Absorption, Distribution and Excretion
In rats, following oral administration, elimination occurs within 2-4 days. The phenyl ring is hydroxylated, the ester bond hydrolyzed, and the acid moiety is eliminated as the glucuronide and glycine conjugates.
Intravenous disposition kinetics /in a female black Bengal goat/ using a dose of 0.2 mg/kg showed that the maximum blood concentration of deltamethrin was recorded at 0.5 min, followed by rapid decline, and a minimum concentration was detected at 6 min after administration. The following values were obtained: Vdarea 0.148 (+ or -0.02) L/kg; t1/2 (a) 0.22 (+ or -0.02) min; t1/2 (beta) 2.17 (+ or -0.37) min; Kel 1.05 (+ or -0.24) /min; AUC 4.30(+ or -0.45)ug min/mL; ClB 0.05 (+ or -0.006) L/kg/min; T~B 1.93 (+ or -0.58); fc 0.40(+ or -0.05). After 10 min, liver retained the maximum residue, and heart, adrenal gland, kidney, spleen, fat and brain also held the insecticide; liver, fat, heart and spleen retained residue after 30 min, and bone, liver and fat retained residue after 60 min of iv administration. Oral absorption of deltamethrin was poor and inconsistent, and approximately 65% of administered dose was recovered from feces and gastrointestinal contents. The excretion of deltamethrin through urine was meager, and only 0.01 and 0.013% of the administered dose was recovered after 3 and 5 days of oral administration respectively. All the tissues retained the residue after 3 days; while fat, rumen, reticulum, omasum, abomasum, large and small intestine and bone retained the residue after 5 days of oral administration; and the percentage recoveries were 1.73 and 0.027 respectively. ...
Three young male human volunteers underwent a complete medical check-up one week prior to the morning of the study. Each of them received a single dose of 3 mg of (14)C deltamethrin mixed in 1 g glucose and diluted first in 10 mL polyethylene glycol300 and again in 150 mL water. Total radioactivity was 1.8 + or - 0.9 mBq. Samples of blood, urine, saliva, and feces were taken at intervals over 5 days. Clinical and biological examinations were performed every 12 hr during the trial and one week after its termination. Radioactivity in the biological samples was measured with a liquid scintillation spectrometer. The clinical and biological checks did not detect any abnormal findings. There were no signs of side effects ... either during or after the trial period. The maximum plasma radioactivity appeared between 1 and 2 hr after administration of the product, and remained over the detection limit (0.2 KBq/L) during the 48 hr. The apparent elimination half-life was between 10.0 and 11.5 hr. The radioactivity of blood cells, as well as the saliva, was extremely low. Urinary excretion was 51-50% of the initial radioactivity; 90% of this radioactivity was excreted during the 24 hr following absorption. The apparent half-life of urinary excretion was 10.0-13.5 hr, which is consistent with the plasma data. Fecal elimination at the end of the observation period represented 10-26% of the dose. The total fecal plus urine elimination was around 64-77% of the initial dose after 96 hr.
In a feeding study, deltamethrin was administered twice daily to lactating dairy cows in portions of their daily feed at the rate of 2 or 10 mg/kg diet for 28 consecutive days. The level of 2 mg/kg diet was the residue level found in a recently treated pasture, whereas 10 mg/kg diet was five times this level. Deltamethrin residues in the milk were dose-dependent and appeared to reach a plateau between 7 and 9 days after the start of treatment. At the high deltamethrin intake of 10 mg/kg diet, the deltamethrin residue in milk was about 0.025 mg/L. Deltamethrin residues in tissues were measured 1, 4, and 9 days after the last dose. At the 10 mg/kg diet intake, very small amounts of deltamethrin residues were found in the liver (<0.005 mg/kg), kidney )<0.002 mg/kg), and muscle (0.002-0.014 mg/kg). Residues in fat were about 0.04 mg/kg and 0.2 mg/kg for the 2 and 10 mg/kg intake, respectively. Depletion of deltamethrin in milk was very rapid (estimated half-life was about 1 day); while in fat (renal and subcutaneous) the half-life was 7-9 days. Br2CA (3-(2,2-dibromovinyl)-2,2-dimethylcyclopro-panecarboxylic acid) and PBacid (3-phenoxybenzoic acid) were the only metabolites detected in the milk and tissues of treated cows. In all cases, they were found at trace levels of < 0.0235 mg/L and < 0.034 mg/L, respectively. These two metabolites were also previously identified in rats and mice as the major degradation products of deltamethrin.
