Pharmacokinetic boosting of olaparib: A randomised, cross-over study (PROACTIVE-study).


Journal

European journal of cancer (Oxford, England : 1990)
ISSN: 1879-0852
Titre abrégé: Eur J Cancer
Pays: England
ID NLM: 9005373

Informations de publication

Date de publication:
11 2023
Historique:
received: 03 08 2023
revised: 07 09 2023
accepted: 09 09 2023
medline: 20 11 2023
pubmed: 9 10 2023
entrez: 8 10 2023
Statut: ppublish

Résumé

Pharmacokinetic (PK) boosting is the intentional use of a drug-drug interaction to enhance systemic drug exposure. PK boosting of olaparib, a CYP3A-substrate, has the potential to reduce PK variability and financial burden. The aim of this study was to investigate equivalence of a boosted, reduced dose of olaparib compared to the non-boosted standard dose. This cross-over, multicentre trial compared olaparib 300 mg twice daily (BID) with olaparib 100 mg BID boosted with the strong CYP3A-inhibitor cobicistat 150 mg BID. Patients were randomised to the standard therapy followed by the boosted therapy, or vice versa. After seven days of each therapy, dense PK sampling was performed for noncompartmental PK analysis. Equivalence was defined as a 90% Confidence Interval (CI) of the geometric mean ratio (GMR) of the boosted versus standard therapy area under the plasma concentration-time curve (AUC Of 15 included patients, 12 were eligible for PK analysis. The GMR of the AUC Boosting a 100 mg BID olaparib dose with cobicistat increases olaparib exposure 1.45-fold, compared to the standard dose of 300 mg BID. Equivalence of the boosted olaparib was thus not established. Boosting remains a promising strategy to reduce the olaparib dose as cobicistat increases olaparib exposure Adequate tolerability of the boosted therapy with higher exposure should be established.

Sections du résumé

BACKGROUND
Pharmacokinetic (PK) boosting is the intentional use of a drug-drug interaction to enhance systemic drug exposure. PK boosting of olaparib, a CYP3A-substrate, has the potential to reduce PK variability and financial burden. The aim of this study was to investigate equivalence of a boosted, reduced dose of olaparib compared to the non-boosted standard dose.
METHODS
This cross-over, multicentre trial compared olaparib 300 mg twice daily (BID) with olaparib 100 mg BID boosted with the strong CYP3A-inhibitor cobicistat 150 mg BID. Patients were randomised to the standard therapy followed by the boosted therapy, or vice versa. After seven days of each therapy, dense PK sampling was performed for noncompartmental PK analysis. Equivalence was defined as a 90% Confidence Interval (CI) of the geometric mean ratio (GMR) of the boosted versus standard therapy area under the plasma concentration-time curve (AUC
RESULTS
Of 15 included patients, 12 were eligible for PK analysis. The GMR of the AUC
CONCLUSIONS
Boosting a 100 mg BID olaparib dose with cobicistat increases olaparib exposure 1.45-fold, compared to the standard dose of 300 mg BID. Equivalence of the boosted olaparib was thus not established. Boosting remains a promising strategy to reduce the olaparib dose as cobicistat increases olaparib exposure Adequate tolerability of the boosted therapy with higher exposure should be established.

Identifiants

pubmed: 37806255
pii: S0959-8049(23)00648-2
doi: 10.1016/j.ejca.2023.113346
pii:
doi:

Substances chimiques

olaparib WOH1JD9AR8
Cytochrome P-450 CYP3A EC 1.14.14.1
Piperazines 0
Cobicistat LW2E03M5PG

Types de publication

Randomized Controlled Trial Multicenter Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

113346

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: RHJM reports research funding paid to the institute from Astellas, Bayer, Boehringer-Ingelheim, Cristal Therapeutics, Novartis, Pamgene, Pfizer, Roche, Sanofi, and Servier. IB reports research funding paid to the institute from GSK. PH reports personal fees from Astellas and consulting or advisory fees from Astellas, MSD, Pfizer AstraZeneca, BMS, Ipsen. GSS reports research funding paid to the institute from Agendia, AstraZeneca, Merck, Novartis, Roche, and Seagen and a consulting role for Biovica and Seagen. NPvE reports research funding paid to the institute from Astellas, Janssen-Cilag, Ipsen. JKO, NADG, MIMA, PBO, HJB, SLWK, ADRH, FLO and RtH declare no potential conflicts of interest.

Auteurs

Joanneke K Overbeek (JK)

Department of Pharmacy, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Gelderland, the Netherlands. Electronic address: Joanneke.Overbeek@radboudumc.nl.

Niels A D Guchelaar (NAD)

Department of Medical Oncology, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, South Holland, the Netherlands.

Ma Ida Mohmaed Ali (MI)

Department of Pharmacy and Pharmacology, The Netherlands Cancer Institute, Amsterdam, North Holland, the Netherlands.

Petronella B Ottevanger (PB)

Department of Medical Oncology, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Gelderland, the Netherlands.

Haiko J Bloemendal (HJ)

Department of Medical Oncology, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Gelderland, the Netherlands.

Stijn L W Koolen (SLW)

Department of Medical Oncology, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, South Holland, the Netherlands; Department of Hospital Pharmacy, Erasmus University Medical Center, Rotterdam, South Holland, the Netherlands.

Ron H J Mathijssen (RHJ)

Department of Medical Oncology, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, South Holland, the Netherlands.

Ingrid A Boere (IA)

Department of Medical Oncology, Erasmus MC Cancer Institute, Erasmus University Medical Center, Rotterdam, South Holland, the Netherlands.

Paul Hamberg (P)

Department of Internal Medicine, Franciscus Gasthuis and Vlietland, Rotterdam, South Holland, the Netherlands.

Alwin D R Huitema (ADR)

Department of Pharmacy and Pharmacology, The Netherlands Cancer Institute, Amsterdam, North Holland, the Netherlands; Department of Pharmacology, Princess Máxima Center for Pediatric Oncology, Utrecht, Utrecht, the Netherlands; Department of Clinical Pharmacy, University Medical Center Utrecht, Utrecht University, Utrecht, Utrecht, the Netherlands.

Gabe S Sonke (GS)

Department of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, North Holland, the Netherlands.

Frans L Opdam (FL)

Department of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, North Holland, the Netherlands.

Rob Ter Heine (R)

Department of Pharmacy, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Gelderland, the Netherlands.

Nielka P van Erp (NP)

Department of Pharmacy, Research Institute for Medical Innovation, Radboud University Medical Center, Nijmegen, Gelderland, the Netherlands.

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Classifications MeSH