Basic & Clinical Pharmacology & Toxicology最新文献

{"title":"Use of STOPPFrail Medications Following Receipt of the Danish Terminal Grant: A Nationwide Descriptive Study","authors":"Daniel Pilsgaard Henriksen, Thomas Øhlenschlæger, Ann-Cathrine Dalgaard Dunvald","doi":"10.1111/bcpt.70285","DOIUrl":"10.1111/bcpt.70285","url":null,"abstract":"<p>Patients with limited life expectancy represent a population where care needs change over time. Therapeutic goals shift, and the rationale for many medications changes, especially for long-term preventive therapies, where time-to-benefit exceeds the remaining years of life [<span>1</span>]. The STOPPFrail criteria provide a validated, explicit list of medication classes considered potentially inappropriate in frail older adults with limited life expectancy, intended as a practical aid to deprescribing [<span>1</span>].</p><p>Recent Danish data from care home residents demonstrate that use of medications listed in STOPPFrail is widespread, with 88% using at least one such medication [<span>2</span>]. Population-level data in patients with a formally documented short life expectancy are sparse. The Danish Terminal Grant (TG) scheme identifies such a cohort nationwide.</p><p>Healthcare utilisation trajectories at the end of life are largely comparable between cancer and non-cancer terminal conditions in Denmark [<span>3</span>], yet palliative care has traditionally been more developed for patients with cancer.</p><p>We aimed to describe the use of STOPPFrail medications among TG recipients stratified by cancer history.</p><p>This nationwide register-based study was conducted in accordance with the <i>Basic & Clinical Pharmacology & Toxicology</i> policy for experimental and clinical studies [<span>4</span>].</p><p>The TG is granted administratively by the municipality upon application from the patient's physician, who certifies short life expectancy (weeks to months) and cessation of curative treatment [<span>5</span>]. The grant runs for 1 year and is available to patients in both home and care home settings. We used nationwide prescription data from a source population of all Danish adults (≥ 18 years) with at least one redeemed prescription for chronic disease medication between 1995 and 2022, defined by an ATC code list adapted from the Rx-Risk Comorbidity Index [<span>6</span>]. From this population, we identified an incident cohort of all adults registered under the TG scheme (patient type code 99) between 1 January 2018 and 31 December 2022. The index date was defined as the date of the first TG redemption.</p><p>Individual-level data were obtained by linking the Danish National Prescription Registry [<span>7</span>], the Danish National Patient Registry (DNPR) [<span>8</span>], the Civil Registration System and the Danish Education Register using the unique Danish personal identification number.</p><p>Baseline covariates were assessed at index date. Education was categorised according to Statistics Denmark definitions. Multimorbidity burden was assessed using the Danish Multimorbidity Index [<span>9</span>], a weighted score based on 39 chronic conditions. Cancer status was defined as any cancer diagnosis (ICD-10: C00-C97, D37-D48) recorded in the DNPR within 5 years before the index date. Total medication count and STOPPFrail cl","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70285","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The History of the Discovery of Vitamin K","authors":"Hanna Nørgaard Tuxen,&nbsp;Laila Zwisler,&nbsp;Allan Linneberg","doi":"10.1111/bcpt.70283","DOIUrl":"10.1111/bcpt.70283","url":null,"abstract":"<p>Vitamin K was discovered during the 1930s when a strange haemorrhagic disorder was observed in chickens fed a cholesterol-free diet. A fat-soluble agent, present in green leafy vegetables and hog liver, was able to restore haemostasis in the chickens. The chemical structure and the physiological role of vitamin K were uncovered resulting in the Nobel Prize being awarded to Henrik Dam and Edward Doisy in 1943. The discovery of vitamin K led to a breakthrough in our understanding of the human coagulation system, where vitamin K plays a pivotal role in activating prothrombin and other coagulation factors. The prevention of vitamin K–dependent bleeding in newborns by vitamin K prophylaxis was introduced in the 1940s and is today a strong recommendation by the World Health Organization. Vitamin K also became crucial to the management of diseases with high risk of vitamin K deficiency due to malabsorption of fat. Later a new type of drug was developed, vitamin K antagonists, counteracting the physiologic effects of vitamin K for the prevention of thrombotic events. Recent research has indicated that vitamin K may have important functions beyond coagulation in extra-hepatic tissues by promoting healthy bone mineralization and preventing vascular calcification.