Escitalopram was developed as an antidepressant of the selective serotonin reuptake inhibitors (SSRIs) from citalopram as its (S)-stereoisomer. It has been known that escitalopram showed the high selectivity to serotonin transporters compared to other SSRIs. However, it has been also considered that escitalopram, including other antidepressants, have a risk to induce seizures, such as epileptic patients. In this study, we examined the effect of escitalopram in Na_v1.2 voltage-gated sodium channels (VGSCs) transfected HEK293 cells. Na_v1.2 VGSCs current decreased by approximately 50.7±8.3 % under treatment with 100 μM escitalopram. The IC₅₀ of escitalopram against Na_v1.2 VGSCs current was 114.17 μM. Moreover, the treatment with 100 µM escitalopram could shift the activation curve toward hyperpolarization side and the voltage at half-maximal activation shifted from -13.8 ± 4.6 mV to -21.5 ± 3.9 mV toward hyperpolarization. In addition, the treatment with 100 μM escitalopram also could shift the inactivation curve toward hyperpolarization side and the voltage at half-maximal inactivation shifted from -50.3 ± 3.7 mV to -56.7 ± 6.0 mV toward hyperpolarization. These findings suggested that escitalopram might be able to inhibit Na_v1.2 VGSCs current and changes the kinetics of both activation and inactivation.