a small start-up company called Follica to create a product that could be applied to injured skin as it heals to “activate the right pathways … [that trigger] follicle formation.” Cotsarelis says the for-profit venture is now only doing preclinical experiments, but if all goes perfectly, there could be a product on the market in two to three years."
Source: http://www.sciam.com/article.cfm?articleID=9AFCFE33-E7F2-99DF-3E38BE66BB0F006E&chanID=sa003

"Cotsarelis is involved with Follica Inc., a privately held start-up company that has licensed the patent on the process from the University of Pennsylvania. He said it probably would be more than five years before a treatment was possible."
Source: http://www.reuters.com/article/healthNews/idUSN1619596120070517?pageNumber=2&virtualBrandChannel=0

"The researchers envisage a commercial application similar to that used to treat teenage acne. A dermabrasion gel gently damages the skin and kicks off the wounding process, together with a topical cream to switch on the follicle-generating genes. It’s still early days according to Dr Cotsarelis: “If it all went perfectly then possibly in two to three years we would have a product, but that’s very optimistic,” he said."
Source: http://www.xpress4me.com/news/international/usa/20001089.html

So, according to Cotsarelis himself, 2-3 years in the case of everything going perfectly, and “more than 5” otherwise. These comments were made in the middle of 2007, which would provide an estimated Entry Into Service date of 2009\2010 or 2012. This in turn is similar to the projected timeline for HM, which raises the question once more: could the two techniques be used together?


#14

If all goes well with human trials,will hairsite add a new section to forum index.Where are JTR & J BOND…?


#15

http://www.hairsite.com/hair-loss/board_entry-id-19051-page-0-category-1-order-last_answer-descasc-DESC.html

Just looking for educated opinions on the linked question. Thanks.


#16

Im just going to cut and paste it:

""EXAMPLE 3

EDIHN-INDUCED HAIR FOLLICLES GENERATE HAIRS

[000196] At 25 and 45 days after wound induction, wound sites contained new hairs (Figure 11 „ left and right panels, respectively). New hairs appeared to lack pigmentation, except when the wnt pathway was inhibited, using Dkk-1 (Dickkopf-1) during the first nine days after wounding (see Example 10).

[000197] These findings indicate that EDIHN-induced HF function normally; Le. are capable of generating"

That simply stated says that after 25 and also 45 (which means they didn’t fall out) after dermabrasion, wound sites contained NEW HAIRS. The new hairs would LACK PIGMENTATION, EXCEPT WHEN THE WNT PATHWAY WAS INHIBITED DRUING THE FIRST NINE DAYS AFTER THE WOUNDING.

We know that some of their experiments were on genetically hairlessmice, so the hairs being created had to be brand new, and not “rejuvinated”. We also know that they used human skin grafted onto immuno deficient mice and grew human hair on the human skin after the wounding.

The big question I have is this…immuno deficient mice dont have the circulating levels of DHT that we have. When Albert Klingman noticed de noveau hair growth after acne dermabrasion on SOME patients, that was hair on the face which obviously likes DHT. WE are trying to grow hair on the head that does not like DHT. Might it be prudent to be on finasteride while attempting this? I have read Bryan Shelton postulate before that if a man got on finasteride before the first signs of hairloss when he was 18, then the hair may not ever entertain enough androgenic stimuli to “become” sensitive to androgens in the first place. However, one could look at this in an entirely different neo-natal way: Perhaps if the hair cold form with the full compliment of adult DHT, they may never be sensitive to DHT in the first place like the very best donor area hair in the very heart of the hippocratic wreath?

I will say this…they have grown real visible hair in the labratory and noted its PIGMENTATION. This means these were not mere “hair germs” or “proto-hairlike-structures”, but real visible hairs that they could see, and they did it on human skin that resulted in human (not mouse) hair. The only thing different would be the amount of hormones the forming dermal unit was confronted with in the experiment. Supposedly by increasing the amount of wnt protien, they could make more and thicker hair appear. Could this be the difference in people who have thick hair (pre-balding years) genetically and those with thinner hair when they are teens, mere wnt-signalling in your mother’s womb. If so, then perhaps that is something that someday scientists will be able to tinker with to make sure any kid born is born with a good mop to start with anyway.


