BAY 60-5521
BAY 60-5521 is an orally active cholesteryl ester transfer protein (CETP) inhibitor with an IC50 of 7 nM. BAY 60-5521 inhibits CETP-mediated transfer of cholesteryl esters from HDL to LDL/VLDL, as well as the transfer of triglycerides from LDL/VLDL to HDL. It dose-dependently increases HDL-C and HDL concentrations, and slightly reduces triglyceride levels. BAY 60-5521 can be used in studies related to dyslipidemia.
For research use only. We do not sell to patients.
- CAS No.: 893409-49-9
- Formula: C30H37F4NO
- Molecular Weight:503.61
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
BAY 60-5521 (4-18 h) inhibits CETP activity in artificial liposome fluorescence assays, with a mean IC50 of 25 nM, and a mean IC50 of 7 nM measured in human lipoprotein SPA assays[2].
BAY 60-5521 (24 h) inhibits CETP activity in human plasma and plasma from CETP transgenic mice, with mean IC50 values of 50 nM and 25 nM, respectively[2].
BAY 60-5521 potently inhibits CETP activity in cell-free CETP fluorescence buffer assays and human plasma, with IC50 values of 0.025 μM and 0.05 μM, respectively[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
BAY 60-5521 (0.5-2 mg/kg; p.o.; single administration; 16 h-3 days) exerts CETP inhibitory activity and increases HDL-C levels in male CETP transgenic mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CETP transgenic mice (male, 18-25 g, transgenic expression of human CETP)[2]
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Dosage:0.5 mg/kg; 1 mg/kg; 2 mg/kg (single dose); 2 mg/kg (daily for 3 days)
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Administration:p.o.; single dose for 16 h and 24 h/once daily for 3 days
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Result:Significantly inhibited CETP activity at 16 h and 24 h post-administration with a single oral 2 mg/kg dose.
Increased HDL levels by 53.7% compared to baseline with daily oral 2 mg/kg for 3 days.
Chemical Information
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CAS No. 893409-49-9
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Molecular Weight 503.61
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Formula C30H37F4NO
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SMILES
F[C@@H](C1=CC=C(C=C1)C(F)(F)F)C2=C(C3CCCC3)N=C(CC(C)(C[C@@H]4O)C)C4=C2C5CCCCC5
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)