Labetalol hydrochloride-d5
Labetalol hydrochloride-d5 (AH-5158 hydrochloride-d5) is deuterium labeled Labetalol hydrochloride (HY-B1108). Labetalol (AH5158) hydrochloride is an orally available, selective α1-adrenergic recepto and non-selective β-adrenergic receptor competitive antagonist. Labetalol hydrochloride is an antihypertensive molecule that partially crosses the blood-brain barrier and has little effect on cardiac output. Labetalol hydrochloride can be used in the study of cardiovascular diseases, such as hypertension during pregnancy.
For research use only. We do not sell to patients.
- CAS No.: 2713514-78-2
- Formula: C19H20D5ClN2O3
- Molecular Weight:369.90
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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]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
Description
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. 2713514-78-2
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Unlabeled CAS 32780-64-6
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Molecular Weight 369.90
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Formula C19H20D5ClN2O3
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SMILES
OC1=CC=C(C=C1C(N)=O)C(O)CNC(CCC2=C(C([2H])=C(C([2H])=C2[2H])[2H])[2H])C.Cl
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Synonyms
AH-5158 hydrochloride-d5; Sch-15719W-d5
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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
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-236. [Content Brief]
[2]. Greenslade FC, et al. Labetalol binding to specific alpha- and beta-adrenergic sites in vitro and its antagonism of adrenergic responses in vivo. J Mol Cell Cardiol. 1979 Aug;11(8):803-11. [Content Brief]
[3]. Erdtsieck-Ernste EB, et al. Changes in adrenoceptors and monoamine metabolism in neonatal and adult rat brain after postnatal exposure to the antihypertensive labetalol. Br J Pharmacol. 1992 Jan;105(1):37-44. [Content Brief]
[4]. Johnson JD, et al. Catecholamines mediate stress-induced increases in peripheral and central inflammatory cytokines. Neuroscience. 2005;135(4):1295-307. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Labetalol hydrochloride-d5 Related Classifications
HY-B1108S Related Classifications
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