Fenpropathrin targets the voltage-gated sodium channels in the nervous system of insects and mites. As a pyrethroid insecticide, it acts by prolonging the opening of sodium channels, which leads to repetitive neuronal firing, hyperexcitation, paralysis, and death of the target pest. Its high efficacy against a wide range of pests is due to its potent action on these channels. Fenpropathrin is an ester and nitrile compound.

In vitro, Fenpropathrin's activity is typically measured using electrophysiological techniques on insect neuronal preparations. The compound is applied to neurons, and its effects on sodium channel currents are measured. It prolongs the opening of sodium channels, leading to a sustained inward sodium current. Its insecticidal activity is confirmed in bioassays, where it causes paralysis and death of target pests. However, specific IC50 or EC50 values are not detailed in standard product descriptions.

In animal modeling, fenpropathrin can be used to create models of Parkinson's disease.

---

In vivo, Fenpropathrin is effective in controlling a wide range of pests on various crops. It has contact action, meaning it kills pests upon direct contact, and also has repellent properties. Its efficacy has been demonstrated in field trials and agricultural use. However, specific in vivo protocols and results are not detailed in standard product descriptions. Its use is established in agriculture.

The in vitro assays for Fenpropathrin measure its effects on voltage-gated sodium channels. Electrophysiological techniques, such as patch-clamp, are used to measure sodium currents in insect neurons. Fenpropathrin is applied, and the prolongation of sodium channel opening is measured. The compound's potency can be determined from the concentration-response curve. However, specific IC50 values are not detailed in standard product descriptions.

In vitro cell-based assays for Fenpropathrin are conducted using insect cell lines or neuronal cultures. In a typical assay, cells are treated with Fenpropathrin, and cell viability is assessed. The compound's ability to cause cell death is measured. However, specific protocols for Fenpropathrin are not detailed in the available literature. Its use is limited to agricultural research.

In vivo animal experiments for Fenpropathrin are conducted in agricultural settings or in laboratory studies on target pests. In a typical efficacy study, pests are exposed to Fenpropathrin, and mortality is recorded. The LC50 (lethal concentration for 50% of the population) is determined. These studies confirm the compound's insecticidal activity.

Absorption, Distribution and Excretion
/Pyrethroids/ Topical LD50 shows they readily penetrate the cuticles of insects (e.g., cockroaches)... /Pyrethroids/
When radioactive pyrethroids are administered orally to mammals, they are absorbed into the animal's intestines and distributed to all examined tissues. Excretion of radioactive material in rats after administration of the trans isomer: Dose: 500 mg/kg; 20-day interval; urine 36%; feces 64%; total 100%. /Pyrethroids/
When applied topically, pyrethroids can be absorbed through intact skin. When animals are exposed to aerosols containing pyrethroids and synergistic ethers, little or no systemic absorption of this mixture occurs. /Pyrethroids/
While limited absorption may be the reason for the lower toxicity of some pyrethroids, rapid biodegradation by mammalian liver enzymes (ester hydrolysis and oxidation) is likely a major factor. Most pyrethroid metabolites are rapidly excreted, at least partially via the kidneys. /Pyrethroids/

---

Metabolism/Metabolites
The metabolism of phenylpropionate esters in rats involves rapid oxidase-catalyzed ester cleavage, followed by hydroxylation.
The metabolic pathways of pyrethroids do not differ significantly among different mammalian species, but vary slightly depending on their structure. …Essentially, pyrethroids and allethrin are primarily degraded via oxidation of the isobutylene side chain of the acid moiety and the unsaturated side chain of the alcohol moiety, with ester hydrolysis also playing a significant role; while other pyrethroids are primarily degraded via ester hydrolysis. /Pyrethroids and Pyrethroids/
The relative resistance of mammals to pyrethroids is almost entirely attributed to their ability to rapidly hydrolyze pyrethroids into inactive acid and alcohol components, as direct injection into the mammalian central nervous system results in susceptibility similar to that of insects. Partial additional resistance in homeothermic organisms can also be attributed to the negative temperature coefficient of pyrethroids, resulting in lower toxicity at mammalian body temperature, but the primary mechanism of action is metabolic. Pyrethroids are metabolized and cleared very rapidly, meaning that intravenous administration results in high toxicity, oral absorption in moderately slow toxicity, and dermal absorption in typically undetectable toxicity. /Pyrethroids/
Primary alcohol esters of trans-substituted acids are the fastest to disintegrate due to rapid hydrolysis and oxidation. For all secondary alcohol esters and primary alcohol esters of cis-substituted cyclopropanecarboxylic acids, oxidation is dominant. /Pyrethroids/
For more complete metabolic/metabolite data on fiproprine (7 metabolites), please visit the HSDB record page.
Fiproprine is well absorbed after oral administration, extensively metabolized, and excreted in the urine as a polar conjugate. As expected, its primary metabolic pathway is via ester bond hydrolysis. The cyclopropanecarboxylic acid moiety is subsequently excreted in the urine as a glucuronide conjugate. (L857)

