Absorption, Distribution and Excretion
Thiacloprid is rapidly absorbed and rapidly excreted after the following metabolic processes, leaving very little residue in tissues. Metabolisms/Metabolites Thiacloprid is rapidly absorbed and rapidly excreted after the following metabolic processes, leaving very little residue in tissues. The metabolic processes can be summarized as follows: 1) hydroxylation of the thiazoline ring and subsequent glucuronidation (as shown in metabolite PIZ 1270); 2) hydroxylation of the cyanamide moiety (metabolite KNO 1891); 3) ring-opening of the thiazoline ring (e.g., metabolites KNO2672, PIZ1297F/WAK 6935); 4) formation of the oxazolium ring (metabolite PIZ 1253); 5) oxidation of the thiazoline ring and subsequent methylation (e.g., PIZ 1297E and PIZ 1269X); and 6) oxidative cleavage of the methylene bridge (PIZ 1243). Only slight sex-related quantitative differences were observed in the metabolite profile.

Toxicity Summary
Identification and Uses: Thiacloprid is a neonicotinoid insecticide. It is used to control aphids, codling moths, leafhoppers, leaf miners, psyllids, and whiteflies on potatoes, rapeseed, pome fruits, vegetables, and ornamental plants. Human Studies: One case report describes a 23-year-old male who intentionally ingested Thiacloprid and suffered poisoning, presenting with status epilepticus, respiratory paralysis, rhabdomyolysis, metabolic acidosis, and acute kidney injury, ultimately leading to refractory shock and death. In cultured human peripheral blood lymphocytes, Thiacloprid significantly increased chromosomal aberrations and sister chromatid exchanges at all concentrations (75, 150, and 300 μg/mL), regardless of metabolic activation. In the absence of metabolic activation, Thiacloprid treatment at all concentrations for 24 hours and at concentrations of 75 and 150 μg/mL for 48 hours significantly induced the formation of micronuclei and nucleocytoplasmic bridges. Furthermore, in the absence of metabolic activation, treatment with 300 μg/mL for 24 hours and 150 μg/mL for 48 hours significantly induced nucleate bud formation; in the presence of metabolic activation, Thiacloprid also significantly induced nucleate bud formation at the two highest concentrations (150 and 300 μg/mL). Animal studies: Increased incidence of thyroid follicular cell adenomas (possibly also in female rats) and uterine tumors (adenocarcinomas) in male rats provide evidence of Thiacloprid's carcinogenicity. Increased incidence of ovarian corpus luteum tumors in mice also confirms Thiacloprid's carcinogenicity. Thiacloprid impairs the development and quality of preimplantation embryos in mice and rabbits, exhibiting embryotoxicity even at acute reference doses. In rats, Thiacloprid exhibits developmental neurotoxicity, manifested as weight loss in both male and female rats before and after weaning, delayed sexual maturation in male rats, and altered passive avoidance test performance. In rats treated with Thiacloprid, serum levels of free triiodothyronine and free thyroxine were significantly elevated. The potential genotoxic effects of Thiacloprid on bovine peripheral blood lymphocytes were assessed using a comet assay and cytogenetic endpoints. Whole blood cultures were treated with insecticides at concentrations of 30, 60, 120, 240, and 480 μg/mL for 24, 48, and/or 2 hours, respectively. Results showed that treatment with insecticides at concentrations from 120 to 480 μg/mL significantly increased the frequency of DNA damage and the percentage of unstable chromosomal aberrations (breakages). Ecotoxicity studies showed that C. elegans was less sensitive to neonicotinoid insecticides than the target pest. Long-term exposure to Thiacloprid during the early developmental stages of carp affected their individual development and growth rate, and inhibited their antioxidant capacity. Pheromones produced by the codling moth were altered, with decreased levels of the major component, codlingone, and a minor component. In worker bees, Thiacloprid (oral exposure over 24 hours at concentrations of 200 μg/L or 2000 μg/L) reduces hemocyte density, cyst reaction, and antimicrobial activity, even at actual field concentrations. As an active substance and formulation, Thiacloprid interferes with the learning and memory functions of bees, posing a significant risk. In the field, bees (Apis mellifera carnica) were chronically exposed to Thiacloprid at sublethal concentrations for several weeks. Results showed impaired foraging behavior, homing success rate, navigation ability, and social communication, with Thiacloprid residue levels increasing over time in both foraging bees and their nest companions. Free-flying bumblebee colonies exposed to Thiacloprid were more prone to premature death, and surviving colonies had lower final body weights and 46% fewer breeding bees than control colonies. Earthworms were exposed to Thiacloprid (1 and 3 mg/kg) for 7, 14, and 28 days, followed by transfer to clean soil for 35, 42, and 56 days. The results showed that the activity of the molecular marker was suppressed at one or more sampling time points after Thiacloprid exposure, but its activity increased compared to the control group during the recovery process. Significant DNA damage was also observed in Eisenia fetida during the comet assay.

