SML1930
CORM-401
Synonym(s):
Mn(CO)4{S2CNMe(CH2CO2H)}, Tetracarbonyl[N-(dithiocarboxy-?S,?S′)-N-methylglycine]manganate
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About This Item
Recommended Products
form
powder
Quality Level
storage condition
protect from light
color
light yellow to dark yellow
solubility
DMSO: 10 mg/mL, clear
storage temp.
−20°C
SMILES string
CN(CC(O)=O)C1=S=[Mn-4]([C+]=O)([C+]=O)([C+]=O)([C+]=O)S1
Biochem/physiol Actions
CORM-401 (Mn(CO)4(S2CNMe(CH2CO2H))) is a manganese-containing carbon monoxide-releasing molecule (CORM) that generates at least three molar equivalents of CO. Due to reversible binding of CO, CORM-401 is relatively stable in solution (0.33 mol eq of CO loss after 4 h in PBS; [CORM-401] = 1 mM at time zero), while increased CO release occurs in the presence of a CO receptor or a ligand to prevent the rebinding of CO (3.2 mol eq of CO transferred to iron with a t1/2 of 0.8 min in the presence of 44 μM myoglobin; [CORM-401] = 10 μM at time zero). CO administration by CORM-401 is reported to uncouple mitochondrial respiration and inhibit glycolysis in human endothelial cells (10-100 μM), and relax isolated rat aortic rings (25 μM) pre-contracted with phenylephrine.
wgk_germany
WGK 3
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Dalton transactions (Cambridge, England : 2003), 40(16), 4230-4235 (2011-03-16)
[Mn(CO)(4){S(2)CNMe(CH(2)CO(2)H)}], 1, is shown to be a CO releasing molecule providing at least three moles CO per mole of compound. The mechanism of CO loss is dissociative and reversible and was investigated using Gaussian 09 calculations. The reversible binding of
Biochemical pharmacology, 102, 64-77 (2016-01-02)
Carbon monoxide (CO) is generated by heme oxygenase-1 (HO-1) and displays important signaling, anti-apoptotic and anti-inflammatory activities, indicating that pharmacological agents mimicking its action may have therapeutic benefit. This study examined the biochemical and pharmacological properties of CORM-401, a recently
Biochimica et biophysica acta, 1847(10), 1297-1309 (2015-07-18)
Carbon monoxide (CO), a product of heme degradation by heme oxygenases, plays an important role in vascular homeostasis. Recent evidence indicates that mitochondria are among a number of molecular targets that mediate the cellular actions of CO. In the present
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