Mibefradil (Ro 40-5967) is acalcium channelblocker with moderate selectivity for T-type Ca²⁺channels displayingIC₅₀s of 2.7 μM and 18.6 μM for T-type and L-type currents, respectively^[1].

IC50: 2.7 μM (T-type calcium channel), 18.6 μM (L-type calcium channel)^[1]

Mibefradil inhibits reversibly the T- and L-type currents with IC₅₀values of 2.7 and 18.6 μM, respectively. The inhibition of the L-type current is voltage-dependent, whereas that of the T-type current is not. Ro 40-5967 blocks T-type current already at a holding potential of -100 mV^[1]At a higher concentration (20 μM), Mibefradil reduces the amplitude of excitatory junction potentials (by 37±10 %), slows the rate of repolarisation (by 44±16 %) and causes a significant membrane potential depolarisation (from –83±1 mV to –71±5 mV). At a higher Mibefradil concentration (20 μM) there is significant membrane potential depolarisation and a slowing of repolarisation. These actions of Mibefradil are consistent with K⁺channel inhibition, which has been shown to occur in human myoblasts and other cells^[2].

The hearing thresholds of the 24-26 week old C57BL/6J mice differed following the 4-week treatment period. The hearing threshold at 24 kHz is significantly decreased in the Mibefradil-treated and benidipine-treated groups compared with the saline-treated group (P<0.05)^[3]. Compared with the saline-treated group, rats receiving Mibefradil or Ethosuximide show significant lower Ca_V3.2 expression in the spinal cord and DRG^[4].

495.63

C₂₉H₃₈FN₃O₃

116644-53-2

米贝拉地尔；米贝地尔；咪拉地尔；咪贝地尔

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.