Eszopiclone 2mg tablets
Requires a prescription from a doctor or prescriber
Eszopiclone, marketed by Sepracor under the brand-name Lunesta, is a nonbenzodiazepine hypnotic drug used to treat insomnia.
Minimal controls; includes benzodiazepines and anabolic steroids
Legal requirements and restrictions
Benzodiazepines and similar medicines. Subject to minimal controlled drug requirements.
Legal requirements
- Prescriptions valid for 28 days
- No controlled drugs register required
- No safe custody requirements
- Record keeping requirements for imports/exports
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Eszopiclone
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
MHRA licensed products
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Lunivia 2mg tablets
WHO defined daily dose (DDD)
2 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 15 · Randomised trials: 18 · 2003–2026
Showing the 50 most relevant studies, sorted by most relevant.
Elizabeth K. Stranks, Simon F. Crowe
Journal of Clinical and Experimental Neuropsychology, 2014
- Eszopiclone
- Zolpidem
- Acetamides
Mengzhen Zhou, Jiyou Tang, Shasha Li, et al.
Frontiers in Human Neuroscience, 2023
Background: About one-third of adults have trouble sleeping, ranging from occasional difficulty to chronic insomnia, along with difficulty maintaining sleep. Many studies reported that the long-term use of hypnotics can cause brain dysfunction and damage cognition. Objective: The objective of the study is to evaluate whether low, medium, and high doses of orexin dual receptor antagonists (DORA), zopiclone (ZOP), eszopiclone (ESZ), and zolpidem (ZST) can impair cognition. Methods: From the beginning through September 20, 2022, PubMed, Embase, Scopus, the Cochrane Library, and Google Scholar were searched. Randomized controlled trials (RCTs) assessing the therapeutic effects of DORA, eszopiclone, and zopiclone for sleep and cognitive function were included. The primary outcomes were indices related to the cognitive profile, including memory, alertness, execution and control function, and attention and orientation. The secondary outcomes were indices related to sleep and adverse events. The standard mean difference (SMD) was generated for continuous variables. Certain data were captured from figures by GetData 2.26 and analyzed using RStudio 4.2. Results: Finally, a total of 8,702 subjects were included in 29 studies. Compared with the placebo, the DSST (Digit Symbol Substitution Test) scores of low, medium, and high doses of DORA were SMD = 0.77; 95% CI: 0.33-1.20; SMD = 1.58; 95% CI: 1.11-2.05; and SMD = 0.85; 95% CI: 0.33-1.36, respectively. The DSST scores of zolpidem at low, medium, and high doses were SMD = -0.39; 95% CI: 0.85-0.07; SMD = -0.88, 95% CI: -2.34-0.58; and SMD = -0.12, 95% CI: -0.85-0.60, respectively. Zopiclone's DSST scale score was SMD = -0.18; 95% CI: -0.54-0.18. In addition, the total sleep time (TST) of low, medium, and high doses of DORA was SMD = 0.28, 95% CI: -0.15-0.70; SMD = 1.36, 95% CI: 0.87-1.86; and SMD = 2.59, 95% CI: 1.89-3.30, respectively. The TST of zolpidem with low, medium, and high doses was SMD = 1.01, 95% CI: 0.18-1.83; SMD = 1.94, 95% CI: 0.46-3.43; and SMD = 1.71, 95% CI: 0.86-2.56, respectively. The TST of low, medium, and high doses of eszopiclone was relatively SMD = 2.03, 95% CI: -0.21-4.27; SMD = 2.38, 95% CI: 1.35-3.42; and SMD = 1.71, 95% CI: 0.60-2.82. Zopiclone's TST was SMD = 2.47, 95% CI: 1.36-3.58. Conclusion: We recommend DORA as the best intervention for insomnia because it is highly effective in inducing and maintaining sleep without impairing cognition. Although zolpidem has a more pronounced effect on maintaining sleep, it is best to reduce its use because of its side effects. Eszopiclone and zopiclone improved sleep quality, but their safety in cognition remains to be verified.
