Anti-Mouse CD309 (VEGFR2) - Purified <i>in vivo </i>GOLD™ Functional Grade (V173-GRP)

Vascular endothelial growth factors (VEGF) and VEGF receptors (VEGFR) play an essential role in angiogenesis1. There are three VEGFRs: VEGFR-1, VEGFR-2, and VEGFR-3. VEGFR-1 and VEGFR-2 are responsible for angiogenesis, and VEGFR-3 affects lymphogenesis. In the pathogenesis of diseases including diabetes mellitus, rheumatoid arthritis, and cancer, new blood vessel formation is highjacked. Changes at the VEGF/VEGFR-2 axis are particularly potent at allowing VEGF-induced proliferation, migration, and vascular endothelial cell differentiation during tumor angiogenesis. Additionally, VEGFR-2 is upregulated in tumor vascular endothelial cells, and VEGF levels are associated with poor prognosis and resistance to chemotherapy. Consequently, the VEGF/VEGFR axis is a prime anti-cancer target. DC101 greatly reduces melanoma tumor growth and cell proliferation in murine mouse models without adverse effects as well as promotes tumor vessel normalization2. Additionally, DC101 therapy enhances immune cell penetration of melanoma cells by increasing the proportion of CD19+ B cells, CD11c+ dendritic cells, and CD3+ and CD8+ T cells. DC101 treatment also increases expression of PD-1 and PD-L1 in CD45+ immune cells and tumors. Additionally, DC101 directly inhibits angiogenesis in vivo, and, in tumors, reduces xenograft tumor growth, decreases endothelial cells and microvessel density, and increases tumor cell apoptosis3. DC101 binds to an extracellular, ligand-binding domain on the amino-terminal of VEGFR-2, thereby blocking ligand binding and preventing VEGF165-induced receptor phosphorylation4. DC101 has been used in Cy5.5-, FITC, and HYNIC-labeled chitosan conjugates to study VEGFR-2 expression in ischemia5.