If its not DHT then what is the main problem? As of today your only practical choice is take propecia or dont. There arent any things in existence that can alter this CXXC5 yet.
DHT is still a huge player in preventing male pattern baldness.
South Korean Scientists Has Developed A New Type Of Biochemical Material To Prevent Hair Loss
- Thread starter Xaser94
- Start date
DHT is still a huge player in preventing male pattern baldness.
Guys I have been following this thread since its beginning with being obsessed because this seems legit. Respected Dermatology Foundations referred to this study. Their study paper seems logical. We saw it in the news much more than the other treatments.
We find out from the study that a protein called CXXC5 is negative regulator of Wnt Pahtway which is important for hair growth and that they developed a compound called PTD-DBM. They are testing it on mice for toxicity.
So, Let's come to the point that I want to say. We don't know exactly if it will work on humans. In clincals %80 of the compounds don't work on humans. Therefore, We must make them aware of this study and encourage them to work on new CXXC5 inhibitors as alternative to PTD-DBM by contacting them.
I'm going to start by mailing the pharmatics in my country. So, I want your help. You can help me (also yourself) by contacting them about this.
Thanks
Keep your positive, goal-oriented thinking off of this site or I will not hesitate to report you. You've been warned, bucko.
This is what I thought you were going to say, but to me it sounds like just connecting the dots without knowing for sure if you're following the right path.
Can anyone point out in the text where exactly it makes this connection? I can't read the full paper without paying, apparently.
Also, when they say "inhibits" hair growth, do they mean "stops" it or "miniaturizes" it? Because if it's the former, then it's clearly not the same as male pattern baldness.
As it presently stands, unless this study proves successful in humans in vivo, DHT is most definitely the main problem (aside from faulty genes). There is currently nothing else that factors into it that, when removed entirely, stops hairloss or even restores it. Even kingjohn, the most hated of English kings up there, stated that DHT is "the messenger" and not the message. Which, if the link between the two is applicable to humans, would be a correct statement.
People keep coping by saying that DHT isn't the problem, because it gives hope to the idea that a simpler solution to the problem is out there, but all evidence thus far indicates otherwise.
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PLEASE .... THE LAST STUDIES DO NOT SAY THE SAME. DHT IS NOT THE MAIN PROBLEM. You are attacking the consequence, not the cause.
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Poor results with alpha 5 reductase inhibitors....Agree with this: DHT is "the messenger" and not the message. Remember that....@That Guy. Proof of this is that with the alpha 5 reductase inhibitors, total hair growth is not achieved ... only 15% with Dustasteride 20-25%. Very bad results.
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I will, because it means that DHT is indeed the problem. Shoot the messenger because there is no message to be received without one.
If you have no follicles left in a particular area, you cannot really be mad at 5-ar inhibs for failing to regrow it as they're not intended to regrow hair; they just slow or stop the process of miniaturiziation and can save some follicles if they aren't too far gone.
Lastly, they produce neither bad nor good results because whether a percentage is good or not depends on the baseline it's compared to. For someone with minimal loss, 15 - 20% regrowth is a large amount of hair; not so much for someone with advanced thinning and loss.
Anyway, @InBeforeTheCure or @Swoop I'm dying to hear, just straight up, explain like I'm five: Scientifically speaking, is there any reason to be hopeful about this?
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Let's see...@That Guy.
Finasteride: Gives you a full head of hair? Do not. Sorry.
Dutasteride: No
Minoxidil: No
I think I have answered your questions. That they are many by what I see...
Hematuria and Hematospermia Associated with the Use of Finasteride for the Treatment of Androgenic Alopecia: A Case Report. It's a serious study. Read it. You need it.
https://www.ncbi.nlm.nih.gov/pubmed/29090364
There are many reasons to be hopeful.
https://www.nextbigfuture.com/2017/...kin-tissue-and-other-tissues-will-follow.html Look at the pipeline.
Follica: Phase 3
Shiseido: Phase 3
Breezula: Phase II-III
Setipiprant: Phase 3 the next year (2018-2019)
There are so many competitors that I lost the account. I counted as 15. Truly amazing. We will have better treatments soon. We have never been in a situation like now.
