Product |
Cholecystokinin Octapeptide (desulfated), CCK-8 |
Synonym |
CCK-8 |
Species |
Human |
Protein Accession |
P09150 |
Purity |
> 95% |
Endotoxin Level |
< 1.0 EU per μg |
Biological Activity |
≥ 95 nmol/mg |
Expression System |
Synthetic |
Fusion Tag |
None |
Predicted Molecular Mass |
1076.2 Da |
Formulation |
Lyophilized from a 0.2 μm filtered solution in 30% acetonitrile and 0.1% TFA |
Reconstitution |
Centrifuge vial before opening. Reconstitute in sterile distilled water or aqueous buffer
containing 0.1% TFA to a concentration of 0.1-1.0 mg/ml. |
Storage & Stability |
Store at -20°C. Store under desiccating conditions. The product can be stored for up to 12
months. |
FAQ
What is Cholecystokinin Octapeptide (desulfated) and how does it differ from regular
CCK-8?
Cholecystokinin Octapeptide (desulfated), commonly known as CCK-8 desulfated, is a
derivative of the natural peptide hormone cholecystokinin (CCK). This particular peptide form lacks the
sulfate group typically present in the tyrosine residue of the full peptide chain. CCK plays a crucial
role in stimulating the digestion of fat and protein, influencing satiety, and acting as a neuropeptide
within the central nervous system. The desulfated version, CCK-8, retains many of these functions but
differs in certain biochemical interactions and physiological effects due to the absence of the sulfate
group. This structural modification can affect how the peptide is recognized by various receptors,
potentially altering its potency, duration of action, or even the spectrum of biological activities it
can influence. Scientists often use CCK-8 desulfated in research settings to explore the specific
pathways mediated by cholecystokinin by observing how desulfated variants interact with cells compared
to their sulfated counterparts. Understanding these differences is critical for developing targeted
interventions or therapies that modulate digestive and neurophysiological processes. Despite these
variations, both forms of the peptide play vital roles in appetite regulation and gastrointestinal
function, contributing to broader research in obesity management, digestive health, and neurological
studies.
How is Cholecystokinin Octapeptide (desulfated) used in research
settings?
Cholecystokinin Octapeptide (desulfated) is prominently utilized in scientific
research, specifically in studies focusing on appetite regulation, digestive processes, and neurological
applications. Researchers employ CCK-8 desulfated to dissect its role in various physiological systems,
leveraging its structural nuances to compare against the traditional CCK peptides. The desulfated form
interacts differently with CCK receptors, providing insight into the mechanisms of receptor binding and
activation. This can be pivotal in understanding how digestive hormones modulate pancreatic secretion,
gallbladder contraction, and appetite suppression. In neurological studies, CCK-8 desulfated offers a
tool to discern how CCK influences anxiety, pain perception, and satiety in the brain. Furthermore, it
is often used to observe the desensitization of receptors or to determine the specific pathways
activated in metabolic studies. By shedding light on the distinctive roles and mechanisms of action
within CCK pathways, this peptide variant assists scientists in the development of drugs aimed at
alleviating digestion-related disorders or optimizing appetite control. Comprehensive exploration of its
actions also aids in understanding broader physiological interactions and potential therapeutic
targets.
What potential clinical applications can arise from the study of Cholecystokinin
Octapeptide (desulfated)?
The study of Cholecystokinin Octapeptide (desulfated) reveals potential
clinical applications that could significantly impact fields like metabolic disorders, obesity, and
gastrointestinal diseases. By understanding how CCK-8 desulfated interacts with specific receptors
differently than traditional CCK, researchers can discover new pathways for therapeutic interventions.
In obesity, exploring its role in appetite suppression may lead to the development of weight management
medications that leverage these unique interactions to help modulate hunger and enhance satiety without
adverse effects. Gastrointestinal disorders, including those related to enzyme secretions and digestive
fluid balance, could also benefit from targeted therapies that optimize CCK activity to achieve desired
clinical outcomes without disrupting natural biochemical balances. In neurological domains, because CCK
is implicated in functions such as reducing anxiety or modulating pain, desulfated CCK variants might
provide alternatives for treating conditions where these symptoms are prevalent. The insights gained
from ongoing research can thus inform the creation of innovative pharmacological solutions necessitating
refined specificity and minimized side effects.
What are the biochemical implications of removing
the sulfate group from Cholecystokinin Octapeptide?
From a biochemical perspective, the removal
of the sulfate group from Cholecystokinin Octapeptide leads to significant implications regarding its
interaction with cellular receptors and subsequent activation patterns. With the removal of this moiety,
CCK-8 desulfated exhibits altered biophysical properties that can influence its affinity and selectivity
for the CCK receptor subtypes, CCK-A, and CCK-B. This structural change may affect the peptide's charge
and hydrophilicity, impacting how it interacts with the surrounding environment within the cellular
membrane or how it is handled by enzymes responsible for peptide metabolism. These changes also
influence the peptide's stability, resistance to enzymatic degradation, or ease of penetration through
cellular barriers. As a consequence, the desulfated form may have a prolonged action or require
different dosing levels to achieve similar effects as the traditional sulfated form. Such biochemical
nuances render CCK-8 desulfated a critical variant in research looking to address the receptor
specificity, ligand-effector coupling, and subsequent signaling pathways initiated within target cells,
ultimately broadening our understanding of peptide-receptor dynamics.
How does the removal of
sulfate from CCK-8 potentially affect its interaction with receptors?
The desulfation of CCK-8
potentially alters its interaction with G-protein coupled receptors, such as the CCK-A and CCK-B
receptors, which mediate the peptide's biological activities. Sulfation typically enhances binding
affinity for these receptors, suggesting that the absence of the sulfate group in CCK-8 desulfated might
result in reduced binding affinity and changes in receptor selectivity. This modification could thus
affect the potency and efficacy of CCK-8 in activating downstream signaling cascades. Additionally,
without the sulfate group, alterations in receptor conformation upon binding could occur, thereby
modifying the normal physiological effects triggered by receptor activation. These changes are crucial
for researchers trying to delineate the functional differences between peptide variants, providing an
opportunity to explore the receptor's active sites in more detail. Consequently, alterations in the
interaction profile also invite investigations into potential therapeutic benefits where modulation of
receptor sensitivity or selectivity could play a role in treating diseases involving dysregulated
peptide signaling pathways, such as those related to digestion and mood disorders.