Zuclopenthixol acetate 50mg/1ml solution for injection ampoules
Requires a prescription from a doctor or prescriber
Zuclopenthixol, also known as Zuclopentixol or Zuclopenthixolum, is an antipsychotic agent.
Official documents, adverse reaction reporting, and safety monitoring
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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 Zuclopenthixol acetate
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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.
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Suspected adverse reactions reported for Zuclopenthixol acetate
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.
1 branded products available
Part of the Clopixol brand family (generic: Zuclopenthixol acetate)
MHRA licensed products
View all licensed products for Zuclopenthixol acetate on the MHRA register
Clopixol Acuphase 50mg/1ml solution for injection ampoules
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
30 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 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
Check stock at pharmacies and supply information
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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. 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: 14 · Randomised trials: 3 · 1998–2026
Showing the 50 most relevant studies, sorted by most relevant.
Manuel A. González Hernández, E. Canfora, J. Jocken, et al.
Nutrients, 2019
Michele Cândida Carvalho de Oliveira, A.C.A Cardoso, M. Viana, et al.
Renewable & Sustainable Energy Reviews, 2018
V. Vatanpour, M. Pasaoglu, Hossein Barzegar, et al.
Chemosphere, 2022
Kamyar Khoshnevisan, H. Maleki, H. Samadian, et al.
Carbohydrate polymers, 2018
Shree Bose, Vijyendra Ramesh, J. Locasale
Trends in cell biology, 2019
Śladowska K, Moćko P, Brzostek T, et al.
2025
- Multiple Sclerosis
- Multiple Sclerosis, Relapsing-Remitting
- Immunologic Factors
ObjectiveThis study aimed to review the efficacy and safety profile of disease-modifying therapies (DMTs) in patients with relapsing pediatric-onset multiple sclerosis (POMS).MethodsA systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Published randomized controlled trials (RCTs), nonrandomized studies with a control group, large single-arm studies, and ongoing (unpublished) studies investigating the use of approved and unapproved DMTs in POMS were included. Eligible published studies were identified in MEDLINE (via PubMed), EMBASE, and the Cochrane Library, and unpublished studies were identified in a clinical trials registry (www.Clinicaltrialsgov).ResultsA total of 13 published studies were included in the systematic review: 4 RCTs, 3 observational studies with a control group, and 6 large single-arm studies. The following DMTs for the treatment of POMS were evaluated in the included studies: interferon beta-1a, interferon beta-1b, teriflunomide, dimethyl fumarate, fingolimod, natalizumab, glatiramer acetate, and ocrelizumab. All DMTs were shown to be effective in reducing relapse rates, preventing disability progression, and reducing disease activity in MRI in patients with POMS. DMTs that are considered highly effective in adults with multiple sclerosis (natalizumab, fingolimod) were also shown to be more effective than interferon beta-1a in POMS. A total of 9 ongoing (unpublished) studies were identified, including 5 RCTs. The following drugs were evaluated: ozanimod, fingolimod, peginterferon beta-1a, ocrelizumab, ofatumumab, siponimod, alemtuzumab, and natalizumab.ConclusionThe number of DMTs approved for the treatment of POMS is limited, and some of the available DMTs are used off-label. The available evidence from published studies of varying reliability supports the efficacy of DMTs in POMS. However, well-designed, long-term RCTs in the pediatric population are needed. The results of ongoing studies may fill the existing gap in clinical evidence, possibly leading to the approval of more highly effective DMTs for patients with POMS.
Abstract licence: CC BY-NC-ND
Qian Song, Xiang Zhang, Weixin Liu, et al.
Journal of hepatology, 2023
Liu Y, Cao M, Ren Y, et al.