None of this has anything to do with any of my posts
If you are a serious professional. You will embrace new technologies and new treatments. It's easy
I'm not a professional and I will embrace new technologies when they come to market and have efficacy.
I'm not yet convinced that the subject of this thread will work on male pattern baldness
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In the chain of events that happen that lead to your hair miniaturizing we have just discovered a potentially new one, CXXC5. CXXC5 has been shown to be an inhibitor of the main cellular pathway (wnt) that controls cell proliferation, cell migration and stuff like that.
So what? There's lot's of things in the chain, why's CXXC5 so special? Because it's something we could potentially actually effectively get at, and we've already shown how we can neutralise its effect in human cells.
Worst case, it's just some side effect whose inhibition will have little to no effect at all.
Best case, it's the bottleneck that's stopped other modes of treatment from work effectively as they might.
There's the question InBeforeTheCure raised about what actually the mechanism controlling CXXC5 is (as this is where the "real" problem could be). It's an important question, but one that could be potentially academic if hitting CXXC5 is enough reverse Androgenetic Alopecia.
But there's still so much we need to know. We simply don't know if this will work, and we don't understand what's driving CXXC5 to overexpress, and we don't know if we really can get at it effectively and safely yet. There could be a better target in the chain that this study will lead us to. But it's exciting because it's shiny and new and no one's really tried doing it yet.
I'd actually like the throw the reverse of this question out and ask why there's no good "theoretical" reason to be excited about this? But I don't want the answer to be based on emotion or about industry regulation or social victimhood.
(Also the full study is available on reddit if you search for it)
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Sanchez1234
Experienced Member
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I asked LUO to make the compound but he replied;
The compound PTD-DBM is a peptide. But the artical has not released the amino acid sequence. So we are not able to produce it now. If we know, maybe we can produce it. Thank you very much
The compound PTD-DBM is a peptide. But the artical has not released the amino acid sequence. So we are not able to produce it now. If we know, maybe we can produce it. Thank you very much
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Why I'm not excited?
-İt's a study..
-Not one company actually claimed to start trials anytime soon..
-it would take years if they actually would start now
-no significant results in human trials are available at the moment
Maybe it's gamechanger maybe not, but it's sooooo early that nobody ain't even an idea of how to start this.
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How else would you expect them to discover this?
industry regulation
Would you usually expect these before the first study?
Rub it on bald guys heads and see if it works?
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Still not available in the near future, maybe never, so no hype for me.
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This isn't only related to Androgenetic Alopecia and there's several drugs with the same method of action. So it's essentially available now.
And I specifically asked for a theoretical reason, not your ignorant, pessimistic feelz.
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Cry me a River baby...
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No, I just find it interesting.
?
Explain.
Somewhat. It's definitely more relevant than most other studies in the past year or so that been randomly hyped. Amplifying Wnt signaling could be useful for:
1) Making existing hair follicles larger. The Wnt pathway controls the size of the dermal papilla, the size of the hair follicle in general, and the thickness of the hair shaft.
2) Making new hair follicles. Wnt is the first signal in hair follicle morphogenesis, and in this experiment, the mice treated with VPA (a weak to moderate Wnt agonist) plus the peptide grew five times as many new follicles as the mice treated with VPA alone. So apparently, amplifying the signal does make a real difference. But keep in mind that because of differences in immune system, mice are much better at growing new follicles than we are.
So this is something to follow, but let's not get our hopes up too much until we see real results in baldies.
Maybe some day, but I'll settle for unmodified clones of M.P.B-resistant hairs. I'm not greedy.
Amino acid sequence RKTGHQICKFRKC with the carboxyl group (n terminal may also work) linked to the amino acid sequence RRRRRRRR with a glycerin linker GGGG.
