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Dynorphin (1-17)

CAT#
10-101-81
Synonyms/Alias
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
CAS No.
80448-90-4
Sequence
H-Tyr-Gly-Gly-Phe-Leu-Arg-Arg-Ile-Arg-Pro-Lys-Leu-Lys-Trp-Asp-Asn-Gln-OH
M.W/Mr.
2147.48
Molecular Formula
C99H155N31O23
Source
Synthetic
Long-term Storage Conditions
−20°C
Application
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).
Description
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.
Areas of Interest
Analgesia

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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.

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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