BMS-182123, a fungal metabolite that inhibits the production of TNF-alpha by macrophages and monocytes

J Antibiot (Tokyo). 1996 Mar;49(3):234-40. doi: 10.7164/antibiotics.49.234.

Abstract

A fungal metabolite, BMS-182123, which inhibited bacterial endotoxin-induced production of tumor necrosis factor (TNF-alpha) in murine macrophages and human peripheral blood monocytes (in vitro), was isolated from the culture broth of Penicillium chrysogenum strain V39673. The effective BMS-182123 concentration (IC50) resulting in 50% inhibition of lipopolysaccharide-induced TNF-alpha production in murine macrophages and human monocytes was 600 ng/ml and 4.0 microgram/ml, respectively. BMS-182123 suppressed the lipopolysaccharide-induced TNF-alpha promoter activity and did not affect the stability of posttranscriptional mRNA. Addition of hydrophobic resin, Amberlite XAD-8 (1%), to the fermentation enhanced the production of BMS-182123 by 5.5 fold. A total of 577 mg pure BMS-182123 was recovered from a 250-liter fermentation supplemented with 1% Amberlite XAD-8.

MeSH terms

  • Animals
  • Base Sequence
  • Bridged-Ring Compounds / chemistry
  • Bridged-Ring Compounds / metabolism
  • Bridged-Ring Compounds / pharmacology*
  • DNA Probes / genetics
  • Fermentation
  • Humans
  • In Vitro Techniques
  • Lipopolysaccharides / pharmacology
  • Macrophages / drug effects*
  • Macrophages / metabolism*
  • Mice
  • Molecular Sequence Data
  • Molecular Structure
  • Monocytes / drug effects*
  • Monocytes / metabolism*
  • Penicillium / classification
  • Penicillium / metabolism*
  • Promoter Regions, Genetic / drug effects
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Bridged-Ring Compounds
  • DNA Probes
  • Lipopolysaccharides
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • trichodimerol