Absorption, Distribution and Excretion
In rats, the drug is eliminated within 2–4 days after oral administration. The benzene ring is hydroxylated, the ester bond is hydrolyzed, and the acidic moiety is excreted as a glucuronide and glycine conjugate. In female Bengal goats, a kinetic study after intravenous injection at a dose of 0.2 mg/kg showed that deltamethrin plasma concentrations peaked at 0.5 minutes, then rapidly declined, reaching a minimum concentration 6 minutes after administration. The following values were obtained: Vdarea 0.148 (±0.02) L/kg; t1/2 (a) 0.22 (±0.02) min; t1/2 (beta) 2.17 (±0.37) min; Kel 1.05 (±0.24) /min; AUC 4.30 (±0.45) μg·min/mL; ClB 0.05 (±0.006) L/kg/min; T~B 1.93 (±0.58); fc 0.40 (±0.05). Ten minutes after intravenous administration, the highest residue was observed in the liver, followed by the heart, adrenal glands, kidneys, spleen, adipose tissue, and brain tissue. Residues were still present in the liver, adipose tissue, heart, and spleen 30 minutes after intravenous administration, and in bone, liver, and adipose tissue after 60 minutes. Deltamethrin has low and unstable oral absorption, with approximately 65% of the administered dose recovered from feces and gastrointestinal contents. Very little deltamethrin is excreted in urine, with only 0.01% and 0.013% of the administered dose recovered after 3 and 5 days, respectively. Residue remained in all tissues after 3 days; however, residues remained in fat, rumen, reticulum, omasum, abomasum, large intestine, small intestine, and bones after 5 days, with recovery rates of 1.73% and 0.027%, respectively. …
Three young male volunteers underwent comprehensive physical examinations one week prior to the start of the study. Each volunteer received a single dose of 3 mg of deltamethrin, mixed with 1 g of glucose, diluted first with 10 mL of polyethylene glycol 300, and then diluted with 150 mL of water. The total radioactivity was 1.8 ± 0.9 mBq. Blood, urine, saliva, and stool samples were collected at intervals over 5 days. Clinical and biological examinations were performed every 12 hours during the trial and again one week after the trial. Radioactivity in biological samples was measured using a liquid scintillation counter. No abnormalities were found in the clinical and biological examinations. No side effects occurred during or after the trial. Plasma radioactivity reached peak 1 to 2 hours after administration and remained above the detection limit (0.2 KBq/L) for 48 hours. The apparent elimination half-life was 10.0 to 11.5 hours. Radioactivity in blood cells and saliva was extremely low. Urinary excretion was 51% to 50% of the initial radioactivity; 90% of the radioactivity was eliminated within 24 hours of absorption. The apparent half-life of urinary excretion was 10.0 to 13.5 hours, consistent with plasma data. At the end of the observation period, fecal excretion was 10% to 26% of the administered dose. After 96 hours, the total excretion in feces and urine was approximately 64-77% of the initial dose. In a feeding trial, deltamethrin was added twice daily to the diets of lactating dairy cows for 28 consecutive days at doses of 2 mg/kg and 10 mg/kg. The 2 mg/kg dose represented the residue levels found in recently treated pastures, while the 10 mg/kg dose was five times that amount. Deltamethrin residues in milk were dose-dependent, reaching a plateau between 7 and 9 days after treatment initiation. In the high-dose group (10 mg/kg), the deltamethrin residue in milk was approximately 0.025 mg/L. Deltamethrin residues in tissues were measured on days 1, 4, and 9 after the last administration. At a dietary intake of 10 mg/kg, only trace amounts of deltamethrin residues were detected in the liver (<0.005 mg/kg), kidney (<0.002 mg/kg), and muscle (0.002–0.014 mg/kg). At dietary intakes of 2 mg/kg and 10 mg/kg, the residual amounts in fat were approximately 0.04 mg/kg and 0.2 mg/kg, respectively. The consumption of deltamethrin in milk was very rapid (estimated half-life of approximately 1 day); while the half-life in fat (kidney and subcutaneous tissue) was 7–9 days. Only two metabolites, Br2CA (3-(2,2-dibromoethene)-2,2-dimethylcyclopropanecarboxylic acid) and PBacid (3-phenoxybenzoic acid), were detected in the milk and tissues of the tested cows. In all cases, their detection concentrations were trace, <0.0235 mg/L and <0.034 mg/L, respectively. These two metabolites have previously been identified as major degradation products of deltamethrin in rats and mice. For more complete data on the absorption, distribution, and excretion of deltamethrin (18 in total), please visit the HSDB records page.

