Benzatropine 2mg tablets
Requires a prescription from a doctor or prescriber
Benztropine, with the chemical formula 3alpha-diphenylmethoxytropane, is a tropane-based dopamine inhibitor used for the symptomatic treatment of Parkinson's disease.
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Suspected adverse reactions reported for Benzatropine
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2 branded products available
WHO defined daily dose (DDD)
2 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.
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Codes for healthcare professionals and prescribing systems
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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: 3 · Trials: 3 · 1977–2026
Showing the 50 most relevant studies, sorted by most relevant.
Firda Ridhayani, Ika Puspita Sari, T. Andayani
Indonesian Journal of Pharmacology and Therapy, 2024
Drug-drug interactions among children are a getting along concern in health care settings, specifically intensive care units, as sources of adverse drug events that may affect patient condition. Children admitted to pediatric intensive care unit are more prone to drug-drug interactions owing to the diseases and medications complexity. This condition could put the patient at high risk of harm, particularly with his critical condition, so need intense considerations from clinical practitioners to prevent adverse drug events caused by potential drug-drug interactions. This article’s review attempts to explore the important drug-drug interactions among children, including explaining the drug combination, mechanism, and related adverse drug events to help health practitioners recognize it earlier before prescribing the medication. This article’s review explored previous research results from PubMed and Google Scholar as literature resources and PRISMA flow chart as protocol for article selection process. A total of 9 articles discussed comprehensively about the type of drug combinations, mechanism of drug-drug interactions, and associated adverse drug events with significant drug-drug interactions that commonly occurred in children’s patient during the treatment. The drug-drug interaction including midazolam-phenobarbital, cannabidiol-clobazam, Paxlovid-tacrolimus, inhaled fluticasone propionate-lopinavir/ritonavir, rifampicin-warfarin, clofazimine-moxifloxacin, benzatropine-haloperidol, and enalapril-spironolactone. In conclusion, gaining a better understanding of drug-drug interactions among children will empower healthcare professionals to develop useful strategies to recognize, manage, and prevent various types of pharmacokinetic and pharmacodynamic interactions. Especially at different stages in terms of age, physiology, and complexity of the disease in children.
Abstract licence: CC BY-NC
Janet A. Camp‐Bruno, Bertrand G. Winsberg, A. Green-Parsons, et al.
Developmental Medicine & Child Neurology, 1989
- Benztropine
- Cerebral Palsy
- Clinical Trials as Topic
Ruiz de Villa A, Haider AA, Frimer L, et al.
2022
Bhattacharyya KB, Roy A, Biswas A, et al.
2016
Myoclonic dystonia refers to a clinical syndrome characterized by rapid jerky movements along with dystonic posturing of the limbs. Clinically, it is characterized by sudden, brief, electric shock-like movements, mostly involving the upper extremities, shoulders, neck and trunk. Characteristically, the movements wane with consumption of small dose of alcohol in about 50% of cases. Additionally, dystonic contractions are observed in most of the patients in the affected body parts and some patients may exhibit cervical dystonia or graphospasm as well. It may manifest as an autosomal dominant condition or sometimes, as a sporadic entity, though there are doubts whether these represent cases with reduced penetrance. The condition is usually treated with a combination of an anticholinergic agent like, benztropine, pimozide and tetrabenazine. We report one sporadic case and one familial case where the father and the son are affected. The cases were collected from the Movement Disorders Clinic of Bangur Institute of Neurosciences, Kolkata, West Bengal in a period of ten months. Myoclonic dystonia is a rare condition and to the best of our knowledge, this series is the first one reported from our country. Videos of the patients are also provided with the article.
Abstract licence: CC BY-NC-SA
Abdelmissih S, Ahmed Rashed L, Sharif Ismail Negm M, et al.
2025
BackgroundThe presumed implication of thromboembolic and oxidative stress pathways in parkinsonism guided the current research toward the exploration of the anticoagulant dabigatran etexilate (DE) as a thrombin inhibitor in the cobalt chloride (CoCl2)-induced parkinsonism (CIP) model, a model of significance to industrial toxins-related health issues.MethodsOral CoCl2 (12.5 mg/kg) was administered daily for 60 days, with the introduction of benztropine mesylate (BM) (10 mg/kg) and/or DE (3 mg/kg) on day 31. Rearing, postural instability, and pasta handling were evaluated, followed by histopathologic examination of the substantia nigra (SN) and striatum (STR). The expressions of brain dopamine receptor 2 (D2 ), adenosine receptor 1 (A1) and 2A (A2A), and protease-activated receptor 1 (PAR1), as well as the brain levels of dopamine (DA), endothelin 1 (ET1), malondialdehyde (MDA), and glutathione (GSH), were assessed.ResultsBM+DE restored the number of rears to the control level, compared to being reduced in the CIP model. BM+DE restored the first, second, third, and average displacement distances to the control level, compared to being reduced in the CIP model. BM+DE was superior to either BM or DE in restoring the time to finish eating pasta and the number of adjustments of forepaws while eating to control levels after being affected in the CIP model. BM+DE restored DA to the control level and was superior to DE in restoring D2 to the control level. BM+DE was superior to BM in restoring A1 and A2A , increasing A1/A2A beyond the control level. BM+DE was superior to BM in restoring PAR1 and ET1 to control levels. BM+DE was superior to BM in restoring MDA to the control level and was superior to both BM and DE in increasing GSH beyond the control level. BM+DE exhibited the highest percentage of preserved neurons in SN, which was negatively correlated with MDA.ConclusionBM+DE offers a therapeutic potential for parkinsonism triggered by chronic exposure to CoCl2. The implication of thrombin-related factors and oxidative stress in the modulation of the dopaminergic-adenosinergic crosstalk is plausible.
