Background: The ability to differentiate patient-specific human induced pluripotent stem cells (hiPSC) into cardiac myocytes (hiPSC-CM) offers exciting perspectives for cardiovascular research. A number of studies have used hiPSC-CM to model voltage-gated Na+ channel (Nav) dysfunctions such as long QT and Brugada syndromes. These studies mainly reported current-voltage curves but the expression patterns and precise biophysical and pharmacological properties of Nav channels from hiPSC-CM remain unknown. Objective: We propose to study Nav channels characteristics from hiPSC-CM to assess the appropriateness of this novel cell model. Methods and results: We generated hiPSC-CM using the recently described monolayer-based differentiation protocol. hiPSC-CM expressed cardiac-specific markers, exhibited spontaneous electrical and contractile activities, and expressed several Nav channels. Electrophysiological, pharmacological, and molecular characterizations revealed that, in addition to the main Nav1.5 channel, the neuronal TTX-sensitive Nav1.7 channel was also significantly expressed in hiPSC-CM. Most of the Na+ currents were resistant to blocking by tetrodotoxin (TTX) a specific s Na+ channel blocker, and therapeutic concentrations of lidocaine, a class I antiarrhythmic, also blocked Na+ currents in a use-dependent manner. The Nav1.5 and Nav1.7 expression and maturation patterns of hiPSC-CM and native human cardiac tissues appeared to be similar. The four Navβ regulatory subunits were expressed, with β3 as the preponderant subtype in hiPSC-CM. Conclusions: Based on our results, we propose that Nav channels from hiPSC-CM recapitulate most of characteristics reported for native human cardiomyocytes. hiPSC-CM can also be adapted to model cardiac diseases, perform drug screening, and assess the safety of novel compounds. As with any experimental model, hiPSC-CM have limitations that should be kept in mind in order to benefit from their full potential.