SummaryNimesulide, a nonsteroidal anti-inflammatory drug (NSAID), was shown to be less ulcerogenic [dose inducing ulceration in 50% of rats (UDso) > 20 mg/kg orally] than indomethacin (UDso = 1.6 mg/kg orally) and, in contrast to indomethacin, to affect prostaglandin E2 (PGE2) [dinoprostone] and thromboxane A2 (TXA2) formation more potently in inflammatory exudate than in the gastric mucosa in rats.After administration for 3 consecutive days, nimesulide in doses of up to 9 mg/kg orally (about 7 times the anti-inflammatory dose in the carrageenan rat paw oedema assay) did not modify renal function parameters or urinary PGE2 concentrations. In contrast, indomethacin caused a significant increase in blood urea and urinary N-acetyl-~-glucosaminidase and proteins at doses of 9 mg/kg orally (about 3 times the anti-inflammatory dose in the carrageenan rat paw oedema assay), and also significant inhibition of urinary PGE2 concentrations at doses of 3 and 9 mg/kg orally.These results, which have been confirmed by clinical data, suggest that nimesulide has good gastric and renal tolerability.Nonsteroidal anti-inflammatory drugs (NSAIDs) are a chemically heterogeneous group of compounds, mostly organic acids, that mediate their anti-inflammatory effects largely through inhibition of prostaglandin (PG) synthesis, although other mechanisms also contribute to their clinical effectiveness. However, these drugs are known to induce a number of unwanted effects including inhibition of haemostasis (Dukes 1988; Flower et al.

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