The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

CHEMBL137009     N-[1-[4-(4- fluorophenoxy)butyl]-4...

Synonyms: SureCN933977, AG-D-17026, ACMC-20m7dr, CHEBI:326258, LS-40628, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of R 56865

  • Myocytes were also exposed to hypoxia in the presence of R 56865, a compound that blocks noninactivating components of the Na+ current [1].
  • We conclude that R 56865 delays the onset of cellular uncoupling during ischemia and that this effect is not related to changes of conduction velocity and at most in part to changes of APD80 [2].
  • 1. In isolated cardiac muscle, submicromolar concentrations of R 56865 (N-[1-[4-(4-fluorophenoxy)-butyl]-4-piperidinyl]-N-methyl-2- benzothiazolamine) have been shown to attenuate the toxicity of cardiac glycosides [3].
  • Mechanical signs of intoxication, e.g. extrasystoles and contracture, as well as the development of spike-like action potentials could be prevented by pretreatment with R 56865 (3 X 10(-10)-10(-6) mol/l) [4].
  • No significant differences were observed between placebo and R 56865 (20 mg) concerning time to onset and duration of ST-segment changes and symptomatic angina pectoris, respectively [5].

High impact information on R 56865


Chemical compound and disease context of R 56865


Biological context of R 56865


Anatomical context of R 56865


Gene context of R 56865

  • KC 12291 and R 56865 dose-dependently induced bradycardia (Delta heart rate obtained, -55.1+/-5.2 beat per min, P<0.05, and -71.9+/-8.5 bpm, P<0.05, respectively) [14].
  • The AVP-induced contraction was not affected by R 56865 (10(-5) mol/l) [15].

Analytical, diagnostic and therapeutic context of R 56865


  1. Dependence of hypoxic cellular calcium loading on Na(+)-Ca2+ exchange. Haigney, M.C., Miyata, H., Lakatta, E.G., Stern, M.D., Silverman, H.S. Circ. Res. (1992) [Pubmed]
  2. R 56865 delays cellular electrical uncoupling in ischemic rabbit papillary muscle. Tan, H.L., Netea, A.O., Sleeswijk, M.E., Mazón, P., Coronel, R., Opthof, T., Janse, M.J. J. Mol. Cell. Cardiol. (1993) [Pubmed]
  3. Characterization of the interaction of R 56865 with cardiac Na- and L-type Ca channels. Wilhelm, D., Himmel, H., Ravens, U., Peters, T. Br. J. Pharmacol. (1991) [Pubmed]
  4. R 56865 prevents electrical and mechanical signs of ouabain intoxication in guinea-pig papillary muscle. Vollmer, B., Meuter, C., Janssen, P.A. Eur. J. Pharmacol. (1987) [Pubmed]
  5. The negative inotropic and chronotropic effects of intravenous R 56865 during percutaneous transluminal coronary angioplasty. Pijl, A.J., Van Wezel, H.B., Koolen, J.J., Piek, J.J., Koch, K., Swaan, A., David, G.K., Visser, C.A., Van Zwieten, P.A. British journal of clinical pharmacology. (1995) [Pubmed]
  6. Inhibition of sodium and calcium overload pathology in the myocardium: a new cytoprotective principle. Ver Donck, L., Borgers, M., Verdonck, F. Cardiovasc. Res. (1993) [Pubmed]
  7. Ouabain-induced changes of calcium and potassium in slices of hippocampus of the rat: comparison to hypoxia and effect of R 56865. Scheufler, E., Urenjak, J., Osikowska-Evers, B., Beile, A., Guttmann, I., Wilffert, B., Tegtmeier, F., Peters, T. Neuropharmacology (1992) [Pubmed]
  8. Flunarizine and R 56865 suppress veratridine-induced increase in oxygen consumption and uptake of 45Ca2+ in rat cortical synaptosomes. Wermelskirchen, D., Gleitz, J., Urenjak, J., Wilffert, B., Tegtmeier, F., Peters, T. Neuropharmacology (1992) [Pubmed]
  9. Investigation of electrophysiologic mechanisms for the antiarrhythmic actions of R 56865 in cardiac glycoside toxicity. Damiano, B.P., Stump, G.L., Yagel, S.K. J. Cardiovasc. Pharmacol. (1991) [Pubmed]
  10. Effects of R 56865 on postischemic ventricular function in isolated rat working heart preparations obtained from healthy, diabetic and hypertensive animals. Pijl, A.J., Hendriks, M.G., Kam, K.L., Paffendorf, M., van Zwieten, P.A. Naunyn Schmiedebergs Arch. Pharmacol. (1994) [Pubmed]
  11. R 56865 exerts cardioprotective properties independent of the intracellular Na(+)-overload in the guinea pig heart. Hartmann, M., Decking, U.K. Naunyn Schmiedebergs Arch. Pharmacol. (2003) [Pubmed]
  12. Suppressive effects of R 56865 on triggered propagated contractions and triggered arrhythmias in rat cardiac trabeculae. Daniels, M.C., ter Keurs, H.E. J. Cardiovasc. Pharmacol. (1992) [Pubmed]
  13. Effects of R-56865 on transient inward current, Na(+)-Ca2+ exchange, and Ca2+ release from SR in cardiac myocytes. Ichikawa, H., Hearse, D.J., Coetzee, W.A. Am. J. Physiol. (1994) [Pubmed]
  14. Pharmacological characterisation of sodium channels in sinoatrial node pacemaking in the rat heart. Létienne, R., Vié, B., Le Grand, B. Eur. J. Pharmacol. (2006) [Pubmed]
  15. R 56865 differentiates between contractile agents with respect to the nifedipine-sensitive component in the isolated rat aorta. Koch, P., Wilhelm, D., Wilffert, B., Peters, T. Pharmacology (1989) [Pubmed]
  16. Late sodium current inhibition in human isolated cardiomyocytes by R 56865. Le Grand, B., Coulombe, A., John, G.W. J. Cardiovasc. Pharmacol. (1998) [Pubmed]
WikiGenes - Universities