Hoppi said:
Oh, am I right in saying that most things bind to receptors, not actually REDUCE dht as such? I mean that's fine, maybe I just misunderstood and thought some things worked differently to the way they do.
Topical Flutamide and spironolactone bind to receptors? or? I'm wary of RU58841 of course as it's expensive and untested ._.
Okay, I'm now going to give you a basic primer on drugs and chemicals that are often discussed on hairloss sites like this one -- drugs that reduce the androgenic stimulus in some way, shape, or fashion. They generally fall into two or three distinct categories, and sometimes there's a bit of overlap, since some drugs fall into more than one category. I'll make the following comments about them, in no particular order:
1) Androgen receptor blockers (these are also frequently called "antiandrogens"...either term is acceptable). These are substances which enter cells and bind to androgen receptors, thus preventing real androgens from binding to them. In that way, they reduce the extent to which any real androgenic stimulus can occur within the cell. Well-known examples of androgen receptor blockers include flutamide, casodex, RU58841, cyproterone acetate, and spironolactone.
2) 5a-Reductase inhibitors. These are substances which enter cells and bind to the enzyme 5a-reductase, preventing it from converting testosterone into DHT. Well-known examples of 5a-reductase inhibitors include finasteride and dutasteride. In general, a well-designed and clinically-useful 5a-reductase inhibitor wouldn't bind to androgen receptors, since if it _did_ do that, that would also make it an antiandrogen; that usually wouldn't be desirable. Finasteride and dutasteride have very very little affinity for the androgen receptor, which is why they're such useful drugs.
3) The term "DHT inhibitor" is just something made-up on hairloss sites; it has no real meaning among doctors and scientists, and isn't used in medical journals or medical textbooks. I recommend that people use the same terms used by doctors (see [1] and [2] above).
4) An early experimental drug by Merck was called by its familiar abbreviation "4MA". It was an azasteroid, and an early precursor to finasteride. It was successfully tested on stumptailed macaques, just like finasteride, and found to fight male pattern baldness. Unfortunately, in addition to being a 5a-reductase inhibitor, it was also found to have antiandrogenic properties (it binds to androgen receptors), which is almost certainly why no further development was done on it.
5) There's a third kind of drug which can reduce the androgenic stimulus in the human body, and it's anything that chemically interferes with the production of testosterone in the testes. Examples of that would be ketoconazole and spironolactone. Significant systemic doses of either one of those drugs can reduce levels of testosterone in the blood. (Notice that the action of systemic spironolactone is spread over at least a couple of different categories: it's both an androgen receptor blocker, and a drug which interferes with testosterone production. It may even
conceivably act as a 5a-reductase inhibitor, at least according to one study I've found.)
6) There's still another way I can think of to reduce androgenic stimulation, but let's keep all this as simple as possible!
