Orphenadrine 50mg tablets
Requires a prescription from a doctor or prescriber
A muscarinic antagonist used to treat drug-induced parkinsonism and to relieve pain from muscle spasm.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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 Orphenadrine
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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
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 Orphenadrine
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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.
13 branded products available
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)
200 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
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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
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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 · Randomised trials: 3 · 1975–2026
Showing the 50 most relevant studies, sorted by most relevant.
Christopoulos N, Akinosoglou K
2026
Background/objectivesPostoperative pain remains a significant clinical challenge, often requiring multimodal strategies to mitigate opioid-related adverse events. The fixed-dose combination (FDC) of Diclofenac, a non-steroidal anti-inflammatory drug, and Orphenadrine, a muscle relaxant, targets distinct nociceptive pathways to potentially enhance analgesia and reduce opioid consumption. This systematic review aims to evaluate the analgesic efficacy and safety profile of the fixed-dose combination of Diclofenac and Orphenadrine for postoperative pain management and quantify its opioid-sparing effect compared to standard monotherapies or placebo.MethodsA systematic search of electronic databases (MEDLINE, Scopus) and clinical trial registries (including ClinicalTrials.gov and CTIS) was conducted up to 20 September 2025. Fourteen (14) randomized controlled trials (RCTs) involving 981 adult patients undergoing various surgical procedures were included. Due to high clinical and methodological heterogeneity, a Synthesis Without Meta-analysis (SWiM) approach was utilized. The certainty of evidence was assessed using the GRADE methodology.ResultsThe synthesis demonstrated that the FDC may improve pain relief (measured by the Visual Analog Scale and Numeric Rating Scale scores) and may reduce opioid consumption compared to active comparators and placebo. The opioid-sparing effect could be correlated with a reduced incidence of dose-dependent adverse events, particularly nausea and vomiting. However, the overall certainty of the evidence was graded as "Very Low" due to the high risk of bias and lack of transparency in the included studies.ConclusionsThe FDC of Diclofenac and Orphenadrine is a rational addition to multimodal postoperative analgesic regimens, which may potentially reduce the perioperative opioid burden without compromising pain control. Nevertheless, because almost all included studies suffer from severe methodological flaws, these apparent efficacy findings must be interpreted with caution. Future high-quality, pre-registered, and low-bias randomized controlled trials are required to draw firm clinical conclusions.
Abstract licence: CC BY 4.0
B. Friedman, D. Cisewski, E. Irizarry, et al.
Annals of Emergency Medicine, 2017
B. Friedman, E. Irizarry, M. Davitt, et al.
Annals of Emergency Medicine, 2017
L. Sorokina, M. A. Vyzhigina, M. Semenkov, et al.
Russian Journal of Anesthesiology and Reanimatology, 2024
H. Gombotz, R. Lochner, R. Sigl, et al.
Wiener Medizinische Wochenschrift, 2010
G. Bersani, A. Grispini, S. Marini, et al.
Clinical neuropharmacology, 1990
S. Hunskaar, D. Donnell
Journal of International Medical Research, 1991
Dilauro G, Luccarelli C, Quivelli AF, et al.
2023
Advancing the development of perfecting the use of polar organometallics in bio-inspired solvents, we report on the effective generation in batch of organosodium compounds, by the oxidative addition of a C-Cl bond to sodium, a halogen/sodium exchange, or by direct sodiation, when using sodium bricks or neopentylsodium in hexane as sodium sources. C(sp3 )-, C(sp2 )-, and C(sp)-hybridized alkyl and (hetero)aryl sodiated species have been chemoselectively trapped (in competition with protonolysis), with a variety of electrophiles when working "on water", or in biodegradable choline chloride/urea or L-proline/glycerol eutectic mixtures, under hydrous conditions and at room temperature. Additional benefits include a very short reaction time (20 s), a wide substrate scope, and good to excellent yields (up to 98 %) of the desired adducts. The practicality of the proposed protocol was demonstrated by setting up a sodium-mediated multigram-scale synthesis of the anticholinergic drug orphenadrine.
Abstract licence: CC BY
Tayyaba Kokab, Afzal Shah, M. Khan, et al.
