THALIDOMIDE INHIBITS CORNEAL ANGIOGENESIS INDUCED BY VASCULAR ENDOTHELIAL GROWTH-FACTOR

Background: Ocular diseases caused by neovascularization are among the leading causes of blindness. No specific pharmacological treatment is available. Among potential drugs, thalidomide deserves special intere st since a wide body of clinical experience exists. However, its antia ngiogenic effect is controversial. We therefore investigated the effec t of thalidomide on corneal angiogenesis induced by vascular endotheli al growth factor (VEGF), which has a special role among angiogenic gro wth factors. Methods: Corneal neovascularization was induced in NZW ra bbits by an intrastromal pellet loaded with 500 or 750 ng VEGF. Animal s received two daily feedings of 200 mg/kg thalidomide. Results: Signi ficant inhibition of corneal angiogenesis (P<0.0001) was caused by the teratogenic dose of thalidomide after the 5th day of treatment and pe rsisted for more than 16 days. No obvious side effects were recorded. Conclusions: Thalidomide has a significant antiangiogenic effect again st VEGF-induced neovasclar growth. Together with earlier findings this observation indicates that the drug inhibits two angiogenic pathways which are mediated through integrin adhesion molecules.