Vascular endothelial growth factor receptor 1 (VEGFR-1), Vascular endothelial growth factor receptor 3 (VEGFR-3) (VEGFR-1, VEGFR-3)

Vascular endothelial growth factor receptor 1 (VEGFR-1, FLT-1) and vascular endothelial growth factor receptor 3 (VEGFR-3, FLT-4) are members of the VEGF receptor family of receptor tyrosine kinases that mediate the effects of VEGF ligands. VEGFR-1 is primarily involved in the regulation of angiogenesis, vascular permeability, and immune cell chemotaxis. VEGFR-3 is crucial in the development and maintenance of the lymphatic vasculature, driving lymphangiogenesis. Both receptors are activated via ligand-induced dimerization and autophosphorylation, triggering downstream cascades that influence cell proliferation, survival, migration, and permeability. Dysregulation and overactivation of these pathways contribute to tumor progression, metastasis, and various vascular pathologies. Pharmacologic inhibition of these receptors is a validated strategy in oncology and other disease areas, but can cause vascular and lymphatic side effects due to their physiological roles[3][4][5][6][7][9].

Other names

FLT-1 (Fms-like tyrosine kinase 1)FLT-4 (Fms-like tyrosine kinase 4)

Inhibition of VEGF binding to VEGFR prevents receptor activation and downstream signaling; Direct inhibition of receptor kinase activity blocks phosphorylation and signal transduction; Decoy receptor action sequesters VEGF ligands away from VEGFRs