This study utilized physiologically based pharmacokinetic (PBPK) modeling to explore the pharmacokinetics of BRV and drug interactions between BRV and rifampin (RIF), a CYP2C19 inducer, based on CYP2C19 genetic polymorphisms.  A PBPK model of BRV was developed in the general population and in individuals with different CYP2C19 phenotypes by adjusting catalytic rate constants (kcat), and the model was validated with observed clinical data. 
PBPK
Physiologically based pharmacokinetic modeling of brivaracetam and its interactions with rifampin based on CYP2C19 phenotypes.Brivaracetam (BRV), a third-generation antiepileptic drug (AED), is primarily metabolized through amidase hydrolysis and CYP2C19-mediated hydroxylation in vivo.  A PBPK model of BRV was developed in the general population and in individuals with different CYP2C19 phenotypes by adjusting catalytic rate constants (kcat), and the model was validated with observed clinical data.  The model was then extrapolated to predict BRV steady-state plasma concentration in individuals with different CYP2C19 phenotypes, with or without coadministration of RIF. 
CYP2C19 phenotypes
Physiologically based pharmacokinetic modeling of brivaracetam and its interactions with rifampin based on CYP2C19 phenotypes.Brivaracetam (BRV), a third-generation antiepileptic drug (AED), is primarily metabolized through amidase hydrolysis and CYP2C19-mediated hydroxylation in vivo.  This study utilized physiologically based pharmacokinetic (PBPK) modeling to explore the pharmacokinetics of BRV and drug interactions between BRV and rifampin (RIF), a CYP2C19 inducer, based on CYP2C19 genetic polymorphisms. 
Rifampin
Physiologically based pharmacokinetic modeling of brivaracetam and its interactions with rifampin based on CYP2C19 phenotypes.Brivaracetam (BRV), a third-generation antiepileptic drug (AED), is primarily metabolized through amidase hydrolysis and CYP2C19-mediated hydroxylation in vivo. 
Brivaracetam