Synonym |
CCK-8 (1-4) (desulfated) |
Species |
Human |
Protein Accession |
P06307 |
Purity |
≥ 95% |
Endotoxin Level |
< 1.0 EU per μg |
Biological Activity |
Research grade |
Expression System |
Synthetic |
Fusion Tag |
None |
Predicted Molecular Mass |
1033.2 Da |
Formulation |
Lyophilized from a 0.1 μm filtered solution of acetic acid |
Reconstitution |
Reconstitute in water to a concentration of 0.1-1.0 mg/ml |
Storage & Stability |
Store at -20°C upon receipt, stable for up to 1 year |
FAQ
What is Cholecystokinin Octapeptide (1-4) (desulfated) and how does it differ from other forms of
cholecystokinin?
Cholecystokinin Octapeptide (1-4) (desulfated) is a specific form of the peptide
hormone cholecystokinin (CCK), which is naturally produced in the small intestine. This particular form
has been desulfated, meaning that it lacks the sulfate group on its tyrosine residue, which
distinguishes it from the sulfated version more commonly found in physiological conditions.
Cholecystokinin itself is involved in multiple physiological processes, primarily the digestion of food
in the small intestine and the modulation of satiety. The presence or absence of the sulfate group can
significantly alter the peptide's interaction with receptors and its biological activity. Most notably,
the desulfated form of cholecystokinin tends to have a decreased affinity for certain receptors, mainly
CCK-A, which are predominantly found in the pancreas and gallbladder. As a result, this modification may
lead to differences in the peptide's ability to stimulate digestive enzyme secretion and gallbladder
contraction.
This difference is particularly interesting when examining the role of this peptide
in non-digestive processes, such as satiety regulation. In the brain, cholecystokinin acts as a
neuropeptide involved in signaling fullness and reducing food intake. The exact mechanism by which
desulfation affects this process is not fully understood, but studies suggest that it may have a varied
effect on the central nervous system compared to its sulfated counterpart. Understanding these
differences is crucial for researchers who are exploring therapeutic applications, not only in digestive
disorders but also in conditions such as obesity, where modulation of satiety could be beneficial.
Overall, Cholecystokinin Octapeptide (1-4) (desulfated) represents a unique tool for probing the
multifaceted role of cholecystokinin in human physiology and holds promise in expanding the
understanding of its broader biological functions.
How does the desulfated form of
Cholecystokinin Octapeptide (1-4) impact digestive processes?
Cholecystokinin (CCK) is a key
hormone that facilitates the digestion of nutrients by stimulating the gallbladder to contract and
release stored bile into the small intestine while promoting the secretion of pancreatic enzymes that
help break down fats and proteins. The desulfated form of Cholecystokinin Octapeptide (1-4) presents
some notable differences in its impact on these digestive processes due to its altered receptor
interaction. The absence of the sulfate group results in a lower affinity for CCK-A receptors, which are
the primary mediators of these digestive functions. This reduced receptor binding can lead to a dampened
physiological response in terms of gallbladder contraction and enzyme secretion.
Importantly, the
degree to which these processes are affected varies. For example, while both forms of CCK can
potentially stimulate pancreatic enzyme secretion, the effectiveness of the desulfated version in
triggering such a response is diminished compared to its sulfated counterpart. This differentiation
could make the desulfated version less effective in therapies aimed at enhancing digestion through CCK
pathways. However, it also provides a valuable tool for researchers to selectively study the roles of
CCK in different parts of the digestive system without inducing robust digestive responses that can
complicate experimental outcomes.
Furthermore, the reduced activation of digestive processes by
the desulfated peptide has potential therapeutic implications. In conditions where suppression of
gallbladder contraction or enzyme secretion is desired, such as specific types of gallstone disease or
pancreatitis, a compound that can reduce hyperactivity of these processes without eliminating them may
be beneficial. Therefore, the desulfated form of CCK can be a promising candidate for therapeutic
interventions where modulation rather than complete activation or inhibition of digestive processes is
required. Thus, while the desulfation of Cholecystokinin Octapeptide (1-4) reduces its impact on
digestive processes, this characteristic can be advantageous in both research settings and certain
clinical applications.
Can desulfated Cholecystokinin Octapeptide (1-4) be used in weight
management therapies?
The potential of desulfated Cholecystokinin Octapeptide (1-4) in weight
management therapies is grounded in its role in signaling satiety and reducing food intake, a vital
function of cholecystokinin (CCK) more broadly. Research into CCK and its derivatives, such as the
desulfated octapeptide, has been ongoing due to the hormone’s involvement in the regulation of appetite
and body weight. CCK is released postprandially, meaning it is secreted after meals, where it acts on
the CCK receptors in the brain to signal fullness and satisfaction, prompting a natural end to the
eating process.
The desulfated version of CCK Octapeptide (1-4) presents an opportunity to
explore its efficacy as a therapeutic agent for controlling appetite and, consequently, managing body
weight. Although it has a lower affinity for peripheral CCK-A receptors, which are primarily involved in
digestion, its interaction with CCK-B receptors, found both in the brain and the gut, presents a unique
avenue for appetite regulation. This differential binding can be particularly useful in understanding
the pathways that modulate feeding behavior and energy homeostasis. However, it is important to note
that therapies focused solely on CCK modulation should be carefully evaluated for efficacy and side
effects, given the body’s complex network of hormones and feedback mechanisms regulating appetite and
satiety.