Abstract licence: CC BY 4.0
Maruki T, Takeshima M, Yoshizawa K, et al.
2025
- Sleep Initiation and Maintenance Disorders
- Hypnotics and Sedatives
- Antidepressive Agents
Combination therapy with antidepressants and sleep medications is a promising candidate treatment for major depressive disorder (MDD) with insomnia. This systematic review and meta-analysis examined the efficacy and safety of combination therapy with antidepressants and sleep medication for treating MDD with insomnia compared to antidepressant monotherapy by sleep medication class (benzodiazepine, Z-drug, melatonin receptor agonist, and orexin receptor antagonist). This study was preregistered with PROSPERO (CRD42025636571). PubMed, CENTRAL, and Embase were searched for double-blind randomized controlled trials published until June 2024, resulting in eight eligible studies (1945 participants; eszopiclone = 4, zolpidem = 2, triazolam = 1, ramelteon = 1). Meta-analyses were performed based on six trials of Z-drugs. Compared with antidepressant monotherapy, combination therapy with antidepressants and Z-drugs resulted in higher remission rates from depressive symptoms (risk ratio: 1.25, 95% confidence interval [CI]: 1.08-1.45, P = 0.003), greater improvement in depressive symptoms (standardized mean difference [SMD]: 0.17, 95% CI: 0.01-0.33, P = 0.04) and insomnia symptoms (SMD: 0.43, 95% CI: 0.28-0.59, P < 0.001) in the short-term (within 12 weeks), with no difference in safety outcomes except for dizziness. Combination therapy with antidepressants and Z-drugs may be more useful for MDD with insomnia symptoms than antidepressant monotherapy in the short term. However, this study did not evaluate the benefits and harms of long-term adjunctive Z-drug therapy. Further long-term studies are needed to draw definitive conclusions regarding the efficacy and safety of combination therapy with antidepressants and Z-drugs. Moreover, further research is warranted to assess whether the findings of this study are applicable to other sleep medication classes.
Abstract licence: CC BY-NC
Fuglsang NFB, Madsen NM, Jacobsen SL, et al.
2025
- Sleep Initiation and Maintenance Disorders
- Hypnotics and Sedatives
- Bipolar Disorder
BackgroundA wide range of drugs is used to alleviate insomnia symptoms in individuals with severe mental illness (SMI), including licensed drugs and sedating drugs prescribed off-label. Yet, no review has gathered the evidence on illness-specific or transdiagnostic outcomes of pharmacological interventions for insomnia. We aimed to perform a systematic review and meta-analysis of randomised controlled trials (RCTs) studying the efficacy and acceptability of pharmacological interventions for insomnia among individuals with SMI, defined as schizophrenia, bipolar disorder (BD) or major depressive disorder (MDD).MethodsWe searched for RCTs of pharmacological interventions for insomnia that used either placebo or another medication as inactive control or active comparator. Two independent reviewers performed the literature screening, data extraction and risk of bias assessment (RoB2). We performed random effects meta-analyses on the co-primary outcomes total sleep time (TST), sleep quality and acceptability (all-cause discontinuation) and the secondary outcomes safety and tolerability.ResultsThe search identified 3331 hits, of which 25 RCTs (n = 2476 individuals) were included, with 18 RCTs (n = 2199) in MDD, 4 RCTs (n = 162) in BD and 3 RCTs (n = 115) in schizophrenia. Of 25 RCTs, 22 had a high risk of bias. The most frequently studied drugs were agomelatine (RCTs = 3, n = 686), eszopiclone (RCTs = 3, n = 599) and zolpidem (RCTs = 3, n = 601). Compared to placebo, pharmacological interventions for insomnia were associated with improved sleep quality by a small effect size (RCTs = 8, g = 0.24, 95% CI = 0.05-0.43) and improved TST (RCTs = 10, MD = 30.82 min, 95% CI = 19.13-42.50), with similar acceptability (RCTs = 10, RR = 1.06, 95% CI = 0.90-1.25).DiscussionDespite their frequent use, many licensed and off-label pharmacological interventions for insomnia have never been investigated in patients with SMI. The studies that provided sufficient data for meta-analysis showed better efficacy with similar acceptability compared to placebo, but the generalizability of these results is limited by the high heterogeneity and low quality of the included studies. This underscores the need for high-quality RCTs to provide a better scientific basis for the pharmacological treatment of insomnia in SMI.Trial registrationCRD42023413787.
