Aspirin 325mg / Caffeine 15mg tablets
Available from pharmacies, supermarkets, and retail outlets
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
Yellow Card
Report side effects (MHRA)
Drug safety updates
MHRA alerts for Aspirin + Caffeine
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.
View Drug Analysis Profile
Browse all Drug Analysis Profiles A–Z
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
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.
Search EudraVigilance database
Browse substances A–Z in the European adverse reaction database
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
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 Aspirin + Caffeine on the MHRA register
Anadin Original tablets
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)
Atrial fibrillation: diagnosis and management (NG196)
Generalised anxiety disorder and panic disorder in adults: management (CG113)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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. 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: 10 · Randomised trials: 1 · 1963–2026
Showing the 50 most relevant studies, sorted by most relevant.
Lanteri-Minet M, Pegahi R
2025
- Pain
- Acetaminophen
- Caffeine
T. Kiersch, Milošr. Minić
Current Medical Research and Opinion, 2002
R. Lipton, Walter F. Stewart, R. Ryan, et al.
Archives of neurology, 1998
Saygili S, Hegde S, Shi XZ
2024
- Coffee
- Gastrointestinal Microbiome
- Gastrointestinal Tract
Background and objectives: As one of the most popular beverages in the world, coffee has long been known to affect bowel functions such as motility, secretion, and absorption. Recent evidence obtained in human and animal studies suggests that coffee has modulating impacts on gut microbiota. We aim to present an overview of the specific effects of coffee on gut microbiota composition, diversity, and growth. We will also critically review the impacts of coffee on bowel functions in health and diseases and discuss whether gut microbiota play a role in the coffee-associated functional changes in the gastrointestinal tract. Methods: We searched the literature up to June 2024 through PubMed, Web of Science, and other sources using search terms such as coffee, caffeine, microbiota, gastrointestinal infection, motility, secretion, gut-brain axis, absorption, and medication interaction. Clinical research in patients and preclinical studies in rodent animals were included. Results: A majority of the studies found that moderate consumption of coffee (Bifidobacterium spp. and decreased the abundance of Enterobacteria. Coffee consumption is reported to increase gut microbiota diversity. Although the effects of coffee on bowel functions have been known for a long time, it is not until recently that we have recognized that some of the effects of coffee may be partly due to its impacts on microbiota. Conclusions: The current literature suggests that moderate coffee consumption has beneficial effects on oral and gut microbiota and motility function. However, excessive coffee intake (>5 cups a day) is implicated in reflux disorders, periodontal diseases, and progression of Crohn's disease. Further research in the field is needed, as there are many conflicting results regarding the impacts of coffee in the gastrointestinal tract.
Abstract licence: CC BY
A. Rubin, Leo Winter
Journal of International Medical Research, 1984
Barbanti P, Allais G, Cevoli S, et al.
2024
IntroductionThirty years ago, the first migraine-specific drugs (triptans) appeared. Today two new categories (gepants and ditans) are marketed for acute migraine treatment. That said, is there still a role for conventional therapy? The aim of the present narrative review is to provide an expert overview examining the possible role of the combination paracetamol/caffeine in treatment of acute migraine pain.MethodsTo understand possible settings for more appropriate use of paracetamol/caffeine (1000 mg/130 mg) in treatment of acute migraine, a structured literature search was performed using the PubMed database by a panel of experts from major Italian headache centers; articles not referring to migraine pain were excluded from this review; review articles were prioritized.ResultsOverall response, even to newer specific and selective trigeminal targeted drugs (TTTs), is not over 60%; thus, there is still room for conventional therapies in acute migraine treatment. The panel identified settings in which the use of paracetamol/caffeine combination to treat acute migraine attacks might offer benefit considering the consolidated use through years, despite the lack of studies directly addressing the efficacy of paracetamol/caffeine in the identified populations: subjects > 65 years of age; presence of cardiovascular (CV) comorbidities; TTTs non-responders; pregnancy and breastfeeding; subjects ConclusionsParacetamol is included in the World Health Organization (WHO) essential drug list and has a high level of popularity among patients. Caffeine enhances the analgesic effect of other drugs including paracetamol. In early treatment of acute migraine pain, prescribing physicians might consider using the paracetamol/caffeine combination among other options.
