II-35 Yingying Tian

Physiologically based pharmacokinetic model incorporating genetic polymorphism of CYP2D6 to predict the nonlinear kinetics of paroxetine

Yingying Tian, Sebastian Frechen, Ahmed Abbas Suleiman, Uwe Fuhr

Department of Pharmacology, Clinical Pharmacology Unit, University Hospital of Cologne, Cologne, Germany

Background: Paroxetine exposure increases more than linear with increasing doses and with decreasing number of active CYP2D6 alleles, which precludes individualized dosing by simple methods.

Objectives: To develop a physiological-based pharmacokinetic (PBPK) model for paroxetine able to describe its nonlinear kinetics among different genotypes.

Methods: PK data were obtained from an open, randomized, single-dose, 2-period, crossover pharmacokinetic study with two different formulations of paroxetine involving 40 healthy volunteers. CYP2D6 genotyping was carried out for all subjects. Data were analyzed using nonlinear mixed-effects modeling implemented in NONMEM V7.3.0. First step was to develop a single compartment model incorporating both inter-occasional variability and CYP2D6-mediated clearance. The structural model was then refined and transformed to a PBPK model by the introduction of physiological compartments and parameters and by incorporation of the mechanism-based inhibition process.

Results: A conventional one-compartment PK model with additional compartments for liver and enzyme and combined error model was developed. Among the covariate relationships tested, weight was identified as a significant covariate on volume of distribution of the central compartment. The model produces estimates pooled clearances according to the expected phenotype of CYP2D6*1, *2, *35 and CYP2D6 *9, *41.The model showed some underprediction for high concentrations. When temporarily removing subjects carrying the less frequent CYP2D6 alleles *9, *35 or *41 present in this study, the model was essentially unchanged.

Conclusions: The current model may serve as a promising base for further refinements. In particular, splitting of the pooled clearances into the respective clearances per underlying allele as well as a better description of the mechanism-based inhibition process need to be addressed.

Reference: PAGE 24 (2015) Abstr 3477 [www.page-meeting.org/?abstract=3477]

Poster: Drug/Disease modeling - Absorption & PBPK

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