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Did Anyone Maintain With Setipiprant
- Thread starter Gone
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I don't believe PGD2 is the cause of hair loss, however it could be a factor affecting follicle constriction and hair growth rate, to some extent. I don't think trials that didn't show finasteride levels of regrowth are definitive proof that it won't be beneficial somehow. I'm not expecting it to save hair though.
$illy $ymphony
Member
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I use TM (sodium). For about a year now. And I am not doing it for nothing.
Unlike others (I suppose), I have not just substituted TM for my previous stuff (finasteride, minoxidil, 15+ yrs).
I'd rate TM above the standard stuff. Wish I had it back then. Now, I too am surprised that there seem few if any success with TM (maybe look for it on stopaga.com or similar sites), as the science behind PGD2 seems solid.
Unlike others (I suppose), I have not just substituted TM for my previous stuff (finasteride, minoxidil, 15+ yrs).
I'd rate TM above the standard stuff. Wish I had it back then. Now, I too am surprised that there seem few if any success with TM (maybe look for it on stopaga.com or similar sites), as the science behind PGD2 seems solid.
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- Reaction score
- 950
@KO1 @Folliman
What do you think about this data* presented by Cotsarelis et al. at the 2015 Hair Congress, which seems to show that many hair loss sufferers have hair follicles unresponsive to PGD2? They found SNPs associated with this PGD2 sensitivity, which have also been associated with CRTH2 mRNA stability and asthma susceptibility (Huang et al.). If CRTH2 was necessary for A.G.A to develop, you would of course expect all sufferers to have sensitive follicles. And if it played some role, but not a critical one, would you not still expect genome-wide association studies done on A.G.A to pick those up? Even Cots has been hedging recently, saying things like: "Our findings further underscore the key role of PGD2 in regulating hair growth and indicate that pharmacological antagonism of PTGDR2 [CRTH2] may be an effective approach in preventing and/or treating alopecia in patients sensitive to PGD2." But not even GWAS with high numbers of participants, which are sensitive to variants even with small effects, have associated A.G.A with these PGD2 sensitivity polymorphisms. The one major loophole to this though might be, if we assume those hair samples were taken from donor zones, that maybe this mRNA stability mechanism could be turned off in A.G.A-susceptible regions. Otherwise, these findings would suggest that PGD2 is redundant in A.G.A.
* Photo taken by Hellouser.
What do you think about this data* presented by Cotsarelis et al. at the 2015 Hair Congress, which seems to show that many hair loss sufferers have hair follicles unresponsive to PGD2? They found SNPs associated with this PGD2 sensitivity, which have also been associated with CRTH2 mRNA stability and asthma susceptibility (Huang et al.). If CRTH2 was necessary for A.G.A to develop, you would of course expect all sufferers to have sensitive follicles. And if it played some role, but not a critical one, would you not still expect genome-wide association studies done on A.G.A to pick those up? Even Cots has been hedging recently, saying things like: "Our findings further underscore the key role of PGD2 in regulating hair growth and indicate that pharmacological antagonism of PTGDR2 [CRTH2] may be an effective approach in preventing and/or treating alopecia in patients sensitive to PGD2." But not even GWAS with high numbers of participants, which are sensitive to variants even with small effects, have associated A.G.A with these PGD2 sensitivity polymorphisms. The one major loophole to this though might be, if we assume those hair samples were taken from donor zones, that maybe this mRNA stability mechanism could be turned off in A.G.A-susceptible regions. Otherwise, these findings would suggest that PGD2 is redundant in A.G.A.
* Photo taken by Hellouser.
tress_dreams
Member
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Someone will have to pry my finasteride out of my cold dead hands. So joining the trial is out.
Allergan (AGN) is an 80billion company. I don't think their board would spend millions on trials if their wasn't reason to be hopeful. I'm as much a cynic about all this as the next person but these companies want to make money and that means finding something that works. I would love to wait another 8-12 months+ for results but I'm still losing this game unfortunately. If I'm going to get brave/stupid then it might as well be a drug that's actually in trials. I'll for sure update the board on the progress.
