Effective IRM strategies: Sequences or alternations of MoA
Effective insecticide resistance management (IRM) strategies seek to minimise the selection of resistance to any one type of insecticide. In practice, alternations, sequences or rotations of compounds from different MoA groups provide sustainable and effective IRM. Applications are often arranged into MoA spray windows or blocks that are defined by the stage of crop development and the biology of the lepidopteran species of concern. Local expert advice should always be followed with regard to spray windows and timing. Several sprays may be possible within each spray window, but it is generally essential that successive generations of the pest are not treated with compounds from the same MoA group. Metabolic resistance mechanisms may give cross-resistance between MoA groups; where this is known to occur, the above advice should be modified accordingly.
Inhibit AChE, causing hyperexcitation. AChE is the enzyme that terminates the action of the excitatory neurotransmitter acetylcholine at nerve synapses.
View Acetylcholinesterase (AChE) inhibitors Molecular StructureBlock the GABA-activated chloride channel, causing hyperexcitation and convulsions. GABA is the major inhibitory neurotransmitter in insects.
View GABA-gated chloride channel blockers Molecular StructureKeep sodium channels open, causing hyperexcitation and, in some cases, nerve block. Sodium channels are involved in the propagation of action potentials along nerve axons.
View Sodium channel modulators Molecular StructureBind to the acetylcholine site on nAChRs, causing a range of symptoms from hyper-excitation to lethargy and paralysis. Acetylcholine is the major excitatory neurotransmitter in the insect central nervous system.
View Nicotinic acetylcholine receptor (nAChR) competitive modulators Molecular StructureAllosterically activate nAChRs, causing hyperexcitation of the nervous system. Acetylcholine is the major excitatory neurotransmitter in the insect central nervous system.
View Nicotinic acetylcholine receptor (nAChR) allosteric modulators - Site I Molecular StructureAllosterically activate glutamate-gated chloride channels (GluCls), causing paralysis. Glutamate is an important inhibitory neurotransmitter in insect.
View Glutamate-gated chloride channel (GluCl) allosteric modulators Molecular StructureApplied in the pre-metamorphic instar, these compounds disrupt and prevent metamorphosis.
View Juvenile hormone receptor modulators Molecular StructureBind to and disrupt the gating of Nan-Iav TRPV (Transient Receptor Potential Vanilloid) channel complexes in chrodotonal stretch receptor organs, which are critical for the senses of hearing, gravity, balance, acceleration, proprioception and kinesthesia. This disrupts feeding and other behaviors in target insects.
View Chordotonal Organ TRPV Channel Modulators Molecular StructureInhibit the enzyme that catalyzes the polymerization of Chitin.
View Mite growth inhibitors affecting CHS1 Molecular StructureProtein toxins that bind to receptors on the midgut membrane and induce pore formation, resulting in ionic imbalance and septicemia.
View Microbial disruptors of insect midgut membranes Molecular StructureInhibit the enzyme that synthesizes ATP.
View Inhibitors of mitochondrial ATP synthase Molecular StructureProtonophores that short-circuit the mitochondrial proton gradient so that ATP can not be synthesized.
View Uncouplers of oxidative phosphorylation via disruption of the proton gradient Molecular StructureBlock the nAChR ion channel, resulting in nervous system block and paralysis. Acetylcholine is the major excitatory neurotransmitter in the insect central nervous system.
View Nicotinic acetylcholine receptor (nAChR) channel blockers Molecular StructureInhibit the enzyme that catalyzes the polymerization of Chitin.
View Inhibitors of chitin biosynthesis affecting CHS1 Molecular StructureIncompletely defined MoA leading to inhibition of chitin biosynthesis in a number of insects, including whiteflies.
View Inhibitors of chitin biosynthesis, type 1 Molecular StructureIncompletely defined MoA that leads to moult disruption.
View Moulting disruptor, Dipteran Molecular StructureMimic the moulting hormone, ecdysone, inducing a precocious moult.
