Choroidal Rupture Medication

Updated: Mar 08, 2016
  • Author: Lihteh Wu, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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Medication

Anti-VEGF agents

Class Summary

Vascular endothelial growth factor (VEGF) is essential for angiogenesis. Inhibitors of VEGF that bind to the receptor of VEGF-A isoforms prevent its interaction with Flt-1 and KDR on the endothelial cell surface, and therefore decreases cell proliferation and new blood vessel formation.

Ranibizumab (Lucentis)

Recombinant humanized IgG1-kappa isotype monoclonal antibody fragment designed for intraocular use. Indicated for neovascular (wet) age-related macular degeneration (ARMD). In clinical trials, about one third of patients had improved vision at 12 mo that was maintained by monthly injections. Binds to VEGF-A, including biologically active, cleaved form (ie, (VEGF110). VEGF-A has been shown to cause neovascularization and leakage in ocular angiogenesis models and is thought to contribute to ARMD disease progression. Binding VEGF-A prevents interaction with its receptors (ie, VEGFR1, VEGFR2) on surface of endothelial cells, thereby reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation.

Pegaptanib (Macugen)

Selective vascular endothelial growth factor (VEGF) antagonist that promotes vision stability and reduces visual-acuity loss and progression to legal blindness. VEGF causes angiogenesis and increases vascular permeability and inflammation, all which contribute to neovascularization in age-related wet macular degeneration.

Bevacizumab (Avastin)

Murine derived monoclonal antibody that inhibits angiogenesis by targeting and inhibiting vascular endothelial growth factor (VEGF). Used investigationally for ARMD secondary to choroidal neovascularization.

Aflibercept (Eylea)

Fusion protein of key domains from human VEGF receptors 1 (VEGFR1) and 2 (VEGFR2) with human IgGFc designed for intraocular use. Indicated for neovascular (wet) age-related macular degeneration (ARMD) and macular edema secondary to central retinal vein occlusion. Binds to VEGF-A, including biologically active, cleaved form (ie, (VEGF110) and placental growth factor. VEGF-A has been shown to cause neovascularization and leakage in ocular angiogenesis models and is thought to contribute to ARMD disease progression. Binding VEGF-A prevents interaction with its receptors (ie, VEGFR1, VEGFR2) on surface of endothelial cells, thereby reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation.