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Metabolic & GLP-1 · Reference monograph

Gut hormone regulating bile flow, pancreatic enzymes and satiety

Reference compound — not available from Purity Peptides. Shown for research context.

Overview

Cholecystokinin (CCK) is a peptide hormone and neurotransmitter produced by I-cells of the duodenum and jejunum and by neurons throughout the brain, where it is among the most abundant neuropeptides. It was discovered in 1928 by Andrew Ivy and Eric Oldberg as a gut factor that contracts the gallbladder. A separate activity that stimulated pancreatic enzyme secretion, named pancreozymin in 1943, was later shown to belong to the same molecule.

CCK circulates in several lengths, including CCK-58, CCK-33 and CCK-8, all sharing the same C-terminal sequence; sulfation of a tyrosine residue near the C-terminus is critical for activity at the CCK1 receptor. In 1973, Gerard Smith, James Gibbs and colleagues showed that CCK reduced meal size in rats, making it the first gut hormone identified as a satiety signal. Sincalide, a synthetic form of CCK-8, is an approved diagnostic agent in the United States, used in hepatobiliary imaging and gallbladder function studies. Research uses of CCK span digestion, gallbladder physiology, satiety, anxiety models and the gut-brain axis.

Mechanism studied

  1. Duodenal I-cells
  2. CCK
  3. Gallbladder & pancreas
  4. Early satiety

CCK acts on two G protein-coupled receptors. The CCK1 receptor, formerly CCK-A, binds sulfated CCK with high affinity and is found on gallbladder smooth muscle, pancreatic acinar cells in rodents, vagal afferent neurons and some brain regions. CCK2, formerly CCK-B, is identical to the gastrin receptor, binds sulfated and non-sulfated CCK and gastrin, and predominates in the brain and stomach. Both receptors couple mainly to Gq, stimulating phospholipase C and calcium signalling. Gallbladder contraction and sphincter of Oddi relaxation promote bile delivery. Satiety effects largely depend on CCK1 receptors on vagal afferents relaying to the nucleus of the solitary tract.

Research highlights

  • 01Discovered in 1928 through gallbladder contraction; unified with pancreozymin once both activities were traced to one peptide.
  • 02The 1973 rat studies by Gibbs, Young and Smith established CCK as a prototypical meal-ending satiety signal.
  • 03The fragment CCK-4 has been used in human experimental medicine to provoke panic-like symptoms, linking CCK2 receptors to anxiety research.
  • 04Sincalide, synthetic CCK-8, is used diagnostically to assess gallbladder ejection during hepatobiliary imaging.
  • 05Open questions include why CCK1 receptor agonists did not translate into durable effects on body weight in clinical research.

Latest published research

47,744 papers on PubMed →

  1. Anti-breast cancer effects of the Xingxiao Pill are associated with inhibition of the ErbB3/PI3K/AKT/mTOR pathway, modulation of amino acid metabolism, and promotion of apoptosis

    Zhang J et al. · Journal of ethnopharmacology · 2027 Jan 30 · PMID 42648410

  2. CYP2C19-mediated metabolic activation and OAT3/P-gp-associated transport contribute to Dioscorea bulbifera L.-induced hepatotoxicity

    Tian Y et al. · Journal of ethnopharmacology · 2027 Jan 30 · PMID 42556633

  3. Yishen Tongluo formula regulates apoptosis and autophagy in testicular spermatogenic cells of oligoasthenozoospermic rats via the AMPK/mTOR pathway

    Chen Y et al. · Journal of ethnopharmacology · 2027 Jan 10 · PMID 42486454

  4. Transcription factor CTCF activates KIAA1199 expression to inhibit ferroptosis and promote malignant behaviors in colorectal cancer based on bioinformatics and machine learning

    Fan X et al. · Gene · 2027 Jan 5 · PMID 42858932

  5. PD-1 expression reprograms tumor-associated macrophages polarization and influences progression and clinical outcomes in lung adenocarcinoma

    Deng L et al. · Gene · 2027 Jan 5 · PMID 42838248

  6. Study on the molecular mechanism of bone marrow mesenchymal stem cells inducing epithelial-mesenchymal transition in HPV-associated cervical cancer through activation of miR-129

    Ma N et al. · Pakistan journal of pharmaceutical sciences · 2027 Jan 1 · PMID 42929419

  7. P4HA3 promotes gastric cancer cell proliferation and invasion via the PI3K/AKT/mTOR signaling pathway and regulates glycolytic metabolic reprogramming

    Wang T et al. · Pakistan journal of pharmaceutical sciences · 2027 Jan 1 · PMID 42929411

  8. LINC01116 promotes the progression of papillary thyroid carcinoma by regulating the apoptosis of bone marrow mesenchymal stem cells

    He H et al. · Pakistan journal of pharmaceutical sciences · 2027 Jan 1 · PMID 42929403

Live feed from PubMed (NCBI) for “Cholecystokinin (CCK)”, updated 2026-10-30. Listing a paper is not an endorsement of its findings.

Registered studies

58 on ClinicalTrials.gov →

From the public ClinicalTrials.gov registry for “Cholecystokinin (CCK)”, updated 2026-10-30. Shown for research context only; Purity Peptides products are not for human use.

Key references

  1. [1]Manufacturer's prescribing information — FDA / EMA / ANVISA
  2. [2]PubMed — reviews on cholecystokinin and satiety

FAQ

  • In 1943, Harper and Raper described a duodenal factor that stimulated pancreatic enzyme secretion and named it pancreozymin. Later purification by Mutt and Jorpes showed that cholecystokinin and pancreozymin were the same peptide, and the name cholecystokinin was retained.

  • Sincalide is the synthetic C-terminal octapeptide of CCK, equivalent to CCK-8. It is approved in the United States as a diagnostic agent to stimulate gallbladder contraction and pancreatic secretion during imaging and laboratory assessment. In research it serves as a stable CCK1 receptor agonist.

  • CCK1 receptors are selective for sulfated CCK and mediate gallbladder contraction, pancreatic secretion in rodents and vagal satiety signals. CCK2 receptors bind CCK and gastrin equally, mediate gastric acid regulation and are widely expressed in the brain, where they are linked to anxiety and memory.

FOR RESEARCH USE ONLY.Not for human or veterinary use. Not intended to diagnose, treat, cure, or prevent any disease.

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