What is Cholecystokinin (CCK)?

Triggers gallbladder contraction, pancreatic enzymes, and satiety. Structurally it is Gut peptide (multiple active lengths, e.g. CCK-8).

How strong is the evidence for CCK?

PeptideHormone grades CCK at the "Established" evidence tier — its mechanism and core effects are settled across the peer-reviewed literature. It is catalogued as an endogenous signal the body produces itself, and the tier is an editorial judgment about the public literature that can change as the science does.

What is the half-life of CCK?

The reported circulating half-life of CCK is ~1–2.5 min.

CholecystokininCCK

Triggers gallbladder contraction, pancreatic enzymes, and satiety.

EndogenousEstablished

One signal coordinating gallbladder, pancreas, and appetite at once. Economy, not specialisation, is the organising principle here.

Identity

Class: Gut peptide (multiple active lengths, e.g. CCK-8)
Source: Duodenal I-cells (and CNS neurons)
Receptor: CCK1 (gut) and CCK2 (CNS) receptors

Key properties

Evidence floorClinicalREF1CLIN1

Molecular weight

≈ 1,143.3 Da

REF

Half-life (native)

~1–2.5 min

CLIN

Model dosing

Approximate values for the native hormone; engineered analogs are often deliberately larger and far longer-acting. Each figure carries its own provenance tier, and the floor is the weakest of them - the Standard.

Mechanism

Released in response to dietary fat and protein, CCK stimulates gallbladder contraction and pancreatic enzyme secretion and signals satiety. Its peripheral (CCK1) and central (CCK2) receptors separate its digestive and neural roles.

Reference notes

CCK couples nutrient sensing to the mechanics of digestion (bile and enzymes).
CCK1 vs CCK2 distribution splits its digestive and central effects.
It was one of the earliest gut peptides linked to meal-ending satiety.

Common questions

What is Cholecystokinin (CCK)?: Triggers gallbladder contraction, pancreatic enzymes, and satiety. Structurally it is Gut peptide (multiple active lengths, e.g. CCK-8).
How does CCK work?: Released in response to dietary fat and protein, CCK stimulates gallbladder contraction and pancreatic enzyme secretion and signals satiety. Its peripheral (CCK1) and central (CCK2) receptors separate its digestive and neural roles.
How strong is the evidence for CCK?: PeptideHormone grades CCK at the "Established" evidence tier — its mechanism and core effects are settled across the peer-reviewed literature. It is catalogued as an endogenous signal the body produces itself, and the tier is an editorial judgment about the public literature that can change as the science does.
What is the half-life of CCK?: The reported circulating half-life of CCK is ~1–2.5 min.

Selected literature

Curated peer-reviewed reviews, sourced from PubMed. Selected for relevance, not exhaustive — open any entry on PubMed for the full record and its primary citations.

1.Role of cholecystokinin in satiation: a systematic review and meta-analysis · The British journal of nutrition, 2023 · PMID 35152916
2.Cholecystokinin · Current opinion in endocrinology, diabetes, and obesity, 2007 · PMID 17940422

External references

CCK in the public knowledge graph — the same entity resolved across the authoritative chemistry and protein databases.