Absorption, Distribution and Excretion
Thiacloprid is rapidly absorbed and is rapidly excreted after the following metabolic processes, with little remaining in the tissues.

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Metabolism / Metabolites
Thiacloprid is rapidly absorbed and is rapidly excreted after the following metabolic processes, with little remaining in the tissues. The metabolic processes were summarized as: 1) hydroxylation of the thiazolidine ring and subsequent glucuronidation (as shown by metabolite PIZ 1270), 2) hydroxylation of the cyanamide moiety (metabolite KNO 1891), 3) opening of the thiazolidine ring (e.g., metabolites KNO2672, PIZ1297F/WAK 6935), 4) formation of an oxazole ring (metabolite PIZ 1253), 5) oxidation and subsequent methylation of the thiazolidine ring (e.g., PIZ 1297E and PIZ 1269X), and 6) oxidative cleavage of the methylene bridge (PIZ 1243). Only minor gender-related quantitative differences in metabolite profiles were observed.

Toxicity Summary
IDENTIFICATION AND USE: Thiacloprid is an insecticide of the neonicotinoid class. It is used to control aphids, codling moth, leafhoppers, leafminers, psylla, and whiteflies in potatoes, oilseed rape, pome fruit, vegetables, and ornamentals. HUMAN STUDIES: There is a case report of thiacloprid poisoning resulting from deliberate ingestion in a 23-year-old man, manifesting with status epilepticus, respiratory paralysis, rhabdomyolysis, metabolic acidosis, and acute kidney injury, and ultimately giving rise to refractory shock and death. In human peripheral blood lymphocytes in vitro thiacloprid increased the chromosome aberrations and sister chromatid exchange significantly at all concentrations (75, 150, and 300 ug/mL) both in the absence and presence of the metabolic activation and induced a significant increase in micronucleus and nucleoplasmic bridge formations at all concentrations for 24 hr and at 75 and 150 ug/mL for 48-hr treatment periods in the absence of the metabolic activation. Thiacloprid was also found to significantly induce nuclear bud formation at 300 ug/mL for 24 hr and at 150 ug/mL for 48-hr treatment times in the absence of the metabolic activation and at the two highest concentrations (150 and 300 ug/mL) in the presence of the metabolic activation. ANIMAL STUDIES: Evidence of carcinogenicity reported in rats based on increased incidence of thyroid follicular cell adenomas in males and possibly also in females and increased incidence of uterine tumors (adenocarcinomas). Evidence of carcinogenicity reported in mice based on increased incidence of ovarian luteomas. Thiacloprid impairs development and quality of both mouse and rabbit preimplantation embryos, and shows embryotoxicity even at acute reference dose. Developmental neurotoxicity described in rats based on decreased pre-weaning and post-weaning body weights in both sexes and delayed sexual maturation in the males, and altered performance in passive avoidance testing. In rats treated with thiacloprid, statistically significant increases in free triiodothyronine and free thyroxine serum hormone levels were observed. The potential genotoxic effect of thiacloprid formulation on bovine peripheral lymphocytes was evaluated using the comet assay and the cytogenetic endpoints. Whole blood cultures were treated with the insecticide at concentrations of 30, 60, 120, 240 and 480 ug/mL for 24, 48 hr and/or 2 hr of incubation. A statistically significant increase in the frequency of DNA damage, as well as in unstable chromosome aberrations (% breaks) were found after exposure to the insecticide at concentrations ranging from 120 to 480 ug/mL. ECOTOXICITY STUDIES: Caenorhabditis elegans is less susceptible to neonicotinoids than target species of pest insect. Chronic thiacloprid exposure of early-life stages of carp affected ontogeny and growth rate, and inhibited antioxidant capacity. Pheromone production was altered in moth Cydia pomonella, with a reduction of the major compound, codlemone, and one minor component. In worker bees, thiacloprid (24 hr oral exposure, 200 ug/L or 2000 ug/L) reduced hemocyte density, encapsulation response, and antimicrobial activity even at field realistic concentrations. Thiacloprid, as active substance and as formulation, poses a substantial risk to honey bees by disrupting learning and memory functions. Honey bees (Apis mellifera carnica) were exposed chronically to thiacloprid in the field for several weeks at a sublethal concentration. Foraging behavior, homing success, navigation performance, and social communication were impaired, and thiacloprid residue levels increased both in the foragers and the nest mates over time. Thiacloprid exposed free-flying bumblebee colonies were more likely to die prematurely, and those that survived reached a lower final weight and produced 46% fewer reproductives than colonies placed at control farms. Earthworms were exposed to thiacloprid (1 and 3 mg/kg) for 7, 14, and 28 days and then transferred to the clean soil for 35, 42, and 56 days. Results showed that activities of molecular indicators are inhibited following the exposure to thiacloprid at one or more sample times and then increased during the recovery course compared with the control. Significant DNA damage to E. fetida was also observed by olive tail moments in comet assay.

