Indecainide - CAS 74517-78-5
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Sodium Channel
Indecainide is a Sodium channel antagonists originated by Eli Lilly. Treatment for Arrhythmias and Ventricular arrhythmias was discontinued.
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Ricainid, Indecainida, Indecainidum, Decabid, Ricainide;9-[3-(propan-2-ylamino)propyl]fluorene-9-carboxamide
Soluble in DMSO
-20℃ Freezer
Arrhythmias; Ventricular arrhythmias
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Canonical SMILES:
Current Developer:
Originator Eli Lilly
1.Noninvasive evaluation of indecainide for serious ventricular tachyarrhythmia.
Podrid PJ1, Hohnloser S, Lown B. Am J Cardiol. 1988 Apr 1;61(10):764-9.
Indecainide, a new class 1C agent, was administered to 16 patients with a history of ventricular fibrillation or ventricular tachycardia. Evaluation of drug effect consisted of acute testing with 125 mg followed by a period of maintenance therapy. Efficacy, as evaluated with both ambulatory monitoring and exercise testing, was defined as total elimination of runs of ventricular tachycardia, greater than 90% reduction in couplets and greater than 50% decrease in ventricular premature complex. During acute drug testing 9 of the 16 patients responded to the drug. Four patients did not receive maintenance therapy with indecainide, because of toxic side effects. Of the remaining 12 patients, 7 responded to indecainide based on monitoring, 5 responded judged by exercise testing and 4 when both monitoring and exercise testing were considered. There was no correlation between dose, blood level of drug and effect on arrhythmia. In this small group acute drug testing did not appear to predict the response to the drug during maintenance therapy.
2.Effect of indecainide in patients with left ventricular dysfunction.
Giardina EV1, Saroff AL, Schneider M. Clin Pharmacol Ther. 1990 Nov;48(5):582-9.
Indecainide, a new antiarrhythmic agent classified as type Ic was evaluated in 11 patients with heart disease who had greater than or equal to 30 ventricular premature complexes/hour, moderate-to-marked left ventricular dysfunction, and mean ejection fraction 34% +/- 8%. Patients received indecainide, 50 mg by mouth, every 6 hours and the dose was increased until greater than or equal to 80% suppression was noted, adverse effects occurred, or a maximum dose of 100 mg indecainide was given every 6 hours. Ventricular premature complexes were suppressed greater than or equal to 80% in nine patients (p less than 0.05) and ventricular tachycardia episodes were completely suppressed in five of eight patients. The effective or maximal mean daily indecainide dose was 191 +/- 32 mg; half of the responders achieved achieved efficacy at serum drug concentration greater than or equal to 600 ng/ml. Serum drug concentration was directly related to gender (r = 0.
3.Indecainide: effects on arrhythmias, electrophysiology, and cardiovascular dynamics.
Holland DR1, Lacefield WB, Gonzales CR, Johnston SR, Turk JA. J Cardiovasc Pharmacol. 1989 Sep;14(3):454-61.
The cardiovascular pharmacology of indecainide, a new class I antiarrhythmic agent, was studied in intact animals. Arrhythmias produced by ouabain were converted to sinus rhythm by indecainide (100 micrograms/kg/min, i.v.) at 0.7 +/- 0.1 mg/kg and a corresponding plasma concentration of 1.7 +/- 0.2 micrograms/ml at the time of conversion. Infusion at a slower rate (20 micrograms/kg/min) converted to sinus rhythm at 0.4 +/- 0.1 mg/kg and 0.4 +/- 0.2 micrograms/ml plasma. Arrhythmias produced by prior (24 h) coronary artery occlusion were converted to 50% sinus rhythm by indecainide (100 micrograms/kg/min, i.v.) at 1.3 mg/kg. In conscious dogs, 6 mg/kg indecainide p.o. prolonged the PR and QRS intervals by 31 +/- 5 and 13 +/- 3%, respectively, at a corresponding plasma concentration of 2.8 +/- 0.5 micrograms/ml. His bundle studies revealed that the PR interval prolongation was due to an increase in both A-H and H-V intervals. In anesthetized dogs, indecainide (1-5 mg/kg, i.
4.Indecainide for treatment of ventricular ectopic depolarizations: efficacy, pharmacokinetics, hemodynamic effects and safety.
Salerno DM1, Krejci J, Granrud G, Hodges M. J Am Coll Cardiol. 1988 Apr;11(4):843-50.
Ten patients were treated with oral indecainide for frequent ventricular ectopic depolarizations during a short-term, dose-ranging, single blind inpatient trial followed by open label long-term therapy for 2 years. During dose ranging, patients received placebo followed by 50, 75 and 100 mg of indecainide three times daily. Eight of the 10 patients achieved greater than or equal to 80% reduction in ventricular ectopic depolarizations during inpatient therapy. Mean ventricular ectopic depolarizations decreased from 15,792/24 h to 2,357/24 h on optimal dosage (p less than 0.01). Nine patients had paired ventricular ectopic depolarizations; four of the nine had greater than or equal to 99% reduction of these beats. Among seven patients with nonsustained ventricular tachycardia, five had 100% elimination of these events with indecainide and all had greater than or equal to 90% reduction in these events. Indecainide prolonged the PR interval 44 +/- 27 ms (p less than 0.
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CAS 74517-78-5 Indecainide

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