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Principaux documents

SML0315

Sigma-Aldrich

CORM-A1

≥95% (NMR)

Synonyme(s) :

Sodium boranocarbonate

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About This Item

Formule empirique (notation de Hill) :
CH3BNa2O2
Numéro CAS:
Poids moléculaire :
103.82
Numéro MDL:
Code UNSPSC :
12352200
ID de substance PubChem :
Nomenclature NACRES :
NA.77

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Niveau de qualité

Essai

≥95% (NMR)

Forme

powder

Conditions de stockage

desiccated

Couleur

white to beige

Solubilité

H2O: >15 mg/mL

Température de stockage

room temp

Chaîne 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

Clé InChI

SOFPSQNQOQPAAJ-UHFFFAOYSA-M

Application

CORM-A1 has been used:
  • to deliver carbon monoxide (CO) and to test its cytoprotection in yeast and primary astrocytes culture during oxidative stress[1]
  • as CO donor in murine macrophages J774A.1 cells to test its effect on cellular β-endorphins elevation[2]
  • to test its effect on mitophagy activation in retinal ganglion cells[3]

Actions biochimiques/physiologiques

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.
CORM-A1 is a water-soluble carbon monoxide (CO) releasing molecule.
It mediates the release of CO in a pH and temperature-dependent manner,[1] thus favoring mild vasorelaxation and hypotension.[4] During oxidative stress, CORM-A1 is reported to provide cytoprotection in astrocyte primary cultures.[1] This boron-containing CORM promotes autophagy.[1]

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

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
Sara R Oliveira et al.
The European journal of neuroscience, 52(1), 2771-2780 (2020-03-14)
Previous studies about the modulation of the vasculature by CO were performed exclusively in male or sexually immature animals. Understanding the sex differences regarding systemic drug processing and pharmacodynamics is an important feature for safety assessment of drug dosing and
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
Cláudia Figueiredo-Pereira et al.
Redox biology, 32, 101470-101470 (2020-03-03)
Carbon monoxide (CO) is a gasotransmitter endogenously produced by the activity of heme oxygenase, which is a stress-response enzyme. Endogenous CO or low concentrations of exogenous CO have been described to present several cytoprotective functions: anti-apoptosis, anti-inflammatory, vasomodulation, maintenance of
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

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