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zolpidem tartrate (Intermezzo / zolpidem, TransOral)

✓ Approved

Transcept Pharmaceuticals · GABRA1 · Small Molecule

What is zolpidem tartrate?

zolpidem tartrate is a small molecule developed by Transcept Pharmaceuticals. It is approved for therapeutic indications via oral (po) or sublingual (sl)/oral transmucosal.

Drug Profile

Brand NamesIntermezzo, zolpidem, TransOral
CompanyTranscept Pharmaceuticals
Drug ClassSmall Molecule
Molecular TargetGABRA1
RouteOral (PO), Sublingual (SL)/Oral Transmucosal
StatusApproved
Sources: ClinicalTrials.gov, Transcept Pharmaceuticals

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

PubMedSmall (Weinheim an der Bergstrasse, Germany)2026-07-17

Performance Enhancement of All-Inorganic CsPbI3 Perovskite Solar Cells through Functional Additive and Buried Interface Engineering.

Cai Hengzhuo H, Lin Junfeng J, Lyu Wanyang W, Yi Lingyi L et al.

All-inorganic CsPbI3 perovskite solar cells (IPSCs) are regarded as promising candidates due to their ideal bandgap and excellent thermal stability. However, their practical application is hindered by phase instability and severe interfacial defects, which lead to performance degradation and poor durability. Here, this work proposes a low-temperature synergistic regulation strategy that combines oxamide additive with potassium tartrate interfacial modification to simultaneously optimize interface and adjust bulk crystallization process of CsPbI3 film. The incorporation of oxamide effectively suppresses iodide vacancy defects, promotes uniform crystal growth and reduces non-radiative recombination, while the buried-interface modification by potassium tartrate regulates the energy-level alignment, passivates interfacial traps and promotes carrier extraction. Benefiting from this dual regulation, the modified CsPbI3-based IPSCs achieve a power conversion efficiency of 18.89% and exhibit significantly improved environmental stability. This work provides a simple, effective and scalable approach to address the intrinsic phase instability and interfacial defect problems in CsPbI3-based IPSCs.

PMID 42464936
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PubMedOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2026-07-17

Serum activin A and bone metabolism in patients undergoing hemodialysis.

Nakagawa Yosuke Y, Takahashi Hiroo H, Takahashi Yuichiro Y, Hyodo Toru T et al.

Activin A, which promotes osteoclast differentiation, increases with declining kidney function, but its role in bone metabolism in kidney failure remains unclear. We found that higher activin A levels were associated with increased bone turnover markers, independent of parathyroid hormone levels. Activin A, produced by various cells including bone marrow stromal cells, immune cells, and osteoblasts, is thought to promote osteoclast differentiation. Serum activin A levels rise with declining kidney function, but its role in bone metabolism in kidney failure remains incompletely understood. Serum activin A levels were measured in 35 healthy individuals and 654 patients undergoing maintenance hemodialysis. Associations of serum activin A with tartrate-resistant acid phosphatase isoform 5b (TRACP5b), bone-specific alkaline phosphatase (BALP), and metacarpal bone mineral density were assessed using both unadjusted and multivariable-adjusted linear regression analyses. Serum activin A levels were also compared between patients with and without a history of fracture, and between those who developed incident fractures during follow-up and those who did not. The median serum activin A level in hemodialysis patients was 733 pg/mL (interquartile range (IQR), 591-912), approximately 2.6-fold higher than that of healthy controls (277 pg/mL; IQR, 216-289; P < 0.001). Patients with higher activin A levels had longer dialysis durations, a higher prevalence of polycystic kidney disease, and higher serum phosphorus and alkaline phosphatase levels. Higher activin A levels were significantly associated with increased TRACP5b levels independently of intact parathyroid hormone levels, with a similar trend observed for BALP. Serum activin A levels were not associated with metacarpal bone mineral density, history of fracture, or incident fractures. These findings suggest that in patients with kidney failure, elevated activin A may contribute to high bone turnover, although its ability to predict fracture risk appears limited. Further studies are warranted to investigate its potential as a therapeutic target.