Abstract licence: CC BY-NC
Chavez-Mendoza LF, Vázquez-Alvarez AO, Torres-Mendoza BM, et al.
2025
- Dementia
- Benzodiazepines
- Hypnotics and Sedatives
Currently, approximately 40% of patients with dementia develop some form of sleep disorder. Benzodiazepines are widely prescribed but pose the risk of tolerance and cognitive decline; however, Z-drugs may offer safer alternatives. Therefore, this systematic review aimed to analyze the effect of benzodiazepines and Z-drugs on sleep disorders in patients with dementia. Two authors conducted a systematic search in PubMed, Scopus, Web of Science, Espistemonikos, and ACCESSSS for studies published between 2019 and 2024 using the MeSH terms "dementia", "sleep disorders", and "pharmacotherapy". Randomized clinical trials comparing benzodiazepines, Z-drugs, or innovative medications with placebo or other drugs were included. Sleep and cognitive outcomes were assessed using validated instruments; the ROB-2 tool evaluated the risk of bias. The protocol was registered in "PROSPERO". Three randomized clinical trials involving a total of 192 patients were included in the review. Zopiclone increased the main duration of nighttime sleep by 81 min, Zolpidem reduced nighttime awakenings by 21 min, and Eszopiclone improved sleep quality, benefited the progression of sleep architecture, and reduced mental symptoms such as fear and anxiety. Z-drugs show superior efficacy and safety over benzodiazepines, improving sleep and cognitive symptoms in dementia. Personalized treatment and further research across dementia subtypes are needed to optimize long-term outcomes.
Abstract licence: CC BY
Palagini L, Dell'Osso BM, Ferini Strambi L, et al.
2026
- Sleep Initiation and Maintenance Disorders
- Hypnotics and Sedatives
- Mental Disorders
Pham DV, Quante A
2026
ObjectiveThis systematic review aims to evaluate recent evidence on interventions for sleep disturbances in dementia, a major clinical concern, with limited pharmacological and non-pharmacological strategies examined in controlled trials.MethodsWe included eight RCTs (N = 666 participants; 2020 - January 2025) in people with dementia and sleep disturbances. Records were identified via MEDLINE, screened using PRISMA-guidelines, and non-randomized or non-intervention studies were excluded. Risk-of-bias was assessed with Cochrane RoB2, and effect sizes (Cohen's d) were calculated in R.ResultsZ-drugs indicated small-large benefits, with eszopiclone significantly improving sleep efficiency and latency. Orexin receptor antagonists indicated mixed evidence, with low-dose lemborexant (2.5 mg) most favorable, meeting benchmarks for nocturnal awakenings. Circadian modulation light therapy was associated with reduced nocturnal awakenings in small trials, while relaxation-based music therapy indicated little to no effect. Social stimulation with PARO indicated increased sleep time and large positive effects on sleep efficiency, despite missing clinical benchmarks.ConclusionsEvidence is limited by sparse reporting and few trials per intervention. Z-drug eszopiclone, low-dose ORA lemborexant, and social stimulation PARO show the most favorable profile across outcomes and benchmarks, but pharmacological options require careful risk-benefit consideration. Non-pharmacological approaches appear safer but under-researched. Future trials should standardize outcomes and tailor strategies to patient needs. No external funding. The review was registered in INPLASY: https://doi.org/10.37766/inplasy2025.1.0097.
Abstract licence: CC BY
Kishi T, Ikuta T, Sakuma K, et al.
