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Submit ReviewThe overall effect of this much-investigated compound is the result of the actions of the two enantiomers: glycine-NMDA antagonism by the (+)-isomer and sedative and ataxic effects of the (-)-isomer. See separate isomers 0281 and 0282.
分子量 | 116.12 |
储存 | Store at RT |
CAS Number | 1003-51-6 |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
参考文献是支持产品生物活性的出版物。
Evans et al (1978) Mg2+-like selective antagonism of excitatory amino acid - induced responses by α,ε-diaminopimelic acid, D-α-aminoadipate and HA-966 in isolated spinal cord of frog and immature rat. Brain Res. 148 536 PMID: 207392
Foster and Kem (1989) HA-966 antagonises NMDA receptors through a selective interaction with the glycine modulatory site. J.Neurosci. 9 2191 PMID: 2542488
Lodge (1989) Non-competitive NMDA antagonists. The NMDA Receptor (2nd edition). Eds. G.L.Collingr 37
关键词: (±)-HA-966, (±)-HA-966 supplier, NMDA, Receptors, 0198, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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This product guide provides a background to Huntington's disease research and lists around 100 products for the study of:
Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
Huntington's disease (HD) is a severe monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the effects of mutant huntingtin aggregation implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.