Imiquimod 3.75% cream 250mg sachets
Requires a prescription from a doctor or prescriber
Imiquimod is an immune response modifier that acts as a toll-like receptor 7 agonist.
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MHRA alerts for Imiquimod
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 Imiquimod
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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 Imiquimod
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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.
3 branded products available
MHRA licensed products
View all licensed products for Imiquimod on the MHRA register
Zyclara 3.75% cream 250mg sachets
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.
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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(2)
Melanoma: assessment and management (NG14)
VivaScope 1500 and 3000 imaging systems for detecting skin cancer lesions (HTG388)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & safety information
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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
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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. 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: 19 · Randomised trials: 11 · 1998–2026
Showing the 50 most relevant studies, sorted by most relevant.
M. Jansen, K. Mosterd, A. Arits, et al.
The Journal of investigative dermatology, 2017
M. H. Roozeboom, A. Arits, K. Mosterd, et al.
The Journal of investigative dermatology, 2016
Edith Hanna, R. Abadi, O. Abbas
International Journal of Dermatology, 2016
H. Williams, F. Bath-Hextall, M. Ozolins, et al.
The Journal of investigative dermatology, 2017
Scharner MK, Walker AM, Nguyen SA, et al.
2026
- Leukoplakia, Oral
- Imiquimod
- Administration, Topical
ObjectiveImiquimod, a toll-like receptor 7 agonist, is currently FDA-approved for treatment of actinic keratoses, superficial BCC, and external genital warts. It has also demonstrated promise in off-label use in the treatment of oral cavity leukoplakia and dysplasia. The aim of this scoping review is to summarize the current literature on this novel treatment strategy.Data sourcesCINAHL, Cochrane Library, PubMed, and SCOPUS.Review methodData sources were searched from inception through December 2024. The search was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Extension for Scoping Reviews. Studies reporting on oral leukoplakia or dysplasia treated with topical imiquimod were included, with primary outcome being lesion resolution or reduction.ResultsA total of 9 studies reporting on (N = 89) patients with (n = 99) lesions were included. The average age was 48.4 (range 43-66), and 48.6% were male. 5% topical imiquimod was used in varying treatment regimens, most commonly for 6 weeks in duration (7/9 papers). 34.3% of lesions had complete resolution, 43.4% had incomplete resolution, and 22.2% had no change in the lesion. The most commonly reported adverse effects were burning/soreness at the site (73.0%), fatigue (22.5%), oral lichen planus development or flare (11.2%), and flu-like symptoms (2.2%).ConclusionTopical imiquimod for the treatment of oral cavity leukoplakia and dysplasia is a promising new treatment strategy. Efficacy has been demonstrated in reducing lesion size and even complete lesion resolution, with minimal adverse effects. Further research is needed on this innovative therapeutic approach.
Abstract licence: CC BY-NC-ND
Fay JW, Kimball KM, Hartman NW, et al.
2026
Maqsood M, Nadeem AA, Shahid A, et al.
2026
Tian Y, Yao Y, Zhang J
2026
- Photochemotherapy
- Keratosis, Actinic
- Imiquimod
Saib R, Joly E, Fouere S, et al.
2026
IntroductionInternational guidelines for the management of anogenital warts (AGWs) propose multiple first-line options but do not prioritize treatments based on safety or tolerability. This study aimed to compare the safety profiles of topical, systemic, and ablative treatments used for external AGWs in immunocompetent adults.MethodsA systematic review and frequentist network meta-analysis of randomized controlled trials published through August 2025 was performed. Adverse events (AEs) were classified as low-, moderate-, or high-grade local AEs (LGL, MGL, HGL) and low-grade general AEs (LGG). Relative risks were estimated using random-effects models with placebo as the reference.ResultsWe included 107 RCTs involving 12,423 participants. Ablative procedures were associated with higher rates of moderate-to-severe local AEs compared with topical therapies. Among topical treatments, imiquimod 5% and cidofovir cream were associated with lower rates of severe AEs, whereas podophyllotoxin was more often associated with LGL. SUCRA rankings placed topical treatments above ablative therapies in terms of tolerability. Cidofovir cream demonstrated the best safety profile, followed by imiquimod 5%.ConclusionThis network meta-analysis highlights significant differences in tolerability across AGW treatments and offers a comparative framework for patient-centered therapeutic decision-making. It also emphasizes the need for standardized AE reporting in future trials.
Abstract licence: CC BY-NC
Hamanishi, Junzo, Yamaguchi, Ken, Yamanoi, Koji, et al.
Wolters Kluwer Health, 2023
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
20 hours
Mechanism
Imiquimod's mechanism of action is via stimulation of innate and acquired immune…
Food interactions
1 warning
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
20 hours
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 35 of 35 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:14976261 PMID:32433612
Controls host immune response against pathogens through recognition of uridine-containing single strand RNAs (ssRNAs) of viral origin or guanosine analogs .
PMID:12738885 PMID:27742543 PMID:31608988 PMID:32706371 PMID:35477763
Upon binding to agonists, undergoes dimerization that brings TIR domains from the two molecules into direct contact, leading to the recruitment of TIR-containing downstream adapter MYD88 through homotypic interaction .
PMID:27742543
In turn, the Myddosome signaling complex is formed involving IRAK4, IRAK1, TRAF6, TRAF3 leading to activation of downstream transcription factors NF-kappa-B and IRF7 to induce pro-inflammatory cytokines and interferons, respectively .
PMID:27742543 PMID:32706371
In plasmacytoid dendritic cells, RNASET2 endonuclease cooperates with PLD3 or PLD4 5'->3' exonucleases to process RNA and release 2',3'-cyclic guanosine monophosphate (2',3'-cGMP) and cytidine-rich RNA fragments that occupy TLR7 ligand-binding pockets and trigger a signaling-competent state
PMID:25297876 PMID:32433612
Controls host immune response against pathogens through recognition of RNA degradation products specific to microorganisms that are initially processed by RNASET2 .
PMID:31778653
Recognizes GU-rich single-stranded RNA (GU-rich RNA) derived from SARS-CoV-2, SARS-CoV-1 and HIV-1 viruses .
PMID:33718825
Upon binding to agonists, undergoes dimerization that brings TIR domains from the two molecules into direct contact, leading to the recruitment of TIR-containing downstream adapter MYD88 through homotypic interaction .
PMID:23520111 PMID:25599397 PMID:26929371 PMID:33718825
In turn, the Myddosome signaling complex is formed involving IRAK4, IRAK1, TRAF6, TRAF3 leading to activation of downstream transcription factors NF-kappa-B and IRF7 to induce pro-inflammatory cytokines and interferons, respectively PMID:16737960 PMID:17932028 PMID:29155428
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC D06BB10
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)
Imiquimod
Additional database identifiers
Drugs Product Database (DPD)
11834
ChemSpider
51809
BindingDB
50240849
PDB
6T0
ZINC
ZINC000019632912
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15631
GenAtlas
TLR7
GeneCards
TLR7
GenBank Gene Database
AF240467
GenBank Protein Database
7330281
Guide to Pharmacology
1757
UniProt Accession
TLR7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15632
GenAtlas
TLR8
GeneCards
TLR8
GenBank Gene Database
BC101077
Guide to Pharmacology
1758
UniProt Accession
TLR8_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:
- 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