丙戊酸诱导的抗惊厥作用、致畸性和肝毒性的鉴别。物种变异、药代动力学、代谢和结构特异性对开发替代抗癫痫药物如2-丙戊酸三角洲的影响。

H Nau, H Siemes
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引用次数: 13

摘要

丙戊酸通过各种代谢途径代谢成大量化合物。代谢谱取决于物种和年龄。肝毒性可能与代谢异常有关,尤其是在年轻时。致畸性与特定的结构要求有关:一个游离的羧基原子与一个碳原子相连,碳原子还携带一个氢和两条碳链。这为开发替代性抗癫痫药物提供了线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Differentiation between valproate-induced anticonvulsant effect, teratogenicity and hepatotoxicity. Aspects of species variation, pharmacokinetics, metabolism and implications of structural specificity for the development of alternative antiepileptic agents such as delta 2-valproate.

Valproate is metabolized into a large number of compounds via various metabolic routes. Metabolic profiles depend on species and age. Hepatotoxicity may be correlated with abnormal metabolism, especially in young age. Teratogenicity is associated with specific structural requirements: a free carboxyl atom connected to a carbon atom which also carries a hydrogen, and two carbon chains. This provides a clue for the development of alternative antiepileptic agents.

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