CCG 258001
CCG 258001 is a GRK inhibitor with IC50 values of 0.29, 51.8, and 33 µM against GRK2, GRK1, and GRK5, respectively. CCG 258001 inhibits GRK activity in cardiomyocytes and other muscle cells. CCG 258001 is applicable to the research of heart diseases, including heart failure, myocardial hypertrophy, and hypertension.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- CAS. Nr.: 2055990-96-8
- Formel: C20H22FN3O
- Molecular Weight:339.41
-
Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biologische Aktivität
-
Chemical Information
- Protokoll
- Reinheit & Dokumentation
- Verweise
-
Help & FAQs
Biologische Aktivität
Beschreibung
IC50 & Target
[1]|
GRK2 0.29 μM (IC50) |
GRK5 33 μM (IC50) |
In Vitro
CCG 258001 (5 min) potently inhibits GRK2 with an IC50 of 0.29 µM, while it shows weak inhibitory effects on GRK1 and GRK5[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
CAS. Nr. 2055990-96-8
-
Molecular Weight 339.41
-
Formel C20H22FN3O
-
SMILES
C(OC=1C=C2C(=CC1)NN=C2)[C@H]3[C@@H](CCN(C)C3)C4=CC=C(F)C=C4
-
Versand
Room temperature in continental US; may vary elsewhere.
-
Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
-
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)
CCG 258001 Related Classifications
HY-120168 Related Classifications
Powered by Bioz