Temazepam 10mg/5ml oral solution unit dose vials sugar free
Some safe custody exemptions; written records required
Legal requirements and restrictions
Medicines with lower misuse potential than Schedule 2. Subject to special prescription requirements but reduced record-keeping.
Legal requirements
- Safe custody requirements apply (locked storage)
- No controlled drugs register required
- Prescriptions valid for 28 days
- Can be emergency supplied by pharmacists
Other medicines in this category
Safety information for pregnancy and breastfeeding
Pregnancy
Breastfeeding
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Temazepam
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Temazepam
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
2 branded products available
MHRA licensed products
View all licensed products for Temazepam on the MHRA register
Temazepam 10mg/5ml oral solution unit dose vials sugar free
Alliance Healthcare (Distribution) Ltd
WHO defined daily dose (DDD)
20 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
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: 4 · Randomised trials: 6 · 1975–2026
Showing the 50 most relevant studies, sorted by most relevant.
Yu DJ, Recchia F, Bernal JDK, et al.
2023
Despite the well-established treatment effectiveness of exercise, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy on improving sleep, there have been no studies to compare their long-term effectiveness, which is of clinical importance for sustainable management of chronic insomnia. This study compared the long-term effectiveness of these three interventions on improving sleep in adults with chronic insomnia. MEDLINE, PsycINFO, Embase, and SPORTDiscus were searched for eligible reports. Trials that investigated the long-term effectiveness of these three interventions on improving sleep were included. The post-intervention follow-up of the trial had to be ≥6 months to be eligible. The primary outcome was the long-term effectiveness of the three interventions on improving sleep. Treatment effectiveness was the secondary outcome. A random-effects network meta-analysis was carried out using a frequentist approach. Thirteen trials were included in the study. After an average post-intervention follow-up period of 10.3 months, both exercise (SMD, -0.29; 95% CI, -0.57 to -0.01) and CBT-I (-0.48; -0.68 to -0.28) showed superior long-term effectiveness on improving sleep compared with control. Temazepam was the only included pharmacotherapy, which demonstrated superior treatment effectiveness (-0.80; -1.25 to -0.36) but not long-term effectiveness (0.19; -0.32 to 0.69) compared with control. The findings support the use of both exercise and CBT-I for long-term management of chronic insomnia, while temazepam may be used for short-term treatment.
Abstract licence: CC BY
BMJ, 1980
- Benzodiazepines
- Chlordiazepoxide
- Clorazepate Dipotassium
R. Mendis, A. Wong, Simon Frenkel, et al.
Journal of Palliative Medicine, 2024
- Neoplasms
- Sleep Initiation and Maintenance Disorders
- Temazepam
Schenker MT, Zeng LZ, Lynskey J, et al.
2025
- Azepines
- Triazoles
- Fear
Post-traumatic stress disorder (PTSD) is a highly debilitating condition that develops after trauma exposure. Dysregulation in extinction memory consolidation (i.e., the ability to remember that trauma-related stimuli no longer signal danger) is proposed to underlie PTSD development. Disruptions in rapid eye movement (REM) sleep are thought to be the key contributor to this dysregulation, as REM sleep is suggested to play a vital role in the processing of emotional memories. While previous literature has investigated the role of natural REM sleep variations or REM sleep disruptions on extinction recall capacities, none have attempted to increase REM sleep to improve extinction recall. In this pilot, randomised controlled trial, we investigated the effect of 20 mg suvorexant to increase REM sleep, 20 mg temazepam to decrease REM sleep, and a placebo on extinction recall in 30 healthy adults (age: M = 26.93 years, SD = 7.54). Overall, no difference in REM percentage (p = 0.68, η 2 = 0.0.03, small effect), nor in extinction recall (p = 0.58, η 2 = 0.04, small effect) was observed between the drug conditions. However, increased REM percentage was associated with decreased conditioned fear response at recall, indicating better extinction recall (β = -0.71, p = 0.03, η p 2 = 0.10; moderate effect) across the sample. These findings suggest that increasing REM sleep in populations with REM disruptions such as PTSD to optimal levels could improve extinction recall. This underscores the potential of enhancing REM sleep as a therapeutic target for improving PTSD outcomes, warranting further investigation of suvorexant in clinical populations where REM sleep deficits are prevalent.
