text: A<unk>  is a specific type of receptor<unk>  which blocks the receptor sites for the peptide hormone<unk>  (CCK).
  There are two subtypes of this receptor known at present, defined as CCKA and CCKB (also called CCK-1 and CCK-2). CCKA is mainly expressed in the small intestine, and is involved in the regulation of enzyme secretion by the pancreas, secretion of gastric acid in the stomach, intestinal motility and signaling of satiety (fullness). CCKB is expressed mainly in the central nervous system, and has functions relating to anxiety and the perception of pain.<unk> s for the CCK receptors can thus have multiple functions in both the gut and brain.
  The best known CCK<unk>  is the non-selective<unk>  proglumide, which blocks both CCKA and CCKB, and was originally developed for the treatment of stomach ulcers. This action derived from its blockade of CCKA in the gut and consequent reduction in secretion of gastric acid, however an interesting side effect of proglumide was found, namely that it increases the analgesic effects of opioid painkillers, and decreases the development of tolerance. This was subsequently found to result from its blockade of CCKB receptors in the brain.
  Newer drugs have since been developed which are selective for one or other of the CCK receptors. Selective CCKA<unk> s such as lorglumide and devazepide have been developed both for their anti-ulcer effects and as potential drugs to limit the development of gastrointestinal cancers such as colon cancer.
  However by far the main focus of CCK<unk>  research has focused on the development of selective CCKB<unk> s 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. The first selective CCKB<unk> s were peptide molecules such as CI-988 and the more metabolically stable CI-1015, however these were disadvantaged by only being able to be administered by injection and rapid breakdown inside the body, which led to a short half-life and limited utility. Non-peptide CCKB<unk> s such as L-365,260, YF-476, RP-69758, LY-288,513, PD-145,942 and the CCKB inverse agonist L-740,093 have since been developed, and while all of the drugs developed so far have suffered from limited bioavailability or other issues which have hindered their clinical development, research in this area continues.
  CCKA receptors are also expressed in the brain to some extent, and interestingly IQM-95333, an<unk>  selective for this population of CCKA receptors, was also found to reduce anxiety in animal models. Conversely, inhibition of CCKB receptors in the gut produces similar inhibition of secretion of gastric acid and pepsinogen enzymes as is seen with inhibition of CCKA receptors, suggesting that while the CCKA and CCKB receptors comprise two structurally distinct families which bind different ligands and are primarily expressed in different tissues, they produce similar effects, and the distinction between their gastrointestinal and anxiolytic actions depends mainly on where they are expressed in the body.
option_0: Cholecystokinin antagonist
option_1: H₂-receptor antagonist
option_2: Serotonin antagonist
option_3: Glucagon-like peptide-1 analog
option_4: Muscarinic antagonist
option_5: Muscarinic agonist
option_6: Dopamine agonist
option_7: Alpha-adrenergic agonist