A 131701
A 131701 is a selective α1a- (Ki: 0.22 nM for human α1a) and α1d-adrenoceptor antagonist. A 131701 antagonizes epinephrine-induced increases in intraurethral pressure (IUP). A 131701 causes transient decreases in mean arterial blood pressure (MABP) and transient tachycardia. A 131701 can be used in the research of spontaneous hypertension.
For research use only. We do not sell to patients.
- CAS No.: 181490-18-6
- Formula: C24H24N4O3S
- Molecular Weight:448.54
-
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 Adrenergic Receptor Isoforms
More
Biological Activity
Description
IC50 & Target
[1]|
α1A-adrenergic receptor 0.22 nM (Ki) |
Alpha-1D adrenergic receptor |
Chemical Information
-
CAS No. 181490-18-6
-
Molecular Weight 448.54
-
Formula C24H24N4O3S
-
SMILES
O=C1NC(C2=NC=CC=C2S3)=C3C(N1CCN4C[C@]5([H])CCC6=C(OC)C=CC=C6[C@]5([H])C4)=O
-
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)
A 131701 Related Classifications
HY-135488 Related Classifications
Powered by Bioz