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70283","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRPA1 Regulates Fibrosis-Associated Transcriptional Pathways in Human Lung Epithelial Cells","authors":"Leevi Halonen,&nbsp;Samu Luostarinen,&nbsp;Ida Valjus,&nbsp;Julia Vistbacka,&nbsp;Antti Pemmari,&nbsp;Eeva Moilanen","doi":"10.1111/bcpt.70276","DOIUrl":"10.1111/bcpt.70276","url":null,"abstract":"<p>Transient receptor potential ankyrin 1 (TRPA1) is a cation channel originally identified in lung fibroblasts and extensively studied in sensory neurons, where it is associated with pain and neurogenic inflammation. We and others have recently shown that TRPA1 is also expressed in lung epithelial cells and that its expression is regulated by the cytokine environment. In the present study, we used next-generation sequencing to analyse the role of TRPA1 and the effects of its inhibition on human A549 lung epithelial cell phenotype under inflammatory conditions. Two different TRPA1 inhibitors (HC-030031 and A-967079) were used and found to alter the expression of 968 genes: 576 genes were downregulated, and 392 upregulated. Ingenuity Pathway Analysis (IPA) predicted that TRPA1 inhibitors significantly suppress the activity of <i>pulmonary fibrosis idiopathic signalling</i> and <i>wound healing</i> pathways. In these pathways, altered genes included matrix metalloproteinases (MMPs), growth factors, collagens and transcription factors. The major profibrotic mediators MMP-12 and MMP-7 were among the most strongly inhibited genes by TRPA1 inhibitors. STRING network analysis suggests that TRPA1 regulates fibrosis-related genes through FOS gene and AP-1 transcription factor. These findings together with previous data propose TRPA1 as a factor and therapeutic target in fibrotic lung diseases, which are associated with poor survival and critical need for novel disease-modifying therapies.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13443396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deprescription of Psychotropics in Children and Adolescents: Systematic Review of Guidelines and Development of a Deprescribing Algorithm","authors":"Paul-Benoît Fargier,&nbsp;Mark Horowitz,&nbsp;Rodolphe Charles,&nbsp;Valérie Rousselon,&nbsp;Erik Fakra,&nbsp;Marie-Noëlle Beyens,&nbsp;Marie-Laure Laroche","doi":"10.1111/bcpt.70278","DOIUrl":"https://doi.org/10.1111/bcpt.70278","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Psychotropics are increasingly prescribed in paediatrics despite limited evidence regarding their benefits and effectiveness. Although deprescribing approaches are established in adults, structured paediatric strategies remain poorly defined.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>To identify and evaluate clinical practice guidelines (CPGs) on psychotropic deprescribing in youth, to describe and discuss recommendations regarding when and how to deprescribe in practice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We systematically searched PubMed, Embase, PsycInfo, Scopus, Web of Science and grey literature (2015–2025). Two reviewers independently screened and evaluated the quality of the guidelines (AGREE II). We derived from this a psychotropic deprescribing algorithm in youth, supplemented with clinical expertise.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among the 1390 records identified, none strictly met the methodological criteria for formal CPGs. Nevertheless, we assessed two papers that provided practical deprescribing recommendations and shared several characteristics with CPGs. One systematic review focused on antidepressant discontinuation, recommending tapering after remission with gradual dose reduction and monitoring to distinguish withdrawal from relapse. One narrative review provided child-specific guidance for stimulants, recommending reassessment and possible discontinuation after 1 year of stability. Both were rated as ‘moderate’ using the AGREE II tool and provided limited practical detail on stepwise deprescribing procedures.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Critical gap and urgent need for paediatric-specific deprescribing guidelines. We propose an expert-informed stepwise deprescribing algorithm.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70278","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148565149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Technology-Driven Decision Support for Opioid Tapering: A Scoping Review","authors":"Laurits Valberg Hemmingsen,&nbsp;Lærke Karner Overgaard,&nbsp;Uffe Kock Wiil,&nbsp;Daniel Pilsgaard Henriksen","doi":"10.1111/bcpt.70275","DOIUrl":"https://doi.org/10.1111/bcpt.70275","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>General practitioners manage most opioid tapering. This process requires time-consuming, individualised planning accounting for patient preferences, dose options and costs. Consequently, clinicians need tools to support tapering. This review explores existing international digital decision support systems for opioid tapering.