PMID 42463974
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PubMedArthritis & rheumatology (Hoboken, N.J.)2026-07-16

A Multi-Center Integrative Cohort Characterizing the Genetic, Clinical, and Transcriptomic Features of ACP5 Deficiency.

Zhong Shiling S, Ma Shuangyue S, El Chazli Yasmine Y, Zheng Jika J et al.

Spondyloenchondrodysplasia with immune dysregulation (SPENCDI) is a rare disorder caused by biallelic mutations in ACP5. This study systematically evaluates genetic landscape, clinical features, treatment, and transcriptomics in SPENCDI. Whole-exome sequencing was performed for genetic diagnosis of patients from multiple centers, and tartrate-resistant acid phosphatase (TRAP) activity was measured for novel variants. Previously reported cases were integrated with the current cohort for analysis of genotypes, clinical characteristics, laboratory findings, and treatment responses. Bulk and single-cell RNA sequencing investigated immune signaling alterations. We identified 17 patients with ACP5 deficiency from Egypt and China, discovering five novel pathogenic variants (A260D, L257P, G32D, K190Nfs*22, and T305Nfs*12). Three novel missense variants were detected with loss of TRAP activity. Clinical manifestations involve multiple systems, with the skeletal system most frequently involved (32.31%), where skeletal dysplasia (94.32%) and short stature (81.82%) are the predominant features. Patients showed elevated inflammatory activity, with enrichment of the NF-κB, MAPK, and cell death pathways, as well as upregulation of type I interferon genes in monocytes. Enhanced IFN-γ signaling interactions between monocytes and Natural Killer cells were observed. Therapeutically, Prednisolone and Azathioprine were the most common effective drugs, while patients treated with the Janus kinase inhibitors Ruxolitinib or Upadacitinib achieved a partial response. This study expanded the genetic and clinical spectrum of ACP5 deficiency. An upregulated interferon signature was revealed, and monocytes were identified as a major cellular source of inflammation. These results provide valuable insights for improving the diagnosis and treatment of SPENCDI.

PMID 42459138
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PubMedCellular & molecular biology letters2026-07-16

TLR4-dependent upregulation of IL-22-producing T cells in the bone niche links to the imbalance of bone homeostasis.

Kim Ji-Eun JE, Go Jinyoung J, Lee Eun-Jin EJ, Kim Sang-Min SM et al.

Toll-like receptor 4 (TLR4) activation within the bone marrow (BM) microenvironment regulates proinflammatory cytokines and chemokines, which influence immune activity and bone remodeling. However, the immune cell factors mediating TLR4-dependent cross-talk in the bone/BM microenvironment remain insufficiently defined. We provide a transcriptomic analysis of significant cellular and immune changes in total BM cells of wild-type mice following lipopolysaccharide (LPS)-induced TLR4 activation in vivo compared with TLR4 knockout (KO) mice. To obtain direct evidence that interleukin (IL)-22 contributes to TLR4-driven bone destruction, we analyzed their bone phenotypes following LPS injection into IL-22 KO mice. In addition, co-culture of pre-osteoblasts (OBs) and BM cells was conducted to evaluate the effect of IL-22 in osteoclast (OC) formation in a pre-OB-dependent manner. Differentially expressed gene analysis from BM cells of wild-type (WT) mice revealed an increase in IL-22-producing cells, along with increased IL-22 production in a TLR4-dependent manner. Flow cytometry confirmed that LPS enhanced the number of CD4+IL-22+ cells in the BM and decreased in TLR4-deficient BM. LPS also enhanced the differentiation of CD4+IL-22+ T cells and promoted IL-22 induction in T cells. IL-22 KO mice showed minimal LPS-induced bone loss, whereas WT mice exhibited severe bone destruction with increased formation of tartrate-resistant acid phosphatase-positive OCs. Interestingly, while IL-22 did not directly affect OC differentiation, IL-22 enhanced OC differentiation only when BM cells were co-cultured with pre-OBs through the elevation of the receptor activator of nuclear factor-κB ligand (RANKL) in pre-OBs during osteogenesis. Mechanistically, IL-22 induced cyclooxygenase-2 in pre-OBs through extracellular signal-regulated kinase and p38 signaling, driving prostaglandin E2 production and subsequent RANKL induction. TLR4 activation enhanced IL-22 production in T cells, which stimulates RANKL production in pre-OBs to further induce OC formation. These results support that IL-22 acts as a TLR4-driven mediator to shift bone remodeling toward catabolic bone degeneration.

