The Reason Why Setipiprant Failed In Trials

[dethlol]

So I heard that Setipiprant failed the trials for hair loss, as well as allergies and asthma. In short, the CRTH2 blockade didn't do sh*t.

However, Ramatroban, another CRTH2 antagonist, DOES work for allergies:

http://www.ncbi.nlm.nih.gov/m/pubmed/11778458/

In my opinion, Setipiprant is just a sh*t drug and too weak to stop hair loss.

If trials on hair loss were conducted on TM30089, a chemical analogue of Ramatroban that is far more potent with INSURMOUNTABLE blockade to the receptor, meaning it doesn't let any PGD2 bind to the receptor at all, I have a feeling we would have much better results.

I personally take it orally, 1 - 3mg a day (yes it's THAT potent) and it's certainly reduced, if not entirely stopped itch and shedding. No side effects. I've experimented with up to 10mg a day for months at a time, no side effects. Some fearmongers were spreading hysteria about it having a half life of like a million years; I notice return of itch after a few days cessation.

I read a post of someone who took it topically at 0.1% once a day, and claimed it did way better than RU at 5%.

 

[Ollie]

So I heard that Setipiprant failed the trials for hair loss, as well as allergies and asthma. In short, the CRTH2 blockade didn't do sh*t.

However, Ramatroban, another CRTH2 antagonist, DOES work for allergies:

https://www.ncbi.nlm.nih.gov/m/pubmed/11778458/

In my opinion, Setipiprant is just a sh*t drug and too weak to stop hair loss.

If trials on hair loss were conducted on TM30089, a chemical analogue of Ramatroban that is far more potent with INSURMOUNTABLE blockade to the receptor, meaning it doesn't let any PGD2 bind to the receptor at all, I have a feeling we would have much better results.

I personally take it orally, 1 - 3mg a day (yes it's THAT potent) and it's certainly reduced, if not entirely stopped itch and shedding. No side effects. I've experimented with up to 10mg a day for months at a time, no side effects. Some fearmongers were spreading hysteria about it having a half life of like a million years; I notice return of itch after a few days cessation.

I read a post of someone who took it topically at 0.1% once a day, and claimed it did way better than RU at 5%.

Any links to that topical post ?

Where have you gotten your TM from ?

 

[ihatebackstabbers]

Any links to that topical post ?

Where have you gotten your TM from ?

Link

 

[Ollie]

Link

Broken dude

 

[ihatebackstabbers]

Broken dude

i have to delete it after you copy it

copy it instead of clicking on it

 

[Ollie]

Seems that guy had such bad sleep sides he legit couldn't sleep properly for a week lol. Interesting you haven't had those sides OP.

 

[dethlol]

I fixed the link. Yes the guy did have insomnia, but I'd rather have sleep issues than erectile dysfunction. I get my TM from Kane.

If you want to wait for fevipiprant, go for it. My point of the thread was that just because Seti didn't work doesn't mean that CRTH2 blockade doesn't help hair.

 

[dethlol]

And here is the link to the post about TM working:

http://www.hairlosstalk.com/interact/threads/has-anyone-here-used-tm-30089-huge-half-life.111893/

 

[dethlol]

Also, it might be possible that CRTH2 blockade alone might not be enough to stop hair loss entirely, at least with some users. There was an old post I found somewhere where a guy was regrowing some hair while just taking montelukast.

Also, here's a post on another forum:


Leukotriene E4 activates human Th2 cells for exaggerated pro-inflammatory cytokine production in response to PGD2


We found that cysLTs markedly potentiated pro-inflammatory cytokine production from human Th2 cells in response to PGD2. The potency of LTE4 in the enhancing effect was significantly higher than that of LTD4 or LTC4 and this enhancing effect of LTE4 was inhibited by montelukast. Although the CRTH2 antagonist TM30089 alone substantially inhibited IL-13 production in response to both exogenous and endogenous PGD2 and LTE4, a combination of TM30089 and montelukast was required to completely inhibit the response.

In other words, montelukast/zafirlukast and a CRTH2 antagonist is just about one of the most nuclear synergies you can get in regards to male pattern baldness. Add in an anti-androgen, and you've essentially shut down the entire male pattern baldness process.

I'm currently on TM, montelukast dutasteride and pyrithone zinc shampoo, and my hair has never felt this good and shedded the least since before I started thinning or receding ever.

I'm also using taking CLA 10,12 rally daily and dermastamping in some of the stuff once or twice a month, and the sparse hairs in front of my transplanted hairline have gone fully terminal. At this point it's hard to distinguish between the the native and transplanted hair in that are, except the native hairs have had less time to thrive in the anagen phase and reach the same length as the transplanted ones.

