SML0496
CORM-3
Nitric oxide release inhibitor, powder
Synonym(s):
Carbon monoxide releasing molecule 3, Tricarbonylchloro(glycinato)ruthenium (II)
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About This Item
Empirical Formula (Hill Notation):
C5H4ClNO5Ru
CAS Number:
Molecular Weight:
294.61
UNSPSC Code:
12352200
NACRES:
NA.77
Product Name
CORM-3,
SMILES string
[Ru+2].[Cl-].NCC(=O)[O-].O=[C].O=[C].O=[C]
InChI key
BICHHHDSEZXKNN-UHFFFAOYSA-L
InChI
1S/C2H5NO2.3CO.ClH.Ru/c3-1-2(4)5;3*1-2;;/h1,3H2,(H,4,5);;;;1H;/q;;;;;+2/p-2
form
powder
storage condition
desiccated
color
white to beige
solubility
H2O: 20 mg/mL, clear
shipped in
wet ice
storage temp.
−20°C
Quality Level
Related Categories
Application
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. It has also been used to study its protective function against H2O2-induced apoptosis using primary rabbit lens epithelial cells.
Biochem/physiol Actions
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.
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.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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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)
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)
Do Won Lee et al.
Biochemical and biophysical research communications, 493(2), 957-963 (2017-09-25)
Low dose of carbon monoxide (CO) has anti-inflammatory role through various signaling pathways. Cellular metabolism has been implicated in the activation of inflammation in immune cells. However, the mechanisms by which CO-dependent metabolic regulation affect the immune response remain unclear.
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
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