Thiamethoxam is the first commercial neonicotinoid insecticide from the thianicotinyl subclass. It was discovered in the course of our optimisation program on neonicotinoids started in 1985. Novel variations of the nitroimino-heterocycle of imidacloprid led to 4-nitroimino-1,3,5-oxadiazinanes exhibiting high insecticidal activity. Among these, thiamethoxam (CGA 293433) was identified as the best compound and selected for worldwide development. The compound can be synthesised in only a few steps and high yield from easily accessible starting materials. Thiamethoxam acts by binding to nicotinic acetylcholine receptors. It exhibits exceptional systemic characteristics and provides excellent control of a broad range of commercially important pests, such as aphids, jassids, whiteflies, thrips, rice hoppers, Colorado potato beetle, flea beetles and wireworms, as well as some lepidopteran species. In addition, a strong preventative effect on some virus transmissions has been demonstrated. Thiamethoxam is developed both for foliar/soil applications and as a seed treatment for use in most agricultural crops all over the world. Low use rates, flexible application methods, excellent efficacy, long-lasting residual activity and favourable safety profile make this new insecticide well-suited for modern integrated pest management programmes in many cropping systems.

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Abstract:The insect nicotinic acetylcholine receptor (nAChR) is a major target for insecticide action. The rapidly expanding use of neonicotinoid insecticides of varied structures makes it increasingly important to define similarities and differences in their action, particularly for the first-generation chloropyridinyl compounds versus the second-generation chlorothiazolyl derivatives. We have shown with Musca domestica that a convenient and relevant determination of the neonicotinoid insecticide target is a binding site assay with. This study uses membranes from the aphids Myzus persicae and Aphis craccivora and from heads of the flies Drosophila melanogaster and Musca domestica to characterize the [ 3 H]IMI binding sites relative to their number and possible species variation in structure-activity relationships. With emphasis on commercial neonicotinoids, six potent chloropyridinyl compounds are compared with the corresponding six chlorothiazolyl analogues (syntheses are given for chemicals prepared differently than previously described). The preference for chloropyridinyl versus chlorothiazolyl is not dependent on the insect species examined but instead on other structural features of the molecule. The chlorothiazolyl substituent generally confers higher potency in the clothianidin and desmethylthiamethoxam series and the chloropyridinyl moiety in the imidacloprid, thiacloprid, acetamiprid, and nitenpyram series. Two chlorothiazolyl compounds compete directly with the chloropyridinyl [ 3 H]IMI for the same binding sites in Myzus and Drosophila membranes. This study shows conserved neonicotinoid specificity of the [ 3 H]IMI binding site in each of the four insect species examined.

: Pymetrozine, a pyridine azomethine compound, represents a novel insecticide with a selective activity against homopteran insects. It acts in a unique way : aphids are not knocked down on contact but seem to die of starvation. This implies an e †ect of pymetrozine on feeding behaviour. The aim of the present work was to elucidate how and at which step pymetrozine interferes with the complex mechanisms underlying phloem feeding. The e †ect of pymetrozine, applied in various ways, on di †erent phases of stylet penetration and feeding activity of individual aphids was studied using the Electrical Penetration Graph technique (EPG). Initial choice experiments indicated that pymetrozine does not have a deterrent or antifeedant action. Topical application (150 ng pymetrozine mg~1 fresh weight) inhibited stylet insertion into the plant. When injected, less than 30 ng mg~1 was sufficient to produce the same e †ect. When pymetrozine was systemically applied via plant spraying or root uptake, aphids started feeding normally. After some time, however, they withdrew their stylets from the phloem and walked around with una †ected locomotion. At low doses aphids eventually recovered and resumed feeding. High doses, however, irreversibly disrupted feeding and prevented stylet reinsertion. Aphid motility was not a †ected up to an estimated haemolymph concentration of 1 mM pymetrozine. Aphids which eventually stopped feeding on pymetrozine-treated plants showed EPGs with distorted salivation/ingestion patterns. It is concluded that pymetrozine does not have a general toxic e †ect on aphids but selectively interferes with the nervous regulation of feeding behaviour which consequently results in death due to starvation after a few days.