Kintor Pharmaceutical Announced U.S. FDA Has Greenlighted Phase II Clinical Trial for Pyrilutamide to Treat Androgenetic Alopecia

[trialAcc]

Ahhh I feel for you bro, you’re just going to be heavily disappointed

btw no one with any level of aggressive hairloss is maintaining on RU at all. They’re all combing it with finasteride, minx, dutasteride, etc etc

Where did they publish a comparison of this drugs binding affinity with CB? You also need to account for the ic50 and a bunch of other factors as well. Don’t get your hopes up too high

Binding affinity is 3-4x that of RU, by Kintor's own admission in their preclinical data where they listed out several compounds. RU was found to have a 40x higher binding affinity then CB. I just rounded down to 100 to be conservative.

Why do you assume that everyone has aggressive hairloss? The vast majority of men who will lose their hair don't. You're just speaking to that 5-10% of hairloss suffers that won't get results from this alone.

 

[Chads don't bald]

Even those with aggressive hair loss should be able to maintain on Kintor + finasteride theoretically, no matter how DHT sensitive they are

 

[Will Be an Egg in 5 years]

Hopium?

 

[hemingway_the_mercenary]

Binding affinity is 3-4x that of RU, by Kintor's own admission in their preclinical data where they listed out several compounds. RU was found to have a 40x higher binding affinity then CB. I just rounded down to 100 to be conservative.

Why do you assume that everyone has aggressive hairloss? The vast majority of men who will lose their hair don't. You're just speaking to that 5-10% of hairloss suffers that won't get results from this alone.

RU is not 40x more potent than CB, there is the ka binding affinity which varies from experiment to experiment and you will notice the huge variance if you read multiple preclinical publications on Enza, Daro, Bica, Flut, etc... in almost every experiment a different binding affinity was found. There is also the IC50, which is more important arguably. I won't go into it much more but you need to do a lot more research. RU is one of the weakest and worst anti androgens from experience.

 

[Diffused_confidence]

RU is not 40x more potent than CB, there is the ka binding affinity which varies from experiment to experiment and you will notice the huge variance if you read multiple preclinical publications on Enza, Daro, Bica, Flut, etc... in almost every experiment a different binding affinity was found. There is also the IC50, which is more important arguably. I won't go into it much more but you need to do a lot more research. RU is one of the weakest and worst anti androgens from experience.

Weaker than cb?

 

[trialAcc]

RU is not 40x more potent than CB, there is the ka binding affinity which varies from experiment to experiment and you will notice the huge variance if you read multiple preclinical publications on Enza, Daro, Bica, Flut, etc... in almost every experiment a different binding affinity was found. There is also the IC50, which is more important arguably. I won't go into it much more but you need to do a lot more research. RU is one of the weakest and worst anti androgens from experience.

Yes it is. RU has a 1:1 binding affinity for T as stated in their own pre-clinical research. In the CB phase 2 paper they state that CB is 1:40 of T. You can draw your own conclusions from this if you'd like.

You're telling me to do research yet you seem to just be denying numbers and not stating any of your own.

 

[Diffused_confidence]

Isn't there another US company with a similar idea as kintor? I think the company name begins with O.

 

[Diffused_confidence]

If you're referring to Olix, they're using RNAi technology not a PROTAC. They're both targeting the AR but a PROTAC degrades it, RNAi silences it. Also Olix are South Korean.

I'd imagine the RNAi is better, but its also likely to be more expensive and take longer to come to market should it successfully make it through trials - thats just pure speculation on my part though.

What's the difference between silence and degrade? Is silence like pyrilutamide?

 

[hemingway_the_mercenary]

Yes it is. RU has a 1:1 binding affinity for T as stated in their own pre-clinical research. In the CB phase 2 paper they state that CB is 1:40 of T. You can draw your own conclusions from this if you'd like.

You're telling me to do research yet you seem to just be denying numbers and not stating any of your own.

you have no idea what you’re talking about, I’m done

“The potency of RU58841 was comparable to that of hydroxyflutamide.”

Evaluation of RU58841 as an anti-androgen in prostate PC3 cells and a topical anti-alopecia agent in the bald scalp of stumptailed macaques - PubMed

The effect of androgen receptor transcriptional activation by RU58841, a nonsteroidal anti-androgen, was studied in the human prostate cancer PC3 cell line by cotransfection with wild-type androgen receptor (wt AR) and an androgen-responsive reporter (MMTV-ARE-CAT) construct. Anti-and rogens...

pubmed.ncbi.nlm.nih.gov

(About CB)
“As topical antiandrogen, the steroid resulted about 4 times more active than progesterone (CAS 57-83-0) and, when compared to known antiandrogen standards, it was about 3 times more potent than flutamide (CAS 13311-84-7), about 2 times more effective than finasteride (CAS 98319-26-7) and approximately as active as cyproterone acetate (CAS 427-51-0).”