Abstract licence: CC BY
Reactions Weekly, 2025
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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
36 hours
Mechanism
Benztropine is an agent with anti-muscarinic and antihistaminic effects.
Food interactions
2 warnings
Human targets
5 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.5 mg
Half-life
36 hours
Protein binding
95%
Volume of distribution
12-30 L/kg
[A175126]
Metabolism
[A175087]…
Elimination
[A1628]
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
The extrapyramidal symptoms are defined as drug-induced disorders that include symptoms of dystonia, akathisia, parkinsonism, bradykinesia, tremors, and dyskinesia.
[A175120]
Parkinsonism is a general term that refers to the group of neurological disorders that produce symptoms similar to Parkinson's disease such as tremors, slow movement, and stiffness. The parkinsonism includes a large number of disorders and some of them have not been clearly defined.
[L5509]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1603 interactions
It is widely known that benztropine is a potent inhibitor of presynaptic carrier-mediated dopamine transport. As well, it is known to be an analog of atropine and hence, it has a large affinity for muscarinic receptors M1 in the human brain. Once bound, benztropine blocks the activity of the muscarinic receptors mainly in the striatum.[A1628]
The increased advantage of benztropine lays on the antagonism of acetylcholine activity which corrects the imbalance between dopamine and acetylcholine in Parkinson patients.F3679
Clinically the activity of benztropine is observed after 1-2 hours of oral administration and after a few minutes of intramuscular administration with a last-longing effect of about 24 hours. Reports have indicated that benztropine has a very large sedative effect.[A1628]
The antihistaminic effect of benztropine is very similar to the effect found in [pyrilamine] and the anticholinergic activity was found to be equal to [atropine] ex vivo and of about 50% activity in vivo.F3679
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A175087]
It has an approximate oral bioavailability of 29%.T445
[A175126]
[A175087]
The extensive metabolism of benztropine produces eight phase-I metabolites plus four glucuronide conjugates.
[A1628]
[A1628]
Proteins and enzymes this drug interacts with in the body
PMID:10375632 PMID:11093780 PMID:1406597 PMID:15505207 PMID:19478460 PMID:39112701 PMID:39112703 PMID:39112705 PMID:8302271
Also mediates sodium- and chloride-dependent transport of norepinephrine (also known as noradrenaline) (By similarity). Regulator of light-dependent retinal hyaloid vessel regression, downstream of OPN5 signaling (By similarity)
PMID:33828102 PMID:8280179
Through the H1 receptor, histamine mediates the contraction of smooth muscles and increases capillary permeability due to contraction of terminal venules. Also mediates neurotransmission in the central nervous system and thereby regulates circadian rhythms, emotional and locomotor activities as well as cognitive functions (By similarity)
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Essential for serotonin homeostasis in the central nervous system. In the developing somatosensory cortex, acts in glutamatergic neurons to control serotonin uptake and its trophic functions accounting for proper spatial organization of cortical neurons and elaboration of sensory circuits.
In the mature cortex, acts primarily in brainstem raphe neurons to mediate serotonin uptake from the synaptic cleft back into the pre-synaptic terminal thus terminating serotonin signaling at the synapse (By similarity). Modulates mucosal serotonin levels in the gastrointestinal tract through uptake and clearance of serotonin in enterocytes. Required for enteric neurogenesis and gastrointestinal reflexes (By similarity).
Regulates blood serotonin levels by ensuring rapid high affinity uptake of serotonin from plasma to platelets, where it is further stored in dense granules via vesicular monoamine transporters and then released upon stimulation .
PMID:17506858 PMID:18317590
Mechanistically, the transport cycle starts with an outward-open conformation having Na1(+) and Cl(-) sites occupied. The binding of a second extracellular Na2(+) ion and serotonin substrate leads to structural changes to outward-occluded to inward-occluded to inward-open, where the Na2(+) ion and serotonin are released into the cytosol. Binding of intracellular K(+) ion induces conformational transitions to inward-occluded to outward-open and completes the cycle by releasing K(+) possibly together with a proton bound to Asp-98 into the extracellular compartment.
Na1(+) and Cl(-) ions remain bound throughout the transport cycle .
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Additionally, displays serotonin-induced channel-like conductance for monovalent cations, mainly Na(+) ions. The channel activity is uncoupled from the transport cycle and may contribute to the membrane resting potential or excitability (By similarity)
PMID:2008212 PMID:8125921 PMID:38750358
Is responsible for norepinephrine re-uptake and clearance from the synaptic cleft, thus playing a crucial role in norepinephrine inactivation and homeostasis (By similarity). Can also mediate sodium- and chloride-dependent transport of dopamine PMID:11093780 PMID:8125921 PMID:39395208 PMID:39048818
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 N04AC01
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)
Benzatropine
Additional database identifiers
Drugs Product Database (DPD)
5922
ChemSpider
16736541
BindingDB
50366775
PDB
CXQ
ZINC
ZINC000100036536
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:11049
GenAtlas
SLC6A3
GeneCards
SLC6A3
GenBank Gene Database
M96670
GenBank Protein Database
553260
Guide to Pharmacology
927
UniProt Accession
SC6A3_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:11050
GenAtlas
SLC6A4
GeneCards
SLC6A4
GenBank Gene Database
X70697
GenBank Protein Database
36433
Guide to Pharmacology
928
UniProt Accession
SC6A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11048
GenAtlas
SLC6A2
GeneCards
SLC6A2
GenBank Gene Database
M65105
GenBank Protein Database
189258
Guide to Pharmacology
926
UniProt Accession
SC6A2_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
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q415026), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.