Bopindolol-d9
Bopindolol-d9 ((±)-Bopindolol-d9) is the deuterium labeled Bopindolol (HY-B1562). Bopindolol ((±)-Bopindolol) is an orally active antagonist of β-adrenoceptors (ARs) with partial agonist activity. Bopindolol is non-selective for β1- and β2-ARs and has low affinity for β3-AR subtype. Bopindolol has intrinsic sympathomimetic as well as membrane stabilizing actions, inhibits renin secretion, and interacts with 5-HT receptors. Bopindolol is a proagent of Pindolol (HY-B0982). Bopindolol can be used for essential and renovascular hypertension research.
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- CAS No.: 1794891-82-9
- Formule: C23H19D9N2O3
- Masse moléculaire:389.54
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
In Vitro
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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CAS No. 1794891-82-9
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Unlabeled CAS 62658-63-3
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Masse moléculaire 389.54
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Formule C23H19D9N2O3
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SMILES
[2H]C([2H])([2H])C(C([2H])([2H])[2H])(C([2H])([2H])[2H])NCC(COC1=CC=CC2=C1C=C(N2)C)OC(=O)C3=CC=CC=C3
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Synonyms
(±)-Bopindolol-d9
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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.
Pureté et documentation
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)