Human and Cynomolgus Monkey Vascular Endothelial Growth Factor A (VEGF-A) is a member of the vascular endothelial growth factor (VEGF) family, which includes VEGF-A, VEGF-B, VEGF-C, VEGF-D, and placental growth factor (PlGF)—key regulators of angiogenesis, vascular permeability, and endothelial cell growth. In both humans (Homo sapiens) and cynomolgus monkeys (Macaca fascicularis), the VEGF-A protein is identical at the amino acid level, reflecting strong evolutionary conservation and similar biological functions in these primate species. VEGF-A is produced by many cell types including endothelial cells, macrophages, fibroblasts, epithelial cells, smooth muscle cells, and tumor cells, particularly in response to hypoxia, inflammation, and tissue injury. VEGF-A exerts its biological effects primarily through binding to VEGF receptor-1 (VEGFR-1/Flt-1) and VEGF receptor-2 (VEGFR-2/KDR) on endothelial cells, activating intracellular signaling pathways such as MAPK/ERK, PI3K/AKT, and PLCγ, which promote endothelial cell proliferation, migration, vascular permeability, and new blood vessel formation. In primates, VEGF-A plays essential roles in embryonic vascular development, wound healing, tissue regeneration, and reproductive physiology, including placental vascularization during pregnancy. Dysregulated VEGF-A expression is strongly associated with tumor angiogenesis, diabetic retinopathy, age-related macular degeneration, and other vascular diseases. Because cynomolgus monkeys are widely used as preclinical models for human vascular biology and therapeutic development, the identical VEGF-A sequence between these species supports their use in translational studies of angiogenesis and evaluation of anti-VEGF therapies such as monoclonal antibodies and receptor inhibitors used in cancer and ophthalmic diseases.