2025
Abstract Background To systematically assess the impact of disease-modifying therapy (DMT) on the risk of uveitis in patients with multiple sclerosis (MS) and to investigate potential variations among different DMT types, MS types, and clinical characteristics. Methods A systematic search was conducted across PubMed, Embase, Cochrane Library, CNKI, Wanfang, and VIP databases from the self-established database up to September 2025. This search aimed to identify randomized controlled trials, cohort studies, and observational studies that reported the incidence of uveitis following disease-modifying therapy (DMT) in patients with multiple sclerosis (MS). Meta-analysis was performed using Stata 18.0. Bivariate outcomes were expressed as odds ratios (OR) with 95% confidence intervals (CI). Heterogeneity was evaluated using the I² test, applying a random effects model when I² was ≥ 50%. Publication bias was assessed through funnel plots and the Egger test, while sensitivity analysis was conducted using the leave-one-out method to confirm the stability of the results. Results A total of 8 studies (1 RCT, 7 observational studies) involving patients with multiple sclerosis (MS) from various regions were included. The pooled analysis indicated that disease-modifying therapy (DMT) significantly reduced the prevalence of uveitis (SMD = -0.42, 95% CI: -0.83 to -0.01, P = 0.04). In the one-arm rate analysis, the combined prevalence was approximately 1% (95% CI: 0.00–0.01, I² = 88.09%). Subgroup analysis revealed that interferon beta and glatiramer acetate were associated with the highest risk of uveitis (~ 0.32), while fingolimod and rituximab were linked to the lowest risk (~ 0.01), with significant differences observed between groups ( P
Abstract licence: CC BY
Wang X, Zhao M, Liu P, et al.
2025
- Multiple Sclerosis
- Immunosuppressive Agents
- Immunologic Factors
Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system (CNS) and the leading cause of non-traumatic neurological disability in young adults. Although current disease-modifying therapies (DMTs), such as interferon beta (IFNβ) and glatiramer acetate, can reduce inflammation and delay disease progression, many patients continue to experience relapses. Given the complexity and variability of MS, combination therapy targeting multiple disease mechanisms is being explored as a more effective treatment approach. A comprehensive search of Medline and EMBASE databases was conducted using keywords related to MS, immunomodulatory agents, and combination therapy. Additional clinical trials were identified through the National MS Society database. A limited number of studies have investigated the use of IFNβ with or without immunosuppressive agents. Preliminary findings suggest potential benefits of combination therapy, though evidence is constrained by small sample sizes, lack of randomization, and limited follow-up periods. Combination therapies may offer enhanced therapeutic effects in MS management. However, more rigorous and large-scale clinical trials are required to confirm their safety and efficacy.
Abstract licence: CC BY-NC
N. Yadav, Minna Hakkarainen
Chemosphere, 2020
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
37 found
Half-life
20 hours
Mechanism
Zuclopenthixol is a typical antipsychotic neuroleptic drug of the thioxanthene class.
Food interactions
2 warnings
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
20 hours
Protein binding
98-99%
Volume of distribution
20 L/kg
Metabolism
Elimination
10%
Clearance
0.9 L
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1779 interactions
Neuroleptic malignant syndrome may occur. Zuclopenthixol may potentiate anticholinergic effects of concurrent medications. Zuclopenthixol has a demonstrated antiemetic effect in animals, and may mask signs of toxicity due to other drug overdoses, or may mask symptoms of disease.
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N05AF05
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)
Additional database identifiers
Drugs Product Database (DPD)
11264
Drugs Product Database (DPD)
191
Drugs Product Database (DPD)
190
ChemSpider
4470984
BindingDB
79209
ZINC
ZINC000000601293
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3020
GenAtlas
DRD1
GeneCards
DRD1
GenBank Gene Database
X55760
GenBank Protein Database
30397
Guide to Pharmacology
214
UniProt Accession
DRD1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3026
GenAtlas
DRD5
GeneCards
DRD5
GenBank Gene Database
X58454
GenBank Protein Database
32049
Guide to Pharmacology
218
UniProt Accession
DRD5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3023
GenAtlas
DRD2
GeneCards
DRD2
GenBank Gene Database
M30625
GenBank Protein Database
181432
Guide to Pharmacology
215
UniProt Accession
DRD2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:277
GenAtlas
ADRA1A
GeneCards
ADRA1A
GenBank Gene Database
D25235
GenBank Protein Database
433201
Guide to Pharmacology
22
UniProt Accession
ADA1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:281
GenAtlas
ADRA2A
GeneCards
ADRA2A
GenBank Gene Database
M23533
GenBank Protein Database
178196
Guide to Pharmacology
25
UniProt Accession
ADA2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5293
GenAtlas
HTR2A
GeneCards
HTR2A
GenBank Gene Database
S42168
GenBank Protein Database
36431
Guide to Pharmacology
6
UniProt Accession
5HT2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5182
GenAtlas
HRH1
GeneCards
HRH1
GenBank Gene Database
Z34897
GenBank Protein Database
510296
Guide to Pharmacology
262
UniProt Accession
HRH1_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:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_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