Description
Dynorphin A(1-13), a tridecapeptide of the endogenous opioid peptides, has modest effects in reducing mild opiate withdrawal in humans. Previous studies revealed that dynorphin also potentiates the analgesic effect of morphine in morphine-tolerant rats and mice. The therapeutic potential of dynorphin A(1-13) is limited due to extensive metabolism by human metabolic enzymes resulting in an in vivo half-life of less than one minute. Chemical modifications of dynorphin A(1-13), such as N-methylation of Tyr1 and amidation of the C-terminus have been shown to be effective in protecting against the proteolytic enzymes in human plasma
[1].
Uses
Porcine dynorphin A (1-13) is a potent, endogenous κ opioid receptor agonist and is antinociceptive at physiological concentrations.
Application
Dynorphin A (1-13) has been used as a test compound in the field asymmetric waveform ion mobility spectrometry coupled to mass spectrometry (FAIMS/IMS/MS).
Biochem/physiol Actions
Dynorphin A (1-13), a bioactive product of dynorphin A displays interaction with N-methyl- D-aspartate (NMDA) as well as with opioid receptors. It elevates intracellular calcium [Ca
2+]i level and contributes to the loss of neurons affecting neuronal viability.
in vivo
Dynorphin A (1-13) exposure (33 μM) causes a significant loss in neuronal viability at 4 h with a visible destruction in neuronal morphology seen at 16 h. Exposure to dynorphin A (1-13) causes acute increases in [Ca2+]i in individual neurons similar to increases seen with acute NMDA treatment. Continuous exposure to dynorphin A (1-13) (100 μM) causes a significant loss of neurons over time[1].
IC 50
κ Opioid Receptor/KOR
References
[1] B BRUGOS; G H. Metabolism of dynorphin A(1-13).[J]. Pharmazie, 2004.
