Procyclidine 10mg/2ml solution for injection ampoules
Requires a prescription from a doctor or prescriber
A muscarinic antagonist that crosses the blood-brain barrier and is used in the treatment of drug-induced extrapyramidal disorders and in parkinsonism.
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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 Procyclidine
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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 Procyclidine
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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.
4 branded products available
MHRA licensed products
View all licensed products for Procyclidine on the MHRA register
Procyclidine 10mg/2ml solution for injection ampoules
Procyclidine 10mg/2ml solution for injection ampoules
Procyclidine 10mg/2ml 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)
25 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
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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. 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: 1 · Trials: 1 · 1965–2025
Showing the 50 most relevant studies, sorted by most relevant.
Hayder Ameer Jabor
Systematic Reviews in Pharmacy, 2021
Jihye Nam, Min‐Soo Kim, Young‐Jo Song, et al.
Archives of Toxicology, 2023
- Nerve Agents
- Soman
- Acetylcholinesterase
Elnoor M, Bokhari SA, Singh M, et al.
2024
Antipsychotic medications, while crucial in managing severe psychiatric disorders such as schizophrenia and bipolar disorder, are frequently associated with extrapyramidal symptoms (EPS) and tardive dyskinesia (TD). TD, characterized by repetitive, involuntary movements, especially of the face and limbs, poses a substantial clinical challenge due to its often irreversible nature. Conventional management strategies, including dose reduction and switching to atypical antipsychotics, frequently offer limited success, prompting exploration of alternative therapies. This case report highlights the effectiveness of vitamin E, a potent antioxidant, in treating a 28-year-old male with severe antipsychotic-induced EPS and TD, unresponsive to traditional therapies. The patient, who had been receiving paliperidone injections as part of his psychotic disorder treatment regimen, developed marked EPS, including muscle rigidity, a parkinsonian gait, significant motor disturbances as well as tardive dyskinesia. Despite discontinuation of paliperidone and initiation of procyclidine, propranolol, clonazepam, and omega-3 supplements, his symptoms persisted. Introduction of oral vitamin E at 400 IU daily led to a dramatic improvement, with an 80% reduction in EPS and TD symptoms within weeks. The patient's Abnormal Involuntary Movement Scale (AIMS) score decreased from 24 to 4, and his overall quality of life improved significantly. Gradual increase of vitamin E dosage to 1200 IU daily, coupled with tapering of other medications, eventually led to complete resolution of symptoms, as evidenced by an AIMS score of 0. The patient maintained symptom-free status during follow-up, with no recurrence of psychotic symptoms. This case underscores the potential role of vitamin E as a viable adjunctive treatment for TD, particularly in patients who do not respond adequately to conventional therapies. While the literature presents mixed evidence regarding vitamin E's effectiveness, this case adds to the growing body of research suggesting its benefits, especially when introduced early in the disease course. Further large-scale studies are warranted to establish the most effective treatment protocols and identify patient populations most likely to benefit from vitamin E therapy.
Abstract licence: CC BY
Meaad Nasser Hussein, Ali Noory Fajer
Asian Pacific Journal of Cancer Prevention, 2024
- Antioxidants
- Alanine Transaminase
- Aspartate Aminotransferases
Minsun Moon, Jihyun Won, Yun‐Woo Lee, et al.
