['To determine the effect of therapeutic loading doses of halofantrine and chloroquine on CYP2D6 activity in healthy black Zambians.', "Twenty healthy black male Zambians were phenotyped for CYP2D6 activity by measuring the debrisoquine/4-hydroxydebrisoquine ratio in a 0-8 h urine sample after a 10 mg oral dose of debrisoquine hemi-sulphate. The subjects (all 'extensive metabolizer' phenotype with respect to CYP2D6) were randomized into two groups of 10, and 24 h later one group received 1500 mg halofantrine hydrochloride and the other group 1500 mg chloroquine phosphate both orally in divided doses. All subjects were given further 10 mg doses of debrisoquine at 2 h, 1 week and 2 weeks after the last dose of the antimalarial drug, and phenotyped as described above.", 'The median debrisoquine/4-hydroxydebrisoquine 0-8 h urinary ratio was increased by halofantrine (1.39 to 6.05; P<0.01; 95% confidence intervals 4.00-11.7) and chloroquine (1.96 to 3.91; P<0.01; 95% confidence intervals 1.34-2.66) when debrisoquine was given 2 h after treatment. The decrease in CYP2D6 activity remained statistically significant for 1 week after both drugs. Halofantrine was a significantly more potent inhibitor of CYP2D6 than chloroquine (P=0.037). Phenocopying occurred in two subjects taking halofantrine and one taking chloroquine (i.e. the debrisoquine/4-hydroxydebrisoquine ratios became consistent with the poor metabolizer phenotype).'] Do halofantrine and chloroquine inhibit CYP2D6 activity in healthy Zambians?