title: [Ranibizumab versus bevacizumab. Pharmacological considerations].
abstract: Bevacizumab is able to cross ocular barriers when administered through the intravitreal route and to generate plasma concentrations with an inhibitory effect on plasma vascular endothelial growth factor (VEGF). Consequently, systemic effects cannot be ruled out. The fact that bevacizumab is a full-length IgG explains this phenomenon through the participation of FcRn receptors, whose binding-like that of all IgGs-implies their internalization, transfer to the cell membrane, and externalization to the intracellular space and blood. This process occurs in all tissues with cells expressing this type of receptor, such as the eye. Moreover, because of the absence of a specific formulation for intravitreal administration, an intravenous formulation must be manipulated, generating large-sized aggregates, leading to potential problems of the solution's sterility and reducing the pharmacological effect. Ranibizumab is not a full-length IgG but is rather a variable IgG fraction with anti-VEGF activity. Because of the absence of a constant fraction in its structure, this drug cannot bind to the FcRn receptor and, as a result, cannot be transported to the blood. Consequently, its systemic bioavailability after intravitreal administration is nil, thus avoiding effects in parts of the body other than the eye. Moreover, the formulation is specifically prepared for intraocular administration, avoiding problems due to manipulation. The experience gained with these drugs allows the differences in their efficacy and tolerability to be transferred to daily practice.
authors: Servicio de Farmacología Clínica, Clínica Universidad de Navarra, Pamplona, España; Sociedad Española de Retina y Vítreo (SERV). Electronic address: jrazanza@unav.es.
authors: J R
authors: JR
authors: Azanza Perea
authors: A
authors: A
authors: García Layana
mesh_terms: D020533:Angiogenesis Inhibitors / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D000068258:Bevacizumab; D001682:Biological Availability; D001692:Biological Transport; D020256:Choroidal Neovascularization / Q000188:drug therapy; D002986:Clinical Trials as Topic; D006470:Hemorrhage / Q000139:chemically induced; D015395:Histocompatibility Antigens Class I / Q000378:metabolism; D006801:Humans; D058449:Intravitreal Injections; D008268:Macular Degeneration / Q000188:drug therapy; D008269:Macular Edema / Q000188:drug therapy; D015201:Meta-Analysis as Topic; D015337:Multicenter Studies as Topic; D000069579:Ranibizumab; D011961:Receptors, Fc / Q000378:metabolism; D017452:Receptors, IgG / Q000378:metabolism; D013923:Thromboembolism / Q000139:chemically induced; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014822:Vitreous Body / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D015395:Histocompatibility Antigens Class I; D011961:Receptors, Fc; D017452:Receptors, IgG; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; C100688:Fc receptor, neonatal; D000069579:Ranibizumab