Lintitript inhibited the CCK 2 site in guinea pig cortex with an IC2 of 479 nM. lintitript (0.5 nM) increased the dissociation constant of CCK on CCKA receptors with Kds between 1.8 and 7.2 nM without altering the maximum number of receptors. lintitript antagonized CCK-stimulated isolated rat pancreatic follicles in (amylase release and CCK-induced gallbladder contraction in guinea pigs with pA2s of 7.50 and 9.57). lintitript inhibited the binding of [125I]CCK to the rat pancreatic CCK1 receptor site with IC50 of 0.58 nM in a concentration-dependent manner[1].

Lintitript (1 mg/kg, i.v.) completely reversed CCK-induced amylase secretion. lintitript inhibited CCK-induced gastric and gallbladder emptying in mice with ED50s of 3 μg/kg and 72 μg/kg. lintitript (p.o.) was active in the gallbladder emptying protocol of egg yolk-induced endogenous CCK release, with an ED50 of 27 μg/kg [1].