 

[Vinc2097]

So I heard that Setipiprant failed the trials for hair loss, as well as allergies and asthma. In short, the CRTH2 blockade didn't do sh*t.

However, Ramatroban, another CRTH2 antagonist, DOES work for allergies:

http://www.ncbi.nlm.nih.gov/m/pubmed/11778458/

In my opinion, Setipiprant is just a sh*t drug and too weak to stop hair loss.

If trials on hair loss were conducted on TM30089, a chemical analogue of Ramatroban that is far more potent with INSURMOUNTABLE blockade to the receptor, meaning it doesn't let any PGD2 bind to the receptor at all, I have a feeling we would have much better results.

I personally take it orally, 1 - 3mg a day (yes it's THAT potent) and it's certainly reduced, if not entirely stopped itch and shedding. No side effects. I've experimented with up to 10mg a day for months at a time, no side effects. Some fearmongers were spreading hysteria about it having a half life of like a million years; I notice return of itch after a few days cessation.

I read a post of someone who took it topically at 0.1% once a day, and claimed it did way better than RU at 5%.

the fact you are on dutasteride could do ALL the work.. to be 100 % it is working you would have to drop duta for couple of weeks and pursue the rest of you regimen to see.

no ?

 

[Alex Contee]

the fact you are on dutasteride could do ALL the work.. to be 100 % it is working you would have to drop duta for couple of weeks and pursue the rest of you regimen to see.

no ?

You would have to drop dutasteride for a lot longer than a couple weeks.

As for the OP, I agree that the Seti test didn’t kill the theory for me. I always knew Seti would at best maintain and guess what? The subjects that used Seti maintained. It’s just a shame they didn’t use a finasteride group for comparison.

I have used OC topically with succes. Although it’s expensive as hell and kills my sleep quality. Btw not getting sleep with kill your testosterone levels and can contribute to ed.

I would be very nervous taking something from Kane orally but I’ll look into TM again.

 

[Vinc2097]

You would have to drop dutasteride for a lot longer than a couple weeks.

As for the OP, I agree that the Seti test didn’t kill the theory for me. I always new Seti would at best maintain and guess what? The subjects that used Seti maintained. It’s just a shame they didn’t use a finasteride group for comparison.

I have used OC topically with succes. Although it’s expensive as hell and kills my sleep quality. Btw not getting sleep with kill your testosterone levels and can contribute to ed.

I would be very nervous taking something from Kane orally but I’ll look into TM again.

How much is TM daily ? (103 mg like in the thread).. anyway is fevi is as strong and kill your sleep its not any better no ?..

 

[itsjustsimon]

1g of TM is $200 @ kane. Are you a billionaire or smth?

 

[BaldLion]

I fixed the link. Yes the guy did have insomnia, but I'd rather have sleep issues than erectile dysfunction. I get my TM from Kane.

If you want to wait for fevipiprant, go for it. My point of the thread was that just because Seti didn't work doesn't mean that CRTH2 blockade doesn't help hair.

How long is TM half life?
Are you sure it’s not due to dutasteride that you at least maintain?

 

[jamesbooker1975]

So I heard that Setipiprant failed the trials for hair loss, as well as allergies and asthma. In short, the CRTH2 blockade didn't do sh*t.

However, Ramatroban, another CRTH2 antagonist, DOES work for allergies:

http://www.ncbi.nlm.nih.gov/m/pubmed/11778458/

In my opinion, Setipiprant is just a sh*t drug and too weak to stop hair loss.

If trials on hair loss were conducted on TM30089, a chemical analogue of Ramatroban that is far more potent with INSURMOUNTABLE blockade to the receptor, meaning it doesn't let any PGD2 bind to the receptor at all, I have a feeling we would have much better results.

I personally take it orally, 1 - 3mg a day (yes it's THAT potent) and it's certainly reduced, if not entirely stopped itch and shedding. No side effects. I've experimented with up to 10mg a day for months at a time, no side effects. Some fearmongers were spreading hysteria about it having a half life of like a million years; I notice return of itch after a few days cessation.

I read a post of someone who took it topically at 0.1% once a day, and claimed it did way better than RU at 5%.

" In short, the CRTH2 blockade didn't do sh*t."

No, what really explain is that Setipiprant is a useless drug, while Fevipiprant is a success .

 

[baldco]

" In short, the CRTH2 blockade didn't do sh*t."

No, what really explain is that Setipiprant is a useless drug, while Fevipiprant is a success .

