Mefruside
Based on 1 Customer Validation
Mefruside is an orally active diuretic and has a mild hypotensive effect. Mefruside inhibits the synthesis of urea in an isolated rat liver perfusion model. Mefruside can be used in studies of oedema and hypertension.
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- Pureté : 99.9%
- CAS No.: 7195-27-9
- Formule: C13H19ClN2O5S2
- Masse moléculaire:382.88
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Stockage:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
In Vitro
Mefruside (0.3 mM; 50 min) shows 34% inhibition of urea synthesis in isolated perfused rat liver[1].
Mefruside (0.25, 0.5, 0.75, 1, 1.25 mM) inhibits urea synthesis in a concentration-dependent manner in isolated perfused rat liver[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Rat liver (from male Wistar rats of 120-220 g body weight; isolated perfused model)
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Concentration:0.3 mM
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Incubation Time:50 min
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Result:Exhibited inhibition rate of urea synthesis of 34%.
Chemical Information
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CAS No. 7195-27-9
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Appearance Solid
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Masse moléculaire 382.88
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Formule C13H19ClN2O5S2
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Color White to off-white
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SMILES
O=S(C1=CC=C(C(S(=O)(N)=O)=C1)Cl)(N(CC2(OCCC2)C)C)=O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
Protocole
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Pureté et documentation
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Fiche technique (269 KB)
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SDS (557 KB)
- English - EN (557 KB)
- Français - FR (557 KB)
- Deutsch - DE (557 KB)
- Norwegian - NO (557 KB)
- Español - ES (557 KB)
- Swedish - SV (557 KB)
- Italian - IT (557 KB)
- Korean - KR (557 KB)
- Portuguese - PT (557 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Häussinger D, et al. Liver carbonic anhydrase and urea synthesis. Hepatology. 1988 Mar-Apr;8(2):435. [Content Brief]
[2]. Brogden RN, et al. Mefruside: a preliminary report of its pharmacological properties and therapeutic efficacy in oedema and hypertension. Drugs. 1974;7(6):419-25. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Mefruside Related Classifications
HY-123179 Related Classifications
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