Talzenna (talazoparib)

Using Bayesian evidence synthesis with prespecified borrowing levels, the Japanese subgroup results were compatible in direction and magnitude with the overall TALAPRO-2 effect. These findings reduce uncertainty around local extrapolation; a dedicated randomized study would be required to establish efficacy independently in Japanese patients.

In recurrent ovarian cancer, niraparib+pembrolizumab showed modest activity with durable responses in homologous recombination-deficient (HRD) tumors; olaparib+durvalumab demonstrated high activity in gBRCA platinum-sensitive relapse, and adding bevacizumab broadened benefit in non-BRCA cohorts. In the newly diagnosed disease, rucaparib+nivolumab maintenance failed to improve PFS versus rucaparib alone. Endometrial trials (olaparib+durvalumab; talazoparib+avelumab in mismatch repair-proficient disease) showed limited activity overall, with signals restricted to biomarker-selected subgroups...PARP+PD-1/PD-L1 combinations are most compelling in ovarian cancer, particularly in BRCA/HRD tumors and, in selected settings, with the addition of bevacizumab, while frontline maintenance benefit remains unproven and endometrial activity is modest. Biomarker-guided selection, rational triplets with non-cytotoxic partners, and optimized sequencing warrant further evaluation.

Talazoparib combined with ATR inhibitor possesses potential application as a therapeutic option for SS.

P2, N=24, Active, not recruiting, University of Miami | Recruiting --> Active, not recruiting | N=500 --> 24

Treatment with the PARP inhibitor talazoparib produced a durable growth suppression both in vitro and in multiple ILC xenografts in vivo. Together, these findings reveal that ILC-specific ER:MDC1 activity comes at the cost of DNA repair dysfunction, which may be therapeutically targetable.

Taken together, our findings indicate that Alt-NHEJ inhibitors are potential immune-stimulating agents for MM with hyperactivation of cGAS-STING pathway, coherently with our working hypothesis.

Furthermore, individual knockdown of PARP1, P300, or GCN5 reduced VEGFA expression, indicating their important role in regulating tumor angiogenesis. In conclusion, the QC and Talazoparib combination effectively prevents the activation and secretion of angiogenic factors, thereby suppressing angiogenesis, and may serve as a promising therapeutic approach for oral cancer by targeting PARP1 and associated chromatin remodelers.

In total, 62 MBC patients treated with olaparib (N = 55), talazoparib (N = 4), pamiparib (N = 2), and fluzoparib (N = 1) were enrolled. Hematologic toxicity was the most common grade ⩾3 AEs. PARPis showed promising PFS and tolerable toxicity in the real-world treatment of Chinese MBC patients with HRR-related gene mutations.

The patient received four cycles of induction chemotherapy with carboplatin and etoposide, achieving a partial radiographic response; however, treatment was complicated by cytopenias and significant fatigue. This case illustrates the potential role of PARP inhibitors in the management of BRCA2-mutated high-grade rectal NEC. Molecular profiling techniques may uncover actionable genetic targets in rare, aggressive cancers without standard treatment options or in patients with co-morbidities that preclude standard treatment regimens.

P2, N=150, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

The patient received androgen deprivation therapy, followed by a combination of talazoparib and enzalutamide. Six months later, imaging revealed fewer lung metastases. This case illustrates the diagnostic challenges of low-prostate-specific antigen ductal adenocarcinoma and demonstrates the potential of molecular profiling to guide personalized treatment with targeted therapies for rare prostate cancer subtypes.

Clinically, PARP inhibitors (PARPi), such as olaparib, niraparib, rucaparib, and talazoparib, exploit synthetic lethality in homologous recombination-deficient tumors and are increasingly applied in ovarian, breast, prostate, and pancreatic cancers. By integrating canonical DNA repair roles with non-canonical signaling and host-virus interactions, PARPs represent pivotal regulators. Similarly, the versatile therapeutics of PARPi have implications that extend beyond oncology into a broader and diverse range of other human diseases.