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Metabolism/Metabolites
Deuterium cypermethrin (1 μg) was incubated with the following mouse microsomal formulations at 37 °C for 30 min: a) microsomes treated with tetraethyl pyrophosphate (TEPP) (no esterase and oxidase activity); b) normal microsomes (esterase activity); c) TEPP-treated microsomes with NADPH (oxidase activity); and d) normal microsomes with NADPH (esterase and oxidase activity). Deuterium cypermethrin was metabolized faster in the oxidase system than in the esterase system. The major cyclohydroxylation site was the 4' position, and the minor site was the 5' position. The trans-methyl group is an important hydroxylation site for esters, while cis-methyl oxidation is also observed in the metabolites of the cleaved acidic moiety. Preferred hydroxylation sites are: the trans site of dimethyl, the 4' position of the phenolic hydroxyl group, and the cis site of dimethyl (equivalent to the 5' position of the phenoxy group). Since the amount of cleavage products is greater in the oxidase system, the cleavage of deltamethrin into cyanohydrins is likely the result of the combined action of esterases and oxidases. ... However, at concentrations much higher than (approximately 35 times) of the deltamethrin concentrations in the aforementioned studies, no hydrolysis was detected. In the blood, brain, kidneys, and stomach of mice, esterases hydrolyze deltamethrin to produce PBald and PBacid. In a metabolic study, lactating cows were orally administered (14)C-labeled deltamethrin at a dose of 10 mg/kg body weight/day for three consecutive days. The substance was poorly absorbed and was mainly excreted in feces as unmetabolized deltamethrin. Only 4–6% of (14)C was excreted in urine, and 0.42–1.62% was secreted into milk. Radiocarbon levels were generally low in tissues other than the liver, kidneys, and adipose tissue, where radiocarbon levels were higher. Degradation of deltamethrin occurs via ester bond cleavage, consistent with previous reports in rats and mice. In vitro studies have shown that the enzymes responsible for ester bond cleavage are present in bovine liver homogenate, primarily in the microsomal fraction. Metabolites from ester bond cleavage are further metabolized and/or conjugated, ultimately leading to the excretion of large amounts of these compounds in urine. In breast milk, the main radiolabeled compound is deltamethrin. The main metabolic pathways of deltamethrin in mice are similar to those in rats, but some differences exist. For example, the content of unmetabolized deltamethrin in mouse feces is higher than in rat feces. Four monohydroxy ester metabolites (2'-OH-, 4'-OH-, 5-OH-, and trans-OH-deltamethrin) and one dihydroxy metabolite (4'-OH-trans-OH-deltamethrin) were detected in mouse feces, while these metabolites were not detected in mouse urine. The main metabolites of the acidic fraction in mice are Br₂CA, trans-OH-Br₂CA, and their glucuronide and sulfate conjugates. Trans-OH-Br₂CA sulfate was detected only in mice and not in rats. Compared to rats, mice produced significantly higher levels of