View Ecdysone receptor agonists Molecular StructureActivate octopamine receptors, leading to hyperexcitation. Octopamine is the insect equivalent of adrenaline, the fight-or-flight neurohormone.
View Octopamine receptor agonists Molecular StructureInhibit electron transport complex III, preventing the utilization of energy by cells.
View Mitochondrial complex III electron transport inhibitors – Qo site Molecular StructureInhibit electron transport complex I, preventing the utilization of energy by cells.
View Mitochondrial complex I electron transport inhibitors Molecular StructureBlock sodium channels, causing nervous system shutdown and paralysis.
Sodium channels are involved in the propagation of action potentials along nerve axons.
Inhibit acetyl coenzyme A carboxylase, part of the first step in lipid biosynthesis, leading to insect death.
View Inhibitors of acetyl-CoA carboxylase Molecular StructureInhibit electron transport complex IV, preventing the utilization of energy by cells.
View Mitochondrial complex IV electron transport inhibitors Molecular StructureInhibit electron transport complex II, preventing utilization of energy by cells.
View Mitochondrial complex II electron transport inhibitors Molecular StructureActivate muscle ryanodine receptors, leading to contraction and paralysis. Ryanodine receptors mediate calcium release into the cytoplasm from intracellular stores.
View Ryanodine receptor modulators Molecular StructureDisrupt the function of chrodotonal stretch receptor organs, which are critical for the senses of hearing, gravity, balance, acceleration, proprioception and kinesthesia. This disrupts feeding and other behaviors in target insects. In contrast to Group 9, Group 29 insecticides do not bind to the Nan-lav TRPV channel complex.
View Chordotonal organ nicotinamidase inhibitors Molecular StructureAllosterically inhibit the GABA-activated chloride channel, causing hyperexcitation and convulsions. GABA is the major inhibitory neurotransmitter in insects.
View GABA-gated chloride channel allosteric modulators Molecular StructureA baculovirus-unique Per os Infectivity Factor (PIF) protein complex on the virus promotes host-specific infection by binding to PIF targets on midgut cells that are unknown but believed to be unique for each baculovirus type. Infection is ultimately lethal.
View Baculoviruses Molecular StructureAllosterically activate nAChRs (at a site distinct from Group 5 - Site I), causing hyperexcitation of the nervous system. Acetylcholine is the major excitatory neurotransmitter in the insect central nervous system.
View Nicotinic Acetylcholine Receptor (nAChR) Allosteric Modulators - Site II Molecular StructureNegative modulation of KCa2 causes hyperexcitation and convulsions. KCa2 channels are activated by increase of the intracellular calcium concentration and are involved in the regulation of action potentials.
View Calcium‐activated potassium channel (KCa2) modulators Molecular StructureInhibit electron transport complex III, preventing the utilization of energy by cells. In contrast to Group 20, Group 34 insecticides bind to the Qi site.
View Mitochondrial complex III electron transport inhibitors – Qi site Molecular StructureMultiple biological processes govern the accumulation of proteins critical to supporting a wide variety of functions within insects. Protein suppressors act through reduction of specific protein levels in the pest species. Insecticides that act in this manner are generally moderately slow acting.
View RNA Interference mediated target suppressors Molecular StructureDisrupt the function of chordotonal stretch receptor organs, which are critical for the senses of hearing, gravity, balance, acceleration, proprioception and kinesthesia. This disrupts feeding and other behaviors in target insects. Group 36 insecticides act at a site different from Group 9 and Group 29 insecticides and are neither affecting TRPV channels nor nicotinamidase.
View Chordotonal organ modulators – undefined target site Molecular StructureBind to VAChTs, causing cholinergic synaptic transmission block resulting in nervous system shutdown and paralysis. VAChTs are involved in loading acetylcholine into synaptic vesicles
View Vesicular acetylcholine transporter (VAChT) inhibitor Molecular StructureModes of action are colour-coded according to the physiological functions affected. This informs the symptomology, speed of action and other properties of the actives therein and not for any resistance management purpose. Base rotations for resistance management on the mode of action number only.