Peptides›Cognitive, Metabolic›Cholecystokinin-33

Cholecystokinin-33

/ Endogenous 33-residue gut peptide; CCK-A and CCK-B receptor agonist; full-length form (the 8mer sincalide is the synthetic clinical analog)

TIER 3 · PreclinicalN = 0 · TESTING PENDINGMW 3866.00 g·mol⁻¹

ALIAS · CCK-33 · Cholecystokinin (33-residue form)

—

Pass rate

Samples

Suppliers

Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

Terms in this page you can click for a plain-English popup: , , , , , , , .

§ A · Identity

Primary sequenceKAPSGRVSMIKNLQSLDPSHRISDRDYMGWMDF (sulfated Tyr; C-terminal amidated)

MW · 3866.00CLASS · Endogenous 33-residue gut peptide; CCK-A and CCK-B receptor agonist; full-length form (the 8mer sincalide is the synthetic clinical analog)CATEGORY · Cognitive, Metabolic

Tier 3. CCK-33 is the foundational endogenous gut peptide for the cholecystokinin family; the synthetic 8mer sincalide (Kinevac) is the FDA-approved clinical analog used for gallbladder imaging and pancreatic function testing. CCK-33 itself has extensive preclinical pharmacology but is not a marketed therapeutic.

§ B · Mechanism of action

Cholecystokinin is released from intestinal I cells in response to luminal fat and protein and acts at two G-protein-coupled receptors: CCK-A (predominantly peripheral — gallbladder smooth muscle, pancreatic acinar cells, vagal afferents) and CCK-B (predominantly central nervous system, also gastric parietal cells where it is shared with gastrin). Sulfation of the tyrosine seven residues from the C-terminus is required for full CCK-A potency. Peripheral CCK-33 release drives gallbladder contraction, pancreatic enzyme secretion, and vagally mediated satiety signalling.

§ C · Human clinical evidence

Tier 3 for CCK-33 itself. The synthetic 8mer sincalide is approved (Kinevac) for cholecystokinetic and pancreatic-function diagnostic use. CCK-33 has been administered in research settings to characterise satiety, gallbladder, and anxiety-related endpoints but is not a clinical product.

§ D · Primary literature

PubMed28450850Rehfeld JF et al. — Cholecystokinin-From Local Gut Hormone to Ubiquitous Messenger · Frontiers in Endocrinology · reviewComprehensive review of CCK biology covering molecular forms (CCK-83, -58, -39, -33, -22, -8), tissue-specific processing, receptor pharmacology, and physiological roles across gut, pancreas, and CNS.Limitations: Narrative review; expert synthesis not systematic.2017

PubMed9074762Liddle RA et al. — Cholecystokinin cells · Annual Review of Physiology · reviewFoundational review of intestinal I cell biology, CCK release mechanisms, and the regulatory role of CCK in pancreatic exocrine secretion and gallbladder contraction.Limitations: Pre-2000 review; subsequent receptor and processing detail elaborated in later literature.1997

§ F · Safety signal

Acute infusion of CCK in research settings has been generally well tolerated. CCK-B receptor agonism (notably by CCK-4) is a recognised experimental panicogen — relevant to research design in anxiety pharmacology but not to peripheral CCK-33 satiety studies at low doses.

§ H · Regulatory status

Regulatory status

FDA status:: Not FDA-approved

§ I · Notable gaps and controversies

Vendor 'CCK-33' is sold as a research chemical without identity or sulfation-state characterisation. Non-sulfated CCK-33 has substantially reduced CCK-A receptor potency, and vendor preparations rarely report sulfation status. Translational claims for satiety or weight management based on CCK biology should be read as referring to the broader CCK-receptor pharmacology, of which CCK-33 itself is a research tool rather than a clinical agent.