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You are here:Home-Research Areas-Cardiovascular Disease-Heart Arrhythmia

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An arrhythmia (also known as cardiac dysrhythmia) is defined as an irregular heartbeat, and results from abnormal electrical activity in the heart. There are various different types of arrhythmia, often resulting in a heartbeat that is too fast (tachycardia) or too slow (bradycardia). Atrial and ventricular fibrillation, which are the most common cardiac arrhythmias, account for 10-20% of all deaths among adults in the Western world. The incidence of atrial fibrillation increases with age; it not only affects cardiac function, but also increases the risk of stroke and may worsen heart failure.

Normal heartbeat

A normal heartbeat is driven by various stages of membrane depolarization and repolarization in single heart cells, propagating from the sinoatrial (SA) node to the atrium and the ventricle. There are two types of action potentials: the fast response action potential, which occurs in cardiac muscle and Purkinje fibers; and the slow response, evident in the SA and atrioventricular (AV) nodes. Action potentials enable rapid changes in heart rate. Contraction of the cardiac muscle occurs in response to depolarization. By generating action potentials and setting off a wave of depolarization, the SA node thus acts as a pacemaker, setting the rate of contraction of the heart. Dysfunction of the SA node may therefore result in an irregular heartbeat. The effective refractory period (ERP) is a mechanism that helps protect the heart from arrhythmias, by preventing the generation of new action potentials during the propagation of an existing one.

In addition to SA node dysfunction, arrhythmias can also occur as a result of abnormalities in the electrophysiology of heart cells or in cell-to-cell (impulse) propagation, which takes place through gap junctions. These enable conduction of a wave of depolarization between cells. Ion channels are responsible for the conduction of coordinated electrical impulses, and consequently dysregulation of their activity has been linked to the development of arrhythmias. For example, mutations in genes encoding the KV11.1 (hERG) potassium channel, the sodium NaV1.5 channel, and the calcium CaV1.2 channel have been linked to long QT syndrome (LQTS).

Treatment of Arrhythmia

Antiarrhythmic drug therapy aims to restore normal cardiac rhythm and conduction, and to prevent more serious arrhythmias from occurring. Vaughan Williams created one of the most widely used classification schemes for antiarrhythmic drugs. The scheme divides antiarrhythmic drugs into five classes (I-V), each of which concerns a different target:

1.Class I - Na+ channel blockers

~Class Ia - intermediate association/dissociation

~Class Ib - fast association/dissociation

~Class Ic - slow association/dissociation

2.Class II - Beta-adrenergic receptor blockers

3.Class III - K+ channel blockers

4.Class IV - Ca2+ channel blockers

5.Class V - Work by other, or unknown mechanisms

The lack of new molecular targets and toxicity problems has resulted in few novel antiarrhythmic agents being introduced in recent years, and further research is needed to develop novel, more efficacious antiarrhythmic drugs with greater selectivity and lower toxicity.

Cat. No. Product Name CAS No. Information
GY03945

Pirmenol hydrochloride

61477-94-9

An orally effective, long-acting antiarrhythmic agent that interacts with cardiac muscarinic receptors.

GY05219

JTV-519 fumarate

1883549-36-7

JTV-519 (K201) is a Ca2+-dependent blocker of SERCA and a partial agonist of ryanodine receptors (RyRs); displays Ca(2+)-dependent inhibition of SERCA-dependent ATPase activity with IC50 of 9 uM at 0.25 Ca2+ in cardiac muscle; may prevent abnormal Ca(2+) leak from the sarcoplasmic reticulum (SR) in the ischemic heart and skeletal muscle (SkM) by stabilizing the ryanodine receptors (RyRs; RyR1 and RyR2, respectively).

GY05374

JTV-519 HCl

1038410-88-6

JTV-519 (K201) is a Ca2+-dependent blocker of SERCA and a partial agonist of ryanodine receptors (RyRs); displays Ca(2+)-dependent inhibition of SERCA-dependent ATPase activity with IC50 of 9 uM at 0.25 Ca2+ in cardiac muscle; may prevent abnormal Ca(2+) leak from the sarcoplasmic reticulum (SR) in the ischemic heart and skeletal muscle (SkM) by stabilizing the ryanodine receptors (RyRs; RyR1 and RyR2, respectively).

GY05276

JTV-519

145903-06-6

JTV-519 (K201) is a Ca2+-dependent blocker of SERCA and a partial agonist of ryanodine receptors (RyRs); displays Ca(2+)-dependent inhibition of SERCA-dependent ATPase activity with IC50 of 9 uM at 0.25 Ca2+ in cardiac muscle; may prevent abnormal Ca(2+) leak from the sarcoplasmic reticulum (SR) in the ischemic heart and skeletal muscle (SkM) by stabilizing the ryanodine receptors (RyRs; RyR1 and RyR2, respectively).

GY05105

Vanoxerine

67469-69-6

Vanoxerine (GBR-12909, I-893, Boxeprazine) is a highly potent inhibitor of dopamine uptake in vitro in tissue slices obtained from rat neostriatum with IC50 of 40-50 nM, also inhibits norepinephrine uptake with IC50 of 560-2600 nM; Vanoxerine also is a potent hK(v)11.1 blocker, and at submicromolar concentrations, it blocks Ca and Na currents in a strongly frequency-dependent manner possesses anticonvulsant activity in zebrafish and rodent models of generalized epilepsy but with cardiac ion channel effects.

GY05104

Vanoxerine 2HCl

67469-78-7

Vanoxerine (GBR-12909, I-893) is a highly potent inhibitor of dopamine uptake in vitro in tissue slices obtained from rat neostriatum with IC50 of 40-50 nM, also inhibits norepinephrine uptake with IC50 of 560-2600 nM; Vanoxerine also is a potent hK(v)11.1 blocker, and at submicromolar concentrations, it blocks Ca and Na currents in a strongly frequency-dependent manner possesses anticonvulsant activity in zebrafish and rodent models of generalized epilepsy but with cardiac ion channel effects.

GY06454

Danegaptide Hydrochloride

943133-81-1

Danegaptide Hydrochloride is a potent, orally active gap-junction modifier; prevents significantly conduction velocity slowing at 10 nM compared with vehicle; has highly desirable in vitro and in vivo safety profile including (1) lack of direct effects on membrane ion currents, hERG inhibition, and CYP450 liabilities, (2) negative AMES result, (3) a benign NovaScreen profile, and (4) no effects on systemic hemodynamics.

GY06453

Danegaptide

943134-39-2

Danegaptide is a potent, orally active gap-junction modifier; prevents significantly conduction velocity slowing at 10 nM compared with vehicle; has highly desirable in vitro and in vivo safety profile including (1) lack of direct effects on membrane ion currents, hERG inhibition, and CYP450 liabilities, (2) negative AMES result, (3) a benign NovaScreen profile, and (4) no effects on systemic hemodynamics.

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