Your Health, We Care
Release date: 2024-11-25 15:22:33 Recommended: 112
Capmatinib has been approved for the treatment of MET exon 14-mutated non-small cell lung cancer based on demonstrated efficacy in a patient population that has not received targeted therapy. To further explore its therapeutic potential, we conducted a Phase 2 clinical study to evaluate the efficacy of capmatinib in patients who had previously received MET inhibitor therapy.
In this study, we included patients with advanced non-small cell lung cancer with MET amplification or MET exon 14 skipping mutations and gave them Capmatinib 400 mg twice daily. The primary endpoint of the study was objective response rate, while secondary endpoints included progression-free survival, disease control rate (DCR), intracranial response rate, and overall survival. To gain insight into the mechanisms of resistance to Capmatinib capmatinib, we also performed an analysis of circulating tumor DNA.
A total of 20 patients participated in the study, of which 15 had MET skipping variants and 5 had MET amplification. Notably, all patients had received crizotinib before, while three of them had received other treatments for MET. The median interval between treatment with crizotinib and capmatinib was 22 days (range 4-374 days).
The results of the study showed that 2 patients (10%) experienced an objective response to capmatinib treatment, while 14 patients remained stable, resulting in a DCR of 80%. Among the five patients who discontinued crizotinib due to intolerance, the DCR was as high as 83%, with two patients achieving the most significant tumor shrinkage at -25% and -28%, respectively. For four patients with measurable brain metastases, the intracranial DCR rate was 100%, but unfortunately we did not observe an objective intracranial response. Overall, median progression-free survival and overall survival were 5.5 months (95% CI: 1.3 to 11.0 months) and 11.3 months (95% CI: 5.5 months to not reached), respectively. In addition, we repeatedly detected METD1228 and Y1230 mutations and alterations in the MAPK pathway in plasma samples after crizotinib treatment and before capmatinib treatment. As Capmatinib progressed, new and persistent MET mutations and MAPK pathway alterations were detected in plasma.
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