Dexpramipexole improves bioenergetics and outcome in experimental stroke

Dexpramipexole, a drug recently tested in patients with amyotrophic lateral sclerosis (ALS,) is able to bind F1Fo ATP synthase and increase mitochondrial ATP production. Here, we have investigated its effects on experimental ischaemic brain injury.

[1]  Adam J Pawson,et al.  The Concise Guide to PHARMACOLOGY 2015/16: Transporters , 2015, British journal of pharmacology.

[2]  Christopher Southan,et al.  The Concise Guide to PHARMACOLOGY 2015/16: G protein‐coupled receptors , 2015, British journal of pharmacology.

[3]  Joanna L. Sharman,et al.  The IUPHAR/BPS Guide to PHARMACOLOGY in 2016: towards curated quantitative interactions between 1300 protein targets and 6000 ligands , 2015, Nucleic Acids Res..

[4]  G. Lippe,et al.  The Mitochondrial Permeability Transition Pore: Channel Formation by F-ATP Synthase, Integration in Signal Transduction, and Role in Pathophysiology. , 2015, Physiological reviews.

[5]  G. Porter,et al.  Cell death disguised: The mitochondrial permeability transition pore as the c-subunit of the F(1)F(O) ATP synthase. , 2015, Pharmacological research.

[6]  Paul M. George,et al.  Novel Stroke Therapeutics: Unraveling Stroke Pathophysiology and Its Impact on Clinical Treatments , 2015, Neuron.

[7]  John C McGrath,et al.  Implementing guidelines on reporting research using animals (ARRIVE etc.): new requirements for publication in BJP , 2015, British journal of pharmacology.

[8]  Paul A Insel,et al.  Experimental design and analysis and their reporting: new guidance for publication in BJP , 2015, British journal of pharmacology.

[9]  Gérard Hopfgartner,et al.  Quantification in MALDI-MS imaging: what can we learn from MALDI-selected reaction monitoring and what can we expect for imaging? , 2015, Analytical and Bioanalytical Chemistry.

[10]  V. Gribkoff,et al.  The Mitochondrial Complex V–Associated Large-Conductance Inner Membrane Current Is Regulated by Cyclosporine and Dexpramipexole , 2015, Molecular Pharmacology.

[11]  L. Galluzzi,et al.  Molecular mechanisms of cell death: central implication of ATP synthase in mitochondrial permeability transition , 2014, Oncogene.

[12]  Joel Stein,et al.  Executive summary: heart disease and stroke statistics--2014 update: a report from the American Heart Association. , 2014, Circulation.

[13]  O. Hardiman,et al.  Dexpramipexole versus placebo for patients with amyotrophic lateral sclerosis (EMPOWER): a randomised, double-blind, phase 3 trial , 2013, The Lancet Neurology.

[14]  D. Attwell,et al.  Synaptic Energy Use and Supply , 2012, Neuron.

[15]  V. Gribkoff,et al.  Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency , 2012, Brain Research.

[16]  A. Minassi,et al.  Ischemic Neuroprotection by TRPV1 Receptor-Induced Hypothermia , 2012, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[17]  V. Gribkoff,et al.  The effects of dexpramipexole (KNS-760704) in individuals with amyotrophic lateral sclerosis , 2011, Nature Medicine.

[18]  I. Macrae,et al.  Preclinical stroke research – advantages and disadvantages of the most common rodent models of focal ischaemia , 2011, British journal of pharmacology.

[19]  V. Gribkoff,et al.  Safety, Tolerability, and Pharmacokinetics of KNS‐760704 (Dexpramipexole) in Healthy Adult Subjects , 2011, Journal of clinical pharmacology.

[20]  M. Kiernan,et al.  Dexpramipexole, the R(+) enantiomer of pramipexole, for the potential treatment of amyotrophic lateral sclerosis. , 2010, IDrugs : the investigational drugs journal.

[21]  M. Moskowitz.  Brain protection: maybe yes, maybe no. , 2010, Stroke.

[22]  I. Cuthill,et al.  Animal Research: Reporting In Vivo Experiments: The ARRIVE Guidelines , 2010, British journal of pharmacology.

[23]  J. Barbosa,et al.  Ionic liquid matrices for MALDI-TOF-MS analysis of intact glycoproteins , 2010, Analytical and bioanalytical chemistry.

[24]  Maurizio Memo,et al.  Mitochondria-targeted antioxidant effects of S(-) and R(+) pramipexole , 2010, BMC pharmacology.

