Abstract
Following the oral administration of [14C] pranoprofen to mice, 70-80% of radioactivity was excreted in the urine, and 15-25% in the feces within 3 d at 5, 25, 50, 100 and 200 mg/kg. This showed that no significant change in urinary and fecal excretion was observed among these doses. The radioactivity levels in the blood also increased in proportion to the doses, indicating that no repression of the absorption of pranoprofen was found even at increased doses. The major metabolites in mouse urine were acyl glucuronide and the glucoside of pranoprofen. At low doses acyl glucoside was predominantly excreted in urine, whereas acyl glucoside decreased relative to acyl glucuronide at increased doses. Although 43.2% of the acyl glucoside was recovered in the 24 h urine samples after the intravenous administration of acyl glucuronide, no acyl glucuronide was found in the urine after the intravenous administration of acyl glucoside. These results demonstrated the interesting observation that pranoprofen had a preference for glucosidation rather than glucuronidation in mice at low doses in spite of having a higher capacity of glucuronidation.
