| A brief history of categories and their development | representative | Mode of action | Site of action (target) | Manifestations of intoxication | remark |
| Organophosphorus: In 1932, scientists discovered the biological activity of organophosphorus compounds, in 1941 the British and Germans discovered the toxicity of some compounds to insects when synthesizing organophosphorus nerve agents, in 1944 the German Schrader synthesized the first systemic organophosphorus insecticide OMPA and TEPP, and in 1944 synthesized parathion code-named E605. | Dichlorvos, chlorpyrifos, propromophos, triazoliphos, octylthion, oxyleconium, phosphorus killing, etc | 1. Fumigation: the agent enters from the valve on the wall of the pest body; 2. Touch killing: through the body wall, mouth organ, body wall (internodular membrane), foot (tarsal joint), antennae and wings; 3. Gastric toxicity: chewable mouthparts enter the stomach and intestines of insects when they feed on plant tissues; 4. Internal suction: after the agent is absorbed by the plant, the pest enters the insect body when it eats the plant juice; | Acetylcholinesterase: Adsorb acetylcholinesterase released by neurons in insects, so that acetylcholine, which conducts insect nerve impulses, cannot be hydrolyzed, and accumulates in large quantities at synapses, thereby interfering with the normal conduction of nerve impulses, inducing neurotoxins, resulting in insect death. | Excitement, convulsions | 1. Human and animal poisoning should be induced to vomit first, and then intravenously or oral atropine should be injected immediately, and then sent to the hospital for treatment; 2. Positive correlation between efficacy and temperature; 3. The toxicity and mode of action between different types are quite different; 4. More sensitive crops; 5. Most of them are broad-spectrum insecticides. |
| Carbamates: In 1925, scientists discovered that the toxin in toxic lentils, physostigmine, belongs to natural carbamate compounds. In the 1940s, Gysin developed the first carbamate insecticide- dimavir, and in 1953, he combined with the carbonization company to synthesize methanafran (ciivine). | Amidoxil, Isopropylvir, Sedentine, Chlorpyrifos, CRU, Buttix, Butyrox, etc., as well as DuPont's indigovir | 1. Touch killing; 2. Stomach poisoning; 3. Suction; 4. Fumigation. | Similar to organophosphorus Indigovir is a sodium channel inhibitor | ditto | 1. The treatment method before sending people and animals to the hospital after poisoning is similar to organophosphorus; 2. The efficacy is not sensitive to temperature response; 3. The knockdown speed is faster than that of organophosphorus; 4. The toxicity varies greatly, and the aldicarbic, carbofuran and adodovir are highly toxic agents; 5. Some species are invalid for mites. |
| Pyrethroids: simulate the chemical structure of pyrethroids in natural pyrethroid plants, and synthesize insecticidal activity and stability of agents with better stability. Americans first synthesized the world's first pyrethroid insecticide - propenophrene in 1947, commercially produced in 1949, followed by the Japanese, in the early 70s developed phenyl ether esters and cyanophenoxyspermide containing α- cyanoid; In 1972, the British developed the second generation of permethrin, dichlorophenoxyfenthrin, and then the Japanese and Germans developed a number of new types of drugs. | Type I. type: the structure does not contain α-cyano, amoxymethrin, propylmethrin, phenylether ester, dichlorophenyl ether bacteriostide, etc.; Type II. contains α-cyano, etc., cypermethrin, cypermethrin, high-efficiency cypermethrin, high-efficiency cypermethrin, high-efficiency cypermethrin, high-efficiency cypermethrin, methrin, bifenthrin, etc | 1. Touch killing; 2. Stomach poisoning; | Sodium ion channels: During the conduction of nerve impulses in insects, the axons of neurons have a large number of sodium and potassium ions in and out, and are controlled by ion channels. This type of agent is to destroy the ion channels of neuronal axons to disturb the entry and exit of sodium ions, resulting in neurological disorders and poisoning and death. | Type I: excited, uncoordinated movements; Type II: spasms, paralysis | 1. There is no specific antidote after human and animal poisoning, and it is sent to the hospital for treatment as soon as possible after inducing vomiting; 2. The efficacy of some types of drugs is negatively correlated with the temperature reaction; 3. Touch killing is the mainstay, and the knockdown speed is faster; 4. Most of them are poisoned or low-toxic; 5. The resistance and interaction resistance are obvious; 6. Some of the effects on mites are poor; |
| Nicotine chloride: belongs to heterocyclic compounds. Bayer developed the world's first nicotinoid insecticide, imidacloprid in the mid-1980s, Cao Da of Japan developed acetamidine in the late 1980s, Takeda developed acetamidine in 1989, and Novartis of Switzerland (one of Syngenta's predecessor companies) developed thiamethoxazine in 1991. | Imidacloprid, acetamiprid, alenoptoxate, thiamethoxazine, thiamethoxam, etc | 1. Root suction; 2. Touch killing; 3. Avoidance. | Acetylcholinesterase receptor: Selectively controls nicotinic acetylcholinesterase receptors in the insect nervous system, blocking the conduction of the insect central nervous system. | Paralyzed to death. | 1. High efficiency and low toxicity, but toxic to bees; 2. Acetamidine is sensitive to temperature and is positively correlated; 3. Invalid for mites. |
