Research compounds
Cholecystokinin
CCK, sincalide
Cholecystokinin is a gut hormone released after fat and protein ingestion, causing gallbladder contraction, pancreatic enzyme secretion and satiety. A synthetic fragment, sincalide, is FDA-approved as a diagnostic agent.
Also known as: sincalide, Kinevac, CCK-8, cholecystokinin octapeptide
- Status
- Cholecystokinin is approved by the U.S. FDA and has official prescribing information.
- Evidence
- Approved labeling. Official prescribing information exists, based on clinical trials in people.
- Half-life
- Approximately 2.5 minutes for sincalide.
- How it's taken
- Intravenous injection in a diagnostic setting
- Mechanism
- Metabolic (non-incretin)
How Cholecystokinin works
CCK is released from duodenal I cells and acts at CCK-A receptors on the gallbladder and pancreas and CCK-B receptors in the brain. Peripherally it contracts the gallbladder and stimulates pancreatic enzyme release; via vagal afferents it produces meal-related satiety. The C-terminal octapeptide carries full activity, which is what sincalide reproduces.
What research has looked at
- Sincalide is FDA-approved to stimulate gallbladder contraction for imaging and to assess gallbladder ejection fraction.
- CCK is one of the best-characterised endogenous satiety signals, and its vagal afferent mechanism explains meal termination.
- It is used diagnostically to stimulate pancreatic secretion during function testing.
Evidence level: Approved labeling. Official prescribing information exists, based on clinical trials in people. These are areas studied or reported, not promised effects.
Reported side effects and risks
- CCK-based agents failed as obesity therapies: the satiety effect is short-lived, tachyphylaxis develops rapidly, and doses producing meaningful appetite suppression cause nausea and abdominal cramping.
- Sincalide commonly causes abdominal pain, nausea and diarrhea during the diagnostic procedure.
- CCK-B receptor activation in the brain is anxiogenic and has been used experimentally to provoke panic attacks — an effect directly opposed to what a consumer seeking appetite control would want. No regulator has approved it, the human evidence base is limited, and material sold under this name is research chemical supply with unverified identity, purity, sterility and dose accuracy.
- Native CCK is degraded within minutes.
Sources
- FDA approved-drug listing for sincalide · U.S. Food & Drug Administration
- DailyMed prescribing information for sincalide · NIH · DailyMed
- PubMed research on cholecystokinin sincalide gallbladder satiety · NIH · National Library of Medicine
- DrugBank record for sincalide · DrugBank
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Cholecystokinin FAQ
What is Cholecystokinin?
Cholecystokinin is a gut hormone released after fat and protein ingestion, causing gallbladder contraction, pancreatic enzyme secretion and satiety. A synthetic fragment, sincalide, is FDA-approved as a diagnostic agent.
How does Cholecystokinin work?
CCK is released from duodenal I cells and acts at CCK-A receptors on the gallbladder and pancreas and CCK-B receptors in the brain. Peripherally it contracts the gallbladder and stimulates pancreatic enzyme release; via vagal afferents it produces meal-related satiety. The C-terminal octapeptide carries full activity, which is what sincalide reproduces.
Is Cholecystokinin FDA approved?
Yes. Cholecystokinin is approved by the U.S. FDA and has official prescribing information. Evidence level: approved labeling. Official prescribing information exists, based on clinical trials in people.
What is the half-life of Cholecystokinin?
Reported half-life: Approximately 2.5 minutes for sincalide.
How is Cholecystokinin taken?
Intravenous injection in a diagnostic setting.
What side effects have been reported with Cholecystokinin?
Reported in the sources: CCK-based agents failed as obesity therapies: the satiety effect is short-lived, tachyphylaxis develops rapidly, and doses producing meaningful appetite suppression cause nausea and abdominal cramping; Sincalide commonly causes abdominal pain, nausea and diarrhea during the diagnostic procedure; CCK-B receptor activation in the brain is anxiogenic and has been used experimentally to provoke panic attacks — an effect directly opposed to what a consumer seeking appetite control would want. No regulator has approved it, the human evidence base is limited, and material sold under this name is research chemical supply with unverified identity, purity, sterility and dose accuracy; Native CCK is degraded within minutes.
Educational summary compiled from the sources listed above. Not medical advice. Peptide Vault does not sell, source or recommend any compound. Talk to a qualified clinician before starting or changing anything.