| Synonym | Dyn A (1-10) amide | 
                
                    | Species | Human | 
                
                    | Protein Accession | P01261 | 
                
                    | Purity | Greater than 95% | 
                
                    | Endotoxin Level | Less than 1 EU/μg | 
                
                    | Biological Activity | Not available | 
                
                    | Expression System | Chemical Synthesis | 
                
                    | Fusion Tag | None | 
                
                    | Predicted Molecular Mass | 1241.4 Da | 
                
                    | Formulation | Supplied as a lyophilized powder | 
                
                    | Reconstitution | Reconstitute in water to a concentration of 0.1-1.0 mg/ml | 
                
                    | Storage & Stability | Store at -20°C. For long term storage, store at -80°C. Stable for up to 3 months when stored at
                        -20°C. | 
            
            FAQ
            
                What is Dynorphin A (1-10) amide, and how does it function in the body?
Dynorphin A (1-10) amide
                is a naturally occurring peptide fragment of the endogenous opioid peptide, dynorphin, derived from the
                precursor protein prodynorphin. The sequence of this peptide consists of the first ten amino acids of
                dynorphin A, with an additional modification at the C-terminal end known as amidation. This modification
                increases the peptide's stability and affinity for opioid receptors, enhancing its physiological
                effects. Dynorphin A (1-10) amide primarily interacts with the kappa-opioid receptor (KOR) but can also
                have varying degrees of affinity towards delta and mu-opioid receptors, though these interactions are
                typically weaker.
Dynorphins are vital in regulating numerous physiological processes, most
                notably those associated with pain perception, stress response, mood regulation, and addiction. Upon
                binding to the kappa-opioid receptors located in the central and peripheral nervous systems, dynorphin A
                (1-10) amide can modulate neurotransmitter release, thereby influencing signal transmission in neuronal
                pathways responsible for pain and reward. This modulation can result in analgesic effects, making it a
                target for therapeutic applications aimed at treating different types of pain, particularly neuropathic
                pain which is usually resistant to traditional analgesics.
Moreover, the activity of dynorphin A
                (1-10) amide at kappa-opioid receptors is linked with stress-related behavioral responses. Activation of
                these receptors has been associated with inducing dysphoric states, which contrasts with the often
                euphoric effects exerted by mu-opioid receptor agonists. This property might be leveraged
                therapeutically to help manage addiction. By mitigating the rewarding effects of addictive substances,
                dynorphin A (1-10) amide potentially could be developed as part of treatment strategies aimed at
                preventing relapse in individuals recovering from substance abuse disorders. Additionally, the peptide
                also influences various neuroendocrine functions, contributing to its complex role in the body.
                
