Vascular endothelial growth factor A isoform 165 (VEGF-A165) (VEGF-A165)

Vascular endothelial growth factor A isoform 165 (VEGF-A165) is the predominant and most biologically active splice variant of the VEGF-A protein [Source: UniProt P15692]. It plays a critical role in both physiological and pathological angiogenesis by stimulating the growth, migration, and survival of vascular endothelial cells [Source: PubMed PMID: 15159444]. VEGF-A165 exerts its effects primarily through binding to the tyrosine kinase receptors VEGFR-1 (Flt-1) and VEGFR-2 (KDR/Flk-1), as well as the co-receptor neuropilin-1 [Source: UniProt P15692]. In many cancers, tumor cells overexpress VEGF-A165 to induce the formation of a blood supply necessary for tumor expansion and metastasis [Source: PubMed PMID: 15159444]. Additionally, it is a major driver of pathological neovascularization in ocular diseases such as wet age-related macular degeneration and diabetic retinopathy [Source: StatPearls, VEGF Inhibitors]. Therapeutic interventions, including monoclonal antibodies like bevacizumab and decoy receptors like aflibercept, target VEGF-A165 to inhibit its pro-angiogenic signaling and treat these conditions [Source: DrugBank DB00112].

Other names

VEGF165Vascular permeability factorVPFVEGF-A

Neutralization of the VEGF-A165 protein to prevent its binding to VEGFR-1 and VEGFR-2 receptors, thereby inhibiting downstream signaling pathways that promote angiogenesis and vascular permeability [Source: DrugBank DB00112, StatPearls].