Abnormal Ca²⁺ handling is essential in the pathophysiology of muscular dysgenesis such as muscular dystrophy (MD) or/and dilated cardiomyopathy (DCM). One of Ca²⁺ permeable channels, transient receptor potential cation channel, subfamily V, member 2 (TRPV2) has been suggested as a principal candidate for Ca²⁺ entry pathways and a potential therapeutic target for muscular dysgenesis. Recently, we produced functional antibodies against TRPV2 with remarkable protective effects against DCM as well as MD animal models. However, the antibodies were rodent TRPV2 specific. Here, we produced selective antibodies recognizing humanTRPV2 from the outside of cells using phage display. One of antibodies inhibited the Ca²⁺ influx via humanTRPV2 in cultured cells and caused TRPV2 to disappear from the plasma membrane via cellular internalization. We measured the change in [Ca²⁺]_i induced by TRPV2 activator.  Although cannabidiol induced massively increased [Ca²⁺]_i in the Duchenne muscular dystrophy (DMD) cell line, this increase was almost completely abolished by treatment with the functional antibody. These results suggest that the functional antibody we developed has therapeutic potential for treating MD or/and DCM.