S. Korea Hair Cm3 / Ngf-574h Cosmetic Due Q1 2019

[EndlessPossibilities]

Nice find. Maybe thats another working mechanism for minoxidil against hair loss, by increasing elastin

Elastin is bad. The study looking at male bald scalps found that they had way more fibrosis due to elastic collagen.
https://www.ncbi.nlm.nih.gov/m/pubmed/18286292/

Straight up one of the reasons why I think minoxidil in the long run will do more harm. Without finasteride.

 

[Bitless]

Looks like the reason for the delay was because of medipost’s cosmetic department’s financial losses through out the years.

 

[NotInmywatch]

i don't think the fibrosis theory is valid tbh. it's pretty clear the derma papilla cells are the reason why we go bald, their signaling gets impaired by androgenic action and in addition their numbers go down and down because dermal sheath cells can't fill up the DP after the end of the cycle anymore. they too interact with androgens. don't see where fibrosis is going to fit in there and i can't finasteride anything in modern day serious literature either

fibrosis can occur as a consequence of constant microinflammation. Useful and crucial cells for the continuous production of hair are annihilated and replaced by stromal or structural cells without any other function but serve as physical filling/scarring tissue. so the fibrosis theory would be more like fibrosis as a result of the DHT-initiated pro-inflammatory environment regulated by a myriad of subsequent molecules.

this is where NGF-574H comes in. it can in theory override these harmful molecules by anti-inflammatory, celullar reparation and growth factors ones.

the thing is, skin is a formidable barrier so the only hope is to take advantage of the deep tunnels that the hair roots make in the skin by existing.

some literature report that this method of penetration is feasible and real.

biological products do not resist ethanol as a vehicle.

 

[GotHair?]

The CEO of Celino Inc. the spin off company for Ngf-574H said that price should be around the price of minoxidil.
So I don't expect it to be expensive. I am willing to fly to South Korea and try it. Since I wanted to go there as a tourist anyways. trial results tell us that it should be decent. But I guess we will see...

 

[TK421]

Will this product be able to slow down hairloss or would you still need to be using an anti androgen?

 

[Ollie]

Will this product be able to slow down hairloss or would you still need to be using an anti androgen?

You'll need an AA just like you would with minoxidil. Growth factors can only fight and hold back the root problem for so long.

 

[Ollie]

thats ridiculous. the theory is that androgens influence the realize of growth factors so with that you would be much more close to "underlying issue" then with anti androgens. AA is a very shallow and outdated view

Growth factors wont do sh*t long term. If you have surging DHT causing / helping chronic inflammation thats restricting the follicle, then growth factors wont do anything after a certain point. Just like minoxidil peaks after a couple of years.

If you want to talk about the very root problem then you need a substance that prevents the communication of proteins and other various signalling...we're decades from that. Choi has just scratched that surface.

 

[itsjustsimon]

thats ridiculous. the theory is that androgens influence the realize of growth factors so with that you would be much more close to "underlying issue" then with anti androgens. AA is a very shallow and outdated view

Btw, this sh*t looks good especially for those who do not respond well to minoxidil. I hope it's real.

 

[itsjustsimon]

Cmon dude, how can you dislike this old lady?

It's semantics dude, who cares.

 

[Ollie]

your problem is that you don't know what you are talking about. what do you think samumed is doing? wnt signaling is altered due to androgens, THATS the underlying issue. not stupid dht. and it turns out their compound grows hair as well. even new follicles. how are we decades away from that? if tsuji succeeds, nobody will ever do further research into this as it won't be worth it

growth factors are many levels lower than androgens, minoxidil is something *completely* different

https://www.ncbi.nlm.nih.gov/pubmed/29482481

Are you completely retarded. WNT is one tiny piece of the puzzle. These WNT drugs thus far have proven fruitless because unlike the mouse studies we don’t have the same level of cell proliferation as mice. Sm04554... 10% increase in hair density. That . Is . Nothing. Not to mention the dosing had diminishing marginal returns anyway.
Still AA’s will be the go to until the stem cell treatments then they’ll be made obsolete.

