Tat-NR2B9c (Synonyms: Tat-NR2Bct; NA-1) |
Catalog No.GC30774 |
Tat-NR2B9c is designed to prevent nitric oxide (NO) production by preventing postsynaptic density protein 95 (PSD-95) binding to N-methyl-D-aspartate (NMDA) receptors and neuronal nitric oxide synthase.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 500992-11-0
Sample solution is provided at 25 µL, 10mM.
Tat-NR2B9c is designed to prevent nitric oxide (NO) production by preventing postsynaptic density protein 95 (PSD-95) binding to N-methyl-D-aspartate (NMDA) receptors and neuronal nitric oxide synthase. Tat-NR2B9c dissociates NMDA glutamate receptors from downstream excitotoxic signaling pathways without affecting normal glutamate receptor function. Neuroprotective effects of Tat-NR2B9c have been demonstrated in a diverse range of stroke models in several species including rodents, primates, and humans. Moreover, Tat-NR2B9c peptide has shown clinical efficacy as a neuroprotective agent in acute stroke.[1][2]
In vitro study indicated that Tat-NR2B9c have no measurable effect on the rate or magnitude of NMDA-induced calcium influx. However, Tat-NR2B9c prevented NMDA-induced DNA breaks, and the neuronal death could be significantly reduced by Tat-NR2B9c. Tat-NR2B9c also prevented NMDA-induced superoxide p47phox formation by blocking phosphorylation, and neuroprotective effect of Tat-NR2B9c may be partly or wholly attributable to its suppression of NOX2 activation. In addition, Tat-NR2B9c, which targets the PDZ domain of PSD-95, disrupts the functional coupling between NR2B and NOX2.[2]
In vivo experiments demonstrated that Tat-NR2B9c would be effective in treating or preventing perinatal and neonatal hypoxic-ischemic brain injury, as well as its related brain disorders. Results indicated that Tat-NR2B9c reduced brain damage caused by hypoxic-ischemic injury when administered either before or after ischemia and improved post-HI neurobehavioral outcomes when delivered before or after ischemia. Moreover, Tat-NR2B9c might exert neuroprotective effects through the promotion of pro-survival signaling and inhibition of pro-apoptotic signaling.[1]
References:
[1]. Xu B, et al. Neuroprotective Effects of a PSD-95 Inhibitor in Neonatal Hypoxic-Ischemic Brain Injury. Mol Neurobiol. 2016 Nov;53(9):5962-5970.
[2]. Chen Y, et al. Tat-NR2B9c prevents excitotoxic neuronal superoxide production. J Cereb Blood Flow Metab. 2015 May;35(5):739-42.
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