北京若生智能科技有限公司
Drug Database
ZO

zolpidem tartrate (Stilnox CR / FK199B / Stilnoxium)

✓ Approved

Astellas Pharma · GABRA1 · 小分子

什么是 zolpidem tartrate？

zolpidem tartrate 是一种小分子，由Astellas Pharma研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Stilnox CR, FK199B, Stilnoxium
公司Astellas Pharma
药物类别小分子
分子靶点GABRA1
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Astellas Pharma

作用机制

分子靶点

zolpidem tartrate 作用于 1 个分子靶点：

GABRA1gamma-aminobutyric acid type A receptor alpha1 subunit (DEE19, ECA4)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

zolpidem tartrate 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Psychiatric disordersInsomnia✓ Approved

相关研究文献

PubMedAdvances in clinical and experimental medicine : official organ Wroclaw Medical University2026-10-26

Genetic evidence linking gout to increased risk of epilepsy: A two-sample Mendelian randomization study.

Chen Zhen Z, Wang Ying Y, Yao Shan S

While observational studies have explored the association between gout, uric acid (UA) levels, and the risk of epilepsy, their findings remain inconsistent. To clarify the potential causal relationship, we performed a Mendelian randomization (MR) analysis. We conducted a bidirectional MR analysis using genome-wide association study (GWAS) summary data. Epilepsy data were sourced from the International League Against Epilepsy (ILAE), gout data from the FinnGen consortium and a GWAS of clinically defined gout and its subtypes, and UA data from the BioBank Japan (BBJ) and a genome-wide meta-analysis of serum UA levels in Japanese individuals. The inverse-variance weighted (IVW) method served as the primary causal inference approach. To ensure robustness, we complemented this with 3 additional methods: MR-Egger, weighted median, and MR using Robust Adjusted Profile Score (MR-RAPS) - the latter specifically employed to account for potential weak instrument bias due to the limited number of single-nucleotide polymorphisms (SNPs) included in this analysis. Our analysis identified a causal association between genetically predicted gout and an increased risk of epilepsy (odds ratio (OR) = 1.014, 95% confidence interval (95% CI): 1.011-1.017, p < 0.001), generalized epilepsy (OR = 1.009, 95% CI: 1.000-1.018, p = 0.042), and focal epilepsy (OR = 1.044, 95% CI: 1.002-1.088, p = 0.041) in Europeans. In contrast, UA levels showed no significant association with epilepsy or its subtypes in this population. Similarly, neither gout nor UA levels were linked to epilepsy in East Asians. Sensitivity analyses generally supported the robustness of the primary findings. This MR study provides genetic evidence supporting a potential causal role of gout in increasing the risk of epilepsy, including generalized and focal epilepsy, in European populations. In contrast, genetically predicted UA levels showed no significant association with epilepsy. These findings support a potential role of gout in epilepsy risk and warrant further investigation into the underlying mechanisms.

PMID 42929092
阅读全文 →
PubMedClinical epigenetics2026-10-26

Multi-omics analysis reveals MICB promotes cerebral atherosclerosis through FTMT suppression in NK and plasma cells.

Dai Yonggang Y, Liu Ye Y, Yan Yunjun Y, Ji Haoran H et al.

Ferroptosis, an iron-dependent form of regulated cell death, is implicated in vascular injury, but how immune-related proteins modulate ferroptosis and cerebral atherosclerosis (CeA) remains unclear. We performed multi-step Mendelian randomization (MR) integrating plasma proteomics, single-cell eQTL, and FinnGen CeA GWAS data. Mediation MR quantified the role of the ferroptosis regulator FTMT. Cell-type-specific MR was conducted across 14 immune subtypes. Functional enrichment and RT-qPCR of clinical blood samples validated findings. Four immune proteins (KIR2DL3, HLA-E, LTA, MICB) were identified as causal risk factors for CeA, acting primarily by downregulating FTMT (all β1 < 0, P < 0.001). Mediation analysis revealed FTMT explained up to 53% of the immune protein effect. Single-cell MR demonstrated striking cell-type specificity for MICB: higher MICB in NK cells and IgJ+ B cells was strongly associated with CeA risk (e.g., β = 0.90, P = 4.3 × 10-6), while higher MICB in dendritic cells was protective (β = - 0.57, P = 2.1 × 10-30). In clinical samples, RT-qPCR confirmed reduced FTMT expression, and plasma ELISA showed elevated circulating LTA, soluble MICB, and soluble HLA-E in CeA patients. Network analysis highlighted NK cell cytotoxicity as a central pathway. In summary, our study demonstrates that four immune-related proteins, including MICB, promote cerebral atherosclerosis by downregulating the ferroptosis-protective factor FTMT. Importantly, single-cell MR reveals that MICB acts as a risk factor for CeA specifically in NK cells and plasma cells, providing new mechanistic insight into cell-type-dependent immune regulation of vascular disease.

