Pharmacogenetics and genomics最新文献

{"title":"Association of Genetic Variation in CES, UGT, ABC, and SLCO with Irinotecan Infusion Reactions and Severe Toxicity: Corrigendum.","authors":"Kelly I Nugent, Lyucheng Huang, Maisa Nazzal, Amy L Pasternak, Daniel L Hertz","doi":"10.1097/FPC.0000000000000578","DOIUrl":"https://doi.org/10.1097/FPC.0000000000000578","url":null,"abstract":"","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":"36 1","pages":"23"},"PeriodicalIF":1.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145431967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NFIB rs28379954 does not affect CYP2D6-mediated metabolism of prototypical substrates, tamoxifen or solanidine.","authors":"Samantha Medwid, Ute I Schwarz, Richard B Kim","doi":"10.1097/FPC.0000000000000590","DOIUrl":"https://doi.org/10.1097/FPC.0000000000000590","url":null,"abstract":"<p><strong>Background: </strong>Cytochrome P450 2D6 (CYP2D6) is a highly polymorphic drug-metabolizing enzyme involved in the metabolism of many clinically important medications. CYP2D6 is affected by genetic variation as well as drug interactions; however, this does not account for all the variability seen in CYP2D6. Previously, a single-nucleotide variant in the nuclear factor 1-B (NFIB), rs28379954 T>C, was linked to increased CYP2D6 activity and metabolism of CYP2D6 substrates. Thus, we investigated the effect of NFIB rs28379954 on the metabolism of CYP2D6 substrates, solanidine and tamoxifen.</p><p><strong>Methods: </strong>Patients (N = 759) were genotyped for CYP2D6 genetic variants and NFIB rs28379954. Solanidine, tamoxifen, and their metabolites were measured with ultra-HPLC-tandem mass spectrometry.</p><p><strong>Results: </strong>NFIB rs28379954 genotype (T/T versus T/C) was not associated with metabolism of solanidine to its CYP2D6-generated metabolites, 4-OH-solanidine or SSDA irrespective of CYP2D6 phenotype (poor metabolizer, intermediate metabolizer, or normal metabolizer; P > 0.05). Similarly, the ratio of endoxifen to tamoxifen was not affected by NFIB rs28379954 genotype in any CYP2D6 phenotypic group (P > 0.05). Multivariable linear regression modeling demonstrated that CYP2D6 phenotypes were associated with solanidine metabolic ratios as well endoxifen to tamoxifen ratios. However, the addition of NFIB genotype to the model did not significantly improve the predictability of solanidine or tamoxifen metabolites in plasma.</p><p><strong>Conclusion: </strong>In conclusion, we did not observe any significant impact of NFIB rs28379954 genetic variation on CYP2D6 activity in vivo, when assessed using tamoxifen or solanidine metabolites as prototypical CYP2D6 substrates.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145763577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacogenomic analysis of low-density lipoprotein receptor 3' untranslated region genetic variants influencing rosuvastatin efficacy in Chinese dyslipidemia patients.","authors":"Keke Wang, Yihua Zhu, Yan Tian, Jingli Qin, Zhuo Wang, Guoqiang Zhang, Luyan Wang, Yanwei Zhang, Hong Yuan, Ningling Sun, Songnian Hu, Yayu Ma","doi":"10.1097/FPC.0000000000000575","DOIUrl":"10.1097/FPC.0000000000000575","url":null,"abstract":"<p><strong>Objectives: </strong>Dyslipidemia is a crucial risk factor for atherosclerotic cardiovascular disease. Although rosuvastatin is widely used, treatment response varies significantly due to genetic variation. This study investigated the pharmacogenomic impact of low-density lipoprotein receptor (LDLR) 3' untranslated region (UTR) variants on rosuvastatin efficacy in a Chinese Han adult cohort with dyslipidemia.</p><p><strong>Methods: </strong>A cohort of 113 Chinese participants receiving 10 mg rosuvastatin daily was sequenced for LDLR 3'UTR variants. Haploview was used to assess linkage disequilibrium (LD) patterns and haplotype structures. Multivariate regression modeling was employed to assess the influence of genetic variants on therapeutic outcomes.</p><p><strong>Results: </strong>Seventeen LDLR 3'UTR variants were identified. A crosspopulation comparative assessment revealed significant variation in allele frequencies across distinct ethnic groups. Five variants (rs14158, rs2738466, rs5742911, rs17249057, and rs17249064) were in complete LD ( D ' = 1 and r2  = 1). CHANGE analysis revealed that rosuvastatin efficacy was significantly influenced by rs2738465, rs55903358, rs186461273, and rs751672818, while ANCOVA indicated that baseline triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and patient age, alongside rs2738467, rs143587805, and rs751672818 significantly impacted treatment response. Given the bias correction properties and well-established efficiency, results derived from ANCOVA were preferred. These findings were first reported, highlighting LDLR variants can be used as predictive markers for precision medicine for rosuvastatin in the Chinese population.</p><p><strong>Conclusions: </strong>These findings highlight the role of LDLR 3'UTR as a critical pharmacogenomic locus. Our results advance understanding of genetic predictors for personalized statin therapy.