May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Anti–Angiogenic Effect of Linomide Analogue
Author Affiliations & Notes
  • Y. Yang
    Ophthalmology,
    The Ohio State University, Columbus, OH
  • S. Meadows
    Ophthalmology,
    The Ohio State University, Columbus, OH
  • P.–K. Li
    Division of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, The Ohio State University, Columbus, OH
  • F.H. Davidorf
    Ophthalmology,
    The Ohio State University, Columbus, OH
  • M.H. Abdel–Rahman
    Ophthalmology,
    Human Cancer Genetics Program,
    The Ohio State University, Columbus, OH
  • Footnotes
    Commercial Relationships  Y. Yang, None; S. Meadows, None; P. Li, None; F.H. Davidorf, None; M.H. Abdel–Rahman, None.
  • Footnotes
    Support  Patti Blow Research Fund in Ophthalmology; Ohio Lion's Eye Research Foundation
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 4166. doi:
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      Y. Yang, S. Meadows, P.–K. Li, F.H. Davidorf, M.H. Abdel–Rahman; Anti–Angiogenic Effect of Linomide Analogue . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4166.

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

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Abstract

Abstract: : Purpose: Linomide (Roquinimex, LS 2616), is an orally absorbed, immunomodulatory drug that has been shown to have antiangiogenic activity. Recently, a series of linomide analogues has been reported with more potent anti–angiogenic activity than the original compound both in–vitro and in–vivo. We hypothesize that linomide analogues represent potential agents for the treatment of eye diseases associated with pathological neovascularization such as age related macular degeneration (AMD) and diabetic retinopathy (DR). The aims of this study are to test the selectivity and to explore potential mechanism of action of the leading compound (Lin05). The efficiency of systemic administration of Lin05 in inhibition of experimental choroidal neovascularization (ECNV) was also tested. Methods: The selectivity of the leading compound was tested on 2 endothelial cell lines, human retinal endothelial cells (HREC) and human umbilical vein endothelial cells (HUVEC), 1 normal epithelial cell line, human retinal pigmented epithelial cells (RPE) and two cancer cell lines SKMEL–28 and ZR–75–1. The effect of Lin05 on the inhibition of VEGF induced phosphorylation of KDR and ERK1/2 were tested by Western blot analysis. In vivo anti–angiogenic effect of Lin05 was tested using the laser induced ECNV model in adult Brown Norway rats. Quantification of lesion sizes were carried out at day 10 and 14 using fluorescent angiography and histopathology. Results: The Linomide (Lin 05) has at least 8–fold selective inhibition of endothelial cells proliferation compared to normal and neoplastic epithelial cells. The antiproliferative effects of the Lin05 on endothelial cells are apparently not through the blockage of VEGF induced KDR phosphorylation nor through inhibition of KDR downstream signaling through ERK1/2. Systemic administration of Lin05 was associated with a significant decrease in both vascular leakage, assessed by fluorescent angiography, and lesion size assessed by histopathology (p=0.02). No systemic toxicity was detected for Lin05 in major organs such as liver, lung and kidneys. Conclusions: Linomide analogues are potential anti–angogenic agents for the treatment of eye diseases associated with pathological neovascularization. Our results also indicate that the selectivity of linomide analogue on endothelial cells could be through an alternative pathway not involving VEGF/KDR, and such mechanism should be further studied.

Keywords: neovascularization • drug toxicity/drug effects • age-related macular degeneration 
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