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As rifampicin can cause the induction and inhibition of multiple metabolizing enzymes and transporters, it has been challenging to accurately predict the complex drug–drug interactions ( DDI s). We previously constructed a physiologically‐based pharmacokinetic ( PBPK ) model of rifampicin accounting for the components for the induction of cytochrome P450 ( CYP ) 3A/ CYP 2C9 and the inhibition of organic anion transporting polypeptide 1B ( OATP 1B). This study aimed to expand and verify the  PBPK  model for rifampicin by incorporating additional components for the induction of  OATP 1B and  CYP 2C8 and the inhibition of multidrug resistance protein 2. The established  PBPK  model was capable of accurately predicting complex rifampicin‐induced alterations in the profiles of glibenclamide, repaglinide, and coproporphyrin I (an endogenous biomarker of  OATP 1B activities) with various dosing regimens. Our comprehensive rifampicin  PBPK  model may enable quantitative prediction of  DDI s across diverse potential victim drugs and endogenous biomarkers handled by multiple metabolizing enzymes and transporters.

cpt: pharmacometrics and systems pharmacology

Expanded Physiologically‐Based Pharmacokinetic Model of Rifampicin for Predicting Interactions With Drugs and an Endogenous Biomarker via Complex Mechanisms Including Organic Anion Transporting Polypeptide 1B Induction