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Cholecystokinin (CCK-8)8 residuesDYMGWMDFEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: CCK-8S, CCK-8, sincalide
Your body already makes CCK-8 every time you eat fat or protein. This sulfated octapeptide fires from duodenal I-cells and tells your brain to stop eating, usually within minutes. Cholecystokinin (CCK-8) is one of the strongest short-term satiety signals in human physiology, and its synthetic twin sincalide (Kinevac) has been FDA-approved since 1976 for gallbladder imaging. The catch: a plasma half-life of 2 to 5 minutes makes it nearly useless outside a clinical IV setting. Researchers still study it to understand appetite regulation and gut-brain signaling, but nobody is pinning this one at home.
A single IV infusion of CCK-8 can cut meal size by 20 to 30 percent in healthy adults. That finding, confirmed by Drewe and colleagues in a controlled human study [1], captured what the gut already knew: cholecystokinin is the body's fastest brake on eating. CCK-8 (also called CCK-8S for its sulfated form; CAS 25126-32-3) is the most bioactive circulating fragment of the 33-amino-acid hormone cholecystokinin, first isolated from porcine intestinal mucosa in the 1960s. Duodenal and jejunal I-cells release it within minutes of detecting dietary fat and protein. It locks onto CCK1 receptors on vagal nerve endings and sends satiety signals straight to the brainstem. Simultaneously, it contracts the gallbladder, pumps pancreatic enzymes, and slows gastric emptying. Think of it as a coordinated digestive and satiety broadcast that peaks in under 15 minutes and vanishes in under five. The synthetic version, sincalide (Kinevac), received FDA approval in 1976 for gallbladder ejection fraction testing. Radiologists still use it daily. Native CCK-8 has no therapeutic approval; its 2 to 5 minute half-life and IV-only validated route make chronic dosing impractical. Rehfeld's 2025 review [2] confirmed that current obesity research has shifted toward protease-resistant CCK1-selective analogs rather than native CCK-8. Community use is nonexistent: zero Reddit threads, zero biohacker protocols, zero self-administration reports exist anywhere online.
CCK-8 binds two G-protein-coupled receptor subtypes. CCK1 receptors sit mostly in the periphery: gallbladder smooth muscle, pancreatic acinar cells, and vagal afferent nerve terminals lining the stomach and duodenum. CCK2 receptors concentrate in the central nervous system. When CCK-8 docks with either receptor, it kicks off a Gq/11 signaling cascade. Phospholipase C generates IP3 and DAG. IP3 releases calcium from the endoplasmic reticulum; DAG activates protein kinase C. In pancreatic acinar cells, that calcium surge triggers exocytosis of zymogen granules packed with digestive enzymes. In gallbladder smooth muscle, the same cascade produces contraction and bile ejection. The satiety pathway runs through CCK1 receptors on vagal afferent nerve endings. Receptor activation fires action potentials up the vagus nerve to the nucleus tractus solitarius in the brainstem. From there, signals relay to hypothalamic feeding centers to suppress appetite and terminate meals. CCK-8 also slows gastric emptying through both vagal reflexes and direct smooth muscle action, keeping nutrients in contact with absorptive epithelium longer. In the brain, CCK-8 modulates dopaminergic, serotonergic, and GABAergic neurotransmission. The closely related fragment CCK-4 is a validated panicogenic agent in human studies; CCK-8 has weaker anxiogenic properties through CCK2 receptors. Some tissues also see adenylyl cyclase activation via Gs coupling, raising cAMP and activating protein kinase A.
CCK-8 is a validated endogenous satiety hormone with strong IV human evidence for meal termination, gallbladder contraction, and gastric emptying delay. Its 2-5 min half-life makes it impractical as a therapeutic agent. All validated human administration is IV only. The FDA-approved synthetic equivalent (sincalide/Kinevac) is approved solely for diagnostic gallbladder imaging since 1976.
Drewe J et al. Am J Physiol Endocrinol Metab 2009; PMID 18957613: dose-dependent effects of CCK-8 on antropyloroduodenal motility, GI hormones, appetite, and energy intake in healthy men (gold-standard human pharmacodynamic study)
All validated human data is IV only. No SC bioavailability data in humans. No approved obesity or therapeutic indication for native CCK-8. Extremely short half-life precludes sustained effect. Tachyphylaxis with repeated use via CCK1 receptor desensitization. 2025 research interest has shifted toward long-acting CCK1-selective analogs (not native CCK-8).
No community use exists. Zero Reddit threads on r/peptides or r/Nootropics, zero biohacker protocols, zero self-administration reports found. IV-only validated route and 2-5 min half-life create insurmountable practical barriers. No recreational, anabolic, or nootropic appeal.
