By J. R. Vane, R. M. Botting (auth.), Dr Nicolas Bazan, Dr Jack Botting, Sir John Vane (eds.)
ISBN-10: 940106265X
ISBN-13: 9789401062657
ISBN-10: 9401153868
ISBN-13: 9789401153867
For the earlier a hundred years the mainstay of treatment for rheumatoid arthritis (RA) has been aspirin or different medicines of the non-steroid anti inflammatory crew. In 1971 Vane seasoned posed that either the useful and poisonous activities of those medicinal drugs was once via inhibition of prostaglandin synthesis. the new discovery that prostaglandins answerable for ache and different indicators at inflammatory foci are synthesized via an inducible cyclooxygenase (COX-2) that's encoded by way of a gene targeted from that of the consti tutive enzyme (COX-I) supplied a brand new aim for remedy of RA. A drug that will selectively inhibit COX-2 could with a bit of luck produce the symptomatic profit supplied by way of latest NSAIDs with out the gastrointestinal and renal toxicity because of the inhibition of COX-I. medicines selective for COX-2 at the moment are on hand. Experimental experiences have proven them to be potent with minimum toxicity, and in medical trials gastric and renal toxicities are much less. hugely selective COX-2 inhibitors, might be designed with wisdom of the crystal constructions of COX-I and COX-2, also are on hand. different experimental reviews, together with these in animals missing potent genes for COX-lor COX-2 and in experimental carcinomas, recommend there's nonetheless a lot to be discovered of the pathophysiological features of those enzymes. The inflammatory reaction is a fancy response concerning many mediators that derive from white blood cells, endothelial cells and different tissues. initial facts have published that inhibitors of the cytokines and adhesion molecules that play a vital function within the migration of white cells to inflammatory websites should be important in RA.
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Additional resources for New Targets in Inflammation: Inhibitors of COX-2 or Adhesion Molecules Proceedings of a conference held on April 15–16, 1996, in New Orleans, USA, supported by an educational grant from Boehringer Ingelheim
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Expression and selective inhibition of the constitutive and inducible forms of human cyclo-oxygenase. Biochem 1. 1995;305:479-84. 17. Dullet M, Percival MD. Effect of inhibitor time-dependency and selectivity towards cyclooxygenase isoforms. Biochem J. 1995;306:247-51. 18. Glaser K, Sung ML, O'Neill K et al. Etodolac selectively inhibits human prostaglandin G/H synthase-2 (PGHS-2) versus human PGHS-1. Eur J Pharmacol. 1995;281: 107-11. 19. Laneuville 0, Breuer DK, Dewitt DL, H1a T, Funk CD, Smith WD.
9. Loll PI, Picot D, Ekabo 0, Garavito RM. The synthesis and use of iodinated non-steroidal antiinflammatory drug analogs as crystallographic probes of the prostaglandin H2 synthase cyclooxygenase active site. Biochemistry. 1996;35:7330-40. 10. Garavito RM, Picot D, Loll PJ. 1 A X-ray crystal structure of the integral membrane enzyme prostaglandin H2 synthase-I. Adv Prostaglandin, Thromboxane Leukotriene Res. 1995; 23:99-103. II. Marshall PJ, Kulmacz RJ. Prostaglandin H synthase: Distinct binding sites for cyclooxygenase and peroxidase substrates.
Patoia L, Santucci L, Furno P et al. 5 mg, meloxicam 15 mg, piroxicam 20mg and placebo by means of faecal blood loss, endoscopy and symptom evaluation in healthy volunteers. Br J Rheumatol. I 996;35(Suppl 6):61-7. 29. Distel M, Mueller C, Bluhmki E, Fries J. Safety of meloxicam, a global analysis of clinical trials. Br J Rheumatol. I 996;35(Suppl 6):68-77. 30. Wiesenberg-Boettcher I, Schweizer A, Green JR, Mueller K, Maerki F, Pfeilschifter J. The phannacological profile of CGP 28238, a novel highly potent anti-inflammatory compound.
New Targets in Inflammation: Inhibitors of COX-2 or Adhesion Molecules Proceedings of a conference held on April 15–16, 1996, in New Orleans, USA, supported by an educational grant from Boehringer Ingelheim by J. R. Vane, R. M. Botting (auth.), Dr Nicolas Bazan, Dr Jack Botting, Sir John Vane (eds.)
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