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Documentos Principais

SML0496

Sigma-Aldrich

CORM-3

Sinônimo(s):

Carbon monoxide releasing molecule 3, Tricarbonylchloro(glycinato)ruthenium (II)

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R$ 611,00
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10 MG
R$ 611,00
50 MG
R$ 2.467,00

About This Item

Fórmula empírica (Notação de Hill):
C5H4ClNO5Ru
Número CAS:
Peso molecular:
294.61
Código UNSPSC:
12352200
NACRES:
NA.77

R$ 611,00


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Formulário

powder

Nível de qualidade

condição de armazenamento

desiccated

cor

white to beige

solubilidade

H2O: 20 mg/mL, clear

Condições de expedição

wet ice

temperatura de armazenamento

−20°C

cadeia de caracteres SMILES

[Ru+2].[Cl-].NCC(=O)[O-].O=[C].O=[C].O=[C]

InChI

1S/C2H5NO2.3CO.ClH.Ru/c3-1-2(4)5;3*1-2;;/h1,3H2,(H,4,5);;;;1H;/q;;;;;+2/p-2

chave InChI

BICHHHDSEZXKNN-UHFFFAOYSA-L

Aplicação

CORM-3 (carbon monoxide (CO) releasing molecule-3) has been used to study its effect on NLRP3 (leucine-rich-repeat-containing receptor, pyrin-domain-containing 3) inflammasome activation via glycolysis in macrophages and also on hyperglycemia-induced IL-1β (interleukin-1 β) production.[1] It has also been used to study its protective function against H2O2-induced apoptosis using primary rabbit lens epithelial cells.[2]

Ações bioquímicas/fisiológicas

CO possesses anti apoptotic function and offers protection against oxidative damage, promoting endothelial healing. CORM-3 is known to have therapeutic effects in transplantation, myocardial infarction and rheumatoid arthritis.[3]
CORM-3 is a water-soluble carbon monoxide (CO) releasing molecule that can be used to study the effects of CO on cellular systems. Carbon monoxide (CO), produced during the degradation of heme by the enzyme heme oxygenase, has recently been found to be an important gaseous signaling mediator in mammalian cells CORM-3 has been shown to have anti-inflammatory and cardioprotective activity.
CORM-3 is a water-soluble carbon monoxide releasing molecule.

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


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Carbon monoxide (CO) inhibits hydrogen peroxide (H2O2)?induced oxidative stress and the activation of NF-?B signaling in lens epithelial cells.
Huang Y, et al.
Experimental Eye Research, 166, 29-39 (2018)
CORM-3 Reactivity toward Proteins: The Crystal Structure of a Ru (II) Dicarbonyl? Lysozyme Complex.
Santos-Silva T, et al.
Journal of the American Chemical Society, 133(5), 1192-1195 (2011)
Carbon monoxide regulates glycolysis-dependent NLRP3 inflammasome activation in macrophages.
young S H, et al.
Biochemical and Biophysical Research Communications, 493(2), 957-963 (2017)
Eric K Patterson et al.
Experimental biology and medicine (Maywood, N.J.), 246(21), 2338-2345 (2021-07-23)
In sepsis-induced inflammation, polymorphonuclear neutrophils (PMNs) contribute to vascular dysfunction. The serine proteases proteinase 3 (PR3) and human leukocyte elastase (HLE) are abundant in PMNs and are released upon degranulation. While HLE's role in inflammation-induced endothelial dysfunction is well studied
Ricardo Coletti et al.
Journal of neuroendocrinology, 31(2), e12686-e12686 (2019-01-12)
Nitric oxide (NO) negatively modulates the secretion of vasopressin (AVP), oxytocin (OT) and atrial natriuretic peptide (ANP) induced by the increase in extracellular osmolality, whereas carbon monoxide (CO) and hydrogen sulphide (H2 S) act to potentiate it; however, little information

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