N-Acetylprocainamide - CAS 32795-44-1
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
N-Acetylprocainamide, the N-acetylated metabolite of Procainamide, is a Class III antiarrhythmic agent. N-Acetylprocainamide is also a model drug in the study of establishing a quantitative approach to predict the renal clearances of basic drugs.
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Solid powder
Soluble in DMSO
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -92℃ for long term (months to years).
Shelf Life:
2 years
Boiling Point:
500.0±35.0 °C | Condition: Press: 760 Torr
Melting Point:
210 °C
1.097±0.06 g/cm3
Canonical SMILES:
1.Copper-catalyzed oxidative amidation of aldehydes with amine salts: synthesis of primary, secondary, and tertiary amides.
Ghosh SC1, Ngiam JS, Seayad AM, Tuan DT, Chai CL, Chen A. J Org Chem. 2012 Sep 21;77(18):8007-15. Epub 2012 Aug 30.
A practical method for the amidation of aldehydes with economic ammonium chloride or amine hydrochloride salts has been developed for the synthesis of a wide variety of amides by using inexpensive copper sulfate or copper(I) oxide as a catalyst and aqueous tert-butyl hydroperoxide as an oxidant. This amidation reaction is operationally straightforward and provides primary, secondary, and tertiary amides in good to excellent yields for most cases utilizing inexpensive and readily available reagents under mild conditions. In situ formation of amine salts from free amines extends the substrate scope of the reaction. Chiral amides are also synthesized from their corresponding chiral amines without detectable racemization. The practicality of this amide formation reaction has been demonstrated in an efficient synthesis of the antiarrhythmic drug N-acetylprocainamide.
2.Drug-herb interaction: effect of St John's wort on bioavailability and metabolism of procainamide in mice.
Dasgupta A1, Hovanetz M, Olsen M, Wells A, Actor JK. Arch Pathol Lab Med. 2007 Jul;131(7):1094-8.
CONTEXT: St John's wort induces the activity of the cytochrome P450 enzyme system causing treatment failure because of increased metabolism of many drugs. Procainamide is metabolized by a different pathway to N-acetyl procainamide.
3.Effect of drugs on defibrillation capacity.
Dopp AL1, Miller JM, Tisdale JE. Drugs. 2008;68(5):607-30.
Over 300,000 people die of sudden cardiac death (SCD) in the US annually. Implantable cardioverter-defibrillators (ICDs) have been shown to be more effective than antiarrhythmic drugs for the prevention of SCD in specific susceptible populations. Many patients in whom ICDs have been implanted receive concomitant therapy with antiarrhythmic drugs, for the purpose of reducing the frequency of appropriate and inappropriate defibrillation shocks. Drugs may influence defibrillation capacity and therefore influence the function of ICDs. The objective of this article is to review and update the literature regarding the effects of drugs on defibrillation capacity.A literature search was performed using PubMed (1966 to December 2007) to identify clinical studies, case reports and animal studies describing the effects of drugs on defibrillation capacity. Search terms included: antiarrhythmic drugs; cardiovascular drugs; amiodarone; sotalol; flecainide; propafenone; dofetilide; ibutilide; beta-blockers; lidocaine; procainamide; N-acetylprocainamide; mexiletine; disopyramide; moricizine; calcium channel blockers; defibrillation threshold; defibrillation energy requirements; defibrillation energy changes; defibrillation efficacy; implantable cardioverter defibrillators; and external defibrillators.
4.1-Aminobenzotriazole, a known cytochrome P450 inhibitor, is a substrate and inhibitor of N-acetyltransferase.
Sun Q1, Harper TW, Dierks EA, Zhang L, Chang S, Rodrigues AD, Marathe P. Drug Metab Dispos. 2011 Sep;39(9):1674-9. doi: 10.1124/dmd.111.039834. Epub 2011 Jun 15.
1-Aminobenzotriazole (ABT) has been used widely as a nonselective in vitro and in vivo inhibitor of cytochrome P450 enzymes. To date, however, it has not been evaluated as an inhibitor of UDP-glucuronosyltransferase (UGT), sulfotransferase (SULT), and N-acetyltransferase (NAT). In the present study, ABT was shown not to inhibit UGT and SULT activity (acetaminophen and 7-hydroxycoumarin as substrates) in rat liver microsomes and rat liver 9000 g supernatant fraction (RLS9), respectively. However, it did inhibit the RLS9-catalyzed N-acetylation of procainamide (IC(50) ∼ 30 μM), and no preincubation time dependence was evident. In agreement, oral ABT (100 mg/kg, 2 h predose) decreased the clearance of intravenous procainamide (45%) in rats, accompanied by a decreased N-acetylprocainamide-to-procainamide ratio in urine (0.74 versus 0.21) and plasma (area under the curve ratio 0.59 versus 0.11). Additional studies with human forms of NAT (hNAT1 and hNAT2) revealed that ABT is a more potent inhibitor of hNAT2 compared with hNAT1 (IC(50) 158 μM versus > 1 mM).
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CAS 32795-44-1 N-Acetylprocainamide

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