Ask about this productRelated genes to: CYP2B6 antibody
- Gene:
- CYP2B6 NIH gene
- Name:
- cytochrome P450 family 2 subfamily B member 6
- Previous symbol:
- CYP2B
- Synonyms:
- CPB6, CYPIIB6
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-13
- Date modifiied:
- 2019-04-23
Related products to: CYP2B6 antibody
Related articles to: CYP2B6 antibody
- A sensitive and selective LC-MS/MS bioanalytical method was developed, optimized, and validated for the simultaneous quantification of bupropion and hydroxybupropion in human plasma using ultrasound-assisted dispersive liquid-liquid microextraction (UA-DLLME) as the sample preparation technique. Four critical UA-DLLME parameters - extraction solvent volume, disperser solvent volume, sample pH, and ultrasonication time - were simultaneously optimized using Central Composite Design and response surface methodology, yielding extraction recoveries of 93.8 ± 1.2% and 95.6 ± 0.9% for bupropion and hydroxybupropion, respectively. Chromatographic separation of both analytes and the internal standard carbamazepine was achieved on an Agilent Poroshell 120 EC-C18 column (50 × 4.6 mm, 2.7 μm) using an isocratic mobile phase of 10 mM ammonium formate (pH 4.0) and acetonitrile (35:65, v/v) at 0.4 mL/min, with a total runtime of 5 min. Detection was performed by triple quadrupole mass spectrometry in positive electrospray ionization mode using multiple reaction monitoring transitions of m/z 240.1 → 184.1 for bupropion and m/z 256.1 → 238.1 for hydroxybupropion. Comprehensive validation following ICH M10 guideline recommendations demonstrated linearity across 2-1000 ng/mL, LLOQ of 2 ng/mL, intraday and interday precision within 14.13% CV, accuracy within ±8.92% RE, and stability under all evaluated conditions for both analytes. The method was successfully applied to a single-dose pharmacokinetic study in five healthy volunteers following bupropion SR 150 mg administration. The assay measures total (non-stereoselective) hydroxybupropion, and the hydroxybupropion/bupropion AUC metabolic ratios of 6.55-11.68 serve as surrogate indices of CYP2B6 hydroxylation activity, classifying all subjects as CYP2B6 extensive metabolizers and demonstrating the method's utility for CYP2B6 phenotyping and precision pharmacotherapy applications. - Source: PubMed
Publication date: 2026/06/11
Serag AhmedRamzy SherifAlosaimi Manal EAbduljabbar Maram HAlaqel Saleh IAlanazi Mashael NAlqahtani AbdulateefAlmalki Atiah H - Clopidogrel therapy is recommended to prevent recurrent ischemic stroke. However, clopidogrel resistance exists. This study examines which enzymes are involved in clopidogrel resistance. The study group includes 402 neurology patients who had experienced a recurrent ischemic stroke while receiving clopidogrel monotherapy. Patients were genotyped for CYP2C19, CYP2C9, CYP2B6, CYP3A4, CYP3A5, CYP1A2, ABCB1 and CES1A1. Phenotype frequencies were compared with those of a Global(G), European(E) and a local patient control(C) group. Only for ABCB1 a significant difference in phenotype distribution was seen (pG = 0.003, pE = <0.001, pC = 0.019). In patient with ABCB1 rapid efflux activity (3435TT), no other enzyme was significantly associated. In patients with ABCB1 normal efflux activity (3435CT/CC), CYP2C19 intermediate and poor metabolism were significantly associated (pE = <0.001, pG = <0.001, pC = 0.002). In patients with normal CYP2C19 metabolism, CYP2C9 intermediate and poor metabolism were significantly associated (pG = <0.001, pE = <0.001, pC = <0.001). Besides CYP2C19 clinical guidelines, also for ABCB1 and CYP2C9 guidelines are needed to prevent clopidogrel resistance. - Source: PubMed
Publication date: 2026/06/16
Deiman BirgitHermans Mikede Rijk MaartenBras AnneScharnhorst Volkher - Amphetamine-type stimulants (ATS) remain a major group among internationally misused psychostimulants. Prolintane (1-(1-phenylpentan-2-yl)pyrrolidine) is one representative historically applied in clinical settings. Recently, 2-, 3-, and 4-methylprolintane, structurally related prolintane analogs, have been identified as inhibitors of monoamine reuptake, prompting the need for detailed toxicological and analytical characterization. To explore their metabolic transformation and assess their detectability in urine, we analyzed rat samples collected over 24 h following oral administration (2 mg/kg) of each isomer, as well as human liver S9 incubations (25 μM; 1 h and 6 h). Metabolites were tentatively assigned using liquid chromatography-high-resolution tandem mass spectrometry (LC-HRMS/MS). Complementary isoenzyme-specific incubations with 11 human phase I monooxygenases enabled mapping of the primary biotransformation routes. The same in vivo samples were subsequently evaluated with commonly used urine screening strategies, including gas chromatography-MS, LC-ion trap MS, and LC-HRMS/MS. Across all isomers, metabolism was extensive, yielding 95 distinct metabolites. Initial hydroxylation and oxidation reactions were mainly linked to the activity of CYP1A2, CYP2B6, CYP2C19, and CYP3A4, followed by conjugation through glucuronidation, sulfation, or O-methylation. Each screening platform successfully detected the compounds via their metabolites; however, the high degree of overlap in the metabolic profiles limits the ability to distinguish between the three isomers. These results provide essential analytical reference data and contribute to toxicological risk assessment of these emerging ATS derivatives. - Source: PubMed
