Etomidate 20mg/10ml solution for injection ampoules
Requires a prescription from a doctor or prescriber
Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system.
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Drug safety updates
MHRA alerts for Etomidate
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.
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Suspected adverse reactions reported for Etomidate
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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 Etomidate
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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
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View all licensed products for Etomidate on the MHRA register
Hypnomidate 20mg/10ml solution for injection ampoules
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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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
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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. 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: 19 · Randomised trials: 31 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
Takatoshi Koroki, Yuki Kotani, Takahiko Yaguchi, et al.
Critical Care, 2024
Alisha Greer, M. Hewitt, Parsa T. Khazaneh, et al.
Critical Care Medicine, 2024
Y. Kotani, Gioia Piersanti, Giacomo Maiucci, et al.
Journal of critical care, 2023
Y. Feng, X-B Chen, Y. Zhang, et al.
European review for medical and pharmacological sciences, 2023
Zampieri FG, Schmidt RC, Besen BAMP, et al.
2026
- Intubation, Intratracheal
- Critical Illness
- Ketamine
BackgroundEtomidate, ketamine, and propofol are all used as induction agents for emergency tracheal intubation in critically ill adults but it remains uncertain which agent should be preferable.MethodsWe searched MEDLINE and Embase (inception to December 2025) for randomized controlled trials comparing etomidate, ketamine, propofol, or ketamine-propofol combination (ketofol) for emergency or rapid sequence intubation in critically ill adults. We performed random-effects network meta-analysis using the frequentist framework. The primary outcome was short-term mortality (28-30 day, or ICU/in-hospital mortality when unavailable). Secondary outcomes included cardiovascular collapse, post-induction hypotension, vasopressor use, first-pass intubation success, and peri-intubation cardiac arrest. Certainty of evidence was assessed using the CINeMA framework.ResultsNine trials (4,672 patients, four treatments) were included. Ketamine and etomidate probably result in similar mortality (OR 0.96, 95% CI 0.80-1.16; [Formula: see text] = 30%; moderate certainty). Evidence for other mortality comparisons was very uncertain: ketamine vs propofol (OR 1.53, 0.80-2.93; 1 trial; low certainty) and etomidate vs propofol (OR 0.63, 0.32-1.24; indirect only; very low certainty). Compared with etomidate, ketamine probably increases cardiovascular collapse (OR 1.44, 1.20-1.71; moderate certainty) and may increase post-induction hypotension (OR 1.34, 1.07-1.68; low certainty) and peri-intubation vasopressor use (OR 1.45, 1.21-1.74; low certainty). There was probably little or no difference in first-pass intubation success or cardiac arrest.ConclusionsEtomidate and ketamine probably result in similar mortality, but confidence intervals are compatible with clinically important differences in either direction-ketamine probably causes more peri-intubation hemodynamic instability. Beyond one trial, no randomized evidence exists for propofol in emergency intubation of critically ill adults.
Abstract licence: CC BY
Bandyopadhyay A, Haldar P, Sawhney C, et al.
2025
ObjectiveEtomidate and ketamine are hemodynamically stable induction agents for rapid sequence intubation (RSI) of critically ill patients. Despite their relative stability in terms of hemodynamics, how the choice of agent affects mortality and the success of the procedure is debatable and has not yet been explored via systematic review and meta-analysis. The objective of this systematic review is to compare the efficacy of ketamine and etomidate for RSI in terms of mortality, hemodynamic parameters, and success rate.MethodsA comprehensive search of PubMed, Embase, and the Web of Science was conducted from the starting date of each database until April 2024. Randomized controlled trials comparing the safety and efficacy of ketamine and etomidate as induction drugs for critically ill patients undergoing RSI were included. The primary outcome was the risk of 28-day mortality, and the secondary outcomes included the success rate and postinduction hypotension. Pooled relative risks (RRs) with 95% confidence intervals (CIs) were calculated using a random-effects meta-analysis.ResultsFour studies with 1,663 patients were meta-analyzed, and no statistically significant difference between the two drugs was found for 28-day mortality (RR, 0.95; 95% CI, 0.72-1.25; heterogeneity I2=39%; level of certainty of evidence per GRADE, moderate), first-pass success rate (RR, 1.00; 95% CI, 0.97-1.03), or postinduction cardiac arrest (RR, 1.10; 95% CI, 0.62-1.96). Postinduction hypotension was higher in the ketamine group (RR, 1.30; 95% CI, 1.03-1.64), but the result was not statistically significant.ConclusionMortality outcomes did not differ when ketamine or etomidate was used for RSI in critically ill patients. Ketamine, however, was associated with a non-significantly higher risk of postinduction hypotension.
