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The tolerance of the gastric mucosa to a new anti-inflammatory product, ketoprofen (19.583 R.P., Orudis, Profenid N.D.) was compared to the tolerance of acetylsalicylic acid in a double-blind cross-over trial using selected healthy volunteers. The effect of the medication on the gastric mucosa was examined by the use of a gastrocamera technique. The volunteers received during 2 one-week periods either acetylsalicylic acid 3 g daily or ketoprofen 100 mg daily. The sequential diagram shows that the upper barrier was crossed (preference for ketoprofen) when 10 volunteers had been analysed.

In a 4-week double-blind multi-crossover trial 12 healthy volunteers received 1-week treatment with aspirin (3.6 g daily) and 1-week treatment with ketoprofen (200 mg daily). Before and after each active drug treatment the volunteers received 1-week of placebo treatment. The gastrointestinal blood loss was quantitatively determined by use of the radioactive chromiun (Cr51) technique. It is concluded that the gastrointestinal blood loss during the ketoprofen treatment was significantly less than during the aspirin period but significantly greater than during the placebo periods.

Ketoprofen possesses the typical pharmacological properties of non-steroidal anti-inflammatory agents i.e. anti-inflammatory, analgesic and antipyretic activity, as well as antibradykinin activity and ability to inhibit prostaglandin synthesis. Ketoprofen is as potent as indomethacin in the tests for anti-inflammatory and analgesic activity, but its antipyretic and antibradykinin activities and its inhibitory activity against prostaglandin synthesis is respectively 4, 8 and 8 times greater than that of indomethacin. It seems very likely that the pituitary-adrenal axis is not involved in the mechanism of the anti-inflammatory action of ketoprofen, since in the carrageenan abscess test, the compound shows the same activity both in adrenalectomized and in normal rats and, when locally applied to the inflamed area, it is more active than when administered systemically. In the mouse the acute oral toxicity of ketoprofen is about one twentieth that of indomethacin. Like all powerful steroidal or non-steroidal antiinflammatory agents, ketoprofen shows some gastrointestinal toxicity, but its effect is mild and distinctly less than that of indomethacin. Pharmacokinetic studies in the rat, dog and monkey have shown that gastro-intestinal absorption of the drug is rapid and almost complete; the compound and its metabolites are excreted from the body fairly rapidly.