Commentary on: “Influence of OATP1B1 Function on the Disposition of Sorafenib‐β‐D‐Glucuronide”

In Bins et al., through the use of in vitro transporter assays and mouse models, the authors demonstrate that SG is a substrate of mouse Oatp1b2 and human OATP1B1, and its uptake into liver cells is inhibited by rifampin, resulting in enhanced SG concentrations in plasma and a 90% reduction of the l...

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Bibliographic Details
Published in:Clinical and translational science 2017-07, Vol.10 (4), p.240-241
Main Authors: Morrissey, KM, Benet, LZ, Ware, JA
Format: Article
Language:English
Subjects:
Animal models
Bile
Cancer therapies
Curcumin
Drugs
Enzymes
Glibenclamide
Hepatocytes
Herbal medicine
Liver
Metabolism
Metabolites
Patients
Plasma levels
Rifampin
Statins
Substrates
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Summary:In Bins et al., through the use of in vitro transporter assays and mouse models, the authors demonstrate that SG is a substrate of mouse Oatp1b2 and human OATP1B1, and its uptake into liver cells is inhibited by rifampin, resulting in enhanced SG concentrations in plasma and a 90% reduction of the liver‐to‐plasma ratio of SG in mice. In Bins et al., despite the observed increase in SG plasma concentrations and the potential for SG eliminated into the bile to undergo hydrolysis to sorafenib, plasma levels of sorafenib are unchanged with rifampin coadministration. [...]the clinical relevance of this observed DDI between rifampin and SG may be limited. [...]commonly administered concomitant drugs (e.g., statins and glibenclamide), complementary alternative medicines (e.g., curcumin, St. John's wort), and endogenous substrates may differentially impact sorafenib and SG disposition and response.
ISSN:1752-8054
1752-8062
DOI:10.1111/cts.12476