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Dynorphin (1-17)

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Dynorphin (1-17); Dynorphin(1-17); Dynorphin 1-17; Dynorphin1-17; Dynorphins; Dynorphin A (1-17); Dynorphin A 1-17; Dynorphin A1-17; DynorphinA 1-17; DynorphinA1-17; DynorphinA(1-17); D004399; LS-185865; LS185865; LS 185865
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Dynorphin A-(1- 17) is an endogenous opioid peptide that has been implicated in the pathophysiology of both traumatic brain injury (TBI) and spinal cord injury (SCI).
Dynorphin A-( 1- 17) is an endogenous opioid derived from the prohormone prodynorphin. It acts as endogenous κ-agonist that is resistant to enzymatic degradation. And it is a neuroactive peptide with potent analgesic effects.
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Dynorphin A 1–17 (DYN A) is an endogenous neuropeptide that is of interest due to its diverse roles in analgesia, inflammation and addiction. Upon release, DYN A is subject to metabolism by a range of enzymes and its biotransformation is dependent on the site and environment into which it is released.

CAS: 72957-38-1 (net)
Sequence: H-Tyr-Gly-Gly-Phe-Leu-Arg-Arg-Ile-Arg-Pro-Lys- Leu-Lys-OH acetate salt
M.W: 1603.99
Molecular Formula: C75H126N24O15

Dynorphin 1–17, (DYN 1–17) opioid peptide produces antinociception following binding to the kappa-opioid peptide (KOP) receptor. Upon synthesis and release in inflamed tissues by immune cells, DYN 1–17 undergoes rapid biotransformation and yields a unique set of opioid and non-opioid fragments. Some of these major fragments possess a role in immunomodulation, suggesting that opioid-targeted therapeutics may be effective in diminishing the severity of inflammatory disorders.

Rahiman, S. S. F., Morgan, M., Gray, P., Shaw, P. N., & Cabot, P. J. (2016). Dynorphin 1-17 and Its N-Terminal Biotransformation Fragments Modulate Lipopolysaccharide-Stimulated Nuclear Factor-kappa B Nuclear Translocation, Interleukin-1beta and Tumor Necrosis Factor-alpha in Differentiated THP-1 Cells. PloS one, 11(4), e0153005.

Dynorphin A (1–17), an endogenous opioid neuropeptide, can have pathophysiological consequences at high concentrations through actions involving glutamate receptors. Despite evidence of excitotoxicity, the basic mechanisms underlying dynorphin-induced cell death have not been explored. To address this question, we examined the role of caspase-dependent apoptotic events in mediating dynorphin A (1–17) toxicity in embryonic mouse striatal neuron cultures. In addition, the role of opioid and/or glutamate receptors were assessed pharmacologically using MK(+)801, a non-equilibrium N-methyl-D-aspartate (NMDA) antagonist; CNQX, a competitive α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate antagonist; or (−)-naloxone, a general opioid antagonist.

Singh, I. N., Goody, R. J., Goebel, S. M., Martin, K. M., Knapp, P. E., Marinova, Z., ... & Hauser, K. F. (2003). Dynorphin A (1–17) induces apoptosis in striatal neurons in vitro through α-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptor-mediated cytochrome C release and caspase-3 activation. Neuroscience, 122(4), 1013-1023.

Opioids inhibit release of primary afferent transmitters but it is unclear whether the converse occurs. To test the hypothesis that primary afferent transmitters influence opioid-ergic tone, we studied the functional and anatomical relationships between pituitary adenylyl cyclase-activating polypeptide (PACAP) and dynorphin 1-17 (Dyn) in spinal cord. We found that activation of the PACAP-specific receptor PAC1 (PAC1R) inhibited, whereas PAC1R blockade augmented, spinal release of Dyn. It is noteworthy that in the formalin-induced pain model PAC1R blockade (via PACAP6-38) also resulted in antinociception that was abolished by spinal κ-opioid receptor blockade.

Liu, N. J., Schnell, S. A., Schulz, S., Wessendorf, M. W., & Gintzler, A. R. (2011). Regulation of spinal dynorphin 1-17 release by endogenous pituitary adenylyl cyclase-activating polypeptide in the male rat: relevance of excitation via disinhibition. Journal of Pharmacology and Experimental Therapeutics, 336(2), 328-335.

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