Prostate Cancer

P1, N=60, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

P3, N=370, Recruiting, Jiangsu HengRui Medicine Co., Ltd. | Not yet recruiting --> Recruiting

P=N/A, N=250, Not yet recruiting, Chinese University of Hong Kong

P=N/A, N=24, Recruiting, Inova Health Care Services | Not yet recruiting --> Recruiting

P=N/A, N=112, Completed, Assistance Publique Hopitaux De Marseille | Recruiting --> Completed | N=200 --> 112

P=N/A, N=180, Not yet recruiting, Unity Health Toronto

P=N/A, N=411, Completed, Centre Paul Strauss | Recruiting --> Completed | Trial completion date: Feb 2025 --> Jan 2026 | Trial primary completion date: Nov 2024 --> Nov 2025

P1, N=7, Completed, Godavari Biorefineries Limited | Not yet recruiting --> Completed | N=27 --> 7 | Trial completion date: Jan 2023 --> Jan 2026 | Trial primary completion date: Dec 2022 --> Jan 2026

At the same time, known ferroptosis inhibitors, ferrostatin-1 and deferoxamine, effectively prevented cell death, indicating the specificity of the mechanism of action. Transcriptomic analysis of cell lines differing in sensitivity to the combination revealed activation of antioxidant systems in more resistant cells (in particular, pronounced expression of the NQO1 and GCLM genes responsible for the reduction of quinones to hydroquinones and the synthesis of glutathione, respectively). The obtained results indicate the high synergistic potential of the erastin-DHA combination for ferroptosis induction and open new possibilities for the development of combined approaches to the therapy of resistant tumors.

Repurposed drugs such as flubendazole and the ezetimibe derivative L14-8, along with natural compounds including evodiamine and luteolin, demonstrate translational potential for ferroptosis induction. Collectively, ferroptosis represents a promising therapeutic vulnerability for precision treatment of advanced prostate cancer.

Notably, the combination of NXPH4 knockdown and enzalutamide treatment showed potent synergistic effects, significantly suppressing cell proliferation in vitro and substantially inhibiting tumor growth in vivo. These findings reveal a previously unrecognized mechanism of EnzR and identify the NXPH4-ALDH1L2 complex as a promising therapeutic target for CRPC treatment.

Results showed a mild, though non-significant, trend toward increased [18 F]F-PSMA-1007 in most groups compared to the control, except for those exposed to short pulses associated with high-pressure. These findings highlight the potential of USMB to enhance drug delivery for PSMA uptake but also underscore the necessity for careful consideration of ultrasound parameters to prevent tissue damage.