Abstract licence: CC BY
L. Showler, Yasmine Ali Abdelhamid, M. Ankravs, et al.
Critical Care and Resuscitation, 2026
Objective Patients in the intensive care unit (ICU) suffer from disturbed sleep and pharmacological sleep aids are frequently prescribed despite limited data on their efficacy. The objective of this study was to assess the effect of a single nocturnal dose of the benzodiazepine temazepam on sleep duration and quality in ICU patients. Design Prospective, single-centre, blinded, placebo-controlled, parallel-group, randomised clinical trial. Setting A tertiary ICU in Australia. Participants Adult ICU patients whose treating clinician considered that a pharmacological sleep aid was indicated. Interventions A single weight- and age-adjusted dose of temazepam (10–30 mg) or a matching placebo was administered enterally at 21:00 h. Main outcome measures The primary outcome was total sleep time between 21:00 and 07:00 h by hourly structured nurse assessment. Secondary outcomes included the evaluation of sleep quality, independently determined by the bedside nurse and patient using the Richards-Campbell Sleep Questionnaire. Results Between October 2020 and May 2024, 56 patients received temazepam (n = 28) or placebo (n = 28). The mean (standard deviation) total sleep time with temazepam was 349 (120) vs. placebo 291 (124) minutes; difference = 57 min (95% confidence intervals: −11 to 130); p = 0.10. No differences in total Richards-Campbell Sleep Questionnaire sleep quality were observed when assessed by the nurse (57 (17) vs. 49 (23), p = 0.15) or by the patient (50 (28) vs. 51 (23), p = 0.70). Conclusion A single dose of temazepam was not observed to improve the duration or quality of nocturnal sleep for patients in the ICU. Trial registration Retrospectively registered with the Australian and New Zealand Clinical Trials Registry on 11th June 2021 (ACTRN 12621000742875).
Abstract licence: CC BY-NC-ND
Emma L Arbon, Malgorzata Knurowska, Derk‐Jan Dijk
Journal of Psychopharmacology, 2015
- Zolpidem
- Delayed-Action Preparations
- Electroencephalography
G. Mooter, P. Augustijns, N. Blaton, et al.
International Journal of Pharmaceutics, 1998
R.C. Heel, Rex N. Brogden, T.M. Speight, et al.
Drugs, 1981
- Hypnotics and Sedatives
- Kinetics
- Temazepam
Gerald Dubowitz
BMJ, 1998
- Altitude
- Mountaineering
- Oxygen
S. Verheyen, N. Blaton, R. Kinget, et al.
International journal of pharmaceutics, 2002
- Chemistry, Pharmaceutical
- Delayed-Action Preparations
- Diazepam
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
2 found
Half-life
3.5-18 hours
Mechanism
Gamma-Aminobutyric acid (GABA) is considered the principal inhibitory neurotrans…
Food interactions
2 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
90 to 100%
Half-life
3.5-18 hours
Protein binding
96%
Volume of distribution
1.3-1.5 L/kg
[L5539]
Metabolism
5-8%
Elimination
80-90%
Clearance
1.03 ml/min/kg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Although the chemical synthesis of temazepam was established by 1965 [A175333], mainstream contemporary use of the medication did not occur until it's legitimate use as treatment for insomnia was accepted and approved later on. In particular, before temazepam saw regular prescription use in civilians it was - and still is - employed by the US military as a sedative-hypnotic medication to be taken by soldiers, pilots, etc. to obtain the necessary rest required for medical recovery or scheduled maneuvers and operations [A175339]. Regardless, temazepam has become one of the most frequently prescribed medications internationally and sees millions of prescriptions every year. Unfortunately, however, given its frequent use and the inherent nature of its pharmacological effects, temazepam - like many other benzodiazepines - possesses a high potential for misuse and is genuinely capable of developing drug tolerance, physical dependence, and addiction in users.
[L5539]
Furthermore, such management is generally predominantly associated with the symptomatic relief of transient and short-term insomnia characterized by difficulty in falling asleep, frequent nocturnal awakenings and/or early morning awakenings F3718. In particular, the official prescribing information for temazepam typically specifies that the instructions issued for dispensed prescriptions of the medication should indicate specifically that patients are only expected to use the therapy for short periods of time - usually 7-10 days in general [FDA Label, F3718]. Subsequently, treatment with temazepam should usually not exceed 7 to 10 consecutive days and nor should it be prescribed in quantities exceeding a one-month supply F3718.
Some regional prescribing information also notes that temazepam may be used for premedication prior to minor surgery or other related procedures .
[L5539]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1341 interactions
Benzodiazepines like temazepam might cause fetal harm when administered to a pregnant woman. Transplacental distribution has in the past resulted in neonatal CNS depression following the ingestion of therapeutic doses of related benzodiazepine hypnotics like diazepam during the last weeks of pregnancy [FDA Label] [L5539, F3718, F3721].
It is not known whether this drug is excreted in human milk [FDA Label] [L5539, F3718, F3721].
Caution should, therefore, be exercised when temazepam is administered to a nursing woman [FDA Label] [L5539, F3718, F3721].