trans-OH-Br2CA and its conjugates. The major metabolite of alcohols in mice was a taurine conjugate of PBacid in urine, which was not detected in rats. Overall, mice produced lower levels of phenolic compounds than rats. In addition, 3-phenoxybenzaldehyde (PBald) and 3-phenoxybenzyl alcohol were also detected. Benzoic acid (PBalc) and its glucuronide, as well as glucuronides of 3-(4-hydroxyphenoxy)benzyl alcohol (4'-OH-PBalc) and 5-hydroxy-3-phenoxybenzoic acid (5-OH-PBacid), were detected in mice but not in rats. When mice were intraperitoneally injected with (14)C-deltamethrin, with or without injection of piperonyl butyl ether (PBO) and/or S,S,S-tributyl thiophosphate (DEF), the metabolites obtained were the same as those obtained with oral administration. However, compared to the control group, DEF reduced the content of hydrolysis products, while PBO reduced the content of oxidation products. The sulfate of 4'-OH-PBacid accounts for approximately 50% of the administered dose, in addition to small amounts of free form (4%) and glucuronide (2%). The cyano group is mainly converted to thiocyanate, with a small amount converted to isothiocyanate (ITCA). The trans isomer of deltamethrin is also rapidly metabolized. Its metabolites are almost identical to those of deltamethrin, but a 5-hydroxy derivative was found in the cis isomer, while it was not found in the trans isomer.
For more complete metabolite/metabolite data for deltamethrin (19 in total), please visit the HSDB record page.
Known human metabolites of deltamethrin include 4'-hydroxydeltamethrin.
Deltamethrin is readily absorbed orally, but less so through the skin; absorbed deltamethrin is readily metabolized and excreted. The primary degradation pathway of deltamethrin is ester bond hydrolysis, ultimately yielding 3-phenoxybenzoic acid and 3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylic acid. (The cis isomer yields both cis and trans-cyclopropanecarboxylic acids.) A secondary degradation pathway involves cyclohydroxylation to α-cyano-3-(4-hydroxyphenyl)benzyl ester, followed by hydrolysis to the corresponding hydroxycarboxylic acid (A558).
Biological Half-Life
After intravenous injection, the distribution half-life and elimination half-life of deltamethrin were 1.39 hours and 33.0 hours, respectively.
In rats intravenously injected with deltamethrin and its metabolite (4-OH-deltamethrin), the elimination half-lives were 33 hours and 25 hours, respectively.
The half-life of deltamethrin in the rat brain was 1–2 days, but it was more persistent in body fat, with a half-life of 5 days.
Three young male volunteers underwent comprehensive physical examinations one week prior to the start of the study. Each volunteer received a single dose of 3 mg of 14C-labeled deltamethrin, which was mixed with 1 g of glucose and diluted. The sample was first dissolved in 10 mL of polyethylene glycol 300 solution, and then in 150 mL of water. The total radioactivity was 1.8 ± 0.9 mBq. …The apparent elimination half-life was 10.0 to 11.5 hours. …The apparent urinary excretion half-life was 10.0 to 13.5 hours, consistent with plasma data.

