Genomic and sex contributions to interindividual variability in pitavastatin bioavailability

Aim: This study investigates pharmacogenetic determinants of pitavastatin disposition using a candidate-gene approach. Methods: In 48 healthy volunteers, 138 variants across 40 genes involved in drug metabolism and transport were analysed to assess their relationship with pitavastatin pharmacokineti...

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Authors: González Iglesias, Eva, Moreno-Pérez de Villar, Sofía, Ochoa Mazarro, María Dolores, Román, Manuel, Novalbos, Jesús, Martín Vílchez, Samuel, Miguel, Alejandro de
Format: article
Publication Date:2026
Country:España
Institution:Universidad Autónoma de Madrid
Repository:Biblos-e Archivo. Repositorio Institucional de la UAM
Language:English
OAI Identifier:oai:dnet:biblosearchi::43062ba00fc9337ed4e991bd3e7c8980
Online Access:https://hdl.handle.net/10486/775000
https://dx.doi.org/10.1111/bcpt.70251
Access Level:Open access
Keyword:bioequivalence trial
pharmacogenetics
pharmacokinetics
pitavastatin
SLCO1B1
Medicina
Description
Summary:Aim: This study investigates pharmacogenetic determinants of pitavastatin disposition using a candidate-gene approach. Methods: In 48 healthy volunteers, 138 variants across 40 genes involved in drug metabolism and transport were analysed to assess their relationship with pitavastatin pharmacokinetics, alongside the influence of sex and biogeographical origin. Results: Women exhibited 35% higher AUC and Cmax values than men; however, these differences disappeared after adjusting for the dose/weight (DW) ratio, with only a 22% increase in t1/2 remaining. The most prominent finding was the 50%–65% increase in AUC/DW and Cmax/DW observed in decreased function (DF) individuals compared with increased function (IF) and normal function (NF) carriers of SLCO1B1 phenotype, reinforcing its role as the primary hepatic uptake transporter for pitavastatin. Additional variants in efflux transporters such as ABCB1, ABCC3 and ABCG2 may also contribute to interindividual variability, albeit to a lesser extent. Among drug-metabolising enzymes, CYP4F2 emerged as a candidate for further investigation, given the 36% reduction in AUC48h/DW associated with the rs3093200 variant. No significant associations were detected for CYP2D6 or CYP2C9 genes. Evidence to date does not indicate a meaningful impact of UGT enzymes on pitavastatin pharmacokinetics. Conclusion: Overall, these findings highlight several genetic factors that may modulate pitavastatin disposition, warranting confirmation through functional studies or larger population cohorts