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Toxicity Data
LC50 (rat) = 1,223 mg/m3/4h

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Interactions
Disturbance regimes determine communities' structure and functioning. Nonetheless, little effort has been undertaken to understand interactions of press and pulse disturbances. In this context, leaf-shredding macroinvertebrates can be chronically exposed to wastewater treatment plant effluents (i.e., press disturbance) before experiencing pesticide exposure following agricultural runoff (i.e., pulse disturbance). It is assumed that wastewater pre-exposure alters animals' sensitivity to pesticides. To test this hypothesis, we exposed model-populations of the shredder Gammarus fossarum to wastewater at three field-relevant dilution levels (i.e., 0%, 50%, and 100%). After 2, 4, and 6 weeks, survival, leaf consumption, dry weight, and energy reserves were monitored. Additionally, animals were assessed for their sensitivity toward the neonicotinoid insecticide thiacloprid using their feeding rate as response variable. Both wastewater treatments reduced gammarids' survival, leaf consumption, dry weight, and energy reserves. Moreover, both wastewater pre-exposure scenarios increased animals' sensitivity toward thiacloprid by up to 2.5 times compared to the control. Our results thus demonstrate that press disturbance as posed by wastewater pre-exposure can enhance susceptibility of key players in ecosystem functioning to further (pulse) disturbances. Therefore, applying mitigation measures such as advanced treatment technologies seems sensible to support functional integrity in the multiple-stress situation.
Microbial pathogens are thought to have a profound impact on insect populations. Honey bees are suffering from elevated colony losses in the northern hemisphere possibly because of a variety of emergent microbial pathogens, with which pesticides may interact to exacerbate their impacts. To reveal such potential interactions, we administered at sublethal and field realistic doses one neonicotinoid pesticide (thiacloprid) and two common microbial pathogens, the invasive microsporidian Nosema ceranae and black queen cell virus (BQCV), individually to larval and adult honey bees in the laboratory. Through fully crossed experiments in which treatments were administered singly or in combination, we found an additive interaction between BQCV and thiacloprid on host larval survival likely because the pesticide significantly elevated viral loads. In adult bees, two synergistic interactions increased individual mortality: between N. ceranae and BQCV, and between N. ceranae and thiacloprid. The combination of two pathogens had a more profound effect on elevating adult mortality than N. ceranae plus thiacloprid. Common microbial pathogens appear to be major threats to honey bees, while sublethal doses of pesticide may enhance their deleterious effects on honey bee larvae and adults. It remains an open question as to whether these interactions can affect colony survival.
Deltamethrin (DEL) and thiacloprid (THIA) are two insecticides that are widely used in agriculture either separately or in combination. Studies on genotoxicity and cytotoxicity of TIA and the mixture of DEL and THIA insecticides have not been reported so far. Therefore, we investigated the cytotoxic and genotoxic effects of commercial formulations DEL and/or THIA in rat bone marrow cells, using mitotic index (MI), micronucleus (MN) and chromosome aberrations (CA) assay. In vivo cytokinesis-block micronucleus (CBMN) assay using cytochalasin-B in bone marrow cells was performed ... . Rats were orally gavaged with a single dose of DEL (15 mg/kg), THIA (112.5 mg/kg) or DEL + THIA (15 + 112.5 mg/kg) for 24 hr (acute treatments), or DEL (3 mg/kg/day), THIA (22.5 mg/kg/day) or DEL + THIA (3 + 22.5 mg/kg/day) for 30 days (subacute treatments). A corn oil vehicle control group and cyclophosphamide (50 mg/kg) positive control group were also included. All DEL and/or THIA treatments significantly decreased MI and binucleated (BN) cell numbers, and significantly increased CA, as compared to the vehicle control group. The results of CBMN assay indicated that the combination of DEL and THIA for both treatment times and the 30-day treatment with THIA alone caused a significant increase in micronucleus formation in BN cells. The present findings indicated the combined exposure of DEL and THIA showed genotoxic and cytotoxic effects more than those of individual exposure of DEL or THIA in rat bone marrow cells.
BACKGROUND: The honeybee, Apis mellifera, is undergoing a worldwide decline whose origin is still in debate. Studies performed for twenty years suggest that this decline may involve both infectious diseases and exposure to pesticides. Joint action of pathogens and chemicals are known to threaten several organisms but the combined effects of these stressors were poorly investigated in honeybees. Our study was designed to explore the effect of Nosema ceranae infection on honeybee sensitivity to sublethal doses of the insecticides fipronil and thiacloprid. METHODOLOGY/FINDING: Five days after their emergence, honeybees were divided in 6 experimental groups: (i) uninfected controls, (ii) infected with N. ceranae, (iii) uninfected and exposed to fipronil, (iv) uninfected and exposed to thiacloprid, (v) infected with N. ceranae and exposed 10 days post-infection (p.i.) to fipronil, and (vi) infected with N. ceranae and exposed 10 days p.i. to thiacloprid. Honeybee mortality and insecticide consumption were analyzed daily and the intestinal spore content was evaluated 20 days after infection. A significant increase in honeybee mortality was observed when N. ceranae-infected honeybees were exposed to sublethal doses of insecticides. Surprisingly, exposures to fipronil and thiacloprid had opposite effects on microsporidian spore production. Analysis of the honeybee detoxification system 10 days p.i. showed that N. ceranae infection induced an increase in glutathione-S-transferase activity in midgut and fat body but not in 7-ethoxycoumarin-O-deethylase activity. CONCLUSIONS/SIGNIFICANCE: After exposure to sublethal doses of fipronil or thiacloprid a higher mortality was observed in N. ceranae-infected honeybees than in uninfected ones. The synergistic effect of N. ceranae and insecticide on honeybee mortality, however, did not appear strongly linked to a decrease of the insect detoxification system. These data support the hypothesis that the combination of the increasing prevalence of N. ceranae with high pesticide content in beehives may contribute to colony depopulation.
Deltamethrin (DEL) and thiacloprid (THIA) are the two commonly used synthetic insecticides applied either separately or as a mixture. The aim of this study was to assess thyroid stimulating hormone (TSH) and the serum levels of thyroid hormones exposure to these compounds in rats. The animals were orally gavaged with a single dose of DEL (15 mg/kg), THIA (112.5 mg/kg) or DEL + THIA (15 + 112.5 mg/kg) for 24 hr (acute treatments) or DEL (3 mg/kg per day), THIA (22.5 mg/kg per day) or DEL + THIA (3 + 22.5 mg/kg per day) for 30 days (subacute treatments). ... Statistically significant increases in free triiodothyronine (FT3) and free thyroxine (FT4) serum hormone levels were observed in the independent treatment with THIA and the combined treatment with DEL and THIA for 30 days. The results of this study suggest that in vivo exposure to subacute treatments of commercial formulations of THI and mixture of DEL + THIA increased serum FT3 and FT4 levels in rats. Further studies are required to determine the effects of endocrine disruptors and potential health risks of these insecticides in human, especially in children because of the importance of these hormones during growth and development.

