Summarizing, it looks like the TMPRSS2 protein is necessary for the virus to replicate, and the Androgen Receptor modulates its transcription. But where I'm co

Summarizing, it looks like the TMPRSS2 protein is necessary for the virus to replicate, and the Androgen Receptor modulates its transcription. But where I'm confused is why this drug in particular was studied, instead of an approved AR antagonist like bicalutamide or enzalutamide. Way easier to dispense those than some clinical trial drug, right? And is it important that the drug is a silent antagonist of AR rather than an inverse agonist? Also, how does this affect women? Are we at less risk of mortality through this mechanism? My T levels are very low, but all of us have androgens and their receptors. Maybe TMPRSS2 gets transcribed even when T or DHT levels are low?