Cholecystokinin (CCK-8) Dosage Calculator
Cholecystokinin (CCK-8) is a sulfated octapeptide fragment of the 33-amino-acid gut hormone cholecystokinin, first isolated from porcine intestinal mucosa in the 1960s.
1mcg · Daily
Summary: Add 2mL BAC water to your 0.5mg vial. Draw to 0.4 units on a U-100 syringe for a 1mcg dose. This vial will last 500 doses.
Cycle Planner
Cholecystokinin (CCK-8) Pharmacokinetics
Pharmacokinetics — Active Dose Over Time
t½ = 2-5 minutes (IV)Disclaimer: This curve is a simplified first-order exponential decay model. Actual pharmacokinetics vary based on injection site, individual metabolism, body composition, and other factors. Half-life values are approximate and based on available preclinical and clinical literature. Many research peptides lack formal human pharmacokinetic studies. This is for educational purposes only — not medical advice.
Cholecystokinin (CCK-8) Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 1mcg | Daily |
| Moderate | 2mcg | Daily |
| Aggressive | 4mcg | 2x Daily |
Note: Cholecystokinin-8 (CCK-8) is the sulfated octapeptide form of the endogenous gut-brain hormone cholecystokinin. It is one of the most potent naturally occurring satiety signals in mammalian physiology. CCK-8 binds both CCK1 (peripheral) and CCK2 (central) G-protein-coupled receptors, triggering gallbladder contraction, pancreatic enzyme secretion, gastric emptying delay, and vagal afferent satiety signaling. In clinical medicine, its synthetic analog sincalide (Kinevac) is FDA-approved as a diagnostic agent for gallbladder function testing. Research interest in CCK-8 extends to appetite regulation, anxiety modulation, pain processing, and neuroprotection. However, its extremely short plasma half-life of 2-5 minutes limits therapeutic utility, driving development of longer-acting CCK1-selective analogs for obesity treatment. All investigational use of native CCK-8 remains research-only.
About Cholecystokinin (CCK-8)
Cholecystokinin (CCK-8) is a sulfated octapeptide fragment of the 33-amino-acid gut hormone cholecystokinin, first isolated from porcine intestinal mucosa in the 1960s. It is the most bioactive circulating form of CCK and plays a central role in the gut-brain axis, acting as a primary short-term satiety signal released by I-cells in the duodenal and jejunal mucosa in response to dietary fat and protein. CCK-8 exerts its physiological effects through two receptor subtypes: CCK1 receptors (formerly CCK-A), which predominate in the gastrointestinal tract, pancreas, and vagal afferent neurons, and CCK2 receptors (formerly CCK-B), which are widely distributed in the central nervous system. Activation of peripheral CCK1 receptors stimulates gallbladder contraction, relaxation of the sphincter of Oddi, secretion of pancreatic digestive enzymes, and inhibition of gastric emptying. Vagal CCK1 receptor activation transmits satiety signals to the nucleus tractus solitarius in the brainstem, reducing meal size and promoting meal termination. In the central nervous system, CCK-8 acts as a neuromodulator with roles in anxiety, panic responses, pain modulation, memory, and dopaminergic neurotransmission. The related fragment CCK-4 is a well-established panicogenic agent in human research, and elevated brain CCK levels are implicated in anxiety and panic disorders. The synthetic C-terminal octapeptide of CCK, known as sincalide (marketed as Kinevac), received FDA approval in 1976 as a diagnostic agent for assessing gallbladder ejection fraction and stimulating pancreatic secretion during imaging studies. Native CCK-8 remains a critical research tool for studying appetite regulation, gastrointestinal motility, and neuropeptide signaling. Its rapid enzymatic degradation in plasma (half-life of 2-5 minutes) has spurred development of protease-resistant, long-acting CCK1 receptor agonists as potential anti-obesity therapeutics.