Cisatracurium besilate 20mg/10ml solution for injection ampoules
Requires a prescription from a doctor or prescriber
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Cisatracurium besilate 20mg/10ml solution for injection ampoules
Cisatracurium besilate 20mg/10ml solution for injection ampoules
Cisatracurium besilate 20mg/10ml solution for injection ampoules
Cisatracurium besilate 20mg/10ml solution for injection ampoules
Cisatracurium besilate 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.
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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.
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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: 4 · Randomised trials: 19 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
Mengya Cao, Hui-qiong Huang, Jianbin Tong, et al.
BMC Anesthesiology, 2023
Behzad Nazemroaya, Sahand Taei
Archives of Anesthesia and Critical Care, 2024
Dong R, Song C, Li J, et al.
2025
ObjectiveDesflurane is the most commonly suitable volatile anesthetic for elderly patients due to its low blood solubility, suggesting faster induction and awakening time. This study compared the safety and efficacy of desflurane versus sevoflurane in terms of postoperative cognitive function and early recovery quality in elderly orthopedic patients.MethodsEighty elderly patients undergoing orthopedic surgery were included in this prospective, randomized controlled trial. After preoxygenation with a 5 L/min fresh oxygen flow via a facial mask for 5 min, anesthesia was induced using 0.2 μg/kg sufentanil, 1-2 mg/kg etomidate, and 0.2 mg/kg cisatracurium. General anesthesia was maintained through continuous infusion of remifentanil (0.05-0.20 μg/kg/min) and a sevoflurane expiratory concentration of 1-2% or desflurane 2-5%, in combination with air containing 40% oxygen to maintain bispectral index (BIS) values 40-60. Data collected included hemodynamic parameters, time to eye-opening, extubation, following commands, orientation, post-anesthesia care unit (PACU) length of stay, opioid consumption, patient and surgeon satisfaction scores, number of patients willing to repeat surgery with the same anesthesia regimen, and adverse events. Additionally, white blood cell counts, percentages of neutrophils and lymphocytes, and troponin I levels were recorded at baseline and 24 h post-surgery.ResultsThe Mini-Mental State Examination (MMSE) scores were lower at 1 h post-surgery in the desflurane group (D group) than in the sevoflurane group (S group), although the difference was not clinically significant (p > 0.05). Over 70% of patients in both groups returned to baseline MMSE levels 24 h postoperatively. There were no significant differences in MMSE scores at baseline, 6, 24, or 48 h post-surgery between the groups (p > 0.05). Patients in the D group recovered significantly faster, indicated by shorter times to eye-opening, extubation, following commands, and reduced PACU length of stay (p p p p > 0.05).ConclusionDesflurane was not associated with reduced MMSE scores or postoperative respiratory complications. However, it demonstrated faster recovery times and higher patient satisfaction scores than sevoflurane.Clinical trial registrationChiCTR2400093852.
Abstract licence: CC BY
Swati Taneja, Amardeep Kaur, Shalvi Mahajan, et al.
Archives of Anesthesia and Critical Care, 2023
F. Rokhtabnak, Saeed Safari, Soudabeh Djalali Motlagh, et al.
Iranian Journal of Medical Sciences, 2023
Suresh S, Hrishi AP, Thiruvathra J, et al.
2025
Rui An, Chunnan Lin, Ze-Guang Lu, et al.
BMC Anesthesiology, 2025
- Ketamine
- Propofol
- Atracurium
Gegal Pruthi, K. Bharathi, P. Simha, et al.
The Indian Anaesthetists Forum, 2025
Karimi M, Ghaheri A, Saleh K, et al.
2024
- Atracurium
- Electrocardiography
- Anesthesia, General
Neto AJMM, Benette GL, Siqueira LC, et al.
