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Practical preclinical model for assessing the potential for unconjugated hyperbilirubinemia produced by human immunodeficiency virus protease inhibitors.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。
Antimicrob Agents Chemother. 2006 Feb;50(2):762-4. doi: 10.1128/AAC.50.2.762-764.2006.
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Pharmacokinetics of concurrent administration of fosamprenavir and atazanavir without ritonavir in human immunodeficiency virus-negative subjects.在人类免疫缺陷病毒阴性受试者中同时给予福沙普那韦和阿扎那韦（不联用利托那韦）的药代动力学
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Anti-HIV agents. Atazanavir as a booster for protease inhibitors.
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Hyperbilirubinaemia in HIV-HCV co-infected patients on antiretroviral therapy: drug effect or liver disease severity?接受抗逆转录病毒治疗的HIV-HCV合并感染患者的高胆红素血症：药物作用还是肝脏疾病严重程度？
BMJ Open Gastroenterol. 2016 Mar 2;3(1):e000072. doi: 10.1136/bmjgast-2015-000072. eCollection 2016.
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Biomarkers, metabonomics, and drug development: can inborn errors of metabolism help in understanding drug toxicity?生物标志物、代谢组学与药物研发：先天性代谢缺陷有助于理解药物毒性吗？
AAPS J. 2007 Jul 20;9(3):E284-97. doi: 10.1208/aapsj0903031.

本文引用的文献

1
In vitro inhibition of UDP glucuronosyltransferases by atazanavir and other HIV protease inhibitors and the relationship of this property to in vivo bilirubin glucuronidation.阿扎那韦及其他HIV蛋白酶抑制剂对尿苷二磷酸葡萄糖醛酸基转移酶的体外抑制作用及其该特性与体内胆红素葡萄糖醛酸化的关系。
Drug Metab Dispos. 2005 Nov;33(11):1729-39. doi: 10.1124/dmd.105.005447. Epub 2005 Aug 23.
2
Inhibition of human organic anion transporting polypeptide OATP 1B1 as a mechanism of drug-induced hyperbilirubinemia.抑制人类有机阴离子转运多肽OATP 1B1作为药物性高胆红素血症的一种机制。
Chem Biol Interact. 2004 Nov 20;150(2):179-87. doi: 10.1016/j.cbi.2004.08.008.
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.
4
Pharmacokinetic enhancement of inhibitors of the human immunodeficiency virus protease by coadministration with ritonavir.与利托那韦共同给药对人免疫缺陷病毒蛋白酶抑制剂的药代动力学增强作用。
Antimicrob Agents Chemother. 1997 Mar;41(3):654-60. doi: 10.1128/AAC.41.3.654.
5
The 3-methylcholanthrene-inducible UDP-glucuronosyltransferase deficiency in the hyperbilirubinemic rat (Gunn rat) is caused by a -1 frameshift mutation.高胆红素血症大鼠（冈恩大鼠）中3-甲基胆蒽诱导的尿苷二磷酸葡萄糖醛酸基转移酶缺乏是由一个-1移码突变引起的。
J Biol Chem. 1989 Dec 15;264(35):21302-7.

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.

DOI:10.1128/AAC.50.2.762-764.2006
PMID:16436740
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1366866/
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。