May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Topically Applied Src Kinase/VEGFR Prodrug Reduces Retinal Vascular Permeability
Author Affiliations & Notes
  • E. Aguilar
    Cell Biology, The Scripps Research Institute, La Jolla, CA
  • E.L. Scheppke
    Cell Biology, The Scripps Research Institute, La Jolla, CA
  • M. Dorrell
    Cell Biology, The Scripps Research Institute, La Jolla, CA
  • J. Hood
    TargeGen, Inc., La Jolla, CA
  • R. Soll
    TargeGen, Inc., La Jolla, CA
  • S. Yee
    TargeGen, Inc., La Jolla, CA
  • M. Friedlander
    Cell Biology, The Scripps Research Institute, La Jolla, CA
  • Footnotes
    Commercial Relationships  E. Aguilar, TargeGen, Inc., F; E.L. Scheppke, TargeGen, Inc., F; M. Dorrell, None; J. Hood, TargeGen, Inc., E; R. Soll, TargeGen, Inc., E; S. Yee, TargeGen, Inc., E; M. Friedlander, TargeGen, Inc., F.
  • Footnotes
    Support  EY11254
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 136. doi:
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      E. Aguilar, E.L. Scheppke, M. Dorrell, J. Hood, R. Soll, S. Yee, M. Friedlander; Topically Applied Src Kinase/VEGFR Prodrug Reduces Retinal Vascular Permeability . Invest. Ophthalmol. Vis. Sci. 2006;47(13):136.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To determine the efficacy of topically applied src kinase/VEGFR antagonists at reducing retinal vascular permeability. Vascular leakage and edema in ischemic retinal diseases is caused, in part, by local up–regulation of Vascular Endothelial Growth Factor (VEGF). VEGF–induced vascular leakage is dependent on both VEGFR activity and the cytoplasmic protein kinase members of the src proto–oncogene family. Inhibitors of src kinase activity prevent VEGF–induced vascular leakage. We hypothesized that it is possible to use a targeted, non–invasively delivered agent to specifically block the activity of VEGF.

Methods: : Balb/cByJ mice were treated with a single dose of a topically applied ATP–competitive multi–targeted tyrosine kinase prodrug (TG100801, 10 ul @ 10 mg/ml) in an HPMC vehicle or with vehicle alone. Based on its activity against kinases known to regulate vascular barrier function including VEGFR, Src, and Yes, we hypothesized that TG100801 should inhibit VEGF–mediated retinal vascular permeability. After two hours, eyes were flushed with PBS and single intravitreal injections of PBS (0.3 ul, left eye) and VEGF (100 ng/ul, 0.3 ul, right eye) were administered to each animal in both groups. One hour after PBS/VEGF injections, a solution of Evans Blue (20 mg/ml, 150 ul) was injected into the tail vein of each mouse. Four hours later, blood samples were drawn and the animals sacrificed. Retinas were dissected and dissolved in formamide. Retinal vascular leak was assessed by quantifying the amount of Evans Blue in the retina spectrophotometrically and normalizing it to the amount of Evans Blue circulating in the blood.

Results: : In eyes receiving HPMC–vehicle eyedrops, VEGF–injection induced a 3.3–fold increase in retinal vascular leak over PBS–injection. In eyes receiving TG100801 eyedrops, the increase in retinal vascular leak due to VEGF vs. PBS–injection was reduced to a 1.6–fold increase. Topical application of TG100801 is responsible for 73% (n=8, t test p<0.001) and 98% reduction (n=7, t test p<0.004) in two separate VEGF–induced vascular leak experiments.

Conclusions: : The topically applied src kinase/VEGFR prodrug TG100801 significantly inhibits the vaso–permeable effects of VEGF, suggesting that such eyedrop therapy may be useful in the treatment of retinal vascular diseases associated with altered vascular permeability such as diabetic macular edema.

Keywords: retina • diabetic retinopathy • neovascularization 
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