Trihexyphenidyl 2mg/5ml oral solution sugar free
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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.
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2 branded products available
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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(3)
Spasticity in under 19s: management (CG145)
Cerebral palsy in under 25s: assessment and management (NG62)
Severe sialorrhoea (drooling) in children and young people with chronic neurological disorders: oral glycopyrronium bromide (ES5)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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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
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0.
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: 9 · Randomised trials: 3 · 1986–2026
Showing the 50 most relevant studies, sorted by most relevant.
Garcia Ron A, Arias Vivas E, Arriola Pereda G, et al.
2026
- Sialorrhea
- Cerebral Palsy
- Spain
IntroductionAnterior sialorrhoea, or "drooling," is the involuntary loss of saliva due to an inability to manage oral secretions. In cerebral palsy (CP), drooling results from oral motor dysfunction, significantly impacting the quality of life of both patients and their caregivers. Despite its physical and psychological repercussions, the clinical approach to sialorrhoea remains poorly defined.ObjectivesThis document aims to provide a guideline for the evaluation and management of sialorrhoea in children with CP, based on the best available evidence and expert consensus. Additionally, it seeks to identify gaps in the literature and propose future research directions.MethodologyA working group was formed, composed of paediatric neurologists from the Spanish Society of Paediatric Neurology (SENEP). A systematic review of the literature was conducted in databases such as MEDLINE, PubMed, and Cochrane, prioritising randomised clinical trials and systematic reviews. Clinical evidence was included when higher-level evidence was unavailable, and recommendations were formulated based on expert consensus.Consensus and discussionThe management of sialorrhoea should be multidisciplinary, including thorough clinical evaluations and assessment scales for severity and impact. Treatment should follow a stepwise approach, starting with non-pharmacological strategies (oromotor therapy, postural correction) and, if necessary, pharmacological interventions with anticholinergics (glycopyrrolate, trihexyphenidyl) or botulinum toxin injection. Surgical options and radiotherapy are reserved for refractory cases.ConclusionSialorrhoea is a clinically relevant issue in children with CP, requiring an individualised approach based on the best available evidence. This consensus provides a useful guideline for clinical practice and highlights the need for further studies to optimise treatment.
Abstract licence: CC BY-NC-ND
Pichon E, Alioth A, Catalano Chiuvé S, et al.
2026
- Dystonic Disorders
- Dystonia
- Intellectual Disability
BackgroundBilateral focal hand dystonia is an almost pathognomonic sign of Partington syndrome, frequently accompanied by intellectual disability and oromotor dyspraxia. However, a few studies have focused on the treatment of this focal dystonia, making patient management uncertain.CasesWe present 2 cases of Partington syndrome featuring Aristaless-related homeobox (ARX) gene mutations, hand dystonia, and other clinical signs. Various drug treatments were attempted, including levodopa (l-dopa), trihexyphenidyl, tetrabenazine, and benzodiazepines, as well as botulinum toxin. Additionally, a blinded dystonia protocol was used to assess l-dopa's efficacy in 1 patient, which confirmed only mild benefit.Literature reviewThrough a systematic review of the literature, we found that only l-dopa and baclofen might result in mild improvement, whereas propranolol, gabapentin, and haloperidol were reported as ineffective. The descriptions in those studies were, however, imprecise and the improvement rather mild, hindering definitive conclusions about their effectiveness.ConclusionsTreatment options in Partington syndrome-associated dystonia remain elusive. Further research and additional case studies are needed to fully characterize the clinical features of Partington syndrome and to identify effective treatments.
Abstract licence: CC BY
Prateek Kumar Panda, Vetoni Moirangthem, Apurva Tomar, et al.
Pediatric Neurology, 2024
- Cerebral Palsy
- Dystonia
- Trihexyphenidyl
Romana Akter Happy, Bithi Debnath, Narayan Chandra Saha, et al.
Journal of Bangladesh College of Physicians and Surgeons, 2026
N. Dayan, E. Touítou
Biomaterials, 2000
J. Brans, R. Lindeboom, PhD Snoek J.W. MD, et al.
Neurology, 1996
Sonu Kumar, Jaya Shankar Kaushik, S. Verma, et al.
