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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

PubMedAngewandte Chemie (International ed. in English)2026-09-10

Five-Boron Multiple-Resonance TADF Emitter With Accelerated Reverse Intersystem Crossing for High-Performance Narrowband Green OLEDs.

Lee Taehwan T, Ochi Junki J, Zhang Zishun Z, Kondo Yasuhiro Y et al.

Multiple-resonance thermally activated delayed fluorescence (MR-TADF) emitters are promising candidates for organic light-emitting diodes owing to their narrowband emission and high exciton utilization. While π-conjugated framework expansion has been extensively explored for tuning excited-state properties, five-boron MR-TADF emitters have not yet been realized. Herein, we report the first five-boron MR-TADF emitter, M-DABNA-Mes, featuring an unprecedented odd-numbered boron-rich multiple-resonance framework. Theoretical investigations of one-, three-, and five-boron MR frameworks reveal that incorporation of the fifth boron atom reduces the singlet-triplet energy gap, preserves spin-orbit coupling, and reduces the total reorganization energy while maintaining favorable narrowband emission characteristics. Consistent with these predictions, M-DABNA-Mes doped in a polystyrene film exhibits a sub-microsecond delayed fluorescence lifetime (τTADF = 0.93 µs), a reverse intersystem crossing rate of 2.6 × 106 s-1, and narrow green emission at 512 nm with a full width at half maximum of 19 nm. OLEDs based on M-DABNA-Mes achieve a maximum external quantum efficiency of 34.3% with remarkably low efficiency roll-off (32.3% at 10,000 cd m-2) and a maximum luminance of 275,800 cd m-2. These results demonstrate that the five-boron MR framework enables rapid spin conversion, high spectral purity, and excellent OLED performance, providing a new platform for high-performance MR-TADF emitters.

PMID 42717847
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PubMedCardiovascular diagnosis and therapy2026-09-10

Association of left ventricular global longitudinal strain with outcomes of severe mitral regurgitation due to severe mitral annular calcification: a retrospective cohort study.

Al Zein Mohammad M, Okushi Yuichiro Y, Unai Shinya S, Pettersson Gösta B GB et al.

Mitral annular calcification (MAC) is associated with increased mortality and a heightened risk of complications such as stroke, myocardial infarction, and arrhythmias. In advanced stages, MAC can cause severe mitral regurgitation (MR), further worsening outcomes. Prognostic markers to guide therapy in this population remain unclear. Left ventricular global longitudinal strain (LVGLS) has been linked to outcomes in MR, but its role in severe MR due to severe MAC is not well established. This study evaluated the prognostic value of LVGLS in this setting. We conducted a single-center, retrospective study of patients with severe MAC identified from the Cleveland Clinic echocardiographic database between January 2010 and August 2023. From these, patients with mild or moderate MR and those with concomitant significant mitral stenosis (MS) were excluded. Subsequently, patients with isolated severe MR due to severe MAC were identified. Clinical and echocardiographic parameters, including LVGLS, were recorded at baseline. The primary outcome was all-cause mortality. Patients were stratified by the median LVGLS value for analysis. Survival was assessed using Kaplan-Meier analysis and Cox proportional hazards models. Restricted cubic spline was used to evaluate potential non-linear associations between LVGLS and mortality. During the study period, 10,061 patients were diagnosed with severe MAC on echocardiography at our institution. Of these, 8,912 with mild or moderate MR and 1,021 with concomitant significant MS were excluded, and 128 patients with isolated severe MR due to severe MAC were included in our study. The median follow-up was 134 days [interquartile range (IQR), 33-1,812 days]. The median age was 81 years (IQR, 71-88 years), and 35 (27.3%) were male. The median left ventricular ejection fraction (LVEF) was 63% (IQR, 56-69%), mean MR regurgitant volume was 60±20.8 mL, and median right ventricular systolic pressure was 54 mmHg (IQR, 42-71 mmHg). The median LVGLS was -14.8%±4.5%. Of the 128 patients, 45 (35.2%) underwent mitral valve intervention, 42 (93.3%) surgery and 3 (6.7%) mitral clip implantation, while 83 (64.8%) received conservative management. Among surgical cases, 37 underwent valve replacements (34 bioprosthetic) and 5 valve repairs. During follow-up, 63 patients (49.2%) died. LVGLS worse than -14.8% was associated with higher 12-month mortality (log-rank P=0.043) but not over the entire follow-up period (P=0.11). On multivariable cox regression, LVGLS was not a predictor of mortality after adjusting for other covariates [hazard ratio (HR) 1.046, 95% confidence interval (CI): 0.983-1.112]. In severe MR due to MAC, impaired LVGLS was associated with increased short-term but not long-term mortality. The limited long-term prognostic value may reflect the low myocardial reserve in patients with severe valvular dysfunction due to MAC, the progressive and systemic nature of the disease, and the influence of non-cardiac comorbidities.

