异常的 c-MET（间质-上皮转化）信号传导有助于非小细胞肺癌 (NSCLC) 的癌细胞发育、增殖和转移。大约 4% 的 NSCLC 病例中发现了 MET 外显子 14 (METex14) 跳跃突变，最近批准的酪氨酸激酶抑制剂卡马替尼和替泊替尼可作为靶向突变。卡马替尼是这篇综述文章的重点，是一种高选择性 MET 抑制剂，被批准用于 METex14 突变 NSCLC 患者。在这篇综述中，我们讨论了 cMET 作为靶点、卡马替尼的药理学、卡马替尼治疗 MET 改变肺癌的关键试验以及毒性概况。我们重点介绍一些正在进行的卡马替尼临床试验，这些试验将其作用扩展到其他患者亚群，特别是那些具有 EGFR 突变的患者，这些患者将 MET 改变作为耐药途径。我们进一步提供了我们对 METex14 NSCLC 管理、测序药物策略和毒性管理的看法。© 2023 Fraser 等人。

Aberrant c-MET (Mesenchymal-Epithelial Transition) signaling contributes to cancer cell development, proliferation, and metastases of non-small cell lung cancer (NSCLC). MET exon 14 (METex14) skipping mutation is noted in approximately 4% of NSCLC cases and is targetable with the recently approved tyrosine kinase inhibitors capmatinib and tepotinib. Capmatinib, the focus of this review article, is a highly selective MET inhibitor approved for use in patients with METex14 mutated NSCLC. In this review, we discuss cMET as a target, the pharmacology of capmatinib, key trials of capmatinib in MET-altered lung cancer, and toxicity profile. We highlight some ongoing capmatinib clinical trials that expand their role to other subsets of patients, especially those with EGFR mutations, who develop MET alterations as a resistance pathway. We further provide our perspective on the management of METex14 NSCLC, strategies for sequencing agents, and toxicity management.© 2023 Fraser et al.