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Cardiac late Na+ current: Proarrhythmic effects, roles in long QT syndromes, and pathological relationship to CaMKII and oxidative stress

Heart rhythm, 2015-02, Vol.12 (2), p.440-448

2015

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A novel, potent, and selective inhibitor of cardiac late sodium current suppresses experimental arrhythmias

The Journal of pharmacology and experimental therapeutics, 2013-01, Vol.344 (1), p.23

2013

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The Selective Cardiac Late Sodium Current Inhibitor GS-458967 Suppresses Autonomically Triggered Atrial Fibrillation in an Intact Porcine Model

Journal of cardiovascular electrophysiology, 2015-12, Vol.26 (12), p.1364-1369

2015

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Effect of ranolazine on ventricular repolarization in class III antiarrhythmic drug-treated rabbits

Heart rhythm, 2012-12, Vol.9 (12), p.2051-2058

2012

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Use-dependent block of cardiac late Na+ current by ranolazine

Heart rhythm, 2009-11, Vol.6 (11), p.1625-1631

2009

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Reduction of repolarization reserve unmasks the proarrhythmic role of endogenous late Na+ current in the heart

American journal of physiology. Heart and circulatory physiology, 2009-09, Vol.297 (3), p.H1048-H1057

2009

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New Insights into the Beneficial Electrophysiologic Profile of Ranolazine in Heart Failure: Prevention of Ventricular Fibrillation With Increased Postrepolarization Refractoriness and Without Drug-Induced Proarrhythmia

Journal of cardiac failure, 2012-12, Vol.18 (12), p.939-949

2012

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Block of Tetrodotoxin-sensitive, Nav1.7, and Tetrodotoxin-resistant, Nav1.8, Na+ channels by Ranolazine

Channels (Austin, Tex.), 2008-11, Vol.2 (6), p.449-460

2008

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Ranolazine selectively blocks persistent current evoked by epilepsy‐associated NaV1.1 mutations

British journal of pharmacology, 2010-11, Vol.161 (6), p.1414-1426

2010

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Blockade of Na+ channels in pancreatic α-cells has antidiabetic effects

Diabetes (New York, N.Y.), 2014-10, Vol.63 (10), p.3545-3556

2014

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Antiepileptic activity of preferential inhibitors of persistent sodium current

Epilepsia (Copenhagen), 2014-08, Vol.55 (8), p.1274-1283

2014

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Rapid Kinetic Interactions of Ranolazine With HERG K+ Current

Journal of cardiovascular pharmacology, 2008-06, Vol.51 (6), p.581-589

2008

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Mechanisms of atrial-selective block of Na⁺ channels by ranolazine: I. Experimental analysis of the use-dependent block

American journal of physiology. Heart and circulatory physiology, 2011-10, Vol.301 (4), p.H1606-H1614

2011

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Sodium channel block by ranolazine in an experimental model of stretch-related atrial fibrillation: prolongation of interatrial conduction time and increase in post-repolarization refractoriness

Europace (London, England), 2013-05, Vol.15 (5), p.761-769

2013

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Mechanisms of atrial-selective block of Na⁺ channels by ranolazine: II. Insights from a mathematical model

American journal of physiology. Heart and circulatory physiology, 2011-10, Vol.301 (4), p.H1615-H1624

2011

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Ranolazine reduces neuronal excitability by interacting with inactivated states of brain sodium channels

Molecular pharmacology, 2014-01, Vol.85 (1), p.162-174

2014

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Mechanisms by Which Ranolazine Terminates Paroxysmal but Not Persistent Atrial Fibrillation

Circulation. Arrhythmia and electrophysiology, 2019-10, Vol.12 (10), p.e005557-e005557

2019

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Block of Na+ currents and suppression of action potentials in embryonic rat dorsal root ganglion neurons by ranolazine

Neuropharmacology, 2012-06, Vol.62 (7), p.2250-2259

2012

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Discovery of triazolopyridinone GS-462808, a late sodium current inhibitor (Late INai) of the cardiac Nav1.5 channel with improved efficacy and potency relative to ranolazine