Bottom line in this instance is the application of growth factors won’t mean sh*t if the onset of DHT and AR sensitivity ultimately fucks the blood supply and starves the follicle into non existence.

 

[vanomastormoz]

Are you completely retarded. WNT is one tiny piece of the puzzle. These WNT drugs thus far have proven fruitless because unlike the mouse studies we don’t have the same level of cell proliferation as mice. Sm04554... 10% increase in hair density. That . Is . Nothing. Not to mention the dosing had diminishing marginal returns anyway.
Still AA’s will be the go to until the stem cell treatments then they’ll be made obsolete.

Bottom line in this instance is the application of growth factors won’t mean sh*t if the onset of DHT and AR sensitivity ultimately fucks the blood supply and starves the follicle into non existence.

This is total bullshit. Why then so many people still balding on finasteride/dutasteride? And don't have results. Why this happen if main problem is DHT .

 

[Ollie]

This is total bullshit. Why then so many people still balding on finasteride/dutasteride? And don't have results. Why this happen if main problem is DHT .

Because ANDROGENS are the problem . Super sensitive people are also subject to the process from testosterone.

Some people are born with no 5ar enzyme .. guess what ... no hairloss. Women who have very low both test and DHT .. most have no hairloss until later in life when there is heightened AR sensitivity in old age.

 

[Tom4362]

@Ollie are already on the CB from Wuhan currently?

 

[Ollie]

@Ollie are already on the CB from Wuhan currently?

I am indeed

 

[Ollie]

thats not very nice. WNT signaling DOES show effectiveness in humans. what the f*** are you talking about. 10% increase in density is better than finasteride do you not understand that? finasteride has 9% increase in hair count after 6 months lol.. androgens are the problem in so far as they cause downstream reactions, nothing more.

http://www.nwpii.com/ajbms/papers/AJBMS_2015_2_05.pdf

you are one level too high.


"Changes in hair follicle and hair size are believed to involve signalling between the hair follicle components via paracrine factors. It is believed that androgens exert their effects on hair follicles via the mesenchyme-derived dermal papilla cells by altering the regulatory paracrine factors produced by the dermal papilla itself and affect the other follicular components.
"

they enter the dermal papilla cells, cause transcription of certain genes which trigger see signaling effect. growth factors are absolutely included in thsi. we don't know much about it but to say androgens are the problem is ridiculous. cell signaling is the answer. they also enter dermal sheath cells which are responsible for repopulating the dermal papilla with DP cells that themselves induce hair growth. so you have two types of cells as a target and the androgens are not the direct issue, they just trigger something in people who are prone to it.

" The mesenchyme-derived dermal papilla in the center of the hair bulb (Fig. 1F) (4,–6, 25) initiates and regulates much follicular growth activity via paracrine signaling (26). Androgens are believed to act via androgen receptors in dermal papilla cells that form hormone-receptor complexes that act as gene switches, which activate cell-specific gene transcription and alter dermal papilla production of short-distance paracrine signals that influence other follicular cells. This closely resembles androgen action via the mesenchyme/stroma in developing and cancerous prostates (2, 27)."


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928870/

finasteride is only a 9% average because there are a lot of people who don’t really respond so it drags the average down. I literally regrew 30% of my hair and hairline back from finasteride.

Drugs upregulatjng WNT won’t mean anything if Androgens keep downregulating it. It’s like minoxidil, it allows for increased blood flow to fight the problem temporarily until it can no longer hold back the increasing problem.

 

[NotInmywatch]

this is a multifactorial disease. DHT and T are one powerful cause (95% of cases), age is another, disregulated paracrine factors are another, and so on.
in women alopecia finasteride does nothing. a lot of women do not respond at all to powerful antiandrogens and still lose their hair. in 30% of cases of chronic tellogen effluvium there is no detectable cause with all lab parameters being normal. some men still lose hair despite dutasteride, etc.

the human body doesnt give a sh*t about head hair.

so every possible angle should be attacked. future clascoterone users will use follicum FOL-005 and NGF-574H as ancillary treatments. so it's pointless to argue about this.

