Lurbinectedin, a selective inhibitor of oncogenic transcription, has shown preclinical antitumor activity against homologous recombination repair-deficient (HRD) models and preliminary clinical activity in BRCA1/2 breast cancer.
Two PARP inhibitors are available as the therapeutic option (Lynparza and Talzenna), but many patients do not derive benefit because of multiple primary and secondary resistance mechanisms and toxicities.
Lurbinectedin is a selective inhibitor of oncogenic transcription that leads to cell death. Lurbinectedin has antitumor activity against homologous recombination repair-deficient (HRD) cell lines.
About the Study
This cohort was evaluated because, in a previous phase II study, lurbinectedin had shown antitumor activity in patients with advanced breast cancer and germline BRCA1/2 pathogenic variants: Response Rate was 41% and median Survival was 20.0 months compared to 9% and 12.5 months, respectively, in patients with BRCA1/2 wild-type or unknown status.
Lurbinectedin was active in both BRCA mutations: four PRs in 11 patients (36.4%) with BRCA2 and two PRs in 10 patients (20.0%) with BRCA1.
47.6% had Stable Disease (SD, meaning the disease was controlled and the lesions stayed the same volume and size)
This brings us to 76.2% of patients with clinical benefit
Median Survival was 16.1 months.
The most common treatment-related side effects were nausea, fatigue and vomiting.
These side effects were mostly mild.
The most common harsh toxicity was neutropenia.
Lurbinectedin has previously shown antitumor activity in breast cancer patients with mutations in BRCA2.
This phase II basket study included a cohort of 21 patients with BRCA-mutated breast cancer treated with lurbinectedin.
The study showed antitumor activity and clinical benefit to BRCA-mutated patients who failed on previous treatment lines.
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