Drug Database
ZO

zolpidem tartrate (Stilnox CR / FK199B / Stilnoxium)

✓ Approved

Astellas Pharma · GABRA1 · Small Molecule

What is zolpidem tartrate?

zolpidem tartrate is a small molecule developed by Astellas Pharma. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesStilnox CR, FK199B, Stilnoxium
CompanyAstellas Pharma
Drug ClassSmall Molecule
Molecular TargetGABRA1
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Astellas Pharma

Mechanism of Action

Molecular Targets

zolpidem tartrate acts on 1 molecular target:

GABRA1gamma-aminobutyric acid type A receptor alpha1 subunit (DEE19, ECA4)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

zolpidem tartrate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Psychiatric disordersInsomnia✓ Approved

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Pure-green OLEDs with CIEy over 0.7 via employing multi-resonance thermally activated delayed fluorescence sensitizers.

Nie Yufang Y, Jiang Chao C, Cao Chi C, Liang Jie J et al.

Multiple-resonance thermally activated delayed fluorescence (MR-TADF) materials have emerged as key candidates for next-generation ultra-high-definition (UHD) display organic light-emitting diodes (OLEDs) owing to their narrowband emission and high efficiency. Due to their long delayed fluorescence lifetimes, most MR-TADF devices suffer from severe efficiency roll-off at high brightness. Incorporating sensitizers into the emissive layer has been proven to be the most feasible and effective solution. Nevertheless, many sensitized devices suffer from incomplete energy transfer, which compromises the color purity of electroluminescence. Herein, we propose an ultra-low concentration doping MR-TADF-sensitized fluorescence (MR-TSF) strategy. Three new MR-TADF sensitizers exhibit reverse intersystem crossing rates (k RISC) of 1.42-1.58 × 105 s-1, along with radiative decay rates (k r) exceeding 108 s-1, endowing them with nearly unity photoluminescence quantum yields (PLQYs). When the doping concentration of the sensitizer is only 3.0 wt%, the external quantum efficiency (EQE) roll-offs of the sensitized devices at 1000 cd m-2 are reduced from the original values of 49.2%, 40.7%, and 40.7% to 22.5%, 23.2%, and 23.1%, respectively. Meanwhile, the MR-TSF devices have a minimal impact on the intrinsic color purity of the emitters.

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PubMedMedicine2026-07-25

Cognitive function and knee osteoarthritis: A bidirectional Mendelian randomization study with BMI mediation.

Zhang Yuping Y, Lin Qiuxiang Q, Yu Debiao D, Lu Tianxiang T et al.

This study investigated the causal relationship between cognitive function and knee osteoarthritis (KOA) and whether body mass index (BMI) mediates this effect. A bidirectional Mendelian randomization (MR) analysis was conducted using genome-wide association study summary statistics. The primary analysis used the inverse-variance weighted method, with MR-Egger, weighted median, robust adjusted profile score, and MR-PRESSO applied for sensitivity analyses. Forward MR analyses showed a significant inverse causal effect of cognitive function on KOA risk, with intelligence (OR = 0.843, 95% CI: 0.755-0.941, P = .002) and cognitive performance (OR = 0.850, 95% CI: 0.771-0.937, P = .001) associated with reduced risk. Reverse MR analyses found no evidence that KOA causally affects cognitive function (Intelligence: β = -0.020, 95% CI:-0.048 to 0.008, P = .167; Cognitive performance: β = -0.006, 95% CI:-0.032-0.020, P = .661). Mediation analysis showed that BMI partially mediated the effect of intelligence on KOA (indirect β = -0.047, 95% CI:-0.110 to-0.006, P = .023), accounting for 27.29% of the total effect. In conclusion, these findings support a unidirectional causal effect of cognitive function on KOA, partially mediated by BMI, highlighting the relevance of cognitive function and weight management in high-risk individuals.

PMID 42499075
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Online monitoring of Maillard reaction dynamics using a custom reaction-transfer device and direct analysis in real time mass spectrometry.

Qiu Zhichen Z, Xu Liping L, Geng Xin X, Li Hongli H et al.

Controlling the Maillard reaction (MR) is critical for producing food flavor and color, yet real-time monitoring of its dynamics remains challenging. We developed an online monitoring system by integrating a custom reaction-transfer device with a Direct Analysis in Real Time (DART) ion source and high-resolution mass spectrometry. The system continuously transfers volatile MR products from the reaction headspace via a heated transfer line, enabling real-time, high-resolution analysis. The system successfully captured time-resolved molecular profiles, from early-stage sugar degradation intermediates to late-stage formation of nitrogen-containing heterocycles. Substrate-dependent kinetics and products were clearly differentiated. Elemental composition analysis via Van Krevelen plots further revealed distinct reaction pathways. The method was applied to monitor 12 MR model reactions and 5 real food samples, and correlation analysis linked complex food flavors to specific precursor reaction systems. Method validation confirmed the method's precision and robustness, establishing a simple and informative platform for online MR monitoring.

