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Iza-Bren, a first-in-class bispecific antibody-drug conjugate targeting EGFR and HER3, has delivered an 11.14-month median progression-free survival in EGFR-mutated non-squamous non-small cell lung cancer that progressed after third-generation EGFR TKI treatment. The result comes from PANKU-Lung01, a randomized phase III trial, and the report describes it as the longest second-line PFS in this setting. The drug links the topoisomerase I inhibitor Ed-04 via a tetrapeptide cleavable linker. The data position Iza-Bren as a candidate for patients who have exhausted current targeted options, a population with limited established therapies after third-generation TKI failure.
Written by a model from the reports · updated 3 hours ago
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- thelancet.com[Articles] Izalontamab brengitecan versus platinum-based chemotherapy in EGFR-mutated advanced non-squamous non-small-cell lung cancer after progression on third-generation EGFR tyrosine kinase inhibitors (PANKU-Lung01): a multicentre, randomised, open-label, phase 3 trial in China
The phase 3 PANKU-Lung01 trial showed that izalontamab brengitecan significantly prolonged progression-free survival compared with platinum-based chemotherapy in patients with EGFR-mutated advanced non-squamous NSCLC. The study enrolled patients whose disease had progressed after third-generation EGFR TKI treatment; grade 3 or worse treatment-related adverse events were more frequent than with chemotherapy. The authors state that these results provide the first phase 3 evidence for a bispecific antibody-drug conjugate and support izalontamab brengitecan as a potential treatment option in this population.
- mp.weixin.qq.comPickIza-Bren Reports 11.14-Month PFS in Later-Line EGFR-Mutated NSCLC
Iza-Bren reported an 11.14-month PFS in EGFR-mutated non-squamous NSCLC that progressed after third-generation EGFR TKI treatment, which the article describes as the longest second-line PFS. PANKU-Lung01 is a randomized phase III study. The first-in-class bispecific ADC targets EGFR and HER3, linking the topoisomerase I inhibitor Ed-04 through a tetrapeptide cleavable linker.
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