In summary, dynorphin A (1-10) amide, through its interaction with kappa-opioid receptors,
                exerts significant effects on pain modulation, stress responses, mood, and addiction, highlighting its
                potential in therapeutic applications such as analgesia and addiction management. Understanding its
                mechanism and effects in more detail offers pathways to novel treatment modalities leveraging this
                powerful peptide.
What are the potential therapeutic applications of Dynorphin A (1-10)
                amide?
Dynorphin A (1-10) amide holds promising potential for numerous therapeutic applications,
                particularly in managing pain, treating mood disorders, and addressing substance abuse. Its primary
                function as a modulator of the kappa-opioid receptor (KOR) implies a range of physiological impacts
                relevant to these medical areas. Indeed, one of the most studied aspects of dynorphins, underscored by
                this amide fragment, is their analgesic properties making it a candidate for pain management, especially
                neuropathic and chronic pain forms resistant to typical opioid treatments. Through the activation of
                KORs, Dynorphin A (1-10) amide can reduce the perception of pain by influencing neuronal pathways
                without the risk of addiction associated with mu-opioid receptor agonists.
Mood disorders such as
                depression and anxiety may also benefit from interventions involving Dynorphin A (1-10) amide. The
                peptide's ability to influence neurotransmitter release, particularly involving dopamine systems, means
                it could modulate mood and anxiety levels. Research suggests that kappa-opioid receptor agonists, like
                dynorphin, induce dysphoria and stress, with chronic exposure potentially triggering depressive states.
                Counterbalancing this, however, understanding and modulating this response could provide a framework for
                developing treatments aimed at mood regulation—essentially using the dynorphin pathway to recalibrate
                neurochemical imbalances in affected individuals, though this requires substantial further research to
                ensure therapeutic efficacy and safety.
In the realm of addiction, Dynorphin A (1-10) amide’s
                modulatory effect on reward pathways positions it as a candidate for disrupting addictive behavior
                pathways. By affecting the release of dopamine in key brain areas associated with reward and pleasure,
                it can diminish the rewarding effects of addictive substances such as opioids, alcohol, and
                psychostimulants. This diminished effect could reduce craving and relapse incidence in individuals
                undergoing recovery from substance abuse, making it a tool worth investigating within addiction
                treatment frameworks.
Furthermore, research is expanding into other areas such as epilepsy,
                Parkinson’s disease, and cognitive function where Dynorphin A (1-10) amide might offer benefits through
                its broad-spectrum receptor interactions and regulatory roles. While significant efforts in basic and
                clinical research are necessary to translate these potential applications into validated therapies, the
                existing data underscores the promise held by this peptide. With ongoing advancements in peptide drug
                design, stability, and delivery mechanisms, Dynorphin A (1-10) amide could emerge as a formidable
                component in the new wave of therapeutics targeting complex neurological disorders and managing
                intricate biopsychological processes.
How does Dynorphin A (1-10) amide differ from other opioid
                receptor modulators?
Dynorphin A (1-10) amide, as a fragment of the larger dynorphin peptide, is
                primarily distinguished from other opioid receptor modulators by its specific affinity and activity at
                the kappa-opioid receptor (KOR), marking it as predominantly a kappa-selective agonist. In contrast,
                many traditional opioids, such as morphine and codeine, are mu-opioid receptor (MOR) agonists, making
                their interaction with opioid receptors markedly different from that of dynorphin derivatives. This
                fundamental difference in receptor activity leads to varied physiological and pharmacological outcomes,
                which further delineate their distinct therapeutic profiles and potential side effects.
The
                emphasis on kappa-opioid receptor affinity results in dynorphin A (1-10) amide inducing physiological
                effects that diverge from those typically associated with mu-opioid activation. While mu-opioid receptor
                agonists generally produce analgesia accompanied by euphoric sensations—factors contributing to their
                high abuse potential—dynorphin A (1-10) amide’s activation of KOR often leads to anti-reward effects,
                such as dysphoria and anhedonia. This difference is pivotal in considering the role of such peptides in
                addiction and managing pain without the pronounced risk of dependency and overdose inherent in many
                mu-opioid receptor modulators. Consequently, these kappa-selective properties might be leveraged to
                develop non-addictive analgesics or therapeutic agents aimed at treating addictive disorders by
                mitigating the rewarding effects of drugs of abuse.
Moreover, Dynorphin A (1-10) amide can
                modulate numerous other physiological processes that differentiate it from typical opioid analgesics.
                Its involvement in stress response and modulation of hormonal release further demonstrates its broad
                scope of influence. These distinct activities are underscored by the peptide's ability to induce complex
                changes in neuronal circuitry beyond those observed with standard opioids, offering a nuanced approach
                to disorders involving stress dysregulation, mood disorders, and neurodegenerative diseases.
In
                addition, dynorphins exhibit a variation in their effects on neurotransmitter systems compared to
                classic opioid therapies. While both types of compounds can influence the dopaminergic pathways within
                the central nervous system, the outcomes diverge due to the opposing actions mediated by KOR and MOR
                systems, providing nuanced opportunities for therapeutic manipulation. Considering their unique receptor
                interactions and physiological impact, Dynorphin A (1-10) amide represents a distinct class of opioid
                receptor modulators with potential advantages over traditional opioids, particularly in developing
                non-addictive analgesics and complex neurological disorder therapeutics.
Are there any side
                effects or risks associated with Dynorphin A (1-10) amide?