| Antibiotics: agents that use microbial metabolites to kill insects. Bacillus thuringiensis was discovered by the Japanese in 1901 in bacillus cereus populations. In 1975, the sixteen-element macrolide compound avermectin discovered by the Kitasato Research Institute in Japan became a new milestone in the application of antibiotics in agricultural production. | Avermectin, methylvidine salt, polybactericide, liuyangmycin, bacillus thuringiensis, etc | 1. Touch killing; 2. Stomach poisoning. | Chloride channel (avermectin): AGABAA receptor that acts on the synapses of insect neurons or synapses of muscle neurons, interferes with the information transmission of nerve endings, prolongs the open channel of chloride ions, and the influx of a large number of chloride ions blocks the connection between nerve endings and muscles, which is insect paralysis, food refusal, and death. | Paralysis, refusal to eat, etc | 1. Avermectin original drug is highly toxic to humans and animals; 2. Avermectin and polybactericides are broad-spectrum insecticides, Bacillus thuringiensis has high activity against Lepidoptera larvae, and methylphenidate has a higher contact killing effect than avermectin. |
| Benzoylureas: In the 1970s, when the Dutch developed herbicides, they accidentally discovered a benzoylurea compound that has no herbicide effect but is effective against insects, a chitin inhibitor. | Urea, urea (enemy), pyridoxine (taibao), fluolamide (lid), fiprourea (carame), bodecanide (nongment) and so on | Stomach poisoning | Inhibits the synthesis of insect chitin, thereby disturbing its molting regularity. | Blackening, stiffness, deformity. | 1. High efficiency and low toxicity; 2. The efficacy is slow and long-lasting, and should be used in conjunction with or in advance with fast-acting insecticides; 3. Toxic to silkworms. |
| Amides: In 1998, Japanese pesticides and Bayer jointly developed the first insecticide to induce insect fish nittin receptors - fiproxateramide, or lange. In 2000, DuPont developed a highly effective insecticide of fish nitrate in the upper and lower conduction of the object catheter - chlorobenzamide, Kang Kuan. | Ridge Song: Fiprofenoxamide; Kang Kuan: Chlorpyrifos benzamide; Fogo: chlorhexendox benzamide + thiamethoxazine; Cyanoxamide. | 1. Touch killing; 2. Stomach poisoning; 3. Osmotic conduction (Kang Kuan) | Fish nittin receptor: Induces insects to produce fish nitrate, so that calcium ions are released indefinitely, resulting in severe deficiency, paralysis and death. | Muscle stiffness, refusal to eat, paralysis | 1. High efficiency and low toxicity, less toxic to fish and bees; 2. The efficacy is slow, and the drug should be used in advance or in combination with other quick-acting agents when controlling older larvae; 3. It should not be used continuously. |
| Pyrazole: In 1989, the French company Rhone Planck combined pyrazole heterocyclic and fluorine elements to develop the first pyrazole insecticide - fiproxic cyanide. | Cyanide, butene cyrustani | 1. Stomach poisoning; 2. Touch killing; 3. Suction. | Chloride channels | excited | 1, there is a devastating poison to bees, In July 2009, the mainland banned the production and use of fipronide (which can be used as a seed treatment agent); 2. Tetranefluorosatide cyanide is a new type of phenylpyrazole insecticide developed by Dalian Ruize, which is less toxic to bees. |
| Quaternary ketoacids: Bayer discovered spironate during the development of herbicides, followed by further synthesis of spironoates and ethyl spironoids | Spironoid ethyl ester (muwant), spironite ester, spirothate | Bidirectional suction conduction | Inhibits the activity of acetyl-CoA carboxylase during fat synthesis in pests, thereby inhibiting fat synthesis, blocking the normal energy metabolism of pests, and ultimately leading to death. | The effect is slow and should be sprayed in advance or used in combination with a quick-acting agent. |
| Pyridines: First developed by Cibalgaard käger in 1988. | Pyrazinone (pyrazinone) | Touch killing, two-way conduction and internal suction | The needle penetrates the blockage | Food intake was stopped within 3 hours and most died after 48 hours | 1. It is efficient for sucking mouthpiece pests; 2. Spray evenly; 3. Do not use continuously in large doses to avoid pest resistance |
| Pyrrole: An insecticide containing trifluoromethylpyrrolonitrile developed by the American Cyanamide Company in 1987. | Ceramide nitrile (expended, brominecarbonitrile) | Touch to kill stomach poison Strong permeability and a certain degree of absorption | Interferes with the oxidative phosphorylation process in the mitochondria of insect somatic cells | Due to the lack of energy supply, the activity after poisoning weakens, spots appear on the body, body color changes, paralysis, and death | 1. Insecticide and mite killing; 2. Toxic to fish |
