Translation of Cardiac Myosin Activation With 2-Deoxy-ATP to Treat Heart Failure Via an Experimental Ribonucleotide Reductase-Based Gene Therapy

[1]  J. Goldman,et al.  Dose-dependent augmentation of cardiac systolic function with the selective cardiac myosin activator, omecamtiv mecarbil: a first-in-man study , 2011, The Lancet.

[2]  P. Rahko,et al.  Low-dose enoximone improves exercise capacity in chronic heart failure. Enoximone Study Group. , 2000, Journal of the American College of Cardiology.

[3]  M. Regnier,et al.  2-deoxy-ATP enhances contractility of rat cardiac muscle. , 2000, Circulation research.

[4]  H. Sweeney,et al.  Transendocardial delivery of AAV6 results in highly efficient and global cardiac gene transfer in rhesus macaques. , 2011, Human gene therapy.

[5]  M. Geeves,et al.  Upregulation of Cardiomyocyte Ribonucleotide Reductase Increases Intracellular 2 deoxy-ATP, Contractility, and Relaxation , 2011, Journal of molecular and cellular cardiology.

[6]  M. Regnier,et al.  2-Deoxy adenosine triphosphate improves contraction in human end-stage heart failure. , 2015, Journal of molecular and cellular cardiology.

[7]  P. Chase,et al.  Increased intracellular [dATP] enhances cardiac contraction in embryonic chick cardiomyocytes , 2008, Journal of cellular biochemistry.

[8]  R. Palmiter,et al.  Heparin-binding correlates with increased efficiency of AAV1- and AAV6-mediated transduction of striated muscle, but negatively impacts CNS transduction , 2012, Gene Therapy.

[9]  Akshay S. Desai,et al.  Calcium upregulation by percutaneous administration of gene therapy in patients with cardiac disease (CUPID 2): a randomised, multinational, double-blind, placebo-controlled, phase 2b trial , 2016, The Lancet.

[10]  Md. Faiz Ahmad,et al.  The structural basis for the allosteric regulation of ribonucleotide reductase. , 2013, Progress in molecular biology and translational science.

[11]  P. Buttrick,et al.  Reverse Remodeling With Left Ventricular Assist Devices: A Review of Clinical, Cellular, and Molecular Effects , 2011, Circulation. Heart failure.

[12]  S. Bartholomew,et al.  2-Deoxy-ATP Enhances Multiple Kinetic Parameters to Improve Cardiac Function , 2016 .

[13]  Rian,et al.  A DOSE-DEPENDENT INCREASE IN MORTALITY WITH VESNARINONE AMONG PATIENTS WITH SEVERE HEART FAILURE , 2000 .

[14]  C. Murry,et al.  Thin filament incorporation of an engineered cardiac troponin C variant (L48Q) enhances contractility in intact cardiomyocytes from healthy and infarcted hearts. , 2014, Journal of molecular and cellular cardiology.

[15]  E. Homsher,et al.  The effect of ATP analogs on posthydrolytic and force development steps in skinned skeletal muscle fibers. , 1998, Biophysical journal.

[16]  Piotr Ponikowski,et al.  Chronic Oral Study of Myosin Activation to Increase Contractility in Heart Failure (COSMIC-HF): a phase 2, pharmacokinetic, randomised, placebo-controlled trial , 2016, The Lancet.

[17]  Amit N. Patel,et al.  Intracoronary Gene Transfer of Adenylyl Cyclase 6 in Patients With Heart Failure: A Randomized Clinical Trial. , 2016, JAMA cardiology.

[18]  Piotr Ponikowski,et al.  Acute Treatment With Omecamtiv Mecarbil to Increase Contractility in Acute Heart Failure: The ATOMIC-AHF Study. , 2016, Journal of the American College of Cardiology.

[19]  D. Cox,et al.  Cardiac Myosin Activation: A Potential Therapeutic Approach for Systolic Heart Failure , 2011, Science.

[20]  D. Martin,et al.  Molecular cloning of the cDNA for a mutant mouse ribonucleotide reductase M1 that produces a dominant mutator phenotype in mammalian cells , 1988, Molecular and cellular biology.

[21]  F. Spinale,et al.  Large animal models of heart failure: a critical link in the translation of basic science to clinical practice. , 2009, Circulation. Heart failure.