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Association between pelvic inflammatory disease and ovarian cancer: A bidirectional Mendelian randomization study.

Qin Kaiyun K, Jiang Yan Y, Gao Xingshuang X, Liu Weilan W et al.

Some observational studies have suggested an association between pelvic inflammatory disease (PID) and ovarian cancer (OC), but the causality between PID and OC remains unclear. To investigate the causal association between PID and 7 OCs, we performed two-sample bidirectional Mendelian randomization (MR) analyses using genetic variants associated with PID. Pooled data on OC were obtained from the Ovarian Cancer Association Consortium. Effect estimates were obtained by inverse-variance weighting, the weighted median method, MR-Egger regression, and MR pleiotropy residual sum and outlier (MR-PRESSO) tests. The results of the inverse-variance weighting analysis showed that PID incidence risks were not significantly associated with OC, mucinous OC, low malignant potential OC, low-grade serous OC, high-grade serous OC, endometrioid OC, or clear cell OC. In this study, the causalities between PID and 7 OCs were comprehensively assessed, but the identified genetic evidence suggested no possible causalities between PID and 7 OCs in European populations.

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Causal association between hip osteoarthritis and the risk of pancreatic cancer: A bidirectional two-sample Mendelian randomization study.

Li Wei W, Hu Bo B, Zhuang Hongyu H

The potential causal relationship between hip osteoarthritis (HOA) and pancreatic cancer (PC) is not well understood. To investigate this, our study utilized a two-sample Mendelian randomization (MR) method to examine a possible causal link between HOA and an increased risk of PC. Genome-wide association study summary data for both HOA and PC were sourced from the Integrative Epidemiology Unit OpenGWAS database (https://gwas.mrcieu.ac.uk/datasets/). The single-nucleotide polymorphisms associated with these conditions at a statistically significant level (P value <5 × 10-8) were identified as instrumental variables for subsequent analysis. We conducted bidirectional two-sample MR analyses employing inverse-variance weighting (IVW), weighted median, MR-Egger regression, and weighted mode methods. The robustness of the findings was assessed through sensitivity testing. The IVW analysis indicated that HOA elevated the risk of PC (odds ratio = 1.788; 95% confidence interval: 1.166-2.742; P = .008). Conversely, in the reverse MR analysis, the IVW analysis provided no evidence that PC increased the risk of HOA (odds ratio = 1.016; 95% confidence interval: 0.973-1.060; P = .475). In addition, the weighted mode, weighted median, and MR-Egger regression methods did not uncover a causal relationship. There was no heterogeneity or horizontal pleiotropy among the instrumental variables. The "leave-one-out" analysis revealed that no single-nucleotide polymorphism significantly influenced the overall results. Genetically predicted HOA is significantly associated with an increased risk of PC. However, we found no evidence that PC leads to an increased risk of HOA.

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PubMedMedicine2026-07-25

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Yi Bingqing B, Luo Yaoyue Y, Li Hong H, Nie Yiran Y et al.

Numerous observational studies have suggested a potential shared genetic background between inflammatory bowel disease (IBD) and IgA vasculitis (IgAV). However, the causal relationship between these 2 conditions remains poorly understood. We performed large-scale two-sample and multivariable Mendelian randomization (MR) analyses (MVMR) to examine whether there is a causal relationship between IBD and IgAV. We employed 4 distinct approaches, including MR-Egger, weighted median, random-effects inverse-variance weighted (IVW), and weighted mode, to conduct the MR analysis. The univariable MR analysis demonstrated that IBD and Crohn disease (CD) were associated with an increased risk of IgAV in the International Inflammatory Bowel Disease Genetics Consortium, with an odds ratio (OR) of 1.17 (95% confidence interval [CI]: 1.06-1.28, PIVW = .001) for IBD and an OR of 1.12 (95% CI: 1.01-1.24, PIVW = .016) for CD. Ulcerative colitis was associated with an increased risk of IgAV, which was considered suggestive after Bonferroni correction, with an OR of 1.12 (95% CI: 1.01-1.24, PIVW = .028). Consistent results were observed after adjusting for potential confounders (drug allergy and upper respiratory tract infection) in MVMR. IBD, ulcerative colitis, and CD were associated with an increased risk of IgAV, with an OR of 1.20 (95% CI: 1.08-1.34, PIVW = .001), 1.20 (95% CI: 1.07-1.35, PIVW = .002), and 1.13 (95% CI: 1.03-1.25, PIVW = .0012). Our study identifies a causal relationship between IBD and IgAV, particularly between CD and IgAV, suggesting that IBD is a potential precursor to IgAV rather than the converse. Further studies on the common mechanisms of these 2 diseases are needed.

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