SML0769
Cu-ATSM
≥98% (HPLC), peroxynitrite inhibitor, powder
别名:
CuII(ATSM), [[2,2′-（1,2-二甲基-1,2-乙二亚甲基）双[N-甲基肼甲硫代酰胺基]]]铜, 二乙酰基双（N（4）-甲硫基氨基脲）铜（II）
生化/生理作用
Cu-ATSM是一种口服可生物利用的血脑屏障渗透性复合物，可特异性抑制过氧亚硝酸盐对Cu、Zn超氧化物歧化酶（SOD1）的作用。
Cu-ATSM是一种口服可生物利用的血脑屏障渗透性复合物，可特异性抑制过氧亚硝酸盐对Cu、Zn超氧化物歧化酶（SOD1）的作用以及随后细胞蛋白的硝化作用。在肌萎缩性侧索硬化症（ALS）小鼠模型中，CuII(ATSM)可显著延迟疾病的发作（瘫痪和寿命延长）。并且，据报道Cu-ATSM在缺血再灌注损伤模型中也可降低脂质过氧化。随后，研究显示Cu-ATSM具有类似于Liproxstatin-1的效力，可抑制肥大症。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
Blaine R Roberts et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(23), 8021-8031 (2014-06-06)
Mutations in the metallo-protein Cu/Zn-superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (ALS) in humans and an expression level-dependent phenotype in transgenic rodents. We show that oral treatment with the therapeutic agent diacetyl-bis(4-methylthiosemicarbazonato)copper(II) [Cu(II)(atsm)] increased the concentration of mutant SOD1 (SOD1G37R)
Erin J McAllum et al.
Neurobiology of disease, 81, 20-24 (2015-03-15)
Mutations in the metalloprotein Cu,Zn-superoxide dismutase (SOD1) cause approximately 20% of familial cases of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease for which effective therapeutics do not yet exist. Transgenic rodent models based on over-expression of mutant SOD1 have
Erin J McAllum et al.
Amyotrophic lateral sclerosis & frontotemporal degeneration, 14(7-8), 586-590 (2013-08-21)
Our objective was to assess the copper(II) complex of diacetylbis(4-methylthiosemicarbazone) [Cu(II)(atsm)] for its preclinical potential as a novel therapeutic for ALS. Experimental paradigms used were designed to assess Cu(II)(atsm) efficacy relative to treatment with riluzole, as a function of dose
Adam Southon et al.
British journal of pharmacology, 177(3), 656-667 (2019-10-28)
Diacetyl-bis(4-methyl-3-thiosemicarbazonato)copperII (CuII (atsm)) ameliorates neurodegeneration and delays disease progression in mouse models of amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), yet the mechanism of action remains uncertain. Promising results were recently reported for separate Phase 1 studies in ALS
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