NNC 55‐0396 is a structural analog of mibefradil (Ro 40‐5967) that inhibits both T‐type and high‐voltage‐activated (HVA) Ca²⁺ channels with a higher selectivity for T‐type Ca²⁺ channels. The inhibitory effect of mibefradil on HVA Ca²⁺ channels can be attributed to a hydrolyzed metabolite of the drug: the methoxy acetate side chain of mibefradil is removed by intracellular enzymes, thus it forms (1 S,2S)‐2‐(2‐(N‐[(3‐benzoimidazol‐2‐yl)propyl]‐N‐methylamino)ethyl)‐6‐fluoro‐1,2,3,4‐tetrahydro‐1‐isopropyl‐2‐naphtyl hydroxy dihydrochloride (dm‐mibefradil), which causes potent inhibition of HVA Ca²⁺ currents. By replacing the methoxy acetate chain of mibefradil with cyclopropanecarboxylate, a more stable analog was developed (NNC 55‐0396). The acute IC₅₀ of NNC 55‐0396 to block recombinant Cav3.1 T‐type channels expressed in HEK293 cells is ∼7 μM, whereas 100 μM NNC 55‐0396 has no detectable effect on high voltage‐activated currents in INS‐1 cells. Block of T‐type Ca²⁺ current was partially reduced by membrane hyperpolarization and was enhanced at high stimulus frequency. Washing NNC 55‐0396 out of the recording chamber did not reverse the T‐type Ca²⁺ current activity, suggesting that the compound dissolves in or passes through the plasma membrane to exert its effect; however, intracellular perfusion of the compound did not block T‐type Ca²⁺ currents, arguing against a cytoplasmic route of action. We conclude that NNC 55‐0396, by virtue of its modified structure, does not produce the metabolite that causes inhibition of L‐type Ca²⁺ channel channels, thus rendering it more selective to T‐type Ca²⁺ channels.