Kane is offering Setipiprant now

Ziggyz123

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The only problem with the ******** group by his people flaking and not paying..

- - - Updated - - -

The only problem with the ******** group by his people flaking and not paying..

- - - Updated - - -

The only problem with the ******** group by his people flaking and not paying..

- - - Updated - - -

I think seti might work but you have to wait for it to finish trials and they figure out dosing and all that stuff.


Correct, but that's what everyone is doing in the group buys. Testing topically, orally, dosing ranges, etc..
 

I.D WALKER

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That and those whom are respectively trialing Seti. in conjunction with an array of treatment regimen's abound, inevitably skewers it's (Seti.) efficacy finding(s). Still I'm grateful for their progress report initiative all the same. I would not expect or encourage anyone to drop their original regimen (especially if it's effective) for the purpose of trying a questionable treatment.
 

cupido

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That and those whom are respectively trialing Seti. in conjunction with an array of treatment regimen's abound, inevitably skewers it's (Seti.) efficacy finding(s). Still I'm grateful for their progress report initiative all the same. I would not expect or encourage anyone to drop their original regimen (especially if it's effective) for the purpose of trying a questionable treatment.



@ziggy,

Nah it was about other issues with cb and kb from ********. there are some topics about them on other forums. I can defenitly dig them up if you insist It's a big joke.

Oc000459 is 3-5 * stronger then sepi, and still limited. It needs to be used in conjunction with ru and fina .
Stepping down to weaker brother like seti just doesn't make sense.
You need a very high dose obviously.

Moral of the story. Don't waste your money on any source. On saga there is even a gb from European source but its Not worth it IMO.

300usd/30g for groupbuy price is still too much considering oral dose of 1g a day vs 200mg oc000459

I believe something like tooical ibuprofen will do as much for the pgd nflammation puzzle.

This all is a big hype don't buy into it brothers.

Btw if someone want their stuff tested let me know. I have contact with an university who also tested my batch.
 

KiNGTyreZe

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@ziggy,

Nah it was about other issues with cb and kb from ********. there are some topics about them on other forums. I can defenitly dig them up if you insist It's a big joke.

Oc000459 is 3-5 * stronger then sepi, and still limited. It needs to be used in conjunction with ru and fina .
Stepping down to weaker brother like seti just doesn't make sense.
You need a very high dose obviously.

Moral of the story. Don't waste your money on any source. On saga there is even a gb from European source but its Not worth it IMO.

300usd/30g for groupbuy price is still too much considering oral dose of 1g a day vs 200mg oc000459

I believe something like tooical ibuprofen will do as much for the pgd nflammation puzzle.

This all is a big hype don't buy into it brothers.

Btw if someone want their stuff tested let me know. I have contact with an university who also tested my batch.

TM30089 is 1000 times stronger than Setipiprant. 1 mg is enough.
 

Ziggyz123

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Yeah TM is supposedly good at getting rid of ALL pgd2. Honestly, I'm not putting shot on my head anymore. My scalp hates it. Supposedly the half life of that stuff is like 13 years or something lol.
 

lmg7

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What do you mean CONTINUES to work ?Do we have any update from the forum users of seti ?
 

Dench57

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That and those whom are respectively trialing Seti. in conjunction with an array of treatment regimen's abound, inevitably skewers it's (Seti.) efficacy finding(s). Still I'm grateful for their progress report initiative all the same. I would not expect or encourage anyone to drop their original regimen (especially if it's effective) for the purpose of trying a questionable treatment.

Nobody should advise dropping a treatment and replacing it with Seti. It's for people still losing ground on existing treatments (and I know there are a lot of you), unable to use current treatments for whatever reason, or for people to add to their existing regimen. I'm one of the few who will be using it solely on its own so I will be able to judge it easily. Not expecting miracles but from my own reading it looks like the most promising treatment since RU, without the topical hassle and androgenic sides.

There's a lot of misinformation in this thread. People throwing around the 1g used in Seti trials and assuming that dose is needed for efficacy - those were doses used for asthma, and to test SAFETY in humans. The same way the early Finasteride trials used way, way above the therapeutic ceiling of 1.25mg to test for safety in humans.

