Bevacizumab contains human framework regions with antigen binding regions of a humanised murine antibody that binds to VEGF. Bevacizumab is produced by recombinant DNA technology in a Chinese hamster ovary mammalian cell expression system in a nutrient medium containing the antibiotic gentamicin and is purified by a process that includes specific viral inactivation and removal steps. Bevacizumab binds VEGF and prevents the interaction of VEGF to its receptors (Flt-1 and KDR) on the surface of endothelial cells. This prevents blood vessel proliferation and in response retardation of metastatic tumor growth occurs.

Bevacizumab is an antineoplastic agent and prevents or reduces the formation of blood vessels (angiogenesis) thereby preventing or reducing metatstatic disease progressing. Bevacizumab binds VEGF and prevents vascular endothelial growth and endothelial cell proliferation.

Most likely removed by opsonization via the reticuloendothelial system when bound to endothelial cells, or by human antimurine antibody production

Category C in pregnancy. No studies on lactating patients: recommended to discontinue the drug or discontinue lactation. No extensive studies in pediatrics. In geriatrics: increased risk of proteinuria, arterial thromboembolic events, as well as GI bleeding and sepsis among others.

Velcheti V, Viswanathan A, Govindan R: The proportion of patients with metastatic non-small cell lung cancer potentially eligible for treatment with bevacizumab: a single institutional survey. J Thorac Oncol. 2006 Jun;1(5):501. [PubMed:17409907]