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Effects of Thalidomide and Related Metabolites in a Mouse Corneal Model of Neovascularization

Authors
Journal
Experimental Eye Research
0014-4835
Publisher
Elsevier
Publication Date
Volume
64
Issue
6
Identifiers
DOI: 10.1006/exer.1997.0292
Keywords
  • Thalidomide
  • Angiogenesis
  • Neovascularization
  • Tumor Necrosis Factor-Alpha
  • Growth Factor
  • Cornea

Abstract

Abstract Thalidomide, when administered orally, is an inhibitor of angiogenesis in the basic fibroblast growth factor (bFGF)-induced rabbit cornea micropocket assay. We now show in the mouse that thalidomide given intraperitoneally but not orally significantly inhibits bFGF-induced and vascular endothelial growth factor (VEGF)-induced corneal neovascularization. We further demonstrate that this inhibition is independent from thalidomide's ability to suppress tumor necrosis factor-alpha (TNF-alpha) production. Experiments examining thalidomide's enantiomers reveal that the S(-)-enantiomer has the strongest antiangiogenic activity in VEGF-induced and bFGF-induced corneal neovascularization. Structure activity studies suggest that thalidomide's anti-angiogenic activity is related to the open ring metabolites resulting from hydrolysis. Together these data support a correlation between thalidomide's antiangiogenic and teratogenic activities.

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