Using desulfated CCK Octapeptide (1-4) as a weight management therapy would involve its
administration in a form that can precisely target brain receptor sites associated with satiety without
causing unintended triggers in the digestive tract. Current research efforts are concentrating on
developing delivery mechanisms that can enhance this specificity. Moreover, understanding patient
variability, such as genetic differences in receptor expression and endocrine feedback, is crucial in
assessing the peptide’s potential as a weight management tool on a broader scale.
Critically, any
therapeutic development would need to pass rigorous clinical trials to establish its safety, efficacy,
and long-term impacts. The peptide may function best as part of a multifaceted weight management
program, potentially including lifestyle interventions and other medical treatments. Thus, while the
desulfated Cholecystokinin Octapeptide (1-4) presents an intriguing possibility for appetite modulation,
its application in weight management therapies requires further extensive research to fully understand
and harness its capabilities.
What potential roles does desulfated Cholecystokinin Octapeptide
(1-4) have in neuroscience research?
In the realm of neuroscience research, desulfated
Cholecystokinin Octapeptide (1-4) offers a unique window into the complex interactions of neuropeptides
within the central nervous system. Cholecystokinin (CCK), to which the octapeptide belongs, has been
implicated in various neurological and psychiatric conditions, making its desulfated form a potentially
powerful tool for both exploratory and applied neuroscience. Understanding the distinct roles of
different CCK forms, including desulfated versions, helps elucidate the intricate mechanisms of brain
signaling pathways and their wider physiological and behavioral effects.
One of the primary
interests in neuroscience is the role of CCK in modulating mood and emotional states. Given the
peptide’s involvement in anxiety and stress responses, its desulfated form can be employed to examine
its effects on neurotransmission, particularly its interaction with other neurotransmitter systems such
as dopamine and serotonin. Research has suggested that disruptions in CCK signaling could be linked to
anxiety disorders, and accurately characterizing how the desulfated peptide modulates relevant pathways
could pave the way for developing novel therapeutic approaches.
In addition, studying the
desulfated octapeptide in the context of cognitive functions such as memory and learning represents
another promising area. CCK and its derivatives have been found to influence neural plasticity and
synaptic connectivity, key factors in cognitive processing. Whether the desulfated octapeptide
influences these cognitive processes differentially compared to its sulfated counterpart remains an open
question that neuroscience research aims to address.
Moreover, the characterization of this
peptide in research models can refine our understanding of CCK’s role in feeding behaviors and energy
homeostasis, areas with significant implications for addressing obesity and metabolic disorders.
Exploring the neural circuits through which desulfated CCK Octapeptide (1-4) exerts its effects can help
map out specific targets for intervention, improving the therapeutic strategies employed in treating
metabolic and psychological conditions.
In summary, the desulfated form of Cholecystokinin
Octapeptide (1-4) serves as a multifaceted research tool in neuroscience, extending its application to
various domains including mood regulation, cognitive function, and energy metabolism. Continued
investigation into this peptide could enhance our understanding of CCK-related pathways, offering novel
insights into brain function and potential avenues for clinical interventions.
What are the
challenges and considerations in developing Cholecystokinin Octapeptide (1-4) (desulfated) as a
therapeutic agent?
Developing Cholecystokinin Octapeptide (1-4) (desulfated) as a therapeutic
agent involves navigating several challenges and considerations, including its pharmacokinetics,
specificity, dosing, and the potential for unwanted side effects. Here we delve into each of these
factors to provide a comprehensive picture of what is entailed in bringing this compound from the
research bench to a therapeutic setting.
One of the primary challenges lies in the
pharmacokinetics of the peptide. As with many peptide-based drugs, desulfated CCK Octapeptide (1-4)
might face issues related to stability and half-life in the human body. Peptides are often rapidly
degraded by proteases, limiting their duration of action. Innovative delivery systems, such as
encapsulation in nanoparticles or the development of stable analogs, could be necessary to enhance the
peptide's stability and bioavailability. These technological advancements would help ensure that the
compound reaches its target site in sufficient quantities to exert its therapeutic
effect.
Specificity is another important consideration. While the desulfated form of the peptide
offers a reduced affinity for certain receptors, ensuring that it selectively modulates only the
intended pathways is crucial. The brain, where CCK acts as a neuropeptide, comprises a complex network
of receptors and signaling pathways. Ensuring that the therapeutic agent reaches these sites without
interacting adversely with other systems is vital. This need for specificity extends to addressing
individual variability in patient populations, as genetic differences could affect receptor expression
and sensitivity to the peptide.
Determining the appropriate dosing is also critical. Due to its
modified activity, establishing an effective dose that achieves the desired therapeutic outcomes without
causing adverse effects presents a complex balancing act. Clinical trials must rigorously assess these
parameters, accounting for the varying pharmacodynamic responses across populations.
Furthermore,
potential side effects must be thoroughly investigated. While the peptide may have beneficial effects,
its role in diverse physiological processes means that unintended consequences could arise, particularly
with long-term use. For instance, unintended modulations of mood or cognitive processes would be
undesirable in a therapeutic aimed solely at regulating appetite.
Lastly, understanding the
regulatory path for peptide-based therapies is paramount. Given the increasing interest in peptides as
therapeutics, navigating the regulatory requirements necessitates a clear demonstration of safety,
efficacy, and quality. This often involves extensive clinical testing and collaboration with regulatory
bodies to facilitate approval processes.
Overall, while Cholecystokinin Octapeptide (1-4)
(desulfated) shows promise, its development as a therapeutic agent demands careful consideration of many
scientific, technical, and regulatory challenges to ensure safe and effective treatments for patients.