[25]  F. Pedata,et al.  The adenosine A2A receptor antagonist ZM241385 enhances neuronal survival after oxygen‐glucose deprivation in rat CA1 hippocampal slices , 2009, British journal of pharmacology.

[26]  D. Nicholls,et al.  Bioenergetics of mitochondria in cultured neurons and their role in glutamate excitotoxicity , 2007, Journal of neuroscience research.

[27]  M. Bianchi,et al.  High mobility group box 1 protein is released by neural cells upon different stresses and worsens ischemic neurodegeneration in vitro and in vivo , 2007, Journal of neurochemistry.

[28]  I. Sayeed,et al.  Patch clamp reveals powerful blockade of the mitochondrial permeability transition pore by the D2‐receptor agonist pramipexole , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[29]  A. Ludolph,et al.  Targeted Antioxidative and Neuroprotective Properties of the Dopamine Agonist Pramipexole and Its Nondopaminergic Enantiomer SND919CL2x [(+)2-Amino-4,5,6,7-tetrahydro-6-lpropylamino-benzathiazole Dihydrochloride] , 2006, Journal of Pharmacology and Experimental Therapeutics.

[30]  A. Vannacci,et al.  Nuclear Poly(ADP-ribose) Polymerase-1 Rapidly Triggers Mitochondrial Dysfunction* , 2005, Journal of Biological Chemistry.

[31]  Walter A. Korfmacher,et al.  Direct analysis of drug candidates in tissue by matrix-assisted laser desorption/ionization mass spectrometry. , 2003, Journal of mass spectrometry : JMS.

[32]  R. Corradetti,et al.  Brief, repeated, oxygen‐glucose deprivation episodes protect neurotransmission from a longer ischemic episode in the in vitro hippocampus: role of adenosine receptors , 2003, British journal of pharmacology.

[33]  G. Costantino,et al.  Novel Isoquinolinone-Derived Inhibitors of Poly(ADP-ribose) Polymerase-1: Pharmacological Characterization and Neuroprotective Effects in an in Vitro Model of Cerebral Ischemia , 2003, Journal of Pharmacology and Experimental Therapeutics.

[34]  A. Chiarugi.  Characterization of the molecular events following impairment of NF-kappaB-driven transcription in neurons. , 2002, Brain research. Molecular brain research.

[35]  G. Perkins,et al.  Differential Neuroprotection by Cyclosporin A and FK506 Following Ischemia Corresponds with Differing Abilities to Inhibit Calcineurin and the Mitochondrial Permeability Transition , 2002, Neurobiology of Disease.

[36]  P. Romagnoli,et al.  Poly(ADP-ribose) polymerase inhibitors attenuate necrotic but not apoptotic neuronal death in experimental models of cerebral ischemia , 2001, Cell Death and Differentiation.

[37]  G. Somjen.  Mechanisms of spreading depression and hypoxic spreading depression-like depolarization. , 2001, Physiological reviews.

[38]  E. Meli,et al.  1‐Aminoindan‐1,5‐dicarboxylic acid and (S)‐(+)‐2‐(3′‐carboxybicyclo[1.1.1] pentyl)‐glycine, two mGlu1 receptor‐preferring antagonists, reduce neuronal death in in vitro and in vivo models of cerebral ischaemia , 1999, The European journal of neuroscience.

[39]  E. Meli,et al.  Protection with metabotropic glutamate 1 receptor antagonists in models of ischemic neuronal death: time-course and mechanisms , 1999, Neuropharmacology.

[40]  M. Moskowitz,et al.  Pathobiology of ischaemic stroke: an integrated view , 1999, Trends in Neurosciences.

[41]  C. Fall,et al.  Pramipexole Reduces Reactive Oxygen Species Production In Vivo and In Vitro and Inhibits the Mitochondrial Permeability Transition Produced by the Parkinsonian Neurotoxin Methylpyridinium Ion , 1998, Journal of neurochemistry.

[42]  J. Garcìa,et al.  Neurological deficit and extent of neuronal necrosis attributable to middle cerebral artery occlusion in rats. Statistical validation. , 1995, Stroke.

[43]  Eng H. Lo,et al.  The Science of Stroke: Mechanisms in Search of Treatments , 2010, Neuron.

[44]  G. D. del Zoppo.  Stroke and neurovascular protection. , 2006, The New England journal of medicine.