2005 Association for Research in Vision and Ophthalmology Meeting

(455/B429) A VEGF121-Gelonin Fusion Protein
(VEGF121/rGel) Induces Regression of Subretinal and Choroidal Neovascularization (CNV)

H.Akiyama1, R.L. Silva1, S.Kachi1, N.Umeda1, S.Aslam1, S.F. Hackett1, K.Mohamedali2, M.G. Rosenblum2, P.A.

Campochiaro1. 1Ophthalmology, Wilmer Eye Inst, Baltimore, MD; 2MD Anderson Cancer Institute, Houston, TX.

Purpose: Intravascularly injected VEGF121/rGel selectively binds and damages tumor vessels. In this study, the effect of intravascular or intravitreous injection of VEGF121/rGel was tested in two models of ocular neovascularization (NV).

Methods: One week after rupture of Bruch's membrane the baseline amount of CNV was measured in a group of mice and remaining mice received injection of VEGF121/rGel or rGel and after one week the amount of CNV was measured. A similar protocol was used in rho/VEGF mice. VEGF121/rGel was localized in ocular sections by immunohistochemistry.

Results: In rho/VEGF mice, intravitreous injections of 0.005 mg VEGF121/rGel starting at postnatal day (P) 21 resulted in a significant reduction in total area of subretinal NV per retina at P25 compared with vehicle-injected mice. In mice with established CNV one week after rupture of Bruch's membrane, tail vein injections of 45 mg/kg of VEGF121/rGel every two days for 1 week or a single intravitreous injection of 0.005 mg of VEGF121/rGel resulted in significant reductions in CNV area at rupture sites compared with the baseline area before treatment. After intravascular or intravitreous injections, VEGF121/rGel was localized to CNV lesions with no staining of normal retinal or choroidal vessels.

Conclusions: These data indicate that after either intravascular or intravitreous injections of VEGF121/rGel, it localizes to new vessels in the eye and causes regression of the neovascularization.
Vascular targeting with VEGF121/rGel provides a new approach for inducing regression of ocular NV.

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