B-007
B-007 is an AplnR agonist with G protein-biased signaling (EC50 = 11.6 nM). B-007 activates the G protein pathway while abolishing β-arrestin1 and β-arrestin2 signaling. B-007 serves as a scaffold for development of G protein-biased apelin receptor agonists. B-007 can be used for the research of heart failure.
For research use only. We do not sell to patients.
- Formula: C32H24F5N5O7S
- Molecular Weight:717.62
-
Storage:
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]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
All Arrestin Isoforms
More
Biological Activity
Description
IC50 & Target
[1]|
Arrestin-2/β-Arrestin 1 |
Arrestin-3/β-Arrestin 2 |
In Vitro
B-007 potently activates the AplnR G protein pathway in cell systems expressing the Apelin receptor (AplnR), with an EC50 of 11.6 nM and an Emax of 118.0%[1].
B-007 completely fails to activate the β-arrestin1 or β-arrestin2 pathways of the AplnR in AplnR-expressing cell systems, thereby exhibiting prominent G protein-biased characteristics[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
-
Molecular Weight 717.62
-
Formula C32H24F5N5O7S
-
SMILES
COC1=CC=CC(OC)=C1C2=NC(C(NS(C(C3=CC=CC=C3)COC(C4=C(F)C(F)=C(F)C(F)=C4F)=O)(=O)=O)=O)=NN2C5=CN=CC(C)=C5
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
B-007 Related Classifications
HY-183777 Related Classifications
Powered by Bioz