PMID 42718883
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PubMedAsia-Pacific journal of clinical oncology2026-09-10

Augmented Reality, Mixed Reality, Virtual Reality, and Extended Reality Applications in Personalized Oncology and Patient-Centered Cancer Care: A Narrative Review.

Velraj Malarkodi M, Mani Deepalakshmi D, Parthasarathy Arun Kanniyappan AK, Murugesan Vijayakumar V et al.

Extended reality (XR) technologies, including augmented reality (AR), mixed reality (MR), and virtual reality (VR), are an appealing technology in clinical oncology. This narrative review evaluates the current evidence of XR applications throughout the cancer care continuum in terms of the clinical implementation, patient outcome, and the relevance of the practice to practicing clinical oncologists. A literature search on PubMed, Scopus, Web of Science, and Cochrane Library (January 2015-December 2025) was conducted at the right time to select the articles related to AR, VR, MR, XR, and cancer/oncology. Randomized controlled trials (RCTs), systematic reviews, meta-analyses, and clinical implementation studies were given priority. VR contains the strongest evidence base in which 15 RCTs meta-analysis (n = 864) found large reductions in the level of anxiety related to chemotherapy (standardized mean difference [SMD] = -1.40) among adult patients with cancer and fatigue (SMD = -3.85). Cancer-related pain (SMD = -0.86, 95% CI: -1.89 to -0.85, p < 0.001) affected significantly VR interventions as well when implemented in 28 RCTs. In hepatic, glioma, and gastrointestinal tumor resection, AR-guided surgical navigation has been clinically workable, and prospective research has indicated that it is capable of better tumor localization. Depression (SMD = -1.86, p < 0.001) was also reduced. The 3D holographic visualization with the help of MR enables the treatment planning of the multidisciplinary type. The XR technologies possess immense potential in the field of personalized oncology. The sphere of VR-based supportive care intervention is clinically prepared, and still the uses of AR and MR in surgical oncology require confirmation of multicenter trials. Standardization of the protocols, cost-effectiveness studies and its integration into the clinical processes are yet to remain on the list of the top priorities.

PMID 42717530
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PubMedFrontiers in nutrition2026-09-10

FODMAP intake, gut microbiota, and gastroesophageal reflux disease: a triangulated study of Mendelian randomization and clinical validation.

Chen Yuanchun Y, Lu Shiyun S

Dietary factors related to fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and gut microbiota may influence gastroesophageal reflux disease (GERD), but causal evidence and clinical consistency remain uncertain. We tested whether FODMAP-related and GERD-relevant dietary traits influence GERD risk using Mendelian randomization (MR), and whether gut microbiota mediate these associations. We integrated UK Biobank dietary GWAS, MiBioGen microbiota GWAS, and FinnGen GERD summary statistics using inverse-variance weighted MR, multivariable MR, Benjamini-Hochberg false discovery rate (BH-FDR) correction, MR-Steiger filtering, and two-step mediation analysis. A 525 matched-pair retrospective case-control cohort provided clinical validation. After BH-FDR correction, genetically predicted cheese, cereal, oily fish, fresh/dried fruit, and salad/raw vegetables were associated with lower GERD risk (ORs, 0.46-0.77), whereas tea and poultry were associated with higher risk (ORs, 1.28-2.14). Microbiota-wide and mediation signals did not survive FDR correction. The oily fish-Erysipelatoclostridium indirect effect was small and statistically imprecise (indirect effect, -0.015; 95% CI, -0.034 to 0.005), corresponding to a mediated proportion of 4.1% (95% CI, -1.2 to 9.5%); therefore, it was interpreted as an exploratory signal rather than evidence of a confirmed microbial pathway. Clinical data directionally supported the main dietary signals: tea, poultry, processed meat, and sweets were associated with higher GERD risk (ORs, 1.04-1.19), while cheese, cereal, fruit, and oily fish were protective (ORs, 0.80-0.94). Dietary associations with GERD were more robust than microbiota-associated signals. These findings suggest that oily fish-related dietary patterns may be associated with lower GERD risk, while exploratory analyses provide preliminary evidence that gut microbiota may contribute to these associations. Further studies are required to validate these potential biological pathways.