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":"233-242"},"PeriodicalIF":1.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145001227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of pharmacogenomics and opioid prescribing for infants with surgical congenital heart disease.","authors":"Rabab M Barq, Shadassa Ourshalimian, Simran Maggo, Olivia A Keane, Jenny Q Nguyen, Matthew A Deardorff, Tamorah Lewis, Ashwini Lakshmanan, Scott A Mosley, Lorraine I Kelley-Quon","doi":"10.1097/FPC.0000000000000588","DOIUrl":"10.1097/FPC.0000000000000588","url":null,"abstract":"<p><strong>Objectives: </strong>Pharmacogenomic (PGx) variants associated with opioid metabolism and reward pathways may influence pain response and risk of opioid dependence. Infants undergoing surgery routinely receive opioids, and prolonged exposure impacts health outcomes. This study evaluated relationships between PGx variants and opioid utilization in infants undergoing surgery for congenital heart disease (CHD).</p><p><strong>Methods: </strong>This retrospective cohort study included infants <1 year who underwent CHD surgery and had exome sequencing at a quaternary children's hospital from 2009 to 2020. PGx variants associated with opioid-response (COMT, DRD2/ANKK1, ABCB1, OPRM1, and CYP2D6) were evaluated. Median cumulative morphine milliequivalents (MMEs) administered were calculated over each hospitalization, and median MMEs corresponding with each variant were analyzed using Kruskal-Wallis tests.</p><p><strong>Results: </strong>Overall, 48 infants were identified (54.2% male, 47.9% Hispanic/Latino, and 6.3% preterm). Most (n = 34, 70.8%) underwent open surgery, and 14 (29.2%) underwent minimally invasive procedures. Forty infants (83%) were homozygous for at least one opioid-related PGx variant. Infants who underwent open surgery and were homozygous for OPRM1: rs1799971, COMT: rs4633, rs4680, and ABCB1: rs1045642 demonstrated increased cumulative MMEs compared to wild type. Infants who underwent minimally invasive surgery and were homozygous for ABCB1: rs1045642 also had increased cumulative MMEs. No relationship between CYP2D6 metabolizer phenotypes and MMEs was observed.</p><p><strong>Conclusion: </strong>Most infants undergoing CHD surgery who had exome sequencing were homozygous for an opioid-related PGx variant. Additionally, infants who were homozygous received increased MMEs during hospitalization. Routine reporting of PGx variants could inform future innovation in precision medicine and opioid stewardship efforts.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12915561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145918166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exome-wide association study identifies a phosphatidylethanolamine-binding protein 4 variant associated with idiopathic pulmonary fibrosis risk in Koreans.","authors":"Jong-Uk Lee, Min Kyung Kim, Hun Soo Chang, Seung-Lee Park, Eunjeong Seo, Choon-Sik Park","doi":"10.1097/FPC.0000000000000580","DOIUrl":"https://doi.org/10.1097/FPC.0000000000000580","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with poor prognosis, shaped by both environmental and genetic factors. While genome-wide association studies have identified several IPF risk loci, the genetic basis remains incomplete, especially in non-European populations.</p><p><strong>Methods: </strong>We performed an exome-wide association study in 186 Korean IPF patients and 262 healthy controls using the Illumina HumanExome v1.1 BeadChip to discover novel exonic variants linked to IPF susceptibility. Logistic regression was used to test associations, adjusting for age, sex, and smoking history. Functional implications were evaluated through structural modeling and protein stability predictions.</p><p><strong>Results: </strong>After quality control, 23 737 single-nucleotide polymorphisms (SNPs) were analyzed. The variant rs1047406 (T>C) in the PEBP4 gene was significantly associated with IPF under a codominant model (odds ratio = 1.94, 95% confidence interval = 1.42-2.65, P < 0.05 after correction). Haplotype analysis, including three nearby SNPs, further supported this association. In-silico analyses predicted that the E11G substitution caused by rs1047406 reduces protein stability and may disrupt proper folding. GTEx eQTL data showed that the minor allele is linked to altered PEBP4 expression in several tissues. PEBP4 is known to regulate phosphoinositide 3-kinase/protein kinase B and nuclear factor kappa B pathways, both implicated in fibrotic remodeling.</p><p><strong>Conclusion: </strong>A novel PEBP4 variant associated with IPF was identified in a Korean population, likely affecting protein function and expression. These findings underscore the importance of ethnic-specific studies and support PEBP4 as a candidate gene in IPF, meriting further validation.