ifedipind(NF) competitively and stereoselectively inhibited the metabolism of praziquantel(PQT)enantiomers in human liver microsomes。 Ki value of NF for the(-)-PQT measuredeither by parent drug disappearance of by the MI formation was 1. 4 and 1. 5μmol/L

respec-tively

both of which was much less than the Ki value of 6. 1μmol/L for(+)-PQT measuredby parent drug disappearance. The inhibitory effect of NF on(-)-PQT metabolism in the ratliver microsomes was much less than in human liver microsomes. The Ki value for(-)-PQTand(+)-PQT disappearance were 11.6 and 10. 0μmol/L. and Ki for MI formation from(-)-PQT was 10 μmol/L。 NF had no or a little inhibitory effect on the activities of metoprolol-hy-droxylase

ethylmorphine N-demethylase and 7-ethoxycoumarin O-deethylase. Metoprolol

arepresentative substrate of P450 IID6

had little effect on(-)-PQT and(+)-PQTmetabolism;furthermore

quinidine as a specific inhibitor of P450 IID6 only exhibited a very weakinhibitory effect on(-)-PQT and(+)-PQT metabolim These findings indicated that thepossidility of P450 IID6 involved in the metabolism of PQT enantiomers might be very low.