VEGF-A, PlGF, VEGF-B

The **Vascular endothelial growth factor (VEGF) family** consists of secreted glycoproteins critical for the regulation of angiogenesis and vascular permeability. **VEGF-A** is the prototypical member, essential for blood vessel formation and frequently termed simply "VEGF" in the literature. **Placenta growth factor (PlGF)** is primarily active in vasculogenesis, tissue repair, and pathological angiogenesis, especially during ischemia or inflammation. **VEGF-B** has a specialized role in embryonic myocardial angiogenesis and is also implicated in endothelial cell survival. These growth factors exert their effects by binding to the receptor tyrosine kinase **VEGFR-1** (FLT1) on endothelial cells; VEGF-A can also signal through **VEGFR-2 (KDR/Flk-1)**—the main driver of mitogenic and permeability effects. All three are targets for anti-angiogenic drugs in cancer and ophthalmology, and their circulating levels serve as biomarkers in some disease settings[2][7][1][4][5]. The grouping as "VEGF-A, PlGF, VEGF-B" is non-canonical—they are distinct proteins that sometimes overlap in function and therapeutics, but are not a single molecular target. **Note**: For best accuracy and structured data downstream, each VEGF ligand should be handled as an individual target.

Other names

VEGFVEGFAVascular permeability factorPGFVEGFB

Inhibition of ligand-receptor binding to VEGFR-1 and/or VEGFR-2, preventing downstream angiogenic signaling Neutralization of growth factor by antibody or fusion protein (trapping ligand) Inhibition of endothelial cell proliferation, migration, and new vessel formation