Chemistry: modes of action, explained at the target site

Section: Chemistry

A mode of action is the biological mechanism by which an active ingredient kills or disables a pest. Two products with different brand names may share one mode of action — and, for resistance purposes, count as the same treatment. This page explains the major groups in plain terms; the Explorer tabulates them.

Nerve targets

Sodium-channel modulators — pyrethroids and pyrethrins

Voltage-gated sodium channels carry nerve impulses. Pyrethroids (synthetic relatives of natural pyrethrins from chrysanthemum) hold these channels open, causing repetitive firing, paralysis (“knockdown”), and death. They are fast, widely used, and — as the Resistance section documents — widely resisted through target-site (kdr) mutations and metabolic detoxification.

Neonicotinoids and the nicotinic acetylcholine receptor (nAChR)

Neonicotinoids (for example imidacloprid, dinotefuran) bind nicotinic acetylcholine receptors in the insect nervous system, overstimulating them. Their selectivity for insect over mammalian receptors is relative, not absolute, and their environmental profile — particularly effects on pollinators — is a substantial regulatory and scientific topic in its own right. In urban pest management they appear notably in ant and cockroach baits and in some fly baits.

GABA antagonists — fipronil

Fipronil (a phenylpyrazole, IRAC Group 2B) blocks GABA-gated chloride channels, removing inhibitory control in the insect nervous system; it also blocks glutamate-gated chloride channels (GluCl), an insect-specific channel family that is part of its selectivity story. It is slow enough to allow social transfer in ants, which is why it appears in ant and cockroach baits. Its established termite use is different: a non-repellent liquid soil treatment, not a bait — termite baits use chitin-synthesis inhibitors (Group 15, below). That non-repellent, transferable profile demands careful label-directed placement.

Sodium-channel blockers — indoxacarb (22A) and the spinosyns (5)

Blocking a channel is not the same as holding it open. Indoxacarb (Group 22A, an oxadiazine) is a pro-insecticide: insect enzymes convert it to a metabolite that blocks voltage-dependent sodium channels — the mechanistic opposite of the Group 3A modulators — which is why it is a genuine rotation partner for pyrethroids in cockroach and ant baits. The spinosyns (Group 5: spinosad, spinetoram, fermentation products of a soil bacterium) are allosteric modulators of the nicotinic acetylcholine receptor at a site (Site I) distinct from the neonicotinoids' — again, a different tool for rotation purposes, despite the shared receptor.

Muscle and glutamate-gated targets — diamides (28) and avermectins (6)

The diamides (Group 28, e.g. chlorantraniliprole) act on the ryanodine receptor of muscle cells, locking calcium channels open until the muscle can no longer contract. The avermectins (Group 6, e.g. abamectin) are allosteric modulators of glutamate-gated chloride channels; their slow action makes them useful in ant and cockroach baits, where transfer matters more than speed.

IRAC grouping: why the numbers exist

The Insecticide Resistance Action Committee (IRAC) classifies insecticides by mode of action into numbered groups (for example, Group 3A pyrethroids, Group 4A neonicotinoids, Group 2B fipronil). The purpose is practical resistance management: rotating products within the same group is not rotation. Labels and extension guidance increasingly print the IRAC group so users can alternate genuinely different mechanisms. Our Explorer uses IRAC groups as its organising spine.

Boric acid and borates (IRAC Group 8D)

Borates sit inside the numbered IRAC scheme — Group 8D, among the multi-site inhibitors — even though their action is unlike a nerve poison's. Boric acid and borate dusts/gels act principally as stomach poisons: a cockroach or ant that grooms after walking through dust, or feeds on a borate bait, ingests borate that disrupts gut and metabolic function. Action is slow, there is no quick knockdown, and the material remains effective as long as it stays dry and in place — which is why placement in wall voids and behind appliances, out of occupied surfaces and strictly per label, is the established use pattern.

Desiccant dusts: a physical mode

Silica gel and diatomaceous earth both kill by destroying the cuticle's waterproofing so the insect loses water and desiccates — but by different mechanisms, and the difference is practical, not pedantic. Silica gel (amorphous silica) is a sorptive dust: its particles absorb the cuticular lipids on contact, without needing to abrade anything. Diatomaceous earth works by abrasion plus sorption — its sharp fossil particles scratch the cuticle and take up lipids. The sorptive mechanism is one reason silica gel outperforms diatomaceous earth in several bed-bug studies. Diatomaceous earth varies by grade and formulation, and only label-specified grades may be used as pesticides. Neither is a stomach poison — that is boric acid (above), which belongs in Group 8D and must not be filed with the physical dusts. Because the mode is physical rather than biochemical, conventional metabolic/target-site resistance is considered unlikely — though avoidance behaviour and harborage choice still limit real-world results. Dusts must stay dry to work.