| Juvenile carcinoids and molting hormones: Lycostyl esters, the first commercially available sparing hormone insecticides in 1973; In 1985, The American Rohm and Haas was the first to develop a molting hormone insecticide - suppressor hydrazine. | Juvenile conservation hormones: mosquito fly ether, dioxil, phenylene ether --- mainly used for health pest control; Molting hormones: suppressor hydrazine (insect death net), carnohydrazide (rice man) | Stomach poison touch kill | Interferes with the process of insect metamorphosis | Deformity, death | The effect is slow and should be used in advance or in combination with a quick-acting insecticide |
| Sand silkworm toxins: heteropod sand silkworm, Japanese fishing bait, is a kind of link worm living in the beach sediment, at first found that this insect is toxic to mosquitoes and flies, people who have more contact also have nausea, headache and other reactions, in 1934 Nitta isolated an active ingredient - sand silkworm toxin NTX, in 1962 Hagriwara was first synthesized, in 1965 Takeda company first developed the first sand silkworm toxin insecticide: Bataan. | Bataan, Insecticidal Single, Insecticidal Double, Borer Dan | Touch to kill stomach poison Weaker suction and fumigation | Blocking the transmission of cholinergic synapses Bataan not only kills leafhoppers quickly, but also inhibits feeding (reduces the frequency of extension, reduces honeydew secretion) at sub-lethal doses, inhibits its toxic behavior, and thus prevents the occurrence of rice virus disease. In addition, Bataan also has a certain bactericidal activity, as an insecticide, in the field can also produce a certain inhibition reaction to pathogenic bacteria. | Sluggish, paralyzed death (no spasticity and excitatory response) | 1. Outstanding effect on lepidoptera pests such as leafhoppers and planthoppers on rice, fruit trees, vegetables and other crops; 2. High toxicity to silkworms; 3. The seedlings of cruciferous vegetables such as Chinese cabbage and kale are both sensitive to borericide and insecticidal, and are more sensitive when the summer temperature is high or the crop growth is weak; Beans, cotton, etc. are particularly sensitive to insecticidal rings and insecticidal rings, and are susceptible to drug damage. |
| Plant-derived insecticides: Insecticidal active ingredients extracted from plant organs or tissues | Terpenes: Neem - terpenoids extracted from neem trees; | Touch killing, stomach poisoning, sterilization, refusal to eat, etc | Directly or indirectly by destroying the chemical sensing organs of the insect mouth organs, food refusal effects are generated; Through the action of digestive enzymes in the midgut, the nutritional conversion of food is insufficient, affecting the vitality of insects. High doses of neem can directly kill insects, while low doses can lead to the emergence of permanent larvae, or deformed pupae, adults, etc. By inhibiting the synthesis and release of pre-thymus hormone (PTrH) by neurosecretion cells in the brain, it affects the synthesis and release of anterior thymus to molting steroids, as well as the synthesis and release of priming hormones by the pharyngeal lateral body. The destruction of normal concentrations of infant hormone in insect hemolymphatics also results in insufficient synthesis of ovantin required for insect egg maturation, leading to infertility | 1, almost all plant pests have an effect; 2. The efficacy is slow, pay attention to the timing of medication or use with other insecticides; 3. Many products marked with neem insecticides on the domestic market today have hidden ingredients. | |
| Organones, esters: rotenone - ketones extracted from fish vines. Pyrethroids – ester compounds extracted from pyrethroids; | Touch killing, stomach poisoning, food refusal, repellent, inhibition of growth, etc | Inhibits electron transport in insect cells | Slowness of movement, paralysis; | 1. Aphids, green worms, jumping nails, thrips and other medicinal effects are remarkable (fish vine ketone); 2. Rapid insecticide and long effectiveness; 3, see the light is easy to decompose; 4. High toxicity to fish. | |
| Alkaloids: matrine - alkaloids extracted from organs such as the rhizomes and leaves of matrine; Quinoa alkali - an alkaloid compound extracted from plants of the genus Quinoa in the family Liliaceae; | Stomach poisoning, touch killing, refusal to eat, sterilization | Matrine: paralyzes the nerve center, coagulates proteins, causes its stomata to block and suffocate to death | Death by suffocation | 1. It is effective for vegetables, fruit trees, aphids on the field, vegetable green insects, small cabbage moths, borers, mites and other pests; 2. The efficacy is slow, pay attention to the timing of application or use in combination with other agents. 3. Most of the matrine insecticides in the domestic pesticide market today have hidden components. | |
| Microbial insecticide In 1901, the Japanese discovered Bacillus thuringiensis in the Bacillus cereus population. | Thuringiensis, White Zombie, Green Zombie, Nuclear Polyhedral Virus, Granular Virus, etc | Touch killing, stomach poisoning | Parasitic destruction of insects disrupts their metabolic processes | Illness and death | 1. Safety of the environment, people and livestock; 2. The efficacy is slow but has cumulative efficacy; 3. Pay attention to the use of technology and its environmental conditions at that time. |