PMID 42718703
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PubMedBone research2026-09-10

WDR23 prevents bone loss by promoting autophagic degradation of TRAF6 in osteoclastogenesis.

Park Hye-Won HW, Yu Jungeun J, Yu Jiyeon J, You Jinseon J et al.

Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a pivotal adaptor molecule in the receptor activator of nuclear factor-κB (RANK) and its ligand (RANKL) signaling pathways, which are essential for osteoclastogenesis. In this study, we identified WD40 repeat-containing protein 23 (WDR23), also known as DDB1-CUL4 associated factor 11 (DCAF11), as a novel binding partner of TRAF6. Our findings demonstrate that WDR23/DCAF11 acts as a negative feedback regulator of RANK/RANKL-induced osteoclastogenesis by promoting the autophagy-dependent degradation of TRAF6. Notably, RANKL induced the upregulation of WDR23 expression during osteoclastogenesis. WDR23 physically interacted with the TRAF domain of TRAF6 via the WD40 repeat domains 1 and 2 of WDR23, resulting in reduced TRAF6 protein stability by its autophagy-dependent degradation during osteoclastogenesis. By modulating TRAF6 protein levels, WDR23 attenuated RANKL signaling cascades, including nuclear factor-κB and mitogen-activated protein kinases, thereby downregulating the expression of osteoclastogenic markers, such as nuclear factor of activated T-cell c1, tartrate-resistant acid phosphatase, dendritic cell-specific transmembrane protein, V-ATPase subunit d2 and cathepsin K. Conversely, WDR23 knockdown or deficiency enhanced RANKL-induced osteoclastogenesis by preventing the autophagy-dependent degradation of TRAF6. WDR23-deficient mice exhibit an osteoporotic bone phenotype characterized by elevated osteoclast formation and reduced bone mass. Collectively, these results establish WDR23 as a key negative feedback regulator of RANKL-induced osteoclastogenesis via autophagy-mediated TRAF6 degradation and underscore its potential as a therapeutic target for bone disorders associated with aberrant osteoclast formation and function.

PMID 42717193
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PubMedAnnals of human genetics2026-09-10

Genetically Proxied Leukocyte Telomere Length and Epigenetic Age Acceleration in Relation to Healthspan: A Mendelian Randomization Study.

Feng Bowen B, Yang Robert R, Wang Gabriella R GR, Hu Qiu Q et al.

Leukocyte telomere length (LTL) and epigenetic age acceleration (EAA) are widely studied biomarkers of biological aging, but their potential roles in healthspan remain unclear. We evaluated whether genetically proxied LTL and EAA show evidence of potential effects on healthspan. We conducted a two-sample Mendelian randomization study. Genetic instruments for LTL and four EAA biomarkers were obtained from published genome-wide association studies, including up to 472,174 individuals for LTL and approximately 35,000 individuals for each EAA biomarker. Summary statistics for healthspan, defined as age at first diagnosis of any of eight major chronic conditions or death, were derived from 300,447 unrelated European-ancestry participants in the UK Biobank. We used inverse-variance-weighted (IVW) models for the main analysis, with complementary MR estimators and sensitivity analyses to evaluate consistency, pleiotropy, instrument heterogeneity, and robustness. Genetically proxied longer LTL was associated with extended healthspan (IVW β = 0.106; 95% CI: 0.054-0.158; p = 6.9 × 10-5). The association was robust across multiple sensitivity analyses. In contrast, the four genetically proxied EAA biomarkers did not show consistent MR evidence of an association with healthspan. These findings provide genetic evidence consistent with a potential role of LTL in healthspan, while providing little support for comparable associations involving the genetically proxied components of the evaluated EAA biomarkers. The findings do not exclude potential associations with environmentally or physiologically acquired EAA.

PMID 42717711
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