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E9156

Sigma-Aldrich

Encainide hydrochloride

≥98% (HPLC), powder

Synonym(s):

(+/-)-4-Methoxy-N-[2-[2-(1-methyl-2-piperidinyl)ethyl]phenyl]benzamide hydrochloride, MJ-9067

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About This Item

Empirical Formula (Hill Notation):
C22H28N2O2 · HCl
CAS Number:
Molecular Weight:
388.93
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Assay

≥98% (HPLC)

form

powder

solubility

H2O: >25 mg/mL

originator

Bristol-Myers Squibb

storage temp.

2-8°C

SMILES string

Cl.COc1ccc(cc1)C(=O)Nc2ccccc2CCC3CCCCN3C

InChI

1S/C22H28N2O2.ClH/c1-24-16-6-5-8-19(24)13-10-17-7-3-4-9-21(17)23-22(25)18-11-14-20(26-2)15-12-18;/h3-4,7,9,11-12,14-15,19H,5-6,8,10,13,16H2,1-2H3,(H,23,25);1H

InChI key

OJIIZIWOLTYOBS-UHFFFAOYSA-N

Biochem/physiol Actions

Encainide hydrochloride is a sodium channel blocker and class Ic antiarrhythmic. Encainide is a non-chiral antiarrhythmic and benzanilide derivative.

Features and Benefits

This compound was developed by Bristol-Myers Squibb. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

Pictograms

Skull and crossbones

Signal Word

Danger

Hazard Statements

Hazard Classifications

Acute Tox. 3 Oral - Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

Target Organs

Respiratory system

Storage Class Code

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

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S Goldstein et al.
Circulation, 91(1), 79-83 (1995-01-01)
We tested the hypothesis that patients whose ventricular arrhythmias are easy to suppress have a lower rate of arrhythmic death, defined as arrhythmic death and nonfatal cardiac arrest, the primary end point in the Cardiac Arrhythmia Suppression Trials (CAST-I and
H J Duff et al.
The Journal of pharmacology and experimental therapeutics, 274(1), 508-515 (1995-07-01)
Encainide treatment in patients after myocardial infarction is associated with increased risk of sudden cardiac death. This may relate to drug-induced changes in the electrophysiologic milieu, thus predisposing the patient to sustained ventricular tachyarrhythmias. The goals of this study were
L Gorkin et al.
The American journal of cardiology, 71(4), 263-267 (1993-02-01)
Psychosocial variables predict the recurrence of clinical events in symptomatic patients, controlling for measures of disease severity. The Cardiac Arrhythmia Suppression Trial-1, a pharmacologic test of the arrhythmia suppression and mortality hypothesis among postmyocardial infarction patients, allowed a prospective test
A E Epstein et al.
JAMA, 270(20), 2451-2455 (1993-11-24)
To test the hypothesis that in survivors of myocardial infarction, the suppression of ventricular premature depolarizations improves survival free of cardiac arrest and arrhythmic death. International, prospective, multicenter, randomized, placebo-controlled trial. University and community hospitals. A total of 3549 patients
J C Kellen et al.
American journal of critical care : an official publication, American Association of Critical-Care Nurses, 5(1), 19-25 (1996-01-01)
Care of patients with ventricular arrhythmia after myocardial infarction requires careful nursing management, including assisting with arrhythmia monitoring and testing. Because ventricular premature depolarization is a known risk factor for sudden cardiac death, it was hypothesized that the suppression of

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Voltage-gated sodium channels are present in most excitable cell membranes and play an important role in generating action potentials.

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