Anyone who has read the Cotsarelis studies will have an idea just how important PGD2 is in the miniaturization of the follicle, whether that's downstream from DHT or separate entirely. People can use less selective and less safe compounds like OC and TM, the latter of which has no human studies whatsoever, compared to Seti which has a proven excellent safety profile. The fact is it has been proven safe ORALLY, unlike OC and TM. It's got $27m worth of backing as a hairloss treatment ahead of any other CRTH2 antagonist for a reason. Personally I think these factors, plus the reports of early users saying it has reduced Androgenetic Alopecia inflammation within a few weeks, make it worth a punt for $350 for a 3-5 month trial. People have no right to complain about losing ground on finasteride/dutasteride/RU if they're not willing to try this.
 

Parsia

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Nobody should advise dropping a treatment and replacing it with Seti. It's for people still losing ground on existing treatments (and I know there are a lot of you), unable to use current treatments for whatever reason, or for people to add to their existing regimen. I'm one of the few who will be using it solely on its own so I will be able to judge it easily. Not expecting miracles but from my own reading it looks like the most promising treatment since RU, without the topical hassle and androgenic sides.

There's a lot of misinformation in this thread. People throwing around the 1g used in Seti trials and assuming that dose is needed for efficacy - those were doses used for asthma, and to test SAFETY in humans. The same way the early Finasteride trials used way, way above the therapeutic ceiling of 1.25mg to test for safety in humans.

Anyone who has read the Cotsarelis studies will have an idea just how important PGD2 is in the miniaturization of the follicle, whether that's downstream from DHT or separate entirely. People can use less selective and less safe compounds like OC and TM, the latter of which has no human studies whatsoever, compared to Seti which has a proven excellent safety profile. The fact is it has been proven safe ORALLY, unlike OC and TM. It's got $27m worth of backing as a hairloss treatment ahead of any other CRTH2 antagonist for a reason. Personally I think these factors, plus the reports of early users saying it has reduced Androgenetic Alopecia inflammation within a few weeks, make it worth a punt for $350 for a 3-5 month trial. People have no right to complain about losing ground on finasteride/dutasteride/RU if they're not willing to try this.

Thanks Dench for your info , nice post as always :) I still not sure how people say OC OR TM is much powerful than Seti , I didn't see any study about that yet . I'm not really sure about Seti if Low dosage will be work or not , but I really enjoyed to read your thoughts and your logic about Seti , As I always love your posts :) But Just a quick update and a little bit off-topic ! I have start using Rama a few days ago , Do you use it 1ml and spread it in 2X0.5ml in a day?
 

I.D WALKER

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Dench I'll be the watching your progress extra closely.

Yes the safety profile of Seti is totally exciting. Even if it were to performance only marginally better than finasteride. Best of luck.
 

champpy

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Cupido, any idea what the cost would be of getting compounds tested at your university
 

Mageirast

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Nobody should advise dropping a treatment and replacing it with Seti. It's for people still losing ground on existing treatments (and I know there are a lot of you), unable to use current treatments for whatever reason, or for people to add to their existing regimen. I'm one of the few who will be using it solely on its own so I will be able to judge it easily. Not expecting miracles but from my own reading it looks like the most promising treatment since RU, without the topical hassle and androgenic sides.

There's a lot of misinformation in this thread. People throwing around the 1g used in Seti trials and assuming that dose is needed for efficacy - those were doses used for asthma, and to test SAFETY in humans. The same way the early Finasteride trials used way, way above the therapeutic ceiling of 1.25mg to test for safety in humans.

Anyone who has read the Cotsarelis studies will have an idea just how important PGD2 is in the miniaturization of the follicle, whether that's downstream from DHT or separate entirely. People can use less selective and less safe compounds like OC and TM, the latter of which has no human studies whatsoever, compared to Seti which has a proven excellent safety profile. The fact is it has been proven safe ORALLY, unlike OC and TM. It's got $27m worth of backing as a hairloss treatment ahead of any other CRTH2 antagonist for a reason. Personally I think these factors, plus the reports of early users saying it has reduced Androgenetic Alopecia inflammation within a few weeks, make it worth a punt for $350 for a 3-5 month trial. People have no right to complain about losing ground on finasteride/dutasteride/RU if they're not willing to try this.