CXXC5
MSSLGGGSQDAGGSSSSSTNGSGGSGSSGPKAGAADKSAVVAAAAPASVADDTPPPERRNKSGIISEPLNKSLRRSRPLSHYSSFGSSGGSGGGSMMGGESADKATAAAAAASLLANGHDLAAAMAVDKSNPTSKHKSGAVASLLSKAERATELAAEGQLTLQQFAQSTEMLKRVVQEHLPLMSEAGAGLPDMEAVAGAEALNGQSDFPYLGAFPINPGLFIMTPAGVFLAESALHMAGLAEYPMQGELASAISSGKKKRKRCGMCAPCRRRINCEQCSSCRN[RKTGHQICKFRKC]EELKKKPSAALEKVMLPTGAAFRWFQ
CXXC4
MNTNVCVEPGPSPEAPGLPKESHLPEGALNSLVDYNSEMERYRSFATSFYKTNGGAFPQAAKIARITTPIFPSSAAAAAAAARIGMSPWNCDNAATAAAATAMLWGSGGGGGGGGGGGGGGGGGGGGGGGGGGGRKSSSAAASSSASSSSAILPAGGGGGGGGGGSRTSMHHRNDSQRLGKAGCPPEPSLQMANTNFLSTLSPEHCRPLAGECMNKLKCGAAEAEIMNLPERVGTFSAIPALGGISLPPGVIVMTALHSPAAASAAVTDSAFQIANLADCPQNHSSSSSSSSGGAGGANPAKKKRKRCGVCVPCKRLINCGVCSSCRN[RKTGHQICKFRKC]EELKKKPGTSLERTPVPSAEAFRWFF
Other possibilities for the protein transduction domain:
Example:
PTD(RRRRRRRR) <GGGG> DBM(RKTGHQICKFRKC)
RRRRRRRR
YGRKKRRQRRR
DAATATRGRSAASRPTERPRAPARSASRPRRPVE
RQIKIWFQNRRMKWKK
AGYLLGKINLKALAALAKKIL
Vehicle: 50% ethanol, 20% propylene glycol, 30% water
We can reproduce the mouse study to verify which PTD sequence works.
CXXC5
MSSLGGGSQDAGGSSSSSTNGSGGSGSSGPKAGAADKSAVVAAAAPASVADDTPPPERRNKSGIISEPLNKSLRRSRPLSHYSSFGSSGGSGGGSMMGGESADKATAAAAAASLLANGHDLAAAMAVDKSNPTSKHKSGAVASLLSKAERATELAAEGQLTLQQFAQSTEMLKRVVQEHLPLMSEAGAGLPDMEAVAGAEALNGQSDFPYLGAFPINPGLFIMTPAGVFLAESALHMAGLAEYPMQGELASAISSGKKKRKRCGMCAPCRRRINCEQCSSCRN[RKTGHQICKFRKC]EELKKKPSAALEKVMLPTGAAFRWFQ
CXXC4
MNTNVCVEPGPSPEAPGLPKESHLPEGALNSLVDYNSEMERYRSFATSFYKTNGGAFPQAAKIARITTPIFPSSAAAAAAAARIGMSPWNCDNAATAAAATAMLWGSGGGGGGGGGGGGGGGGGGGGGGGGGGGRKSSSAAASSSASSSSAILPAGGGGGGGGGGSRTSMHHRNDSQRLGKAGCPPEPSLQMANTNFLSTLSPEHCRPLAGECMNKLKCGAAEAEIMNLPERVGTFSAIPALGGISLPPGVIVMTALHSPAAASAAVTDSAFQIANLADCPQNHSSSSSSSSGGAGGANPAKKKRKRCGVCVPCKRLINCGVCSSCRN[RKTGHQICKFRKC]EELKKKPGTSLERTPVPSAEAFRWFF
Other possibilities for the protein transduction domain:
Example:
PTD(RRRRRRRR) <GGGG> DBM(RKTGHQICKFRKC)
RRRRRRRR
YGRKKRRQRRR
DAATATRGRSAASRPTERPRAPARSASRPRRPVE
RQIKIWFQNRRMKWKK
AGYLLGKINLKALAALAKKIL
Vehicle: 50% ethanol, 20% propylene glycol, 30% water
We can reproduce the mouse study to verify which PTD sequence works.
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my weak finasteride boners become rock hard whenever someone with scientific knowledge drops wisdom in threads like these