EGFR x c-MET

Class

EGFR/c-MET bispecific antibody (full-length human IgG1)

Pathway

simultaneously blocks EGFR and c-MET receptor tyrosine kinase signaling, addressing MET-amplification-driven resistance to EGFR-targeted therapy in NSCLC

EGFR and c-MET are both receptor tyrosine kinases (RTKs) that sit on the cell surface and, when activated by their ligands, initiate intracellular signaling cascades that promote cell growth, survival, and migration. In many epithelial cancers, particularly non-small cell lung cancer (NSCLC), mutations in EGFR make this receptor constitutively active, driving uncontrolled proliferation. Anti-EGFR therapies can effectively suppress this, but tumors frequently develop resistance by amplifying c-MET, which reactivates the same downstream growth pathways through a parallel receptor. A bispecific antibody engineered to bind both EGFR and c-MET simultaneously blocks ligand-driven activation of each receptor and can trigger their removal from the cell surface, addressing tumor growth through two convergent nodes at once. This dual-targeting strategy is designed to treat EGFR-mutant tumors upfront while also suppressing the c-MET-mediated escape route that limits the durability of EGFR-only therapies, and to address tumors that already show combined EGFR/c-MET dysregulation. Beyond NSCLC, this mechanism has relevance in other EGFR-driven or c-MET-amplified carcinomas. Because the molecule is a full antibody rather than a small molecule, it also carries an antibody's characteristic properties, including engagement of immune effector functions to help eliminate targeted cells.