This technology describes a dual-pathway targeting approach that induces cell death via ferroptosis to treat castration-resistant prostate cancer.
Treatment approaches for advanced prostate cancer often involves surgery and radiation combined with androgen deprivation therapy and medical castration. However, approximately one-third of patients progress to castration-resistant prostate cancer (CRPC), where treatment options are severely limited. Currently, approved therapies for CRPCs target the androgen receptor, but many CRPC tumors develop resistance to this treatment. Therefore, there is a critical need for CRPC treatments capable of inhibiting tumor growth independently of the androgen receptor pathway.
This technology identifies dual signaling and metabolic pathways as therapeutic targets to overcome castration-resistance in prostate cancer without targeting the androgen receptor. By targeting these pathways, this approach induces ferroptosis, programmed cell death caused by loss of iron homeostasis, in prostate epithelial cells that have become resistant to androgen deprivation therapy. This method bypasses directly targeting the androgen receptor and provides a foundation for developing new combination therapies to inhibit the regression of CPRC.
This technology has been validated in vivo using mouse models.
Patent Pending (WO/2026/064521)
IR CU25059
Licensing Contact: Joan Martinez
