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Chemical Compound Review

Rilmakalim     1-[(3S,4S)-3-hydroxy-2,2- dimethyl-6...

Synonyms: rimalkalim, Rilmakalime, Rilmakalimum, HOE-234, CHEMBL275758, ...
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High impact information on Rilmakalim


Biological context of Rilmakalim


Anatomical context of Rilmakalim


Associations of Rilmakalim with other chemical compounds

  • The rilmakalim-induced shortening of the APD90 was half-maximally antagonized by glibenclamide and HMR 1883 with 10 nM and 0.4 microM, respectively (pHo = 6.5) [13].
  • Adenosine triphosphate-dependent K currents activated by metabolic inhibition in rat ventricular myocytes differ from those elicited by the channel opener rilmakalim [14].
  • 4. Stable early afterdepolarizations induced in Purkinje fibers by berberine (100 microM) were reversibly blocked by rilmakalim (2.4 microM), which also suppressed late afterdepolarizations induced in Purkinje fibers treated with ouabain (0.3-0.5 microM) [10].
  • Levcromakalim induced a concentration-dependent and equipotent inhibition of contraction of HIMA and HSV preconstricted by EFS and exogenoulsy applied NA, while rilmakalim produced a stronger inhibition of EFS- than NA-evoked contractions [12].

Gene context of Rilmakalim

  • In conclusion, after metabolic inhibition the amplitude of the activated KATP current is about twice as high as under saturating concentrations of the opener rilmakalim [14].
  • They also suggest that the effect of rilmakalim on EFS-evoked contractions involves K(ATP) channels located pre-synaptically [12].

Analytical, diagnostic and therapeutic context of Rilmakalim

  • 1. The effects of rilmakalim, a potassium channel opener, were studied on rabbit cardiac Purkinje, ventricular muscle and atrial fibers, with the use of conventional microelectrode techniques [10].


  1. Effects of a novel cardioselective ATP-sensitive potassium channel antagonist, 1-[[5-[2-(5-chloro-o-anisamido)ethyl]-beta-methoxyethoxyphenyl]sulfonyl]-3-methylthiourea, sodium salt (HMR 1402), on susceptibility to ventricular fibrillation induced by myocardial ischemia: in vitro and in vivo studies. Billman, G.E., Houle, M.S., Englert, H.C., Gögelein, H. J. Pharmacol. Exp. Ther. (2004) [Pubmed]
  2. Mechanisms of L-NG nitroarginine/indomethacin-resistant relaxation in bovine and porcine coronary arteries. Graier, W.F., Holzmann, S., Hoebel, B.G., Kukovetz, W.R., Kostner, G.M. Br. J. Pharmacol. (1996) [Pubmed]
  3. Effect of rilmakalim on detrusor contraction in the presence and absence of urothelium. Wuest, M., Kaden, S., Hakenberg, O.W., Wirth, M.P., Ravens, U. Naunyn Schmiedebergs Arch. Pharmacol. (2005) [Pubmed]
  4. KATP channel openers reverse immune complex-induced airways hyperreactivity independently of smooth muscle relaxation. Buchheit, K.H., Hofmann, A. Naunyn Schmiedebergs Arch. Pharmacol. (1996) [Pubmed]
  5. Selective block of sarcolemmal IKATP in human cardiomyocytes using HMR 1098. Kääb, S., Zwermann, L., Barth, A., Hinterseer, M., Englert, H.C., Gögelein, H., Näbauer, M. Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy. (2003) [Pubmed]
  6. Selective inhibition of pinacidil effects by estrogen in guinea pig heart. Kocić, I., Gruchała, M., Petrusewicz, J. International journal of cardiology. (2006) [Pubmed]
  7. Ca2+-transients induced by K+ channel openers in isolated coronary capillaries. Langheinrich, U., Mederos y Schnitzler, M., Daut, J. Pflugers Arch. (1998) [Pubmed]
  8. Cardiovascular effects of the novel potassium channel opener (3S,4R)-3-hydroxy-2,2-dimethyl-4-(2-oxo- 1-pyrrolidinyl)-6-phenylsulfonylchromane hemihydrate. Linz, W., Klaus, E., Albus, U., Becker, R., Mania, D., Englert, H.C., Schölkens, B.A. Arzneimittel-Forschung. (1992) [Pubmed]
  9. Cellular mechanisms controlling EDRF/NO formation in endothelial cells. Busse, R., Lückhoff, A., Mülsch, A. Basic Res. Cardiol. (1991) [Pubmed]
  10. Antiarrhythmic and electrophysiological effects of the novel KATP channel opener, rilmakalim, in rabbit cardiac cells. Riccioppo Neto, F., Mesquita Júnior, O., Olivera, G.B. Gen. Pharmacol. (1997) [Pubmed]
  11. Hypotonic stress increases efficacy of rilmakalim, but not pinacidil, to activate ATP-sensitive K(+) current in guinea pig ventricular myocytes. Kocic, I., Hirano, Y., Hiraoka, M. J. Pharmacol. Sci. (2004) [Pubmed]
  12. Differential antivasoconstrictor effects of levcromakalim and rilmakalim on the isolated human mammary artery and saphenous vein. Novaković, A., Gojković-Bukarica, L., Beleslin-Cokić, B., Japundzić-Zigon, N., Sajić, Z., Nezić, D., Perić, M., Djukanović, B., Kazić, T. J. Pharmacol. Sci. (2003) [Pubmed]
  13. HMR 1883, a novel cardioselective inhibitor of the ATP-sensitive potassium channel. Part I: effects on cardiomyocytes, coronary flow and pancreatic beta-cells. Gögelein, H., Hartung, J., Englert, H.C., Schölkens, B.A. J. Pharmacol. Exp. Ther. (1998) [Pubmed]
  14. Adenosine triphosphate-dependent K currents activated by metabolic inhibition in rat ventricular myocytes differ from those elicited by the channel opener rilmakalim. Krause, E., Englert, H., Gögelein, H. Pflugers Arch. (1995) [Pubmed]
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