Anti-Human VEGF-A (Ranibizumab) - 50 mg

All|Recombinant Antibodies>Biosimilar Recombinant Antibodies|Primary Monoclonal Antibodies

2 - 8°C Wet Ice

Vascular endothelial growth factor (VEGF), a potent proangiogenic cytokine1, is the key signalused by oxygen-hungry cells to promote the growth of blood vessels. VEGF binds to specializedreceptors on the surfaces of endothelial cells and directs them to build new vessels2. VEGF arecrucial regulators of vascular development during embryogenesis (vasculogenesis) and blood-vessel formation in the adult (angiogenesis). Abnormal VEGF function is associated withinflammatory diseases including atherosclerosis and hyperthyroidism3, 4, 5, 6. VEGF-A is a memberof 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 variousophthalmic conditions, including age-related macular degeneration8. Ranibizumab is a high-affinity recombinant, humanized antibody that neutralizes all isoforms ofVEGF-A8, 9. Ranibizumab was derived from a murine monoclonal anti-VEGF antibody10andconsists of a nonbinding human sequence and a high affinity murine binding epitope11. Wheninjected intravitreously, ranibizumab can penetrate the internal limiting membrane and access thesubretinal space. Ranibizumab reduces the proliferation of endothelial cells as well as vascularpermeability and formation of new blood vessels by preventing VEGF-A from interacting withits receptors on the endothelial cell surface9. Ranibizumab is also able to inhibit humanumbilical vein endothelial cell proliferation in vitro. Ranibizumab does not bind to mouseVEGF-A in vitro by Western blot, nor does it have a measurable biological effect afterintraperitoneal or intravitreal injection in oxygen-induced-retinopathy mouse models12.Intravitreal injections of ranibizumab in cynomolgus monkeys reduces choroidalneovascularization11. Ranibizumab is also known as RhuFab V2 in the literature10.

≥ 5.0 mg/ml

VEGF-A is a secreted protein produced by diverse cell types, includingaortic vascular smooth muscle cells, keratinocytes, macrophages, and many tumor cells.Expression begins during embryogenesis and declines after birth. VEGF-A expression isrelatively low in most adult organs, except for the brain choroid plexus, lung alveoli, kidneyglomeruli, and heart vascular beds. VEGF-A is also up-regulated during the development of theendocrine corpus luteum in pregnancy, wound healing, tissue repair, as well as during disease-related neovascularization.