#17

I don’t quite get the follicle growth thing.

It takes a lot more than mild dermabrasion to cause balded skin to start reproducing vast swaths of terminal hairs at 100/cm2 that eventually grow to a foot long if left uncut.

Whatever they’re doing, the chemicals they’re adding to the process must be causing a hell of a lot more changes than just than pigmentation increases.

Either way, is the chemical basis of this stuff already available in some way? Can we somehow try this out ourselves right now?


#18

Okay I re-read some more of this stuff on both threads.

Off the cuff, it sounds like Lithium Chloride would theoretically do the job of a topical WNT-expressing drug (after the critical 9 days). Whether the second topical step is really necessary or not.

The topical WNT-inhibiting substance (the first nine days) would seem to be the only thing we don’t already have access to for this process. So is there a specific perscription drug that would really do this correctly if re-mixed into a topical form? Or some other substance out there that will adequately do the job?


#19

» Okay I re-read some more of this stuff on both threads.
»
»
» Off the cuff, it sounds like Lithium Chloride would theoretically do the
» job of a topical WNT-expressing drug (after the critical 9 days). Whether
» the second topical step is really necessary or not.
»
»
» The topical WNT-inhibiting substance (the first nine days) would seem to
» be the only thing we don’t already have access to for this process. So is
» there a specific perscription drug that would really do this correctly if
» re-mixed into a topical form? Or some other substance out there that will
» adequately do the job?

ECGC in green tea inhibits wnt signalling, but it also inhibits angiogenesis (new blood capillary formation), so I dont know how this might effect this wounding-healing process during the first nine day re-eplithialization period.

Curcumin also can inhibit wnt signalling, but also inhibits angiogenesis. Curcumin needs to be taken with piperine (black pepper extract) or taken with food seasoned with a healthy amount of black pepper if you can stand it in order for it to be metabolized. I do not know how long grean tea catechin ECGC is active in the body, but curcumin is only active for about 12 hours, so supplementation would have to be done twice a day for 9 days with the curcumin

Then again if you dont mind white hair…One could start putting the topical lithium chloride on the wounds from the get go I suppose

I can tell this however, these wounds on mousebacks WERE NOT TOUCHED IN ANY WAY. These little guys dont shampoo or anything. Men would have to keep that in mind and touch their heads as little as possible, keep any kind of shampoo or chemical off the abraded area in all probabiliity for a couple of weeks I’d imagine. Any chemical interference might screw up the skin signalling taking place in the are. New hairs were seen by the 25th day, so after 20 days perhaps it would be OK to touch the area, etc. Until then though…covering up the wound with a band aid or ointment would probably invalidate the whole process because if it didnt we’d have new hair everytime we cut ourselves and placed a band aid on top.

I can tell you this one thing for certain Cal. They wouldn’t have went to the trouble of this patent and be engaging in human trials with the backing of Gillette if they though this was bullshiiit. Proctor&Gamble also does not need hoaxes and the like to raise investor money. These people think this works. If it only produces small hairs, then they were genuinely wrong about it in an honest misevaluation or mistake based on the evidence they have. Im excited because its another way (other than HM) for men to get hair on their heads, which is something I want for humanity to have, male and female.


#20

I wonder if the process even has to be that well done to get some kind of results.

We’re talking about WNT “inhibition.” It hasn’t been termed “complete WNT deprivation” though. I wonder how total the WNT suppression really has to be just to get something happening hair-wise.

And what happens when you grow a “half-correct” hair follicle with this process? Is it fixable? What might this process do to your original existing hairs that are partly miniaturized? Kill them and replace them? Fix them?

I dunno. The whole thing sure bears more attention though. It makes perfect sense to me that mild abrasion could cause follicular regeneration.

I’ve personally gotten a couple of (terminal) hairs growing in my receded areas just from experimenting with needling & sandpapering a small spot a few months ago. And I didn’t make any effort to protect the abraded areas in any way whatsoever. I remember putting some salicylic acid on the spot once or twice, but nothing resembling the kind of perfect 9-day regimen & protections they’re talking about. Such a sloppy job, and yet I have a couple of legit dark hairs to show for this. One of them has grown 3-4cm long.