From:  Innovative immunotherapies for prostate cancer: understanding the synergies between checkpoint inhibition, CAR T-cell therapy, and next-generation therapeutic modalities

 Analysis of pivotal Phase III immunotherapy trials in mCRPC: efficacy outcomes and future implications.

NCT numberTrial namePhaseDescriptionUpdated resultsKey insight & implication for future developmentReference
1NCT00861614CA184-043IIIIpilimumab + RT vs. placebo + RT in mCRPCMedian OS: 11.5 months vs. 10.3 months. HR: 0.88, p = 0.049The narrow survival benefit, which barely missed statistical significance, suggests CTLA-4 inhibition may only be effective in a subset with more favorable prognoses (e.g., no visceral disease, normal ALP). Future efforts require robust biomarkers for patient selection.[19]
2NCT01057810CA184-095IIIIpilimumab vs. placebo in mCRPCMedian OS: 29.1 months vs. 28.0 months. HR: 1.09, p = 0.34Lack of efficacy in an earlier-line, less heavily pretreated population indicates that a mere “cold” TME is not the only barrier. Intrinsic resistance mechanisms or the immunosuppressive role of continuous androgen signaling may need concurrent targeting.[19]
3NCT02312557Single-Arm Phase II StudyIIPembrolizumab + enzalutamide in mCRPC progressing on enzalutamide alonePrimary endpoint (ORR): Limited activity observed in this biomarker-unselected, post-enzalutamide populationDemonstrated that PD-1 inhibition after ARSI progression has minimal efficacy without patient selection, highlighting the need for biomarkers and questioning combination timing.[15]
4NCT03834519KEYLYNK-010IIIPembrolizumab + olaparib vs. NHA in mCRPCMedian OS: 16.0 months vs. 14.7 months. HR: 0.95, p = 0.24The failure in a biomarker-unselected population confirms that the immunogenic potential of PARP inhibition is likely restricted to tumors with HRR deficiencies. Future trials must be strictly biomarker-driven.[30]
5NCT03834506Keynote-921IIIPembrolizumab + docetaxel vs. docetaxel in mCRPCMedian OS: 20.1 months vs. 18.9 months. HR: 0.89, p = 0.15Unlike in NSCLC, chemo-immunotherapy synergy is not universal. In mCRPC, docetaxel may not induce sufficient immunogenic cell death or may concurrently deplete immune cells, negating the benefit of PD-1 blockade.[31]
6NCT03016312IMbassador250IIIAtezolizumab + enzalutamide vs. placebo + enzalutamide in mCRPCMedian OS: 15.8 months vs. 16.7 months. HR: 1.14, p = 0.21The trend toward worse survival in the combination arm raises a critical safety flag. It suggests the potential for antagonism between PD-L1/PD-1 blockade and enzalutamide, necessitating a deeper investigation into their interplay on the immune landscape.[32]
7NCT03338790CheckMate 9KD (Cohort B)IINivolumab + docetaxel in chemotherapy-naive mCRPCPrimary endpoint (ORR): Encouraging anti-tumor activity and acceptable safety, warranting further investigation.This Phase II signal contrasted with subsequent Phase III failures, suggesting chemotherapy combination efficacy may be context-dependent and not sufficient as a broad strategy in mCRPC.[33]

NCT: National Clinical Trial; NHA: next-generation hormonal agent monotherapy; OS: overall survival; ORR: objective response rate; mCRPC: metastatic castration-resistant prostate cancer; RT: radiotherapy; ARSIs: androgen receptor signaling inhibitors; HR: hazard ratio; TME: tumor microenvironment; ALP: alkaline phosphatase; HRR: homologous recombination repair. Adapted from Meng et al. [6] with added critical analysis (CC-BY).