SML2988
Tat-NR2B9c trifluoroacetate
≥95% (HPLC)
Synonym(s):
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
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About This Item
Empirical Formula (Hill Notation):
C105H188N42O30 · xC2HF3O2
CAS Number:
Molecular Weight:
2518.88 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77
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Biochem/physiol Actions
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).
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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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;
Gabriella MacDougall et al.
Journal of molecular neuroscience : MN, 61(2), 235-246 (2016-11-21)
We have previously reported that cationic poly-arginine and arginine-rich cell-penetrating peptides display high-level neuroprotection and reduce calcium influx following in vitro excitotoxicity, as well as reduce brain injury in animal stroke models. Using the neuroprotective peptides poly-arginine R12 (R12) and
Diego Milani et al.
Brain research bulletin, 135, 62-68 (2017-10-02)
Following positive results with the poly-arginine peptide R18 when administered intravenously 30 or 60min after permanent and/or transient middle cerebral artery occlusion (MCAO; 90min) in the rat, we examined the effectiveness of the peptide when administered 2h after MCAO. R18
Karen Tse et al.
Journal of neuroscience research, 97(11), 1378-1392 (2019-05-16)
Antiepileptogenic agents that prevent the development of epilepsy following a brain insult remain the holy grail of epilepsy therapeutics. We have employed a label-free proteomic approach that allows quantification of large numbers of brain-expressed proteins in a single analysis in
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