Is capmatinib not an anti-angiogenic drug?

Capmatinib (Capmatinib), a highly selective and potent oral small molecule MET (methionine) inhibitor, has shown significant inhibitory effects on the methionine pathway in in vivo and in vitro experiments, and has demonstrated anti-tumor activity in the treatment of non-small cell lung cancer. Especially in the GEOMETRY Mono-1 study, capmatinib showed a higher treatment response rate for patients with stage IV non-small cell lung cancer with MET exon 14 skipping mutations, especially in patients receiving first-line treatment. This finding emphasizes the importance of detecting this biomarker at the time of diagnosis.

However, it should be clear that capmatinib does not fall into the category of anti-angiogenic drugs. Anti-angiogenic drugs are drugs specifically designed to inhibit the formation of new blood vessels in tumors by cutting off the blood supply that tumors need to grow and spread. This class of drugs inhibits the formation of new blood vessels by interfering with the interaction between tumor cells and vascular endothelial cells.

In contrast, capmatinib has a completely different mechanism of action. It interferes with the proliferation and spread of cancer cells mainly by inhibiting the activity of tyrosine kinases. Tyrosine kinases play a key role in tumor cell proliferation and invasion. Capmatinib can selectively inhibit overactive tyrosine kinases on tumor cells, thereby effectively preventing further growth and spread of cancer cells.

In summary, although capmatinib performs well in anti-tumor therapy, it does not act through anti-angiogenesis. Understanding this is critical to correctly understanding the therapeutic rationale and scope of application of capmatinib.