Anti-Mouse CD309 (VEGFR2) – DyLight® 594

Recombinant full-length Mouse VEGFR2 protein

This DyLight® 594 conjugate is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative.

Liquid

This DyLight® 594 conjugate is stable when stored at 2-8°C. Do not freeze.

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.