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Merck
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Key Documents

Autres documents

SML1828

Sigma-Aldrich

EMD-87580

≥98% (HPLC)

Synonyme(s) :

EMD87580, N-[2-methyl-4,5-bis(methylsulfonyl)-benzoyl]-guanidine

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About This Item

Formule empirique (notation de Hill):
C11H15N3O5S2
Numéro CAS:
187870-78-6
Poids moléculaire :
333.38
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Pureté

≥98% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 20 mg/mL, clear

Température de stockage

−20°C

Chaîne SMILES 

NC(NC(C1=CC(S(=O)(C)=O)=C(S(=O)(C)=O)C=C1C)=O)=N

Application

EMD-87580 has been used as a selective and potent sodium-hydrogen antiporter 1 (NHE-1) inhibitor in cardiac ventricular myocytes to test its effect on the hypertrophic response.

Actions biochimiques/physiologiques

EMD-87580 is a selective inhibitor of the Na+/H+ exchanger subtype 1 (NHE-1), also known as the Na+/H+ antiporter. EMD-87580 has shown cardioprotective effects, and has been investigated as a possible treatment for Duchenne′s muscular dystrophy.

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

Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Ghassan Bkaily et al.
Canadian journal of physiology and pharmacology, 93(11), 923-934 (2015-08-21)
Using the UM-X7.1 hereditary cardiomyopathic and muscular dystrophy hamsters (HCMH), we tested the effects of lifelong preventive or curative treatments during the heart failure phase with the NHE-1 inhibitor EMD 87580 (EMD) or with the angiotensin-converting enzyme inhibitor cilazapril on
Juliana Fantinelli et al.
European journal of pharmacology, 737, 125-132 (2014-05-27)
Previous results show that prolonged treatment with EMD-87580 (EMD) NHE-1 blocker attenuates and reverses postinfarction remodelling. Our aim was to evaluate the effects of the treatment of EMD compared to ischemic postconditioning (IPO) in a model of regional ischemia. Isolated
Sabzali Javadov et al.
The Journal of pharmacology and experimental therapeutics, 317(3), 1036-1043 (2006-03-04)
Although inhibition of Na+/H+ exchanger isoform 1 (NHE-1) reduces cardiomyocyte hypertrophy, the mechanisms underlying this effect are not known. Recent evidence suggests that this may be associated with improved mitochondrial function. To understand the mechanistic bases for mitochondrial involvement in
Mohamed Mlih et al.
Molecular and cellular biochemistry, 404(1-2), 211-220 (2015-03-12)
Osteopontin (OPN), a multifunctional glycophosphoprotein, has been reported to contribute to the development and progression of cardiac remodeling and hypertrophy. Cardiac-specific OPN knockout mice were protected against hypertrophy and fibrosis mediated by Ang II. Recently, transgenic mice expressing the active

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