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Abstract

Nonsteroid anti-inflammatory drugs (NSAIDs) are a structurally diverse group of agents with similar therapeutic effects. They reduce pain, fever and inflammation, and are also associated with lowered risks of cardiovascular disease1 and colon cancer2,3. The biological basis for the therapeutic effects of NSAIDs is their ability to inhibit prostaglandin biosynthesis. The NSAIDs specifically target the bifunctional cyclooxygenase enzyme (COX) which is responsible for the initial rate-limiting conversion of arachidonic acid to prostaglandin G (PGG) and its subsequent conversion to PGH2. This is then converted to other prostanoids4,5.

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© 1996 Kluwer Academic Publishers and William Harvey Press

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Herbette, L.G., Vecchiarelli, M., Trummlitz, G. (1996). NSAID mechanism of action: the role of intracellular pharmacokinetics. In: Vane, J., Botting, J., Botting, R. (eds) Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-9029-2_5

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  • DOI: https://doi.org/10.1007/978-94-010-9029-2_5

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-9031-5

  • Online ISBN: 978-94-010-9029-2

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