Vascular endothelial growth factor receptor‑2 (VEGFR-2)

Vascular endothelial growth factor receptor‑2 (VEGFR-2) is a transmembrane receptor tyrosine kinase primarily expressed on vascular endothelial and lymphatic endothelial cells, where it binds vascular endothelial growth factor (VEGF) ligands, particularly VEGF-A, VEGF-C, and VEGF-D, to mediate critical biological processes including angiogenesis, vasculogenesis, and vascular permeability[1][3][7]. VEGFR-2 plays a fundamental role in embryonic development and adult vascular homeostasis, and its activation leads to endothelial cell proliferation, migration, and survival, as well as growth and maintenance of blood and lymphatic vessels[1][3][7]. Dysregulation and overactivation of VEGFR-2-mediated signaling contribute significantly to tumorigenesis through the promotion of tumor angiogenesis, making VEGFR-2 a validated and clinically important therapeutic target in oncology[2][4][6]. Multiple anti-cancer drugs—including monoclonal antibodies (e.g., ramucirumab) and small-molecule inhibitors (e.g., axitinib, cabozantinib)—have been developed and approved to block VEGFR-2 activity and thereby inhibit tumor blood vessel growth[4][6]. Pharmacodynamic biomarkers such as VEGFR-2 expression levels and circulating VEGF-A are under investigation for patient selection and therapy monitoring, though anti-angiogenic therapies are associated with notable risks such as hypertension, proteinuria, bleeding, and impaired wound healing[4][6].

Other names

Kinase insert domain receptor (KDR)Fetal liver kinase 1 (Flk-1, in mouse)CD309

Inhibition of VEGFR-2 ligand binding (antibody blockade); Inhibition of VEGFR-2 tyrosine kinase activity (small molecule tyrosine kinase inhibitors); Inhibition of downstream angiogenic signaling pathways