Cholecystokinin receptors (CCK1 and CCK2, a.k.a. CCK-A and CCK-B respectively) are activated by gastrin as well as by cholecystokins (CCK) CCK-4; CCK-8; and CCK-33. Activation of these receptors evokes secretion of amylase by pancreatic acinar cells, acid and pepsin by stomach mucosal cells, and contraction of the pylorus and galbladder. Several CCK-A (CCK1) antagonists have been developed over the years for the treatment of stomach ulcers (Proglumide, Lorglumide, and Devazepide), but also for their potential as drugs to limit the development of gastrointestinal cancers such as colon cancer. However, by far the main focus of CCK antagonist research has focused on the development of selective CCK-B antagonists as novel medications which have been primarily investigated for the treatment of anxiety and panic attacks, as well as for other roles such as analgesic effects, sexual behavior, learning, and memory.
 SelectiveCCK-A but notCCK-B receptor antagonists inhibit HT-29 cell proliferation: synergism with pharmacological levels of melatonin. C. González-Puga et al. J. Pineal Res. 2005, 39, 243-250.
 The CCKB antagonist CI988 reduces food intake in fasted rats via a dopamine mediated pathway. L. Frommelt. Peptides, 2013, 39, 111-118.