 

[klerik]

Growth factors wont do sh*t long term. If you have surging DHT causing / helping chronic inflammation thats restricting the follicle, then growth factors wont do anything after a certain point. Just like minoxidil peaks after a couple of years.

If you want to talk about the very root problem then you need a substance that prevents the communication of proteins and other various signalling...we're decades from that. Choi has just scratched that surface.

You don't know that. Nobody knows exaclty how hairloss works, if we did then we would probably have a cure already. The only thing we know is that dht is bad for hair in certain people, those affected by hairloss.

It may well be that dht lowers growth factors produced by the body and that leads to hairloss or just that in people with hairloss their body produces less growth factors to counter the dht which damages hair. One good way to eliminate this is the usual antiandrogens like finasteride, cb, ect. The other one may as well be adding more growth factors so that it counters the dht problems.

This may very well be sh*t, but the numbers are very sound, we need to see how it works on Androgenetic Alopecia though.

 

[NotInmywatch]

well, 85% of people respond to finasteride. in other words, if androgens are THE key why do some people not respond to finasteride? anyway it doesn't matter because you apparently have not read the paper that I have linked.

"Drugs upregulatjng WNT won’t mean anything if Androgens keep downregulating it. It’s like minoxidil, it allows for increased blood flow to fight the problem temporarily until it can no longer hold back the increasing problem."

what? what do you think was the theory behind seti? androgens up regulate pgd2 and seti can help that. with your type of argument this wouldn't make any sense. I don't even understand what you are talking about and neither do you if you are completely honest. I don't know what im talking about myself as I am not a biologist that understands how these complex cell signaling things take place in detail. even researchers don't understand it properly. but just from a purely argumentative perspective you are already wrong. minoxidil gives you better nutrition to keep it alive. altering the cell signaling pathway completely undercuts all the damage androgens could ever do. I don't understand why you don't get this. imagine androgens up regulate wnt whatever that means. then you take a drug that down regulates it again. that would stop the androgen hairloss chain right there. why does it matter that androgens still act on it when you counteract them. it's like the argument "CB can't work because while it might competitively block the androgen receptor, dht is still trying to dock onto it" whaaat

I'm trying to understand what you're saying. your point is that..... we should focus on discovering the destructive pathways that are activated by DHT and block them without using an AA ?

but.. .what if I told you that there are more than 100 pathways activated by DHT? then you would need 100 different topical agents.... maybe you could try to fix the top 5 , but a simpler option would always be to block the androgen receptor.

 

[Ollie]

n



no question that we do not understand the picture of how it actually goes down on a cellular level. that will take years and more of research. it's not even a question of what is the bests way to treat this.it's a question of how does it actually work and what is involved.

what ollie is saying though is complete nonsense

"Bottom line in this instance is the application of growth factors won’t mean sh*t if the onset of DHT and AR sensitivity ultimately fucks the blood supply and starves the follicle into non existence."

like what, this suggest a big lack of understand in biology. just like the rest of us. this is quite complicated, you might think uh its just hair and people have thought so in the past. there is a reason why no cure has come out yet... it's hard. but androgens are the most upper layer and superficial understanding of it. also there might be100 pathways activated by dht, the trick is to figure out which ones do the hair damage

Dude you’re missing the whole point. DHT as notinmywatch has said May very well contribute to 100’s of pathways. Meaning that the androgen angle is the only realistic angle unless you have tons of topical drugs.

We will have drugs that BENEFIT the pathways but we can’t control them. If you benefit WNT by x but over time the androgens affect it by an increasly disproportionate amount, then the WNT drug (or whatever angle) becomes less effective and in the end does nothing.
The only real topical cure would be what Choi is has written about. A substance that completely prevents the protein cxxc5 and other various signals from being communicated by androgens.

 

[Ollie]

maybe we should destry the cxxc5 gene that encodes the protein lol

No lol cxxc5 is one of the proteins that does the signalling and acts as a downregulator of the WNT pathway. Choi’s compound successfully prevents androgens from affecting cxxc5. But still that’s just one protein that has an effect on Wnt .

We’ve literally just got to hope for stem cells. Hopefully shiseido can share something worthwhile next week .