You guys should give this study a quick glance as to why Seti or Fevi might not work

Garza et al. described overexpression of prostaglandin synthase (PTGDS) on baldness areas and its product, the prostaglandin D2 (PGD2), as an inducer of the premature catagen phase. [1] PGD2 (Prostaglandin D2) activity is mediated by the prostaglandin D2 receptor PTGDR2 (GPR44) [1, 2] A Mantel et al. suggested that ROS (reactive oxygen species) -driven function in hair follicles keratinocytes is the molecular mechanism by which PGD2 induced testosterone synthesis [3]. Induction of ROS by PGD2 is attributed to 15 -deoxy -delta -12,14 -prostaglandin J2 (15d -PGJ2), a spontaneous electrophilic metabolite of PGD2 [4, 5] . Therefore, high PGD2 levels found in the bald scalp of Androgenetic Alopecia may lead to increased testosterone, which can be converted locally to dihydrotestosterone by 5a -reductases to induce Androgenetic Alopecia . It has been suggested that inhibitors of PTGDR2 may reverse hair growth through inhibition by PGD2 activity[6]. A multicenter, randomized, double -blind, placebo -controlled, Phase 2A study of setipiprant (oral PTGD2 receptor antagonist) 500 mg tablets BID in Androgenetic Alopecia is being performed (ClinicalTrials.gov Identifier: NCT02781311). It is interesting that this receptor is not overexpressed in our patients. Perhaps research on treatment should focus on drugs that target PTGDS activity and not PTGDR2

 

[AllerganSaveUs]

You guys should give this study a quick glance as to why Seti or Fevi might not work

The earlier studies on PGD2 in male pattern baldness such as this one https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982925/ as well as the one you posted
suggest that inhibiting PTGDS (aka PGD2 synthase) could work to prevent and treat male pattern baldness. I know that tretinoin inhibits PTGDS and has been shown clinically to increase hair growth when used with Minoxidil. Hopefully someone with intelligence can tell us if inhibiting PTGDS is truly realistic to treat male pattern baldness and what can be done to inhibit PTGDS. Good post, thank u

 

[tomJ]

So I heard that Setipiprant failed the trials for hair loss, as well as allergies and asthma. In short, the CRTH2 blockade didn't do sh*t.

However, Ramatroban, another CRTH2 antagonist, DOES work for allergies:

http://www.ncbi.nlm.nih.gov/m/pubmed/11778458/

In my opinion, Setipiprant is just a sh*t drug and too weak to stop hair loss.

If trials on hair loss were conducted on TM30089, a chemical analogue of Ramatroban that is far more potent with INSURMOUNTABLE blockade to the receptor, meaning it doesn't let any PGD2 bind to the receptor at all, I have a feeling we would have much better results.

I personally take it orally, 1 - 3mg a day (yes it's THAT potent) and it's certainly reduced, if not entirely stopped itch and shedding. No side effects. I've experimented with up to 10mg a day for months at a time, no side effects. Some fearmongers were spreading hysteria about it having a half life of like a million years; I notice return of itch after a few days cessation.

I read a post of someone who took it topically at 0.1% once a day, and claimed it did way better than RU at 5%.

How does this compare to fevi?...and unfortunately many dumb dumbs consider these failures as they are mostly maintanance drugs, not growth drugs.

 

[HairlossCurse]

I think it failed either because the PGD2 increase was actually to do with the hairs being in the resting phase, not actually the cause. Alternatively, the inhibitor needs to be at a high dose locally (i.e injected right into follicle or a custom topical made that can pierce the human skin and fatty layer), similar to what Aclaris did with the JAK-STAT inhibitors, simply converting the pills to topical was not good enough as it did not pierce skin down to follicles, they made a custom topical that did this.

 

[jamesbooker1975]

The earlier studies on PGD2 in male pattern baldness such as this one https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3982925/ as well as the one you posted
suggest that inhibiting PTGDS (aka PGD2 synthase) could work to prevent and treat male pattern baldness. I know that tretinoin inhibits PTGDS and has been shown clinically to increase hair growth when used with Minoxidil. Hopefully someone with intelligence can tell us if inhibiting PTGDS is truly realistic to treat male pattern baldness and what can be done to inhibit PTGDS. Good post, thank u

I think that tretinoin works even without minoxidil, I am wrong ?

How does this compare to fevi?...and unfortunately many dumb dumbs consider these failures as they are mostly maintanance drugs, not growth drugs.

At really lower doses, fevipiprant was more effective, much more, than Setipiprant in Asthma . For me, is like comparing something even weaker than saw palmeto to dutasteride.

Lets put this for example, We know that DHT cause hair loss, what about a drug that will only inhibit 30 % of the systemic DHT ( compare to 70 % finasteride, almost 100 % of dutasteride ) it should work ? For me, setipiprant have to be see it in this way.