2026
- Neostigmine
- Atracurium
- Cholinesterase Inhibitors
BackgroundNeostigmine is widely used to reverse nondepolarizing neuromuscular blockade in children, but the optimal dose under total intravenous anesthesia is uncertain.AimsThe primary aim was to compare the time to full neuromuscular recovery (TOF ratio of 1.0) following administration of neostigmine at doses of 0, 10, 20, and 30 μg/kg in children at a TOF count of 3. Secondary objectives were full reversal within 10 min and adverse events.MethodsThis prospective, randomized, double-blind, parallel-group, superiority trial enrolled 120 children (2-10 years; ASA I-II) undergoing tonsillectomy. Participants received 0, 10, 20, or 30 μg/kg neostigmine at a TOF count of 3 measured by quantitative acceleromyography. The primary outcome was the time from TOF count of 3 to full reversal (TOF ratio = 1.0). Secondary outcomes were the proportion of patients achieving full reversal within 10 min and adverse events. Comparisons among active groups used the Kruskal-Wallis test.ResultsA total of 118 patients were analyzed. Median [IQR] time to full reversal was 20.2 [14.8-24.1], 14.0 [10.7-16.8], 11.0 [8.2-15.5], and 11.2 [7.9-14.6] min in the 0, 10, 20, and 30 μg/kg groups, respectively. Reversal was significantly slower in the control group compared with all neostigmine doses. However, there was no statistically significant difference among the active doses (Kruskal-Wallis, p = 0.33). At 10 min, full reversal had occurred in 10.7%, 23.3%, 43.3%, and 33.3% of patients in the respective groups. Adverse events were uncommon, occurring in 10 of 118 patients, and consisted exclusively of transient bradycardia and tachycardia, without differences among groups.ConclusionsAt TOF count of 3, neostigmine 10-30 μg/kg shortened reversal compared with no reversal, but doses above 10 μg/kg conferred no additional benefit. Quantitative monitoring remains essential, as fewer than half of patients achieved a TOF ratio of 1.0 within 10 min.Trial registryhttps://ensaiosclinicos.gov.br/rg/RBR-4xrx2g3.
Abstract licence: CC BY
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
22 minutes
Mechanism
Like other non-depolarising neuromuscular blocking agents, cisatracurium binds c…
Food interactions
None known
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
6%
[A253602][L43577]
…
Half-life
22 minutes
[L43577]
Protein binding
[L43577]
Volume of distribution
145 mL
[L43577]
…
Metabolism
Elimination
80%
Clearance
4.57 mL/min/kg
[L43577]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L43577]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1379 interactions
If complete neuromuscular blockade is evident or suspected, cholinesterase inhibitors should not be administered. The reversal of paralysis may not be sufficient to maintain a patent airway and an appropriate level of spontaneous ventilation.
[L43577]
The long-term carcinogenicity of cisatracurium has not been evaluated. In an in vitro mouse lymphoma forward gene mutation assay, cisatracurium besylate led to mutations in the presence and absence of exogenous metabolic activation.
Other assays did not show evidence of mutagenicity or clastogenicity.
[L43577]
The use of cisatracurium may lead to residual paralysis, as well as a higher risk of seizure. Medication errors increase the risk of death, and the use of certain drugs may potentiate the neuromuscular blocking action of cisatracurium.[L43577]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A253602][L43577]
Cisatracurium is metabolized into laudanosine and monoquaternary alcohol metabolite (MQA). Following the IV infusion of cisatracurium, the Cmax of laudanosine and MQA were 6% and 11% of the parent compound, respectively.
[L43577]
Compared to young patients, the volume of distribution of cisatracurium is slightly larger in elderly patients, which also leads to longer half-life values. The plasma clearance of cisatracurium was not affected by age.
Patients with hepatic impairment have a slightly higher volume of distribution and plasma clearance values; however, these minor pharmacokinetic differences are not considered clinically significant. Additionally, the pharmacokinetic parameters of cisatracurium in patients with end-stage renal disease were similar to those detected in healthy adult patients.
[L43577]
[L43577]
[L43577]
[L43577]
The volume of distribution of cisatracurium besylate is small due to its relatively large molecular weight and high polarity.
[A253602]
The MQA can also undergo Hofmann elimination, but the rate of this process is slower than the one detected for cisatracurium. Laudanosine is further metabolized to desmethyl metabolites that are conjugated with glucuronic acid and excreted in the urine. Laudanosine may cause transient hypotension and, in higher doses, cerebral excitatory effects when administered to several animal species; however, the effects of laudanosine in humans have not been established.
