Anti-Human VEGF-A (Brolucizumab) (V210-GRP)

Vascular endothelial growth factor (VEGF), a potent proangiogenic cytokine1, is the key signal used by oxygen-hungry cells to promote the growth of blood vessels. VEGF binds to specialized receptors on the surfaces of endothelial cells and directs them to build new vessels2. VEGF are crucial regulators of vascular development during embryogenesis (vasculogenesis) and blood-vessel formation in the adult (angiogenesis). Abnormal VEGF function is associated with inflammatory diseases including atherosclerosis and hyperthyroidism3,4,5,6. VEGF-A is a member of the VEGF gene family, and several isoforms can be generated by alternative splicing7. Additionally, VEGF-A is a major mediator of angiogenesis and plays a key role in various ophthalmic conditions, including age-related macular degeneration8. RTH-258 (Brolucizumab) is a low molecular weight, humanized single-chain variable antibody fragment that inhibits the three major isoforms of VEGF-A9. Brolucizumab prevents the interaction of VEGF-A with its receptors VEGFR-1 and VEGFR-2, thereby suppressing endothelial cell proliferation, neovascularization, and vascular permeability. Brolucizumab was developed for the treatment of wet age-related macular degeneration and macular edema9. It is formerly known as ESBA100810.