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Merck

SML0315

Sigma-Aldrich

CORM-A1

≥95% (NMR)

Sinónimos:

Sodium boranocarbonate

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10 MG
US$ 160,00
50 MG
US$ 634,00

US$ 160,00

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10 MG
US$ 160,00
50 MG
US$ 634,00

About This Item

Fórmula empírica (notación de Hill):
CH3BNa2O2
Número de CAS:
Peso molecular:
103.82
Número MDL:
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
NACRES:
NA.77

US$ 160,00

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Ensayo

≥95% (NMR)

Formulario

powder

condiciones de almacenamiento

desiccated

color

white to beige

solubilidad

H2O: >15 mg/mL

temp. de almacenamiento

room temp

cadena 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

Clave InChI

SOFPSQNQOQPAAJ-UHFFFAOYSA-M

Aplicación

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]

Acciones bioquímicas o fisiológicas

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]

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


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Jianxiong Liu et al.
Pediatric research, 82(5), 881-887 (2017-07-01)
BackgroundThe potential contribution of sex-related variables to cerebrovascular functions in neonates remains elusive. Newborn piglets provide a translationally relevant model for studying the effects of seizures in the neonatal brain. The present study investigated whether sex differences contribute to cerebrovascular
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
Bhavisha A Bakrania et al.
American journal of physiology. Regulatory, integrative and comparative physiology, 314(3), R427-R432 (2017-12-08)
Preeclampsia is a pregnancy-specific disorder of maternal hypertension and reduced renal hemodynamics linked to reduced endothelial function. Placental ischemia is thought to be the culprit of this disease, as it causes the release of factors like tumor necrosis factor (TNF)-α
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
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

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