The mode-of-action of the insecticidal crop protection product, flonicamid, has not been elucidated at this time. However, various enzyme assays, ligand binding studies, neurophysiology, genetic assays and phenotypic observations rule out all known in insecticide mode-of-actions. An important feature of a piercing-sucking insecticide is it's ability to rapidly inhibit feeding. Feeding studies in which the amount of 14C-inuln in honeydew was monitored clearly demonstrated that Myzus periscae stopped feeding immediately after Flonicamid exposure. Conversely, mortality occurred about 40 hours following Flonicamid exposure. In addition, the effects of Flonicamid on isolated ligand-a and voltage-gated ion channels were recorded from Heliothis virescens and from Drosophila melanogaster neurons. Direct measurements of ionic currents flowing in living neurons as they were exposed to Flonicamid revealed that flonicamid is not highly active against the nicotinic acetylcholine receptor. These results clearly demonstrate that the mode-of-action of flonicamid differs from that of the nicotinic compounds.