Setipiprant

[Canuck]

I'll give you guys an update closer to the end of the month.

I mostly lurk but really looking forward to your update, hellouser!

[Farkhairloss]

Expect delays, as per usual.

Hellouser looking forward to your updates. Also what is the story behind the guy from Switzerland with the t3mple regrowth? His posts keep getting d3leted. He mentions you on his blog. Is he legit?

[burtandernie]

I just want to see a study with results on what one of these things like seti can do in humans. How well does it prevent hair loss? Does it regrow anything? Right now we are completely blind there is no info on any real human results

[hellouser]

I just want to see a study with results on what one of these things like seti can do in humans. How well does it prevent hair loss? Does it regrow anything? Right now we are completely blind there is no info on any real human results

You'll find out pretty soon.

[baldybald]

You'll find out pretty soon.

Still using oraly is more effective and recommend in their website

[chongmet]

Still using oraly is more effective and recommend in their website

Users in forums say that taking it orally wasting 50% of the substance. I'm sure Kythera can solve it if they just find out the right dosage for taking it orally. But I'm not sure if we can afford it right now (economically). Then we might want to use it topically in order to not waste much of the substance. But am not sure about it.

[baldybald]

Users in forums say that taking it orally wasting 50% of the substance. I'm sure Kythera can solve it if they just find out the right dosage for taking it orally. But I'm not sure if we can afford it right now (economically). Then we might want to use it topically in order to not waste much of the substance. But am not sure about it.

Not true. Timid the same as finasteride, use it oraly or topically?

[baldybald]

Users in forums say that taking it orally wasting 50% of the substance. I'm sure Kythera can solve it if they just find out the right dosage for taking it orally. But I'm not sure if we can afford it right now (economically). Then we might want to use it topically in order to not waste much of the substance. But am not sure about it.

Not true. It is the same as finasteride, use it oraly or topically?

[chongmet]

Not true. It is the same as finasteride, use it oraly or topically?

I'm not sure if it's the same situation. But anyway, even if it is, Fin is something we already know by clinical trials the right dosage. In Seti, we don't know it yet, so it might be better to use it topically, as for now (for saving reasons)

[baldybald]

I'm not sure if it's the same situation. But anyway, even if it is, Fin is something we already know by clinical trials the right dosage. In Seti, we don't know it yet, so it might be better to use it topically, as for now (for saving reasons)

Yes I agree for saving reason. Again minoxidil is more effective oraly than topically but it is not safe at all. In general, most of time oraly is more effective. Just my opinion.

[baldybald]

I'm not sure if it's the same situation. But anyway, even if it is, Fin is something we already know by clinical trials the right dosage. In Seti, we don't know it yet, so it might be better to use it topically, as for now (for saving reasons)

Yes I agree for saving reason. Again minoxidil is more effective oraly than topically but it is not safe at all. In general, most of time oraly is more effective. Just my opinion.

[Swooping]

I just want to see a study with results on what one of these things like seti can do in humans. How well does it prevent hair loss? Does it regrow anything? Right now we are completely blind there is no info on any real human results

This is not true. You are not always blind. You can look for observational evidence in vivo. Setipiprant is a selective DP2 antagonist. So the first question you could ask yourself; "Are there other selective DP2 antagonists?"

That would give you an answer; "Yes there are many selective DP2 antagonists in clinical trials and some are even close to be released into the market.".

So that would mean that these other compounds would need to show evidence of regrowth of hair because their primary intention is all the same (selectively antagonizing the DP2 receptor). Yet none of the clinical trials showed this as a side effect. Furthermore we haven't even seen a case study whatsoever of evidence of regrowth of hair with DP2 antagonists.

The thing is many people suffer from androgenetic alopecia. This means that many people are automatically a test subject for it unwillingly in clinical trials that are not even related to hair growth. That's the beauty of it. That's what happened with minoxidil too. Hair growth showed up as an side effect. Other potassium channel openers like like minoxidil, for instance diazoxide and pinacidil have shown to induce hair growth too. Hair regrowth doesn't go by unnoticed.

This will actually tell you immediately that DP2 antagonists like setipiprant won't regrow your hair pretty much. Why? Well just like I said because the evidence would already been shown through these other compounds that have the same biological activity as setipiprant. This is just logical thinking and how science works. So this isn't being blind or speculative. You can already be pretty damn sure of this.

We should clap our hands and be extremely lucky if this will actually even maintain hair or even somewhat approach a treatment like finasteride in terms of effectiveness. At least such is my opinion.

[JSmith120]

This is not true. You are not always blind. You can look for observational evidence in vivo. Setipiprant is a selective DP2 antagonist. So the first question you could ask yourself; "Are there other selective DP2 antagonists?"

That would give you an answer; "Yes there are many selective DP2 antagonists in clinical trials and some are even close to be released into the market.".

So that would mean that these other compounds would need to show evidence of regrowth of hair because their primary intention is all the same (selectively antagonizing the DP2 receptor). Yet none of the clinical trials showed this as a side effect. Furthermore we haven't even seen a case study whatsoever of evidence of regrowth of hair with DP2 antagonists.

The thing is many people suffer from androgenetic alopecia. This means that many people are automatically a test subject for it unwillingly in clinical trials that are not even related to hair growth. That's the beauty of it. That's what happened with minoxidil too. Hair growth showed up as an side effect. Other potassium channel openers like like minoxidil, for instance diazoxide and pinacidil have shown to induce hair growth too. Hair regrowth doesn't go by unnoticed.