PMID 42928267
阅读全文 →
PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-10-26

Integrative Genetic, Transcriptomic, and Single-Cell Analyses Prioritize Druggable Candidate Genes in Knee Osteoarthritis.

Zheng Yiping Y, Xuan Yingying Y, Li Yi Y, Deng Changxu C et al.

Knee osteoarthritis (KOA) is a common degenerative joint disease with a complex pathogenesis and a lack of effective molecular targets. This study aimed to prioritize druggable genes associated with KOA and investigate their expression patterns and cellular localization by integrating genetic, transcriptomic, and single-cell analyses. We first screened for potential druggable genes genetically associated with KOA using MR analysis. Subsequently, batch-corrected synovial transcriptomic data were analyzed using weighted gene co-expression network analysis (WGCNA), and the genes of the most relevant module were integrated with the MR candidates. A total of 127 machine-learning pipelines were evaluated using repeated nested cross-validation, followed by external validation and SHapley Additive exPlanations (SHAP) interpretation. The expression levels of key genes were further validated by experiments. Single-cell RNA sequencing, immune-cell deconvolution, and peripheral immune-cell-specific eQTL-MR were used to investigate the cellular contexts potentially associated with the candidate genes. Finally, potential drug-gene interactions were retrieved from DGIdb, and selected target-compound pairs were evaluated using molecular docking and molecular dynamics simulations. A total of 315 druggable genes showed nominal MR associations with KOA. After integrating KOA-associated WGCNA module, we identified 15 candidate genes. Next, the random forest was selected as the optimal machine-learning model, achieving a mean outer-cross-validation AUC of 0.929 (95% CI, 0.913-0.945). SHAP and differential-expression analyses prioritized four genes. JUN, ADAMTS1, and CRISPLD2 were downregulated in KOA synovium, whereas CX3CR1 was upregulated, and these expression patterns were supported by experimental validation. Single-cell analysis revealed that JUN, ADAMTS1, and CRISPLD2 were predominantly expressed in fibroblast-related populations and CX3CR1 was mainly expressed in myeloid cells, with their expression varying across fibroblast and macrophage states. Peripheral immune-cell-specific eQTL-MR identified nominal associations for JUN in plasma cells, ADAMTS1 in NK_R cells, and CX3CR1 in NK cells. However, none remained significant after correction for multiple testing. Molecular docking and molecular dynamics simulations showed that the ADAMTS1-pravastatin and CX3CR1-Rugocrixan complexes maintained stable protein-ligand contacts during their respective simulations. Integrative multi-omics analyses identified JUN, ADAMTS1, CRISPLD2, and CX3CR1 as prioritized candidate genes associated with KOA. These genes were associated with distinct states of synovial fibroblasts and myeloid cells. These findings provide a foundation for further mechanistic validation and experimental evaluation of candidate drug-target interactions.

PMID 42929463
阅读全文 →
PubMedCells2026-10-26

Temporal Dynamics of Emerging Cardiovascular Biomarkers in the Early Phase After Acute ST-Segment Elevation Myocardial Infarction: A Prospective Single-Center Pilot Study.

Zivkovic Stefan S SS, Misevic Vojko V VV, Krupnikovic Kosta S KS, Obradovic Aleksa D AD et al.

Acute ST-segment elevation myocardial infarction (STEMI) remains a major cause of cardiovascular morbidity and mortality. Despite successful primary percutaneous coronary intervention (pPCI), early myocardial injury and stress may contribute to left ventricular dysfunction. The optimal timing of biomarker assessment after STEMI remains uncertain. To characterize the early kinetics of soluble suppression of tumorigenicity-2 (sST2), galectin-3 (Gal-3), mid-regional pro-adrenomedullin (MR-proADM), and growth differentiation factor 15 (GDF-15) during the first 96 h after STEMI and identify potentially informative sampling time points for future prognostic assessment. Secondary, exploratory objectives were to evaluate differences in biomarker concentrations according to symptom duration, left ventricular ejection fraction (LVEF), and infarct-related artery. In this prospective, single-center, exploratory pilot study, patients aged 18-75 years with first STEMI treated with pPCI within 6 h of symptom onset were enrolled between September 2024 and November 2025. Blood samples were collected at admission and 12 ± 4, 24 ± 4, 48 ± 8, and 96 ± 8 h after pPCI. Biomarkers were measured by ELISA, with high-sensitivity cardiac troponin I (hs-cTnI) as a reference marker of myocardial injury. Of 46 enrolled patients, 16 were excluded, mostly due to early discharge, and 30 patients with complete samples at all five time points were included in the analysis (mean age 57.9 ± 11.1 years; 66.7% male). sST2, MR-proADM, and hs-cTnI showed significant temporal variation (all p < 0.001), with the highest measured concentrations of sST2 at 12 h and of MR-proADM at 24 h. No significant change over time was found for Gal-3 and GDF-15. In exploratory analyses, sST2 and MR-proADM concentrations were higher in patients with LVEF < 40%, and sST2 concentrations were higher in patients with left anterior descending artery (LAD) infarction. Symptom duration was not associated with biomarker concentrations. sST2 and MR-proADM show distinct early post-STEMI kinetics, suggesting potentially informative sampling windows for future prognostic studies. Larger prospective studies are needed to confirm these kinetics and the exploratory differences according to left ventricular function and infarct location, and to evaluate the prognostic value of these sampling windows with echocardiographic and clinical follow-up.

