Abstract
The NSAIDs are potent anti-inflammatory and analgesic agents. It is now believed that the NSAIDs exert their therapeutic activity through the inhibition of COX-2 at the site of inflammation. Unfortunately, these compounds are equally capable of inhibiting constitutively expressed COX-1 in tissues such as the gastrointestinal tract and kidney, which results in serious, mechanism-based toxicities that limit the drug's therapeutic utility. With the identification of selective COX-2 inhibitors, alternatives to traditional NSAID therapy should be available that will provide clinical usefulness with reduced toxicity.
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / pharmacology*
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Digestive System / drug effects*
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Digestive System / enzymology
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Gastrointestinal Diseases / drug therapy
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Gastrointestinal Diseases / enzymology
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Humans
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Isoenzymes / biosynthesis
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Isoenzymes / drug effects*
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Membrane Proteins
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Peroxidases / biosynthesis
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Peroxidases / drug effects*
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Prostaglandin-Endoperoxide Synthases / biosynthesis
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Prostaglandin-Endoperoxide Synthases / drug effects*
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Membrane Proteins
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Peroxidases
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Cyclooxygenase 2
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases