Encainide
(Synonyms: MJ9067) 目录号 : GC68017Encainide (MJ9067) 是一种具有 IC 类活性的抗心律失常药物。Encainide 有可能用于危及生命的室性心律失常、症状性室性心律失常和室上性心律失常研究。
Cas No.:66778-36-7
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Encainide (MJ9067) is an antiarrhythmic drug with class IC activity. Encainide has the potential for life-threatening ventricular arrhythmias, symptomatic ventricular arrhythmias and supraventricular arrhythmias research[1].
Encainide (0.3, 0.9, 2.7 mg/kg; infusion of single doses) prolongs His-Purkinje conduction time (HV interval) and intra-ventricular conduction time (QRS duration) but has no effect on sinus nodal recovery time or AV nodal conduction, or on refractoriness of atrium, AV node, or ventricular myocardium or on QT interval[1].
[1]. R N Brogden, et al. Encainide. A review of its pharmacological properties and therapeutic efficacy. Drugs. 1987 Nov;34(5):519-38.
| Cas No. | 66778-36-7 | SDF | Download SDF |
| 别名 | MJ9067 | ||
| 分子式 | C22H28N2O2 | 分子量 | 352.47 |
| 溶解度 | DMSO : 200 mg/mL (567.42 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.8371 mL | 14.1856 mL | 28.3712 mL |
| 5 mM | 0.5674 mL | 2.8371 mL | 5.6742 mL |
| 10 mM | 0.2837 mL | 1.4186 mL | 2.8371 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Encainide
Cardiovasc Drugs Ther 1989 Oct;3(5):691-710.PMID:2518680DOI:10.1007/BF01857621.
Encainide is a class IC antiarrhythmic agent having little or no effect on action-potential duration or maximum diastolic potential but decreasing the maximum rate of phase O depolarization as well as increasing atrial and ventricular effective refractory periods. In intact animals or humans, Encainide increases the AH, PR, QRS, and H-V intervals while not affecting the sinus node cycle length or JT interval. QT interval increases only by the concomitant increase in the QRS interval. Encainide is metabolized to O-demethyl Encainide (ODE) and 3-methoxy-ODE (MODE), both of which are also antiarrhythmics with similar pharmacology to Encainide. Encainide and its metabolites have little negative inotropic activity and ancillary pharmacology. Consequently, Encainide has little or no effect on hemodynamic variables in patients with either normal or compromised cardiac function. The drug is well tolerated, with side effects being mainly those associated with its local anesthetic activity such as blurred vision and dizziness. Encainide is particularly effective in patients with excessive premature ventricular complexes (PVCs) and less so in patients with sustained ventricular tachycardia (VT). Like all antiarrhythmics, Encainide may aggravate or precipitate new arrhythmias (proarrhythmia). The overall incidence of proarrhythmia is about 10%, with less occurring in patients with PVCs and more in those with sustained VT; also, the incidence of proarrhythmia is higher in patients with underlying heart disease. Encainide is also effective for the treatment of supra-ventricular arrhythmias, including atrial fibrillation, PSVT (both PAF as well as reentry of the nodal or W-P-W type), and ectopic atrial tachycardia. Its dosage and role in antiarrhythmic therapy are discussed.
Encainide for ventricular arrhythmias: placebo-controlled and standard comparison trials
Am J Cardiol 1986 Aug 29;58(5):74C-82C.PMID:3092623DOI:10.1016/0002-9149(86)90108-6.
Efficacy data obtained from the use of Encainide in the treatment of patients with benign or potentially lethal ventricular arrhythmias are reviewed. These include an oral dose multicenter titration study involving 111 patients in whom Encainide was given from 25 to 75 mg, 4 times/day, which was followed by a 3-center, reduced dose study in which 35 patients received a forced escalation of Encainide from 10 to 30 mg, 4 times/day. Frequent Holter monitoring was used to judge efficacy. An 8-center, double-blind, parallel, placebo-controlled outpatient trial was conducted using Encainide from 10 to 50 mg, 3 times/day, in 125 patients. This trial defined the lower end of the dose response curve for Encainide to be 25 mg, 3 times/day. The data from all these trials show that when properly titrated, Encainide is effective in decreasing ventricular premature complex frequency by at least 75% in about 80% of patients. A similar percentage will have abolition of ventricular tachycardia. When Encainide was compared with quinidine in a 9-center placebo-controlled crossover study, Encainide demonstrated more efficacy at 25 mg, 4 times/day, compared with quinidine at 200 mg, 4 times/day, in all arrhythmia parameters. Encainide was also better tolerated than quinidine and there was no statistically significant difference in the prevalence of asymptomatic proarrhythmia as detected by Holter monitoring between these 2 drugs. Long-term data in 220 patients over 36-month follow-up show continued Encainide efficacy. Thus, Encainide is a potent, effective class 1C antiarrhythmic agent and it has minimal negative inotropic effects and is well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
Flecainide and Encainide
Eur Heart J 1987 Mar;8 Suppl A:33-40.PMID:3107989DOI:10.1093/eurheartj/8.suppl_a.33.
