Levomenthol 6.25mg/5ml oral solution
Menthol is a covalent organic compound made synthetically or obtained from peppermint or other mint oils.
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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 Levomenthol
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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 Levomenthol
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1 branded products available
Part of the Vicks brand family (generic: Levomenthol)
MHRA licensed products
View all licensed products for Levomenthol on the MHRA register
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
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.
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 all 11 studies.
2007–2026
Showing all 11 studies, sorted by most relevant.
Adebowale A. Alade, Samad A. Ahmed, Somdutt Mujwar, et al.
Journal of Biomolecular Structure and Dynamics, 2023
Marjan Piponski, Antonija Beneta, Gjose Stefkov, et al.
SEPARATION SCIENCE PLUS, 2025
Serwat Naz, Sumia Akram, R. Naeem, et al.
International Journal of Molecular Sciences, 2026
Cannabis sativa L. leaves (CSL) are a rich in bioactive compounds and known for their medicinal and recreational uses. In this study, a natural hydrophobic deep eutectic solvent (HDES) system composed of menthol and thymol (1:1) was employed for the efficient extraction of bioactive compounds from CSL. Extraction of bioactives was optimized at various conditions involving DES/ethanol ratio, temperature, and extraction time, as well as shaking speed through statistical models including response surface methodology (RSM) and artificial neural network (ANN). The maximum bioactive yield, equal to 70% (w/w) of powdered CSL, was achieved at optimized values of 5.5 mL DES, 4.5 mL ethanol, and 225 rpm shaking speed at 55 °C for 107.5 min. It was observed that slightly adjusting the shaking speed and temperatures customized the nature of bioactives with more antioxidant, antidiabetic, and antimicrobial properties. The extracts of CSL produced while applying natural HDES were found to be non-toxic during hemolytic assay. Overall, HDES when mixed with ethanol in 55:45 ratio produced CSL extracts with an ample level of phenolics (133.75 mg GAE/g) and flavonoids (120.05 mg QE/g). GC-MS analysis of CSL extracts produced by HDES revealed the presence of multiple bioactives like tetrahydrocannabivarin, cannabidiol, cannabinol, cannabidivarol, dl-menthol, levomenthol, and 4-hydroxy-3-methylacetophenone. Based on these findings, it can be concluded that HDES in combination with ethanol may work as an efficient extraction solvent to recover CSL bioactives without compromising their antioxidant features and safety for use in food and pharmaceutical applications.
Abstract licence: CC BY
A. Wade, G. Crawford, D. Young, et al.
The Journal of International Medical Research, 2019
Objective To determine whether 3% w/w levomenthol added to ibuprofen gel (5% w/w) improves its efficacy compared with ibuprofen gel alone or diclofenac gel (1.16%) for the treatment of soft-tissue injuries. Methods A total of 182 patients with acute soft-tissue injuries participated in a randomised, single-blind, single-dose study to assess the efficacy and safety of three topical analgesic gels. Efficacy was assessed as the score change in a numeric rating scale for pain. Results The median time to significant pain relief was 20 minutes for the ibuprofen/levomenthol and diclofenac gels but 25 minutes for ibuprofen gel. At 2 hours, significantly more patients treated with ibuprofen/levomenthol gel reported a cooling sensation (45.8%) compared with diclofenac (16.4%) or ibuprofen (14.7%) gels, and both ibuprofen/levomenthol and diclofenac gels provided significantly more effective global pain relief compared with ibuprofen gel. Few adverse events and no serious adverse events related to study medication were recorded. Conclusions Although all gels effectively relieved pain, both ibuprofen/levomenthol and diclofenac gels provided superior global pain relief compared with ibuprofen gel, with a shorter median time to significant pain relief. Only ibuprofen/levomenthol gel provided cooling for up to 2 hours. None of the gels were associated with serious safety concerns. EudraCT No 2015-005240-33 EU Clinical Trials Register URL: https://www.clinicaltrialsregister.eu/ctr-search/search
Abstract licence: CC BY-NC 4.0
Olivera Blažeska, Elena Kazandzievska, Packa Antovska, et al.
Macedonian Pharmaceutical Bulletin, 2022
J. Köhnlein, F.v. Rheinbaben, S. Werner
Krankenhaus-Hygiene + Infektionsverhütung, 2016
I. Kosalec, M. Klarić, S. Pepeljnjak
Planta Medica, 2007
Reactions Weekly, 2012
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
Menthol primarily activates the cold-sensitive TRPM8 receptors in the skin.
Food interactions
None known
Human targets
5 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 724 interactions
Proteins and enzymes this drug interacts with in the body
PMID:15306801 PMID:15852009 PMID:16174775 PMID:25559186 PMID:37857704
TRPM8 is a voltage-dependent channel; its activation by cold or chemical ligands shifts its voltage thresholds towards physiological membrane potentials, leading to the opening of the channel .
PMID:15306801
In addition to its critical role in temperature sensing, regulates basal tear secretion by sensing evaporation-induced cooling and changes in osmolality (By similarity).
May plays a role in prostate cancer cell migration PMID:16174775 PMID:25559186
PMID:17259981 PMID:21195050 PMID:21873995 PMID:23199233 PMID:25389312 PMID:33152265
Has a relatively high Ca(2+) selectivity, with a preference for divalent over monovalent cations (Ca(2+) > Ba(2+) > Mg(2+) > NH4(+) > Li(+) > K(+)), the influx of cation into the cytoplasm leads to membrane depolarization .
