DRL-17822
DRL-17822 is a selective cholesteryl ester transfer protein (CETP) inhibitor. DRL-17822 increases high-density lipoprotein levels. The exposure of DRL-17822 nanocrystal formulation increases significantly after a high-fat breakfast. The exposure of DRL-17822 in the fasted state is higher than that of its nanocrystal formulation. DRL-17822 can be used in the research of type II hyperlipidemia and atherosclerotic cardiovascular disease.
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: 898911-09-6
- 分子式: C30H31F6N7
- 分子量:603.60
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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
体外実験
DRL-17822 does not cross Caco-2 cell monolayers in measurable amounts, and may moderately inhibit recombinant human CYP3A4[1].
DRL-17822 is highly lipophilic, water-insoluble, and extensively bound to plasma proteins across species[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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:Wistar rats (male)[1]
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Dosage:10 mg/kg
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Administration:i.v.; single dose
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Result:Recovered approximately 0.004% of the dose in urine within 24 hours.
Recovered approximately 12.5% of the dose in feces within 24 hours.
化学情報
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CAS 番号 898911-09-6
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分子量 603.60
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分子式 C30H31F6N7
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SMILES
FC(F)(C1=CC(CN(CC2=CC3=C(N=C2N(CC4CC4)CC5CC5)C(C)=CC=C3)C6=NN(C)N=N6)=CC(C(F)(F)F)=C1)F
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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)
DRL-17822 関連分類
HY-182320 関連分類
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