Blocking Effect of NIP-142 on the KCNQ1/KCNE1 Channel Current Expressed in HEK293 Cells

  • Namekata Iyuki
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
  • Tsuruoka Noriko
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
  • Tsuneoka Yayoi
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
  • Matsuda Tomoyuki
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University Biological Research Laboratories, Nissan Chemical Industries, Ltd.
  • Takahara Akira
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
  • Tanaka Yoshio
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Toho University
  • Suzuki Takeshi
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University School of Material Science, Japan Advanced Institute of Science and Technology (JAIST)
  • Takahashi Tetsuo
    Department of Biophysical Chemistry, Faculty of Pharmaceutical Sciences, Toho University
  • Iida-Tanaka Naoko
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University Department of Food Science, Otsuma Women's University
  • Tanaka Hikaru
    Department of Pharmacology, Faculty of Pharmaceutical Sciences, Toho University

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抄録

We examined the effect of NIP-142, a benzopyran compound with terminating effect on experimental atrial arrhythmia, on the KCNQ1/KCNE1 channel, which underlies the slow component of the cardiac delayed rectifier potassium channel (IKs). NIP-142, as well as chromanol 293B, showed concentration-dependent blockade of the current expressed in HEK293 cells; the EC50 value of NIP-142 and chromanol 293B for the inhibition of tail current was 13.2 μM and 4.9 μM, respectively. These results indicate that NIP-142 has blocking effect on the KCNQ1/KCNE1 channel current.

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