1. Membrane Transporter/Ion Channel
  2. Sodium Channel
  3. Recainam hydrochloride

Recainam hydrochloride  (Synonyms: Wy-42362 hydrochloride)

Cat. No.: HY-105454A
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Recainam (Wy-42362) hydrochloride is a potent orally active antiarrhythmic agent and a sodium channel inhibitor. Recainam hydrochloride elevates ventricular fibrillation threshold, suppresses induced cardiac dysrhythmias, and may accentuate cardiac tissue refractoriness heterogeneity. Recainam hydrochloride can be used for the research of arrhythmias.

For research use only. We do not sell to patients.

Recainam hydrochloride

Recainam hydrochloride Chemical Structure

CAS No. : 74752-07-1

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Description

Recainam (Wy-42362) hydrochloride is a potent orally active antiarrhythmic agent and a sodium channel inhibitor. Recainam hydrochloride elevates ventricular fibrillation threshold, suppresses induced cardiac dysrhythmias, and may accentuate cardiac tissue refractoriness heterogeneity. Recainam hydrochloride can be used for the research of arrhythmias[1][2][3][4].

In Vitro

Recainam (10-300 μM; ≥30 min) hydrochloride has no significant effect on key electrophysiologic variables of isolated rabbit sinoatrial node preparations, aside from modestly shortening action potential duration[2].
Recainam (10-100 μM; ≥30 min) hydrochloride significantly reduces the maximal rate of rise of phase 0 (V̇max) in isolated rabbit atrial muscle preparations without altering other key electrophysiologic variables[2].
Recainam (10-300 μM; ≥30 min) hydrochloride causes concentration-dependent reductions in the maximal rate of rise of phase 0 (V̇max) in isolated canine ventricular muscle preparations without altering action potential duration or effective refractory period[2].
Recainam (1-300 μM; ≥30 min) hydrochloride causes concentration-dependent reductions in the maximal rate of rise of phase 0 (V̇max), action potential amplitude, action potential duration, and effective refractory period in isolated canine Purkinje fiber preparations[2].
Recainam (10-60 μM; ≥30 min) hydrochloride shifts the membrane responsiveness curve in the hyperpolarizing direction in isolated canine Purkinje fiber preparations, with higher concentrations abolishing premature responses from depolarized membrane potentials[2].
Recainam (300 μM; ≥30 min) hydrochloride induces a frequency-dependent reduction in the maximal rate of rise of phase 0 (V̇max) in isolated canine Purkinje fiber, canine ventricular muscle, and rabbit atrial muscle preparations, and abolishes responses at frequencies >3 Hz in Purkinje fibers[2].
Recainam (100 μM; ≥10 min) hydrochloride depresses phase 4 depolarization and slows isoproterenol-induced automaticity in isolated canine Purkinje fiber preparations[2].
Recainam (300 μM; ≥30 min) hydrochloride does not affect slow channel-dependent potentials induced by high potassium and isoproterenol in isolated canine ventricular muscle and Purkinje fiber preparations[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Parmacokinetics
Species Dose Route AUC0-∞ T1/2 MRT Vss Cmax Bioavailability Tmax
Dog[3] 15 mg/kg i.v. 20.9 μg·h/mL 1.8 h 2.3 h 1.2 L/kg / / /
Dog[3] 15 mg/kg p.o. 18.1 μg·h/mL / / / 8.5 μg/mL 89 % 2.0 h
Mice[3] 100 mg/kg p.o. 16.6 μg·h/mL 0.8 h / / 13.5 μg/mL / /
Mice[3] 120 mg/kg p.o. 26.9 μg·h/mL 1.2 h / / 23.5 μg/mL / /
Mice[3] 208 mg/kg p.o. 64.3 μg·h/mL 1.0 h / / 48.7 μg/mL / /
Mice[3] 54 mg/kg p.o. / / / / 6.4 μg/mL / /
Rabbit[3] 100 mg/kg p.o. 39.6 μg·h/mL 3.4 h / / 16.0 μg/mL / /
Rabbit[3] 25 mg/kg i.v. 5.0 μg·h/mL 0.6 h 0.7 h 3.6 L/kg / / /
Rabbit[3] 50 mg/kg p.o. / / / / 4.1 μg/mL / /
Rat[3] 100 mg/kg p.o. 10.5 μg·h/mL 3.1 h / / 1.3 μg/mL 51 % /
Rat[3] 110 mg/kg p.o. 19.9 μg·h/mL 4.5 h / / 6.6 μg/mL / /
Rat[3] 20 mg/kg i.v. 4.1 μg·h/mL 0.6 h 0.6 h 3.2 L/kg / / /
Rat[3] 500 mg/kg p.o. 73.9 μg·h/mL 3.6 h / / 7.8 μg/mL / /
Rhesus monkey[3] 15 mg/kg i.v. 12.8 μg·h/mL 1.6 h 1.9 h 2.2 L/kg / / /
Rhesus monkey[3] 15 mg/kg p.o. 12.0 μg·h/mL 1.9 h / / 3.3 μg/mL 97 % /
In Vivo

Recainam (3.75-7.5 mg/kg loading; 0.0375-0.075 mg/kg per min maintenance; i.v.; loading dose over 20 min; maintenance infusion for remainder of experiment) hydrochloride elevates the energy required for ventricular defibrillation in a dose-dependent manner, with low and high doses increasing E50 by 42% and 92%, respectively, while prolonging QRS duration without altering ventricular effective refractory period[1].
Recainam (p.o.; i.v.) hydrochloride exhibits anti-arrhythmic activity in dogs with experimentally induced cardiac arrhythmias[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Mongrel dogs (male, 14-23 kg, anesthetized with sodium pentobarbital)[1]
Dosage: 3.75 mg/kg (loading) + 0.0375 mg/kg per min (maintenance); 7.5 mg/kg (loading) + 0.075 mg/kg per min (maintenance)
Administration: i.v.; loading dose over 20 min; maintenance infusion for remainder of experiment
Result: Increased sinus QRS duration by 11% and paced QRS duration by 14% at low dose.
Produced no significant change in ventricular effective refractory period or sinus cycle length at low dose.
Increased E50 by 42% at low dose.
Increased sinus QRS duration by 27% and paced QRS duration by 23% at high dose.
Produced no significant change in ventricular effective refractory period or sinus cycle length at high dose.
Increased E50 by 92% at high dose.
Caused changes in E50 that were significantly different from the saline group and between low and high dose groups.
Showed no statistically significant difference in percent change of sinus QRS duration between low and high dose groups.
Molecular Weight

299.84

Formula

C15H26ClN3O

CAS No.
SMILES

CC(C)NCCCNC(NC1=C(C=CC=C1C)C)=O.[H]Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

Purity & Documentation
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Recainam hydrochloride
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HY-105454A
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