Menthol 1.5% in Aqueous cream
Requires a prescription from a doctor or prescriber
Menthol is a covalent organic compound made synthetically or obtained from peppermint or other mint oils.
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MHRA alerts for Menthol
Safety monitoring data
Yellow Card reports
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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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1 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
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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.
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: 25 · Randomised trials: 5 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
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
Clare Meernik, H. Baker, S. Kowitt, et al.
BMJ Open, 2019
Zhu Y, Zhao J, Yao J, et al.
2026
ObjectiveThis study employed a network meta-analysis (NMA) to systematically evaluate and compare the relative efficacy of three menthol administration routes-ingestion (ING), mouth rinsing (MR), and topical application (Top)-on exercise performance and physiological responses in the heat, aiming to explore potential task-oriented personalized supplementation strategies.MethodsDatabases including PubMed, Embase, Web of Science, and CNKI were searched for randomized controlled trials (RCTs) investigating menthol interventions on exercise performance in hot environments (T≥25 °C), with a search deadline of March 2, 2026. Two reviewers independently performed literature screening, data extraction, and risk of bias assessment using the Cochrane RoB 2.0 tool. Network meta-analysis was conducted using Stata 18.0 software.ResultsThe network meta-analysis of the 15 included randomized controlled trials revealed outcome-specific trends in exercise performance, although most pairwise comparisons did not reach statistical significance. Surface under the cumulative ranking curve (SUCRA) analysis indicated that ingestion (ING) demonstrated a potential trend for improving endurance performance (SUCRA = 76.1%), while mouth rinsing (MR) showed a tendency for enhancing mean power output (SUCRA = 66.9%). Regarding physiological responses, the impact of all administration routes on core temperature (Tc) and heart rate (HR) was modest and lacked statistically significant differences compared to control conditions. Specifically, ING ranked relatively higher in maintaining core temperature (SUCRA = 67.0%), whereas topical application (Top) exhibited the weakest potential for thermoregulation (SUCRA = 6.2%) and might even lead to a slight upward trend in temperature due to the physical obstruction of heat dissipation.ConclusionThe interventional efficacy of menthol in the heat appears to be co-regulated by the administration route and the specific exercise task. While the current evidence does not establish definitive superiority among the administration routes due to the lack of statistical significance, ingestion may serve as an exploratory option for long-duration endurance events, whereas mouth rinsing could be considered for tasks focusing on instantaneous power output. Given that menthol may mask actual subjective thermal perception without alleviating objective physiological heat strain, its application must be combined with objective physiological monitoring in practice to ensure exercise safety.Systematic review registrationwww.crd.york.ac.uk/prospero, identifier: CRD420261340546.
Abstract licence: CC BY
Wang Y, Fan X, Li H, et al.
2026
Vázquez-López NI, Falfán-Valencia R, Pérez-Rubio G
2026
- Flavoring Agents
- Electronic Nicotine Delivery Systems
- DNA Damage
ObjectivesThis systematic review evaluated the scientific evidence on the effects of flavors in electronic cigarettes in animal models and their impact on human health, aiming to understand the potential risks associated with their use.MethodsA PubMed search was conducted using MeSH terms such as "e-cigarettes AND flavor AND nicotine AND e-liquid AND cytotoxicity AND cellular damage and health AND adolescent AND young people." We selected original studies that evaluated tissue damage, inflammation, oxidative stress, and DNA damage in animal models, as well as health outcomes in humans. In vitro studies, studies with conflicts of interest related to the tobacco industry, and studies that did not meet our objectives were excluded.ResultsFruity, menthol/mint, and sweet flavors increase nicotine consumption and preference for e-cigarettes in animal models and are also linked to inflammation, cellular damage, and cardiovascular changes. In humans, these flavors have been associated with respiratory symptoms, reduced lung function, and DNA damage in oral cells. Neurological effects, such as activation of reward circuits, have also been observed.ConclusionThe evidence available to date suggests that these products can be as harmful to health as combustible cigarettes.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261346170.
Abstract licence: CC BY
Andrea C. Villanti, Lauren K. Collins, R. Niaura, et al.
BMC Public Health, 2017
Mills SD, Tapp-Hughes N, Zhang Y, et al.
2026
IntroductionThe Food and Drug Administration proposed a rule to ban the sale of menthol cigarettes, but recently withdrew the proposal. This study uses simulation modeling to estimate the impact of a national menthol cigarette ban on tobacco use, life expectancy, and lung cancer.MethodsWe used the Tobacco Use Individual-level Simulation and Tracking (TwIST) Model, a validated microsimulation model of tobacco use in the US adult population. The simulated population and model parameter estimates are primarily informed by data from the Population Assessment of Tobacco and Health Study. We used findings from a published meta-analysis to inform estimates of the impact of a menthol ban on tobacco use in the model.ResultsTen years after a menthol ban, the model projects a 38.5% reduction in tobacco use prevalence among adults. Declines are even greater in the non-Hispanic Black population (70.4% reduction) and among individuals living in poverty (46.0% reduction). Among a cohort of adults, individual life expectancy is projected to increase by 73 days, on average. Among the non-Hispanic Black population and individuals living in poverty, life expectancy will increase by 193 days and 183 days, respectively. In the cohort, 1-year incidence of lung cancer is estimated to decline by 14.4% in the general population, 32.4% among non-Hispanic Black adults, and 22.1% among individuals living in poverty.ConclusionsA menthol ban would reduce tobacco use and lung cancer rates, while increasing life expectancy. The greatest benefits are expected among non-Hispanic Black individuals and people living in poverty.
Abstract licence: CC BY-NC-ND
Patrik Kéringer, N. Farkas, N. Gede, et al.
Scientific Reports, 2020
Ying Yin, Mengyu Wu, L. Zubcevic, et al.
Science (New York, N.Y.), 2017
Mimi Kim, Geoffrey Curtin
2020
Abstract Background: This systematic review followed PRISMA guidelines to examine the Key Question: Does menthol cigarette use have a differential impact on smoking cessation compared with non-menthol cigarette use?Methods: The original protocol was registered on March 22, 2016 (updated January 10, 2019; PROSPERO: CRD42019119301). Six databases were queried from inception to December 14, 2018.Results: Fifty-seven studies (27 rated “good”, 27 rated as “fair”, and three studies rated as “poor” individual study quality) that compared menthol and non-menthol smokers were qualitatively synthesized across the following cessation measures (total adjusted studies; strength of evidence grade): duration of abstinence (2; low); quit attempts (14; insufficient); rate of abstinence/quitting (28; moderate); change in smoking quantity/frequency (3; insufficient); and return to smoking/relapse (2; insufficient). Overall, the qualitative synthesis failed to show a consistent trend for the association of menthol cigarette use and smoking cessation across the outcomes. Further, meta-analytic results found no difference between menthol and non-menthol cigarette use and the two measures of quit attempts and duration of abstinence.Implications: The overall strength of evidence for an association between menthol cigarette use and smoking cessation was graded as “low”, based on deficiencies of indirectness and inconsistency in the available body of evidence. Therefore, there is no consistent, significant, or differential association between menthol cigarette use and smoking cessation.
Abstract licence: CC BY 4.0
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 medicines. 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
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