Clevidipine-d7
Clevidipine-d7 is the deuterium labeled Clevidipine. Clevidipine is a short-acting dihydropyridine calcium channel antagonist (IC50= 7.1 nM, V(H) = -40 mV ) under development for treatment of perioperative hypertension.
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- CAS No.: 2747918-66-5
- Formule: C21H16D7Cl2NO6
- Masse moléculaire:463.36
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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. 2747918-66-5
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Unlabeled CAS 167221-71-8
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Masse moléculaire 463.36
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Formule C21H16D7Cl2NO6
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SMILES
ClC1=CC=CC(C2C(C(OCOC(C(C(C([2H])([2H])[2H])([2H])[2H])([2H])[2H])=O)=O)=C(NC(C)=C2C(OC)=O)C)=C1Cl
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
Références
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. Yi X, Vivien B, Lynch C 3rd. Clevidipine blockade of L-type Ca2+ currents: steady-state and kinetic electrophysiological studies in guinea pigventricular myocytes. [Content Brief]
[3]. Huraux C, Makita T, Szlam F, The vasodilator effects of clevidipine on human internal mammary artery. Anesth Analg. 1997 Nov;85(5):1000-4. [Content Brief]
[4]. Ericsson H, et al. In vitro hydrolysis rate and protein binding of clevidipine, a new ultrashort-acting calcium antagonist metabolised by esterases, in different animal species and man. Eur J Pharm Sci. 1999 Apr;8(1):29-37. [Content Brief]
[5]. Ericsson H, et al. Pharmacokinetics of new calcium channel antagonist clevidipine in the rat, rabbit, and dog and pharmacokinetic/pharmacodynamic relationship in anesthetized dogs. Drug Metab Dispos. 1999 May;27(5):558-64. [Content Brief]
[6]. Schwieler JH, et al. Circulatory effects and pharmacology of clevidipine, a novel ultra short acting and vascular selective calcium antagonist, in hypertensive humans. J Cardiovasc Pharmacol. 1999 Aug;34(2):268-74. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)