Toxicity Summary
Both type I and type II pyrethroids exert their effects 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 hyperactivity, which may result in paralysis and/or death. Other mechanisms of action of pyrethroids include antagonism of γ-aminobutyric acid (GABA)-mediated inhibition, regulation of nicotinic cholinergic transmission, enhancement of norepinephrine release, and action on calcium ions. They also inhibit calcium ion channels and Ca2+,Mg2+-ATPase. (T10, T18, L857)

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Toxicity Data
LC50 (Rat) = 785 mg/m3/2h
LD50: 4123 mg/kg (oral, rat) (A563)
LD50: >2460 mg/kg (skin, rabbit) (A563)

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Interactions
In vitro, deltamethrin can be hydrolyzed by esterases in mouse blood, brain, kidney, liver, and stomach tissues. Pretreatment of mice with the oxidase inhibitor piperonyl butyl ether (PBO) or the esterase inhibitor S,S,S-tributylphosphate trisulfide (DEF) delayed the metabolism of deltamethrin administered intraperitoneally. PBO or DEF made mice more sensitive to deltamethrin.
... Sprague-Dawley rats... /in/ Group A received cottonseed oil as a control, while groups B, C, and D received deltamethrin (DM); DM and DDT; and DM, DDT, phytoestrogens, and p-nonylphenol, respectively. Rats were exposed to these substances in utero and then administered them for 10 weeks. Compared to the control group, seminal vesicle mass (Group B; P = 0.046) and sperm count [Group C (P = 0.013) and Group D (P = 0.003)] were decreased, and anal-genital distance [Group B (P = 0.047), Group C (P = 0.045), and Group D (P = 0.002)] was shortened. Compared with the control group, the diameter of seminiferous tubules [Group B (P < 0.001), Group C (P < 0.001), and Group D (P < 0.001)] and epithelial thickness [Group B (P = 0.030), Group C (P < 0.001), and Group D (P < 0.001)] were all reduced. Histological examination of the testes showed apical detachment and vacuolation. Liver weight [Group C (P = 0.013) and Group D (P = 0.005)] and liver enzymes [Group D (P = 0.013)] were also affected. These findings may suggest that co-exposure to endocrine-disrupting compounds can lead to deterioration of male reproductive health. In addition to hepatic esterases, plasma esterases are also involved in the metabolism of deltamethrin in mammals and contribute to its rapid detoxification via oral administration. In a synergistic study, researchers orally administered a series of esterase inhibitors (mainly organophosphate insecticides) to male rats, which inhibited plasma cholinesterase activity by 50%. After 15 minutes, 2 hours, or 24 hours, rats were given the oral LD50 dose of deltamethrin emulsifiable concentrate, showing a synergistic effect with ethamidophos, dimethoate, and dichlorvos. Given the high toxicity of these combinations, users must handle deltamethrin with extreme caution. Acetaminophen, phosmet, phosphamidon, methyl parathion, and two control agents did not show a synergistic effect. This study investigated the effects of deltamethrin pretreatment on the pharmacokinetics and metabolism of antipyrine in male rats. Deltamethrin pretreatment (20 mg/kg and 40 mg/kg daily for 6 days prior to antipyrine administration) significantly reduced the total plasma clearance of antipyrine while significantly increasing the β-phase elimination half-life, area under the concentration-time curve, and mean residence time of antipyrine. The observed changes were dose-dependent. Following treatment with deltamethrin, the urinary excretion of norantipyrine, 4-hydroxyantipyrine, and 3-hydroxymethylantipyrine decreased by 39%, 32%, and 26%, respectively (p < 0.001). Furthermore, the average rate constants for the formation of these metabolites were significantly reduced by approximately 71%. These results indicate that deltamethrin can inhibit oxidative metabolism, a finding that may have clinical and toxicological significance. For more complete data on interactions with deltamethrin (10 in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 for male rats: 128 mg/kg (soluble in vegetable oil)
Oral LD50 for dogs (male and female): >300 mg/kg (technical grade)
Oral LD50 for dogs (male and female): 2 mg/kg (technical grade)
Dermal LD50 for rabbits: >2000 mg/kg (technical grade)
For more complete (28) non-human toxicity values of deltamethrin, please visit the HSDB record page.

[1]. Deltamethrin toxicity: A review of oxidative stress and metabolism . Environmental research, 2019, 170: 260-281.

[2]. Effect of the pesticide, deltamethrin, on Ca2+ signaling and apoptosis in OC2 human oral cancer cells . Drug and Chemical Toxicology, 2014, 37(1): 25-31.

[3]. Deltamethrin induced an apoptogenic signalling pathway in murine thymocytes: exploring the molecular mechanism . Journal of Applied Toxicology, 2014, 34(12): 1303-1310.

[4]. The modulatory effect of deltamethrin on antioxidants in mice . Clinica Chimica Acta, 2006, 369(1): 61-65.

[5]. Neuromechanical effects of pyrethroids, allethrin, cyhalothrin and deltamethrin on the cholinergic processes in rat brain . Life sciences, 2005, 77(7): 795-807.

[6]. The heart as a target for deltamethrin toxicity: Inhibition of Nrf2/HO-1 pathway induces oxidative stress and results in inflammation and apoptosis . Chemosphere, 2022, 300: 134479.

