BMS-986308
BMS-986308 is a selective and orally active renal outer medullary potassium (ROMK) channel inhibitor. BMS-986308 is selective for ROMK over hERG. BMS-986308 can be used for heart failure research.
For research use only. We do not sell to patients.
- CAS No.: 2254333-97-4
- Formula: C24H25N7O2
- Molecular Weight:443.50
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| HepG2 | IC50 |
>100 μM
Compound: 28; BMS-986308
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Cytotoxicity against human HepG2 cells
Cytotoxicity against human HepG2 cells
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[PMID: 38807539] |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male Sprague-Dawley rats (age: 8-12 weeks, 270-300 g)[1]
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Dosage:0.01 mg/kg, 0.03 mg/kg, 0.1 mg/kg, 0.3 mg/kg, 1 mg/kg and 3 mg/kg
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Administration:p.o; once (10% v/v DMAC, 40% v/v PEG400, 50% v/v of 30% w/v of HPβCD in 50 mM citrate buffer (pH 4.0))
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Result:Led to a robust increase in diuresis.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 2254333-97-4
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Molecular Weight 443.50
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Formula C24H25N7O2
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SMILES
CC1=C(COC2=O)C2=CC=C1[C@@H]3CN(C[C@@H](N3)C)CC4=NN(C5=CC(C)=C(C=N5)C#N)N=C4
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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)
BMS-986308 Related Classifications
HY-162555 Related Classifications
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