Pancreatic β-cells depolarize in response to glucose and fire calcium-dependent actions
potentials that trigger insulin secretion. The major current responsible for action potential
repolarization in these cells is a delayed rectifier and Kv2. 1 subunits are thought be a major
contributor of the delayed rectifier channels. Hence, blockers of Kv2. 1 channels might
prolong action potentials and enhance calcium influx and insulin secretion. However, the
lack of specific small molecule Kv2. 1 inhibitors has hindered the testing of this mechanism …