December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Topical Nepafenac Inhibits Ocular Neovascularization
Author Affiliations & Notes
  • K Takahashi
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • Y Saishin
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • Y Saishin
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • K Mori
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • A Ando
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • S Yamamoto
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • Y Oshima
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • H Nambu
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • D Bingamen
    Alcon Pharmaceutical Products Research Alcon Research Ltd Fort Worth TX
  • PA Campochiaro
    Wilmer Eye Institute Johns Hopkins University School of Medicine Baltimore MD
  • Footnotes
    Commercial Relationships   K. Takahashi, None; Y. Saishin, None; Y. Saishin, None; K. Mori, None; A. Ando, None; S. Yamamoto, None; Y. Oshima, None; H. Nambu, None; D. Bingamen, Alcon E; P.A. Campochiaro, Alcon F; Novartis Ophthalmics F, C, R; GenVec, Inc. F, C, R; RW Johnson F. Grant Identification: EY05951 and EY012609 and a grant from Alcon
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1268. doi:
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    • Get Citation

      K Takahashi, Y Saishin, Y Saishin, K Mori, A Ando, S Yamamoto, Y Oshima, H Nambu, D Bingamen, PA Campochiaro; Topical Nepafenac Inhibits Ocular Neovascularization . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1268.

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

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Abstract

Abstract: : Purpose: Topical Nepafenac readily penetrates the cornea and is metabolized to a potent cyclo-oxygenase-1 (COX-1) and COX-2 inhibitor, AL-6295A. In this study we tested the effect of topical nepafenac in two murine models of ocular neovascularization (NV). Methods: A masked trial was performed to compare the topical effects of vehicle with one of several concentrations of nepafenac (0.01, 0.03, 0.1, or 0.5%), 0.1% diclofenac, or 0.5% ketorolac tromethamine in mice with oxygen-induced ischemic retinopathy or mice with choroidal NV (CNV) due to laser-induced rupture of Bruch's membrane. Mice with ischemic retinopathy were given one drop four times a day between P12 and P17 and then preretinal NV was measured by image analysis. Starting one day after rupture of Bruch's membrane, mice were treated for two weeks with one drop 4 times a day and then the amount of CNV at each rupture site was measured. Results: Mice treated with 0.1% (n=16) or 0.5% (n=16) nepafenac had significantly less CNV (0.0072±0.0012 mm2, p=0.0037 and 0.0074±0.0015 mm2, p=0.0029, respectively) than vehicle-treated mice (0.0254±0.0060 mm2). In the ischemic retinopathy model, compared to vehicle-treated mice (n=7) in which the average area of preretinal NV was 0.0444±0.0079 mm2, mice treated with 0.1% (n=9) or 0.5% (n=13) nepafenac had significantly less preretinal NV (0.0165±0.0029 mm2, p=0.0011 and 0.0186±0.0043 mm2, p=0.0075). In additional studies, compared to vehicle-treated mice (CNV = 0.0279±0.0076 mm2), mice treated with 0.1% or 0.03% nepafenac had significantly less CNV (0.0181±0.0033 and 0.0133±0.0017 mm2, respectively) whereas eyes treated with 0.1% diclofenac had no significant difference (0.0232±0.0038 mm2, p=0.72). Mice treated with 0.5% ketorolac tromethamine for 14 days had high mortality, but when evaluated after 7 days of treatment showed no difference from mice treated with vehicle for 7 days. Conclusion: Topical nepafenac inhibits ocular NV.

Keywords: 346 choroid: neovascularization • 566 retinal neovascularization • 388 diabetic retinopathy 
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