Bisoprolol-d5
Based on 1 Customer Validation
Bisoprolol-d5 is the deuterium labeled Bisoprolol. Bisoprolol is a potent, selective and orally active β1-adrenergic receptor blocker. Bisoprolol has little activity on β2-receptor and has the potential for hypertension, coronary artery disease and stable ventricular dysfunction research.
For research use only. We do not sell to patients.
- CAS No.: 1189881-87-5
- Formula: C18H26D5NO4
- Molecular Weight:330.47
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Storage:
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
All Adrenergic Receptor Isoforms
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Biological Activity
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. 1189881-87-5
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Unlabeled CAS 104344-23-2
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Appearance Oil
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Molecular Weight 330.47
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Formula C18H26D5NO4
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Color Colorless to light yellow
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SMILES
CC(C)NC([2H])([2H])C(O)([2H])C([2H])([2H])OC1=CC=C(C=C1)COCCOC(C)C
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Protocols
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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.
Purity & Documentation
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Data Sheet (266 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. Jillian G Baker, et al. The selectivity of beta-adrenoceptor antagonists at the human beta1, beta2 and beta3 adrenoceptors. Br J Pharmacol. 2005 Feb;144(3):317-22. [Content Brief]
[3]. Maria Hoeltzenbein, et al. Pregnancy outcome after first trimester exposure to bisoprolol: an observational cohort study. J Hypertens. 2018 Oct;36(10):2109-2117. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)