Abstract licence: CC BY-NC
Seyed Pouya Paknezhad, Kavous Shahsavarinia, Morteza Ghojazadeh, et al.
Archives of Anesthesia and Critical Care, 2024
Zhiqiu Xia, Kajal Kamra, Jianghu Dong, et al.
Heliyon, 2024
Zhen Gu, Xiaoli Huang, Aolin Ren, et al.
Frontiers in Medicine, 2026
Objective Explore the clinical efficacy and safety of ciprofol-etomidate (C-E) versus propofol-etomidate (P-E) for gastrointestinal endoscopy sedation, and generate hypotheses for subsequent prospective pre-registered trials. Methods A prospective, double-blind, randomized, positive-controlled exploratory trial enrolled 240 adults (120 per group). Exploratory outcomes included hemodynamics, adverse events, and Chalder Fatigue Questionnaire (CFQ) scores. Intention-to-treat (ITT) analysis was primary, with per-protocol analysis (PPA, n = 223) as sensitivity validation. Results C-E group showed significantly lower CFQ Bimodal scores ≥4, postoperative dizziness incidence, and blood pressure fluctuations (>20% baseline; all p < 0.05). One P-E patient needed respiratory support for SpO₂ = 85%. Other outcomes (e.g., induction time, total dose) were comparable. ITT and PPA results were consistent. Conclusion This retrospective registered exploratory study tentatively suggests C-E may offer potential advantages in hemodynamic stability, respiratory safety, and reduced post-procedural fatigue/dizziness for low-risk (ASA I ~ II) patients. Findings are hypothesis-generating and require validation via prospective pre-registered trials. Systematic review registration https://www.chictr.org.cn/indexEN.html , identifier ChiCTR2500107221.
Abstract licence: CC BY 4.0
Andriazzi VH, Curcio RP, Novais MARA, et al.
2026
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
75 minutes
Mechanism
Etomidate binds at a distinct binding site associated with a Cl- ionopore at the…
Food interactions
None known
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Half-life
75 minutes
Protein binding
76%
Metabolism
Elimination
75%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1601 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
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
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:10227690 PMID:10954735 PMID:18245775 PMID:19449892 PMID:25982116 PMID:27078104 PMID:32860739
Has a very broad substrate specificity; can transport a wide range of aldoses including both pentoses and hexoses .
PMID:18245775 PMID:19449892
Most important energy carrier of the brain: present at the blood-brain barrier and assures the energy-independent, facilitative transport of glucose into the brain .
PMID:10227690
In association with BSG and NXNL1, promotes retinal cone survival by increasing glucose uptake into photoreceptors (By similarity). Required for mesendoderm differentiation (By similarity)
ATC N01AX07
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Etomidate
Additional database identifiers
Drugs Product Database (DPD)
23454
ChemSpider
580864
BindingDB
50125935
PDB
V8D
ZINC
ZINC000000001408
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:282
GenAtlas
ADRA2B
GeneCards
ADRA2B
GenBank Gene Database
M34041
GenBank Protein Database
178198
Guide to Pharmacology
26
UniProt Accession
ADA2B_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:4088
GeneCards
GABRG3
GenBank Gene Database
S82769
GenBank Protein Database
1754749
UniProt Accession
GBRG3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2591
GenAtlas
CYP11B1
GeneCards
CYP11B1
GenBank Gene Database
M32879
GenBank Protein Database
181333
Guide to Pharmacology
1359
UniProt Accession
C11B1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2592
GeneCards
CYP11B2
GenBank Gene Database
X54741
GenBank Protein Database
35200
Guide to Pharmacology
1360
UniProt Accession
C11B2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11005
GenAtlas
SLC2A1
GeneCards
SLC2A1
GenBank Gene Database
K03195
GenBank Protein Database
183303
Guide to Pharmacology
875
UniProt Accession
GTR1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72