FPL 64176 (FPL) is a benzoylpyrrole agonist of Cav1.2 Ca²⁺ channels (LTCC). It was recently proposed that FPL activates LTCC by making inactivated channels conducting. Thus, we examined which inactivated states are made conductive by FPL with recombinant LTCCs composed of Cav1.2, b_2a and a₂d₁ subunits coexpressed in tsA201 cells. LTCC currents were measured in the whole-cell configuration of the patch-clamp technique with Ca²⁺ as a charge carrier. The Ca²⁺-induced inactivation (CDI) was inhibited by coexpression of a dominant negative calmodulin (Cav1.2 CaM_1,2,3,4). The voltage-dependent inactivation (VDI) was inhibited by either a point mutation in the intracellular linker between domains I and II of Cav1.2 (Cav1.2(G436R)) or deletion of the distal C-terminus (DCT) of Cav1.2 (Cav1.2 D1821). The agonistic effect of FPL was significantly inhibited in Cav1.2 CaM_1,2,3,4 and Cav1.2 D1821 but not Cav1.2(G436R). Thus, FPL makes LTCC undergoing CDI and DCT-induced VDI conducting. Because both Ca²⁺/calmodulin on the IQ motif of Cav1.2 and DCT cause inactivation through the EF hand in the proximal C-terminus of Cav1.2, it is likely that there is allosteric interaction between FPL binding sites and the EF hand in Cav1.2.