Anti-Mouse CD309 (VEGFR2) – Purified in vivo GOLD™ Functional Grade

Recombinant full-length Mouse VEGFR2 protein

This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.

Liquid

Functional grade preclinical antibodies are manufactured in an animal free facility using in vitro cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.

Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at -80°C. Avoid Repeated Freeze Thaw Cycles.

Research Use Only

2 - 8°C Wet Ice

DC101 activity is directed against VEGFR-2.

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.

VEGFR-2 is widely expressed by vascular endothelial cells, some vascular tumors, carcinomas, malignant melanomas, and lymphomas. Certain leukemia cells express functional VEGFR on the cell surface.

VEGF-A, VEGF-C, and VEGF-D splice isoforms

1. Spratlin J. Curr Oncol Rep. 13(2):97-102. 2011.
2. Wang Z, Shi X, Zhao Y, et al. Biochem Biophys Res Commun. 661:10-20. 2023.
3. Prewett M, Huber J, Li Y, et al. Cancer Res. 59(20):5209-5218. 1999.
4. Patent EP1602668A1: https://patentimages.storage.googleapis.com/10/da/cb/f945064c422659/EP1602668A1.pdf
5. Lee CM, Kim EM, Cheong SJ, et al. J Biomed Mater Res A. 92(4):1510-1517. 2010.
6. Rockwell P, Neufeld G, Glassman A, et al. Mol Cell Differ. 3(1): 91–109. 1995.