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

Related Research Articles

PubMedMedicine2026-11-11

Association of 14 matrix metalloproteinases and 4 tissue inhibitors of metalloproteinases on ankylosing spondylitis: A bidirectional Mendelian randomization study.

Sun Xiaoyang X, Li Guoqing G, Zhao Huaguo H, Wang Yang Y

Observational studies link matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) to ankylosing spondylitis (AS), but causality is uncertain. We performed a bidirectional, 2-sample Mendelian randomization (MR) analysis using genetic variants to assess causal relationships between genetically predicted circulating levels of 14 MMPs and 4 TIMPs and AS risk, and to evaluate reverse causation. Genetic instruments for circulating MMPs and TIMPs were derived from a large proteogenomic genome-wide association study of 5368 individuals. Summary statistics for AS were obtained from the FinnGen Release 12 GWAS (3838 cases; 353,224 controls). Causal estimates were generated using inverse-variance weighting (primary analysis), complemented by MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses included Cochran's Q test, MR-Egger intercept, MR-PRESSO, and leave-one-out analyses. Forward MR identified a nominal association between genetically predicted higher circulating MMP13 levels and an increased risk of AS (IVW odds ratio = 1.223, 95% confidence interval, 1.048-1.428; P = .011, FDR = 0.198). This association showed a consistent direction in the weighted median estimates and showed no evidence of heterogeneity or horizontal pleiotropy. No other MMPs or TIMPs showed convincing evidence of an association with AS. Reverse MR analyses provided no evidence that genetic liability to AS causally influences circulating MMP or TIMP levels. This bidirectional MR analysis provides genetic support for a potential causal relationship between MMP13 and the development of AS, while suggesting that other MMPs and TIMPs are unlikely to be causal drivers. Further experimental and clinical studies are warranted to clarify the biological relevance of MMP13 in AS.

PMID 43012792
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PubMed[Zhonghua yan ke za zhi] Chinese journal of ophthalmology2026-11-11

[Modifiable risk factors and diabetic retinopathy: a Mendelian randomization analysis].

Wang K K, Miao R J RJ, Qu S S SS, Yu Y B YB et al.

Objective: To investigate the causal relationships of body mass index (BMI), smoking, alcohol and coffee consumption, sleep, physical activity, and educational attainment with diabetic retinopathy (DR) and its subtypes. Methods: We conducted a two-sample Mendelian randomization (MR) study. Genetic instruments were selected from seven large-scale European-descent genome-wide association studies. Summary-level statistics for three DR phenotypes were obtained from the FinnGen consortium. The inverse-variance weighted method was used as the main MR analysis, with weighted median, MR-Egger regression, maximum likelihood, and MR-PRESSO models used for sensitivity analyses to assess the robustness of the findings. The MR study was conducted from September to November 2024. Results: A total of 14 584 patients with DR and 202 082 control participants were included. For analyses of DR subtypes, 2 026 patients with non-proliferative DR and 204 208 control participants, as well as 8 681 patients with proliferative DR and 204 208 control participants, were included. Higher genetically predicted BMI was intensively and independently associated with increased risk of DR and subtypes. The odds ratio (OR) was 1.26 [95% confidence interval (CI): 1.16-1.37, P<0.001] of overall DR, 1.68 (95%CI, 1.38-2.06, P<0.001) of non-proliferative DR, and 1.41 (95%CI, 1.27-1.56, P<0.001) of proliferative DR for 1-SD increase in BMI. Increased coffee consumption was associated with a higher risk of overall DR (OR=1.23; 95%CI, 1.04-1.45, P=0.015), non-proliferative DR (OR=1.72; 95%CI, 1.17-2.53, P=0.006), and proliferative DR (OR=1.33; 95%CI, 1.08-1.63, P=0.007). In addition, genetically predicted educational attainment was inversely associated with non-proliferative DR (OR=0.70; 95%CI, 0.55-0.90, P=0.005). Insufficient evidence was found to support the causal association of smoking, alcohol consumption, sleep, and physical activity with DR (all P>0.05). Conclusions: Based on MR analysis of European populations, higher BMI, increased coffee intake, and lower educational attainment are risk factors for DR.

PMID 43010760
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PubMedMedicine2026-11-11

Causal effects of genetically predicted CCL25 signaling on ovarian cancer risk: A 2-sample Mendelian randomization study.

Zhang Yuqiang Y, Tang Li L, Chen Juan J, Yang Ling L et al.

Ovarian cancer (OC) is a common and highly malignant neoplasm in women, characterized by a poor prognosis and posing a significant threat to both health and quality of life. Despite the unclear pathogenesis of OC, there is growing evidence suggesting an association between OC and inflammatory cytokines. Nevertheless, this potential causal relationship remains insufficiently explored. To enhance early clinical diagnosis and inform therapeutic strategies, we conducted a bidirectional Mendelian randomization (MR) analysis to evaluate the causal relationship between inflammatory cytokines and OC. We identified genetic instrumental variables for inflammatory cytokines and OC utilizing publicly accessible genome-wide association study data. Causal relationships between inflammatory cytokines and OC were assessed using inverse variance weighting as the primary analytical approach. The robustness and validity of the observed causal relationships were further substantiated through multiple sensitivity analyses, including Cochran Q test, MR-Egger intercept test, MR pleiotropy residual sum and outlier, and leave-one-out analysis. Additionally, a random-effects meta-analysis was conducted to enhance statistical power and further identify causal proteins. Finally, colocalization analysis was employed to reinforce the evidence regarding the sharing of common etiological variants. MR analysis indicated that genetically predicted elevated levels of serum C-C motif chemokine 25 (CCL25) were inversely correlated with the risk of developing OC (inverse variance weighting: odds ratio = 0.95, 95% confidence interval = 0.91-0.99, P = .038). The direction of the beta coefficient was consistent across all MR methodologies. There was no evidence of horizontal pleiotropy (Egger intercept = 0.016, P = .145) or heterogeneity (Cochran Q = 8.857, P = .635). A meta-analysis confirmed that the inverse causal relationship between CCL25 and OC remained statistically significant (odds ratio = 0.94, 95% confidence interval = 0.90-0.99, P = .001). Colocalization analysis revealed no shared genetic factors between CCL25 and OC (the sum of the posterior probabilities of hypothesis 3 and hypothesis 4 is equal to 0.05.). Combined MR and meta-analyses indicate that CCL25 functions as a protective factor for OC. Future research should therefore conduct more comprehensive investigations into this relationship.

PMID 43012786
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PubMedZhonghua nan ke xue = National journal of andrology2026-11-11

[Relationship between age at first sexual intercourse and erectile dysfunction: A Mendelian randomization study].

Cheng Yidong Y, Huang Ting T

Objective To investigate the causal relationship between age at first sexual intercourse (AFS) and erectile dysfunction (ED) using a two-sample Mendelian randomization (MR) study. Methods Genetic instruments for AFS as the exposure and ED as the outcome were obtained from genome-wide association studies (GWAS). The inverse variance weighted (IVW) method was used as the primary statistical approach for MR analysis, with Cochran's Q test assessing heterogeneity and the MR-Egger intercept test assessing horizontal pleiotropy. Results The IVW method indicated a causal relationship between AFS and ED risk (Pooled OR: 0.599, 95% CI: 0.492－0.732, P<0.001). And the heterogeneity and pleiotropy analyses confirmed the accuracy and robustness of these findings. Conclusion A younger AFS is associated with a higher risk of ED, which provides a reference for the sex education in adolescents.

PMID 43012247
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PubMedImmunity, inflammation and disease2026-11-11

Rheumatoid Arthritis and Thrombocytopenia: Causal Evidence and Prognostic Implications From Observational and Mendelian Randomization Analyzes.

Wu Yejun Y, Cai Yuyang Y, Yang Anzhen A, Zhang Shuying S et al.

Rheumatoid arthritis (RA) is a systemic autoimmune disease associated with hematological abnormalities, and we aimed to investigate the clinical significance and causal relationship of thrombocytopenia (TP) in RA. We integrated observational data with genetic approaches, characterized the clinical features of RA patients with TP, and evaluated their prognostic implications. Data from the National Health and Nutrition Examination Survey were used to analyze clinical characteristics and survival outcomes of RA patients. Survey-weighted Cox regression models were applied to evaluate the association between TP and mortality. Two-sample Mendelian randomization (MR) analysis was performed to evaluate the causal relationship between RA and TP. Among 2667 RA participants with available platelet measurements, 135 had TP (< 150 × 109/L). In the common complete-case sample, TP remained associated with higher all-cause mortality after full survey-weighted adjustment (HR 1.92, 95% CI 1.17-3.16; p = 0.009). Lower serum albumin and higher urinary albumin concentration were also associated with mortality in the fully adjusted model. In the MR analysis using 52 SNPs, fixed-effect IVW yielded OR 1.054 (95% CI 1.002-1.108; p = 0.042), but alternative estimators were not significant and the MR-Egger intercept indicated directional pleiotropy (p = 0.0016). Thrombocytopenia was associated with poorer survival among RA participants, whereas MR did not provide robust evidence for a causal effect of RA liability on thrombocytopenia. These findings warrant further prospective validation.

PMID 43012374
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PubMedJournal of mass spectrometry and advances in the clinical lab2026-11-11

Integrative Mendelian Randomization and Proteomic Analyses Reveal Genetically Supported Candidate Causal Biomarkers for Non-Traumatic Osteonecrosis of the Femoral Head.

Wang Zhangzheng Z, Mo Liang L, He Wei W, Liu Youwen Y et al.

Non-traumatic osteonecrosis of the femoral head (NONFH) is a highly disabling orthopedic disorder characterized by an insidious onset and significant clinical challenges. Although quantitative proteomic profiling of necrotic and adjacent healthy bone tissues has elucidated aspects of disease mechanisms, fundamental limitations remain in comprehensively understanding NONFH pathogenesis. This study aimed to identify causal biomarkers for NONFH by integrating differentially expressed proteins (DEPs) with transcriptome-wide association study (TWAS) and Mendelian randomization (MR) analyses. Data-independent acquisition (DIA)-based proteomics was performed on necrotic, sclerotic, and healthy bone tissues to identify DEPs. TWAS-prioritized genes were subjected to MR using blood and musculoskeletal tissue-specific expression quantitative trait loci (eQTLs). Reliable causal relationships were retained by excluding pleiotropy or heterogeneity and requiring consistent directions across methods (IVW, WME, and MR-Egger) and multiple analyses. The functional relevance and cell-type specificity of these causal biomarkers were examined using published single-cell RNA sequencing data. Proteomic analysis revealed a total of 846 DEPs. MR identified five causal genes in blood (ACOT1, ALDH1A1, DAG1, STEAP4, LIPA) and four causal genes in musculoskeletal tissue (ACOT1, PPIC, TSC22D4, LIPA). ACOT1 and ALDH1A1 exhibited protective effects (β < 0), whereas DAG1, STEAP4, LIPA, PPIC, and TSC22D4 were associated with increased disease risk (β > 0). Seven genes (ACOT1, LIPA, PPIC, TSC22D4, ALDH1A1, DAG1, and STEAP4) demonstrating both proteomic dysregulation and genetic causality may serve as novel biomarkers or therapeutic targets for NONFH. These findings provide a foundation for further mechanistic studies and hold potential for advancing diagnosis and treatment strategies for NONFH.

PMID 43011886
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