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Document nant human renin kinetics, pH-stability, and peptidomimetic inhibitor binding. J Protein Chem 1991; 10:553–563. Page 342 52. Tong L, Pav S, Lamarre D, Pilote L, Laplante S, Anderson PC, Jung G. High resolution crystalstructures of recombinant human renin in complex with polyhydroxymonoamide inhibitors. J Mol Biol 1995; 250:211–222. 53. Sham HL, Bolis G, Stein HH, Fesik SW, Marcott PA, Plattner JJ, Rempel CA, Greer J. Renin inhibitors. Design and synthesis of a new class of conformationally restricted analogues of angiotensinogen. J Med Chem 1988; 31:284–295. http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_342.html [4/5/2004 5:27:19 PM]
Document Page 343 14 Structural Aspects in the Inhibitor Design of Catechol O-Methyltransferase Jukka Vidgren and Martti Ovaska Orion Corporation Orion Pharma, Espoo, Finland I. Introduction Catechol O-methyltransferase (COMT) plays an important role in the catabolic inactivation of catecholamines. It is present both in extracerebral tissues and in the central nervous system. During the last few years there has been a remarkable interest in COMT. Basic biochemical and molecular biology research has given detailed insights into the function and nature of the enzyme. The knowledge of the crystallographic structure has allowed researchers to analyze the molecular mechanism of the catalytic reaction and to accomplish the structure-based design of inhibitors. The development of potent and selective inhibitors has provided effective pharmacological tools to investigate the physiological role of the enzyme. The main clinical interest has been the possible application of COMT inhibitors as adjuncts in the L-dopa therapy of Parkinson's disease. Parkinson's disease is a dopamine deficiency disorder. The dopamine-producing neurons in striatum are destroyed. The medication strategy is to replenish the missing dopamine. L-Dopa, given together with a peripheral inhibitor of dopa decarboxylase (DDC), for example, carbidopa, is a standard therapy in Parkinson's disease. While dopamine does not penetrate into the brain, L-dopa penetrates the blood-brain barrier and is decarboxylated into dopamine in the brain. The half-life of L-dopa is short and in the presence of DDC inhibitor a large amount of the drug is eliminated by COMT. The COMT enzyme produces the metabolite 3-methoxytyrosine (3-OMD), which has no benefit in the treatment of Parkinson's disease, but has a long elimination half-life and may be harmful during chronical treatment. Also a gradual loss of the efficacy of L-dopa occurs during longterm medication. Since the early 1980s active http://legacy.netlibrary.com/nlreader/nlReader.dll?bookid=12640&filename=Page_343.html [4/5/2004 5:27:21 PM]
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Page 395 and 396: Document 13 Rational Design of Reni
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Page 413 and 414: Document 2. Blundell TL, Cooper J,
Page 415 and 416: Document 17. Szelke M. Chemistry of
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Document D ddI, 152 tumour necrosis
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