Studies on the mechanism of action of cetraxate [4'-(2-carboxyethyl)phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride], a new anti-ulcer agent.

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Abstract
To elucidate mechanisms involved in the anti-ulcer action of cetraxate [4''-(2-carboxyethyl)phenyl trans-4-amino methyl cyclohexane carboxylate hydrochloride], the effects of this agent on the ulcer index (UI), fibrinolytic activity (FA) and contents of several connective tissue components in ulcer tissue were examined using aspirin and acetic acid ulcers in rats. In aspirin ulcers, cetraxate (100 and 300 mg/kg p.o. [per os]), like tranexamic acid (500 mg/kg p.o.), .epsilon.-aminocaproic acid (500 mg/kg p.o.) and gefarnate (200 mg/kg p.o.), inhibited both the UI and FA. Aluminum sucrose sulfate (1000 mg/kg p.o.) was effective only against the UI and L-glutamine (500 mg/kg p.o.) and failed to inhibit both parameters. In acetic acid ulcers, after oral, daily .times. either 5 or 8 administrations, cetraxate (200 and 300 mg/kg), gefarnate (200 mg/kg), aluminum sucrose sulfate (1000 mg/kg) and L-glutamine (500 mg/kg) were effective on both the UI and FA. Tranexamic acid (500 mg/kg) and .epsilon.-aminocaproic acid (500 mg/kg) were ineffective on the UI, but both agents inhibited FA. In acetic acid ulcers, cetraxate induced increases in hexosamine and uronic acid, e.g., acid mucopolysaccharides (AMPS), especially chondroitin sulfate A and -C, but L-glutamine and aluminum sucrose sulfate caused increases in hexosamine and sialic acid, e.g., glycoproteins. Cetraxate may mainly accelerate the ulcer healing by increasing AMPS in ulcer tissue. The local anti-FA property of this agent may be beneficial in treating bleeding ulcers.