Bioorganic & medicinal chemistry letters, 2016-07, Vol.26 (13), p.3207-3211

2016

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Discovery of triazolopyridine GS-458967, a late sodium current inhibitor (Late INai) of the cardiac NaV 1.5 channel with improved efficacy and potency relative to ranolazine

Bioorganic & medicinal chemistry letters, 2016-07, Vol.26 (13), p.3202-3206

2016

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Block of tetrodotoxin-sensitive, Na(V)1.7 and tetrodotoxin-resistant, Na(V)1.8, Na+ channels by ranolazine

Channels (Austin, Tex.), 2008-11, Vol.2 (6), p.449

2008

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Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat

American journal of physiology. Heart and circulatory physiology, 2013-10, Vol.305 (7), p.H1068-H1079

2013

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Nav1.5-dependent persistent Na+ influx activates CaMKII in rat ventricular myocytes and N1325S mice

American Journal of Physiology: Cell Physiology, 2011-09, Vol.301 (3), p.C577-586

2011

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Ranolazine block of human Na v 1.4 sodium channels and paramyotonia congenita mutants

Channels (Austin, Tex.), 2011-03, Vol.5 (2), p.161-172

2011

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Ranolazine selectively blocks persistent current evoked by epilepsy-associated Naν1.1 mutations

British journal of pharmacology, 2010-11, Vol.161 (6), p.1414-1426

2010

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Cardiac late Na+ current: Proarrhythmic effects, roles in long QT syndromes, and pathological relationship to CaMKII and oxidative stress

A novel, potent, and selective inhibitor of cardiac late sodium current suppresses experimental arrhythmias

The Selective Cardiac Late Sodium Current Inhibitor GS-458967 Suppresses Autonomically Triggered Atrial Fibrillation in an Intact Porcine Model

Effect of ranolazine on ventricular repolarization in class III antiarrhythmic drug-treated rabbits

Use-dependent block of cardiac late Na+ current by ranolazine

Reduction of repolarization reserve unmasks the proarrhythmic role of endogenous late Na+ current in the heart

New Insights into the Beneficial Electrophysiologic Profile of Ranolazine in Heart Failure: Prevention of Ventricular Fibrillation With Increased Postrepolarization Refractoriness and Without Drug-Induced Proarrhythmia

Block of Tetrodotoxin-sensitive, Nav1.7, and Tetrodotoxin-resistant, Nav1.8, Na+ channels by Ranolazine

Ranolazine selectively blocks persistent current evoked by epilepsy‐associated NaV1.1 mutations

Blockade of Na+ channels in pancreatic α-cells has antidiabetic effects

Antiepileptic activity of preferential inhibitors of persistent sodium current

Rapid Kinetic Interactions of Ranolazine With HERG K+ Current

Mechanisms of atrial-selective block of Na⁺ channels by ranolazine: I. Experimental analysis of the use-dependent block

Sodium channel block by ranolazine in an experimental model of stretch-related atrial fibrillation: prolongation of interatrial conduction time and increase in post-repolarization refractoriness

Mechanisms of atrial-selective block of Na⁺ channels by ranolazine: II. Insights from a mathematical model

Ranolazine reduces neuronal excitability by interacting with inactivated states of brain sodium channels

Mechanisms by Which Ranolazine Terminates Paroxysmal but Not Persistent Atrial Fibrillation

Block of Na+ currents and suppression of action potentials in embryonic rat dorsal root ganglion neurons by ranolazine

Discovery of triazolopyridinone GS-462808, a late sodium current inhibitor (Late INai) of the cardiac Nav1.5 channel with improved efficacy and potency relative to ranolazine

Discovery of triazolopyridine GS-458967, a late sodium current inhibitor (Late INai) of the cardiac NaV 1.5 channel with improved efficacy and potency relative to ranolazine

Block of tetrodotoxin-sensitive, Na(V)1.7 and tetrodotoxin-resistant, Na(V)1.8, Na+ channels by ranolazine

Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat

Nav1.5-dependent persistent Na+ influx activates CaMKII in rat ventricular myocytes and N1325S mice

Ranolazine block of human Na v 1.4 sodium channels and paramyotonia congenita mutants

Ranolazine selectively blocks persistent current evoked by epilepsy-associated Naν1.1 mutations

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