The first diamide wasflubendiamide. It was invented by Nihon Nohyaku and commercialised in 2007.[1] It is a highly substituted diamide of phthalic acid and is highly active against lepidoptera (caterpillers).[1][2] Later DuPont introducedchlorantraniliprole, which is more active against caterpillers and in addition active against other insect types.[1][2]Cyanthraniliprole, introduced later, shows systemic activity and is also active against sucking pests such asaphids andwhitefly.[2]
According to one review, the first species reported to show resistance to diamides was thediamondback moth in 2012.[4]
The binding of diamides or ryanodine to the calcium channels causes them to remain open, leading to the loss of calcium crucial for biological processes.[9] Specifically, calcium release is essential for muscle contraction and therefore locomotion.[10] Ryanodine receptors are the only major calcium release channels of the sarco/endoplasmic reticulum.[10] The forcing open of these channels then causes insects to act lethargic, stop feeding, and eventually die.[9]
The diamides are classified underIRAC group 28.[11]
^abTeixeira, Luís A; Andaloro, John T (2013). "Diamide insecticides: Global efforts to address insect resistance stewardship challenges".Pesticide Biochemistry and Physiology.106 (3):76–78.Bibcode:2013PBioP.106...76T.doi:10.1016/j.pestbp.2013.01.010.
^abSantulli G, Marks AR (2015). "Essential Roles of Intracellular Calcium Release Channels in Muscle, Brain, Metabolism, and Aging".Current Molecular Pharmacology.8 (2):206–222.doi:10.2174/1874467208666150507105105.PMID25966694.
