- Reaction score
- 531
What about resistance? We do know that androgen receptors in prostate cancer cells like LNCaP-BC2 or LNCaP develop resistance to Bicalutamide when it's used as monotherapy. But I don't know about the androgen receptors of other cells, like those in hair follicles. There have been anecdotal claims that prolonged exposure to anti-androgens, like Finasteride, Dutasteride, RU58841 and perhaps a couple more AAs, has made the hair follicles even more sensitive and they were bound to increase their dosage and finally switch to Flutamide or Cyproterone Acetate. Some claim that Bicalutamide makes their scalps oilier and itchy and had no effect on their hair loss, though my experience is just the opposite.
Is there a possibility that after years of Dutasteride, the androgen receptors were so sensitive to testosterone that they didn't bind to Bicalutamide, just like they do in the testes, where androgen levels are high enough to prevent binding of Bicalutamide?
The only theory that I can possibly think of about the unexpected failure of Bicalutamide is that since Bicalutamide takes around three months to reach its stable serum levels, it's not sufficient enough to dominate over the already flaring testosterone and DHT, that occurred due to withdrawal of Dutasteride. But it still doesn't explain why the dose needs to be increased over time when it seemed to have been working well before.
I'm just concerned about developing resistance to oral Bicalutamide, because if it happens and second generation NSAAs don't become available and affordable by then, then the only option that'd be left to me will be surgical castration or GnRH analogues.
Theres a huge difference between cancer cells and regular cells. Of course cancer cells become resistant, your regular cells do not work this way. Bicalutamide at 50mg or more orally will easily be able to combat hairloss, but the only question is how effective is it topically. The main issue ive run into is I can hardly dissolve it, meaning the dosage is very low.
Think about it like this, the AR need to be binded to by an androgenic molecule for hairloss to occur. If there is competition as to what binds to the AR then the gene expression will be lower. The ideal scenario would be to have a molecule that has as strong of an affinity to the AR as DHT but I am not aware of such a molecule. Howver, bicalutamide compensates for its lack of strenght by volume. There are so many bicalutamide molecules available to bind the the AR that it overpowers testosterone. Thats why it works otherwise it would not be effective as testosterone would just keep binding to the receptors as if bicalutamide wasnt even there