For more Absorption, Distribution and Excretion (Complete) data for DELTAMETHRIN (18 total), please visit the HSDB record page.

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Metabolism / Metabolites
Deltamethrin (1 ug) was incubated at 37 °C for 30 min with each of the following mouse microsome preparations; a) tetraethyl pyrophosphate (TEPP)-treated microsomes (no esterase and oxidase activity); b) normal microsomes (esterase acivity); c) TEPP-treated microsomes plus NADPH (oxidase activity); and d)normal microsomes plus NADPH (esterase plus oxidase activity). Deltamethrin was more rapidly metabolized under the oxidase system than under the esterase system. The major site of ring hydroxylation was 4'-position and the secondary site was the 5-position. The trans methyl group was an important site of hydroxylation of the esters and cis methyl oxidation was evident in the metabolites of the cleaved acid moiety. The preferred sites of hydroxylation were as follows; trans of dimethyl group, 4'-position in the phenol group, and cis of the dimethyl group was equal to the 5-position in the phenoxy group. Cleavage of deltamethrin to cyanohydrin may result from both esterase and oxidase enzyme activities, since larger amounts of the cleaved products were evident in the oxidase system. ... However, at a much higher (approximately 35-fold) concentration of deltamethrin than that in the above study, it was not detectably hydrolysed. ... Deltamethrin was hydrolysed by esterases in the blood, brain, kidney, and stomach of mice yielding PBald and PBacid.
In a metabolic study, (14)C-deltamethrin was administered orally to lactating dairy cows at the rate of 10 mg/kg body weight per day for 3 consecutive days. It was poorly absorbed and mainly eliminated in the feces as unchanged deltamethrin. Only 4-6% of the administered (14)C was eliminated in the urine, and 0.42-1.62% was secreted in the milk. The radiocarbon contents of various tissues were generally very low with the exception of those of the liver, kidney, and fat, which were higher. Deltamethrin degradation occured by cleavage of the ester bond, as already reported in rats and mice. The enzymes responsible for the ester bond cleavage were located in cow liver homogenate, mainly in the microsomal fraction, as seen in an in vitro study. Metabolites resulting from ester bond cleavage further metabolized and/or conjugated, resulting in a large number of compounds excreted in the urine. In the milk, the major identifiable radiolabelled compound was deltamethrin.
The major metabolic pathways of deltamethrin in mice were similar to those in rats, though there were some differences. These included the presence of more unchanged deltamethrin in mouse feces than in rat feces. In mouse feces, there were 4 monohydroxy ester metabolites (2'-OH-, 4'-OH-, 5-OH-, and trans-OH-deltamethrin and one dihydroxy metabolite (4'-OH-trans-OH- deltamethrin) that were not found in mouse urine. Major metabolites from the acid moiety in mice were Br2CA, trans-OH-Br2CA, and their glucuronide and sulfate conjugates. Among them, trans-OH-Br2CA-sulfate was detected only in mice, but not in rats. Compared with rats, much larger amounts of trans-OH-Br2CA and its conjugates were formed in mice. A major metabolite of the alcohol moiety in mice was the taurine conjugate of PBacid in the urine, which was not detected in rats. Generally, mice produced smaller amounts of phenolic compounds compared with rats. Also, 3-phenoxybenzaldehyde (PBald), 3-phenoxybenzyl alcohol (PBalc), and its glucuronide, and glucuronides of 3-(4-hydroxyphenoxy)benzyl alcohol (4'-OH-PBalc) and 5-hydroxy-3-penoxybenzoic acid (5-OH-PBacid) were found in mice, but not in rats. When mice were given an ip dose of (14) C-deltamethrin with or without piperonyl butoxide (PBO) and/or S,S,S-tributylphosphorotrithioate (DEF), the same metabolites were obtained as with oral administration. However, DEF decreased the hydrolytic products relative to the controls, while PBO decreased the oxidation products.
Sulfate of 4'-OH-PBacid accounted for about 50% of the dose, together with small amounts of free (4%) and glucuronide forms (2%). The CN group was converted mainly to thiocyanate and, in small amounts, to ITCA. The trans-isomer of deltamethrin was also rapidly metabolized and yielded almost the same metabolties as deltamethrin, though 5-OH-derivative was found in the cis-isomer, but not in the trans-isomer.
For more Metabolism/Metabolites (Complete) data for DELTAMETHRIN (19 total), please visit the HSDB record page.
Deltamethrin has known human metabolites that include 4'-hydroxy-deltamethrin.