Biological profile of cortexolone 17alpha-propionate (CB-03-01), a new topical and peripherally selective androgen antagonist - PubMed

The aim of this study was to investigate the antiandrogenic activity of a new monoester of cortexolone, cortexolone 17alpha-propionate (CAS 19608-29-8, CB-03-01). Although the compound displayed a strong local antiandrogenic activity in hamster's flank organ test, it did not exhibit...

pubmed.ncbi.nlm.nih.gov

Once again you have no idea what you’re taking about

 

[MrKmass]

you have no idea what you’re talking about, I’m done

“The potency of RU58841 was comparable to that of hydroxyflutamide.”

Evaluation of RU58841 as an anti-androgen in prostate PC3 cells and a topical anti-alopecia agent in the bald scalp of stumptailed macaques - PubMed

The effect of androgen receptor transcriptional activation by RU58841, a nonsteroidal anti-androgen, was studied in the human prostate cancer PC3 cell line by cotransfection with wild-type androgen receptor (wt AR) and an androgen-responsive reporter (MMTV-ARE-CAT) construct. Anti-and rogens...

pubmed.ncbi.nlm.nih.gov

(About CB)
“As topical antiandrogen, the steroid resulted about 4 times more active than progesterone (CAS 57-83-0) and, when compared to known antiandrogen standards, it was about 3 times more potent than flutamide (CAS 13311-84-7), about 2 times more effective than finasteride (CAS 98319-26-7) and approximately as active as cyproterone acetate (CAS 427-51-0).”

Biological profile of cortexolone 17alpha-propionate (CB-03-01), a new topical and peripherally selective androgen antagonist - PubMed

The aim of this study was to investigate the antiandrogenic activity of a new monoester of cortexolone, cortexolone 17alpha-propionate (CAS 19608-29-8, CB-03-01). Although the compound displayed a strong local antiandrogenic activity in hamster's flank organ test, it did not exhibit...

pubmed.ncbi.nlm.nih.gov

Once again you have no idea what you’re taking about

I guess the CB problem is its percentage too low for most people as well as the vehicle problem. Do you know the most suitable vehicle for CB?

 

[hemingway_the_mercenary]

I guess the CB problem is its percentage too low for most people as well as the vehicle problem. Do you know the most suitable vehicle for CB?

Like I’ve been saying, absorption is the problem to all topical AR blockers. If it wasn’t a problem then most of them would be suitable and a better alternative to finasteride. Unfortunately, it’s a major problem regardless of the vehicle and the only way I can see to overcome it is to increase the drug potency by at least 100x.
Finasteride for example is just as effective topically as it is orally because 0.2mg systemically provides around 90% the suppression as 1mg does (forget the exact stats)

it’s very easy to deliver that amount through the scalp. But when an active drug needs 250-750mg orally for example like fllutamdie then delivering a sufficient dose to the follicles is very challenging. I’ve used many different vehicles by the way, not much difference between any of them. None of them were able to get close to the absorption needed.

Now if we were able to make a drug that was effective orally at a dose of 5mg and under, like minoxidil is for example, then it could potentially being a great treatment topically but ideally it would have to be even more potent like 1mg and under

so we need a drug that’s about 500 times more potent than flutamde per mg. You can see why this would be challenging but these new AR degrades are very promising

 

[MrKmass]

Like I’ve been saying, absorption is the problem to all topical AR blockers. If it wasn’t a problem then most of them would be suitable and a better alternative to finasteride. Unfortunately, it’s a major problem regardless of the vehicle and the only way I can see to overcome it is to increase the drug potency by at least 100x.
Finasteride for example is just as effective topically as it is orally because 0.2mg systemically provides around 90% the suppression as 1mg does (forget the exact stats)

it’s very easy to deliver that amount through the scalp. But when an active drug needs 250-750mg orally for example like fllutamdie then delivering a sufficient dose to the follicles is very challenging. I’ve used many different vehicles by the way, not much difference between any of them. None of them were able to get close to the absorption needed.

Now if we were able to make a drug that was effective orally at a dose of 5mg and under, like minoxidil is for example, then it could potentially being a great treatment topically but ideally it would have to be even more potent like 1mg and under

so we need a drug that’s about 500 times more potent than flutamde per mg. You can see why this would be challenging but these new AR degrades are very promising

I understand what you are saying. But even though topical AR blockers are less effective due to the difficulty of penetration, many people report results with RU, more than with CB. If CB is more potent, its absorption must be even more complicated than RU for it to be less effective for most people.

