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用于评估人类免疫缺陷病毒蛋白酶抑制剂产生非结合性高胆红素血症可能性的实用临床前模型。

Practical preclinical model for assessing the potential for unconjugated hyperbilirubinemia produced by human immunodeficiency virus protease inhibitors.

作者信息

Kempf Dale J, Waring Jeffrey F, Morfitt David C, Werner Paige, Ebert Brian, Mitten Michael, Nguyen Bach, Randolph John T, DeGoey David A, Klein Larry L, Marsh Kennan

机构信息

Global Pharmaceutical Research and Development, Abbott, Abbott Park, Illinois 60064, USA.

出版信息

Antimicrob Agents Chemother. 2006 Feb;50(2):762-4. doi: 10.1128/AAC.50.2.762-764.2006.

Abstract

A practical preclinical model for the hyperbilirubinemia produced by human immunodeficiency virus protease inhibitors has been developed. Indinavir and atazanavir produced significant hyperbilirubinemia, whereas amprenavir, the negative control, was indistinguishable from the ritonavir booster dose. This model was used to disqualify an exploratory protease inhibitor from development.

摘要

一种用于人类免疫缺陷病毒蛋白酶抑制剂所致高胆红素血症的实用临床前模型已被开发出来。茚地那韦和阿扎那韦可导致显著的高胆红素血症,而作为阴性对照的安普那韦与利托那韦增效剂量之间没有差异。该模型被用于淘汰一种处于研发阶段的探索性蛋白酶抑制剂。

相似文献

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Mechanism of indinavir-induced hyperbilirubinemia.茚地那韦诱导高胆红素血症的机制。
Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12671-6. doi: 10.1073/pnas.231140698. Epub 2001 Oct 16.

本文引用的文献

3
Mechanism of indinavir-induced hyperbilirubinemia.茚地那韦诱导高胆红素血症的机制。
Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12671-6. doi: 10.1073/pnas.231140698. Epub 2001 Oct 16.

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