Trandolapril-d3
Trandolapril-d3 is the deuterium labeled Trandolapril (HY-B0592). Trandolapril (RU44570) is a nonsulfhydryl proagent that is hydrolysed to the active diacid Trandolaprilat. Trandolapril is an orally administered angiotensin converting enzyme (ACE) inhibitor that has been used in the treatment of hypertension and congestive heart failure (CHF), and after myocardial infarction (MI).
For research use only. We do not sell to patients.
- Formula: C24H31D3N2O5
- Molecular Weight:433.56
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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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Molecular Weight 433.56
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Formula C24H31D3N2O5
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SMILES
[H][C@@](CCCC1)(N2C([C@@H](N[C@H](CCC3=CC=CC=C3)C(OCC)=O)C([2H])([2H])[2H])=O)[C@]1(C[C@H]2C(O)=O)[H]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Trandolapril-d3 Related Classifications
HY-W744298 Related Classifications
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