Aim
MET amplification (METamp) can develop as de novo or acquired resistance to tyrosine kinase inhibitor therapy in patients with NSCLC and actionable genomic alterations. Tepotinib, a highly selective oral MET kinase inhibitor, has shown promise in both settings. In Cohort B of VISION study (data cut off [DCO]: Aug 20, 2021), 24 patients with de novo METamp were treated with tepotinib; ORR was 41.7% (95% CI 22.1–63.4) and mPFS was 4.2 months (95% CI 1.4–15.6). In INSIGHT 2 (DCO: Mar 28, 2023), 98 patients with EGFR-mutant lung cancer and acquired METamp (in tissue by FISH) were treated with osimertinib and tepotinib; ORR was 50.0% (95% CI 39.7–60.3) and mPFS was 5.6 months (95% CI 4.2–8.1). We present preliminary data from a real-world analysis of Australian patients with metastatic NSCLC and METamp in a cost-share program for tepotinib.
Methods
This was a retrospective analysis of adult patients with metastatic NSCLC with METamp detected by NGS or FISH, from the Australian tepotinib cost-share program between May 2023 and May 2025.
Results
As of May 2025, 16 patients were enrolled and received tepotinib. In the de novo group (N=6), median age was 62.5 years, 33.3% were female, and 50.0% had ECOG PS of 1. MET gene copy number (GCN) ranged from 3.9–20.0; ORR was 66.7%; median duration of treatment (mDoT) was 11 months; treatment was ongoing in 3 patients. In the acquired group (N=10), median age was 66.5 years, 50.0% were female, and 70.0% had ECOG PS of 1. MET GCN was 3.9–14; ORR was 70.0%; mDoT was 16 months; treatment was ongoing in 5 patients. No new safety signals were observed in either group.
Conclusions
Analysis of patients in Australian cost-share program showed that tepotinib is an effective and tolerable treatment in MET-amplified NSCLC.