Flecainide acetate

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

一种 Ic 类抗心律失常药，用于预防和治疗快速心律失常，通过阻断心脏中的 Nav1.5 钠通道发挥作用。

A class Ic antiarrhythmic agent used to prevent and treat tachyarrhythmias, works by blocking the Nav1.5 sodium channel in the heart, slowing the upstroke of the cardiac action potential; also inhibits ryanodine receptor 2 (RyR2), reduces calcium sparks and thus arrhythmogenic calcium waves in the heart.Heart Arrhythmia Approved(In Vitro):Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia. Flecainide works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential. in vitro: Under the current-clamp condition, flecainide (1-100 microM) prolonged the action potential duration at both the early and the late phases of repolarization in a concentration-dependent manner without affecting the resting membrane potential . At a holding potential (HP) of -120 mV, flecainide use-dependently blocked WT and G1306E I(Na) equally but was more potent on R1448C channels. For WT, the extent of block depended on a holding voltage more negative than the activation threshold, being greater at -90 mV as compared to -120 and -180 mV . in vivo: Flecainide (80-130 mg/m(2) orally) resulted in termination of the tachycardia in all 8 patients. Acute pharmacological termination of arrhythmia occurred with oral flecainide loading in 1 and temporarily with intravenous esmolol loading in 1 patient.

Flecainide is a class 1C antiarrhythmic drug especially used for the management of supraventricular arrhythmia. Flecainide works by blocking the Nav1.5 sodium channel in the heart, causing prolongation of the cardiac action potential.in vitro: Under the current-clamp condition, flecainide (1-100 microM) prolonged the action potential duration at both the early and the late phases of repolarization in a concentration-dependent manner without affecting the resting membrane potential . At a holding potential (HP) of -120 mV, flecainide use-dependently blocked WT and G1306E I(Na) equally but was more potent on R1448C channels. For WT, the extent of block depended on a holding voltage more negative than the activation threshold, being greater at -90 mV as compared to -120 and -180 mV .in vivo: Flecainide (80-130 mg/m(2) orally) resulted in termination of the tachycardia in all 8 patients. Acute pharmacological termination of arrhythmia occurred with oral flecainide loading in 1 and temporarily with intravenous esmolol loading in 1 patient. Adjuvant therapy in form of propranolol was used in 5 and digoxin in 2 .

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Membrane Transporter/Ion Channel

Sodium Channel

Sodium Channel

Cardiovascular Disease

Heart Arrhythmia

54143-56-5

474.3947

C19H24F6N2O5

>98% (HPLC)

10 mM in DMSO

CC(=O)O.C1CCNC(C1)CNC(=O)C2=C(C=CC(=C2)OCC(F)(F)F)OCC(F)(F)F

Benzamide, N-(2-piperidinylmethyl)-2,5-bis(2,2,2-trifluoroethoxy)-, acetate (1:1)

(-20℃)

With Ice Pack

≥ 2 years