As with any bioactive peptide,
                understanding the potential side effects and risks associated with Dynorphin A (1-10) amide is crucial,
                particularly in light of its interactions with the kappa-opioid receptor (KOR) and the varied
                physiological systems it influences. KOR agonists like Dynorphin A (1-10) amide are generally associated
                with less risk of addiction compared to mu-opioid receptor agonists; however, they do present a unique
                side effect profile that must be considered critically, especially in terms of mood and cognitive
                effects.
One of the primary concerns with Dynorphin A (1-10) amide use is its propensity to
                induce pronounced dysphoric and aversive effects. Unlike the euphoric states often associated with
                mu-opioid receptor activation, kappa-opioid receptor engagement can result in feelings of dysphoria,
                which, although contributing to its potential role in reducing addictive behaviors in substance abuse
                treatment, might limit patient compliance and acceptance in broader therapeutic applications. These
                dysphoric effects stem from the interaction of Dynorphin A (1-10) amide with central nervous system
                pathways involved in mood regulation, highlighting a need for careful management and, possibly,
                co-administration with mood-stabilizing agents to mitigate such adverse outcomes.
Additionally,
                kappa-opioid receptor activation can influence cognition and perception, sometimes manifesting as
                impaired cognitive and motor abilities. While these effects vary depending on dosage and administration
                routes, they necessitate vigilance when considering this peptide for therapeutic purposes, particularly
                in populations where cognitive function is already compromised, or in concurrent usage with other
                central nervous system modulating therapies.
Moreover, physical side effects like sedation and
                nausea can accompany kappa-opioid receptor engagement. While generally of lesser concern than
                complications arising from mu-opioid receptor agonist use, these issues still represent practical
                considerations in therapeutic contexts, requiring tailored dosage strategies and potentially
                necessitating supportive treatment to enhance tolerability and maintain patient
                adherence.
Importantly, like with any pharmacological agents, individual variability in response
                to Dynorphin A (1-10) amide should be anticipated. Genetic, environmental, and existing health status
                factors can significantly influence both the efficacy and the side effect profile, emphasizing the
                importance of personalized medical approaches and robust clinical trials to delineate these variables
                more precisely. Ultimately, while Dynorphin A (1-10) amide holds enticing therapeutic promise across
                several challenging medical domains, careful consideration of its side effects and patient-specific
                factors remains imperative to harness its full potential safely and effectively.
What are the
                research advancements concerning Dynorphin A (1-10) amide?
Research on Dynorphin A (1-10) amide
                continues to advance, opening new windows into its potential therapeutic capabilities and physiological
                roles. Recent studies have delved deeply into its molecular interactions, neuronal pathway impacts, and
                potential clinical applications, with ongoing interest in leveraging its kappa-opioid receptor activity
                to address pain, addiction, and mood disorders.
Significant strides have been made in
                understanding the complex mechanisms underpinning Dynorphin A (1-10) amide’s action at the kappa-opioid
                receptor level and beyond. Scientists utilize advanced molecular biology and neuroimaging techniques to
                map the precise effects of its receptor engagement across various neuronal circuits. This growing
                understanding has illuminated its nuanced role in modulating neurotransmitter systems, particularly
                concerning dopamine pathways related to reward, reinforcement, and pain. These insights are critical as
                they help clarify how Dynorphin A (1-10) amide potentially modulates addictive behaviors and equips
                researchers with valuable knowledge to develop addiction therapeutics focused on mitigating cravings and
                relapse.
In the realm of pain management, researchers are increasingly interested in Dynorphin A
                (1-10) amide’s analgesic capabilities, especially for neuropathic and chronic pain forms that resist
                traditional opioid therapy. Innovative studies employ animal models and advanced imaging to ascertain
                effective, safe dosing parameters and better understand its long-term impacts compared to existing
                opioid options. This research direction presents the prospect of novel therapeutics providing effective
                pain relief without the addictive potential associated with current treatments, addressing a severe
                healthcare challenge amid ongoing opioid crises.
Further noteworthy advancements include
                examining Dynorphin A (1-10) amide’s potential for addressing mood disorders such as depression and
                anxiety. By exploring its complex modulation of emotional pathways and its kappa-induced dysphoric
                effects, scientists aim to develop complementary treatments that balance these aspects to offer
                therapeutic relief for individuals with mood dysregulation. Such exploration is imperative as mood
                disorders remain a critical unmet need globally, necessitating the pursuit of innovative pharmacological
                strategies.
Research continues to progress into optimizing Dynorphin A (1-10) amide’s molecular
                stability and bioavailability, vital steps for transitioning from lab-based findings to viable clinical
                applications. Bioengineering and medicinal chemistry advancements are pivotal, with fresh approaches to
                peptide modification enhancing its therapeutic profile by improving receptor selectivity, minimizing
                side effects, and achieving targeted delivery in the body.
In conclusion, research advancements
                concerning Dynorphin A (1-10) amide illustrate the robust potential of this peptide to offer innovative
                solutions across pain management, addiction treatment, and mood disorder interventions. Combining
                cutting-edge scientific techniques and interdisciplinary collaboration, researchers move closer to
                translating laboratory discoveries into tangible medical advancements, highlighting a promising future
                for Dynorphin A (1-10) amide in clinical practice.