2021
S. Loga, S. Curry, M. Lader
British journal of clinical pharmacology, 1975
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
13-20 hours
Mechanism
Orphenadrine binds and inhibits both histamine H1 receptors and NMDA receptors.
Food interactions
2 warnings
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
13-20 hours
Protein binding
95%
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1537 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:26875626 PMID:27616483 PMID:28126851 PMID:9489750
Participates in synaptic plasticity for learning and memory formation (By similarity). Channel activation requires binding of the neurotransmitter L-glutamate to the GluN2 subunit, glycine or D-serine binding to the GluN1 subunit, plus membrane depolarization to eliminate channel inhibition by Mg(2+) .
PMID:26875626 PMID:27616483 PMID:28126851 PMID:9489750
NMDARs mediate simultaneously the potasium efflux and the influx of calcium and sodium (By similarity). Each GluN2 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators PMID:26875626 PMID:28095420 PMID:28126851 PMID:9489750
PMID:21376300 PMID:26875626 PMID:26919761 PMID:28126851 PMID:28228639 PMID:36959261 PMID:7679115 PMID:7681588 PMID:7685113
NMDARs participate in synaptic plasticity for learning and memory formation by contributing to the long-term potentiation (LTP) .
PMID:26875626
Channel activation requires binding of the neurotransmitter L-glutamate to the GluN2 subunit, glycine or D-serine binding to the GluN1 subunit, plus membrane depolarization to eliminate channel inhibition by Mg(2+) .
PMID:21376300 PMID:26875626 PMID:26919761 PMID:27164704 PMID:28095420 PMID:28105280 PMID:28126851 PMID:28228639 PMID:36959261 PMID:38538865 PMID:7679115 PMID:7681588 PMID:7685113
NMDARs mediate simultaneously the potasium efflux and the influx of calcium and sodium (By similarity). Each GluN2 or GluN3 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators PMID:26875626 PMID:26919761 PMID:36309015 PMID:38598639
GluN3B subunit also binds D-serine and, in the absence of glycine, activates glycinergic receptor complexes, but with lower efficacy than glycine (By similarity). Each GluN3 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators (By similarity)
Forms excitatory glycinergic receptor complexes with GluN1 alone which are activated by glycine binding to the GluN1 and GluN3 subunits .
PMID:38598639
GluN3A subunit also binds D-serine (By similarity). Each GluN3 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators (By similarity). By competing with GIT1 interaction with ARHGEF7/beta-PIX, may reduce GIT1/ARHGEF7-regulated local activation of RAC1, hence affecting signaling and limiting the maturation and growth of inactive synapses (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)
Enzymes involved in drug metabolism — important for understanding drug interactions
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
Involved compounds
ATC M03BC51
ATC N04AB02
ATC M03BC01
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)
Orphenadrine
Additional database identifiers
Drugs Product Database (DPD)
10058
Drugs Product Database (DPD)
10171
ChemSpider
4440
BindingDB
50062614
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4588
GenAtlas
GRIN2D
GeneCards
GRIN2D
GenBank Gene Database
U77783
GenBank Protein Database
2444026
UniProt Accession
NMDE4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4584
GenAtlas
GRIN1
GeneCards
GRIN1
GenBank Gene Database
D13515
GenBank Protein Database
219920
Guide to Pharmacology
455
UniProt Accession
NMDZ1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:16768
GenAtlas
GRIN3B
GeneCards
GRIN3B
GenBank Gene Database
AC004528
GenBank Protein Database
3025446
UniProt Accession
NMD3B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:16767
GenAtlas
GRIN3A
GeneCards
GRIN3A
GenBank Gene Database
AJ416950
GenBank Protein Database
20372905
UniProt Accession
NMD3A_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: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:10582
GenAtlas
SCN10A
GeneCards
SCN10A
GenBank Gene Database
AF117907
GenBank Protein Database
4838145
Guide to Pharmacology
585
UniProt Accession
SCNAA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_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:2631
GeneCards
CYP2E1
GenBank Gene Database
J02625
GenBank Protein Database
181360
Guide to Pharmacology
1330
UniProt Accession
CP2E1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_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
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 the following publications:
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Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q3292273), 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.