Safety and effectiveness in pediatric patients have not been established [FDA Label] [L5539, F3718, F3721].
Lower doses of temazepam, like 7.5 mg is recommended as the initial dosage for patients aged 65 and over since the risk of the development of oversedation, dizziness, confusion, ataxia and/or falls increases substantially with larger doses of benzodiazepines in elderly and debilitated patients [FDA Label] [L5539, F3718, F3721].
No evidence of carcinogenicity was observed in animal studies although hyperplastic liver nodules were observed in female mice exposed to the highest doses of temazepam [FDA Label] [L5539, F3718, F3721]. The clinical significance of this finding is not known [FDA Label] [L5539, F3718, F3721].
Fertility in male and female rats was not adversely affected by temazepam toxicity studies [FDA Label] [L5539, F3718, F3721].
No mutagenicity tests have been done with temazepam [FDA Label] [L5539, F3718, F3721].
Subsequently, benzodiazepines like temazepam can bind to benzodiazepine receptors that are components of various varieties of GABA(a) receptors [A175207, A175210, F3718, F3721]. This binding acts to enhance the effects of GABA by increasing GABA affinity for the GABA(a) receptor, which ultimately enhances GABA ligand binding at the receptors [A175207, A175210, F3718, F3721]. This enhanced ligand binding of the inhibitory neurotransmitter GABA to the receptors increases the aforementioned chloride ion conduction (perhaps reportedly via an increase in the frequency of the chloride channel opening), resulting in a hyperpolarized cell membrane that prevents further excitation of the associated neuron cells [A175207, A175210, F3718, F3721]. Combined with the notion that such benzodiazepine receptor associated GABA(a) receptors exist both peripherally and in the CNS, this activity consequently facilitates various effects like sedation, hypnosis, skeletal muscle relaxation, anticonvulsant activity, and anxiolytic action [A175207, A175210, F3718, F3721].
In sleep laboratory studies, the effect of temazepam was compared to placebo during a two week period F3718. The studies demonstrated a linear dose-response improvement in total sleep time and sleep latency with substantial drug-placebo differences apparent for total sleep time and for sleep latency at higher doses of temazepam F3718. Regardless, REM sleep was ultimately unchanged but slow wave sleep was decreased F3718.
Moreover, a transient syndrome, known as "rebound insomnia", wherein the symptoms that led to treatment with temazepam in the first place recur in an enhanced form, may happen on withdrawal of temazepam treatment F3718. The possibility of this occurrence is in part why long term use of temazepam is not recommended due to worries over tolerance and dependence wherein patients' bodies become physiologically accustomed to the regular presence and pharmacological effect of higher and higher doses of the benzodiazepine used F3718.
The duration of hypnotic effect and the profile of unwanted adverse effects may be influenced by the distribution and elimination half-lives of the administered temazepam and any active metabolites that may be formed F3718. When such half-lives are long, the drug or its metabolite(s) may accumulate during periods of nightly administration and be associated with impairments of cognitive and motor performance during waking hours F3718. Conversely, if half-lives are short, the drug and metabolites would be cleared before the next dose is ingested, and carry-over effects related to sedation or CNS depression should be minimal or not present at all F3718. However, during nightly use and for an extended period, pharmacodynamic tolerance or adaptation to some effects of benzodiazepine hypnotics may develop - which may also contribute to the possibility of 'rebound insomnia' F3718.
Consequently, if the drug has a very short elimination half-life, it is possible that a relative deficiency (for example, in relation to benzodiazepine GABA(a) receptor sites) may occur at some point in the interval between each night's use F3718. This sequence of events may account for certain clinical findings reported happening after several weeks of nightly use of rapidly eliminated benzodiazepine hypnotics, including increased wakefulness during the last third of the night and the appearance of increased daytime anxiety F3718.
How the body processes this drug — absorption, distribution, metabolism, and elimination
Finally, a dose-proportional relationship was established for the area under the plasma concentration/time curve over the 15 to 30 mg dose range [FDA Label].
[L5539]
Less than 5% of the drug is demethylated to oxazepam and subsequently eliminated as the glucuronide [F3718, L5539]. Regardless, the glucuronides of temazepam have no demonstrable CNS activity and it is believed that no active metabolites are formed in general [FDA Label, F3718, L5539]. Since temazepam mainly undergoes Phase II conjugation reactions, it is proposed that it is devoid of CYP450 interactions.
[A38982]
[A175306]
Proteins and enzymes this drug interacts with in the body
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
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N05CD07
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)
Temazepam
Additional database identifiers
Drugs Product Database (DPD)
2014
ChemSpider
5198
BindingDB
50408032
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: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: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: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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q414796), 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.