BLT-3
BLT-3 is an inhibitor of scavenger receptor class B type I (SR-BI) that exerts reversible, non-cell-type-specific inhibitory effects on SR-BI-mediated lipid transport. BLT-3 inhibits SR-BI-mediated selective lipid uptake from HDL as well as cholesterol efflux from cells to HDL. BLT-3 enhances the binding of HDL to SR-BI. BLT-3 is applicable to research related to atherosclerosis and coronary heart disease.
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- CAS No.: 109940-24-1
- Formule: C19H13NO
- Masse moléculaire:271.32
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
In Vitro
BLT-3 inhibits SR-BI-mediated DiI uptake from DiI-HDL in ldlA[mSR-BI] cells, with an IC50 of 0.51 μM[1].
BLT-3 inhibits SR-BI-mediated [3H]CE uptake from [3H]CE-HDL in ldlA[mSR-BI] cells, with an IC50 of 2.3 μM[1].
BLT-3 inhibits SR-BI-mediated [3H]CE uptake from [3H]CE-HDL in Y1-BS1 cells, with an IC50 of 1.7 μM[1].
BLT-3 inhibits SR-BI-mediated [3H]cholesterol efflux to HDL in ldlA[mSR-BI] cells, with an IC50 of 17.2 μM[1].
BLT-3 enhances the binding of 125I-HDL to SR-BI in ldlA[mSR-BI] cells by increasing binding affinity (decreasing Kd and Koff) without altering Bmax, with an IC50 of 46.5 μM for its binding-enhancing effect[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 109940-24-1
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Masse moléculaire 271.32
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Formule C19H13NO
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SMILES
N=1OC(C=2C=CC=CC2)=C3C=CC=C3C1C=4C=CC=CC4
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
BLT-3 Related Classifications
HY-120433 Related Classifications
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