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SML1828

Sigma-Aldrich

EMD-87580

≥98% (HPLC)

Synonym(e):

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

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About This Item

Empirische Formel (Hill-System):
C11H15N3O5S2
CAS-Nummer:
187870-78-6
Molekulargewicht:
333.38
UNSPSC-Code:
12352200
NACRES:
NA.77

Qualitätsniveau

100

Assay

≥98% (HPLC)

Form

powder

Farbe

white to beige

Löslichkeit

DMSO: 20 mg/mL, clear

Lagertemp.

−20°C

SMILES String

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

InChI

1S/C11H15N3O5S2/c1-6-4-8(20(2,16)17)9(21(3,18)19)5-7(6)10(15)14-11(12)13/h4-5H,1-3H3,(H4,12,13,14,15)

InChIKey

GROMEQPXDKRRIE-UHFFFAOYSA-N

Anwendung

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.

Biochem./physiol. Wirkung

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.
Inhibitor of sodium-hydrogen exchanger-1 (NHE-1)

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Hier finden Sie alle aktuellen Versionen:

Analysenzertifikate (COA)

Lot/Batch Number
017M4719V

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Die Dokumentenbibliothek aufrufen

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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