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Y. Saishin, Y. Saishin, K. Takahashi, R. Lima Silva, D. Hylton, J.S. Rudge, S.J. Wiegand, P.A. Campochiaro; VEGF-TRAPR1R2 Suppresses Choroidal Neovascularization(CNV) and VEGF-Induced Breakdown of the Blood-Retinal Barrier(BRB) . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3920.
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Purpose: VEGF-TRAPR1R2 is a fusion protein that combines ligand binding elements taken from the extracellular domains of VEGF receptors 1 and 2 fused to the Fc portion of IgG1. It is a specific inhibitor of VEGF. The purpose of this study was to investigate the effect of VEGF-TRAPR1R2 in models of CNV, subretinal NV, and breakdown of the BRB. Methods: : The effect of subcutaneous injections of VEGF-TRAPR1R2 was tested in mice with laser-induced rupture of Bruch's membrane, transgenic mice that express VEGF in photoreceptors, and in two models of VEGF-induced breakdown of the BRB. Results: Subcutaneous injections or a single intravitreous injection of VEGF-TRAPR1R2 strongly suppressed CNV in mice with laser-induced rupture of Bruch's membrane. Subcutaneous injections of VEGF-TRAPR1R2 also significantly inhibited subretinal NV in rhodopsin/VEGF transgenic mice, and significantly reduced BRB breakdown in mice in which recombinant VEGF was injected into the vitreous cavity and in double transgenic mice with doxycycline-induced expression of VEGF in the retina. Conclusions: These data confirm that VEGF is a critical stimulus for the development of CNV and indicate that VEGF-TRAPR1R2 may provide a new agent for treatment of patients with CNV and diabetic macular edema.
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