VEGF₁₆₄ is one of many splice variants of the VEGF-A gene, and is one amino acid shorter than its human counterpart, VEGF₁₆₅ (1, 2). VEGF₁₆₄ is produced by a number of cells including endothelial cells, macrophages, and T cells (1, 2). VEGF₁₆₄ is involved in angiogenesis, vascular endothelial cell survival, growth, migration, and vascular permeability (1,2). Gene expression is induced by hypoxia, inflammatory cytokines, and oncogenes (1, 2). VEGF₁₆₄ binds to heparan sulfate and is retained on the cell surface and in the extracellular matrix (1-3). VEGFR1 and VEGFR2 are the receptor tyrosine kinases for VEGF₁₆₄ (2). NRP-1 and NRP-2 may function as co-receptors and enhance VEGFR2 signaling (2-3). Binding of VEGF₁₆₄ to VEGFR1 and VEGFR2 leads to activation of the PI3K/AKT, p38 MAPK, FAK, and Paxillin (2).

Less than 0.01 ng endotoxin/1 μg rVEGF₁₆₄.

>98% as determined by SDS-PAGE of 6 μg reduced (+) and non-reduced (-) recombinant rVEGF₁₆₄. All lots are greater than 98% pure.

Recombinant rat VEGF₁₆₄ (rVEGF₁₆₄) Ala27-Arg190 (Accession #NP_001103803) was expressed in human 293 cells at Cell Signaling Technology.

The bioactivity of recombinant rVEGF₁₆₄ was determined in a cell proliferation assay using HUVEC. The ED₅₀ of each lot is between 1-5 ng/ml.