The Cb (breezula [clascoterone]) Community Thread

nick123

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Finasteride and dutasteride do not block the AR, so why would it happen with them? Testosterone, and smaller amounts of DHT, are still attaching to the AR and activating it. AR upregulation is known to occur in prostate cancer cells. They use drugs for prostate cancer that are almost insurmountable. They outcompete DHT for the receptor, and are able to overcome AR upregulation. Then you have mutant AR to deal with, and that's another issue. Why is it so far-fetched to think upregulation might happen in the scalp when we know it happens in prostate cancer cells? It's not the same thing and I'm not saying it happens, but what other explanation is there for these results from Cassiopea? The rigor participation argument doesn't hold water, unless you believe people who sign up for minoxidil trials are more rigorous.

So am I right in thinking if this were true that all androgen receptor antagonists such as breezula, ru58841, fluridil (eucapil) or even kintors upcoming pyrilutamide will eventually upregulate the number of androgen receptors and thus accelerate hair loss?
 

nick123

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But there would be a max threshold of how much AR receptors actually can upregulate? So if I am on a high enough dosage it shouldn’t make a difference if AR upregulates. Im on 120 mg of RU.

Why is there an assumption there's a max threshold to what it can upregulate?

Right. If you increase the dosage enough then it shouldn't matter. Just if you come off the drug you are going to go through a massive shed until it downregulates, if it downregulates.

This also worries me, if it doesn't downregulate and come off your androgen receptor antagonist your hair will loss will accelerate at a much faster pace than if you didn't start your androgen receptor antagonist at all.

This is all starting to really disappoint me, I've never been able to maintain on 4x dutasteride + 3x finasteride per week and there's absolutely nothing in the pipeline that seems useful.
 

Fgsfds

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Right. If you increase the dosage enough then it shouldn't matter. Just if you come off the drug you are going to go through a massive shed until it downregulates, if it downregulates.
If this happens, then you'd want to at least block the downstream factors like PGD2 and DKK1 until your AR receptors normalize
 

LouisSarkozy

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If this happens, then you'd want to at least block the downstream factors like PGD2 and DKK1 until your AR receptors normalize
anything somehow safe to block dkk1? i'm using prostaquinon and ceti for pgd2 but was still receeding on dutasteride
 

nick123

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Ceti as in Setipiprant? It's total garbage even at 2g a day.

I think he means cetirizine hydrochloride, which is known to reduce PGD2.

Edit: I'm pretty sure I read somewhere cetirizine hydrochloride also reduces PGE2 which isn't a good thing? Does anyone else if this is true?
 

LouisSarkozy

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I think he means cetirizine hydrochloride, which is known to reduce PGD2.

Edit: I'm pretty sure I read somewhere cetirizine hydrochloride also reduces PGE2 which isn't a good thing? Does anyone else if this is true?
thanks i saw mixed studies one saying it's a cox2 inhibitor so reducing pge2 and some saying it actually increase pge2 but i'm not sure. got it coumpounded in trichosol recentrly to trial on my hairline
 

nick123

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thanks i saw mixed studies one saying it's a cox2 inhibitor so reducing pge2 and some saying it actually increase pge2 but i'm not sure. got it coumpounded in trichosol recentrly to trial on my hairline

Interesting, well good luck and report back!
 

nick123

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Right. If you increase the dosage enough then it shouldn't matter. Just if you come off the drug you are going to go through a massive shed until it downregulates, if it downregulates.

If the upregulation of androgen receptors when using androgen receptor antagonists is really true, then why haven't we noticed accelerated loss with RU58841 users after 6 months or am i missing something?!
 

pegasus2

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Could the reason to an upregulation in androgen receptors when taking 5 AR inhibitors be because an increase in testosterone upregulates androgen receptors?

Based on this source: https://journals.physiology.org/doi/abs/10.1152/ajpendo.00157.2020

RU and CB are not 5 AR inhibitors, they don't increase testosterone. I don't think there's any evidence of 5-ARIs upregulating AR except in prostate cancer cells. Also, the particular study involves exogenous T + energy deficit. Assuming those findings are even replicable, it's probably not T specifically, but androgens as a whole that have that effect, and finasteride substantially lowers overall androgen activity.
 

nick123

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RU and CB are not 5 AR inhibitors, they don't increase testosterone. I don't think there's any evidence of 5-ARIs upregulating AR except in prostate cancer cells. Also, the particular study involves exogenous T + energy deficit. Assuming those findings are even replicable, it's probably not T specifically, but androgens as a whole that have that effect, and finasteride substantially lowers overall androgen activity.

I'm fully aware CB and RU are not 5 AR inhibitors, I was just under the assumption finasteride/dutasteride also upregulated AR.
 

nick123

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Some forum members have stated they needed to increase the concentration of RU after 6+ months.
Sorry to beat at the anti androgen receptor and AR upregulation theory again but is there any other potential reasons/theories to why the Breezula 7.5% 6-12 month results took such a hit other than possible AR upregulation?

The reason I ask is because surely this theory would then carry over to Winlevi and acne treatment? Surely after a while people using Winlevi to treat acne would have more androgen receptors and thus more acne?
 

nick123

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I've been doing some more digging into the "anti androgen receptor and AR upregulation" theory and I came across a 12 month study of fluridil where between the 6 and 12 months there was not a decrease in efficacy which was seen between the 6-12 months on the Breezula (CB-03-01) 7.5% phase II study.

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Based on this, this either means one these things:
1) The AR upregulation theory does not apply to fluridil
2) The study results were tampered
3) The AR upregulation theory is not true and there is another reason to why breezula (CB-03-01) 7.5% lost efficacy after 6 months.

Source:
 
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Fgsfds

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iirc on the 6 month results a lower concentration outperformed a higher one therefore there's compliance issues going on
 

pegasus2

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Sorry to beat at the anti androgen receptor and AR upregulation theory again but is there any other potential reasons/theories to why the Breezula 7.5% 6-12 month results took such a hit other than possible AR upregulation?

The reason I ask is because surely this theory would then carry over to Winlevi and acne treatment? Surely after a while people using Winlevi to treat acne would have more androgen receptors and thus more acne?

All we have is wild speculation. We need more data.
 
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