PMID 42929840
阅读全文 →
PubMedActas espanolas de psiquiatria2026-10-26

Genetic Liability to Psychiatric Disorder and Risk of Musculoskeletal Diseases: A Bidirectional Mendelian Randomization Study.

Luo Xiaohai X, Wu Ning N, Wang Zhaofu Z, Ma Jingzu J et al.

Psychiatric disorders, particularly major depressive disorder (MDD), are increasingly recognized as systemic diseases that may predispose individuals to a range of physical comorbidities. Epidemiological studies have reported associations between depression and musculoskeletal diseases; however, causal inferences remain limited due to confounding factors and reverse causation. This study aims to investigate the bidirectional causal relationships between common psychiatric disorders and musculoskeletal outcomes using a Mendelian randomization (MR) framework. A bidirectional two-sample MR analysis was conducted using summary statistics from a large-scale genome-wide association study (GWAS) in European ancestry populations. Genetic instruments for seven psychiatric disorders were obtained from the Psychiatric Genomics Consortium, while musculoskeletal outcomes were sourced from the IEU Open GWAS and UK Biobank. Causal effects were primarily estimated using an inverse variance weighted model, with sensitivity analyses conducted using the weighted median (WM) and MR-Egger methods. Established diagnostic methods were employed to assess horizontal pleiotropy, heterogeneity, and robustness, and false discovery rate (FDR) corrections were applied to account for multiple testing. The genetic liability to MDD showed the most consistent evidence of association with osteoarthritis (OA) and osteomyelitis (OM). The association with OA appeared to be the most stable overall, while the findings regarding OM should be interpreted more cautiously due to the relatively limited number of available instrumental variables. Nominal associations were also observed for fracture and osteoporosis (OP) in relation to MDD, as well as between autism spectrum disorder (ASD) and fracture risk and between anorexia nervosa (AN) and fracture risk; however, these findings were either modest in magnitude or did not remain significant after multiple-testing correction, and thus should be considered exploratory results. There was no strong evidence supporting a reverse causal effect of musculoskeletal diseases on psychiatric disorders. This MR study suggests that genetic liability to MDD may be associated with susceptibility to specific musculoskeletal diseases, particularly OA, and more cautiously, OM. These findings should be interpreted with caution, especially for associations based on limited instrumental support or modest effect sizes, and require replication in different populations.

PMID 42928693
阅读全文 →
PubMedMolecular neurobiology2026-10-26

Evaluating the Impacts of Inflammatory Proteins on the Risk of Alzheimer's Disease.

Zhang Ziyao Z, Cao Hongbao H, Baranova Ancha A, Zhang Fuquan F

Accumulating evidence suggests that inflammation contributes to the pathogenesis of Alzheimer's disease (AD). However, the relationship between circulating inflammatory proteins and AD remains incompletely understood. Two-sample Mendelian randomization (MR) was used to assess the associations of 91 circulating inflammatory proteins with AD. The discovery stage protein GWAS included 14,824 participants, and the validation stage analysis used UK Biobank data from 54,219 participants. The AD dataset comprised 85,934 cases and 401,577 controls. The inverse variance weighted (IVW) method was the primary approach, complemented by weighted median, MR-Egger, heterogeneity, and pleiotropy analyses. MR estimates from both stages were subsequently combined by meta-analysis, followed by drug-gene interaction analyses. In the discovery stage, four proteins showed nominal associations with AD: AXIN1 (OR = 1.082, P = 0.026), NGF (OR = 1.061, P = 0.048), CXCL11 (OR = 0.952, P = 0.017), and TNFRSF9 (OR = 0.946, P = 0.048). However, none survived FDR correction (FDR = 0.799). In the validation stage, only TNFRSF9 reached nominal significance (OR = 0.870, P = 0.031), which did not survive FDR correction (FDR = 0.125); AXIN1 showed an opposite direction. Meta-analysis provided suggestive pooled estimates for CXCL11 (OR = 0.956, P = 9.34 × 10⁻3), TNFRSF9 (OR = 0.926, P = 0.034), and NGF (OR = 1.061, P = 0.034), but these should not be regarded as independent confirmation. DGIdb analysis identified interactions between the genes of interest and various drugs or compounds. These findings provide exploratory genetic evidence linking circulating inflammatory proteins to AD, but robust replication was not established after multiple testing correction and requires further validation.

PMID 42928319
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多zolpidem tartrate