KO1
Established Member
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Since these samples were taken from patients undergoing hair transplants, we can probably assume they were donor. While that could point to donor insensitivity, I don't think sensitivity is a "local" phenomenon as the CRTH2 receptor in unsensitive individuals simply doesn't express the required SNPs. Which could mean it is redundant. Or it could also mean that the picture is more complicated than we understand.
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Folliman
Established Member
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Sorry, I didn't fully absorb the data since I'm a little brain dead at the moment, what is GWAS?.
There's so many questions that can branch out from here. What was the thickness of the hair follicles insensitive to PGD2? From what part of the scalp? Are they from the hair loss safe zone? What were their PGE2 levels? were they already having a high CRTH2 expression?
It's hard to tell what is actually going on when so many questions are left unanswered.
There's so many questions that can branch out from here. What was the thickness of the hair follicles insensitive to PGD2? From what part of the scalp? Are they from the hair loss safe zone? What were their PGE2 levels? were they already having a high CRTH2 expression?
It's hard to tell what is actually going on when so many questions are left unanswered.
- Reaction score
- 950
I think there's some possibility it could be local. Hypothetically, the SNPs could for example affect binding of certain microRNAs which are differentially expressed between donor hair follicles and balding hair follicles.
GWAS = Genome-Wide Association Study. Take a large number of baldites, a large number of fullheads, sample maybe a million variants in their genomes, and find the variants which are more frequent in one group or the other. These are likely found near genes or non-coding RNAs which play a role in the disease.
Likely donor given they're from hair transplant patients. The mechanism is potentially mRNA stability of CRTH2, which may or may not be different between occipital and frontal hair follicles. Too bad they didn't profile CRTH2 expression in balding scalp between the two sensitivity groups.
I don't get the dismissiveness towards pgd2. Sure, most things don't do anything, that's why we're still balding. But to act like Allergan spent missions to acquire a compound that was obviously useless and then run phase II trials for it... thats about as much confidence as anything gets around here.
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- 198
0 changes for me.
The real question here is... Has anyone used 2g of setipiprant daily for at least 3 months?
The real question here is... Has anyone used 2g of setipiprant daily for at least 3 months?
How much did you use?
I'm trialling 1g a day soon. 2g would be close to $600 U.S. a month
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Lack of anecdotal reports from other PGD2 trials, lack of supporting scientific hypothesis, lack of success stories from group buys.
ah yes that old scammer trick of running an invite only forum !
pretty sure he doesnt even sell - anything - , ironically I explicitly told him he should sell it when i messaged him on reddit, because he might as well make a buck as the haters are running his name through the mud anyway.
inmyhead
Senior Member
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ah yes that old scammer trick of running an invite only forum !
pretty sure he doesnt even sell - anything - , ironically I explicitly told him he should sell it when i messaged him on reddit, because he might as well make a buck as the haters are running his name through the mud anyway.
yes maybe you should jump on his protocol then and regrow all your hair
- Reaction score
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How much did you use?
I'm trialling 1g a day soon. 2g would be close to $600 U.S. a month
Less than 500mg daily (I slowly increased the dose).
Theres no way a guy with an average income can spend that much each month.
yes maybe you should jump on his protocol then and regrow all your hair
I would if I could reliably source the compounds at a reasonable cost.
I cannot, so I do not.
But sure, he's running an elaborate 4D scam where you not only do not sell stuff yourself, but purposefully limit your customer base and don't even bother to advertise!
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Something I thought was interesting... I recently stopped taking my regular dose of 100mg oral seti daily and after a week or so of no seti I had a huge outbreak of spots and much oilier skin than usual. Could be a coincidence but if it is correlated then it might possibly show that a low amount of seti can do more than one might think.