Nav1.9, a TTX-resistant sodium channel encoded by SCN11A, is a validated but poorly characterized target in human pain signaling, with most data to date drawn from rodent models rather than native human tissue. Using human DRG and TG neurons, we pharmacologically isolated and characterized native Nav1.9 currents and found clear differences between the two populations: TG neurons show a right-shifted inactivation curve, larger window current, and faster activation kinetics than DRG neurons. Inflammatory conditions substantially potentiated Nav1.9 currents in both, consistent with rodent findings. These results provide the first detailed biophysical profile of native human Nav1.9 channels, offering a more translatable foundation for analgesic drug discovery targeting acute and chronic pain.