[22]  M. Gheorghiade,et al.  Agents with inotropic properties for the management of acute heart failure syndromes. Traditional agents and beyond , 2009, Heart Failure Reviews.

[23]  C. Murry,et al.  Cell-based delivery of dATP via gap junctions enhances cardiac contractility. , 2014, Journal of molecular and cellular cardiology.

[24]  D. Martyn,et al.  Calcium regulation of tension redevelopment kinetics with 2-deoxy-ATP or low [ATP] in rabbit skeletal muscle. , 1998, Biophysical journal.

[25]  W. Koch,et al.  Gene therapy in heart failure. , 2008, Circulation research.

[26]  D. Martyn,et al.  Cardiac length dependence of force and force redevelopment kinetics with altered cross-bridge cycling. , 2004, Biophysical journal.

[27]  Ann M Stock,et al.  Structural basis for drug-induced allosteric changes to human β-cardiac myosin motor activity , 2015, Nature Communications.

[28]  Amit N. Patel,et al.  Changes in ventricular remodelling and clinical status during the year following a single administration of stromal cell-derived factor-1 non-viral gene therapy in chronic ischaemic heart failure patients: the STOP-HF randomized Phase II trial , 2015, European heart journal.

[29]  G. Mahairas,et al.  AAV6-mediated Cardiac-specific Overexpression of Ribonucleotide Reductase Enhances Myocardial Contractility. , 2016, Molecular therapy : the journal of the American Society of Gene Therapy.

[30]  R J Barsotti,et al.  Cross-bridge versus thin filament contributions to the level and rate of force development in cardiac muscle. , 2004, Biophysical journal.

[31]  K. Ishikawa,et al.  Cardiac gene therapy in large animals: bridge from bench to bedside , 2012, Gene Therapy.

[32]  W. Koch,et al.  Heart Failure Gene Therapy: The Path to Clinical Practice , 2013, Circulation research.

[33]  P. Chase,et al.  Positive inotropic effects of low dATP/ATP ratios on mechanics and kinetics of porcine cardiac muscle. , 2006, Biophysical journal.

[34]  J. Cleland,et al.  The effects of the cardiac myosin activator, omecamtiv mecarbil, on cardiac function in systolic heart failure: a double-blind, placebo-controlled, crossover, dose-ranging phase 2 trial , 2011, The Lancet.

[35]  J. Teerlink A novel approach to improve cardiac performance: cardiac myosin activators , 2009, Heart Failure Reviews.

[36]  E. Homsher,et al.  ATP analogs and muscle contraction: mechanics and kinetics of nucleoside triphosphate binding and hydrolysis. , 1998, Biophysical journal.

[37]  G. Mahairas,et al.  Ribonucleotide reductase‐mediated increase in dATP improves cardiac performance via myosin activation in a large animal model of heart failure , 2015, European journal of heart failure.

[38]  M. Regnier,et al.  2-Deoxyadenosine triphosphate restores the contractile function of cardiac myofibril from adult dogs with naturally occurring dilated cardiomyopathy. , 2016, American journal of physiology. Heart and circulatory physiology.

[39]  A. Baker Refueling the heart: Using 2-deoxy-ATP to enhance cardiac contractility. , 2011, Journal of molecular and cellular cardiology.

[40]  S. Solomon,et al.  Effect of Cardiac Resynchronization Therapy on Reverse Remodeling and Relation to Outcome: Multicenter Automatic Defibrillator Implantation Trial: Cardiac Resynchronization Therapy , 2010, Circulation.

[41]  R. Hajjar,et al.  Efficiency of eight different AAV serotypes in transducing rat myocardium in vivo , 2007, Gene Therapy.

[42]  R. Weiss,et al.  Transgenic overexpression of ribonucleotide reductase improves cardiac performance , 2013, Proceedings of the National Academy of Sciences.

[43]  B. Greenberg,et al.  Safety and tolerability of omecamtiv mecarbil during exercise in patients with ischemic cardiomyopathy and angina. , 2015, JACC. Heart failure.

[44]  C A Smith,et al.  X-ray structure of the magnesium(II).ADP.vanadate complex of the Dictyostelium discoideum myosin motor domain to 1.9 A resolution. , 1996, Biochemistry.