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a scoping review following the JBI methodology. Five databases (PubMed, Embase, CINAHL, Cochrane and Web of Science) were searched in January 2026. Title/abstract and full-text screening were performed independently by two reviewers based on predefined eligibility criteria. Disagreements were resolved by a third reviewer. Data were extracted and summarised both descriptively and narratively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The search identified 2340 studies, of which four met the eligibility criteria. The studies included described four different technology-driven decision support tools for opioid tapering. The tools varied in format and clinical context (primary and secondary care), but they all aimed to support clinicians in planning and managing opioid tapering. Evidence on clinical effectiveness and real-world implementation was limited across the studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Only few studies have investigated technology-driven decision support for opioid tapering, and only one is set within a European context. While tools exist in different formats and clinical settings, evidence on their effectiveness and real-world implementation remains limited, highlighting a need for further development and evaluation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70275","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148565150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Future Clinical Pharmacological Decision Support","authors":"Jan Schjøtt,&nbsp;Leonora Onarheim Bergsjø,&nbsp;Ylva Böttiger","doi":"10.1111/bcpt.70274","DOIUrl":"10.1111/bcpt.70274","url":null,"abstract":"","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of the Effects of Perfluorooctane Sulfonic Acid (PFOS) and Perfluorooctanoic Acid (PFOA) Exposure on Interleukin-17 Signalling and Poly(I:C)-Induced Lung Inflammation in BALB/c Mice","authors":"Eda Nur İnkaya,&nbsp;Seçil Karahisar Turan,&nbsp;Nurhayat Barlas","doi":"10.1111/bcpt.70272","DOIUrl":"10.1111/bcpt.70272","url":null,"abstract":"<p>The aim of this study was to investigate the effects of co-exposure to perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) on the IL-17-related immune responses and the Poly(I:C)-induced lung inflammation. A total of 66 adult male BALB/c mice were divided into 11 groups, including controls, dose groups receiving PFOS+PFOA (1, 3, 9 mg/kg/day), and combination groups challenged with intratracheal Poly(I:C). Immunological responses were evaluated using flow cytometry, RT-qPCR and ELISA assays. Poly(I:C) stimulation increased Th1, Th17 and Th22 cell percentages, consistent with immune activation. PFOS+PFOA exposure attenuated these responses in a dose-dependent manner under Poly(I:C) (+) conditions. Conversely, increased Th2 cell percentages were observed in PFOS+PFOA exposure groups. Gene expression analyses of <i>Stat3</i>, <i>Il17ra</i> and <i>Ror-γt</i> further suggested tissue-level modulation of IL-17-related signalling pathways. Overall, PFOS+PFOA exposure may modulate the pulmonary immune microenvironment and alter Th1/Th17/Th22-associated responses to Poly(I:C)-induced inflammatory stimulation. These findings suggest that PFAS mixtures may influence pulmonary immune regulation under inflammatory conditions and support the inclusion of immune endpoints in PFAS toxicological evaluation.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70272","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148418350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokines in Alzheimer's Disease: Early Defence, Late Damage and the Impact of Sex and Infection","authors":"Blanca I. Aldana,&nbsp;Kristine Freude","doi":"10.1111/bcpt.70273","DOIUrl":"10.1111/bcpt.70273","url":null,"abstract":"<p>Chemokines constitute a versatile signalling network maintaining homeostasis and glia–neuron communication in the healthy brain but become progressively dysregulated during aging and Alzheimer's disease (AD). This review examines how chemokine systems transition from tightly regulated homeostatic signals to drivers of chronic neuroinflammation in AD. We describe the major chemokine families (CC, CXC, CX3C) and their dominant central nervous system (CNS) receptors (CCR2, CXCR3, CX3CR1), which activate canonical inflammatory pathways including NF-κB, JAK/STAT and PI3K-AKT. In AD, chemokine dysregulation occurs in a coordinated manner across multiple functional modules, including recruitment-associated (CCL2, CXCL1), interferon-inducible (CXCL10), loss-of-restraint (CX3CL1) and vascular-associated chemokines. These alterations shift the network from regulated immune communication to self-sustaining inflammatory circuits perpetuating chronic neuroinflammation. These networks reprogram microglia and astrocytes into disease-associated