Cholecystokinin tetrapeptide (CCK-4, also PTK7) is a peptide fragment derived from the larger peptide hormone cholecystokinin. CCK-4 acts primarily in the brain as an anxiogenic, although it does retain some GI effects, but not as much as CCK-8 or the full length polypeptide CCK-58.
CAT No: 10-101-74
CAS No:35144-91-3
Synonyms/Alias:CCK-4; CCK4; CCK 4; Gastrin Tetrapeptide; Cholecystokinin Octapeptide (5-8); Cholecystokinin Tetrapeptide; Gastrin (14-17) (human)
CCK-4 Acetate, also known as Cholecystokinin Tetrapeptide Acetate or Trp-Met-Asp-Phe-NH2 acetate salt, is a synthetic peptide fragment derived from the larger cholecystokinin family of neuropeptides. Distinguished by its small size and high biological activity, CCK-4 Acetate is widely recognized for its ability to mimic the endogenous actions of cholecystokinin fragments in various research settings. Its structure allows it to interact specifically with cholecystokinin receptors, making it an invaluable tool for probing receptor function, signaling pathways, and neurobiological processes. With high solubility and stability in aqueous solutions, this compound is particularly suited for in vitro studies and diverse experimental protocols. Researchers value CCK-4 Acetate for its reproducibility, ease of handling, and well-characterized mechanism of action, which collectively facilitate the exploration of neuropeptide function in both central and peripheral systems.
Neurobiology Research: CCK-4 Acetate is extensively utilized in neurobiology to investigate the physiological and molecular mechanisms underlying anxiety, panic, and stress responses. By acting as a selective agonist at cholecystokinin-B (CCK-B) receptors in the central nervous system, this peptide enables researchers to induce and measure anxiety-like behaviors in animal models. The ability to precisely control dosing and timing of administration makes it an essential compound for dissecting the neurochemical pathways involved in emotional regulation, neurotransmitter release, and synaptic plasticity. Such studies contribute to a deeper understanding of how neuropeptides modulate behavior and brain function.
Receptor Pharmacology: In the field of receptor pharmacology, Cholecystokinin Tetrapeptide Acetate serves as a reference ligand for characterizing the binding properties and activation profiles of CCK receptors. Its high specificity for CCK-B receptors allows scientists to differentiate between receptor subtypes and assess the efficacy and potency of novel receptor modulators. The peptide is frequently employed in binding assays, signal transduction experiments, and functional studies to elucidate the downstream effects of receptor activation, such as changes in intracellular calcium levels and second messenger cascades.
Gastrointestinal Physiology: The role of CCK-4 Acetate extends to gastrointestinal research, where it is used to mimic the natural actions of cholecystokinin fragments on digestive processes. By stimulating CCK receptors in the gut, it enables the study of mechanisms governing gastric motility, pancreatic secretion, and gallbladder contraction. Researchers utilize this peptide to unravel the complex signaling networks that regulate nutrient digestion and absorption, as well as to identify potential targets for modulating gastrointestinal function in experimental models.
Endocrine System Studies: Trp-Met-Asp-Phe-NH2 acetate salt is also applied in investigations of the endocrine system, particularly in understanding the interplay between neuropeptides and hormone secretion. By activating CCK receptors on endocrine cells, it facilitates the analysis of hormone release dynamics, feedback loops, and the integration of neural and hormonal signals. These studies shed light on how neuropeptides influence metabolic homeostasis, appetite regulation, and energy balance, providing a foundation for further exploration of neuroendocrine control mechanisms.
Behavioral Neuroscience: In behavioral neuroscience, the peptide is a powerful tool for modeling and quantifying behavioral responses to neuropeptide signaling. Its application in behavioral assays allows for the assessment of locomotor activity, exploratory behavior, and conditioned responses following CCK receptor activation. By correlating behavioral outcomes with molecular and cellular changes, researchers gain valuable insights into the functional roles of cholecystokinin fragments in shaping complex behaviors and adaptive responses.