No community use exists for CCK-8. Scientific evidence for its endogenous role is strong; evidence for exogenous therapeutic application is limited to research settings with IV administration. The compound has no biohacker or self-optimization profile.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 1mcg | Single dose |
| Moderate | 2mcg | Single dose |
| Aggressive | 4mcg | Single dose |
CCK-8 is not a typical research peptide. All validated human dosing is intravenous, and most people encounter it only as sincalide (Kinevac) during a gallbladder imaging study. Source from established biochemical suppliers only: Tocris (Cat# 1166), Bachem (4033010), or Cayman Chemical (23371). Do not use gray-market peptide vendors for anything going IV. You need the sulfated form (CCK-8S). The sulfated tyrosine at position 7 is required for full CCK1 receptor potency; the non-sulfated version has roughly 1000-fold lower affinity. If satiety and gallbladder effects don't materialize, wrong form is the first thing to check. Confirm on the Certificate of Analysis before ordering. Reconstitution math for a 1 mg vial: add 2 mL bacteriostatic water to get 500 mcg/mL. A 2.8 mcg dose (0.04 mcg/kg for a 70 kg adult) comes to 0.0056 mL, which is 0.56 units on a U-100 insulin syringe. These volumes are extremely small, so research protocols dilute the stock into 50 mL normal saline for controlled IV infusion. Store lyophilized powder at -20C desiccated. Reconstituted solution goes at 2 to 8C, use within 7 days. The sulfate ester hydrolyzes at room temperature.
Due to its extremely short half-life and rapid clearance, CCK-8 does not accumulate significantly and tachyphylaxis is the primary concern with continuous dosing. Research protocols typically employ intermittent administration around meals rather than continuous cycling. Extended use may lead to CCK1 receptor desensitization, supporting periodic breaks in administration.
CCK1 receptor desensitization occurs with continuous or repeated high-frequency CCK-8 exposure via β-arrestin-mediated receptor internalization. Vagal afferent CCK1 receptors on gastric and duodenal mucosal terminals show reduced sensitivity with sustained stimulation. In research settings, intermittent per-meal administration is standard, not continuous daily cycling. The 4-on/2-off cycling protocol in peptides.ts is loosely derived from this principle but has no published human research precedent for repeated daily dosing.
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Expected: Reduced meal size (~20-30% decrease in energy intake at validated doses), prolonged intermeal interval, gallbladder volume reduction 40-70%, delayed gastric emptying
Monitor: Monitor HR, BP, and GI symptoms (nausea, abdominal cramping, urge to defecate) throughout infusion. Have epinephrine available: anaphylaxis risk from sulfite preservatives in some formulations. Verify gallbladder anatomy by ultrasound before use.
Verify the peptide is CCK-8 sulfated (CCK-8S) with HPLC purity of 98 percent or higher and confirmed molecular weight of 1143.25 Da on the CoA.
For a 1 mg vial, add 2 mL bacteriostatic water to produce a 500 mcg/mL stock solution. Swirl gently; do not shake. Solution should be clear and colorless.
Standard research range is 0.02 to 0.04 mcg/kg IV. For a 70 kg person, that is 1.4 to 2.8 mcg. At 500 mcg/mL, 2.8 mcg equals 0.0056 mL, roughly 0.56 units on a U-100 insulin syringe.
Dilute the withdrawn dose into 50 mL of 0.9 percent normal saline for IV infusion. Direct bolus injection dramatically increases nausea and abdominal cramping. This dilution step is not optional.
Begin the infusion 15 to 30 minutes before meal initiation if studying satiety effects.
Monitor heart rate and blood pressure continuously throughout the infusion and for 15 minutes after completion. Have epinephrine available for anaphylaxis risk from preservatives. Stop immediately for severe abdominal pain, HR below 50 bpm, or systolic BP below 90 mmHg.
Needle gauge: use a 27 to 30 gauge needle for drawing from the vial. IV administration requires appropriate IV access.
Discard after 7 days. Keep lyophilized vials at -20C, protected from light and moisture. Aliquot and freeze at -20C to avoid repeated freeze-thaw cycles.
No human SC bioavailability data available. SC bioavailability likely very low: CCK-8 is rapidly cleaved by plasma peptidases (t½ = 2-5 min IV) and subcutaneous peptidase activity would similarly degrade the peptide before systemic absorption. No dose-equivalency data exists.
P0 SAFETY FLAG: peptides.ts lists SC as a valid administrationRoute, but ALL human dosing data is IV-derived. The FDA-approved sincalide (Kinevac) is IV-only per label. SC use for CCK-8 is not validated and should not be assumed equivalent to IV.
