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Key Documents
SML0315
CORM-A1
≥95% (NMR)
Synonim(y):
Sodium boranocarbonate
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About This Item
Wzór empiryczny (zapis Hilla):
CH3BNa2O2
Numer CAS:
Masa cząsteczkowa:
103.82
Numer MDL:
Kod UNSPSC:
12352200
Identyfikator substancji w PubChem:
NACRES:
NA.77
Polecane produkty
Próba
≥95% (NMR)
Postać
powder
warunki przechowywania
desiccated
kolor
white to beige
rozpuszczalność
H2O: >15 mg/mL
temp. przechowywania
room temp
ciąg SMILES
[Na+].[Na+].[BH3-]C([O-])=O
InChI
1S/CH4BO2.2Na/c2-1(3)4;;/h2H3,(H,3,4);;/q-1;2*+1/p-1
Klucz InChI
SOFPSQNQOQPAAJ-UHFFFAOYSA-M
Zastosowanie
CORM-A1 has been used:
- to deliver carbon monoxide (CO) and to test its cytoprotection in yeast and primary astrocytes culture during oxidative stress
- as CO donor in murine macrophages J774A.1 cells to test its effect on cellular β-endorphins elevation
- to test its effect on mitophagy activation in retinal ganglion cells
Działania biochem./fizjol.
CORM-A1 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 is an important gaseous signaling mediator in mammalian cells CORM-A1 has anti-oxidant and anti-inflammatory activity.
It mediates the release of CO in a pH and temperature-dependent manner, thus favoring mild vasorelaxation and hypotension. During oxidative stress, CORM-A1 is reported to provide cytoprotection in astrocyte primary cultures. This boron-containing CORM promotes autophagy.
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Kod klasy składowania
11 - Combustible Solids
Klasa zagrożenia wodnego (WGK)
WGK 3
Temperatura zapłonu (°F)
Not applicable
Temperatura zapłonu (°C)
Not applicable
Certyfikaty analizy (CoA)
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Kapil K Upadhyay et al.
Redox biology, 28, 101314-101314 (2019-09-13)
Nuclear factor-erythroid 2 related factor 2 (Nrf2)-mediated signaling plays a central role in maintaining cellular redox homeostasis of hepatic cells. Carbon monoxide releasing molecule-A1 (CORM-A1) has been reported to stimulate up-regulation and nuclear translocation of Nrf2 in hepatocytes. However, the
Helena Parfenova et al.
American journal of physiology. Heart and circulatory physiology, 315(4), H978-H988 (2018-07-22)
Neonatal asphyxia leads to cerebrovascular disease and neurological complications via a mechanism that may involve oxidative stress. Carbon monoxide (CO) is an antioxidant messenger produced via a heme oxygenase (HO)-catalyzed reaction. Cortical astrocytes are the major cells in the brain
Kapil K Upadhyay et al.
Toxicology and applied pharmacology, 360, 99-108 (2018-10-03)
Acute liver injury is frequently associated with oxidative stress. Here, we investigated the therapeutic potential of carbon monoxide releasing molecule A-1 (CORM A-1) in oxidative stress-mediated liver injury. Overnight-fasted mice were injected with acetaminophen (APAP; 300 mg/kg; intraperitoneally) and were sacrificed
Rui-Gang Zhang et al.
Molecular immunology, 105, 205-212 (2018-12-16)
Carbon monoxide (CO) is an anti-inflammatory gaseous molecule produced endogenously by heme oxygenases (HOs) HO-1 and HO-2. However, the mechanisms underlying the anti-inflammatory effects of CO in the human bronchial epithelium are still not fully understood. In this study, the
Myrna Constantin et al.
International journal of hypertension, 2012, 859235-859235 (2012-04-21)
Heme oxygenase (HO), a catabolic enzyme, provides the rate-limiting step in the oxidative breakdown of heme, to generate carbon monoxide (CO), iron, and biliverdin-IXα. Induction of the inducible form, HO-1, in tissues is generally regarded as a protective mechanism. Over
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