Stearns R A, Miller R R, Doss G A, Chakravarty P K, Rosegay A, Gatto G J, Chiu S H
Department of Animal and Exploratory Drug Metabolism, Merck Sharp and Dohme Research Laboratories, Rahway, NJ 07065-0900.
Drug Metab Dispos. 1992 Mar-Apr;20(2):281-7.
The in vitro metabolism of DuP 753, a novel nonpeptide angiotensin II receptor antagonist, has been investigated in incubations with liver slice preparations from rats, monkeys and humans. Metabolites were identified by HPLC/MS, FAB/MS, Cl/MS, and/or 1H NMR. In the rat, the primary route of metabolism was oxidative, leading to either monohydroxylated or oxidized (carboxylic acid) metabolites, whereas in monkeys, glucuronidation of the tetrazole moiety predominated. An equal mixture of both oxidized and glucuronic acid-conjugated metabolites was isolated from incubations with human liver slices. All metabolites were tested in an in vitro assay to determine their activity as angiotensin II receptor antagonists. The monohydroxylated products and glucuronic acid conjugates were determined to be much less active than DuP 753. Biotransformation to the carboxylic acid, however, was shown to dramatically increase the activity of this agent. The in vivo duration of action of DuP 753 has been observed to be much longer in the rat than in the monkey. This may be explained, at least in part, by these in vitro metabolism studies. The predominance of glucuronidation observed in incubations with monkey liver slices would yield metabolites with diminished activity and might be expected to shorten the in vivo duration of DuP 753 in that species. The oxidative conversion to the carboxylic acid metabolite, along with the low level of glucuronidation observed in incubations with rat liver slices, may be responsible for the prolonged duration observed in vivo in the rat.
新型非肽类血管紧张素II受体拮抗剂DuP 753的体外代谢情况已在大鼠、猴和人的肝切片制剂孵育实验中进行了研究。通过高效液相色谱/质谱联用仪(HPLC/MS)、快原子轰击质谱(FAB/MS)、化学电离质谱(Cl/MS)和/或核磁共振氢谱(1H NMR)鉴定代谢产物。在大鼠体内,主要代谢途径是氧化,生成单羟基化或氧化(羧酸)代谢产物,而在猴体内,四氮唑部分的葡萄糖醛酸化占主导。在人肝切片孵育实验中分离得到了氧化代谢产物和葡萄糖醛酸结合代谢产物的等量混合物。所有代谢产物都经过体外试验,以确定它们作为血管紧张素II受体拮抗剂的活性。结果表明,单羟基化产物和葡萄糖醛酸结合物的活性比DuP 753低得多。然而,转化为羧酸的生物转化过程显示可显著增加该药物的活性。已观察到DuP 753在大鼠体内的作用持续时间比在猴体内长得多。这至少可以部分地通过这些体外代谢研究来解释。在猴肝切片孵育实验中观察到的葡萄糖醛酸化占主导,会产生活性降低的代谢产物,预计这会缩短DuP 753在该物种体内的作用持续时间。在大鼠肝切片孵育实验中观察到的向羧酸代谢产物的氧化转化以及较低水平的葡萄糖醛酸化,可能是导致在大鼠体内观察到作用持续时间延长的原因。