High throughput screening of potentially selective MMP-13 exosite inhibitors utilizing a triple-helical FRET substrate

Bioorg Med Chem. 2009 Feb 1;17(3):990-1005. doi: 10.1016/j.bmc.2008.03.004. Epub 2008 Mar 6.

Abstract

The major components of the cartilage extracellular matrix are type II collagen and aggrecan. Matrix metalloproteinase 13 (MMP-13) has been implicated as the protease responsible for collagen degradation in cartilage during osteoarthritis (OA). In the present study, a triple-helical FRET substrate has been utilized for high throughput screening (HTS) of MMP-13 with the MLSCN compound library (n approximately 65,000). Thirty-four compounds from the HTS produced pharmacological dose-response curves. A secondary screen using RP-HPLC validated 25 compounds as MMP-13 inhibitors. Twelve of these compounds were selected for counter-screening with 6 representative MMP family members. Five compounds were found to be broad-spectrum MMP inhibitors, 3 inhibited MMP-13 and one other MMP, and 4 were selective for MMP-13. One of the selective inhibitors was more active against MMP-13 triple-helical peptidase activity compared with single-stranded peptidase activity. Since the THP FRET substrate has distinct conformational features that may interact with MMP secondary binding sites (exosites), novel non-active site-binding inhibitors may be identified via HTS protocols utilizing such assays.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Binding Sites
  • Drug Evaluation, Preclinical
  • Fluorescence Resonance Energy Transfer
  • Humans
  • Matrix Metalloproteinase 13 / metabolism
  • Matrix Metalloproteinase Inhibitors*
  • Matrix Metalloproteinases / metabolism
  • Peptides / chemistry
  • Protease Inhibitors / chemistry*
  • Protease Inhibitors / pharmacology
  • Small Molecule Libraries
  • Substrate Specificity

Substances

  • Matrix Metalloproteinase Inhibitors
  • Peptides
  • Protease Inhibitors
  • Small Molecule Libraries
  • Matrix Metalloproteinase 13
  • Matrix Metalloproteinases