PARP抑制剂（PARPi）正在改变转移性去势抵抗型前列腺癌的当前治疗格局。通过对奥拉帕尼、他拉唑帕尼、鲁卡帕尼和尼拉帕尼的已发表数据进行重新分析，我们提供了对分子亚组的响应的简明概述。作为单药治疗，所有PARPi表现出可比较的疗效，并且在响应性方面具有相同的等级：与BRCA1或BRCA2（BRCAm）基因突变相关的肿瘤患者明显表现出优于其他同源重组修复（HRR）相关基因突变的患者的反应。与其他PARPi相比，尼拉帕尼似乎引起更多≥3级不良事件。PARPi还与雄激素受体信号抑制剂（ARSI）联合应用于携带HRR基因的肿瘤患者（HRRm）和分子未选择的患者。与野生型患者相比，BRCAm患者的反应最佳，其次是HRRm。与仅应用ARSI相比，奥拉帕尼-阿比特龙、尼拉帕尼-阿比特龙和他拉唑帕尼-恩扎鲁胺均使HRRm患者的进展无病生存时间延长。在非HRRm亚组中，仅奥拉帕尼-阿比特龙和他拉唑帕尼-恩扎鲁胺有效。鲁卡帕尼与恩扎鲁胺联合应用的结果尚未报告。与仅应用ARSI相比，联合方案的≥3级不良事件发生率增加了10-30％。考虑到对未选择的患者疗效有限，这些PARPi-ARSI联合方案可能最好保留给选择性的患者。版权所有 © 2023。Elsevier B.V.出版。

PARP inhibitors (PARPi) are transforming the current treatment landscape of metastatic castration-resistant prostate cancer. By reanalysing published data on olaparib, talazoparib, rucaparib and niraparib, we provide a concise overview of responses by molecular subgroup. As monotherapy, all PARPi showed comparable efficacy and the same hierarchy in responsiveness: patients with tumours harbouring aberrations in BRCA1 or BRCA2 (BRCAm) evidently demonstrate superior responses when compared to aberrations in other homologous recombination repair (HRR) related genes. Niraparib seems to cause more grade ≥3 adverse events in comparison to other PARPi. PARPi have also been combined with androgen-receptor signalling inhibitors (ARSI) for both patients with tumours harbouring aberrations in HRR genes (HRRm), and molecularly unselected patients. Compared to wildtype, BRCAm patients responded best, followed by HRRm. Olaparib-abiraterone, niraparib-abiraterone, and talazoparib-enzalutamide all prolonged progression-free survival compared to an ARSI alone in HRRm patients. In the non-HRRm subgroup, only olaparib-abiraterone and talazoparib-enzalutamide were effective. Results for the combination of rucaparib with enzalutamide are yet to be reported. The rate of grade ≥3 adverse events for the combination regimens is 10-30% higher when compared to an ARSI alone. Given the limited efficacy in unselected patients, these PARPi-ARSI combinations may be best reserved for selected patients.Copyright © 2023. Published by Elsevier B.V.