Deltamethrin is readily absorbed by the oral route, but less so dermally; absorbed deltamethrin is readily metabolized and excreted. The major degradation pathway of cypermethrin is hydrolysis of the ester linkage to (yield ultimately) 3-phenoxybenzoic acid and 3-(2,2-dichlorovinyl)-2,2- dimethylcyclopropanecarboxylic acid. (From the cis-isomer both cis- and trans- cyclopropanecarboxylic acids are found.) A minor degradative route is ring hydroxylation to give an alpha-cyano-3-(4-hydroxyphenyl)benzyl ester followed by hydrolysis to produce the corresponding hydroxycarboxylic acid (A558).

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Biological Half-Life
Following intravenous administration, the distribution and elimination half-times were ... 1.39 and 33.0 hours for deltamethrin.
In rats administered deltamethrin and its metabolite (4-OH-deltamethrin) intravenously, elimination half-times were 33 and 25 hours, respectively.
Deltamethrin has a half-life in rat brain of 1-2 days, but it is rather more persistent in body fat, with a half-life of 5 days.
Three young male human volunteers underwent a complete medical check-up one week prior to the morning of the study. Each of them received a single dose of 3 mg of (14)C deltamethrin mixed in 1 g glucose and diluted first in 10 mL polyethylene glycol300 and again in 150 mL water. Total radioactivity was 1.8 + or - 0.9 mBq. ... The apparent elimination half-life was between 10.0 and 11.5 hr. ... The apparent half-life of urinary excretion was 10.0-13.5 hr, which is consistent with the plasma data. ...

Toxicity Summary
Both type I and type II pyrethroids exert their effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. They appear to bind to the membrane lipid phase in the immediate vicinity of the sodium channel, thus modifying the channel kinetics. This blocks the closing of the sodium gates in the nerves, and thus prolongs the return of the membrane potential to its resting state. The repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential produces effects quite similar to those produced by DDT, leading to hyperactivity of the nervous system which can result in paralysis and/or death. Other mechanisms of action of pyrethroids include antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, and actions on calcium ions. They also inhibit calium 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 (Dermal, Rabbit) (A563)

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Interactions
Deltamethrin was hydrolysed in vitro by esterases in blood, brain, kidney, liver, and stomach preparations of mice. Pretreatment of mice with the oxidase inhibitor, piperonyl butoxide (PBO), or the esterase inhibitor, S,S,S-tributylphosphorotrithoiate (DEF), delayed metabolism of intraperitoneally administered deltamethrin. PBO or DEF made mice more sensitive to deltamethrin.
... Sprague-Dawley rats ... /in/ Group A received cottonseed oil as control, and Groups B, C and D received deltamethrin (DM); DM and dichlorodiphenyltrichloroethane (DDT); and DM, DDT, phytoestrogens and p-nonylphenol, respectively. Rats were exposed in utero and then received the substances for 10 weeks. The seminal vesicle mass (Group B; P = 0.046) and sperm count [Groups C (P = 0.013) and D (P = 0.003)] were lower and the anogenital distance [Group B (P = 0.047) C (P = 0.045) and D (P = 0.002)] shorter compared with the control group. The seminiferous tubule diameter [Groups B (P = <0.001), C (P = <0.001) and D (P = <0.001)] and epithelium thickness [Groups B (P = 0.030), C (P = <0.001) and D (P = <0.001)] were smaller compared with the control. The histology of the testes showed signs of apical sloughing and vacuolization. Liver weights [Groups C (P = 0.013) and D (P = 0.005)] and liver enzymes [Group D (P = 0.013)] were also affected. These findings may indicate that simultaneous exposure to endocrine disrupting compounds contributes to the deterioration observed in male reproductive health.
Plasma esterases, in addition to hepatic esterases, play a role in the metabolism of deltamethrin in mammals and cause its rapid detoxification by the oral route. In a potentiation study, a range of esterase inhibitors, consisting mainly of organophosphorus insecticides, was given to male rats in oral doses that inhibited 50% of the plasma cholinesterase. After 15 min, or 2 or 24 hr, an oral LD50 dose of deltamethrin EC formulation was given which showed potentiation with azinphos ethyl, omethoate, and dichlorvos. It appears that users must handle deltamethrin in these combinations very carefully because of their high toxicity. Acephate, monocrotophos, phosphamidon, parathion methyl, and the 2 controls did not act as potentiators.
