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Article

Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia.

Clinical cancer research : an official journal of the American Association for Cancer Research - 1 Apr 2012

Peer Cody J, Sissung Tristan M, Kim Aerang, Jain Lokesh, Woo Sukyung, Gardner Erin R, Kirkland C Tyler, Troutman Sarah M, English Bevin C, Richardson Emily D, Federspiel Joel, Venzon David, Dahut William, Kohn Elise, Kummar Shivaani, Yarchoan Robert, Giaccone Giuseppe, Widemann Brigitte, Figg William D

Abstract excerpt

PURPOSE: Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase). We hypothesized that sorafenib inhibits UGT1A1 and individuals carrying UGT1A1*28 and/or UGT1A9 variants experience greater sorafenib exposure and greater increase in sorafenib-induced plasma bilirubin...

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Benzenesulfonates
Bilirubin
Glucuronides
Hyperbilirubinemia

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Multidrug Resistance-Associated Protein 2

UDP-Glucuronosyltransferase 1A9

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Identifiers

PMID: 22307138
DOI: 10.1158/1078-0432.CCR-11-2484
PMCID: PMC6432766

Genes

ABCC2

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

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