IGRs (summary)

The juvenile-hormone analogues split into IRAC subgroups: methoprene and hydroprene are 7A, fenoxycarb is 7B, and pyriproxyfen is 7C. They mimic juvenile hormone; they prevent normal development and reproduction rather than killing adults outright. They are established for fleas, stored-product pests, cockroaches, and mosquito larvae (methoprene in catch basins) and are normally combined with sanitation and, where needed, an adulticide. See Entomology for the biology.

Fumigation, in general terms

Whole-structure fumigation — sealing a building and introducing a fumigant gas such as sulfuryl fluoride (IRAC Group 8C) at a label-calculated dosage for a set exposure period — is reserved for severe, otherwise intractable infestations such as drywood termites or certain stored-product and bed bug situations. It leaves no residual protection, requires evacuation and licensed specialist application, and is treated across the industry as a last resort, not a routine option. This desk describes it in general terms only; it is never a do-it-yourself procedure.

The safety apparatus around it is part of the science. Sulfuryl fluoride is odourless, so fumigators introduce chloropicrin — a lachrymatory warning agent — with it, precisely so that no one can remain in the treated space unaware. After exposure, the structure is aerated and the air is tested and cleared against label criteria before re-entry is permitted; re-entering an uncleared structure is the classic fatal fumigation error. The older structural fumigant methyl bromide has been largely phased out for most uses under the Montreal Protocol, because it depletes stratospheric ozone; its remaining uses are narrow exemptions, in general terms quarantine and critical-use cases. A different fumigant, phosphine, serves stored commodities rather than buildings — see Stored-Product Pests in the Entomology section and Group 24A in the Explorer.

Pollinators and other non-target organisms: an even-handed reading

The neonicotinoids' pollinator profile is the most contested topic in modern insecticide science, and this desk states it as it stands. What is established: neonicotinoids are systemic, so residues occur in the pollen and nectar of treated plants; laboratory studies have repeatedly shown sublethal effects on bees — navigation, learning, foraging and reproduction — at sufficient doses; and exposure is not in doubt. What is contested: how laboratory doses translate to field-realistic exposure, whether effects at the individual-bee level scale into colony-level harm across landscapes and seasons, and how much of observed pollinator decline these compounds explain alongside parasites, disease, habitat loss, and weather. Field studies at realistic exposure have produced mixed results. Regulators have weighed the same evidence differently — outdoor uses of the main neonicotinoids are heavily restricted in the European Union, while the United States has so far relied chiefly on label changes and pollinator-protection language. A science desk does not have to pick a winner to be useful: the honest summary is hazard demonstrated, field-level magnitude debated, regulatory judgement split.

The non-target story is wider than bees. Pyrethroids are highly toxic to aquatic invertebrates and fish, which is why runoff and drain disposal are label issues, not afterthoughts. Broad-spectrum spraying kills the predators and parasitoids that were suppressing other pests — one documented route to secondary-pest flare-ups. And insecticide selectivity claims ("insect-specific") are always relative: fipronil's GluCl action is insect-specific, its GABA action is not unique to insects, and placement and dose are what keep a selective molecule selective in practice.

Microbiologicals: control by microbe

Bacillus thuringiensis (Bt, IRAC Group 11) is a bacterium whose spores carry crystal proteins that, activated in the alkaline insect gut, punch holes in gut cells. The specificity lives in the strain: Bt israelensis targets mosquito and black-fly larvae and is a mainstay of municipal larviciding; Bt kurstaki targets caterpillars. Beauveria bassiana is an entomopathogenic fungus: its spores germinate on the cuticle, penetrate, and grow through the body — a contact infection rather than a poison, which makes it slower and dependent on humidity and temperature, and has made it a researched option against bed bugs and other structural pests in products registered for those uses. Microbiologicals are not "chemicals lite": they are living-system tools with their own resistance record (Bt resistance is documented in some agricultural pests) and their own label law.

Rodenticides, in brief — a neighbouring science

Rodenticides are not insecticides and carry no IRAC groups, but their evidence base belongs on a science desk. The classic chemistry is the anticoagulants, which block vitamin-K recycling and therefore clotting-factor production. First-generation compounds (such as warfarin) generally required feeding on several successive days and break down comparatively quickly. Second-generation compounds were developed against warfarin-resistant rodents: a single feeding can deliver a lethal dose and the compounds persist far longer in tissues. That persistence is the pivot of the modern evidence debate: secondary poisoning — a raptor, owl, or other predator eating a poisoned rodent — is documented for the second-generation compounds, and several jurisdictions have restricted their use on exactly that evidence. Non-anticoagulant alternatives exist with entirely different modes of action (in general terms: compounds causing fatal calcium overload, and acute neurotoxicants); different is not the same as harmless, and all remain governed by their labels. The IPM point survives the chemistry: exclusion, food storage, and sanitation remove the reason rodents are present, and no rodenticide changes that arithmetic.