体外激活氯胍通过人类的肝微粒体是由CYP3A cycloguanil亚型以及S-mephenytoin羟化酶。
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伯DJ,里斯D,安德森T,冈萨雷斯FJ,矿工乔,维罗纳人我
体外激活氯胍通过人类的肝微粒体是由CYP3A cycloguanil亚型以及S-mephenytoin羟化酶。
37 Br中国新药杂志。1994;(5):413 - 20。
- PubMed ID
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8054246 (在PubMed]
- 文摘
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1。激活的氯胍cycloguanil定义,研究了人类肝微粒体的细胞色素P450 (CYP)亚型参与反应。2。明显的氯胍的Km值范围从35 microM 183 microM从四个人类肝脏微粒体。3所示。有6.3倍的活动范围从十七岁人类肝脏微粒体。与CYP3A的氯胍激活率显著相关活动(苯并[a]芘的新陈代谢,咖啡因8-oxidation和奥美拉唑砜形成)和CYP3A免疫反应性的内容。还有一个高度与hydroxyomeprazole形成率显著相关。相关性活动选择性CYP1A2, CYP2C9/10和CYP2E1和免疫反应性的CYP1A2的内容并不重要。4所示。 Proguanil activation was inhibited by R,S-mephenytoin, troleandomycin and by inhibitory anti-CYP3A antiserum and anti-CYP2C IgG and was activated by alpha-naphthoflavone. Inhibitors selective for CYP1A2, CYP2E1, CYP2A6 or CYP2C9/10 had little or no effect on proguanil activation. The extents of inhibition by R,S-mephenytoin, troleandomycin and the two antibodies varied with the immunoreactive CYP3A content of the microsomes used. 5. It is concluded that proguanil activation to cycloguanil by human liver microsomes is mediated both by S-mephenytoin hydroxylase and isoforms of the CYP3A subfamily. This has implications for the use of proguanil as an in vivo probe for the S-mephenytoin poor metaboliser phenotype.
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- 药物反应
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反应 细节
