Analgesics : from chemistry and pharmacology to clinical by Helmut Buschmann; Gregor Bahrenberg; et al
By Helmut Buschmann; Gregor Bahrenberg; et al
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Additional resources for Analgesics : from chemistry and pharmacology to clinical application
The metallated pyridine (vii) is obtained by esterification of 3-hydroxy-2methylpyridine with triflic anhydride to give the corresponding triflate, which is treated with a tin reagent to yield the target tin intermediate. The boron lithium salt (viii) is prepared by treatment of 5-bromo-2-methylpyridine with butyllithium followed by addition of triisopropyl borate. /; viii Scheme 18: Condensation pathways from the key intermediate 2,5-dichloro-3-(4(methylsulfonyl)phenyl) pyridine (iv) with the tin or boronate derivative, respectively, to afford etoricoxib.
W // NH? NO-O-C5HH HI, CH3COOH COX selectivity IC50 [MM] whole blood (1) H 2 CO 3 l CO 2 Scheme 13: Synthesis of diflunisal. 5 (1) Young etal. , 1980) is a nonsteroidal anti-inflammatory drug used in the treatment of mild to moderate pain including osteoarthritis, rheumatoid arthritis and primary dysmenorrhoea. It is used as base or lysine- or arginine-salt for oral or parenteral application. Diflunisal shows weak inhibition of both, COX-1 and COX2 in a whole blood assay. Peak plasma concentrations are reached within 2 to 3 h after oral dosing.
This suggests that the effects of high doses of certain NSAIDs are mediated by cyclooxygenaseIndependent mechanisms. Some of these mechanisms decribed for NSAIDs are summarized below. The enzymatic inhibition of NSAIDs as well as the transcriptional regulation is shown in Fig. 19. Cyclooxygenaseindependent mechanisms of NSAIDs 42 Christoph and Buschmann Summary of mechanisms of actions of NSAIDs as transcriptional regulators on the functional and molecular level Functional level • Inhibition of immune cell activation • Inhibition of cytokine production • Induction of apoptosis Molecular level PPAR (Peroxisome Proliferator-Activated Receptor) • Inhibition of transcription factors NF-KB, NF-AT, and AP-1 • Alteration of MAP kinases cascade • Modulation of the activity of nuclear receptors (PPARs) • Induction of transcription factors and genes (STAG, NAG, NFGI-B) PPAR is a nuclear receptor-transcription factor and Is ligand-dependent and expressed in several tissues.