The in vitro hepatic metabolism of ABT-418, a cholinergic channel activator, in rats, dogs, cynomolgus monkeys, and humans

Drug Metab Dispos. 1994 Sep-Oct;22(5):788-98.

Abstract

The metabolism of the cholinergic channel activator [3H]ABT-418 was studied in 9,000g supernatant (S-9) fractions and precision-cut tissue slices prepared from rat, dog, monkey, and human livers. In rat S-9 fractions and tissue slices, the lactam and trans N'-oxide were detected as major metabolites. The lactam was also the major metabolite in monkey and human S-9 fractions and tissue slices, although the rate of formation was greater in monkey (Vmax' of 428 vs. 103 pmol/min/mg S-9 protein). Trans N'-oxide was not detected in either species, but low levels of the cis N'-oxide were detected in tissue slice preparations from two human subjects. In contrast, trans ABT-418 N'-oxide was identified as a major metabolite in dog S-9 fractions (Vmax' of 266 pmol metabolite formed/min/mg S-9 protein) and tissue slices. Although identified as a minor metabolite in dog S-9 fractions, the lactam metabolite was shown to account for a sizeable proportion of the total radioactivity in the corresponding tissue slice preparations (22% of the total radioactivity at 12 hr); the rank order of lactam formation by the precision-cut liver slices was monkey > human > rat > or = dog. Evidence that N'-oxidation and C-oxidation (to lactam) of ABT-418 was mediated by liver microsomal flavin-containing mono-oxygenase (FMO) and cytochromes P-450 (CYPs), respectively, was obtained with the inhibitors thiobenzamide and clotrimazole. The involvement of cytosolic aldehyde oxidase (AO) was suggested by a significant correlation (r2 = 0.998, p < 0.01) between the observed rate of lactam formation and AO (N1-methylnicotinamide oxidase) activity in rat, dog, monkey, and human S-9 fractions; inhibition of lactam formation by the AO substrate N1-methylnicotinamide; and the lack of lactam formation in the absence of cytosol. Data indicate that the species-related differences in the hepatic metabolism of ABT-418 may be dependent on the relative levels and/or activity of FMO, CYP, and AO. In this regard, ABT-418 is very similar to nicotine. However, unlike nicotine, the N-demethylation of parent drug and the further products of lactam metabolism was not detected.

MeSH terms

  • Adult
  • Animals
  • Anti-Anxiety Agents / metabolism*
  • Dogs
  • Female
  • Humans
  • In Vitro Techniques
  • Ion Channels / drug effects
  • Ion Channels / metabolism*
  • Isoxazoles / metabolism*
  • Liver / enzymology
  • Liver / metabolism*
  • Macaca fascicularis
  • Male
  • Mixed Function Oxygenases / metabolism
  • NADP / metabolism
  • Parasympathetic Nervous System / drug effects
  • Parasympathetic Nervous System / metabolism*
  • Pyrrolidines / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Subcellular Fractions / drug effects
  • Subcellular Fractions / metabolism

Substances

  • Anti-Anxiety Agents
  • Ion Channels
  • Isoxazoles
  • Pyrrolidines
  • 3-methyl-5-(1-methyl-2-pyrrolidinyl)isoxazole
  • NADP
  • Mixed Function Oxygenases