Aims: MET amplification (METamp) is a mechanism of acquired resistance to EGFR-TKIs. Herein, we present a case series highlighting the clinical activity of tepotinib (a potent, highly selective MET-TKI) + EGFR-TKI (gefitinib and/or osimertinib) in patients with EGFR-mutant METamp NSCLC.
Methods: Early access to tepotinib has been provided through compassionate use. Cases include patients with NSCLC and acquired resistance to EGFR-TKIs due to METamp who received tepotinib outside of a clinical trial (500 mg [450 mg active moiety] once daily; first dose before October 2021) plus an EGFR-TKI.
Results: Twelve cases of patients with EGFR-mutant METamp NSCLC, who received tepotinib plus an EGFR-TKI, are presented (five patients received treatment in second line, three in third line, and four in fourth or later line). Patients were aged 47–86 years, five were Asian, eight were female, three had smoking history, and all had adenocarcinoma histology. METamp was detected by tissue and liquid biopsy in ten and two patients, respectively. In seven patients detected by FISH, MET gene copy number ranged from 5.5–33.4 and MET:CEP7 ratio from 1.8–15.1.
Nine patients received tepotinib plus osimertinib, two patients received tepotinib plus gefitinib, and one patient received both combinations sequentially. The treatment duration ranged from 1.3 to 13.8 months. At the time of data collection, treatment was ongoing in four patients. Eleven patients had clinical benefit per the treating physician’s assessment, of whom eight were considered to have a partial response. Of 12 patients with adverse events (AEs) considered related to tepotinib, seven had edema. Three patients had Grade 3 AEs; no Grade 4 or 5 tepotinib-related AEs were reported.
Conclusions: The combination of tepotinib plus EGFR-TKIs showed promising clinical activity for patients with METamp NSCLC who have progressed on previous EGFR-TKIs, including those with several lines of prior treatment.