[L43577]
[L43577]
In healthy male patients (n=6) given 14C-cisatracurium, 4% of the recovered dose was found in feces, and 95% was found in urine, mostly as conjugated metabolites. Less than 10% of the cisatracurium dose was excreted as the unchanged patent drug.
In another group of patients with Foley catheters for surgical management given non-radiolabeled cisatracurium (n=12), 15% of the cisatracurium dose was excreted unchanged in urine.
[L43577]
[L43577]
Proteins and enzymes this drug interacts with in the body
PMID:20881005 PMID:31488329 PMID:8663494 PMID:8906617 PMID:9203638
CHRNB4 forms heteropentameric neuronal acetylcholine receptors with CHRNA2, CHRNA3 and CHRNA4, as well as CHRNA5 and CHRNB3 as accesory subunits .
PMID:11118490 PMID:20881005 PMID:8663494
CHRNA3:CHRNB4 being predominant in neurons of the autonomic ganglia, it is known as ganglionic nicotinic receptor .
PMID:31488329
CHRNA3:CHRNB4 or CHRNA3:CHRNA5:CHRNB4 play also an important role in the habenulo-interpeduncular tract, modulating the mesolimbic dopamine system and affecting reward circuits and addiction (By similarity). Hypothalamic CHRNA3:CHRNB4 nAChR activation by nicotine leads to activation of POMC neurons and a decrease in food intake (By similarity)
PMID:18723036
CHRNA2 forms heteropentameric neuronal acetylcholine receptors with CHRNB2 and CHRNB4 and plays a role in nicotine dependence PMID:24467848 PMID:27493220
ATC M03AC11
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)
Cisatracurium
Additional database identifiers
Drugs Product Database (DPD)
11084
ChemSpider
56615
ZINC
ZINC000238809664
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13800
GenAtlas
CHRNA10
GeneCards
CHRNA10
GenBank Gene Database
AJ278118
GenBank Protein Database
12053839
Guide to Pharmacology
470
UniProt Accession
ACH10_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1956
GenAtlas
CHRNA2
GeneCards
CHRNA2
GenBank Gene Database
U62431
GenBank Protein Database
1458110
Guide to Pharmacology
463
UniProt Accession
ACHA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1957
GeneCards
CHRNA3
GenBank Gene Database
M86383
GenBank Protein Database
177898
Guide to Pharmacology
464
UniProt Accession
ACHA3_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:1959
GeneCards
CHRNA5
GenBank Gene Database
M83712
GenBank Protein Database
177926
UniProt Accession
ACHA5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15963
GeneCards
CHRNA6
GenBank Gene Database
U62435
GenBank Protein Database
1458118
Guide to Pharmacology
467
UniProt Accession
ACHA6_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:14079
GenAtlas
CHRNA9
GeneCards
CHRNA9
GenBank Gene Database
AJ243342
GenBank Protein Database
6688136
Guide to Pharmacology
469
UniProt Accession
ACHA9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1962
GenAtlas
CHRNB2
GeneCards
CHRNB2
GenBank Gene Database
X53179
GenBank Protein Database
32017
UniProt Accession
ACHB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1963
GeneCards
CHRNB3
GenBank Gene Database
U62438
GenBank Protein Database
1458124
UniProt Accession
ACHB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1964
GeneCards
CHRNB4
GenBank Gene Database
U62439
GenBank Protein Database
1458126
UniProt Accession
ACHB4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1956
GenAtlas
CHRNA2
GeneCards
CHRNA2
GenBank Gene Database
U62431
GenBank Protein Database
1458110
Guide to Pharmacology
463
UniProt Accession
ACHA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1955
GeneCards
CHRNA1
Guide to Pharmacology
462
UniProt Accession
ACHA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1951
GenAtlas
CHRM2
GeneCards
CHRM2
GenBank Gene Database
M16404
GenBank Protein Database
177990
Guide to Pharmacology
14
UniProt Accession
ACM2_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