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.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- CAS 番号: 2254333-97-4
- 分子式: C24H25N7O2
- 分子量:443.50
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保管条件:
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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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
製品説明
Cellular Effect
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Cell Line
|
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] |
体内実験
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.
臨床実験
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
化学情報
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CAS 番号 2254333-97-4
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分子量 443.50
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分子式 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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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
BMS-986308 関連分類
HY-162555 関連分類
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