2026
- Sleep Apnea, Obstructive
- Hypnotics and Sedatives
- Outcome Assessment, Health Care
AimThis network meta-analysis of randomized controlled trials (RCTs) aimed to investigate which hypnotics are associated with the most favorable sleep architecture and respiratory outcomes in adults with obstructive sleep apnea.MethodsPrimary outcomes included total sleep time (TST) and apnea-hypopnea index (AHI) during TST. Other outcomes were rapid eye movement (REM) sleep time, latency to persistent sleep (LPS), wake after sleep onset (WASO), sleep efficiency (SE), AHI during non-REM or REM sleep, mean peripheral oxygen saturation (SpO2) during TST, mean SpO2 nadir during TST, arousal index (AI), all-cause discontinuation, adverse event-related discontinuation, and incidence of individual adverse events. Effect sizes with 95% confidence intervals were calculated.ResultsThis systematic review included 32 RCTs (n = 1871, average age = 51.60 years, 62.52% male, mean AHI = 23.60). Our network meta-analysis evaluated brotizolam, daridorexant, eszopiclone, flurazepam, lemborexant, nitrazepam, ramelteon, temazepam, triazolam, zaleplon, zolpidem, zopiclone, and placebo. Compared with placebo, lemborexant increased TST, REM sleep time, and SE and decreased LPS and WASO, whereas both daridorexant and zolpidem increased TST and SE and decreased WASO. These three medications demonstrated respiratory safety and discontinuation profiles similar to those of placebo. Eszopiclone increased TST and SE and decreased LPS, WASO, AHI during TST, and AI, but its effects on LPS, WASO, AHI during TST, and AI disappeared in the sensitivity analysis, excluding continuous positive airway pressure titration studies.ConclusionOur network meta-analysis identified different effects of various hypnotics on sleep architecture and respiratory parameters; however, the lack of data prevented a formal synthesis of subjective outcomes. Therefore, these results should be interpreted with caution in clinical practice.
Abstract licence: CC BY
Jemere T, van der Mei I, Honan C, et al.
2026
- Multiple Sclerosis
- Sleep Wake Disorders
- Outcome Assessment, Health Care
BackgroundPoor sleep is common in people with multiple sclerosis (PwMS). Previous systematic reviews have evaluated intervention effectiveness to improve sleep in PwMS using questionnaires, but no review has comprehensively examined whether sleep interventions improve activity monitor measured sleep outcomes in PwMS.MethodsAdhering to the PRISMA guidelines, we searched PubMed, EMBASE, and PsycINFO databases to identify randomized controlled trials, quasi-experimental and cohort studies published from inception to October 2025. A random-effects model was used to estimate the pooled intervention effects of sleep interventions on objective sleep outcomes.ResultsTen studies were included in the review for narrative synthesis, with five eligible for quantitative meta-analysis. Six sleep parameters were assessed via activity monitors: total sleep time, sleep efficiency, total time in bed, sleep onset latency, wake after sleep onset, and frequency of awakenings. Sleep interventions utilised included physical activity, mindfulness, cognitive behavioral therapy (CBT), melatonin, eszopiclone and transcranial direct current stimulation (tDCS). Only sleep efficiency improved following mindfulness interventions. The median length of actigraph wear time was 7 days (range 4 nights to 16 weeks). Study quality appraisal scores ranged from moderate to high, suggesting a low risk of bias.ConclusionActivity monitors have been used to assess sleep intervention effectiveness in PwMS in studies assessing physical activity, mindfulness and CBT. Objective improvements in sleep were reported following mindfulness and only using one measure (sleep efficiency). However, the small number of included studies limits definitive conclusions. Future trials should consider a wider range of outcome measures and longer time horizons.
Abstract licence: CC BY
Christopher J. Lettieri, Anita A Shah, Aaron B Holley, et al.