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Non-Human Toxicity Values
LD50 Rat (female) oral 444 mg/kg
LD50 Rat (male) oral 836 mg/kg
LD50 Rat dermal >2000 mg/kg
LC50 Rat inhalation (female) 1223 mg/cu m/4 hr
For more Non-Human Toxicity Values (Complete) data for Thiacloprid (9 total), please visit the HSDB record page.

[1]. Effects of Thiacloprid, a New Chloronicotinyl Insecticide, On the Egg Parasitoid Trichogramma cacaoeciae. Ecotoxicology 9, 197–205 (2000).

[2]. The effect of neonicotinoid insecticide thiacloprid on the structure and stability of DNA. Physiol Res. 2019;68(Suppl 4):S459-S466.

Thiacloprid is a nitrile that is cyanamide in which the hydrogens are replaced by a 1,3-thiazolidin-2-ylidene group which in turn is substituted by a (6-chloropyridin-3-yl)methyl group at the ring nitrogen. It has a role as a xenobiotic, an environmental contaminant and a neonicotinoid insectide. It is a member of thiazolidines, a nitrile and a monochloropyridine. It is functionally related to a 2-chloropyridine and a cyanamide.
Thiacloprid has been reported in Streptomyces canus with data available.

C10H9CLN4S

252.72

252.023

111988-49-9

Thiacloprid-d4;1793071-39-2

115224

White to off-white solid powder

1.4±0.1 g/cm3

423.1±55.0 °C at 760 mmHg

136ºC

209.7±31.5 °C

0.0±1.0 mmHg at 25°C

1.691

0.55

0

4

2

16

324

0

HOKKPVIRMVDYPB-UHFFFAOYSA-N

InChI=1S/C10H9ClN4S/c11-9-2-1-8(5-13-9)6-15-3-4-16-10(15)14-7-12/h1-2,5H,3-4,6H2

[3-[(6-chloropyridin-3-yl)methyl]-1,3-thiazolidin-2-ylidene]cyanamide

Thiacloprid; Thiacloprid

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)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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