This will actually tell you immediately that DP2 antagonists like setipiprant won't regrow your hair pretty much. Why? Well just like I said because the evidence would already been shown through these other compounds that have the same biological activity as setipiprant. This is just logical thinking and how science works. So this isn't being blind or speculative. You can already be pretty damn sure of this.

We should clap our hands and be extremely lucky if this will actually even maintain hair or even somewhat approach a treatment like finasteride in terms of effectiveness. At least such is my opinion.

According to my research, and my research only, I have found out that Setipiprant reduces PGD2 levels, which is higher in balding people's scalp. Therefore, Seti will not give regrowth. It's main purpose is to STOP balding.

Minox showed regrowth because it increases PGE1, which is shown to regrow hair. That is why regrowth was shown as a side effect.

I have been doing extensive research, and found that CD-200 and CD-34 are an important piece of the puzzle to reversing hairloss. Do you happen to know what products can be used concerning that? Thanks Swoop.

[chongmet]

According to my research, and my research only, I have found out that Setipiprant reduces PGD2 levels, which is higher in balding people's scalp. Therefore, Seti will not give regrowth. It's main purpose is to STOP balding.

Minox showed regrowth because it increases PGE1, which is shown to regrow hair. That is why regrowth was shown as a side effect.

I have been doing extensive research, and found that CD-200 and CD-34 are an important piece of the puzzle to reversing hairloss. Do you happen to know what products can be used concerning that? Thanks Swoop.

It's strange. As far as I know, Seti blocks one of the receptors of PGD2. If it is true, then it has nothing to do with PGD2 levels, but just making those PGD2's unable to connect , hence preventing the chain reaction.
But 1 thing is sure - Seti's goal is not regrow hair, but maintaining.

[Swooping]

According to my research, and my research only, I have found out that Setipiprant reduces PGD2 levels, which is higher in balding people's scalp. Therefore, Seti will not give regrowth. It's main purpose is to STOP balding.

Minox showed regrowth because it increases PGE1, which is shown to regrow hair. That is why regrowth was shown as a side effect.

I have been doing extensive research, and found that CD-200 and CD-34 are an important piece of the puzzle to reversing hairloss. Do you happen to know what products can be used concerning that? Thanks Swoop.

Jsmith120,

I won't go into too much detail but many things are not correct in your message. Setipiprant doesn't reduce PGD2. See here why https://www.baldtruthtalk.com/thread...l=1#post218979.


You say that minoxidil showed regrowth because it increases PGE1. Was it PGE1? I thought it was PGE2 according to the study; http://www.ncbi.nlm.nih.gov/pubmed/9008235.

We demonstrate here that minoxidil is a potent activator of purified PGHS-1 (AC50 = 80 microM), as assayed by oxygen consumption and PGE2 production. This activation was also evidenced by increased PGE2 production by BALB/c 3T3 fibroblasts and by human dermal papilla fibroblasts in culture.

Nonetheless doesn't matter anyway. What does matter is that you say that minoxidil has shown to increase a prostaglandin and that this the reason is why minoxidil showed hair regrowth as a side effect.

Let me tell you that the action of minoxidil on the hair follicle is extremely complex and mind dazzling. I could show you tons of studies and write a few pages about it. Even the best hair loss researchers in the world don't have a clue why it grows hair. So for you to argue that minoxidil shows hair growth because it increases PGE1 is pretty short sighted don't you think? Also where have you read that PGE1 has shown to regrow hair?

I don't know any products or compounds that increase CD34 and CD200 expression directly, neither do I think they are an important piece of the puzzle to reverse hair loss. In my view it's simply a consequence of other things that happen first. The research that shows the lack of these progenitor cells in bald scalp is from 2011. We know much more in the meantime. Some studies;

http://www.ncbi.nlm.nih.gov/pubmed/23153495

How dermal papilla (DP) niche cells regulate hair follicle progenitors to control hair growth remains unclear.

http://www.ncbi.nlm.nih.gov/pubmed/24985131

The dermal papilla (DP) of the hair follicle is both a chemical and physical niche for epithelial progenitor cells that regenerate the cycling portion of the hair follicle and generate the hair shaft. Here, we review experiments that revealed the importance of the DP in regulating the characteristics of the hair shaft and frequency of hair follicle regeneration. More recent work showed that the size of this niche is dynamic and actively regulated and reduction in DP cell number per follicle is sufficient to cause hair thinning and loss.

The hair follicle bulb: The dermal papilla (green cells at the center of the hair bulb) serves as both a physical and chemical niche that regulates the activity of adjacent epithelial progenitor cells (unlabelled except for a red nuclear stain) that produce the hair shaft and its surrounding inner root sheath.

So what do these studies tell you about the dermal papilla of the hair follicle? Do progenitors regulate the dermal papilla? Or is the dermal papilla crucial for regulation of progenitor cells? I think it's the latter, right?

With this in mind have you ever looked at the morphology of a miniaturized hair follicle, especially the dermal papilla? Let me tell you that it's pretty "broken".

So if you think increasing CD200 and CD34 expression will help while the dermal papilla niche stays altered then that's pretty bold and illogical to me. Obviously anything that reverts a miniaturized hair follicle to a anagen hair follicle will increase CD200 and CD34 expression but that doesn't mean that focusing on CD200 and CD34 directly will have any meaning if it's a secondary event.