PMID:19202543 PMID:21195050
Has a central role in the pain response to endogenous inflammatory mediators, such as bradykinin and to a diverse array of irritants. Activated by a large variety of structurally unrelated electrophilic and non-electrophilic chemical compounds, such as allylthiocyanate (AITC) from mustard oil or wasabi, cinnamaldehyde, diallyl disulfide (DADS) from garlic, and acrolein, an environmental irritant .
PMID:20547126 PMID:25389312 PMID:27241698 PMID:30878828
Electrophilic ligands activate TRPA1 by interacting with critical N-terminal Cys residues in a covalent manner .
PMID:17164327 PMID:27241698 PMID:31866091 PMID:32641835
Non-electrophile agonists bind at distinct sites in the transmembrane domain to promote channel activation .
PMID:33152265
Also acts as an ionotropic cannabinoid receptor by being activated by delta(9)-tetrahydrocannabinol (THC), the psychoactive component of marijuana .
PMID:25389312
May be a component for the mechanosensitive transduction channel of hair cells in inner ear, thereby participating in the perception of sounds (By similarity)
PMID:12077604 PMID:12077606 PMID:26818531 PMID:37648856 PMID:38691614
It is activated by innocuous (warm) temperatures and shows an increased response at noxious temperatures greater than 39 degrees Celsius .
PMID:12077604 PMID:12077606
Activation exhibits an outward rectification .
PMID:12077604
The channel pore can dilate to provide permeability to larger cations .
PMID:37648856
May associate with TRPV1 and may modulate its activity .
PMID:12077606
Is a negative regulator of hair growth and cycling: TRPV3-coupled signaling suppresses keratinocyte proliferation in hair follicles and induces apoptosis and premature hair follicle regression (catagen) PMID:21593771
They are however insensitive to dihydropyridines (DHP)
Signaling leads to the inhibition of adenylate cyclase activity. Inhibits neurotransmitter release by reducing calcium ion currents and increasing potassium ion conductance. Plays a role in the perception of pain.
Plays a role in mediating reduced physical activity upon treatment with synthetic opioids. Plays a role in the regulation of salivation in response to synthetic opioids. May play a role in arousal and regulation of autonomic and neuroendocrine functions
Enzymes involved in drug metabolism — important for understanding drug interactions
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)
Levomenthol
Additional database identifiers
Drugs Product Database (DPD)
265
Drugs Product Database (DPD)
418
Drugs Product Database (DPD)
15195
ChemSpider
15803
BindingDB
50318482
PDB
XUQ
Guide to Pharmacology
2430
ZINC
ZINC000001482164
HUGO Gene Nomenclature Committee (HGNC)
HGNC:17961
GenAtlas
TRPM8
GeneCards
TRPM8
GenBank Gene Database
AY090109
GenBank Protein Database
20147036
Guide to Pharmacology
500
UniProt Accession
TRPM8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:497
GenAtlas
TRPA1
GeneCards
TRPA1
GenBank Gene Database
Y10601
GenBank Protein Database
3287188
Guide to Pharmacology
485
UniProt Accession
TRPA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18084
GenAtlas
TRPV3
GeneCards
TRPV3
GenBank Gene Database
AJ487035
Guide to Pharmacology
509
UniProt Accession
TRPV3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1390
GenAtlas
CACNA1C
GeneCards
CACNA1C
GenBank Gene Database
M92270
Guide to Pharmacology
529
UniProt Accession
CAC1C_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1391
GenAtlas
CACNA1D
GeneCards
CACNA1D
GenBank Gene Database
M76558
GenBank Protein Database
179764
Guide to Pharmacology
530
UniProt Accession
CAC1D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1393
GenAtlas
CACNA1F
GeneCards
CACNA1F
GenBank Gene Database
AJ006216
GenBank Protein Database
3183953
Guide to Pharmacology
531
UniProt Accession
CAC1F_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1397
GenAtlas
CACNA1S
GeneCards
CACNA1S
GenBank Gene Database
U30707
GenBank Protein Database
1698403
Guide to Pharmacology
528
UniProt Accession
CAC1S_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1401
GenAtlas
CACNB1
GeneCards
CACNB1
GenBank Gene Database
M92303
GenBank Protein Database
179806
UniProt Accession
CACB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1402
GenAtlas
CACNB2
GeneCards
CACNB2
GenBank Gene Database
S60415
GenBank Protein Database
300417
UniProt Accession
CACB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1403
GenAtlas
CACNB3
GeneCards
CACNB3
GenBank Gene Database
X76555
GenBank Protein Database
435135
UniProt Accession
CACB3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1404
GenAtlas
CACNB4
GeneCards
CACNB4
GenBank Gene Database
U95020
GenBank Protein Database
2058727
UniProt Accession
CACB4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1388
GenAtlas
CACNA1A
GeneCards
CACNA1A
GenBank Gene Database
AF004884
GenBank Protein Database
2213913
UniProt Accession
CAC1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8154
GenAtlas
OPRK1
GeneCards
OPRK1
GenBank Gene Database
U11053
GenBank Protein Database
532060
Guide to Pharmacology
318
UniProt Accession
OPRK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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
Molecular structure

Linked open data from Wikidata (Q407418), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. Molecular structure images from Wikimedia Commons. WHO INN from the World Health Organization.