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145391983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The prevalence of pharmacogenetic testing in the United States.","authors":"Annika M Czizik, Hannah Burkett, Joshua C Black, Karilynn M Rockhill, Jennifer Jewell, Andrew A Monte","doi":"10.1097/FPC.0000000000000573","DOIUrl":"10.1097/FPC.0000000000000573","url":null,"abstract":"<p><p>It is unknown how many people in the US have had pharmacogenetic (PGx) testing and whether people want to be tested. We conducted a nationally representative survey of the general US adult population to determine the prevalence of adults that have had PGx testing using a validated confidential online survey, the Non-Medical Use of Prescription Drugs Program. A weighted logistic regression was used to test health characteristics associated with PGx testing and determine those who desire to be tested. The analysis included 29 146 individuals who completed the survey, which represents approximately 260 000 000 adults in the US. The prevalence of US adults who have been PGx tested is 6.6% [95% confidence interval (CI): 6.2-7.0]. Only 32.2% (95% CI: 31.5-32.9), an estimated 79 million individuals, desired PGx testing. Adults who had or want PGx testing were more likely to be female, have higher education, be students, current or former members of the military, use medications, and have a mental health disorder. The prevalence of adults who have been PGx tested remains low in the US. There are knowledge gaps about the benefits of PGx testing that must be bridged to increase implementation.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":"221-225"},"PeriodicalIF":1.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12558169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144784956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of genetic variation with irinotecan infusion reactions and severe toxicity.","authors":"Kelly I Nugent, Lyucheng Huang, Maisa Nazzal, Amy L Pasternak, Daniel L Hertz","doi":"10.1097/FPC.0000000000000574","DOIUrl":"10.1097/FPC.0000000000000574","url":null,"abstract":"<p><p>Irinotecan treatment is often complicated by gastrointestinal, hematological, and infusion-related toxicities, the latter of which typically presents as acute cholinergic syndrome (ACS). While genetic variation in UGT1A1 increases toxicity risk, fewer studies have investigated variation in other genes. This study aimed to assess the impact of variation in other genes involved in irinotecan pharmacokinetics with irinotecan-related toxicity. This was a retrospective study of patients receiving standard irinotecan doses (180 mg/m2) with available genetic and clinical data. The primary analysis was to investigate the impact of carboxylesterase (CES) genetic variation on irinotecan infusion-related ACS. Exploratory secondary analyses evaluated variation in CES1, CES2, UGT1A7, UGT1A9, ABCB1, ABCG2, ABCC2, and SLCO1B1 with severe toxicity, treatment modification, diarrhea, and neutropenia. Univariate associations with P less than 0.05 were adjusted for UGT1A1*28 and UGT1A1*6 genotype. A total of 93 patients were included in this analysis. CES1 variants were not associated with infusion-related ACS. In the exploratory analysis, CES1 rs3785161 AA was associated with an increased likelihood of severe irinotecan toxicity (37 vs. 16%; P = 0.034), and ABCG2 rs2231142 AA/AC was associated with an increased likelihood of severe neutropenia (33 vs. 8%; P = 0.017). CES1 and ABCG2 variants may increase the risk of irinotecan toxicity. Further studies are needed to validate these associations to justify prospective studies investigating the clinical benefits of genetics-guided irinotecan dosing.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":"35 8","pages":"226-231"},"PeriodicalIF":1.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144964011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of VKORC1 and CYP2C9 gene polymorphisms with warfarin dose requirements in a representative Iranian population with cardiac valve replacement surgery.","authors":"Omid Maleki, Javad Gharechahi","doi":"10.1097/FPC.0000000000000571","DOIUrl":"10.1097/FPC.0000000000000571","url":null,"abstract":"<p><strong>Background: </strong>Warfarin is a commonly used oral anticoagulant for managing thromboembolic events after cardiac valve surgery. However, its optimal dose varies between individuals, often requiring trial and error to determine. This study aimed to investigate the association of polymorphisms in the CYP2C9 and VKORC1 genes with warfarin dose requirements in an Iranian population undergoing cardiac valve replacement.</p><p><strong>Materials and methods: </strong>A total of 140 patients recieving warfarin after cardiac valve replacement surgery were enrolled. Patients were monitored for their daily warfarin dose and international normalized ratio for at least 3 months post-surgery. Genotyping of CYP2C9 rs1057910 and VKORC1 rs2884737 was conducted using the tetra-primer amplification refractory mutation system -PCR method. Associations between genotypes and warfarin dose were analyzed using linear regression. A P value < 0.05 was considered statistically significant.</p><p><strong>Results: </strong>Patients with the heterozygous AC genotype of CYP2C9 rs1057910 required a significantly lower warfarin dose than those with the wild-type genotype ( P < 0.05). Although variation in warfarin dose was observed among patients with different VKORC1 rs2884737 genotypes, the association was not statistically significant. Including patients' demographic covariates in the regression model did not alter the observed genotype-dose associations.