SML1828
EMD-87580
≥98% (HPLC)
Synonym(s):
EMD87580, N-[2-methyl-4,5-bis(methylsulfonyl)-benzoyl]-guanidine
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About This Item
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Quality Level
Assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 20 mg/mL, clear
storage temp.
−20°C
SMILES string
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.
Biochem/physiol Actions
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.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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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
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
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
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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