Essentially zero systemic bioavailability via oral route: GI proteases degrade the octapeptide entirely before absorption. This is why the body uses endogenous I-cell CCK secretion rather than circulating CCK from oral intake.
Dietary proteins and fats trigger endogenous CCK release from intestinal I-cells: this is the physiological equivalent of "oral CCK supplementation" and is not replicable by ingesting exogenous CCK-8.
Bidirectional antagonism: opioids inhibit gallbladder contraction peripherally (biliary spasm, elevated sphincter of Oddi tone). CCK-8 also opposes opioid analgesia centrally via CCK2 receptor activation in the spinal cord and brain: reducing opioid analgesic efficacy (PMID 1982023). Interaction is clinically relevant in both directions.
Do not combineBlock the downstream parasympathetic pathway through which CCK-8 exerts gallbladder contraction and GI motility effects. Substantially attenuate or abolish efficacy of CCK-8 administration.
Somatostatin inhibits CCK release from duodenal I-cells and suppresses downstream GI responses, opposing satiety and motility effects of exogenous CCK-8.
Same mechanism as native somatostatin: inhibit CCK secretion and blunt GI motility responses. Listed separately because octreotide is commonly used and not in database as a peptide stacking candidate.
Pricing updated 2026-04-09
The most serious documented risk with CCK-8 is anaphylaxis. Post-marketing surveillance of sincalide (Kinevac) has recorded anaphylactic shock attributed to sodium metabisulfite preservative in some formulations (KINEVAC FDA label, DailyMed). This is rare but potentially fatal, and epinephrine must be available during any administration. Gallbladder-related complications deserve equal weight. CCK-8 causes forceful gallbladder contraction. In patients with undiagnosed gallstones, this can dislodge stones into the cystic or common bile duct. The result can be biliary colic, cholangitis, or acute pancreatitis. This is a hard contraindication, not a precaution. Abdominal ultrasound before any CCK-8 use is mandatory. At standard diagnostic IV doses, the most common adverse effects are abdominal discomfort and nausea, occurring in over 20 percent of subjects. Higher or bolus doses amplify gastrointestinal symptoms considerably: cramping, vomiting, diarrhea, and a sudden urge to defecate from increased intestinal motility. Slow IV infusion over 30 to 50 minutes dramatically reduces these effects compared to bolus injection. Skipping the dilution step is the single most common cause of protocol failure. Cardiovascular effects include bradycardia and transient hypotension via vasovagal activation. Heart rate should stay above 50 bpm and systolic blood pressure above 90 mmHg throughout any infusion. Dizziness, flushing, and diaphoresis have been reported. Neurological side effects are uncommon. Headache occurs occasionally; seizures are documented but very rare. All validated human dosing data is IV only. No human subcutaneous bioavailability data exists. CCK-8 is rapidly cleaved by plasma peptidases, and subcutaneous delivery likely produces negligible systemic levels. The FDA-approved sincalide label specifies IV-only administration. The compound's 2 to 5 minute half-life means most side effects resolve within minutes of stopping the infusion. That rapid clearance is reassuring for acute tolerability but also means CCK-8 simply does not lend itself to repeated self-administration protocols. Pregnancy is contraindicated due to risk of preterm labor and spontaneous abortion from smooth muscle stimulation. Active acute pancreatitis and intestinal obstruction are also hard stops. Stop any infusion immediately for severe abdominal pain, hypotension, bradycardia below 50 bpm, or any sign of allergic reaction. Seek emergency medical care if anaphylaxis is suspected.
Verify Cholecystokinin (CCK-8) dosing and safety with a second opinion
CCK-8 is used IV in research: purity is critical. Unlike SC peptides where mild impurities cause local reactions, IV administration of contaminated peptide risks systemic reactions including anaphylaxis. CCK-8 is a specialty biochemical sold by scientific suppliers, not a standard "research peptide" vendor product. Sulfate ester stability, non-sulfated vs. sulfated forms, and lyophilization quality vary significantly across suppliers.
| Test | When | Target |
|---|---|---|
| Abdominal ultrasound (gallbladder) | Before any CCK-8 administration | No gallstones present; normal gallbladder wall thickness and anatomy |
| Vital signs (heart rate, blood pressure) | Continuously throughout IV infusion and 15 min post-infusion | HR >50 bpm, systolic BP >90 mmHg throughout infusion |
| Serum lipase and amylase | If abdominal pain develops during or within 6 hours of infusion | Lipase <3× upper limit of normal; amylase within normal limits |
Rule out cholelithiasis: gallstones are a hard contraindication. CCK-8-induced forceful gallbladder contraction can dislodge stones into the cystic or common bile duct, causing biliary colic, cholangitis, or acute pancreatitis.