Abstract licence: CC BY-NC
Schaeffer E, Becktepe JS, Brockmann K, et al.
2026
Parkinson's disease (PD) is the fastest growing neurological disorder worldwide and, together with other movement disorders, belongs to a group of chronic neurological conditions associated with a substantial burden for affected individuals, caregivers, and healthcare systems. Despite significant advances in symptomatic treatment, disease-modifying therapies remain unavailable, shifting increasing attention toward prevention as a key therapeutic strategy. In this narrative we primarily focus on PD, as the epidemiologically most challenging condition and the one for which the most comprehensive evidence base for preventive strategies has been established. Preventive approaches relevant to other movement disorders are briefly discussed to highlight other promising targets requiring further investigations. In recent years major progress has been achieved in the identification of modifiable factors relevant for primary prevention of PD. Well-supported factors include physical activity, adherence to a Mediterranean diet, and caffeine or tea consumption as protective factors, as well as pesticide exposure as a relevant risk factor. Advances in early and prodromal diagnosis of PD have opened new perspectives for secondary prevention. Earlier identification of individuals at risk may enable timely interventions aimed at attenuating early disease progression. However, despite this progress, the systematic implementation of early therapeutic interventions in the prodromal phase remains limited. Evidence is sparse and largely indirect, mainly inferred from later disease onset associated with physical activity and dietary patterns. Similarly, although early diagnosis and treatment of cognitive impairment are clearly recommended by clinical guidelines, they remain insufficiently integrated into routine clinical care. Finally, tertiary prevention strategies are supported by a broad evidence base. Multidisciplinary rehabilitative care models have demonstrated clear benefits in preventing complications, maintaining daily functioning and quality of life. While such rehabilitative approaches are widely implemented, the strong evidence supporting moderate- to high-intensity physical exercise remains insufficiently translated into routine practice. Looking ahead, a key goal for the coming decades is the development of personalized prevention strategies, including beyond other insights into gene-environment interactions and the integration of multi-omics data to tailor interventions to individual risk profiles. Such approaches hold promise to maximize preventive efficacy and reduce the overall burden of PD and related movement disorders.
Abstract licence: CC BY
Yang Y, Wan Y, Chen H, et al.
2025
Silberstein S, Rapoport AM
2026
- Analgesics
- Anti-Inflammatory Agents, Non-Steroidal
- Migraine Disorders
ObjectiveTo highlight key factors required to optimize multi-mechanistic approaches with oral combination treatments for the acute management of a migraine attack.BackgroundGiven the complex multi-factorial nature of migraine, combining treatments with different mechanisms of action should improve outcomes compared to monotherapies, but this has not been demonstrated with all treatment combinations.MethodsFor this narrative review, we searched PubMed using combinations of these terms: migraine, acute treatment, combination therapy, fixed-dose combination therapy, multi-mechanistic treatment, pharmacokinetics, and pharmacodynamics. All articles considered relevant were included.ResultsNone of the existing migraine acute treatments as monotherapy effectively treat the key pathophysiological processes of migraine completely. Many patients do not achieve 2-h pain freedom, which is key to avoiding migraine recurrence, medication overuse leading to chronification, and migraine-related disability. The development of combination approaches has led to only two combinations with demonstrated superiority over their individual components: aspirin/acetaminophen/caffeine and sumatriptan/naproxen sodium. The latter is the most effective proven combination treatment because it targets peripheral activation of central pain pathways during the early migraine stages and central sensitization that develops later, independent of peripheral input. Other triptan/nonsteroidal anti-inflammatory drug combinations with higher efficacy as monotherapies could be more effective than sumatriptan/naproxen sodium, particularly if their pharmacokinetic profiles align with the vasoactive mediators of peripheral and central sensitization that they target.ConclusionsCombination treatments with different mechanisms of action targeting key distinct pathophysiological processes of migraine may be more effective than monotherapies, particularly if their pharmacokinetic profiles are optimized to target those processes at the right time. Further research in this area is warranted.
Abstract licence: CC BY-NC-ND
Hans-Christoph Diener, C. Gaul, W. Lehmacher, et al.
European Journal of Neurology, 2021
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.
Scientific data (pharmacology, interactions, ADME) is not yet available for this medicine. Clinical sections are sourced from the NHS dm+d database.