Deltamethrin is a cyclopropane carboxylic acid ester, formed by the condensation of 3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid with cyano(3-phenoxyphenyl)methanol. It is the active insecticide of the precursor insecticide deltamethrin. It has multiple functions, including pyrethroid insecticide, agrochemical, EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor, calcium channel agonist, and feed inhibitor. It is an aromatic ether, organobromine compound, nitrile, and cyclopropane carboxylic acid ester. Its structure is related to cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid. Deltamethrin is a type II pyrethroid insecticide. This substance belongs to one of the safest pesticide classes: synthetic pyrethroids. While mammalian exposure to deltamethrin is considered safe, this insecticide is highly toxic to aquatic organisms, especially fish, and therefore must be used with extreme caution near water. Pyrethroids are synthetic compounds similar to the natural chemicals produced in the flowers of pyrethrum plants (such as ginkgo and chrysanthemum). Pyrethroids 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 individuals. They typically decompose within one or two days in sunlight and the atmosphere, and aside from being toxic to fish, they do not significantly affect groundwater quality. Because deltamethrin is a neurotoxin, it temporarily attacks (or, in medical terms, damages) the nervous system of any animal that comes into contact with it. Skin contact may cause localized stinging or redness. If ingested through the eyes or mouth, common symptoms include facial paresthesia, which can manifest as a variety of abnormal sensations, including burning, partial numbness, tingling, and a crawling sensation on the skin.
Mechanism of Action
The lowest deltamethrin concentration affecting sodium channels in crayfish stretch receptor neurons is 1 x 10⁻¹² mol/L, but concentrations as high as 1 x 10⁻⁷ mol/L do not appear to affect the response of this formulation to γ-aminobutyric acid (GABA). Although deltamethrin at a concentration of 1 x 10⁻⁶ mol/L has a slight effect on the GABA response in finger abductor muscles, most of the effects of cyanopyrethroids in invertebrates appear to be attributable solely to their effects on sodium channels.
Synthetic pyrethroids delay the closure of sodium channels, thereby 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. Pyrethroids containing α-cyano groups (e.g., cypermethrin) produce a more persistent sodium tail current than other pyrethroids (e.g., permethrin, bio-permethrin). The former class of pyrethroids induced a stronger dermal sensation than the latter. /Pyrethroids/
The interaction with sodium channels is not the only mechanism of action for 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 increased sodium ion influx. /Pyrethroids/
This study used voltage-clamp techniques to investigate the interaction between a series of pyrethroid insecticides and sodium ion channels in the myelinated nerve fibers of the African clawed frog (Xenopus laevis). Of the 11 pyrethroids, 9 compounds with insecticidal activity induced a slowly decaying sodium tail current at the termination of step depolarization, while the sodium current during depolarization was almost unaffected. /Pyrethroids/
For more complete data on the mechanisms of action of DELTAMETHRIN (11 in total), please visit the HSDB record page.

C22H19BR2NO3

505.2

502.973

52918-63-5

Deltamethrin-d5;2140301-99-9

40585

White to off-white solid powder

1.6±0.1 g/cm3

535.8±50.0 °C at 760 mmHg

98ºC

277.8±30.1 °C

0.0±1.4 mmHg at 25°C

1.653

6.2

0

4

7

28

643

3

CC1([C@H]([C@H]1C(=O)O[C@H](C#N)C2=CC(=CC=C2)OC3=CC=CC=C3)C=C(Br)Br)C

OWZREIFADZCYQD-NSHGMRRFSA-N

InChI=1S/C22H19Br2NO3/c1-22(2)17(12-19(23)24)20(22)21(26)28-18(13-25)14-7-6-10-16(11-14)27-15-8-4-3-5-9-15/h3-12,17-18,20H,1-2H3/t17-,18+,20-/m0/s1

[(S)-cyano-(3-phenoxyphenyl)methyl] (1R,3R)-3-(2,2-dibromoethenyl)-2,2-dimethylcyclopropane-1-carboxylate

Decamethrin; Butoss; Deltamethrin

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 (~197.94 mM)

Solubility in Formulation 1: 2.5 mg/mL (4.95 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
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 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 2.5 mg/mL (4.95 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
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 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (4.95 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.

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