LXR agonist 4
LXR agonist 4 is a selective LXR inverse agonist with IC50 values of 7.6 (LXRα) and 2.9 μM (LXRβ), respectively. LXR agonist 4 exhibits selectivity over RORα and FXR. LXR agonist 4 robustly suppresses SREBP1c expression without altering ABCA1 or APOE. LXR agonist 4 displays antilipogenic properties and resolves fatty acid-induced steatosis. LXR agonist 4 can be used for the research of atherosclerosis and metabolic dysfunction-associated steatotic liver disease (MASLD).
For research use only. We do not sell to patients.
- Formula: C36H31ClF3NO2S
- Molecular Weight:634.15
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
LXRα 7.6 μM (IC50) |
LXRβ 2.9 μM (IC50) |
In Vitro
LXR agonist 4 (compound 3) (30 μM; 4-24 h) does not inhibit the proliferation of HEK293T or HepG2 cells[1].
LXR agonist 4 (30 μM; 24 h) suppresses SREBP1c expression without altering ABCA1 or APOE in HepG2 cells[1].
LXR agonist 4 (30 μM; 72 h) displays antilipogenic properties and resolves fatty acid-induced steatosis in HepG2 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:HEK293T and HepG2
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Concentration:30 μM
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Incubation Time:4, 14, and 24 h
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Result:Showed no significant inhibition of proliferation in HEK293T and HepG2 cells over 24 hours.
Chemical Information
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Molecular Weight 634.15
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Formula C36H31ClF3NO2S
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SMILES
CS(C1=CC=CC(C2=CC=C(C=C2)CN(CC(C3=CC=CC=C3)C4=CC=CC=C4)CC5=CC=CC(C(F)(F)F)=C5Cl)=C1)(=O)=O
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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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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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 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.
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Liver Histomorphometry
Liver histomorphometry is a quantitative histological approach used to measure structural alterations in hepatic tissue, including parenchymal loss, steatosis, fibrosis, and vascular remodeling, by combining stained tissue section analysis with stereological or computerized image-based measurements. Classical morphometric frameworks quantify volume fractions of liver compartments and fibrotic regions using systematic sampling and image analysis, enabling objective comparison of pathological changes across experimental groups. These approaches are widely applied in liver cirrhosis and fibrosis studies to reduce subjectivity in histological scoring and improve reproducibility of tissue evaluation. Recent methodological advances integrate automated image analysis and radiomics-based extraction of histological features from standard liver stains (e. g. , H&E and fibrotic stains), enabling quantitative correlation between morphometric features and fibrosis stages in non-alcoholic fatty live
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)