PubMed, 2009
- Patient Compliance
- Continuous Positive Airway Pressure
- Eszopiclone
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
1 found
Half-life
6.1 hours
Mechanism
The exact mechanism of action of eszopiclone is unknown at this time but is thou…
Food interactions
2 warnings
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 hour
[A179659][L6769]…
Half-life
6.1 hours
Protein binding
52-59%
[L6769]
Volume of distribution
89.9L
Metabolism
[A179641]…
Elimination
10%
[A179659][L6769]…
Clearance
184 mL/min
[A179638]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
One major benefit of eszopiclone is that it is approved by the FDA for the long-term treatment of insomnia. This sets it apart from many other hypnotic sedatives, which are generally approved only for the relief of short-term (6-8 weeks) insomnia. Eszopiclone was initially approved by the FDA in 2004.[L6769]
[L6769]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1653 interactions
[L6853]
Symptoms of overdose may include mental status changes and somnolence, demonstrating general exaggeration of the drug's pharmacological effects. Perform gastric lavage and offer supportive treatment if an overdose is suspected, including intravenous fluids as required. Flumazenil may be used.
Vital signs should be closely monitored in addition to patient symptoms. Appropriate medical interventions should be employed. The possibility of an overdose with multiple drugs should be considered.
Ensure to contact the local poison control center for the most updated management of hypnotic drug overdose.
[L6769]
Eszopiclone is a central nervous system depressant with various effects. These include changes in alertness and motor coordination and the risk of next morning impairment, increasing with the amount of eszopiclone administered. Exercise caution and advise against driving a motor vehicle or activities that require full mental alertness the next morning.[L6769] Complex sleep behaviors may result from eszopiclone use. Eszopiclone should be discontinued in these cases.[L6874] Avoid the use of alcohol and other CNS depressants when eszopiclone is administered. Advise patients to skip the eszopiclone dose if alcohol has been consumed before bed or during the evening. Use the smallest dose of eszopiclone as possible, especially in elderly patients, who may experience exaggerated drug effects. Though the potential for dependence and abuse with eszopiclone is lower than for other hypnotic drugs, this drug has been abused and is known to cause dependence.[L6868]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A179659][L6769]
The mean AUC after a 3 mg dose of eszopiclone was 278 ng/mL × h.
[A179638]
The consumption of a high-fat has been shown to slow absorption. Steady-state concentrations of eszopiclone are reached within 24-48 hours.
[A179662]
[A179638][L6769]
[L6769]
[A179641]
The enzymes involved in the metabolism of eszopiclone are CYP3A (the primary metabolizing enzyme), CYP2C8, and CYP2E1.
[A179641]
The N-oxide derivative shows weak pharmacological activity in animals. The N-desmethyl metabolite is pharmacologically active.
[L6769]
[A179659][L6769]
As much as 75% of an orally administered dose of racemic zopiclone as is found to be excreted in the urine in the form of metabolites. Eszopiclone, the S-isomer of racemic zopiclone, would likely show the same excretion pattern.
[L6769]
[A179638]
Proteins and enzymes this drug interacts with in the body
PMID:23909897 PMID:25489750 PMID:29950725 PMID:30602789
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s) .
PMID:29950725 PMID:30602789
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:23909897 PMID:29950725 PMID:30602789
Alpha-1/GABRA1-containing GABAARs are largely synaptic (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation .
PMID:23909897 PMID:25489750
GABAARs function also as histamine receptor where histamine binds at the interface of two neighboring beta subunits and potentiates GABA response (By similarity).
