Flonicamid mode of action studies

Bruce Black, Joe Argentine, Rathnam Chaguturu, Ratna Dargar, Leo Dungan, Russ Eldridge, Lyle Kinne, Russ Peters, Amy Wrzesinski, and Debbie Yuhas

FMC Corporation, Agricultural Products Group, Princeton, New Jersey, USA

Correspondence: bruce_black@fmc.com

Flonicamid offers a new opportunity to control insects through what appears to be a unique mode of action. Results from a battery of mode of action assays differentiate flonicamid from the most common commercial insecticides used in US crop protection today. Assays performed to date include the inhibition studies of acetylcholinesterase, nicotinic and muscarinic acetylcholine receptors, respiration (including Complex I, II, III, and IV inhibitors, phosphorylation inhibitors, uncouplers of oxidative phosphorylation), GABA-receptor (in vivo and in vitro), glutamate-receptor (agonist and antagonist), octopamine receptor agonist, nitric oxide synthase, nitric oxide receptor agonist, Na-channel, L-type Ca-channel, ryanodine Ca-channel, and calcium ATPase (body wall contraction assay). In addition, the rapid onset of toxicity (<one hour) is inconsistent with chitin synthesis inhibition, juvenile hormone and ecdysone agonist activity. For these reasons, flonicamid does not appear to be an insect growth regulator. In all of the above assays, flonicamid does not act on these targets as do reference commercial standards. Collectively, these modes of action cover the majority (and more) of known insecticide modes of action. Lack of response by flonicamid in these assays compared to known standards suggests a novel mode of action that is differentiated from other insecticides commonly used in American agriculture. In a companion article, Hayashi et al. (2006) presents evidence that flonicamid targets the insect potassium A-type channel. Hence, suggesting a novel mode of action for flonicamid.

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