Biochemical basis for differences in metabolism-dependent genotoxicity by two diazinylpiperazine-based 5-HT2C receptor agonists

Bioorg Med Chem Lett. 2009 Mar 15;19(6):1559-63. doi: 10.1016/j.bmcl.2009.02.032. Epub 2009 Feb 12.

Abstract

The biochemical basis for S9-dependent mutagenic response of the 5-HT(2C) receptor agonist and diazinylpiperazine derivative 1 in the Salmonella Ames assay involves P450-mediated bioactivation to DNA-reactive quinone-methide, aldehyde and nitrone intermediates. Mechanistic information pertaining to the metabolism of 1 was used in the design of diazinylpiperazine 5 to eliminate the safety liability. While 5 was negative in the Ames assay, the compound retained the ability of 1 to form certain electrophilic intermediates. Plausible hypotheses that can collectively account for the differences in mutagenic response of the two piperazine analogs are discussed.

MeSH terms

  • Amides / chemistry
  • Chemistry, Pharmaceutical / methods*
  • Chromatography / methods
  • Drug Design
  • Models, Chemical
  • Mutagenesis
  • Mutagenicity Tests
  • Mutagens
  • Mutation
  • NADP / chemistry
  • Piperazine
  • Piperazines / chemistry*
  • Reproducibility of Results
  • Salmonella / metabolism
  • Serotonin 5-HT2 Receptor Agonists*

Substances

  • Amides
  • Mutagens
  • Piperazines
  • Serotonin 5-HT2 Receptor Agonists
  • Piperazine
  • NADP