April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
BOL-303242-X, a Novel Selective Glucocorticoid Receptor Agonist, Inhibits Hyperosmolarity-Induced Cytokine Release in Human Corneal Epithelial Cells
Author Affiliations & Notes
  • J.-Z. Zhang
    Pharmaceutical R & D, Bausch & Lomb, Rochester, New York
  • M. E. Cavet
    Pharmaceutical R & D, Bausch & Lomb, Rochester, New York
  • K. L. Harrington
    Pharmaceutical R & D, Bausch & Lomb, Rochester, New York
  • K. R. VanDerMeid
    Pharmaceutical R & D, Bausch & Lomb, Rochester, New York
  • F. J. Lopez
    Pharmaceutical R & D, Bausch & Lomb, Rochester, New York
  • K. W. Ward
    Pharmaceutical R & D, Bausch & Lomb, Rochester, New York
  • Footnotes
    Commercial Relationships  J.-Z. Zhang, Bausch & Lomb, E; M.E. Cavet, Bausch & Lomb, E; K.L. Harrington, Bausch & Lomb, E; K.R. VanDerMeid, Bausch & Lomb, E; F.J. Lopez, Bausch & Lomb, E; K.W. Ward, Bausch & Lomb, E.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4859. doi:
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      J.-Z. Zhang, M. E. Cavet, K. L. Harrington, K. R. VanDerMeid, F. J. Lopez, K. W. Ward; BOL-303242-X, a Novel Selective Glucocorticoid Receptor Agonist, Inhibits Hyperosmolarity-Induced Cytokine Release in Human Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4859.

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

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Abstract

Purpose: : The aim of this study was to determine the effects of BOL-303242-X, a novel selective glucocorticoid receptor agonist under clinical evaluation for the treatment of ophthalmic inflammation, on hyperosmolar challenge-induced cytokine release from human corneal epithelial cells (HCEpiC).

Methods: : HCEpiC were challenged with a hyperosmolar stress (440 and 480 mOsm by addition of sucrose to the culture medium) for 24 hours. Cell metabolic activity was measured using the alamarBlue assay and Luminex technology was used to determine the effects of BOL-303242-X on hyperosmolarity-induced cytokine release (IL-6, IL-8, and MCP-1) into the medium. Dexamethasone (DEX) was used as the control.

Results: : Both hyperosmolar conditions, 440 and 480 mOsm, induced measurable cytokine release in HCEpiC without statistically significant effects on cell metabolic activity. BOL-303242-X and DEX significantly reduced hyperosmolarity-induced cytokine release in a dose-dependent manner for IL-6 and MCP-1. BOL-303242-X potency was 0.97 nM, 14.08 nM and that of dexamethasone was 0.38 nM, 7.59 nM for IL-6 and MCP-1, respectively. These differences were not statistically significant. BOL-303242-X was fully efficacious at reducing hyperosmolarity-induced cytokine release as no statistically significant differences were identified when comparing cytokine levels with those after DEX

Conclusions: : . Increasing evidence suggests that tear hyperosmolarity is a central mechanism causing ocular surface inflammation and damage in dry eye patients. Selective glucocorticoid receptor agonists represent a set of molecules that selectively regulate glucocorticoid receptor-mediated gene transcription via transrepression and are believed to possess corticosteroid-like anti-inflammatory activities with reduced transactivation-mediated side effects of steroids such as elevation of intraocular pressure Data from this in vitro model indicate that BOL-303242-X is as efficacious and potent as DEX in reducing hyperosmolarity-induced cytokine release from HCEpiC, supporting clinical evaluation of the compound in reducing inflammation in dry eye patients.

Keywords: cytokines/chemokines • inflammation • receptors: pharmacology/physiology 
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