Flecainide and Encainide (class IC) are presently under clinical evaluation in Italy. They prolong the duration of the QRS but not the period of ventricular repolarisation: the prolongation of QT is due solely to the prolongation of the Q-J. Flecainide and Encainide are extremely powerful and are suitable for the treatment of reciprocating supraventricular paroxysmal tachycardia and of persistent reciprocating tachycardia, the prophylaxis of WPW atrial fibrillation including cases with a short anterograde refractory period of the anomalous pathway and the treatment of ventricular ectopic beats and ventricular tachycardia. Both drugs are probably effective for the treatment of atrial fibrillation. However, in the case of atrial flutter they are of little effect of sinus rhythm cardioversion; on the other hand they significantly prolong the duration of the A-A interval, with variable results on ventricular rate. Flecainide and Encainide have 'parodoxical' arrhythmogenic effects, related to administration dosages, severity of the arrhythmia and seriousness of cardiopathy. Encainide shows peculiar pharmacokinetics due to hepatic oxidating metabolisation and to production of metabolites; among these the O-demethylencainide and the 3-methoxy-O-demethylencainide have an antiarrhythmic activity, which is probably more important than the Encainide parent and is longer-lasting. There are 'extensive', 'poor' and 'non-metaboliser' subjects. This results in wide pharmacokinetic inter- and intraindividual variability which must be taken into account during clinical treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Encainide: a new antiarrhythmic agent
Drug Intell Clin Pharm 1986 Jan;20(1):9-13.PMID:3080301DOI:10.1177/106002808602000101.
Encainide is classified as a type Ic antiarrhythmic agent. Absorption is essentially complete, but bioavailability is variable because of first-pass metabolism. Two metabolic phenotypes, extensive and poor metabolizers, have been identified. O-demethyl Encainide and 3-methoxy-O-demethyl Encainide are active metabolites of Encainide and contribute significantly to its antiarrhythmic effect. In clinical trials, Encainide has been shown to be highly effective in suppressing premature ventricular contractions and ventricular tachyarrhythmias. The drug is useful in treating ventricular arrhythmias refractory to other agents. Encainide is also moderately effective in supraventricular arrhythmias involving an accessory pathway. It is highly effective in cases of Wolff-Parkinson-White syndrome, where the accessory pathway has a short refractory period. Common adverse effects of Encainide are dizziness, visual disturbances, nausea, and headache. Encainide appears to be a safe and effective antiarrhythmic agent with few adverse effects and negligible hemodynamic effects. Encainide may be a useful agent for ventricular and supraventricular arrhythmias, particularly those refractory to other agents.
Clinical pharmacokinetics of Encainide
Clin Pharmacokinet 1988 Mar;14(3):141-7.PMID:3131058DOI:10.2165/00003088-198814030-00002.
The disposition kinetics of the new antiarrhythmic agent Encainide are a function of the genetic polymorphism which also controls debrisoquin 4-hydroxylation. In the majority of subjects (extensive metabolisers) Encainide undergoes extensive first-pass hepatic biotransformation to the active metabolites O-desmethyl Encainide (ODE) and 3-methoxy-O-desmethyl Encainide (MODE). The plasma concentrations of these metabolites are higher than those of Encainide, and pharmacological effects correlate better with plasma metabolite concentrations than they do with those of Encainide itself. In poor metabolisers, who make up to 7% of the population, a first-pass effect is absent, Encainide clearance is lower, and plasma Encainide concentrations are higher than those in extensive metabolisers. In poor metabolisers, plasma concentrations of active metabolites are low or undetectable, and the effects of Encainide therapy can be closely correlated with plasma concentrations of the parent drug. Despite the marked differences in Encainide disposition between extensive and poor metabolisers, the dosages which produce pharmacological effects (QRS prolongation and arrhythmia suppression) are similar in both groups. Encainide biotransformation is impaired in hepatic disease, but no major dosage changes are required. On the other hand, excretion of Encainide and its metabolites is impaired in individuals with renal disease, and starting dosages should be decreased. The time required to achieve steady-state concentrations of metabolites (in extensive metabolisers) and of Encainide itself (in poor metabolisers) is similar (3 to 5 days); therefore, the dosage should be increased no more often than every 3 to 5 days.(ABSTRACT TRUNCATED AT 250 WORDS)