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Original Article

Korean J Physiol Pharmacol 2023; 27(1): 95-103

Published online January 1, 2023

Copyright © Korean J Physiol Pharmacol.

Effects of rosiglitazone, an antidiabetic drug, on Kv3.1 channels

Hyang Mi Lee1, Seong Han Yoon1, Min-Gul Kim1, Sang June Hahn2, and Bok Hee Choi1,*

1Department of Pharmacology, Institute for Medical Sciences, Jeonbuk National University Medical School, Jeonju 54097, 2Department of Physiology, Medical Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea

Correspondence to:Bok Hee Choi

Author contributions: H.M.L. and S.H.Y. performed the experiments and analyzed the data. M.G.K. and S.J.H. coordinated the study. B.H.C. supervised the study. H.M.L. and B.H.C. wrote the manuscript.

Received: August 31, 2022; Revised: October 20, 2022; Accepted: October 22, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Rosiglitazone is a thiazolidinedione-class antidiabetic drug that reduces blood glucose and glycated hemoglobin levels. We here investigated the interaction of rosiglitazone with Kv3.1 expressed in Chinese hamster ovary cells using the whole-cell patch-clamp technique. Rosiglitazone rapidly and reversibly inhibited Kv3.1 currents in a concentration-dependent manner (IC50 = 29.8 μM) and accelerated the decay of Kv3.1 currents without modifying the activation kinetics. The rosiglitazone-mediated inhibition of Kv3.1 channels increased steeply in a sigmoidal pattern over the voltage range of –20 to +30 mV, whereas it was voltage-independent in the voltage range above +30 mV, where the channels were fully activated. The deactivation of Kv3.1 current, measured along with tail currents, was also slowed by the drug. In addition, the steady-state inactivation curve of Kv3.1 by rosiglitazone shifts to a negative potential without significant change in the slope value. All the results with the use dependence of the rosiglitazone-mediated blockade suggest that rosiglitazone acts on Kv3.1 channels as an open channel blocker.

Keywords: Open channel block, Potassium channels, Rosiglitazone, Shaw-type potassium channels