Mecamylamine-d3 hydrochloride
Mecamylamine-d3 hydrochloride is the deuterium labeled Mecamylamine hydrochloride. Mecamylamine hydrochloride is an orally active, nonselective, noncompetitive nAChR antagonist that can treat various neuropsychiatric disorders. Mecamylamine hydrochloride is originally used as a ganglionic blocker in treating hypertension. Mecamylamine hydrochloride can easily crosses the blood-brain barrier.
For research use only. We do not sell to patients.
- CAS No.: 1217625-71-2
- Formula: C11H19D3ClN
- Molecular Weight:206.77
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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
-
CAS No. 1217625-71-2
-
Unlabeled CAS 826-39-1
-
Molecular Weight 206.77
-
Formula C11H19D3ClN
-
SMILES
[2H]C([2H])([2H])NC1(C2CC(CC2)C1(C)C)C.Cl
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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):211-216. [Content Brief]
[2]. Bacher I, et al. Mecamylamine - a nicotinic acetylcholine receptor antagonist with potential for the treatment of neuropsychiatric disorders. Expert Opin Pharmacother. 2009 Nov;10(16):2709-21. [Content Brief]
[3]. Ostroumov K, et al. Modeling study of mecamylamine block of muscle type acetylcholine receptors. Eur Biophys J. 2008 Apr;37(4):393-402. [Content Brief]
[4]. Rabenstein RL, et al. The nicotinic antagonist mecamylamine has antidepressant-like effects in wild-type but not beta2- or alpha7-nicotinic acetylcholine receptor subunit knockout mice. Psychopharmacology (Berl). 2006 Dec;189(3):395-401. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)