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[Chinfloxacin hydrochloride inhibits HERG potassium channel at open state]

Xiang-mei Zhang1, Zhong-hua Zhu, Xiao-li Sun

  • 1Jiangsu Key Laboratory for Molecular and Medical Biotechnology, Nanjing Normal University, Nanjing 210046, China.

Yao Xue Xue Bao = Acta Pharmaceutica Sinica
|March 1, 2011
PubMed

Insights

Chinfloxacin hydrochloride (CFX) inhibits the HERG K+ channel in a concentration-dependent manner. This CFX effect on HERG channels was amplified by changes in extracellular potassium levels.

Area of Science:

  • Pharmacology
  • Ion Channel Physiology

Background:

  • The HERG K+ channel is crucial for cardiac repolarization.
  • Drug-induced HERG channel dysfunction can lead to life-threatening arrhythmias.
  • Chinfloxacin hydrochloride (CFX) is a fluoroquinolone antibiotic with potential cardiac risks.

Purpose of the Study:

  • To investigate the effects of chinfloxacin hydrochloride (CFX) on HERG K+ channel kinetics.
  • To determine the inhibitory concentration (IC50) of CFX on HERG channels.
  • To assess the influence of extracellular potassium on CFX's HERG channel inhibition.

Main Methods:

  • Whole-cell patch clamp technique was employed.
  • HEK293 cells expressing cgi-HERG-GFP plasmids were utilized.
  • HERG K+ currents were recorded in the presence and absence of CFX and moxifloxacin hydrochloride (MOX).

Main Results:

  • CFX inhibited the open state of the HERG K+ channel in a concentration- and time-dependent manner.
  • The IC50 for CFX inhibition was 162.1 +/- 14.2 micromol/L, approximately two-fold higher than MOX.
  • No significant effects on channel kinetics were observed, but CFX inhibition was enhanced by altered extracellular K+ concentrations.

Conclusions:

  • CFX exhibits inhibitory effects on HERG K+ channels.
  • The cardiac safety profile of CFX warrants further investigation due to its HERG channel interaction.
  • Extracellular potassium levels can modulate the inhibitory potency of CFX on HERG channels.

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