Thiopental 500mg powder for solution for injection vials
Requires a prescription from a doctor or prescriber
A barbiturate that is administered intravenously for the induction of general anesthesia or for the production of complete anesthesia of short duration.
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Suspected adverse reactions reported for Thiopental
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Thiopental 500mg powder for solution for injection vials
Thiopental 500mg powder for solution for injection vials
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
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. 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: 7 · Randomised trials: 17 · 1951–2025
Showing the 50 most relevant studies, sorted by most relevant.
N. Abramson
The New England Journal of Medicine, 1986
Hedawy S, E Labeeb E, Aldalahmeh S, et al.
2025
- Hypnotics and Sedatives
- Anesthesia, General
- Anesthesia, Obstetrical
Background and purposeGeneral anesthesia is indicated in emergencies, contraindications, or patient requests. The induction agent to use is an important factor in general anesthesia. We aim to provide an updated systematic review and meta-analysis to compare propofol, ketamine, and thiopental sodium in terms of efficacy and safety profiles in women undergoing cesarean sections under general anesthesia.MethodsWe conducted this systematic review and meta-analysis according to PRISMA guidelines. We searched the following databases (PubMed, Scopus, Cochran Library, and Web of Science) up to 18-8-2024. We used a term for cesarian section, thiopental, ketamine, and propofol.ResultsThirty-six randomized controlled trials met our criteria and were included in our analysis with a total of 1945 patients. In (Thiopentone vs. Propofol) group, the use of thiopentone was associated with higher umbilical artery PH and longer recovery duration, although the certainty of evidence was low for both outcomes, while in the propofol group, the risk of having neonates with Apgar score less than 7 at one minute was higher, but the certainty of evidence was very low. In (Thiopentone vs. Ketamine) group, patients induced with thiopentone reported accidental awareness during general anesthesia (AAGA) more frequently and their neonates revealed higher umbilical vein PvO2. Also, Apgar score ConclusionOur findings suggest that propofol and thiopentone appear to be clinically comparable. Ketamine was favored over thiopentone for its lower risk of AAGA, while thiopentone was associated with a lower risk of Apgar scores < 7 at 1 and 5 min. Additional well-designed trials are needed to support our conclusions more firmly.
Abstract licence: CC BY
Navarro-Altuna V, Purwin S, Ranninger E
2025
- Anesthetics
- Cesarean Section
- Animals, Newborn
ObjectiveTo review and systematically analyse the literature describing the effects of anaesthesia drugs on puppy vitality scores or survival in dogs undergoing caesarean section.AnimalsOverall 13 randomized controlled trials (RCTs) involving 1978 puppies were included.MethodsA comprehensive search using PubMed, Embase and Scopus databases was performed from 1970 until September 2024 to obtain nonrandomized and RCTs examining the effects of anaesthetics on puppy survival rates or vitality scores after caesarean section in dogs. Only studies in English were screened. Search terms included: 'c-section' or 'caesarean section' and 'anaesthesia' and 'dog'. Two authors independently searched, classified and extracted the data. Studies were included if they evaluated the effects of anaesthesia drugs in dogs undergoing general anaesthesia and puppy survival or vitality scores. The level of evidence was scored according to the Oxford Centre for Evidence-based Medicine criteria, and a modified criterion score was used to assess the risk of bias based on the SYRCLE risk of bias tool and the SIGN checklists.ResultsMethodological characteristics varied considerably between studies, including drug doses, titration of anaesthetics, anaesthesia monitoring and puppy outcome scores. Ten studies assessed puppy vitality by using a modified Apgar score (AS). A high risk of bias was identified in six studies, whereas three had a low risk of bias. The scarcity of methodologically consistent studies and the quality of data limit identification of an optimal anaesthetic regimen to improve puppy survival. Low doses of morphine, methadone, dexmedetomidine or meloxicam preoperatively did not produce a significant impact on puppy vitality. Ketamine-midazolam, etomidate or thiopental appear to worsen immediate neonatal outcomes. No difference in neonatal survival was found between alfaxalone and propofol, but AS were higher with alfaxalone than with propofol immediately after birth.ConclusionsThe use of injectable anaesthetics for maintenance of anaesthesia led to lower puppy vitality.
Abstract licence: CC BY
Abdus Samad A, Allah Dad MS, Saeed Z
2025
A. Bhutada, R. Sahni, S. Rastogi, et al.
Archives of Disease in Childhood - Fetal and Neonatal Edition, 2000
Akan M, Çakırgöz M, Demirel İ, et al.