Peptide Mechanism Exploration: Beyond its established uses, CCK-4 Acetate is increasingly employed in studies aimed at delineating the precise molecular mechanisms by which cholecystokinin fragments exert their effects. Through advanced techniques such as receptor mutagenesis, signaling pathway mapping, and structure-activity relationship analysis, scientists utilize this peptide to probe the structural determinants of receptor activation, ligand-receptor interactions, and downstream effector engagement. These investigations not only enhance our understanding of peptide-receptor biology but also inform the rational design of novel ligands with tailored pharmacological properties for experimental use.
Experimental panic induction with cholecystokinin tetrapeptide (CCK-4) is considered as a suitable model to investigate the pathophysiology of panic attacks. While only a few studies investigated the brain activation patterns following CCK-4, no data are available on the putative involvement of the amygdala in the CCK-4 elicited anxiety response. We studied the functional correlates of CCK-4-induced anxiety in healthy volunteers by means of functional magnetic resonance imaging (fMRI) and region of interest (ROI) analysis of the amygdala. Sixteen healthy volunteers underwent challenge with CCK-4 compared with placebo in a single-blind design. Functional brain activation patterns were determined for the CCK-4-challenge, the placebo response and anticipatory anxiety (AA). CCK-4-induced anxiety was accompanied by a strong and robust activation (random effects analysis, P < 0.00001, uncorrected for multiple testing) in the ventral anterior cingulate cortex (ACC), middle and superior frontal gyrus, precuneus, middle and superior temporal gyrus, occipital lobe, sublobar areas, cerebellum, and brainstem. In contrast, random effects group analysis for placebo and AA using the same level of significance generated no significant results. Using a more liberal level of significance, activations could be observed in some brain regions such as the dorsal part of the ACC during AA (random effects analysis, P < 0.005). Overall functional responses did not differ between panickers and nonpanickers. Only 5 of 11 subjects showed strong amygdala activation. However, ROI analysis pointed towards higher scores in fear items in these subjects. In conclusion, while overall brain activation patterns are not related to the subjective anxiety response to CCK-4, amygdala activation may be involved in the subjective perception of CCK-4-induced fear.
Eser, D., Leicht, G., Lutz, J., Wenninger, S., Kirsch, V., Schüle, C., ... & Rupprecht, R. (2009). Functional neuroanatomy of CCK‐4‐induced panic attacks in healthy volunteers. Human brain mapping, 30(2), 511-522.
3alpha-reduced neuroactive steroids such as 3alpha, 5alpha-tetrahydroprogesterone (3alpha, 5alpha-THP) and 3alpha, 5alpha-tetrahydrodeoxycorticosterone (3alpha, 5alpha-THDOC) are potent positive allosteric modulators of gamma-aminobutyric acid type A (GABAA) receptors and display pronounced anxiolytic activity in animal models. Experimental panic induction with cholecystokinin-tetrapeptide (CCK-4) and sodium lactate is accompanied by a decrease in 3alpha, 5alpha-THP concentrations in patients with panic disorder, but not in healthy controls. However, no data are available on 3alpha, 5alpha-THDOC concentrations during experimental panic induction. Therefore, we quantified 3alpha, 5alpha-THDOC concentrations in 10 healthy volunteers (nine men, one woman) before and after panic induction with CCK-4 by means of a highly sensitive and specific gas chromatography/mass spectrometry analysis. CCK-4 elicited a strong panic response as assessed by the Acute Panic Inventory. This was accompanied by an increase in 3alpha, 5alpha-THDOC, ACTH and cortisol concentrations. This increase in 3alpha, 5alpha-THDOC might be a consequence of hypothalamic-pituitary-adrenal (HPA) axis activation following CCK-4-induced panic, and might contribute to the termination of the anxiety/stress response following challenge with CCK-4 through enhancement of GABAA receptor function.
Eser, D., Di Michele, F., Zwanzger, P., Pasini, A., Baghai, T. C., Schüle, C., ... & Romeo, E. (2005). Panic induction with cholecystokinin-tetrapeptide (CCK-4) Increases plasma concentrations of the neuroactive steroid 3 [alpha], 5 [alpha] tetrahydrodeoxycorticosterone (3 [alpha], 5 [alpha]-THDOC) in healthy volunteers. Neuropsychopharmacology, 30(1), 192.
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