Bradycardia and transient hypotension can occur via vasovagal mechanism with CCK-8 administration. Anaphylaxis surveillance required: most dangerous in first 5-10 min.
CCK-8 stimulates pancreatic secretion; in susceptible individuals (subclinical pancreatitis, pancreas divisum, high-dose administration) it can trigger acute pancreatitis.
Onset of gallbladder contraction and initial satiety signaling following IV administration
Peak gallbladder contraction (40-70% reduction in volume); maximal suppression of appetite and gastric emptying
Effects begin to wane as CCK-8 is rapidly cleared from plasma; meal-related satiety persists via downstream neural signaling
Return to baseline gastrointestinal motility; CCK levels normalize to pre-administration values
0 to 5 minutes: Gallbladder contraction starts within 1 to 2 minutes of IV infusion onset. Vagal CCK1 receptors begin transmitting satiety signals to the brainstem nucleus tractus solitarius. A mild heart rate dip may occur through the vasovagal pathway. Some subjects feel abdominal fullness; nausea is likely if the dose was pushed too fast as a bolus. No community user reports exist for this compound. 5 to 15 minutes: Peak effects hit. Gallbladder volume drops 40 to 70 percent from baseline. Appetite suppression and gastric emptying delay reach maximum intensity. Pancreatic enzyme secretion peaks and the sphincter of Oddi relaxes. Energy intake reduction becomes measurable in controlled meal studies. Nausea, abdominal cramping, and the urge to defecate are most pronounced in this window, especially with bolus dosing. Dizziness and flushing can occur. 15 to 30 minutes: Plasma CCK-8 is already cleared given the 2 to 5 minute half-life. Direct GI contractile effects start fading. The downstream neural satiety signal, running through the vagus to the NTS to the hypothalamus, persists beyond peptide clearance. Most GI side effects begin resolving; some residual fullness may linger. 30 to 60 minutes: GI motility, gastric emptying rate, and gallbladder volume return toward baseline. Meal-related satiety may persist via downstream signaling even though the peptide itself is long gone. From a pharmacokinetic standpoint, CCK-8 is functionally absent from circulation well before this window. Any remaining side effects have typically resolved.
Gallbladder contraction begins within 1-2 min of IV infusion start. Vagal afferent CCK1 receptor activation transmits satiety signals to nucleus tractus solitarius. Mild HR decrease may occur via vasovagal mechanism.
No community reports available: compound has no self-administration history.
Gallbladder volume reduces 40-70% from baseline. Maximal appetite suppression and gastric emptying delay. Pancreatic enzyme secretion peaks. Sphincter of Oddi relaxes. Energy intake reduction detectable in meal studies.
No community reports available.
Plasma CCK-8 cleared (t½ = 2-5 min). Direct GI contractile effects wane. Downstream neural satiety signals persist beyond peptide clearance via vagal-NTS-hypothalamic axis activation.
No community reports available.
GI motility, gastric emptying rate, and gallbladder volume return toward pre-infusion baseline. Meal-related satiety may persist beyond peptide clearance via downstream signaling. Energy intake suppression documented through end of meal.
No community reports available.
Source: Hopman et al. Gut 1990; PMID 2378793: CCK-33 elimination t½ = 4.2 min IV in humans; CCK-8 cleared even faster (~2-3 min)
Loading the interactive decay curve.
CCK-8 (cholecystokinin octapeptide, sulfated) has no FDA approval as a therapeutic agent. Its synthetic equivalent sincalide is FDA-approved exclusively as a diagnostic agent (Kinevac, Bracco Diagnostics, approved 1976) for gallbladder ejection fraction testing and pancreatic secretion stimulation during imaging studies. Native CCK-8 is sold by biochemical suppliers (Tocris, Bachem, Cayman Chemical, AnaSpec) as a research reagent, not for human use. It is not scheduled as a controlled substance and carries no DEA restrictions. It is not available from standard peptide vendor channels and has no compounding pharmacy availability. Kinevac is restricted to hospital and nuclear medicine departments. No WADA prohibition exists for CCK specifically, though any peptide used for performance modification may fall under the catch-all prohibition on peptide hormones. This compound has no documented recreational, anabolic, or performance use. This content is for informational and research purposes only. It does not constitute medical advice. Consult a qualified healthcare provider before any investigational use.
Peptide Schedule Research TeamReviewed Apr 20267 Citations
