AL-6556
AL-6556 is a full agonist of the DP receptor and a partial agonist of the EP2 receptor. AL-6556 has an EC50 of 799 nM for bovine DP, a Ki of 3200 nM for human DP, and an EC50 of 1180 nM for human EP2, with selectivity over EP3, FP, IP, TP and 19 non-prostaglandin receptors. AL-6556 stimulates cAMP production via receptor activation and reduces intraocular pressure through aqueous humor inflow and outflow mechanisms. AL-6556 can be used in research related to ocular hypertension and glaucoma.
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: 170552-18-8
- 分子式: C20H33ClO5
- 分子量:388.93
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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
IC50 & Target
[1]|
EP2 1180 nM (EC50) |
DP 799 nM (EC50) |
体外実験
AL-6556 (0.1 nM-100 μM) shows highest affinity for human platelet DP receptors with a Ki of 3200 nM, 21-37-fold selectivity over EP3, FP, IP, and TP prostanoid receptors, and moderate affinity for EP1 and EP4 receptors[1].
AL-6556 (10 μM) weakly interacts with most nonprostanoid receptors, with the strongest inhibition (47.5%) observed at the platelet activating factor receptor[1].
AL-6556 (0.1 nM-100 μM; 15 min) acts as a full agonist at embryonic bovine tracheal fibroblast DP receptors, stimulating cAMP production with an EC50 of 799 nM and 93% maximum efficacy relative to PGD2[1].
AL-6556 (0.1 nM-100 μM; 15 min) acts as a partial agonist at human nonpigmented epithelial cell EP2 receptors, stimulating cAMP production with an EC50 of 1180 nM and 35% maximum efficacy relative to PGE2, with no agonist activity at EP4, IP, or FP receptors[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
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CAS 番号 170552-18-8
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分子量 388.93
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分子式 C20H33ClO5
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SMILES
O[C@@H](C1CCCCC1)CC[C@@H]2[C@H]([C@@H](C[C@H]2O)Cl)C/C=C\COCC(O)=O
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
プロトコル
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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.
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)
Keywords
- AL-6556
- 170552-18-8
- AL6556
- AL 6556
- Prostaglandin Receptor
- human platelet DP receptors
- FP receptor
- IP receptor
- human nonpigmented epithelial cell EP2 receptors
- DP receptor
- platelet activating factor receptor
- embryonic bovine tracheal fibroblast DP receptors
- TP receptor
- EP3 receptor
- EP2 receptor
- Inhibitor
- inhibitor
- inhibit