The effects of a new glutaramic acid derivative, 3,4-dichloro-benzamido-N, N-dipentyl-glutaramic acid (CR-1409), on cholecystokinin-stimulated amylase release and 125I-cholecystokinin octapeptide binding were studied in isolated rat pancreatic acini. CR-1409 at concentrations between 0.3 and 30 microM inhibited cholecystokinin-stimulated amylase release in a dose-dependent manner without appreciable effect on the basal amylase secretion. Biphasic dose-response curves to cholecystokinin for amylase release shifted to the right with an increase in the concentration of the drug. IC50 (half-maximal inhibitory concentration) of CR-1409 for cholecystokinin-stimulated amylase release was 0.64 microM, and the potency of this drug on the inhibition of amylase release was 3400 times greater than that of proglumide. The effect of CR-1409 was rapid, reversible, and selective for cholecystokinin. In addition, CR-1409 at concentrations between 0.1 and 30 microM inhibited 125I-cholecystokinin octapeptide binding to rat pancreatic acini. IC50 of CR-1409 for 125I-cholecystokinin octapeptide binding was 0.22 microM, and the potency of this drug on the effect was 5900 times greater than that of proglumide.