Design and synthesis of seco-oxysterol analogs as potential inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase gene transcription

J Med Chem. 1994 Jul 22;37(15):2343-51. doi: 10.1021/jm00041a013.

Abstract

The synthesis and biological activity of a series of seco-oxysterol analogs designed to be inhibitors of transcription of the gene for 3-hydroxy-3-methylglutaryl-Coenzyme A reductase (HMGR) are described. The compound possessing the most significant activity, [1 alpha (E),4 beta]-3-[2-(4- hydroxy-1-methylcyclohexyl)ethenyl]-alpha,alpha-dimethylbenzenepentan ol (4, U-88156), inhibited (IC50 = 10 microM) the expression of beta-galactosidase (beta-gal) in a transfected human HepG2 cell line wherein the beta-gal gene was driven by a 5 kB segment of the promoter for hamster HMGR. Furthermore, using wild-type HepG2 cells, it was shown that 10 microM 4 reduced HMGR mRNA levels by 73% while stimulating LDL-receptor activity by 47%. In the same system, the related oxysterol, 25-hydroxycholesterol (1), at 10 microM lowered both HMGR mRNA levels and LDL-receptor activity by 58% and 64%, respectively. Overall HMGR activity in wild-type HepG2 cells was inhibited 30% by 4 at 10 microM. These findings collectively demonstrate that a seco-oxysterol analog is capable of regulating HMGR gene expression and that this regulation can occur without a concomitant attenuation of the level of LDL-receptor activity.

MeSH terms

  • Animals
  • Cricetinae
  • Drug Design
  • Gene Expression Regulation, Enzymologic
  • Humans
  • Hydroxymethylglutaryl CoA Reductases / genetics*
  • Oxygen / chemistry
  • Promoter Regions, Genetic
  • Receptors, LDL / metabolism
  • Sterols / chemical synthesis
  • Sterols / pharmacology*
  • Transcription, Genetic / drug effects*
  • Tumor Cells, Cultured

Substances

  • Receptors, LDL
  • Sterols
  • Hydroxymethylglutaryl CoA Reductases
  • Oxygen