NNZ-2591

产品编号: DC11386 Featured
NNZ-2591
结构式
874471-40-6
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中国地区超过5000个高品质化合物库存
应用领域
NNZ-2591是天然存在的神经肽的合成类似物,已显示其在多种动物模型中具有神经保护和促智(记忆增强)作用。
Cas No.: 874471-40-6
名称: (2R)-2-[[(2S)-1-(2-aminoacetyl)-2-prop-2-enylpyrrolidine-2-carbonyl]amino]pentanedioic acid
别名: NNZ-2591,NNZ2591,NNZ 2591
SMILES: C(O)(=O)[C@@H](CCC(O)=O)NC([C@](CC=C)1CCCN1C(=O)CN)=O
分子式: C15H23N3O6
分子量: 341.364
纯度:
保存条件: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description:
In Vivo:
In Vitro:
References: NNZ-2591 is a synthetic analog of the neurotrophic peptide cyclic glycine proline (cGP), which occurs naturally in the brain. NNZ-2591 has demonstrated efficacy in pre-clinical models of Parkinson’s disease, stroke, traumatic brain injury, peripheral neuropathy, Fragile X syndrome, memory impairment and multiple sclerosis. cGP has been shown to regulate the binding of IGF-1 to IGF Binding Protein 3 in the brain. An abnormally high amount of IGF Binding Protein 3 is a feature of Rett syndrome. NNZ-2591 prevents scopolamine-induced acute impairment in memory and modulation of acetylcholine neurotransmission may be the mode of action underlying the memory improvement.NNZ-2591 has shown encouraging results in wellvalidated preclinical models of cognitive impairment, Fragile X syndrome, traumatic brain injury, stroke, Parkinson’s disease, peripheral neuropathy and multiple sclerosis.In rats, cyclo-L-glycyl-L-2-allylproline (NNZ-2591), a diketopiperazine, is neuroprotective after ischemic brain injury and also improves motor function in a rat model of Parkinson's disease. Given nootropic actions of diketopiperazines, we investigated the effects of and potential role for acetylcholine neurotransmission in NNZ-2591 on spatial memory after scopolamine-induced amnesia in rats. Adult male Wistar rats were assigned to four groups: saline/water; saline/NNZ-2591; scopolamine/water and scopolamine/NNZ-2591. Morris Water Maze (MWM) tasks were used to determine spatial learning and memory. Thirty minutes prior to each of four daily acquisition trials, rats were intraperitoneally injected with either scopolamine (0.5 mg/kg) or saline. Either NNZ-2591 (30 mg/kg) or water was administered orally (gavages) 10 min after the injection. Immediately after completion of the day 4 acquisition trial a spatial probe trial was performed. The brains were then collected for immunohistochemical analysis. Scopolamine impaired spatial learning and memory compared to saline treated group, particularly in the day 1 acquisition trial. NNZ-2591 did not reverse this deficit, however it significantly improved memory retention by showing more time spent in the correct quadrant. NNZ-2591 also counteracted the scopolamine-induced up-regulation of choline-acetyltransferase positive neurons in the striatum and similarly counteracted the increased synaptophysin density in the hippocampus. Furthermore, a scopolamine-independent antagonistic effect on muscarinic M2 acetylcholine receptors was found after NNZ-2591 treatment, supporting its modulation of acetylcholine neurotransmission. The data suggest that NNZ-2591 prevents scopolamine-induced acute impairment in memory and modulation of acetylcholine neurotransmission may be the mode of action underlying the memory improvement.
Kinase Assay:
Cell Assay:
Animal Administration:
References:
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
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