SML2988
Tat-NR2B9c trifluoroacetate
≥95% (HPLC)
别名:
NA-1, trifluoroacetate salt, Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Lys-Leu-Ser-Ser-Ile-Glu-Ser-Asp-Val, trifluoroacetate salt, YGRKKRRQRRR-KLSSIESDV, trifluoroacetate salt
登录 查看组织和合同定价。
选择尺寸
关于此项目
经验公式（希尔记法）:
C105H188N42O30 · xC2HF3O2
化学文摘社编号:
分子量:
2518.88 (free base basis)
NACRES:
NA.77
UNSPSC Code:
12352200
Biochem/physiol Actions
NMDAR-PSD-95 interaction blocking peptide with neuroprotective efficacy in vitro and in vivo.
Tat-NR2B9c (NA-1) is a 20-mer peptide composed of a membrane-permeant HIV-1 Tat protein transduction domain sequence (a.a. 47-57) N-terminal to the NMDA receptor (NMDAR) GluN2B carboxyl tail sequence KLSSIESDV that blocks intracellular NMDAR-PSD-95 interaction-induced neurotoxic signaling without affecting NMDAR-mediated synaptic activity or calcium influx. NA-1 protects cultured cortical neurons from NMDA excitotoxicity (50 nM; 20/40/100 μM NMDA) and reduces focal ischemic brain damage in rats in vivo (3 μmol/kg iv. bolus 1 hr post MCAO onset).
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Luka R Srejic et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 33(12), 1937-1943 (2013-09-12)
Since the most significant ischemic sequelae occur within hours of stroke, it is necessary to understand how neuronal function changes during this time. While histologic and behavioral models show the extent of stroke-related damage, only in vivo recordings can illustrate
Yanting Chen et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 35(5), 739-742 (2015-02-12)
The Tat-NR2B9c peptide has shown clinical efficacy as a neuroprotective agent in acute stroke. 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;
Michelle Aarts et al.
Science (New York, N.Y.), 298(5594), 846-850 (2002-10-26)
N-methyl-D-aspartate receptors (NMDARs) mediate ischemic brain damage but also mediate essential neuronal excitation. To treat stroke without blocking NMDARs, we transduced neurons with peptides that disrupted the interaction of NMDARs with the postsynaptic density protein PSD-95. This procedure dissociated NMDARs
Lucy M Teves et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 36(3), 555-561 (2015-12-15)
Tat-NR2B9c, a clinical-stage stroke neuroprotectant validated in rats and primates, was recently deemed ineffective in mice. To evaluate this discrepancy, we conducted studies in mice subjected to temporary middle cerebral artery occlusion (tMCAO) for either 30 or 60 min according to
Diego Milani et al.
Neuroscience research, 114, 9-15 (2016-09-19)
We examined the efficacy of R18 in a transient MCAO model and compared its effectiveness to the well-characterized neuroprotective NA-1 peptide. R18 and NA-1 peptides were administered intravenously (30, 100, 300, 1000nmol/kg), 60min after the onset of 90min of MCAO.
我们的科学家团队拥有各种研究领域经验，包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持