A great post!
 

Swoop

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Nobody should advise dropping a treatment and replacing it with Seti. It's for people still losing ground on existing treatments (and I know there are a lot of you), unable to use current treatments for whatever reason, or for people to add to their existing regimen. I'm one of the few who will be using it solely on its own so I will be able to judge it easily. Not expecting miracles but from my own reading it looks like the most promising treatment since RU, without the topical hassle and androgenic sides.

There's a lot of misinformation in this thread. People throwing around the 1g used in Seti trials and assuming that dose is needed for efficacy - those were doses used for asthma, and to test SAFETY in humans. The same way the early Finasteride trials used way, way above the therapeutic ceiling of 1.25mg to test for safety in humans.

Anyone who has read the Cotsarelis studies will have an idea just how important PGD2 is in the miniaturization of the follicle, whether that's downstream from DHT or separate entirely. People can use less selective and less safe compounds like OC and TM, the latter of which has no human studies whatsoever, compared to Seti which has a proven excellent safety profile. The fact is it has been proven safe ORALLY, unlike OC and TM. It's got $27m worth of backing as a hairloss treatment ahead of any other CRTH2 antagonist for a reason. Personally I think these factors, plus the reports of early users saying it has reduced Androgenetic Alopecia inflammation within a few weeks, make it worth a punt for $350 for a 3-5 month trial. People have no right to complain about losing ground on finasteride/dutasteride/RU if they're not willing to try this.

Dench. Let's get some facts straight. This reminds me of the CB-03-01 discussion when I argued almost as the only one that the dosage was too low because I had a look at the pharmacokinetics and had knowledge of other anti-androgens. People were all so convinced it was a "vehicle" problem which was nonsense obviously. It came as no surprise that COSMO started a trial of CB-03-01 with a 2x 50MG dosage (100mg) a day.

Now on to Setipriprant;



As you can see these are all the trials where Setipiprant was in and proved to be a failure in all basically. Actelion wanted to get rid of the compound, sold it for pocket change and is proceeding with other compounds now. The initial buyover was probably extremely low. The 27 million is only for potential development and regulatory milestones.

You are correct the safety profile does look good of Setipiprant. I did throw in the 1000mg prediction based on the pharmacokinetics of Setipiprant. I can tell you that it's not going to be less than 500mg. Even at 500mg is it a viable solution with these prices? I don't think so.

I mean our goal is to sufficiently antagonize the DP2 receptor (CRTH2) right? In pure principal there is no major difference in doses for rhinitis. The goal is the same antagonize the DP2 receptor sufficiently whether that is in a cell in the hair follicle or somewhere else. What would your argumentation be for a lower dosage then let's say 500mg for example?

After all you want to use a compound that is effective. You can't rub 5mg of RU58841 or CB-03-01 and expect it to work well. Setipiprant is just a very weak compound overall with a low affinity, that's why it requires such a big dosage to "sufficiently" antagonize the DP2 receptor.

I don't exactly understand why you say that OC is "less selective". What off side targets does it have? And on what argumentation do you base that it is less safe?

The question overall and the most important one is if PGD2 blocking is really that important. Look at this point it's nothing more than a hypothesis.

If it really works upstream after AR transcription and has a big role in the pathology of Androgenetic Alopecia then that's awesome. We could all drop our finasteride soon and hop on a DP2 antagonist like setipiprant. Obviously that's a ridiculous scenario to even consider at this point. It could be that PGD2 has a small role in Androgenetic Alopecia and blocking it won't even maintain your hair. My opinion? I think the whole PGD2 angle isn't exciting at all. I don't think blocking PGD2 will even maintain your hair. Time will tell though, I hope I am wrong though so I can drop RU and pop a DP2 antagonist in the future ;).

