In 1971, Vane proposed that the mechanism of action of the aspirin-like drugs was through their inhibition of prostaglandin biosynthesis. Since then, there has been intense interest in the interaction between this diverse group of inhibitors and the enzyme known as cyclooxygenase (COX). It exists in two isoforms, COX-l and COX-2 (discovered some 5 years ago). Over the last two decades several new drugs have reached the market based on COX-l enzyme screens. Elucidation of the three-dimensional structure of COX-l has provided ...
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In 1971, Vane proposed that the mechanism of action of the aspirin-like drugs was through their inhibition of prostaglandin biosynthesis. Since then, there has been intense interest in the interaction between this diverse group of inhibitors and the enzyme known as cyclooxygenase (COX). It exists in two isoforms, COX-l and COX-2 (discovered some 5 years ago). Over the last two decades several new drugs have reached the market based on COX-l enzyme screens. Elucidation of the three-dimensional structure of COX-l has provided a new understanding for the actions of COX inhibitors. The constitutive isoform of COX, COX-l has clear physiological functions. Its activation leads, for instance, to the production of prostacyclin which when released by the endothelium is anti-thrombogenic and anti-atherosclerotic, and in the gastric mucosa is cyto- protective. COX-l also generates prostaglandins in the kidney, where they help to maintain blood flow and promote natriuresis. The inducible isoform, COX-2, was discovered through its activity being increased in a number of cells by pro- inflammatory stimuli. A year or so later, COX-2 was identified as a distinct isoform encoded by a different gene from COX-I. COX-2 is induced by inflammatory stimuli and by cytokines in migratory and other cells. Thus the anti-inflammatory actions of non-steroid anti-inflammatory drugs (NSAIDs) may be due to the inhibition of COX-2, whereas the unwanted side-effects such as irritation of the stomach lining and toxic effects on the kidney are due to inhibition of the constitutive enzyme, COX-I.
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Add this copy of Improved Non-Steroid Anti-Inflammatory Drugs: Cox-2 to cart. $115.52, like new condition, Sold by GreatBookPrices rated 4.0 out of 5 stars, ships from Columbia, MD, UNITED STATES, published 2011 by Springer.
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Fine. Trade paperback (US). Glued binding. 200 p. In Stock. 100% Money Back Guarantee. Brand New, Perfect Condition, allow 4-14 business days for standard shipping. To Alaska, Hawaii, U.S. protectorate, P.O. box, and APO/FPO addresses allow 4-28 business days for Standard shipping. No expedited shipping. All orders placed with expedited shipping will be cancelled. Over 3, 000, 000 happy customers.
Add this copy of Improved Non-Steroid Anti-Inflammatory Drugs: Cox-2 to cart. $49.23, like new condition, Sold by Fireside Bookshop rated 5.0 out of 5 stars, ships from Stroud, GLOUCESTERSHIRE, UNITED KINGDOM, published 1996 by Kluwer Academic Publishers.
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Like New in No d/j as Published jacket. Size: 8vo-over 7¾"-9¾" tall; Type: Book This volume contains the proceedings of the William Harvey Conference held in London, 10-11 October, 1995. It covers the molecular biology and physiological functions of the cyclo-oxygenase enzymes, as well as the experimental and clinical aspects of the recently discovered inhibitors of the inducible cyclooxygenase. Particular attention has been directed at the discussion of the selectivity of non-steroid anti-inflammatory drugs for cyclooxygenase-2 and their propensity to cause gastric and kidney damage. 248pp.
Add this copy of Improved Non-Steroid Anti-Inflammatory Drugs: Cox-2 to cart. $83.48, good condition, Sold by Bonita rated 4.0 out of 5 stars, ships from Newport Coast, CA, UNITED STATES, published 1996 by Kluwer Academic Publishers.
