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Updated: Jul 10, 2026

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
Published on: January 18, 2017
[Therapy with aspirin: a new look at the old problem]
Aspirin resistance, where patients experience cardiovascular events despite aspirin use, lacks clear diagnostic criteria. Research explores mechanisms like gene variations and alternative platelet activation pathways contributing to this phenomenon.
Area of Science:
- Cardiology
- Pharmacology
- Genetics
Context:
- Aspirin is a cornerstone for secondary prevention of atherothrombosis.
- A significant subset of patients exhibit suboptimal response to aspirin therapy.
- The concept of 'aspirin resistance' is recognized but lacks standardized diagnostic criteria.
Purpose:
- To define and explore the phenomenon of aspirin resistance.
- To investigate potential underlying mechanisms contributing to aspirin resistance.
- To understand the variability in aspirin's clinical efficacy.
Summary:
- Aspirin resistance refers to the failure of aspirin to prevent thrombotic events or adequately inhibit platelet function in certain patients.
- Reported incidences of aspirin resistance vary widely (5-70%) depending on the clinical context and laboratory methods employed.
- Potential mechanisms include cyclooxygenase-1 gene variations, alternative thromboxane A2 production pathways (cyclooxygenase-2), platelet receptor polymorphisms (Ilb/IIIa), NSAID interactions, and non-aspirin-mediated platelet activation.
Impact:
- Highlights the need for refined diagnostic criteria for aspirin resistance.
- Informs the development of personalized antiplatelet strategies.
- Suggests potential therapeutic targets for overcoming aspirin resistance.
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