Age-related macular degeneration (AMD) is the major cause of blindness for people over 60. In the wet form of AMD, VEGF is a major stimulator of choroidal neovascularization (CNV) in the posterior pole of the eye. We used a model previously developed in the lab to examine the efficacy of AG13764 and AG13711 (Pfizer, antiangiogenic molecules) to reverse VEGF?induced CNV. These compounds were injected intraperitoneally or intraocularly over a two week period starting at 6 weeks after AAV-VEGF injection. FITC-dextran whole-mounts of RPE-choroid-sclera were prepared after the animals were sacrificed. CNV area was quantified using Neurolucida. In 12/16 animals, the level of CNV was reduced by 16% to 100%, following intravitreal injections of AG13764. In 11/14 animals, the level of CNV was also reduced by 16% to 100%, following intravitreal injection of AG13711. In two groups of IP injected animals (5 per group), AG13764 vs control, the mean CNV level was reduced by 35% (p< 0.04) in the treated eye. This reduction in CNV area is an underestimate since it does not reflect changes in volume. These data indicate that both Pfizer compounds reduce blood vessel proliferation in our AAV-VEGF model of CNV.
| Wang, F E; Shi, G; Niesman, M R et al. (2007) Receptor tyrosine kinase inhibitors AG013764 and AG013711 reduce choroidal neovascularization in rat eye. Exp Eye Res 84:922-33 |