The effect of deltamethrin pretreatment on the pharmacokinetics and metabolism of antipyrine was studied in male rats. The total plasma clearance of antipyrine was significantly decreased by deltamethrin pretreatment (20 mg/kg and 40 mg/kg daily for 6 days prior to antipyrine administration), while the elimination half-life at beta phase, the area under the concentration-time curve and the mean residence time of antipyrine were significantly increased. The magnitude of the observed changes was dose dependent. The urinary excretion of norantipyrine, 4-hydroxyantipyrine and 3-hydroxymethylantipyrine was decreased by 39%, 32% and 26%, respectively (p <0.001) in the presence of deltamethrin. In addition, the rate constants for formation of each of these metabolites were significantly decreased by an average of approximately 71%. These results suggest that deltamethrin is capable of inhibiting oxidative metabolism, a finding which could be of clinical and toxicological significance.
For more Interactions (Complete) data for DELTAMETHRIN (10 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LD50 Rat male oral 128 mg/kg (in vegetable oil)
LD50 Dog (male & female), oral, in capsules >300 mg/kg /Technical grade/
LD50 Dog (male & female), oral, in PEG 200 2 mg/kg /Techanical grade/
LD50 Rabbit, dermal, in PEG 400 >2000 mg/kg /Technical grade/
For more Non-Human Toxicity Values (Complete) data for DELTAMETHRIN (28 total), 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 cyclopropanecarboxylate ester obtained by formal condensation between 3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid and cyano(3-phenoxyphenyl)methanol. It is the active insecticide of the proinsecticide tralomethrin. It has a role as a pyrethroid ester insecticide, an agrochemical, an EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor, a calcium channel agonist and an antifeedant. It is an aromatic ether, an organobromine compound, a nitrile and a cyclopropanecarboxylate ester. It is functionally related to a cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid.
Deltamethrin is a pyrethroid (type 2) ester insecticide. This material is a member of one of the safest classes of pesticides: synthetic pyrethroids. While mammalian exposure to deltamethrin is classified as safe, this pesticide is highly toxic to aquatic life, particularly fish, and therefore must be used with extreme caution around water. A pyrethroid is a synthetic chemical compound similar to the natural chemical pyrethrins produced by the flowers of pyrethrums (Chrysanthemum cinerariaefolium and C. coccineum). Pyrethroids are common in commercial products such as household insecticides and insect repellents. In the concentrations used in such products, they are generally harmless to human beings but can harm sensitive individuals. They are usually broken apart by sunlight and the atmosphere in one or two days, and do not significantly affect groundwater quality except for being toxic to fish. Since deltamethrin is a neurotoxin, it temporarily attacks (in medical terms, insults) the nervous system of any animal with which it comes into contact. Skin contact can lead to tingling or reddening of the skin local to the application. If taken in through the eyes or mouth, a common symptom is facial paraesthesia, which can feel like many different abnormal sensations, including burning, partial numbness, pins and needles, skin crawling, etc.

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Mechanism of Action
The lowest concentration of deltamethrin to have an effect in crayfish stretch receptor neurons on sodium channels was 1X10-12 mol/L, but the response of the preparation to gamma-aminobutyric acid (GABA) appeared to be unaffected by concentrations of deltamethrin up to 1X10-7 mol/L. Although 1X10-6 mol/l deltamethrin had a slight effect on the GABA response of the dactyl abductor muscle, it appears that the majority of the effects of cyano-pyrethroids in invertebrates could be accounted for solely by their action on sodium channels.
The synthetic pyrethroids delay closure of the sodium channel, resulting in a sodium tail current that is characterized by a slow influx of sodium during the end of depolarization. Apparently the pyrethroid molecule holds the activation gate in the open position. Pyrethroids with an alpha-cyano group (e.g., fenvalerate) produce more prolonged sodium tail currents than do other pyrethroids (e.g., permethrin, bioresmethrin). The former group of pyrethroids causes more cutaneous sensations than the latter. /Pyrethroids/
Interaction with sodium channels is not the only mechanism of action proposed for the pyrethroids. Their effects on the CNS have led various workers to suggest actions via antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, or actions on calcium ions. Since neurotransmitter specific pharmacological agents offer only poor or partial protection against poisoning, it is unlikely that one of these effects represents the primary mechanism of action of the pyrethroids, & most neurotransmitter release is secondary to incr sodium entry. /Pyrethroids/
The interaction of a series of pyrethroid insecticides with the sodium channels in myelinated nerve fibers of the clawed frog, Xenopus laevis, was investigated using the voltage clamp technique. Of 11 pyrethroids, 9 insecticidally active cmpd induced a slowly decaying sodium tail current on termination of a step depolarization, whereas the sodium current during depolarization was hardly affected. /Pyrethroids/
For more Mechanism of Action (Complete) data for DELTAMETHRIN (11 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.)