---

Fenpropathrin has a molecular formula of C22H23NO3 and a molecular weight of 349.42 g/mol. It has a melting point of 47°C and a boiling point of approximately 483.6°C. It has a density of 1.17. It is a yellowish to brown liquid or solid, depending on purity and temperature. It is soluble in organic solvents. For storage, it is recommended to keep the compound in a cool, dry place. Detailed pharmacokinetic properties are not relevant as it is a pesticide.

Toxicity Summary
Pyrethroid insecticides work by prolonging the opening time of sodium ion channels during nerve cell excitation. They appear to bind to membrane lipids near sodium ion channels, thereby altering channel dynamics. This blocks the closing of sodium ion channels in the nerve, thus prolonging the time it takes for the membrane potential to return to its resting state. Repetitive (sensory, motor) neuronal firing and prolonged negative afterpotentials produce effects very similar to DDT, leading to nervous system overactivity, which may result in paralysis and/or death. Other mechanisms of action of pyrethroid insecticides include antagonizing GABA-mediated inhibition, modulating nicotinic cholinergic transmission, enhancing norepinephrine release, and acting on calcium ions. (T18, L857)

---

Toxicity Data
LC50 (Rat)> 19,070,000 mg/m3/4h
LD50: 70.6 mg/kg (oral, rat) (T58)

---

Interactions
/Pyrethroid/Detoxification…Important for flies, but the addition of synergists (organophosphates or carbamates) may delay detoxification to ensure lethality. …/Pyrethroid/
Synergist ethers enhance the insecticidal activity of pyrethroids by inhibiting hydrolytic enzymes responsible for pyrethroid metabolism in arthropods. When piperitin is used in combination with pyrethroids, the insecticidal activity of the latter can be increased by 2-12 times. Adding 1000 ppm pyrethroids and 10000 ppm piperonyl butyl ether to the feed resulted in significant enlargement, marginalization, and increased cytoplasmic inclusions in rat hepatocytes within just 8 days, though these changes did not reach their maximum. These changes were dose-proportional and similar to the effects of DDT. The effects of the two drugs had an additive effect. Pyrethroids/

---

Non-human toxicity values
Oral LD50 in male rats: 70.6 mg/kg (soluble in corn oil)
Oral LD50 in female rats: 66.7 mg/kg (soluble in corn oil)
Dermal LD50 in male rats: 1000 mg/kg
Dermal LD50 in female rats: 870 mg/kg
Dermal LD50 in rabbits: >2000 mg/kg

---

Fenpropathrin is toxic to humans and animals. As a pyrethroid, it can cause neurotoxic effects if ingested or absorbed through the skin. Symptoms may include paresthesia, dizziness, and in severe cases, seizures. It is also toxic to aquatic organisms. Appropriate safety measures, including the use of personal protective equipment, should be taken when handling Fenpropathrin. It is a restricted-use pesticide in many countries.

[1]. Fenpropathrin, a Widely Used Pesticide, Causes Dopaminergic Degeneration. Mol Neurobiol. 2016 Mar;53(2):995-1008.

Depending on purity and temperature, fipronil is a pale yellow to brown liquid or solid. It is used as an acaricide and insecticide. Fentrenil is a cyclopropane carboxylic acid ester, formed by the condensation of 2,2,3,3-tetramethylcyclopropane carboxylic acid and cyano(3-phenoxyphenyl)methanol. It is a pyrethroid insecticide, pyrethroid acaricide, and agricultural chemical. It is an aromatic ether and cyclopropane carboxylic acid ester. Its function is related to 2,2,3,3-tetramethylcyclopropane carboxylic acid. Fentrenil is a type I pyrethroid insecticide. Pyrethroids are synthetic compounds whose structure is similar to that of natural compounds produced by the flowers of pyrethroid plants (such as ginkgo and red chrysanthemum). Pyrethroid insecticides are commonly found in commercial products such as household insecticides and repellents. At the concentrations used in these products, they are generally harmless to humans but may cause harm to sensitive populations. They are typically decomposed by sunlight and atmosphere within one or two days and do not significantly affect groundwater quality except for their toxicity to fish. Some insects with mutations in sodium channel genes may develop resistance to pyrethroid insecticides. (L811, L708)