</p><p><strong>Conclusion: </strong>The CYP2C9 rs1057910 variant was significantly associated with daily warfarin dose requirements, suggesting its potential role in guiding idividualized dosing. In contrast, VKORC1 rs2884737 showed no significant association in this population, despite previous findings in other ethnic groups.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":"214-220"},"PeriodicalIF":1.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144286077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microsampling with dried blood spots and mass spectrometry enables PK/PD profiling of responses to praziquantel in a Schistosoma haematobium- exposed Zimbabwean population.","authors":"David Twesigomwe, Grace Zdesenko, Takafira Mduluza, Gavin Blackburn, Richard Burchmore, Francisca Mutapi","doi":"10.1097/FPC.0000000000000572","DOIUrl":"10.1097/FPC.0000000000000572","url":null,"abstract":"<p><strong>Introduction: </strong>Praziquantel (PZQ) is commonly used to treat schistosomiasis; however, there is considerable interindividual variability in its efficacy, partly because of genetic variation. Data on this relationship is scarce across Africa - where schistosomiasis is prevalent. This study aimed to investigate the pharmacokinetic/pharmacodynamic and pharmacogenetic relationship between PZQ and its metabolites in a Zimbabwean population infected with Schistosoma haematobium by leveraging dried blood spots (DBS) and mass spectrometry (MS).</p><p><strong>Methods: </strong>DBS were obtained from 38 Zimbabwean participants on PZQ treatment at four-time points (0.5, 1.5, 2.5, and 4 h). We compared two extraction methods for recovering PZQ and its metabolites from the DBS cards and performed MS analysis to determine the concentrations. A random forest model was used to determine whether CYP1A2 , CYP2C9 , CYP2C19 , CYP2D6 , CYP3A4 , and CYP3A5 known variants were predictive of PZQ efficacy. The relationships between PZQ/metabolite concentration, metabolite ratio, and drug exposure with genotype were determined using a one-way analysis of variance.</p><p><strong>Results: </strong>An acetonitrile and water (4 : 1) mixture was determined to be optimal for recovering PZQ and its metabolites from the DBS cards. Subsequent MS analysis identified PZQ and six metabolite compounds - including phase 1 metabolites (-2H)-O-PZQ, O2-PZQ, and 4-OH-PZQ. Pooled MS sampling was comparable to individual MS sampling for determining pharmacokinetic profiles at the 2.5 and 4-h time points. The (-2H)-O-PZQ and O2-PZQ metabolites had significantly higher concentrations in participants with CYP2C9*1/*9 and *9/*9 versus those with CYP2C9*1/*1. CYP1A2 rs2069514-A (formerly *1C ) and rs762551-A ( CYP1A2*30 ; formerly *1F ) were observed to alter PZQ pharmacokinetic profiles; however, differences in analyte concentrations across the corresponding genotypes were NS.</p><p><strong>Conclusion: </strong>We show that low-cost microsampling using DBS and MS is feasible for detecting and quantifying PZQ and its metabolites. Furthermore, our pharmacogenetics analysis elucidates the impact of known cytochrome P450 variants on PZQ drug response in an African setting.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":"197-213"},"PeriodicalIF":1.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144289590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacogenetic association of CYP enzymes with therapeutic propofol doses during mechanical ventilation.","authors":"Chanel Hsiang, Faisal Shakeel, Nicholas Farina, Ken Johnson, Daniel L Hertz","doi":"10.1097/FPC.0000000000000570","DOIUrl":"10.1097/FPC.0000000000000570","url":null,"abstract":"<p><p>Propofol is commonly used to sedate patients, but variations in how individuals metabolize the drug may affect dosing requirements. The objective of this study was to explore how genetic variations in CYP450 enzymes, particularly CYP2B6 , influence propofol metabolism in ICU patients receiving mechanical ventilation. Genetic variants of CYP2B6 , CYP2C9 , CYP2C19 , and CYP3A5 were collected from an institutional genetic data repository. Patients were dichotomized into low and high metabolic activity for each enzyme, and the mean weight- and time-normalized propofol dose administered was compared between groups via t test. There was no significant difference in average daily propofol dose between patients with low and high CYP2B6 activity (11 vs. 11 mg/kg/h, P  = 0.78), or any of the other CYP enzymes analyzed (all P  > 0.05). This study could not replicate previous studies indicating that patients carrying genetic variants with diminished CYP2B6 activity required lower propofol doses. Future studies with prospectively collected dosing and outcomes data, and measurement of plasma drug concentrations, may provide insights into personalized propofol dosing strategies.</p>","PeriodicalId":19763,"journal":{"name":"Pharmacogenetics and genomics","volume":" ","pages":"192-195"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}