The Cb (breezula [clascoterone]) Community Thread

[Dimitri001]

Consider that studies show minoxidil gains are significantly lost in one month. I see no reason to believe this would be any different, and would one month off of it be enough? I think those looking for a miracle without the potential for side effects better shave their heads and start saving for Tsuji.

Well, it works through a different mechanism than minoxidil, so it's not a foregone conclusion that the gains would go in the same time period.

Would one month off of it be enough, I have no idea, but I don't know that a week off of it wouldn't be enough if you go off before the 6 month mark when the AR desensitization sets in (if that's the proper way to understand the reason for it losing effectiveness). I guess, if this would work at all, it would partly depend on how long CB stays in the follicles.

But, again, I don't know anything about ARs and how any of this works, so my little hypothesis may be a complete non-starter.

 

[telogen]

Upregulating AR with stuff like CB, ru and oh-flut is dead real in my experience. This don't appear to be happening with topical finasteride, which keeps having stable effect over long periods. The problem with finasteride is the unchecked T which accumulates in the scalp and does damage. Upping the dose with something like ru unlimited is also not doable, because you will run into serious sides like gyno in the end.
I've been trying to cycle oh-flut on and off in 30 days spans, and it appears to work, but i don't have anything similarly potent to use
when off oh-flut. Maybe an SFRP1 inhibitor like way-316606??

 

[bucksins6x]

Upregulating AR with stuff like CB, ru and oh-flut is dead real in my experience. This don't appear to be happening with topical finasteride, which keeps having stable effect over long periods. The problem with finasteride is the unchecked T which accumulates in the scalp and does damage. Upping the dose with something like ru unlimited is also not doable, because you will run into serious sides like gyno in the end.
I've been trying to cycle oh-flut on and off in 30 days spans, and it appears to work, but i don't have anything similarly potent to use
when off oh-flut. Maybe an SFRP1 inhibitor like way-316606??

Any sides on oh-flut?

 

[telogen]

Any sides on oh-flut?

Non on 100 mg which maintains.
With ru i was needing 200 mg ed which in the end gave me gyno and forced me to quit.
I'm sure this was a case of upregulated ar

 

[John Difool]

I'd really like to get my hands on some proxalutamide

 

[John Difool]

I suggest trying an Androgen receptor degrader for a while to see if you can reverse that.

Such as ASC-J9?

 

[pegasus2]

Such as ASC-J9?

Yes.

 

[Upnadam10]

Yeah I agree, for me finasteride didnt do much for my hairline but maybe retained the rest but think I would have kept it anyway. but dutasteride stopped it in its tracks, like instantly, zero hairs in shower or on pillow or anything, new hairs growing in my hairline but made me feel like a plank of wood,. Felt ru was similar to dutasteride for hairloss in my opinion but not too sure on reliability for ru, and just generally dont trust those chinese sites

How long have you been on dutasteride? Hard to find success stories on dutasteride on this site. Please share

 

[John Difool]

What? Hard to find success stories?! It depends what you mean by success! If you expect regrowth from popping an AA pill, sure you are in for disappointment. As far as maintenance, it's much better than Fina and there are plenty of material on this. Of course doctors in the US are being greased by Big Pharma to script Fina so that's not as popular in the States.

 

[Jim lahey]

The graph on page 62 of this thread shows it.

I wonder whether cycling off and back on it might not help, as someone suggested.

That graph only goes up to 12 months and is still above baseline so we don't know that happens after 12 months. Its an anti androgen and from what it looks like a pretty mild one so huge gains aren't to be expected.

 

[Jim lahey]

Cycling probably won't give you better results because once you get off it your receptors are going to be very sensitive to androgens.

 

[wilfred]

Anyone in Canda want my unopened CB pm me.

 

[Dimitri001]

That graph only goes up to 12 months and is still above baseline so we don't know that happens after 12 months. Its an anti androgen and from what it looks like a pretty mild one so huge gains aren't to be expected.

Well, the trend is pretty sharply downwards going from 6 to 12 months, so plummeting further seems like the reasonable guess, sadly.

Cycling probably won't give you better results because once you get off it your receptors are going to be very sensitive to androgens.

Are you sure that that's how it works or guessing? It seems like they are getting less sensitive to CB, so the more reasonable assumption seems to be that, if anything, they're gonna be less sensitive.

I wish we had someone in here who was knowledgeable about this stuff and could give us an authoritative answer on this cycling hypothesis.

But anyway, even if what you say is true, it's still possible that you'll be at a net gain with, say, cycles of 6 months being on it and a week or a month of being off it.

 

[Dimitri001]

I know nothing about hormones and ARs, so if I'm conceptualizing this the wrong way someone please set me straight, but regarding this AR desensitization/upregulation explanation of the diminishing effectiveness, my understanding is that CB binds to the AR so that DHT can't. It takes up its place, so to speak.

If that is so, I don't see how desensitization can explain the diminishing returns, because CB isn't having any effect to begin with, it's just taking up space. There's no positive CB effect that can be diminished though desensitization, because CB doesn't have an effect.

Or is it that desensitization is supposed to mean that the ARs' affinity for binding with CB goes down? That also seems kinda dubious, because, in absence of CB, it's exposed to DHT constantly, so that effect should be present with DHT, too. Unless there's a cutoff point - meaning the binding affinity goes down with constant exposure, but it never gets to the point where it won't bind, so it will just keep binding with DHT even as its affinity for it goes down, because DHT is the only game in town.