Publication date: 2026/06/16
Wagmann LeaHerter AnicaDybek Michael BAdejare AdeboyeWallach JasonBrandt Simon DMeyer Markus R - Major depressive disorder (MDD) is treated largely by trial and error, despite marked interindividual variation in antidepressant exposure, efficacy and tolerability. Pharmacogenomics (PGx) has therefore been proposed as a route to stratified antidepressant treatment. This Review asks whether current evidence supports that claim by distinguishing actionable drug-gene guidance, clinical utility in broad trial populations and subgroup evidence for stratified care. Contemporary guidance supports genotype-informed prescribing for selected antidepressants, most consistently through CYP2D6 and CYP2C19 and, for selected serotonin reuptake inhibitors, CYP2B6, whereas SLC6A4 and HTR2A are not clinically actionable for antidepressant prescribing. Randomized and pragmatic trials show that PGx reduces drug-gene mismatched prescribing more reliably than symptom outcomes in unselected MDD samples. Meta-analyses suggest small-to-moderate short-term response or remission gains, with larger signals in treatment-exposed, severe or difficult-to-treat patients. PGx is therefore not simply weakly useful for everyone; its strongest current role is selective, subgroup-enriched prescribing where exposure mismatch is plausible. A practical roadmap is to restrict current interpretation to guideline-supported CYP2D6/CYP2C19/CYP2B6 gene-drug pairs, prioritize testing before affected antidepressants or after nonresponse, intolerance or polypharmacy, avoid broad proprietary class assignment, and validate stratified claims in prospective enriched trials. - Source: PubMed
Publication date: 2026/06/16
Baune Bernhard T - Anti-infective drugs have profoundly transformed the history of medicine. Yet, with the presence of approximately 4.1-5 million interindividual genomic variants in human genome, patients are expected not to respond equally to the same anti-infective drug. This genetic variability, together with nongenetic factors, influences therapeutic outcomes and contributes to drug-induced adverse events in predisposed individuals. Historically, the identification of HLA-B∗57:01 as a predictor of abacavir hypersensitivity in patients with HIV represented the first successful clinical application of pharmacogenomics (PGx) in infectious diseases. Since then, the field has continued to evolve, as evidenced by the discovery of multiple clinically relevant gene-drug pairs, primarily related to immune responses, drug metabolism, and drug transport pathways. The evidence accumulated to date has established a number of mandatory (HLA-B∗57:01-abacavir) and actionable (MT-RNR1-aminoglycosides, CYP2B6-efavirenz, G6PD-nitrofurantoin, G6PD-nalidixic acid, and G6PD-dapsone) gene-drug pairs, whereas most other associations remain informative or exploratory without current guideline-based prescribing recommendations. Despite this progress, robust PGx evidence remains predominantly focused on antiretrovirals, anti-hepatitis C virus, and selected antimicrobial drug classes, such as β-lactams, aminoglycosides, sulfonamides, and antituberculosis drugs. For many other anti-infective agents, current evidence suggests that host genetic variation may have a limited impact on drug efficacy or safety, or that existing studies remain insufficiently powered or replicated to support clinical translation. The narrow ancestral diversity in PGx studies and clinical trials has also restricted the breadth of the knowledge gained and, consequently, the development of inclusive guidelines. This review summarizes the current PGx landscape of antibacterial and antiviral drugs and highlights key challenges and opportunities to improve clinical actionability. Greater inclusion of previously underrepresented populations, coupled with integrative multiomics approaches powered by artificial intelligence and machine learning, could accelerate PGx biomarker identification, validation, and integration into personalized patient care. SIGNIFICANCE STATEMENT: Rapid and effective deployment of anti-infective drugs requires incorporating knowledge of host genetic determinants of drug effectiveness or adverse events, the latter of which is a leading cause of death. The evolution of data science, driven by available genomic data, represents an unprecedented opportunity to accelerate pharmacogenomics discovery in infectious diseases. If acquired at a population level and integrated into medical records, pharmacogenomics data can guide the prescription and/or dosing of anti-infective drugs, shifting infectious disease management toward personalized care. - Source: PubMed
Publication date: 2026/04/10
Smatti Maria KJan ZainabYassine Hadi M