phenotypes, amplify peripheral immune cell infiltration and destabilise synaptic function. Biological sex profoundly influences neuroinflammatory trajectories, with females exhibiting enhanced microglial senescence and interferon signalling, while males show accelerated complement activation. Viral pathogens, particularly neurotropic viruses (HSV-1, HHV-6, VZV) and SARS-CoV-2, actively reprogram chemokine networks, linking infection to amyloid-β accumulation, tau pathology and neurodegeneration. Therapeutically, chemokine axes represent precision targets requiring stage-matched, sex-stratified interventions rather than broad anti-inflammatory approaches. Understanding chemokine network dynamics offers mechanistic insights into AD pathogenesis and could provide pointers for therapeutic strategies.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70273","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Scoping Review of Dehydrozingerone in Preclinical Pharmacology: Activities, Dose Ranges and Toxicity","authors":"Mikee C. Mercado,&nbsp;Norazrina Azmi,&nbsp;Mazlina Mohd Said,&nbsp;Juriyati Jalil,&nbsp;Jamia Azdina Jamal,&nbsp;Nor Syafinaz Yaakob","doi":"10.1111/bcpt.70262","DOIUrl":"10.1111/bcpt.70262","url":null,"abstract":"<div>\u0000 \u0000 <p>Dehydrozingerone, a phenolic compound derived from ginger, has been reported to possess diverse pharmacological activities. This scoping review systematically evaluates the pharmacological and toxicological effects of dehydrozingerone and its analogues across preclinical models, with a focus on dose ranges and safety profiles. A comprehensive literature search was conducted in PubMed and Scopus up to March 2024, supplemented by manual reference checks. Studies investigating the pharmacological or toxicological activities of dehydrozingerone or its analogues in vitro or in vivo were included. Two independent reviewers screened and selected studies based on predefined criteria, and data were extracted on experimental models, dosing regimens and reported outcomes. Fifty-eight experimental studies met the inclusion criteria, predominantly comprising in vitro investigations, with a smaller proportion of in vivo studies. Dehydrozingerone and its analogues demonstrated antioxidant, anticancer, antimicrobial, anti-inflammatory and other pharmacological effects. The most frequently studied in vivo dose was 30–100 mg/kg, with an upper safety threshold of 2000 mg/kg for single-compound oral administration. Toxicity data indicated a favourable safety profile in most preclinical models, although optimal dosages and efficacy varied across studies and experimental conditions. Dehydrozingerone and its analogues demonstrate promising preclinical effects, but inconsistent dosing and limited clinical data hinder translation. Standardised trials are needed to confirm efficacy and safety.</p>\u0000 </div>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148395776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Using Pharmacovigilance Data for Signal Detection of Drug Interactions for Rosuvastatin","authors":"Ronja Levomäki,&nbsp;Päivi Hirvensalo,&nbsp;Aleksi Tornio,&nbsp;Anne M. Filppula","doi":"10.1111/bcpt.70271","DOIUrl":"10.1111/bcpt.70271","url":null,"abstract":"<p>The 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor rosuvastatin is a substrate of breast cancer resistance protein (BCRP). BCRP inhibition increases rosuvastatin plasma concentrations and may result in concentration-dependent muscle toxicity, at worst rhabdomyolysis. We investigated if concomitant use of rosuvastatin and drugs identified as in vitro BCRP inhibitors shows an increased number of rhabdomyolysis events based on pharmacovigilance data. From reports in the US Food and Drug Administration Adverse Event Reporting System for patients using rosuvastatin, we formed interaction (rosuvastatin with inhibitor) and non-interaction (rosuvastatin without inhibitor) groups for 71 BCRP inhibitors. These groups were further divided into subgroups with or without rhabdomyolysis. For each inhibitor, we calculated reporting odds ratio (ROR) and 95% confidence intervals (CIs). We identified 9777 individual rosuvastatin-related reports during 2013–2023, including 815 rhabdomyolysis reports. Of the 71 inhibitors, 19 had enough reports for analysis. Significantly increased RORs were obtained for the clinical BCRP inhibitors febuxostat (ROR 2.47, 95% CI 1.38–4.43) and ticagrelor (ROR 4.15, 95% CI 3.32–5.20). Amiodarone, erlotinib and rifampicin showed significantly increased RORs. Our findings support known interactions involving febuxostat and ticagrelor and suggest that also other BCRP inhibitors may increase the risk of rosuvastatin-induced rhabdomyolysis.</p>","PeriodicalId":8733,"journal":{"name":"Basic & Clinical Pharmacology & Toxicology","volume":"139 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bcpt.70271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}