Vascular endothelial growth factor receptor 2 (VEGFR-2) and vascular endothelial growth factor receptor 3 (VEGFR-3) (VEGFR-2 (also known as KDR or Flk-1) and VEGFR-3 (also known as FLT4))

Vascular endothelial growth factor receptor 2 (VEGFR-2) and vascular endothelial growth factor receptor 3 (VEGFR-3) are cell-surface receptor tyrosine kinases primarily expressed on vascular and lymphatic endothelial cells, respectively[5][7][4]. VEGFR-2 (KDR/Flk-1) is the principal mediator of VEGF-driven angiogenesis, regulating vascular endothelial cell proliferation, migration, survival, and vascular permeability[3][7][5][4]. VEGFR-3 (FLT4) is central to the process of lymphangiogenesis, controlling lymphatic endothelial cell proliferation and development, and is also involved in embryonic vasculogenesis and some aspects of adult vascular biology[7][4][1][9]. Both receptors are activated by their respective VEGF ligands, which induce receptor dimerization and auto-phosphorylation, triggering multiple downstream signaling cascades, notably the MAPK and PI3K-Akt pathways. Aberrant activation of VEGFR-2/VEGFR-3 signaling is implicated in tumor growth, metastasis, chronic inflammation, and vascular/lymphatic malformations, making them key therapeutic targets for anti-angiogenic and anti-lymphangiogenic therapies[4][5][7].

Other names

KDRFlk-1FLT4

Inhibition of receptor tyrosine kinase activity Blockade of downstream VEGF-driven angiogenic and lymphangiogenic signaling Suppression of endothelial cell proliferation, migration, and vessel formation