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British Journal of Clinical Pharmacology logoLink to British Journal of Clinical Pharmacology
. 1997 Dec;44(6):557–564. doi: 10.1046/j.1365-2125.1997.t01-1-00629.x

Characterization of the cytochrome P450 isoenzymes involved in the in vitroN-dealkylation of haloperidol

L P Pan 1, P Wijnant 1, C De Vriendt 1, M T Rosseel 1, F M Belpaire 1
PMCID: PMC2042890  PMID: 9431831

Abstract

Aims The present study was carried out to identify the cytochrome P450 isoenzyme(s) involved in the N-dealkylation of haloperidol (HAL).

Methods In vitro studies were performed using human liver microsomes and c-DNA-expressed human P450 isoforms. N-dealkylation of HAL was assessed by measuring the formation of 4-(4-chlorophenyl)-4-hydroxypiperidine (CPHP).

Results There was a tenfold variation in the extent of CPHP formation amongst the nine human liver microsomal preparations. The CPHP formation rates as a function of substrate concentration, measured in three livers, followed monophasic enzyme kinetics. Km and Vmax values ranged respectively from 50 to 78 μm and from 180 to 412 pmol mg−1 min−1. CPHP formation rates in the nine liver preparations were significantly correlated with dextromethorphan N-demethylase activity (a marker of CYP3A4 activity), but not with the activity of dextromethorphan O-demethylase (CYP2D6), phenacetin O-deethylase (CYP1A2) or tolbutamide hydroxylase (CYP2C9). Ketoconazole, an inhibitor of CYP3A4, inhibited competitively CPHP formation (Ki=0.1 μm ), whereas sulphaphenazole (CYP2C9), furafylline (CYP1A2) and quinidine (CYP2D6) gave only little inhibition (IC50>100 μm ). CPHP formation was, moreover, enhanced by α-naphtoflavone, an effect common to CYP3A4 mediated reactions. Anti-CYP3A4 antibodies strongly inhibited CPHP formation, whereas no inhibition was observed in the presence of CYP2D6 antibodies. Among the recombinant human CYP isoforms tested, CYP3A4 exhibited the highest activity with respect to CPHP formation rate, with no detectable effect of other CYP isoforms (CYP1A2, CYP2D6 and CYP2C9). HAL inhibited dextromethorphan O-demethylase (CYP2D6) with IC50 values between 2.7 and 8.5 μm, but not (IC50>100 μm ) dextromethorphan N-demethylase (CYP3A4), phenacetin O-deethylase (CYP1A2) or tolbutamide hydroxylase (CYP2C9).

Conclusions These results strongly suggest that the N-dealkylation of HAL in human liver microsomal preparations is mediated by CYP3A4.

Keywords: cytochrome P450 isoenzymes, CYP3A4, haloperidol, human liver microsomes, in vitro metabolism

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