July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Treatment with a highly selective Galectin-3 Inhibitor, GAL-200-10, reduces both pathological corneal neovascularization and fibrosis
Author Affiliations & Notes
  • Zhiyi Cao
    Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts, United States
  • Wei-Sheng Chen
    National Institute of Allergy and infectious diseases, National Institute of Health, Bethesda, Maryland, United States
  • Hakon Leffer
    Labrotory Medicine, Lund University, Lund, Sweden
  • Ulf Nilsson
    Chemistry, Lund University, Lund, Sweden
  • Hans Schambye
    Galecto Biotech, Gothenburg, Sweden
  • anders pedersen
    Galecto Biotech, Gothenburg, Sweden
  • Fredrik Zetterberg
    Galecto Biotech, Gothenburg, Sweden
  • Noorjahan A Panjwani
    Ophthalmology, Tufts University School of Medicine, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Zhiyi Cao, Galecto (P); Wei-Sheng Chen, Galecto (P); Hakon Leffer, Galecto (I), Galecto (P); Ulf Nilsson, Galecto (I), Galecto (P); Hans Schambye, Galecto (I), Galecto (P); anders pedersen, Galecto (E); Fredrik Zetterberg, Galecto (E), Galecto (P); Noorjahan Panjwani, None
  • Footnotes
    Support  Galecto Biotech and DOD W81XWH-16-1-0781
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 3332. doi:
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      Zhiyi Cao, Wei-Sheng Chen, Hakon Leffer, Ulf Nilsson, Hans Schambye, anders pedersen, Fredrik Zetterberg, Noorjahan A Panjwani; Treatment with a highly selective Galectin-3 Inhibitor, GAL-200-10, reduces both pathological corneal neovascularization and fibrosis. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3332.

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

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Abstract

Purpose : Corneal neovascularization and scarring are serious conditions that can lead to a profound decline in vision or vision loss. Recent studies have demonstrated that a carbohydrate-binding protein, galectin-3 (Gal-3), promotes angiogenesis as well as fibrosis, and that it does so by independent mechanisms. Therefore, our goal has been to target Gal-3 for developing dual-benefit drugs to control both neovascularization and fibrosis of ocular tissues. We have recently synthesized a new small molecule inhibitor of Gal-3 (Gal-200-10) with improved properties including high Gal-3 selectivity. The Aim of the current study was to test the efficacy of this newly developed inhibitor in reducing corneal neovascularization and fibrosis.

Methods : Corneal neovascularization was induced by silver nitrate (AgNO3) cautery and corneal fibrosis was induced by alkali-burn injury in C57B/6 mice. Vehicle alone (10µl of 1.65% hydroxyethyl cellulose) or GAL-200-10 (10µl in vehicle) were topically applied to the eye twice per day from day 1 until day 13. Corneal opacity was scored by slit lamp examination at day 7 and 14 post-injury. Corneas were harvested on day 7 (for angiogenesis analysis, whole mount staining with CD31, a marker of blood vessels) or 14 post-injury and processed for Western blotting and immunofluorescence staining with anti-α-SMA antibody to reveal and quantify the extent fibrosis in the treated and control groups.

Results : Robust angiogenesis was observed in silver nitrate–cauterized corneas on day 7 post injury, and markedly increased corneal opacification was demonstrated in alkaline burn–injured corneas on days 7 and 14 post injury. Treatment with the inhibitor substantially reduced corneal angiogenesis (n=20, p<0.01, 31% inhibition compared to control) and opacification with a concomitant decrease in a-smooth muscle actin (a-SMA) expression and distribution (0.6677 ± 0.04921, n=3, p<0.01).

Conclusions : The small molecule inhibitor, GAL-200-10, is an ideal candidate for developing a dual-benefit drug to control both corneal neovascularization and fibrosis.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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