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Merck
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SML0769

Sigma-Aldrich

Cu-ATSM

≥98% (HPLC)

Sinonimo/i:

CuII(ATSM), Diacetylbis(N(4)-methylthiosemicarbazonato) copper(II), [[2,2′-(1,2-Dimethyl-1,2-ethanediylidene)bis[N-methylhydrazinecarbothioamidato]]] copper

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About This Item

Formula empirica (notazione di Hill):
C8H14CuN6S2
Numero CAS:
68341-09-3
Peso molecolare:
321.91
Codice UNSPSC:
12352200
NACRES:
NA.77

Livello qualitativo

100

Saggio

≥98% (HPLC)

Forma fisica

powder

Colore

, brown to dark red-brown

Solubilità

DMSO: 0.5 mg/mL, clear (warmed)

Temperatura di conservazione

2-8°C

Azioni biochim/fisiol

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.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Certificati d'analisi (COA)

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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)
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
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

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