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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:
66794-74-9
Molecular Weight:
388.93
MDL number:
MFCD01667688
UNSPSC Code:
12352200
PubChem Substance ID:
329799083
NACRES:
NA.77
Pricing and availability is not currently available.

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

Gene Information

human ... SCN10A(6336) , SCN11A(11280) , SCN1A(6323) , SCN2A(6326) , SCN3A(6328) , SCN4A(6329) , SCN5A(6331) , SCN7A(6332) , SCN8A(6334) , SCN9A(6335)

Biochem/physiol Actions

Encainide hydrochloride is a sodium channel blocker and class Ic antiarrhythmic.
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
GHS06

Signal Word

Danger

Hazard Statements

H301,H315,H319,H335

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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Certificates of Analysis (COA)

Lot/Batch Number
018K46111
018K4611

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J L Anderson et al.
The American journal of cardiology, 79(1), 43-47 (1997-01-01)
In his book Deadly Medicine and on television, Thomas Moore impugns the process of antiarrhythmic drug approval in the 1980s, alleging that the new generation of drugs had flooded the marketplace and had caused deaths in numbers comparable to lives
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
S C Krishnan et al.
Journal of cardiovascular electrophysiology, 9(11), 1167-1172 (1998-12-03)
Three patients in whom Class IC sodium channel blockers induced ST segment elevation in leads V1 through V3 are described. The underlying electrophysiologic mechanism, implications for drug-induced proarrhythmia, and the relationship of the finding to the Brugada syndrome type of
J E Tisdale et al.
Journal of clinical pharmacology, 33(7), 623-630 (1993-07-01)
The efficacy of class 1C antiarrhythmic agents was determined in 36 patients with inducible sustained monomorphic ventricular tachycardia during baseline electrophysiology study (EPS), who continued to have inducible monomorphic ventricular tachycardia during EPS on class 1A antiarrhythmic therapy. Of 12
L Wang et al.
The Journal of pharmacology and experimental therapeutics, 264(3), 1056-1062 (1993-03-01)
Previous studies have reported that enhanced antiarrhythmic effects occur when agents that prolong repolarization are combined with agents that block the sodium channels. The mechanism(s) of this interaction have not been elucidated. In this study, the interactions between the prolongation
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Articles

Sodium Channels

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

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