That depends....the forum will need your clinical history to answer.

For now, the Lupron basically shuts down production of testosterone from the testicles, medical castration. As T is a "fuel" for PCa, those cells generally die off, though not all. Why, some PCa cells adapt to a low T environment. Thus the introduction and use of Xtandi, an ARI, or androgen receptor inhibitor which interferes (blocks) with the PCa's cell ability to bind with and use the remaining T, some of which is produced by the adrenal gland which Lupron does not block.

That's a layman's version, keep in mind I am not a medical professional.