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Tat-NR2B9c
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
包装与价格:
包装价格(元)
1mg电议
5mg电议
10mg电议
25mg电议

产品介绍
Tat-NR2B9c (Tat-NR2Bct; NA-1) 是一种突触后密度 95 (PSD-95) 抑制剂,对 PSD-95d2 (PSD-95 PDZ domain 2) 和 PSD-95d1 的 EC50 值为 6.7 nM 和 670 nM , 分别。

Cell lines

Neuronal cells

Preparation Method

Studies were initiated in cultures at days 10 to 12 in vitro by exchanging the culture medium with a low-magnesium balanced salt solution.10 Peptides and drugs were added from concentrated stocks 15 minutes before the addition of NMDA.

Reaction Conditions

Treated neuronal cell cultures with 100 μmol/L NMDA for 30 minutes together with Tat-NR2B9c over a range of concentrations: 0, 0.05, 0.1, 0.5 μmol/L.

Applications

Tat-NR2B9c showed neuroprotectant efficacy in patients with acute stroke. Tat-NR2B9c is designed to uncouple NO production from NMDAr activation by blocking PSD-95 binding to NMDAr and nNOS. Tat-NR2B9c also prevents NMDA-induced superoxide p47phox formation by blocking phosphorylation.

Animal models

Timed pregnant CD1 mice (7-day-old (P7) pups of either sex)

Preparation Method

Tat-NR2B9c was administered intraperitoneally at a single dose of 15 μg/g body weight in 100–120 μl of saline.

Dosage form

15 μg/g

Applications

Tat-NR2B9c has a neuroprotective effect in the neonatal mouse hypoxic-ischemic brain injury model of stroke. In addition, Tat-NR2B9c reduced brain damage caused by hypoxic-ischemic injury and showed the potential to promote long-term recovery. Tat-NR2B9c would be effective in treating or preventing perinatal and neonatal hypoxic-ischemic brain injury, as well as its related brain disorders.

产品描述

Tat-NR2B9cis 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-NR2B9cdissociates NMDA glutamate receptors from downstream excitotoxic signaling pathways without affecting normal glutamate receptor function. Neuroprotective effects ofTat-NR2B9chave been demonstrated in a diverse range of stroke models in several species including rodents, primates, and humans. Moreover,Tat-NR2B9cpeptide has shown clinical efficacy as a neuroprotective agent in acute stroke.[1][2]

In vitro study indicated thatTat-NR2B9chave no measurable effect on the rate or magnitude of NMDA-induced calcium influx. However,Tat-NR2B9cprevented NMDA-induced DNA breaks, and the neuronal death could be significantly reduced byTat-NR2B9c.Tat-NR2B9calso prevented NMDA-induced superoxide p47phox formation by blocking phosphorylation, and neuroprotective effect ofTat-NR2B9cmay 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 thatTat-NR2B9cwould be effective in treating or preventing perinatal and neonatal hypoxic-ischemic brain injury, as well as its related brain disorders. Results indicated thatTat-NR2B9creduced 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-NR2B9cmight 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-NR2B9cprevents excitotoxic neuronal superoxide production. J Cereb Blood Flow Metab. 2015 May;35(5):739-42.