Basic & Clinical Pharmacology & Toxicology, 2025
- Rivastigmine
- Cholinesterase Inhibitors
- Acetylcholinesterase
Shaimaa Aboelenien, Vinu Cherian, Joel Philip
BJPsych Open, 2024
Aims A recent Cochrane review published in December 2023 concluded that “no trials found that interventions to reduce anticholinergic burden led to any other improvements in cognition compared to usual care”. We describe the case of a 62-year-old lady who developed significant cognitive decline following the initiation of a low dose of procyclidine, which was rapidly reversed upon stopping the medication. Methods We present the case of a 62-year-old lady with a diagnosis of schizo-affective disorder, whose symptoms had been stabilized on a regime of lithium carbonate 500mg nocte, sulpiride 400mg BD and fluoxetine 20mg OD. When the patient presented to the outpatient clinic, she was noted to have bilateral coarse tremors and slight cogwheel rigidity. Procyclidine was started at a dose of 5mg OD to manage these extrapyramidal side-effects. Following this, family members reported that the patient had difficulty initiating and following conversations. Short-term memory was affected and she was observed to have reduced attention span. These problems were reportedly getting worse with time, with a simultaneous decline in functional abilities. She was no longer able to carry out her daily shop, and family members ensured that she was no longer driving as they had concerns about her road safety. She stopped taking procyclidine after 1 month and notably, these problems ceased within one week of stopping the medication. Cognitive testing confirmed that the patient was cognitively intact after procyclidine was stopped. The patient scored 96 on the ‘Addenbrooke's Cognitive Examination’ scale, which falls within the normal range. The ‘Instrumental Activities of Daily Living’ scale was administered to assess functioning at the time of the cognitive impairment. This returned a score of 1/8, indicating that there was significant functional impairment secondary to cognitive impairment when prescribed procyclidine. The ‘Informant Questionnaire on Cognitive Decline in the Elderly’ was administered to objectively quantify the extent of cognitive decline as noted by family. This returned a score of 4.3, confirming that the patient's cognition had indeed been worse when compared with her baseline. Results Our case report highlights the rapid improvement in cognition with the removal of anticholinergic burden in a 62-year-old female. Our report can, therefore, be a harbinger for more robust trials to determine the efficacy of interventions to reduce anticholinergic burden in preserving or improving cognition. Conclusion It is important to monitor for any change in cognition when prescribing anticholinergic medication in at-risk individuals.
Abstract licence: CC BY 4.0
Shalina Mitchell, Prabin Gautam
BJPsych Open, 2025
Aims: Following a Serious Untoward Incident investigation into a patient death where blood tests revealed procyclidine overdose, significant concerns emerged regarding procyclidine prescribing practices. A notable discrepancy was identified between the Summary of Product Characteristics and British National Formulary regarding maximum daily procyclidine dosing, with evidence of 40 mg daily doses being administered. This raised questions about prescribing practices, particularly in patients receiving long-acting injectable antipsychotics. The incident highlighted the need to evaluate current prescribing patterns, assess protocol adherence, monitor effectiveness through GASS scores, and ensure appropriate documentation of procyclidine therapy.
Abstract licence: CC BY 4.0
Prabin Gautam, Titilola Osoba, Shalina Mitchell
BJPsych Open, 2025
Aims: Our aim was to review if procyclidine is being prescribed as per BNF guidelines at DGS CMHT. As per BNF guidelines, procyclidine is recommended to be initiated at 2.5 mg of procyclidine three times per day increasing by 2.5 mg daily until symptoms are relieved. The effective maintenance dose is usually 10–30 mg procyclidine per day. After a period of 3–4 months of therapy, procyclidine should be withdrawn and the patient should be observed to see whether the neuroleptic-induced extrapyramidal symptoms recur.
Abstract licence: CC BY 4.0
Murphy D, Maher S, Kennedy G, et al.
2025
- Akathisia, Drug-Induced
- Palliative Care
Minhal Fatemah, A. Ghaffar, Muhammad Affan Baig
Journal of Clinical and Basic Psychosomatics, 2025
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
None known
Half-life
Not available
Mechanism
The mechanism of action is unknown.
Food interactions
1 warning
Human targets
5 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Protein binding
100%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 552 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
ATC N04AA04
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)
Procyclidine
Additional database identifiers
Drugs Product Database (DPD)
6030
ChemSpider
4750
BindingDB
50062598
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:1950
GenAtlas
CHRM1
GeneCards
CHRM1
GenBank Gene Database
X52068
GenBank Protein Database
34451
Guide to Pharmacology
13
UniProt Accession
ACM1_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
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1953
GenAtlas
CHRM4
GeneCards
CHRM4
GenBank Gene Database
M16405
GenBank Protein Database
61970253
Guide to Pharmacology
16
UniProt Accession
ACM4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1954
GenAtlas
CHRM5
GeneCards
CHRM5
GenBank Gene Database
M80333
GenBank Protein Database
177988
Guide to Pharmacology
17
UniProt Accession
ACM5_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q268997), 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.