Mibefradil dihydrochloride 是一种钙离子通道抑制剂，选择性作用于 T 型 Ca2+通道，对 T 型和 L 型通道的IC50分别为 2.7 和 18.6 μM。

Mibefradil dihydrochloride is an blocker of calcium channel with moderate selectivity for T-type Ca2+ channels (T-type and L-type currents with IC50s of 2.7 μM and 18.6 μM, respectively).

Mibefradil dihydrochloride inhibits reversibly the T- and L-type currents with IC50 values of 2.7 and 18.6 μM, respectively.[1].Mibefradil inhibited Orai1, Orai2, and Orai3 currents dose-dependently. The IC50 for Orai1, Orai2, and Orai3 channels was 52.6, 14.1, and 3.8 μM respectively. Outside-out patch demonstrated that perfusion of 10-μM mibefradil to the extracellular surface completely blocked Orai3 currents and single channel activity evoked by 2-APB. Intracellular application of mibefradil did not alter Orai3 channel activity. Mibefradil at higher concentrations (>50 μM) inhibited Ca2+ release but had no effect on cytosolic STIM1 translocation evoked by thapsigargin. Inhibition on Orai channels by mibefradil was structure-related, as other T-type Ca2+ channel blockers with different structures, such as ethosuximide and ML218, had no or minimal effects on Orai channels. Moreover, mibefradil inhibited cell proliferation, induced apoptosis, and arrested cell cycle progression[3].

Compared with the saline-treated group, rats receiving Mibefradil or Ethosuximide show significant lower CaV3.2 expression in the spinal cord and DRG.

Human Orai1-3 cDNAs in tetracycline-regulated pcDNA4/TO vectors were transfected into HEK293 T-REx cells with stromal interaction molecule 1 (STIM1) stable expression. The Orai currents were recorded by whole-cell and excised-membrane patch clamp. Ca2+?influx or release was measured by Fura-PE3/AM. Cell growth and death were monitored by WST-1, LDH assays and flow cytometry[3].

116666-63-8

C29H39ClFN3O3

532.09

米贝拉地尔;盐酸米贝地尔;Ro 40-5967 (dihydrochloride)

H2O:122 mg/mL (214.58mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years