Taiy Chemical
Cholecystokinin Octapeptide (1-4) (desulfated)
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.
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