Disclosed are methods of enhancing prostate cancer vulnerability to an anti-PSMA targeted therapy by administering an anti-androgen therapy to a subject so that the prostate cancer vulnerability in the subject is enhanced 2-4 weeks after the administration of the anti-androgen therapy and then administering to the subject an antibody or antigen binding fragment thereof that is capable of binding to the extracellular domain of PSMA after the prostate cancer vulnerability is enhanced. The anti-androgen therapy can be a hormonal therapy or surgical castration. The antibody or antigen binding fragment thereof may optionally be conjugated to a cytotoxic agent, e.g., Lutetium-177.
