Dextromethorphan 7.5mg/5ml / Menthol 2.5mg/5ml oral solution
Available from a pharmacy with pharmacist advice
Morphinan antitussive and dissociative drug
Genetic variations that may affect drug response
2 known genetic variations may influence how your body responds to Dextromethorphan 7.5mg/5ml / Menthol 2.5mg/5ml oral solution.Gene involved: CYP2D6
These are known genetic variations. They don't mean the medicine won't work for you — speak to your doctor or a pharmacogenomics specialist for personalised advice. Source: DrugBank (CC BY-NC 4.0).
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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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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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
MHRA licensed products
View all licensed products for Dextromethorphan + Menthol on the MHRA register
Covonia Original Bronchial Balsam oral solution
WHO defined daily dose (DDD)
40 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
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
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: 28 · Randomised trials: 3 · 1994–2025
Showing the 50 most relevant studies, sorted by most relevant.
Andrea C. Villanti, Lauren K. Collins, R. Niaura, et al.
BMC Public Health, 2017
Li-Ling Huang, H. Baker, Clare Meernik, et al.
Tobacco control, 2016
Clare Meernik, H. Baker, S. Kowitt, et al.
BMJ Open, 2019
Sarah D. Mills, Snigdha R Peddireddy, Rachel Kurtzman, et al.
Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco, 2024
Dania Akbar, T. Rhee, Felicia Ceban, et al.
CNS Drugs, 2023
S. Kowitt, Clare Meernik, H. Baker, et al.
International Journal of Environmental Research and Public Health, 2017
H. Tabuteau, A. Jones, Ashley Anderson, et al.
The American journal of psychiatry, 2022
Amna Majeed, Jiaqi Xiong, K. Teopiz, et al.
Expert Opinion on Emerging Drugs, 2021
Owen Jeffries, M. Waldron
Journal of science and medicine in sport, 2019
D. Iosifescu, A. Jones, C. O'gorman, et al.
The Journal of clinical psychiatry, 2022
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
58 found
Half-life
3-30 hours
Mechanism
Dextromethorphan is a low-affinity uncompetitive NMDA antagonist and sigma-1 receptor agonist.
Food interactions
1 warning
Human targets
16 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
30mg
[A34933]
Half-life
3-30 hours
[A215382]
Protein binding
60-70%
[L14363]
Volume of distribution
5-6.7L/kg
[A215382]
Metabolism
[A415]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Dextromethorphan was granted FDA approval before 3 December 1957.[A215412][L14997]
[L14366]
Dextromethorphan is also used in combination with [guaifenesin] as an over-the-counter product to relieve a cough.
[L14369]
Dextromethorphan in combination with [quinidine] is indicated in the treatment of pseudobulbar affect.
[L14363]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1420 interactions
[L14363]
Overdose should be managed through symptomatic and supportive measures.
[L14363]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A34933]
[A215382]
[L14363]
[A215382]
[A415]
Dextrorphan is N-demethylated by CYP3A4 and CYP2D6, while 3-methoxymorphinan is O-demethylated by CYP2D6.
[A415]
Both are metabolized to form 3-hydroxymorphinan.
[A415]
Dextrorphan and 3-hydroxymorphinan are both O-glucuronidated or O-sulfated.
[A415]
Proteins and enzymes this drug interacts with in the body
Plays a role in calcium signaling through modulation together with ANK2 of the ITP3R-dependent calcium efflux at the endoplasmic reticulum. Plays a role in several other cell functions including proliferation, survival and death. Originally identified for its ability to bind various psychoactive drugs it is involved in learning processes, memory and mood alteration .
PMID:16472803 PMID:9341151
Necessary for proper mitochondrial axonal transport in motor neurons, in particular the retrograde movement of mitochondria.
Plays a role in protecting cells against oxidative stress-induced cell death via its interaction with RNF112 (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:27702664 PMID:2848247
Catalyzes three successive oxidations of C19 androgens: two conventional oxidations at C19 yielding 19-hydroxy and 19-oxo/19-aldehyde derivatives, followed by a third oxidative aromatization step that involves C1-beta hydrogen abstraction combined with cleavage of the C10-C19 bond to yield a phenolic A ring and formic acid .
PMID:20385561
Alternatively, the third oxidative reaction yields a 19-norsteroid and formic acid. Converts dihydrotestosterone to delta1,10-dehydro 19-nordihydrotestosterone and may play a role in homeostasis of this potent androgen .
PMID:22773874
Also displays 2-hydroxylase activity toward estrone .
PMID:22773874
Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (CPR; NADPH-ferrihemoprotein reductase) PMID:20385561 PMID:22773874
PMID:18723036
CHRNA2 forms heteropentameric neuronal acetylcholine receptors with CHRNB2 and CHRNB4 and plays a role in nicotine dependence PMID:24467848 PMID:27493220
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)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N06AX62
ATC R05DA09
ATC N07XX59
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q407781), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.