Epidermal growth factor receptor and Hepatocyte growth factor receptor (EGFR/c-Met)

The target "EGFR – HS-20117" refers to the dual inhibition of the Epidermal Growth Factor Receptor (EGFR) and the Hepatocyte Growth Factor Receptor (c-Met, or MET) by the bispecific antibody HS-20117 (also known as PM1080). EGFR and c-Met are transmembrane receptor tyrosine kinases that regulate essential cellular processes including growth, survival, and migration. In many malignancies, particularly non-small cell lung cancer (NSCLC), these receptors are frequently mutated or overexpressed, driving tumor progression and metastasis. Notably, c-Met activation is a common mechanism of resistance to EGFR-targeted tyrosine kinase inhibitors, making dual blockade a promising therapeutic strategy. By simultaneously targeting both receptors, HS-20117 is designed to provide a more potent inhibition of tumor signaling and bypass resistance pathways. This therapeutic approach is currently being investigated in clinical trials for patients with advanced solid tumors, including those harboring EGFR exon 20 insertion mutations. Furthermore, HS-20117 is being utilized as the targeting component in the development of novel antibody-drug conjugates (ADCs) to deliver cytotoxic payloads directly to tumor cells.

Other names

EGFRc-MetMETERBB1HER1HGFREpidermal growth factor receptorHepatocyte growth factor receptorProto-oncogene c-MetEGFR/METEGFR-cMet

Simultaneous binding and inhibition of the EGFR and c-Met receptors, leading to the blockade of downstream oncogenic signaling pathways such as MAPK and PI3K/Akt, and potentially inducing antibody-dependent cellular cytotoxicity (ADCC) and receptor degradation.