Elvin A T, Keenaghan J B, Byrnes E W, Tenthorey P A, McMaster P D, Takman B H, Lalka D, Manion C V, Baer D T, Wolshin E M, Meyer M B, Ronfeld R A
J Pharm Sci. 1980 Jan;69(1):47-9. doi: 10.1002/jps.2600690113.
The metabolism of tocainide, an experimental antiarrhythmic drug, was studied in humans. Urinary excretion of unchanged drug was 28-55% in 24 hr after oral dosing. Urine hydrolysis with hydrochloric acid or beta-glucuronidase increased tocainide recovery to 55-79%. Saccharo-1,4-lactone inhibited the beta-glucuronidase-mediated tocainide recovery increase. Adjustment of urine to pH 13 produced a compound identified as 3-(2,6-xylyl)-5-methylhydantoin. Evidence suggests that it was derived from the same metabolite that formed the additional tocainide after acid or beta-glucuronidase treatment. Tocainide carbamoyl O-beta-D-glucuronide is the structure proposed for the metabolite. The suggested pathway for its formation involves the addition of carbon dioxide to the amino nitrogen of tocainide followed by uridine diphosphate-glucuronic acid conjugation.
对一种实验性抗心律失常药物妥卡尼的代谢情况在人体中进行了研究。口服给药后24小时内，原形药物的尿排泄率为28 - 55%。用盐酸或β-葡萄糖醛酸酶进行尿液水解后，妥卡尼的回收率提高到55 - 79%。1,4-内酯抑制了β-葡萄糖醛酸酶介导的妥卡尼回收率增加。将尿液pH值调至13产生了一种鉴定为3-(2,6-二甲苯基)-5-甲基乙内酰脲的化合物。有证据表明它源自与经酸或β-葡萄糖醛酸酶处理后形成额外妥卡尼的相同代谢物。妥卡尼氨基甲酰O-β-D-葡萄糖醛酸被提议作为该代谢物的结构。其形成的推测途径包括二氧化碳加到妥卡尼的氨基氮上，随后与尿苷二磷酸-葡萄糖醛酸结合。