But suddenly if topical AR blockers are currently unnecessary and finasteride is too dangerous, what type of treatment do you recommend?

 

[Dimitri001]

I'm not aware of prl. Is that kintor?

No, prolactin.

It's explained in this thread https://www.hairlosstalk.com/intera...le-and-female-pattern-hair-loss.127790/unread

 

[trialAcc]

you have no idea what you’re talking about, I’m done

“The potency of RU58841 was comparable to that of hydroxyflutamide.”

Evaluation of RU58841 as an anti-androgen in prostate PC3 cells and a topical anti-alopecia agent in the bald scalp of stumptailed macaques - PubMed

The effect of androgen receptor transcriptional activation by RU58841, a nonsteroidal anti-androgen, was studied in the human prostate cancer PC3 cell line by cotransfection with wild-type androgen receptor (wt AR) and an androgen-responsive reporter (MMTV-ARE-CAT) construct. Anti-and rogens...

pubmed.ncbi.nlm.nih.gov

(About CB)
“As topical antiandrogen, the steroid resulted about 4 times more active than progesterone (CAS 57-83-0) and, when compared to known antiandrogen standards, it was about 3 times more potent than flutamide (CAS 13311-84-7), about 2 times more effective than finasteride (CAS 98319-26-7) and approximately as active as cyproterone acetate (CAS 427-51-0).”

Biological profile of cortexolone 17alpha-propionate (CB-03-01), a new topical and peripherally selective androgen antagonist - PubMed

The aim of this study was to investigate the antiandrogenic activity of a new monoester of cortexolone, cortexolone 17alpha-propionate (CAS 19608-29-8, CB-03-01). Although the compound displayed a strong local antiandrogenic activity in hamster's flank organ test, it did not exhibit...

pubmed.ncbi.nlm.nih.gov

Once again you have no idea what you’re taking about

He sources all of his articles/papers in the bottom. Again, RU has the binding affinity for T. You just posted an abstract comparing finasteride to the effectiveness of CB and expect me to accept that you personally know best? Do some simple math yourself from the actual full studies rather then quoting useless abstracts that are presented in different contexts.

Below, CB binds to the AR with approximately 100 fold lower affinity to DHT (one again from the actual phase 2 Casseopia paper). DHT has a 2.5-10x more potent then T. RU binds approximately 1:1 with T (from the actual RU pre-clinical study). You say you're done with me but you've clearly shown you don't know how to interpret and place data in proper context.

 

[hemingway_the_mercenary]

He sources all of his articles/papers in the bottom. Again, RU has the binding affinity for T. You just posted an abstract comparing finasteride to the effectiveness of CB and expect me to accept that you personally know best? Do some simple math yourself from the actual full studies rather then quoting useless abstracts that are presented in different contexts.

Below, CB binds to the AR with approximately 100 fold lower affinity to DHT (one again from the actual phase 2 Casseopia paper). DHT has a 2.5-10x more potent then T. RU binds approximately 1:1 with T (from the actual RU pre-clinical study). You say you're done with me but you've clearly shown you don't know how to interpret and place data in proper context.

View attachment 165755

View attachment 165754
View attachment 165756

Oh my days man your arrogance is so annoying. So basically all your knowledge is from Derrik's video LOL whereas I just posted a study quoting that in an experiment which compared the two drugs OH-F and RU were found to have a similar potency? You don't even have the background knowledge to understand the concepts I explained.

I understand what you are saying. But even though topical AR blockers are less effective due to the difficulty of penetration, many people report results with RU, more than with CB. If CB is more potent, its absorption must be even more complicated than RU for it to be less effective for most people.

But suddenly if topical AR blockers are currently unnecessary and finasteride is too dangerous, what type of treatment do you recommend?

To my knowledge no one has ever posted pictures of regrowth where they ONLY used RU or any other anti-androgen. Even in cases of maintenance it seems like they all stacked RU with at least one other drug so it's impossible to really tell how effective RU really was. I and many others in our discord server have used RU solo for a significant portion of time and found that it's efficacy is very low and most of us have dropped it.

