Reprint of BMCL_19101

Bioorg Med Chem Lett. 2012 Nov 15;22(22):6821-4. doi: 10.1016/S0960-894X(12)01341-8.

Abstract

The pathogenesis of rheumatoid arthritis is mainly driven by NF-κB-mediated production of cytokines, such as TNF-α. We report herein that the orally available imidazoline-based NF-κB inhibitor, TCH-013, was found to significantly reduce TNF-α signaling and attenuate collagen antibody induced arthritis in BALB/c mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Animals
  • Arthritis, Rheumatoid / chemically induced
  • Arthritis, Rheumatoid / drug therapy*
  • Collagen
  • Dose-Response Relationship, Drug
  • Imidazoles / administration & dosage
  • Imidazoles / pharmacology*
  • Mice
  • Mice, Inbred BALB C
  • Molecular Structure
  • NF-kappa B / antagonists & inhibitors
  • Signal Transduction / drug effects
  • Structure-Activity Relationship
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Imidazoles
  • NF-kappa B
  • TCH-013
  • Tumor Necrosis Factor-alpha
  • Collagen