topical anti androgens ?

[just some dude]

topical anti-androgens seem appealing because you think you will get the benefits of oral fin/dut without the consequences of oral fin/dut.

however, have any of them actually done anything for anyone here? have you noticed meaningful progress since you’ve implemented topical solution(s)?

personally:
i’m not seeing as aggressive results as i wanted with oral dut + topical minoxidil, i’m thinking of adding oral minoxidil and topical anti-androgens

edit: this is about hairline / hair loss treatment - there’s a lot of data on minoxidil, dut, & fin, but not enough on some of these topical anti-androgens; they could def use more anecdotal evidence. for example ru-58841, some people saying it’s kept their hair for years, others swearing it off with chest pains. there’s not as much objective information on them it seems.

 

[Ghoul]

topical anti-androgens seem appealing because you think you will get the benefits of oral fin/dut without the consequences of oral fin/dut.

however, have any of them actually done anything for anyone here? have you noticed meaningful progress since you’ve implemented topical solution(s)?

personally:
i’m not seeing as aggressive results as i wanted with oral dut + topical minoxidil, i’m thinking of adding oral minoxidil and topical anti-androgens

Problem I have with topical anti androgens is variability in systemic effects. Unlike minoxidil, there are potential serious consequences to variability in absorption of a 5-ar inhibitor. I think it’s best to go oral so you always have precise control over the dose.

As far as topical minox, a pretty substantial minority have insufficient, or even none, of the enzyme required to convert it to the active form as it penetrates skin, so its effectiveness is diminished or eliminated entirely,

Oral is converted to active form 100% in everyone. Just have to give any sides some time to subside, if they occur. A lot cheaper and far less time consuming too.

Best clinically proven hair loss prevention and regrowth is via Dut/Minox combo. Boring but highly effective over time.

 

[ProgestegenicWarrior88]

Problem I have with topical anti androgens is variability in systemic effects. Unlike minoxidil, there are potential serious consequences to variability in absorption of a 5-ar inhibitor. I think it’s best to go oral so you always have precise control over the dose.

As far as topical minox, a pretty substantial minority have insufficient, or even none, of the enzyme required to convert it to the active form as it penetrates skin, so its effectiveness is diminished or eliminated entirely,

Oral is converted to active form 100% in everyone. Just have to give any sides some time to subside, if they occur. A lot cheaper and far less time consuming too.

Best clinically proven hair loss prevention and regrowth is via Dut/Minox combo. Boring but highly effective over time.

Nattys being scared of anti-androgens makes sense. But if youre on gear ur already carring like 2-10x rhe androgen load off a natty. Worrying about a fraction of percent of RU going systemic when youre on tren is just goofy.

 

[littletommybhoy]

Problem I have with topical anti androgens is variability in systemic effects. Unlike minoxidil, there are potential serious consequences to variability in absorption of a 5-ar inhibitor. I think it’s best to go oral so you always have precise control over the dose.

As far as topical minox, a pretty substantial minority have insufficient, or even none, of the enzyme required to convert it to the active form as it penetrates skin, so its effectiveness is diminished or eliminated entirely,

Oral is converted to active form 100% in everyone. Just have to give any sides some time to subside, if they occur. A lot cheaper and far less time consuming too.

Best clinically proven hair loss prevention and regrowth is via Dut/Minox combo. Boring but highly effective over time.

Could a perimenopausal woman who has been sterilized be able to take that combo safely?

 

[HUGE McBIGLARGE]

Topicals can still dramatically lower serum DHT.

Efficacy and safety of topical finasteride spray solution for male androgenetic alopecia: a phase III, randomized, controlled clinical trial - PubMed

Topical finasteride significantly improves hair count compared to placebo and is well tolerated. Its effect is similar to that of oral finasteride, but with markedly lower systemic exposure and less impact on serum DHT concentrations.

pubmed.ncbi.nlm.nih.gov

“reduction from baseline in mean serum DHT concentration was lower (34.5 vs. 55.6%), with topical vs. oral finasteride”

Nattys being scared of anti-androgens makes sense. But if youre on gear ur already carring like 2-10x rhe androgen load off a natty. Worrying about a fraction of percent of RU going systemic when youre on tren is just goofy.

RU can produce metabolites. What they do is anyone’s guess.

“Anti-androgen” can be a little misleading. What a lot of people think is that it merely displaces androgens at the receptor, acting as a “silent antagonist”. But in my 5 seconds of Googling, I cannot find anything to suggest this is the case. In my experience, I’ve seen very few drugs with “silent antagonism” of receptors.

In all likelihood, RU is either a partial agonist or inverse agonist of the androgen receptor. This would make it a de-facto displacer of androgens, but the drug still exerts a pharmacological effect at the receptor. If this is the case, then who knows just what the androgen receptors do when agonised.

In some sense, 5ARis are less scary than RU, as at least we know more about them, and they don’t affect receptors directly.

None of this is to suggest that RU is totally awful and it’s gonna make you kill yourself. But at the same time, I wouldn’t feel confident thinking it merely displaces androgens at the receptor level.

 

[ProgestegenicWarrior88]

Bro bro, rhere is no secret "Negative receptor activation" a ligand can only bind or not binding to a receptor. The point of an antagonist, OF ANY RECEPTOR, is to bind to it and do nothing. Denying it from being occupied by an agonist which would actually activate the receptor. Ur 5 second googling did not need to mentioned...

Topicals can still dramatically lower serum DHT.

Efficacy and safety of topical finasteride spray solution for male androgenetic alopecia: a phase III, randomized, controlled clinical trial - PubMed

Topical finasteride significantly improves hair count compared to placebo and is well tolerated. Its effect is similar to that of oral finasteride, but with markedly lower systemic exposure and less impact on serum DHT concentrations.

pubmed.ncbi.nlm.nih.gov

“reduction from baseline in mean serum DHT concentration was lower (34.5 vs. 55.6%), with topical vs. oral finasteride”



RU can produce metabolites. What they do is anyone’s guess.

“Anti-androgen” can be a little misleading. What a lot of people think is that it merely displaces androgens at the receptor, acting as a “silent antagonist”. But in my 5 seconds of Googling, I cannot find anything to suggest this is the case. In my experience, I’ve seen very few drugs with “silent antagonism” of receptors.

In all likelihood, RU is either a partial agonist or inverse agonist of the androgen receptor. This would make it a de-facto displacer of androgens, but the drug still exerts a pharmacological effect at the receptor. If this is the case, then who knows just what the androgen receptors do when agonised.

In some sense, 5ARis are less scary than RU, as at least we know more about them, and they don’t affect receptors directly.

None of this is to suggest that RU is totally awful and it’s gonna make you kill yourself. But at the same time, I wouldn’t feel confident thinking it merely displaces androgens at the receptor level.

 

[HUGE McBIGLARGE]

Bro bro, rhere is no secret "Negative receptor activation" a ligand can only bind or not binding to a receptor. The point of an antagonist, OF ANY RECEPTOR, is to bind to it and do nothing. Denying it from being occupied by an agonist which would actually activate the receptor.

A lot of so-called antagonists are partial agonists that displace stronger agonists. Some beta blockers are like this.

Strictly speaking, most drugs that are silent antagonists exert some signalling effect at the receptor, albeit incredibly small.

And some drugs can be functional agonists in some tissues, function antagonists in others, and functional inverse agonists in others. Such as with SERMs.

Ur 5 second googling did not need to mentioned...

lol