ABSTRACT
Introduction ................................................................................................ 229 Inhibition of intracellular VEGF expression ......................................... 232 Inhibition of extracellular VEGF ............................................................. 232
Pegaptanib sodium (Macugen, Eyetech/OSI Pharmaceuticals).. 232 Ranibizumab (Lucentis, Genentech, Inc.) ................................. 236 Intravenous (systemic) bevacizumab (Avastin®, Genentech, Inc.) ......................................................... 241 Intravitreal bevacizumab (Avastin, Genentech, Inc.).............. 243 VEGF-Trap (Regeneron Pharmaceuticals) ................................ 247
Inhibition of VEGF signaling at target cells.......................................... 247 Summary ..................................................................................................... 248 References .................................................................................................. 249
Introduction VEGF has been implicated as the major stimulus responsible for ocular neovascularization in diseases such as age-related macular degeneration (AMD), diabetic retinopathy (DR), retinopathy of prematurity (ROP), and neovascular glaucoma.1-4 VEGF may also be responsible for the macular edema associated with a variety of ocular diseases such as AMD, DR, vein occlusions, post-operative cystoid macular edema (CME), and uveitis.5 By
promoting vascular permeability, inflammation, and neovascularization, VEGF causes vision loss by irreversibly damaging the retina. The clinician observes this retinal damage as the formation of macular scars, retinal atrophy, traction retinal detachments, and/or intractable glaucoma, all likely resulting from the pathologic expression of VEGF. One approach to treating these blinding diseases is to inhibit VEGF.