PMID 42458258
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PubMedMaterials (Basel, Switzerland)2026-07-15

In Situ Catalytic Modification of Phenolic Resin Pyrolytic Carbon Using Cupric Tartrate-Derived Cu Nanoparticles: Microstructure Evolution and Oxidation Behavior.

Jiang Pengcheng P, Tang Huidong H, Xiong Xin X, Wu Zhi Z et al.

Phenolic resin is widely used as a binder in high-temperature industries; however, its pyrolysis generally yields isotropic glassy carbon, which strongly influences its high-temperature oxidation behavior. In this work, cupric tartrate was introduced as a catalyst precursor to investigate its effects on the thermal decomposition behavior, microstructural evolution, and oxidation behavior of the phenolic resin pyrolytic carbon. Upon heating, cupric tartrate decomposed at 250-320 °C into nanoscale Cu/Cu2O composites, which were then converted into metallic Cu nanoparticles through reduction by gaseous products generated during the pyrolysis of phenolic resin. The in situ formed Cu nanoparticles were associated with the growth of tapered carbon nanofibers (CNFs), reaching maximum lengths of 30-50 μm at 700 °C. Based on the observed microstructural features and established literature reports, a dissolution-precipitation pathway is proposed to rationalize the formation of these CNFs. The presence of Cu-catalyzed CNFs correlates with enhanced structural ordering of the pyrolytic carbon, as reflected by reduced ID/IG ratios, and with an increased apparent oxidation activation energy in the selected fitting region (from 103.73 to 137.45 kJ/mol). Overall, this work demonstrates a facile strategy in which cupric tartrate serves as an effective catalyst precursor that generates Cu nanoparticles in situ; these nanoparticles then catalyze CNF growth from phenolic resin, enabling the construction of low-dimensional carbon nanostructures.

PMID 42451901
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PubMedInternational journal of molecular sciences2026-07-15

Inhibition of CD38 by 78c Enhanced NAD+ and Alleviated Alveolar Bone Loss in Mice with Experimental Periodontitis.

Yarbrough Jon Stephen JS, Pandruvada Subramanya S, Hill William D WD, Yu Hong H

Old murine bone marrow-derived monocytes and macrophages (BMMs) display enhanced CD38 protein, a nicotinamide adenine dinucleotide (NAD+) glycohydrolase, and reduced NAD+ level after infection with oral pathogens compared to young controls. We aimed to determine whether treatment with a CD38-specific inhibitor (78c) in mice with experimental periodontitis could alleviate alveolar bone loss and enhance NAD+ levels in tissues compared with vehicle treatment. Twenty young (2-month-old) and twenty old (18-month-old) male C57BL/6J mice with experimental periodontitis were treated with either vehicle or 78c twice daily via intraperitoneal injection for 4 weeks. The liver, spleen, and right maxillary tissues were harvested to analyze NAD+ levels. The left maxillary tissues were scanned by micro-CT. Then, the left maxillary tissues were processed for tissue sectioning and stained with hematoxylin and eosin (H&E) and tartrate-resistant acid phosphatase (TRAP). Treatment with 78c significantly enhanced NAD+ levels in the liver and spleen of both young and old mice, and significantly increased NAD+ in the right maxilla of old mice compared with vehicle treatment. Additionally, treatment with 78c alleviated alveolar bone loss in both young and old mice. Our results support the notion that 78c is a promising therapeutic strategy for treating periodontal disease.

PMID 42450104
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