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.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 170552-18-8
- Formel: C20H33ClO5
- Molecular Weight:388.93
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
EP2 1180 nM (EC50) |
DP 799 nM (EC50) |
In Vitro
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.
Chemical Information
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CAS. Nr. 170552-18-8
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Molecular Weight 388.93
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Formel 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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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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.
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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