I'm not sure about many more people reporting results from RU than CB but in any case CB is much less frequently used especially at a comparable dosage to RU so how can that comparison even be made? As far as treatment, maybe try a low dose of topical finasteride if you do not want to risk oral finasteride and try to hold your hair for as long as possible in the hopes that something better comes out in the next 10 years

 

[MrKmass]

To my knowledge no one has ever posted pictures of regrowth where they ONLY used RU or any other anti-androgen. Even in cases of maintenance it seems like they all stacked RU with at least one other drug so it's impossible to really tell how effective RU really was. I and many others in our discord server have used RU solo for a significant portion of time and found that it's efficacy is very low and most of us have dropped it.

I'm not sure about many more people reporting results from RU than CB but in any case CB is much less frequently used especially at a comparable dosage to RU so how can that comparison even be made? As far as treatment, maybe try a low dose of topical finasteride if you do not want to risk oral finasteride and try to hold your hair for as long as possible in the hopes that something better comes out in the next 10 years

Thank you for your reply.
Well, I myself am a CB user and so far I haven't seen any improvement, but I'm using a very low percentage.

I already apply what you say, dose of mazzarella in topical finasteride. I have also asked you a few questions about this on your post dedicated to your experience with topical finasteride. For the moment that is not enough to maintain.

I also use 5% spironolactone cream on my hairline.

 

[trialAcc]

Oh my days man your arrogance is so annoying. So basically all your knowledge is from Derrik's video LOL whereas I just posted a study quoting that in an experiment which compared the two drugs OH-F and RU were found to have a similar potency? You don't even have the background knowledge to understand the concepts I explained.


To my knowledge no one has ever posted pictures of regrowth where they ONLY used RU or any other anti-androgen. Even in cases of maintenance it seems like they all stacked RU with at least one other drug so it's impossible to really tell how effective RU really was. I and many others in our discord server have used RU solo for a significant portion of time and found that it's efficacy is very low and most of us have dropped it.

I'm not sure about many more people reporting results from RU than CB but in any case CB is much less frequently used especially at a comparable dosage to RU so how can that comparison even be made? As far as treatment, maybe try a low dose of topical finasteride if you do not want to risk oral finasteride and try to hold your hair for as long as possible in the hopes that something better comes out in the next 10 years

Are you just purposely being ignorant or something? I literally posted pictures from the studies and labeled exactly which studies presented each data point I posted. Who cares if it's from his video, he showed his sources and linked to all the studies.

I'm not telling you here that a topical AA will solve hairloss or get regrowth, just that KX is stronger then RU, and that both are a lot stronger then CB. You're the one who literally got the binding affinities wrong and are still standing here defending your incorrect positions and insulting me when all I am saying is that KX has a better chance of achieving maintenance due to it's binding affinity being closer to DHT itself when compared to the others mentioned.

 

[Jakejr]

So it’s a Chinese study…
Another acne therapy segueing into alopecia by blocking androgen receptors.
So where are the photos?

Pyrilutamide is KX-826​

It’s a topical at varying strengths.


Cohort Dose of KX-826 Subjects

1. 2.5 mg QD for 14 days 10 (8 active + 2 placebo)
2. 5 mg QD for 14 days 10 (8 active + 2 placebo)
3. 10 mg QD for 14 days 10 (8 active + 2 placebo)
4. 20 mg QD for 14 days 10 (8 active + 2 placeo

 

[trialAcc]

So it’s a Chinese study…
Another acne therapy segueing into alopecia by blocking androgen receptors.
So where are the photos?

Pyrilutamide is KX-826​

It’s a topical at varying strengths.


Cohort Dose of KX-826 Subjects

1. 2.5 mg QD for 14 days 10 (8 active + 2 placebo)
2. 5 mg QD for 14 days 10 (8 active + 2 placebo)
3. 10 mg QD for 14 days 10 (8 active + 2 placebo)
4. 20 mg QD for 14 days 10 (8 active + 2 placeo

You're quoting/referencing the phase 1. There are no photos because they applied it on their backs lol

Phase 2 was 6 months at the 5 and 2.5 mg concentrations. Data with photos is due in September.

 

[Diffused_confidence]

What are you at right now?

I'm about a NW1.5 with thinning all over and I plan to wait for the prlr antagonist + wnt agonist in combination with the AR antagonist. Those 3 combined could probably cure hair loss for someone not too far gone. And this is not even taking into account hair cloning.

I might still get a transplant to rock a NW0 lol. I can't believe that in like the next 10 years I might have better hair than I did in my teens

I'm at norwood 2.5 or 3. I have photos here https://www.hairlosstalk.com/interact/threads/25mg-finasteride-journey.132724/

I started at .25mg of finasteride but now I'm at 1mg. I recommend getting on finasteride now and try to save as much hair as possible immediately. These companies are not guaranteed to succeed. At norwood 2 or lower you are going to get the best results possible.