M353-0039
M353-0039 is a selective UT-A2 inhibitor with a human IC50 of 0.35 μM. M353-0039 blocks urea transport mediated by UT-A2. M353-0039 can be used for the study of hyponatremia and edema associated with congestive heart failure, nephrotic syndrome, and cirrhosis.
For research use only. We do not sell to patients.
- CAS No.: 1185074-29-6
- Formula: C16H15N3O3S2
- Molecular Weight:361.44
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
M353-0039 (50 seconds) potently and selectively inhibits UT-A2 in human UT-A2-overexpressing HEK293F cells with an IC50 of 0.35 μM, showing no activity against UT-A3 or UT-B[1].
M353-0039 (10-100 μM; 30 minutes) does not inhibit rat UT-A1-mediated urea transport in stably expressing MDCK cells[1].
M353-0039 (10 nM-100 μM; 6 minutes) does not inhibit mouse UT-B-mediated urea transport in erythrocytes[1].
M353-0039 (10 μM; 5 minutes) inhibits urea transport in human HepG2 cells, confirming UT-A2-mediated urea efflux in these hepatic cells[1].
M353-0039 (50 μM) binds deeply to UT-A2, forming more interactions than prior inhibitors, including critical contacts in the unique "T-T" subpocket, which underpins its superior inhibitory potency[1].
M353-0039 (50 seconds) demonstrates that the C285 residue in UT-A2 is critical for its binding and inhibitory activity, as mutating it to alanine reduces potency and mutating it to tryptophan abolishes activity[1].
M353-0039 (100 μM; 24 hours) exhibits no cytotoxicity toward MDCK cells[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:MDCK cells
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Concentration:100 μM
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Incubation Time:24 hours
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Result:Did not reduce MDCK cell viability compared to vehicle controls.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 8 weeks old)[1]
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Dosage:80 mg/kg
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Administration:i.p.; single dose
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Result:Significantly reduced kidney medulla urea concentration (P=0.0186) and osmolarity (P=0.0037).
Significantly reduced urine urea concentration (P<0.0001) and osmolarity (P<0.0001).
Caused only a minor decrease in kidney medulla urea concentration (P=0.0310) in mice on normal diet plus water deprivation.
Produced no significant changes in urine urea concentration or osmolarity in mice on normal diet plus water deprivation.
Chemical Information
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CAS No. 1185074-29-6
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Molecular Weight 361.44
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Formula C16H15N3O3S2
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SMILES
CC1=CSC(C2=CC(NC(CNC(C3=CC=CO3)=O)=O)=C(S2)C)=N1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)