Abstract
Purpose: :
To investigate the effects of tivozanib, an inhibitor of vascular endothelial growth factor receptors, on experimental choroidal neovascularization (CNV) model.
Methods: :
C57BL/6 mice were treated with tivozanib (1 mg/kg/day) or vehicle at the onset (day 0) of study. Experimental CNV was induced by laser photocoagulation the following day. In other groups of mice, tivozanib or vehicle treatment was started 7 days after the laser application to determine the effect of the drug on established CNV. After 14 days, the extent of CNV was assessed from choroidal flat mounts perfused with fluorescein-labeled dextran. Immunofluorescence staining with isolectin IB4 was also used to quantify the CNV lesions.
Results: :
Tivozanib suppressed the development of CNV lesions, reducing the area by 80.7 % compared to vehicle-treatment (p < 0.001). Tivozanib caused a significant regression of established CNV, reducing the area by 67.7 % compared to vehicle-treatment (p < 0.001). Isolectin IB4-labeled area was smaller in the tivozanib-treated mice compared to the vehicle-treatment (p < 0.001).
Conclusions: :
Tivozanib effectively inhibits the progression of CNV in mice CNV model. These results suggest that tivozanib could constitute a therapeutic alternative for the treatment of neovascular AMD.
Keywords: choroid: neovascularization • vascular endothelial growth factor • age-related macular degeneration