 

[sonictemples]

Wouldn't bica cure that

 

[Throwaway94]

@Dimitri001 What people are talking about is more receptors being created. CB doesn't bind to every receptor. The more receptors there are the more CB is needed. Worse, but unlikely, would be receptors mutating to be activated by CB.

I *think* the main question there is why people believe CB would cause upregulation to begin with whereas other things that bind to the same receptor don't.

I know there's broscience out there talking about upregulation due to some people's experience of it becoming less effective over time and the decline in the breezula trial, but we have yet to see evidence of upregulation beyond that of what people who are going bald seem to have naturally. What's your take on this?

 

[Throwaway94]

Who says other things don't? A lot of people believe that RU does the same thing. None of the other topical AAs have ever gained much popularity. There's certainly no evidence that there is AR up regulation in the HF, but I don't see any other reasonable explanation for CB getting outperformed by placebo. People talking placebo are already going bald too.

I don't know if other things do or don't that part was my interpretation of Dimitri's question.

I don't doubt there is upregulation, but what is there to suggest it wouldn't happen either way? As far as some concs of Breezula being outperformed by placebo, we know it was a small sample and don't have any other details regarding the measurements so I'll reserve judgement there

 

[Dimitri001]

Ok, so AR upregulation = creation of new receptors.

So, the fact that folks are suspecting upregulation might be happening here leads me to believe there are precedents for that, that's known to happen under certain conditions?

I *think* the main question there is why people believe CB would cause upregulation to begin with whereas other things that bind to the same receptor don't.

Who says other things don't? A lot of people believe that RU does the same thing. None of the other topical AAs have ever gained much popularity. There's certainly no evidence that there is AR up regulation in the HF, but I don't see any other reasonable explanation for CB getting outperformed by placebo. People talking placebo are already going bald too.

Yeah, that's what I was thinking, but I meant why doesn't DHT cause upregulation when it binds, because I was understanding upregulation as desensitization. Now that I know it's new receptors, I realize I can't know that it doesn't.

However, upregulation reads to me like an adaptive response - the HF isn't getting the effect it expects from DHT binding, because CB is binding instead, so it grows more ARs (this is complete broscience and speculation, obviously) and I don't see why the normal course of events (just DHT binding with no AA intervention) would induce an adaptive response.

If that's right, the cycling theory could still stand.

[UPDATE: Incidentally, I was just reading this study on ginseng and it says:

"We proved this speculation by showing that RGE and its ginsenosides inhibit the DHT-induced upregulation of androgen receptor in hDPCs."

So, IDK, maybe ginseng to fight the upregulation and ride the CB gains?]

But on what measurement was CB outperformed by placebo? I just looked at TAHC.

I don't think anyone knows what really goes on with the AR, but whether there's AR upregulation in the placebo group or not, it's not to the same degree as the CB group, if that's what's going on here. Results need to be replicated of course.

Hopefully they'll care enough to find out why their product goes useless after a year.


I have another question, and this is getting a little off the topic, but I'm trying to understand this: When 5ar inhibitors wipe DHT out from the scalp, you get more testosterone - can't it bind to ARs? Or does it bind but not have the effect DHT does?

 

[Throwaway94]

Ok, so AR upregulation = creation of new receptors.

So, the fact that folks are suspecting upregulation might be happening here leads me to believe there are precedents for that, that's known to happen under certain conditions?




Yeah, that's what I was thinking, but I meant why doesn't DHT cause upregulation when it binds, because I was understanding upregulation as desensitization. Now that I know it's new receptors, I realize I can't know that it doesn't.

However, upregulation reads to me like an adaptive response - the HF isn't getting the effect it expects from DHT binding, because CB is binding instead, so it grows more ARs (this is complete broscience and speculation, obviously) and I don't see why the normal course of events (just DHT binding with no AA intervention) would induce an adaptive response.

If that's right, the cycling theory could still stand.

[UPDATE: Incidentally, I was just reading this study on ginseng and it says:

"We proved this speculation by showing that RGE and its ginsenosides inhibit the DHT-induced upregulation of androgen receptor in hDPCs."

So, IDK, maybe ginseng to fight the upregulation and ride the CB gains?]

But on what measurement was CB outperformed by placebo? I just looked at TAHC.



Hopefully they'll care enough to find out why their product goes useless after a year.


I have another question, and this is getting a little off the topic, but I'm trying to understand this: When 5ar inhibitors wipe DHT out from the scalp, you get more testosterone - can't it bind to ARs? Or does it bind but not have the effect DHT does?

Anything that binds to the AR will trigger a change in structure and depending on what binds, certain androgenic factors will then be transcribed. DHT is far more androgenic than testosterone, and things like CB are less androgenic than both of these. Also to be taken into account is each molecule's binding affinity.

 

[John Difool]

@Dimitri001 you just rediscovered what topical Bica does overtime.

The androgen receptor (AR), also known as NR3C4 (nuclear receptor subfamily 3, group C, member 4), is a type of nuclear receptor that is activated by binding any of the androgenic hormones, including testosterone and dihydrotestosterone in the cytoplasm and then translocating into the nucleus.

If you want to learn more you should at a minimum read this page:

https://www.google.com/url?sa=t&source=web&rct=j&url=https://en.m.wikipedia.org/wiki/Androgen_receptor#:~:text=The%20androgen%20receptor%20(AR)%2C,then%20translocating%20into%20the%20nucleus.&ved=2ahUKEwjuxMbCktzqAhXgoXIEHUf8ADIQFjAEegQIDBAI&usg=AOvVaw2B5er6cSlM4Ck75DVLKlt6