Evidence map›Paper›PMID 40662264›Full record

ArticleSchizophrenia bulletin2026

Influence of CYP2D6 Genotypes and Phenotypes on the Plasma Levels and Clinical Response to Aripiprazole.

Cécile Gras, Marianna Piras, Setareh Ranjbar, Claire Grosu, François R Girardin, Frederik Vandenberghe, Nicolas Ansermot, Carole Grandjean, Stefan Kaiser, Franziska Gamma and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Schizophrenia bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Genetic PolymorphismsPharmaceuticals (Basel, Switzerland) · 2026
    Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Cécile GrasUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Marianna PirasUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Setareh RanjbarCenter for Psychiatric Epidemiology and Psychopathology, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Claire GrosuUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
François R GirardinService of Clinical Pharmacology, Department of Laboratory Medicine and Pathology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Frederik VandenbergheUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Nicolas AnsermotUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Carole GrandjeanUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Stefan KaiserAdult Psychiatry Division, Department of Psychiatry, Geneva University Hospitals, Geneva, Switzerland.
Franziska GammaLes Toises Psychiatry and Psychotherapy Center, Lausanne, Switzerland.
Kerstin Jessica PlessenService of Child and Adolescent Psychiatry, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Armin von GuntenService of Old Age Psychiatry, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Philippe ConusService of General Psychiatry, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Séverine CrettolUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.
Chin B EapUnit of Pharmacogenetics and Clinical Psychopharmacology, Centre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.

Funding

National Research Foundation
6 · The paper itself

Abstract

backgroundThe antipsychotic aripiprazole is mainly metabolized by the cytochrome P450 (CYP) 2D6. The main objective of this study was to evaluate the influence of CYP2D6 phenotypes on aripiprazole plasma levels and treatment duration.

design466 patients treated with aripiprazole for up to 12 months and with at least one aripiprazole plasma level in steady-state condition were selected. CYP2D6 genotypes and phenoconversion to poor metabolizer status due to strong CYP2D6 inhibition were considered. Aripiprazole plasma level-to-dose ratios and treatment duration up to discontinuation, defined as switching to another psychotropic drug and/or stopping the follow-up, were analyzed using robust linear models and Cox regression, respectively. Akaike variable selection was applied.

resultsCYP2D6 poor metabolizers (genetically determined n = 19 and phenoconverted, n = 52) showed higher aripiprazole concentration-to-dose (P < .001) and aripiprazole plus dehydroaripiprazole concentration-to-dose (P < .001) ratios when compared to normal metabolizers (n = 255). CYP2D6 extreme metabolizers (ie, poor and ultrarapid metabolizers) had higher risk of treatment discontinuation versus intermediate and normal metabolizers after 3, 6, and 12 months of treatment (HR: 2.08, 1.75, 1.59, respectively; P = .013, P = .019, and P = .047, respectively). For a pharmacogenetic-guided treatment, the number of patients needed to genotype to prevent 1 patient from aripiprazole discontinuation was 15.

conclusionCYP2D6 poor metabolism was associated with increased aripiprazole and aripiprazole plus dehydroaripiprazole concentrations-to-dose. CYP2D6 extreme phenotypes were associated with increased risk of treatment discontinuation over 1 year of treatment. This finding supports the applicability of pre-emptive CYP2D6 genotyping, which is expected to decrease aripiprazole adverse events and inefficacy that would probably lead to treatment discontinuation.

Indexed as

Antipsychotic AgentsAripiprazoleCytochrome P-450 CYP2D6SchizophreniaAdultFemaleFollow-Up StudiesGenotypeHumansMaleMiddle AgedPhenotypePiperazinesQuinolonesYoung AdultAntipsychotic AgentsAripiprazoleCytochrome P-450 CYP2D6dehydroaripiprazolePiperazinesQuinolonesaripiprazoleCYP2D6genetic polymorphismsphenotypepre-emptive genotyping

Identifiers

PMID40662264
PMCPMC12996889

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.