2025
Background: Remifentanil, an ultra-short-acting μ-receptor agonist, is used with propofol or thiopental for tracheal intubation without muscle relaxants. While effective with both, its combination with thiopental provides better hemodynamic stability. Thiopental has long been a standard intravenous agent for anaesthesia induction and remains a cost-effective alternative to propofol in resource-limited settings. To date, no study has directly compared the effects of thiopental-remifentanil and propofol-remifentanil combinations on LMA insertion conditions. This study aims to compare the effects of thiopental or propofol with 2 µg·kg-1 remifentanil on laryngeal mask airway (LMA) insertion conditions and success in a prospective, randomised double-blind study. Method: The study included 80 premedicated ASA I-II patients, aged 18-65, randomised into Group P (propofol) and Group T (thiopental). Anaesthesia induction was with 2 μg·kg-1 remifentanil, followed by 5 mg·kg-1 thiopental or 2.5 mg·kg-1 propofol. LMA insertion occurred 90 s post-induction. LMA insertion conditions were evaluated using a six-variable scale. Systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), heart rate (HR), and bispectral index monitor (BIS) values were recorded at baseline, 1 min pre-insertion, and at 1, 2, 3, 4, and 5 min after insertion. Apnoea duration, loss of eyelash reflex duration, insertion duration, number of attempts, and perioperative complications were also documented. Results: Demographic data were similar. Group P showed significantly shorter eyelash reflex loss and LMA insertion durations, longer apnoea duration, and higher rates of full mouth opening, excellent LMA insertion condition, and hypotension or bradycardia compared to Group T (p p p > 0.05). Conclusions: In our study, administration of 2 μg·kg-1 remifentanil before induction along with thiopental or propofol was shown to provide acceptable LMA insertion conditions at comparable levels. As hemodynamic parameters were less affected, we believe the remifentanil-thiopental combination may be a suitable alternative.
Abstract licence: CC BY
J. Pérez-Bárcena, J. A. Llompart-Pou, J. Homar, et al.
Critical Care, 2008
Çakırgöz M, Demirel İ, Akan M, et al.
2025
R. Melamed, S. Bar-Yosef, G. Shakhar, et al.
Anesthesia & Analgesia, 2003
J. Michenfelder
Anesthesiology, 1974
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
24 found
Half-life
3-8 hours
Mechanism
Thiopental binds at a distinct binding site associated with a Cl- ionopore at th…
Food interactions
1 warning
Human targets
12 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
3-8 hours
Protein binding
80%
Metabolism
0.3%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1440 interactions
Lethal blood levels may be as low as 1 mg/100 mL for short-acting barbiturates; less if other depressant drugs or alcohol are also present.
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L32434]
Ring desulfuration leads to the generation of an active metabolite, [pentobarbital], that exists in concentrations approximately 3-10% that of the parent concentration.
[A35309]
Thiopental and pentobarbital are also subject to both oxidation and hydroxylation to carboxylic acids and alcohols, respectively, all of which are pharmacologically inert.
[A35309]
While many of the specifics regarding thiopental biotransformation have not been elucidated, including the enzymes responsible, the oxidation of thiopental to its carboxylic acid may be the major driver of thiopental detoxification as this product appears to account for 10-25% of renally excreted drug.
[A35309]
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: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
PMID:35355020
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:35355020
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:35355020
GABAARs containing alpha-4 are predominantly extrasynaptic, contributing to tonic inhibition in dentate granule cells and thalamic relay neurons (By similarity). Extrasynaptic alpha-4-containing GABAARs control levels of excitability and network activity (By similarity). GABAAR containing alpha-4-beta-3-delta subunits can simultaneously bind GABA and histamine where histamine binds at the interface of two neighboring beta subunits, which may be involved in the regulation of sleep and wakefulness PMID:35355020
PMID:14993607 PMID:29961870 PMID:30140029 PMID:31056671
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:30140029
When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient .
PMID:14993607 PMID:30140029
GABAARs containing alpha-5/GABRA5 subunits are mainly extrasynaptic and contribute to the tonic GABAergic inhibition in the hippocampus (By similarity). Extrasynaptic alpha-5-containing GABAARs in CA1 pyramidal neurons play a role in learning and memory processes (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N01AF03
ATC N05CB01
ATC N05CA19
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)
Thiopental
Additional database identifiers
Drugs Product Database (DPD)
8249
ChemSpider
2272258
BindingDB
50058058
Guide to Pharmacology
2579
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:1958
GenAtlas
CHRNA4
GeneCards
CHRNA4
GenBank Gene Database
L35901
GenBank Protein Database
755648
Guide to Pharmacology
465
UniProt Accession
ACHA4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1960
GenAtlas
CHRNA7
GeneCards
CHRNA7
GenBank Gene Database
X70297
GenBank Protein Database
496607
Guide to Pharmacology
468
UniProt Accession
ACHA7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4572
GenAtlas
GRIA2
GeneCards
GRIA2
GenBank Gene Database
L20814
GenBank Protein Database
493134
Guide to Pharmacology
445
UniProt Accession
GRIA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4580
GenAtlas
GRIK2
GeneCards
GRIK2
GenBank Gene Database
U16126
GenBank Protein Database
790532
Guide to Pharmacology
451
UniProt Accession
GRIK2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3553
GenAtlas
FAAH
GeneCards
FAAH
GenBank Gene Database
U82535
GenBank Protein Database
2149156
Guide to Pharmacology
1400
UniProt Accession
FAAH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1952
GenAtlas
CHRM3
GeneCards
CHRM3
GenBank Gene Database
X15266
GenBank Protein Database
32324
Guide to Pharmacology
15
UniProt Accession
ACM3_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:17450
GeneCards
CYP3A43
GenBank Gene Database
AF319634
GenBank Protein Database
12642642
UniProt Accession
CP343_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q55186498), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.