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.
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: 109940-24-1
- 分子式: C19H13NO
- 分子量:271.32
-
保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
製品説明
体外実験
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.
化学情報
-
CAS 番号 109940-24-1
-
分子量 271.32
-
分子式 C19H13NO
-
SMILES
N=1OC(C=2C=CC=CC2)=C3C=CC=C3C1C=4C=CC=CC4
-
輸送条件
Room temperature in continental US; may vary elsewhere.
-
保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
-
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)