CYP2C8/9 mediate dapsone N-hydroxylation at clinical concentrations of dapsone.

Article Details

Citation

Winter HR, Wang Y, Unadkat JD

CYP2C8/9 mediate dapsone N-hydroxylation at clinical concentrations of dapsone.

Drug Metab Dispos. 2000 Aug;28(8):865-8.

PubMed ID
10901692 [ View in PubMed
]
Abstract

Using selective cytochrome P450 (CYP) inhibitors and clinical concentrations (4 microM) of dapsone (DDS), we found a major contribution of CYP2C9 and little or no contribution (< or = 10%) of CYP3A4 and CYP2E1 to dapsone N-hydroxylation (DDS-NHY) in human liver microsomes. Sulfaphenazole (2.16 microM) and tolbutamide (500 microM), selective inhibitors of CYP2C9 (or 2C8/9), inhibited DDS-NHY by 48 +/- 14 and 41 +/- 15%, respectively. The apparent Michaelis-Menten Km values for DDS-NHY by cloned CYP2C8, CYP2C9, CYP2C18, and CYP2C19 were 75 microM, 31 microM, 25 microM, and greater than 1 mM, respectively. CYP3A4 and CYP2E1 were incapable of DDS-NHY at 4 microM DDS. S-mephenytoin (360 microM) activated DDS-NHY by human liver microsomes and by CYP2C8 by 43 +/- 36 and 193 +/- 16%, respectively. This activation was cytochrome b5-dependent. In contrast, S-mephenytoin inhibited DDS-NHY by CYP2C9, CYP2C18, and CYP2C19 by 27 +/- 2, 49 +/- 1, and 32 +/- 4%, respectively. Because CYP2C18 and CYP19 are expressed at low concentrations in the human liver, these observations indicate that at clinical DDS concentrations, CYP2C9 is a major and CYP2C8 is a likely minor contributor to DDS-NHY in human liver microsomes.

DrugBank Data that Cites this Article

Drug Enzymes
DrugEnzymeKindOrganismPharmacological ActionActions
DapsoneCytochrome P450 2C18ProteinHumans
Unknown
Substrate
Details
DapsoneCytochrome P450 2C8ProteinHumans
Unknown
Substrate
Details
MephenytoinCytochrome P450 2C8ProteinHumans
Unknown
Substrate
Details