文拉法辛CYP2D6在体外是催化氧化。
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Otton SV,球,张西南,稻叶型T,鲁道夫RL,卖家
文拉法辛CYP2D6在体外是催化氧化。
Br中国新药杂志。1996年2月,41 (2):149 - 56。
- PubMed ID
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8838442 (在PubMed]
- 文摘
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1。有几个选择性5 -再摄取抑制剂(SSRIs)基因多态药物代谢酶的抑制剂,CYP2D6。我们研究了文拉法辛的互动,一个新的SSRI, CYP2D6在人类肝脏微粒体。2。文拉法辛是一种少有效的抑制剂的酶活性比其他ssri类药物体外测试。平均明显Ki值决定使用CYP2D6-dependent右美沙芬O-demethylation是:33岁,52和22 microM rac-venlafaxine, R(+)文拉法辛和S(-)文拉法辛,分别vs 0.065到1.8 microM帕罗西汀、氟西汀,norfluoxetine、氟伏沙明和舍曲林。3所示。从人类肝脏微粒体从酵母转化(n = 3)和一个包含人类CYP2D6 cDNA表达质粒催化O-demethylation文拉法辛,这是体内主要代谢途径。内在代谢间隙值(Vmax /公里)表明,S(-)文拉法辛了优先通过这个途径。4所示。 In microsomes from CYP2D6-deficient livers (n = 2), Vmax/Km of O-demethylation of venlafaxine was one to two orders of magnitude lower and was similar to the rate of N-demethylation. 5. Studies with chemical probes which preferentially inhibit P450 isoforms suggested that CYP3A3/4 is involved in venlafaxine N-demethylation. 6. These in vitro findings predict phenotypic differences in the kinetics of venlafaxine in vivo, although the clinical importance of this is unclear as O-demethylvenlafaxine is pharmacologically similar to the parent drug. The findings also predict relatively limited pharmacokinetic interaction between venlafaxine and other CYP2D6 substrates.
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- 药物酶
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药物 酶 类 生物 药理作用 行动 文拉法辛 细胞色素P450 3 a4 蛋白质 人类 未知的底物细节 - 药物反应
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反应 细节
