Concomitant use of isavuconazole and CYP3A4/5 inducers: Where pharmacogenetics meets pharmacokinetics.


Journal

Mycoses
ISSN: 1439-0507
Titre abrégé: Mycoses
Pays: Germany
ID NLM: 8805008

Informations de publication

Date de publication:
Sep 2021
Historique:
revised: 16 04 2021
received: 12 02 2021
accepted: 30 04 2021
pubmed: 9 5 2021
medline: 7 1 2022
entrez: 8 5 2021
Statut: ppublish

Résumé

Isavuconazole is a triazole antifungal drug, approved for the treatment of invasive aspergillosis and mucormycosis. Isavuconazole is metabolised by CYP3A4 and CYP3A5, and it has been shown that the CYP3A inducer rifampin reduces isavuconazole exposure. By extrapolation, the concomitant use of isavuconazole with moderate and strong CYP450 inducers is contraindicated, although it is known that some CYP450 inducers are less potent in comparison with rifampin. We aim to document exposure to isavuconazole in patients concomitantly treated with a CYP450 inducer that is less potent compared to rifampin. Moreover, although it is well known that CYP3A enzymes are important for the metabolism of isavuconazole, this induction effect has never been studied in combination with the patient's CYP3A genotype. We report three patients treated with both isavuconazole and a CYP3A inducer that is less potent compared to rifampin (rifabutin or phenobarbital), in whom we determined isavuconazole concentrations. These cases suggest that the CYP3A4/5 genotype is an important determinant for isavuconazole exposure and that it might also influence the CYP450 induction interaction. CYP3A inducers that are less potent compared to rifampin, may be combined with isavuconazole in patients with loss of CYP3A5 activity (CYP3A5*3/*3). Therapeutic drug monitoring is recommended during this combination. However, low-isavuconazole exposure was observed in the extensive metaboliser with CYP3A4*1/*1 and CYP3A5*1/*3 alleles.

Sections du résumé

BACKGROUND BACKGROUND
Isavuconazole is a triazole antifungal drug, approved for the treatment of invasive aspergillosis and mucormycosis. Isavuconazole is metabolised by CYP3A4 and CYP3A5, and it has been shown that the CYP3A inducer rifampin reduces isavuconazole exposure. By extrapolation, the concomitant use of isavuconazole with moderate and strong CYP450 inducers is contraindicated, although it is known that some CYP450 inducers are less potent in comparison with rifampin.
OBJECTIVES OBJECTIVE
We aim to document exposure to isavuconazole in patients concomitantly treated with a CYP450 inducer that is less potent compared to rifampin. Moreover, although it is well known that CYP3A enzymes are important for the metabolism of isavuconazole, this induction effect has never been studied in combination with the patient's CYP3A genotype.
PATIENTS METHODS
We report three patients treated with both isavuconazole and a CYP3A inducer that is less potent compared to rifampin (rifabutin or phenobarbital), in whom we determined isavuconazole concentrations.
RESULTS RESULTS
These cases suggest that the CYP3A4/5 genotype is an important determinant for isavuconazole exposure and that it might also influence the CYP450 induction interaction.
CONCLUSIONS CONCLUSIONS
CYP3A inducers that are less potent compared to rifampin, may be combined with isavuconazole in patients with loss of CYP3A5 activity (CYP3A5*3/*3). Therapeutic drug monitoring is recommended during this combination. However, low-isavuconazole exposure was observed in the extensive metaboliser with CYP3A4*1/*1 and CYP3A5*1/*3 alleles.

Identifiants

pubmed: 33963620
doi: 10.1111/myc.13300
doi:

Substances chimiques

Cytochrome P-450 CYP3A Inducers 0
Nitriles 0
Pyridines 0
Triazoles 0
isavuconazole 60UTO373KE
Cytochrome P-450 CYP3A EC 1.14.14.1
CYP3A4 protein, human EC 1.14.14.55
Rifampin VJT6J7R4TR

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1111-1116

Subventions

Organisme : Fonds Wetenschappelijk Onderzoek
ID : 12X9420N

Informations de copyright

© 2021 Wiley-VCH GmbH.

Références

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Auteurs

Ruth Van Daele (R)

Department of Pharmaceutical and Pharmacological Sciences, KU Leuven and Pharmacy Department, University Hospitals Leuven, Leuven, Belgium.

Yves Debaveye (Y)

Intensive Care Unit, University Hospitals Leuven and Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium.

Robin Vos (R)

Clinical Department of Laboratory Medicine, Respiratory Diseases, University Hospitals Leuven and Chrometa Department, BREATHE, KU Leuven, Leuven, Belgium.

Pascal Van Bleyenbergh (P)

Clinical Department of Laboratory Medicine, Respiratory Diseases, University Hospitals Leuven, Leuven, Belgium.

Roger J Brüggemann (RJ)

Department of Pharmacy and Radboud Institute for Health Sciences, Radboudumc and Radboudumc Center for Infectious Diseases, Radboudumc, Nijmegen, The Netherlands.

Erwin Dreesen (E)

Department of Pharmaceutical and Pharmacological Sciences, KU Leuven, Leuven, Belgium.
Uppsala Pharmacometrics Research Group, Department of Pharmacy, Uppsala University, Uppsala, Sweden.

Omar Elkayal (O)

Department of Pharmaceutical and Pharmacological Sciences, KU Leuven, Leuven, Belgium.

Henk-Jan Guchelaar (HJ)

Department of Clinical Pharmacy & Toxicology, Leiden University Medical Center, Leiden, The Netherlands.

Pieter Vermeersch (P)

Clinical Department of Laboratory Medicine and National Reference Centre for Mycosis, Excellence Centre for Medical Mycology (ECMM), University Hospitals Leuven, Leuven, Belgium.

Katrien Lagrou (K)

Clinical Department of Laboratory Medicine and National Reference Centre for Mycosis, Excellence Centre for Medical Mycology (ECMM), University Hospitals Leuven and Department of Microbiology, Immunology and Transplantation, KU Leuven, Leuven, Belgium.

Isabel Spriet (I)

Department of Pharmaceutical and Pharmacological Sciences, KU Leuven and Pharmacy Department, University Hospitals Leuven, Leuven, Belgium.

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