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Significance Molecularly targeted α-therapy is an emerging therapeutic option for prostate cancer patients. We previously developed [225 Ac]hu11B6, an α-particle–emitting antibody conjugate, which specifically internalizes into prostate cancer cells by binding to human kallikrein-related peptidase 2. Here, we explore methods to enhance its therapeutic efficacy, prospective treatment strategies, and potential resistance mechanisms in preclinical models. We demonstrate that switching the antibody subclass to IgG3 can be applied to radioimmunotherapy and may enhance efficacy. Second, repeat [225 Ac]hu11B6 administration is effective, even in tumors relapsing after initial treatment. Third genetic profiling revealed radio-biological mechanisms associated with relapse after α-radioimmunotherapy that could appropriate combination therapies. Our findings support the clinical translation of [225 Ac]hu11B6 as a highly effective, urgently needed treatment option for prostate cancer.

Genetic signature of prostate cancer mouse models resistant to optimized hK2 targeted α-particle therapy