Several reports credit mibefradil with tumor suppressing properties arising from its known inhibition of Ca2+ currents. Given that mibefradil (Mb) is also known to inhibit K+ channels, we decided to study the interaction between this organic compound and the tumor‐related Kv10.1 channel. Here we report that Mb modulates the gating of Kv10.1. Mb induces an apparent inactivation from both open and early closed states where the channels dwell at hyperpolarized potentials. Additionally, Mb accelerates the kinetics of current activation, in a manner that depends on initial conditions. Our observations suggest that Mb binds to the voltage sensor domain of Kv10.1 channels, thereby modifying the gating of the channels in a way that in some, but not all, aspects opposes to the gating effects exerted by divalent cations. J. Cell. Physiol. 232: 2019–2032, 2017. © 2016 Wiley Periodicals, Inc. Several reports credit mibefradil, a T‐type calcium channel inhibitor, with tumor suppressing properties. Given that mibefradil also inhibits some potassium channels, we studied the interaction of this compound with the tumor related Kv10.1 channel. We found that mibefradil induces an apparent inactivation both from the open and early closed states, and accelerates current activation in a manner that depends on the holding potential. We hypothesize that mibefradil binds to the voltage‐sensor module altering the gating of the channels.