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• W2123138631 abstract "The discovery of leukotrienes dates back to the period between 1938 and 1940. During this period Kellaway, Feldberg, Trethewie, and Holden published the results of a series of experiments on snake venoms that led them to conclude that there is formed from tissue constituents by enzymic action of the venoms a 'slow-reaction smooth muscle-stimulating substance' which may largely determine the nature of the responses (1, 2). It was, however, in their seminal paper in 1940, using guinea pigs sensitized to egg albumin, that Kellaway and Trethewie (3) coined the term SRS and concluded that SRS was formed by the action of antigen upon sensitized tissue. It was not until some 20 yr later, when Brocklehurst was performing elegant experiments on perfused guinea pig lungs, that he confirmed the release of SRS-like activity on anaphylactic challenge of sensitized tissue (4). In his article Brocklehurst named this biological material slow-reacting substance of anaphylaxis (SRS-A) to differentiate it from other material that could induce slow-reacting contractions. Thus, the term SRS-A was born. Despite intensive research efforts by a wide variety of scientists it was not until 1979 that the chemical constituents of SRS-A were identified, by B. Samuelsson and colleagues at the Karolinska Institute in Stockholm, as the cysteinyl leukotrienes (LTs), namely LTC 4 , LTD 4 , and LTE 4 (5, 6). In the period up until the chemical elucidation of SRS-A it had become progressively more widely accepted that SRS-A played a pivotal role in the bronchoconstriction that is one of the hallmarks of acute asthma attacks. Thus, the seminal discovery that the cysteinyl leukotrienes were the active principle of SRS-A and the elucidation of their biosynthetic pathway from arachidonic acid were key events that provided a rational basis for the design of molecules designed to interfere with these events. Not surprisingly, several pharmaceutical companies (e.g., Merck, ICI [now Zeneca], Abbott, Smith Kline & French [now SmithKline Beecham], Bayer, Lilly, Ono, Ciba Geigy [now Novartis]) mounted research programs that were designed to discover molecules that either inhibited leukotriene biosynthesis or blocked the receptors via which the leukotrienes exerted their effects. The purpose of this article is to review some of the hurdles that are an inevitable component of the drug discovery process. In the interests of brevity, focus is directed particularly at the discovery of drugs by Merck designed to antagonize the cysteinyl leukotriene receptors. This focus, however, in no way diminishes or dismisses the significance of the complementary approach of inhibiting leukotriene biosynthesis, far from it. Indeed, 5-lipoxygenase-activating protein (FLAP) inhibitors have been developed by several companies including Merck (7, 8), and a direct 5-lipoxygenase inhibitor, zileuton, by Abbott (9)." @default.
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• W2123138631 date "2000-02-01" @default.
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• W2123138631 title "From Bench to Bedside" @default.
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• W2123138631 doi "https://doi.org/10.1164/ajrccm.161.supplement_1.ltta-2" @default.
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