To reiterate my point about setipiprant is that it's not really economically feasible to use enough of a dosage to antagonize the DP2 receptor at a sufficient level with these prices. So if people are interested in the PGD2 angle there are many other compounds to consider which are more potent and cheaper. That's all. If it will help anyone at a low dosage then that's great though obviously.
 

Parsia

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Dench. Let's get some facts straight. This reminds me of the CB-03-01 discussion when I argued almost as the only one that the dosage was too low because I had a look at the pharmacokinetics and had knowledge of other anti-androgens. People were all so convinced it was a "vehicle" problem which was nonsense obviously. It came as no surprise that COSMO started a trial of CB-03-01 with a 2x 50MG dosage (100mg) a day.

Now on to Setipriprant;



As you can see these are all the trials where Setipiprant was in and proved to be a failure in all basically. Actelion wanted to get rid of the compound, sold it for pocket change and is proceeding with other compounds now. The initial buyover was probably extremely low. The 27 million is only for potential development and regulatory milestones.

You are correct the safety profile does look good of Setipiprant. I did throw in the 1000mg prediction based on the pharmacokinetics of Setipiprant. I can tell you that it's not going to be less than 500mg. Even at 500mg is it a viable solution with these prices? I don't think so.

I mean our goal is to sufficiently antagonize the DP2 receptor (CRTH2) right? In pure principal there is no major difference in doses for rhinitis. The goal is the same antagonize the DP2 receptor sufficiently whether that is in a cell in the hair follicle or somewhere else. What would your argumentation be for a lower dosage then let's say 500mg for example?

After all you want to use a compound that is effective. You can't rub 5mg of RU58841 or CB-03-01 and expect it to work well. Setipiprant is just a very weak compound overall with a low affinity, that's why it requires such a big dosage to "sufficiently" antagonize the DP2 receptor.

I don't exactly understand why you say that OC is "less selective". What off side targets does it have? And on what argumentation do you base that it is less safe?

The question overall and the most important one is if PGD2 blocking is really that important. Look at this point it's nothing more than a hypothesis.

If it really works upstream after AR transcription and has a big role in the pathology of Androgenetic Alopecia then that's awesome. We could all drop our finasteride soon and hop on a DP2 antagonist like setipiprant. Obviously that's a ridiculous scenario to even consider at this point. It could be that PGD2 has a small role in Androgenetic Alopecia and blocking it won't even maintain your hair. My opinion? I think the whole PGD2 angle isn't exciting at all. I don't think blocking PGD2 will even maintain your hair. Time will tell though, I hope I am wrong though so I can drop RU and pop a DP2 antagonist in the future ;).

To reiterate my point about setipiprant is that it's not really economically feasible to use enough of a dosage to antagonize the DP2 receptor at a sufficient level with these prices. So if people are interested in the PGD2 angle there are many other compounds to consider which are more potent and cheaper. That's all. If it will help anyone at a low dosage then that's great though obviously.

Ok Swoop , Thanks for your post , its nice to see your logic as well , Can you please tell me what other PGD2 Options we have in order of potency ? is our option limited

to OC / TM / RAMA ? And if it is , do you have any opinion which one is more potent ? In order please.
 

Swoop

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Ok Swoop , Thanks for your post , its nice to see your logic as well , Can you please tell me what other PGD2 Options we have in order of potency ? is our option limited

to OC / TM / RAMA ? And if it is , do you have any opinion which one is more potent ? In order please.

I don't know honestly Parsia. I haven't looked into these compounds that well to determine which one are more potent. OC for sure is more potent though. You have to consider in safety too obviously. There are many compounds acting on the DP2 receptor so your options are not limited. Enough to research for you I guess :). From the patent of Cotsarelis http://www.google.com/patents/EP2827952A1?cl=en

Table 4 Clinical Stage DP-2 Antagonists

Actelion ACT- 129968 Phase lib NCT01225315
(Setipiprant)
Actimis AP768 Phase I
Amira AM211 Phase I
Amira AM461 Phase I
Amgen AMG853 Discontinued after NCT01018550
Phase Π (2011)
Array BioPharma ARRY-502 Phase I NCT01349725
AstraZeneca AZD1981 Phase Π NCT01197794
AstraZeneca AZD8075 Discontinued after NCT00787072
Phase I (2010)
AstraZeneca AZD5985 Discontinued after NCT00967356
Phase I (2010)
Merck MK-7246) Phase I
Novartis QAV680 Phase Π completed NCT00814216
Oxagen OC000459 Phase lib NCT01057927
Oxagen OC002417 Back-up candidate
Pulmagen ADC3680B Phase I NCT01173770
Shionogi S-555739 Phase lib (Japan)
aNCT numbers can be searched at the website: www.clinicaltrials.gov

It will be appreciated that many of the antagonists described herein are strong inhibitors of their targets. For example, an antagonist may have a binding inhibitory activity (IC[SUB]50[/SUB] value) for its desired molecular target (i.e., DP-2) of 1000 μΜ or less, 1000 nM or less, 100 nM or less, 10 nM or less, or especially 1 nM or less.
 

KiNGTyreZe

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Dench. Let's get some facts straight. This reminds me of the CB-03-01 discussion when I argued almost as the only one that the dosage was too low because I had a look at the pharmacokinetics and had knowledge of other anti-androgens. People were all so convinced it was a "vehicle" problem which was nonsense obviously. It came as no surprise that COSMO started a trial of CB-03-01 with a 2x 50MG dosage (100mg) a day.

Now on to Setipriprant;



As you can see these are all the trials where Setipiprant was in and proved to be a failure in all basically. Actelion wanted to get rid of the compound, sold it for pocket change and is proceeding with other compounds now. The initial buyover was probably extremely low. The 27 million is only for potential development and regulatory milestones.

You are correct the safety profile does look good of Setipiprant. I did throw in the 1000mg prediction based on the pharmacokinetics of Setipiprant. I can tell you that it's not going to be less than 500mg. Even at 500mg is it a viable solution with these prices? I don't think so.

I mean our goal is to sufficiently antagonize the DP2 receptor (CRTH2) right? In pure principal there is no major difference in doses for rhinitis. The goal is the same antagonize the DP2 receptor sufficiently whether that is in a cell in the hair follicle or somewhere else. What would your argumentation be for a lower dosage then let's say 500mg for example?

After all you want to use a compound that is effective. You can't rub 5mg of RU58841 or CB-03-01 and expect it to work well. Setipiprant is just a very weak compound overall with a low affinity, that's why it requires such a big dosage to "sufficiently" antagonize the DP2 receptor.

I don't exactly understand why you say that OC is "less selective". What off side targets does it have? And on what argumentation do you base that it is less safe?

The question overall and the most important one is if PGD2 blocking is really that important. Look at this point it's nothing more than a hypothesis.

If it really works upstream after AR transcription and has a big role in the pathology of Androgenetic Alopecia then that's awesome. We could all drop our finasteride soon and hop on a DP2 antagonist like setipiprant. Obviously that's a ridiculous scenario to even consider at this point. It could be that PGD2 has a small role in Androgenetic Alopecia and blocking it won't even maintain your hair. My opinion? I think the whole PGD2 angle isn't exciting at all. I don't think blocking PGD2 will even maintain your hair. Time will tell though, I hope I am wrong though so I can drop RU and pop a DP2 antagonist in the future ;).

To reiterate my point about setipiprant is that it's not really economically feasible to use enough of a dosage to antagonize the DP2 receptor at a sufficient level with these prices. So if people are interested in the PGD2 angle there are many other compounds to consider which are more potent and cheaper. That's all. If it will help anyone at a low dosage then that's great though obviously.

Thank you. Great post. However supressing PGD2 can never be bad.

Prostaglandin D2 Inhibits Hair Growth and Is Elevated in Bald Scalp of Men with Androgenetic Alopecia

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3319975/
 

cupido

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Cupido, any idea what the cost would be of getting compounds tested at your university

Hello brother

It depends on the chemical but
between 50 and 150. It takes about 2 days.
Besides the test report you get a full analysis report by a PhD.