---

Mechanism of Action
Synthetic pyrethroid insecticides delay the closing of sodium channels, thus generating a sodium tail current, characterized by a slow influx of sodium ions at the end of depolarization. Clearly, pyrethroid molecules keep the activation gate open. Pyrethroid insecticides containing α-cyano groups (e.g., cypermethrin) produce a more persistent sodium tail current than other pyrethroid insecticides (e.g., permethrin, bio-permethrin). The former class of pyrethroids is more likely to cause dermal paresthesia than the latter. /Synthetic Pyrethroids/
Interaction with sodium channels is not the only mechanism of action of pyrethroids. Their effects on the central nervous system have led many researchers to propose that their mechanisms of action may include antagonism of GABA-mediated inhibition, regulation of nicotinic cholinergic transmission, enhancement of norepinephrine release, or action on calcium ions. Since the protective effect of neurotransmitter-specific drugs against poisoning is limited or incomplete, these effects are unlikely to be the primary mechanisms of action for pyrethroids; most neurotransmitter release is secondary to an increase in sodium ion influx. /Pyrethroids/
Symptoms of pyrethroid poisoning follow a typical pattern: (1) excitation, (2) convulsions, (3) paralysis, (4) death. The effects of pyrethroids on the insect nervous system are very similar to those of DDT, but their persistence appears to be much less. Regular, rhythmic, and spontaneous neural discharges were observed in neuromuscular specimens of insects and crustaceans poisoned with pyrethroids. The primary target of pyrethroids appears to be the ganglia of the insect central nervous system, although some pyrethroid poisoning effects were also observed in detached legs. /Pyrethroids/
From an electrophysiological perspective, pyrethroids cause repetitive discharges and conduction block. /Pyrethroids/
For more complete data on the mechanisms of action of FENPROPATHRIN (12 types), please visit the HSDB record page.

---

Therapeutic Use
Pyrethroids in combination with synergist can be used for the topical treatment of lice (lice infestation). The combination of pyrethroids and synergist is ineffective in treating scabies (mite infestation). Although there are currently no well-controlled studies, many clinicians consider 1% lindane to be the first-line lice killer. However, some clinicians recommend the use of the combination of pyrethroids and synergist, especially in infants, children, and pregnant or lactating women… If used properly, 1-3 treatments usually achieve 100% efficacy… Oil-based (e.g., petroleum fraction) combinations… have the fastest onset of action. ...When treating head lice, apply sufficient gel, shampoo, or solution...covering the affected area and surrounding area...after 10 minutes...thoroughly wash the hair...repeat the treatment after 7-10 days to kill any newly hatched lice. /pyrethroids/

---

Fenpropathrin is a broad-spectrum, high-efficacy pyrethroid insecticide and acaricide used in agriculture. It is used to control Lepidopteran, Hemipteran, and mite pests on vegetables, cotton, and cereal crops. It has contact and repellent action. Its mechanism of action involves targeting voltage-gated sodium channels in the nervous system of pests. Fenpropathrin is an agricultural chemical and is not a therapeutic drug. It is a research compound and a commercial pesticide.

C22H23NO3

349.43

349.167

C, 75.62; H, 6.63; N, 4.01; O, 13.74

39515-41-8

Fenpropathrin-d5

47326

Pale yellow oil
Yellow brown liquid or solid

1.1±0.1 g/cm3

448.2±35.0 °C at 760 mmHg

50 - 51ºC

195.5±16.2 °C

0.0±1.1 mmHg at 25°C

1.552

5.48

0

4

6

26

553

0

CC1(C)C(C(=O)OC(C#N)C2=CC(=CC=C2)OC3=CC=CC=C3)C1(C)C

XQUXKZZNEFRCAW-UHFFFAOYSA-N

InChI=1S/C22H23NO3/c1-21(2)19(22(21,3)4)20(24)26-18(14-23)15-9-8-12-17(13-15)25-16-10-6-5-7-11-16/h5-13,18-19H,1-4H3

[cyano-(3-phenoxyphenyl)methyl] 2,2,3,3-tetramethylcyclopropane-1-carboxylate

Fenpropathrin; S-3206; S3206; XE938; XE 938; Fenpropathrin; 39515-41-8; Meothrin; Rody; Danimen; XE-938; S 3206

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~286.19 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (7.15 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

 (Please use freshly prepared in vivo formulations for optimal results.)