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品質水準
アッセイ
≥98% (HPLC)
フォーム
powder
色
, brown to dark red-brown
溶解性
DMSO: 0.5 mg/mL, clear (warmed)
保管温度
2-8°C
生物化学的／生理学的作用
Cu-ATSM is an orally bioavailable, blood-brain barrier permeable complex that specifically inhibits the action of peroxynitrite on Cu,Zn superoxide dismutase (SOD1) and subsequent nitration of cellular proteins. CuII(ATSM) significantly delayed onset of disease (paralysis and prolonged lifespan) in amyotrophic lateral sclerosis (ALS) mice model. Also, Cu-ATSM was reported to lower lipid peroxidation in a model of ischemicreperfusion injury. Cu-ATSM subsequently was shown to inhibit ferroptosis with a potency similar to Liproxstatin-1.
Cu-ATSM is an orally bioavailable, blood-brain barrier permeable complex that specifically inhibits the action of peroxynitrite on Cu,Zn superoxide dismutase (SOD1).
保管分類コード
11 - Combustible Solids
WGK
WGK 3
引火点(°F)
Not applicable
引火点(℃)
Not applicable
適用法令
試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。
労働安全衛生法名称等を表示すべき危険物及び有害物
名称等を表示すべき危険物及び有害物
労働安全衛生法名称等を通知すべき危険物及び有害物
名称等を通知すべき危険物及び有害物
Jan Code
SML0769-25MG:4548173983721
SML0769-5MG:4548173983738
SML0769-VAR:
SML0769-BULK:
SML0769-IP:
最新バージョンのいずれかを選択してください：
試験成績書（COA）
Lot/Batch Number
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
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
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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