Epidermal growth factor receptor (EGFR) and Mesenchymal-epithelial transition factor (MET) (EGFR/MET)

The Epidermal Growth Factor Receptor (EGFR) and Mesenchymal-epithelial transition factor (MET) are transmembrane receptor tyrosine kinases that regulate essential cellular processes including proliferation, survival, and migration [1, 2]. EGFR and MET signaling pathways are frequently dysregulated in various cancers, most notably non-small cell lung cancer (NSCLC), where they drive tumor progression and contribute to therapeutic resistance [3, 4]. Amivantamab is a fully human bispecific antibody that targets the extracellular domains of both EGFR and MET [3]. Its mechanism of action involves blocking ligand binding, inducing receptor internalization and degradation, and promoting immune-mediated tumor cell death through antibody-dependent cellular cytotoxicity (ADCC) and trogocytosis [4, 5]. By simultaneously inhibiting these two pathways, Amivantamab addresses resistance mechanisms that often emerge during treatment with single-target EGFR inhibitors [3]. This therapeutic strategy is specifically indicated for patients with NSCLC harboring EGFR exon 20 insertion mutations, providing a targeted option where conventional therapies have limited efficacy [5].

Other names

ErbB-1HER1c-MetHepatocyte growth factor receptorHGFRProto-oncogene c-Met

Amivantamab is a bispecific antibody that binds to the extracellular domains of EGFR and MET. It blocks ligand binding to both receptors, triggers receptor internalization and lysosomal degradation, and facilitates immune-mediated tumor cell killing through antibody-dependent cellular cytotoxicity (ADCC) and trogocytosis.