April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Drug Binding to Sclera
Author Affiliations & Notes
  • S. Patel
    Chemical and Biomolecular Engineering, Georgia Institute of Technology, Atlanta, Georgia
  • N. Devlin
    Chemical and Biomolecular Engineering, Georgia Institute of Technology, Atlanta, Georgia
  • S. Bandari
    Chemical and Biomolecular Engineering, Georgia Institute of Technology, Atlanta, Georgia
  • H. F. Edelhuaser
    Department of Ophthalmology, Emory University, Atlanta, Georgia
  • M. R. Prausnitz
    Chemical and Biomolecular Engineering, Georgia Institute of Technology, Atlanta, Georgia
  • Footnotes
    Commercial Relationships  S. Patel, None; N. Devlin, None; S. Bandari, None; H.F. Edelhuaser, None; M.R. Prausnitz, None.
  • Footnotes
    Support  NEI Grant R24-EY017045
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 5968. doi:
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    • Get Citation

      S. Patel, N. Devlin, S. Bandari, H. F. Edelhuaser, M. R. Prausnitz; Drug Binding to Sclera. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5968.

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

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Abstract

Purpose: : Transcleral drug delivery has become an important research area. Studies have determined the permeability of molecules across the sclera and these values have been used in pharmacokinetic modeling. The effect of drug binding to the sclera has not been examined or quantified. Binding can influence transcleral diffusion; extensive binding can decrease the effective permeability of the drug and create a drug depot within the tissue. A drug depot coupled with slow release kinetics may provide an avenue for sustained delivery from the sclera. Our aim is to (1) quantify the extent of binding for pilocarpine, timolol, clonidine, prednisone, tiramcinolone acetonide, and testosterone to the sclera tissue, (2) determine if there is a relationship between the extent of binding and physiochemical properties of the molecule and (3) examine the kinetics of the bound molecules release.

Methods: : A reservoir of known concentration of drug was prepared in balanced salt solution (BSS). Human sclera was soaked in this reservoir at 37 C (±2 C) for 24 hrs to saturate scleral binding sites with drug. The tissue was then removed from this reservoir and placed in a reservoir of BSS also at 37 C (±2 C). The reservoir was well mixed and small aliquots were removed at various time points to determine the kinetics and extent of drug release from binding sites in the tissue. The aliquots were assayed using high performance liquid chromatography. Calculations were performed to determine the ratio of the bound to free drug concentration, Keq , and the time to release, tR. Each drug was tested a minimum of three times.

Results: : Calculations reveal the following rank for Keq from highest to lowest: testosterone > clonidine > prednisone > triamcinolone acetonide > timolol > pilocarpine. The largest value was 11.7, indicating high levels of binding. Kinetic analysis revealed times for release of the drugs ranging from 1 hour up to 40 hours. Some drugs displayed a combination of large Keq values and slow release kinetics. Properties examined for relationships to binding include logP, hydrogen bond acceptors and donors, polar surface area, and charge.

Conclusions: : These results indicate that some drugs can bind significantly to the sclera and have release times that are on the order of tens of hours. This data can have an impact on effective scleral permeability and indicates that binding effects need to be considered when studying transcleral drug delivery. Some drugs may be used in the future to form a drug depot in the sclera that can slowly release the bound drug.

Keywords: sclera • drug toxicity/drug effects 
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