-conotoxin GVIA (CTX) is a specific blocker of N-type calcium (CaV2.2) channels that inhibits neuropathic pain. While the toxin appears to be an open channel blocker, we show that N-channel gating charge movement is modulated. Gating currents were recorded from N-channels expressed along with _2a and ₂ subunits in HEK293 cells in external solutions containing either lanthanum and magnesium (La-Mg) or 5 mM Ca²⁺ plus CTX (CTX-Ca). A comparison showed that CTX induced a 10 mV right-shift in the gating charge vs. voltage (Q-V) relationship, smaller Off-gating current time constant ( Q_Off), a lower Q_Off voltage dependence, and smaller On-gating current (Q_On) . We also examined gating current in La-Mg plus CTX and found no significant difference from that in CTX-Ca, which demonstrates that the modulation was induced by the toxin. A model with strongly reduced open state occupancy reproduced the CTX effect on gating current, and showed that the gating modulation alone would inhibit N-current by 50%. This mechanism of N-channel inhibition could be exploited to develop novel analgesics that induce only a partial block of N-current, which may limit some of the side effects associated with the toxin analgesic currently approved for human use (i.e. Prialt).