Pharmacy

Anti-Inflammatory Drug Discovery by Jeremy I Levin; Stefan Laufer

By Jeremy I Levin; Stefan Laufer

Content material: part 1. Arachidonic acid cascade -- part 2. Kinases -- part three. GPCRs -- part four. Sphingolipids -- part five. Steroid hormone receptors

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Avis, S. H. Hong, A. Martinez, T. Moody, Y. H. Choi, J. Trepel, R. Das, M. Jett and J. L. , 2001, 15, 2007. 32 Chapter 1 169. M. Romano, A. Catalano, M. Nutini, E. D’Urbano, C. Crescenzi, J. Claria, R. Libner, G. Davi and A. , 2001, 15, 2326. 170. J. Ghosh and C. E. Myers, Proc. Natl Acad. Sci. USA, 1998, 95, 13182. 171. M. Mehrabian and H. Allayee, Curr. Opin. , 2003, 14, 447. 172. C. D. Funk, Nat. Rev. , 2005, 4, 664. 173. F. Celotti and S. Laufer, Pharmacol. , 2001, 43, 429. 174. B. K. Lam, J.

S. Gilmour and M. D. Mitchell, Mol. , 2005, 68, 169. 1–7 When the liberated fatty acid is arachidonic acid, subsequent metabolism through the cyclooxygenase (COX) and the lipoxygenase (LOX) pathways leads to the formation of eicosanoids, including prostaglandins and leukotrienes. A subset of lysophospholipids (1-O-alkyl-substituted choline glycerophospholipids) can be acetylated to the platelet-activating factor (PAF). 12–20 The special attraction of this approach is based on the evidence that, unlike cyclooxygenase inhibitors, inhibitors of PLA2 not only reduce the formation of prostaglandins, but also suppress the generation of leukotrienes, lysophospholipids and the PAF.

Myers, Proc. Natl Acad. Sci. USA, 1998, 95, 13182. 171. M. Mehrabian and H. Allayee, Curr. Opin. , 2003, 14, 447. 172. C. D. Funk, Nat. Rev. , 2005, 4, 664. 173. F. Celotti and S. Laufer, Pharmacol. , 2001, 43, 429. 174. B. K. Lam, J. F. Penrose, J. Rokach, K. Xu, M. H. Baldasaro and K. F. Austen, Eur. J. , 1996, 238, 606. 175. A. Koeberle, U. Siemoneit, H. Northoff, B. Hofmann, G. Schneider and O. Werz, Eur. J. , 2009, 608, 84. 176. A. Koeberle, U. Siemoneit, U. Buehring, H. Northoff, S. Laufer, W.

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