GABAARs containing alpha, beta and epsilon subunits also permit spontaneous chloride channel activity while preserving the structural information required for GABA-gated openings (By similarity). Alpha-1-mediated plasticity in the orbitofrontal cortex regulates context-dependent action selection (By similarity). Together with rho subunits, may also control neuronal and glial GABAergic transmission in the cerebellum (By similarity)
PMID:10449790 PMID:16412217
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interfaces (By similarity). When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient PMID:10449790 PMID:16412217
Was initially identified as peripheral-type benzodiazepine receptor; can also bind isoquinoline carboxamides PMID:1847678
PMID:10449790 PMID:29961870 PMID:31032849
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interfaces (By similarity). When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:10449790
Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). The alpha-2 subunit exhibits synaptogenic activity together with beta-2 and very little to no activity together with beta-3, the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation (By similarity)
PMID:16412217 PMID:29053855
GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s) (By similarity). When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:16412217 PMID:29053855
Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission PMID:16412217 PMID:29053855
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N05CF04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Eszopiclone
Additional database identifiers
Drugs Product Database (DPD)
22704
ChemSpider
839530
BindingDB
50247998
ZINC
ZINC000019632834
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4075
GenAtlas
GABRA1
GeneCards
GABRA1
GenBank Gene Database
X13584
GenBank Protein Database
31631
Guide to Pharmacology
404
UniProt Accession
GBRA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4075
GenAtlas
GABRA1
GeneCards
GABRA1
GenBank Gene Database
X13584
GenBank Protein Database
31631
Guide to Pharmacology
404
UniProt Accession
GBRA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4076
GenAtlas
GABRA2
GeneCards
GABRA2
GenBank Gene Database
S62907
GenBank Protein Database
386422
Guide to Pharmacology
405
UniProt Accession
GBRA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4077
GenAtlas
GABRA3
GeneCards
GABRA3
GenBank Gene Database
S62908
GenBank Protein Database
386424
Guide to Pharmacology
406
UniProt Accession
GBRA3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4078
GenAtlas
GABRA4
GeneCards
GABRA4
GenBank Gene Database
U30461
GenBank Protein Database
905393
Guide to Pharmacology
407
UniProt Accession
GBRA4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4079
GenAtlas
GABRA5
GeneCards
GABRA5
GenBank Gene Database
L08485
GenBank Protein Database
182916
Guide to Pharmacology
408
UniProt Accession
GBRA5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4080
GenAtlas
GABRA6
GeneCards
GABRA6
GenBank Gene Database
S81944
GenBank Protein Database
1470364
Guide to Pharmacology
409
UniProt Accession
GBRA6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4081
GenAtlas
GABRB1
GeneCards
GABRB1
GenBank Gene Database
X14767
GenBank Protein Database
31635
UniProt Accession
GBRB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4082
GenAtlas
GABRB2
GeneCards
GABRB2
GenBank Gene Database
S67368
GenBank Protein Database
455946
UniProt Accession
GBRB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4083
GenAtlas
GABRB3
GeneCards
GABRB3
GenBank Gene Database
M82919
GenBank Protein Database
182925
Guide to Pharmacology
412
UniProt Accession
GBRB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4084
GeneCards
GABRD
GenBank Gene Database
AF016917
GenBank Protein Database
2388693
UniProt Accession
GBRD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4085
GeneCards
GABRE
GenBank Gene Database
U66661
GenBank Protein Database
1857126
UniProt Accession
GBRE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4086
GeneCards
GABRG1
GenBank Gene Database
AK122845
GenBank Protein Database
193783776
UniProt Accession
GBRG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4087
GeneCards
GABRG2
GenBank Gene Database
X15376
GenBank Protein Database
31637
UniProt Accession
GBRG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4088
GeneCards
GABRG3
GenBank Gene Database
S82769
GenBank Protein Database
1754749
UniProt Accession
GBRG3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4089
GeneCards
GABRP
GenBank Gene Database
U95367
GenBank Protein Database
2197001
UniProt Accession
GBRP_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14454
GeneCards
GABRQ
GenBank Gene Database
AF189259
GenBank Protein Database
7861736
UniProt Accession
GBRT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1158
GenAtlas
TSPO
GeneCards
TSPO
GenBank Gene Database
M36035
GenBank Protein Database
306883
Guide to Pharmacology
2879
UniProt Accession
TSPO_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4076
GenAtlas
GABRA2
GeneCards
GABRA2
GenBank Gene Database
S62907
GenBank Protein Database
386422
Guide to Pharmacology
405
UniProt Accession
GBRA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4077
GenAtlas
GABRA3
GeneCards
GABRA3
GenBank Gene Database
S62908
GenBank Protein Database
386424
Guide to Pharmacology
406
UniProt Accession
GBRA3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4079
GenAtlas
GABRA5
GeneCards
GABRA5
GenBank Gene Database
L08485
GenBank Protein Database
182916
Guide to Pharmacology
408
UniProt Accession
GBRA5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q413184), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.