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.
For research use only. We do not sell to patients.
- CAS No.: 898911-09-6
- Formula: C30H31F6N7
- Molecular Weight:603.60
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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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
In Vitro
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.
In Vivo
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.
Chemical Information
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CAS No. 898911-09-6
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Molecular Weight 603.60
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Formula 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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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)
DRL-17822 Related Classifications
HY-182320 Related Classifications
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