The Cb (breezula [clascoterone]) Community Thread

sonictemples

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Some peope can’t get irony smh
 

sonictemples

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Jim lahey

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I am aware that Google exists but in case you haven't noticed there's a lot of conflicting information and I was hoping to find something more reliable here.
Sorry I forgot about all the conflicting data on whether breezula is an anti androgen or not. If only Cassiopea had a website where they held all the official information on the drug.
 

John Difool

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From the manufacturer page:
Clascoterone solution 7.5% is a novel AR inhibitor that targets androgen receptors in the scalp and is currently being studied for the treatment of androgenetic alopecia (Androgenetic Alopecia).

I am not sure what else you are looking for.
 

Breyfogle

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Best case scenario: They start the trial in 01.09.2020 take half a year trial 01.03.2021 and wait one year for approval which takes in best case 1 year. So best case 01.03.2022.

Now lets take a look at a realistic timeline:
Start 01.09.2020
End of enrolement (sasumed needed 15 month for phase 3 enrolement) 01.12.2021
End of trial (6 month later) 01.06.2022
Getting approval (takes 12-18 month so lets assume 15) 01.09.2023
And that is really a realistic approximation and not a conservative. And keep in mind that half of the phase 3 trial candidates are droped by the developing company during or after the pase 3 trial and half of the ones, that are not droped are rejected by the fda.



So a realistically we have a 25% chance it hits the market 01.09.2023 and best case it hits the market 01.03.2022.

Thx byebyehair your math seems about right. Helpful post.
 

Dimitri001

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Breezula is indeed safer than finasteride, not that finasteride is dangerous.

Why do you say that finasteride is not dangerous? I know people talk about sexual dysfunction and post finasteride syndrom all the time, is it that the rates of that are very low?
 

Dimitri001

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One point regarding judging a future treatment by comparing it to Minoxidil:

While this is certainly informative and important, keep in mind that there is a wide spectrum in terms of how effective M is for people. For some people M does nothing and for others it gives great results.

So, if some study shows that some future drug is 1/2 as effective as M, well, maybe you're a Minoxidil non responder for whom this drug will overperform the way M overperforms for some people relative to what you'd normally expect from M.

That's kind of praying for it, but for any drug that works to some degree for some people, there's a possibility you'll be among the people who are on the extreme high end of that.
 

pegasus2

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i am not a minoxidil responder, my end pattern will be a NW7, I couldn't take finasteride due to sides (peyronies), hair systems seem to be not as great as the sound of it, I have a ridiculously terrible head shape and look heinous bald. I dont know, CB-03-01 was supposed to be the big alternative to all this mess but I dont believe in it anymore
They all declined sharply after 6 months. That's statistically significant. They still remained above baseline, but minoxidil remains above baseline for 2+ years, and finasteride for 10 years.
Breezula phase two data vs baseline.png
 

Dimitri001

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They all declined sharply after 6 months. That's statistically significant. They still remained above baseline, but minoxidil remains above baseline for 2+ years, and finasteride for 10 years.
View attachment 143659

Yikes, was not aware of this.

I wonder why. You mentioned androgen receptor upregulation, but seems strange to me that that would happen - that's what ARs do, they have things bind to them. They don't react that way to constant DHT binding (or presumably they don't). But then I don't know squat about this stuff.
 

GRme11

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I'm in a good mood so I'm going to help you out on the off chance that your DNS has Cassiopea's website blocked. If you're betting your money on Breezula saving you then you're going to go bankrupt. Better to bet your money on a hair system. Breezula is indeed safer than finasteride, not that finasteride is dangerous. Hair loss is caused by DHT binding to androgen receptors in the hair follicle. Finasteride inhibits the systemic production of DHT. Breezula works by binding to the androgen receptors in your scalp, which prevents DHT from binding to them. Within minutes of hitting the bloodstream Breezula is metabolized into an inert substance, which means it only has effects where it is locally applied. Sounds great so far, right? The problem is that Breezula has a weak affinity for the androgen receptor. It is easily outcompeted by DHT. That's why you have to use so much of it(75mg twice a day). You have to flood your scalp with it so that it will attach to enough receptors to make a difference before DHT does. At such a high dose it is very effective over the short-term, but its effects don't last as long as minoxidil's. We need confirmation of this from their next trial, but in their last trial its effectiveness quickly declined after 6 months. This might be due to androgen receptor upregulation caused by blocking the androgen receptors continuously, thus requiring higher doses to block greater numbers of receptors. So it is certainly an effective and safe treatment in the short-term, but in the long-term it may not be very effective.

There is no release date, but it could be released in a few years. The acne version, which contains the same active ingredient, should be released next year. However, the concentration of the active drug in the acne version is only 1%, whereas you need a concentration of 7.5% to effectively combat hair loss. It should be fairly easy to get the acne version prescribed off-label for hair loss, but it will probably be very expensive since the pricing will be based on a marketed concentration of 1%, and you will have to get it compounded at 7.5%. SM04554 is the other new drug on the horizon. I think that one is more promising as a long-term treatment, but don't expect that to outperform minoxidil either.


Have you found something about AR upregulation in healthy cells? Because many studies show AR upregulation deriving from cancer cells. As long as I searched, I couldn't find something mentioning AR upregulation for healthy cells, or maybe it's happening anyway since you start blocking the AR receptor continuously (like you mention above). So I think if you can cycle your treatment with RU, or other anti-androgens, for example, 3/2/2 times per week, then stop for 1-2 weeks and restart. Maybe sounds stupid though with the logic that receptors could upregulate, and let's say they will go into a crisis-shock situation requesting more of the drug?(seems confusing or maybe I do not understand the things properly). Thank you very much @pegasus2
 

GRme11

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I don't know. I'm just speculating as to the reason. DHT may upregulate the AR over time, and that's why baldness starts later in life. It may be the epigenetic clock that up regulates it. It may be that some activation of the AR is enough to keep it happy so to speak, while blocking it completely causes it to upregulate. I'm not aware of any conclusive studies that can give us the answer.
Thanks for response. Guess it's all about again down to the genetics and a trial-error thing. I think though that the cycling method maybe it's safer for preventing the AR upregulation(if it's possible to happen).I don't know if you agree or disagree with this. Thanks again
 

pegasus2

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Theoretically RU should also cause AR up regulation but many have great results and maintain with RU alone for years.
Yes. People also seem to need increasingly higher doses of RU. That is concerning. RU has a higher affinity for the AR than CB though, so it's better able to compete with DHT
 

pegasus2

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Something that degrades the receptor would be better, but then I wonder what happens if you stop using that.
 

GRme11

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Theoretically RU should also cause AR up regulation but many have great results and maintain with RU alone for years.
Yes but the key here that it won't cause maybe it lies in the fact that it is not having such a great affinity to the AR receptor(compared to Bicalutamide,CPA etc). So you end with some results like:
1)Preventing AR and treatment it's working
2)Treatment it's not working(non responder/maybe higher dosage?)
3)Upregulation of AR(but let's say way less possible)

(Though, since everyone it is different you can only make speculations of what will happen or won't.)

Thanks
 
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GRme11

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Something that degrades the receptor would be better, but then I wonder what happens if you stop using that.
Probably the shock-crisis situation to the AR, which translates again to upregulation ?
(Sorry if my question is stupid I haven't search and read for degradation of AR receptor)
 
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