Indian Journal of Pediatrics, 2022
Gloire Chubaka Magala, É. Aka-Anghui Diarra, Sac Agbo-Panzo, et al.
Journal Africain des Cas Cliniques et Revues, 2025
Gimeno H, Scott H, Sanchez RM, et al.
2026
AimTo identify the outcomes reported in published studies of intervention approaches used with non-degenerative childhood hyperkinetic movement disorders, including dystonia, dyskinesia, hypertonia, athetosis, chorea, cerebral palsy, involuntary movement, and kernicterus, and map them to the International Classification of Functioning, Disability and Health (ICF) framework.MethodThis was a scoping review that used the Arksey and O'Malley's framework. Medline, CINAHL plus, and EMBASE were searched from 2001 (when the ICF was approved for use by the World Health Assembly) to February 2025. Data were extracted and mapped to the ICF framework.ResultsA total of 294 studies included 159 surgical (e.g. deep brain stimulation, intrathecal baclofen pump), 81 pharmacological (e.g. levodopa, trihexyphenidyl, toxin injections), 51 non-pharmacological and non-surgical studies, and three studies reporting outcomes longitudinally. Neuromodulation, particularly deep brain stimulation, was reported in 122 studies. Over half of the non-pharmacological/non-surgical studies described the management of the underlying impairments. Outcomes were reported as measured objectively 650 times with 209 unique tools. The most evaluated ICF domain was body functions and structures (375 of 635, 59%), followed by activity (165 of 635, 26%), and participation (37 of 635, 5.8%). The least assessed domains were quality of life (28 of 635, 0.04%), goals (25 of 635, 0.04%), and environment (5 of 635, 0.007%).InterpretationThe major focus of assessment of interventions for children with non-degenerative hyperkinetic movement disorders is on body structure and function. The voices of children remain unheard across all studies, with a lack of individualized measurement. Partnering with children to understand what meaningful outcomes mean to them will go a long way to address this gap.
Abstract licence: CC BY
A. Harvey, L. Baker, D. Reddihough, et al.
The Cochrane database of systematic reviews, 2016
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
0.3 hours
Mechanism
Trihexyphenidyl is a non-selective muscarinic acetylcholine receptor antagonist…
Food interactions
1 warning
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
7.2 ng/mL
Half-life
0.3 hours
[A229078]
Protein binding
36.13-41.92%
Metabolism
[A222358]
However, it is likely not heavily metabolized.
[A222358]
Elimination
[A222358]
…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Trihexyphenidyl was granted FDA approval on 13 May 1949.[L31768]
[L31773][L31778]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 552 interactions
Respiratory depression and cardiac arrest may be seen as premortal signs.
Patients experiencing an overdose of trihexyphenidyl may experience dry mouth, anhidrosis, mydriasis, nausea, vomiting, tachycardia, hyperpyrexia, reduced gastrointestinal motility, urinary hesitancy or retention, rash, hyperthermia, confusion, restlessness, agitation, poor coordination, paranoia, psychosis, delirium, hallucinations, coma, respiratory failure, circulatory failure, and death.
[A222358]
Patients should be treated with symptomatic and supportive care which may include airway maintenance and the use of [physostigmine].
[A222358]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A229078][A229088]
[A229078]
[A229068]
[A222358]
However, it is likely not heavily metabolized.
[A222358]
[A222358]
However, it is likely eliminated predominantly in the urine.
[A222358]
Proteins and enzymes this drug interacts with in the body
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC N04AA01
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Trihexyphenidyl
Additional database identifiers
Drugs Product Database (DPD)
9845
ChemSpider
5371
BindingDB
81462
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: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: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
HUGO Gene Nomenclature Committee (HGNC)
HGNC:288
GenAtlas
ADRB3
GeneCards
ADRB3
GenBank Gene Database
M29932
GenBank Protein Database
178896
Guide to Pharmacology
30
UniProt Accession
ADRB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_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