I tested 2 batches ru, 1 batch cb and bima bought from multiple sources inuding Kane. All legit and 99% pure.

Testing made me feel comfortable knowing the sources are legit.

Let me know if you want help with testing.

- - - Updated - - -

Dench. Let's get some facts straight. This reminds me of the CB-03-01 discussion when I argued almost as the only one that the dosage was too low because I had a look at the pharmacokinetics and had knowledge of other anti-androgens. People were all so convinced it was a "vehicle" problem which was nonsense obviously. It came as no surprise that COSMO started a trial of CB-03-01 with a 2x 50MG dosage (100mg) a day.

Now on to Setipriprant;



As you can see these are all the trials where Setipiprant was in and proved to be a failure in all basically. Actelion wanted to get rid of the compound, sold it for pocket change and is proceeding with other compounds now. The initial buyover was probably extremely low. The 27 million is only for potential development and regulatory milestones.

You are correct the safety profile does look good of Setipiprant. I did throw in the 1000mg prediction based on the pharmacokinetics of Setipiprant. I can tell you that it's not going to be less than 500mg. Even at 500mg is it a viable solution with these prices? I don't think so.

I mean our goal is to sufficiently antagonize the DP2 receptor (CRTH2) right? In pure principal there is no major difference in doses for rhinitis. The goal is the same antagonize the DP2 receptor sufficiently whether that is in a cell in the hair follicle or somewhere else. What would your argumentation be for a lower dosage then let's say 500mg for example?

After all you want to use a compound that is effective. You can't rub 5mg of RU58841 or CB-03-01 and expect it to work well. Setipiprant is just a very weak compound overall with a low affinity, that's why it requires such a big dosage to "sufficiently" antagonize the DP2 receptor.

I don't exactly understand why you say that OC is "less selective". What off side targets does it have? And on what argumentation do you base that it is less safe?

The question overall and the most important one is if PGD2 blocking is really that important. Look at this point it's nothing more than a hypothesis.

If it really works upstream after AR transcription and has a big role in the pathology of Androgenetic Alopecia then that's awesome. We could all drop our finasteride soon and hop on a DP2 antagonist like setipiprant. Obviously that's a ridiculous scenario to even consider at this point. It could be that PGD2 has a small role in Androgenetic Alopecia and blocking it won't even maintain your hair. My opinion? I think the whole PGD2 angle isn't exciting at all. I don't think blocking PGD2 will even maintain your hair. Time will tell though, I hope I am wrong though so I can drop RU and pop a DP2 antagonist in the future ;).

To reiterate my point about setipiprant is that it's not really economically feasible to use enough of a dosage to antagonize the DP2 receptor at a sufficient level with these prices. So if people are interested in the PGD2 angle there are many other compounds to consider which are more potent and cheaper. That's all. If it will help anyone at a low dosage then that's great though obviously.

Great post. Sepi is weak as I said before.

I'm looking to tm it looks 10.000 times stronger, anyone experience with it ?
 

Mako17

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I have some TM sitting in my freezer. I just don't have DMSO. I tried to dissolve it in neogenic but didn't work well. Thinking about adding a few drops of DMSO to the neogenic then adding the TM to it.
 

cupido

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I have some TM sitting in my freezer. I just don't have DMSO. I tried to dissolve it in neogenic but didn't work well. Thinking about adding a few drops of DMSO to the neogenic then adding the TM to it.

Try ethanol 95% . dmso can be dangerous.

Oc000459 passed the safety and efficacy trials, however tm looks stronger in studies. Oh I read on hlh someone preferred oc over tm but one experience isn't enough.

I might swich my oc with tm soon see which one works better.
 

KiNGTyreZe

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I have some TM sitting in my freezer. I just don't have DMSO. I tried to dissolve it in neogenic but didn't work well. Thinking about adding a few drops of DMSO to the neogenic then adding the TM to it.

You can dissolve TM in water. I don't know about the penetration though.

Just take it orally.
 
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