---

Toxicity Data
LC50 (rat) = 1,223 mg/m³/4h
Interactions
Disturbing mechanisms determine the structure and function of a community. However, research on the interaction between persistent and impulsive disturbances is currently scarce. In this context, large foliage-feeding invertebrates may be exposed to wastewater treatment plant effluents (i.e., persistent disturbance) prior to exposure to pesticide pollution from agricultural runoff (i.e., impulsive disturbance). It is thought that prior exposure to wastewater alters the animal's susceptibility to pesticides. To test this hypothesis, we treated a model population of the detritivorous animal Gammarus fossarum with three field-environment-relevant wastewater dilution levels (i.e., 0%, 50%, and 100%). Animal survival, leaf consumption, dry weight, and energy reserves were monitored at 2, 4, and 6 weeks. Furthermore, we assessed the animals' susceptibility to the neonicotinoid insecticide Thiacloprid using feed intake as a response variable. Both wastewater treatments reduced Gammarus survival, leaf consumption, dry weight, and energy reserves. Moreover, both wastewater pre-exposure treatments increased animal susceptibility to Thiacloprid by 2.5-fold compared to the control group. Therefore, our results suggest that persistent disturbances caused by wastewater pre-exposure increase the susceptibility of key ecosystem players to subsequent (pulsating) disturbances. Thus, under multiple stress conditions, mitigation measures such as advanced treatment technologies to maintain functional integrity appear prudent. Microbial pathogens are believed to have profound impacts on insect populations. The increased colony loss rate of honeybees in the Northern Hemisphere may be due to a variety of emerging microbial pathogens, and insecticides may interact with these pathogens, exacerbating their effects. To reveal this potential interaction, we applied sublethal and field-scale doses of a neonicotinoid insecticide (Thiacloprid) and two common microbial pathogens—the invasive microsporidia ceranae and black bee queen cell virus (BQCV)—to bee larvae and adults in the laboratory. Through fully crossover experiments (treatments applied alone or in combination), we found an additive effect of BQCV and Thiacloprid on host larval survival, likely due to the insecticide significantly increasing viral load. In adult bees, two synergistic effects increased individual mortality: one between N. ceranae and BQCV, and the other between N. ceranae and Thiacloprid. The combination of these two pathogens had a more significant effect on adult bee mortality than the combination of N. ceranae and Thiacloprid. Common microbial pathogens appear to be the primary threat to bees, and sublethal doses of insecticides may enhance their harmful effects on bee larvae and adults. Whether these interactions affect bee colony survival remains an open question.
Dexamethasone (DEL) and Thiacloprid (THIA) are two widely used insecticides in agriculture, used alone or in combination. Currently, there are no reported studies on the genotoxicity and cytotoxicity of Thiacloprid or mixtures of deltamethrin and Thiacloprid. Therefore, we investigated the cytotoxic and genotoxic effects of commercially available formulations DEL and/or THIA on rat bone marrow cells using mitotic index (MI), micronucleus (MN), and chromosomal aberration (CA) assays. We also performed an in vivo cell division arrest micronucleus (CBMN) assay, which used cytochalasin B to induce bone marrow cell division arrest… Rats were administered DEL (15 mg/kg), THIA (112.5 mg/kg), or DEL+THIA (15 + 112.5 mg/kg) by gavage for 24 hours (acute treatment), or DEL (3 mg/kg/day), THIA (22.5 mg/kg/day), or DEL+THIA (3 + 22.5 mg/kg/day) by gavage for 30 days (subacute treatment). A corn oil solvent control group and a cyclophosphamide (50 mg/kg) positive control group were also included. Compared with the carrier control group, all DEL and/or THIA treatments significantly reduced the number of micronuclei (MI) and binucleated (BN) cells and significantly increased cardiac activity (CA). CBMN assay results showed that the combined treatment with DEL and THIA (both treatment durations) and THIA treatment alone for 30 days significantly increased micronucleus formation in BN cells. These results indicate that combined exposure to DEL and THIA has stronger genotoxic and cytotoxic effects on rat bone marrow cells than exposure to DEL or THIA alone. Background: Honeybees (Apis mellifera) are facing a global decline, the causes of which remain controversial. Two decades of research suggest this decline may be linked to infectious diseases and pesticide exposure. The combined effects of pathogens and chemicals are known to threaten a variety of organisms, but the impact of these combined stressors on honeybees is poorly studied. This study aimed to investigate the effects of Nosema ceranae infection on the susceptibility of honeybees to sublethal doses of the insecticides fipronil and Thiacloprid. Methods/Results: Five days after emergence, honeybees were divided into six experimental groups: (i) uninfected control group; (ii) Nosema ceranae-infected group; (iii) uninfected but exposed to fipronil group; (iv) uninfected but exposed to Thiacloprid group; (v) Nosema ceranae-infected group and exposed to fipronil 10 days post-infection group; (vi) Nosema ceranae-infected group and exposed to Thiacloprid 10 days post-infection group. Honeybee mortality and pesticide consumption were analyzed daily, and intestinal spore content was assessed 20 days post-infection. When bees infected with N. ceranae were exposed to sublethal doses of pesticides, bee mortality increased significantly. Surprisingly, exposure to fipronil and Thiacloprid had opposite effects on N. ceranae spore production. Analysis of the bee detoxification system 10 days post-infection showed that N. ceranae infection induced increased glutathione-S-transferase activity in the midgut and fat body, but not increased 7-ethoxycoumarin-O-deethylase activity. Conclusion/Implication: N. ceranae-infected bees had higher mortality rates than uninfected bees after exposure to sublethal doses of fipronil or Thiacloprid. However, the synergistic effect of N. ceranae and pesticides on bee mortality did not appear to be closely associated with a decline in the insect detoxification system. These data support the hypothesis that increased N. ceranae infection rates in bees, combined with high concentrations of pesticides in the hive, may lead to a decline in bee colony numbers.
Demeton-methyl (DEL) and Thiacloprid (THIA) are two commonly used synthetic insecticides that can be used alone or in combination. This study aimed to evaluate changes in thyroid-stimulating hormone (TSH) and serum thyroid hormone levels in rats after exposure to these compounds. Experimental animals received a single oral gavage administration of DEL (15 mg/kg), THIA (112.5 mg/kg), or DEL + THIA (15 + 112.5 mg/kg) for 24 hours (acute treatment); 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 treatment). …Statistically significant increases in serum levels of free triiodothyronine (FT3) and free thyroxine (FT4) were observed after 30 days of treatment with THIA alone and in combination with DEL and THIA. The results of this study indicate that subacute in vivo exposure to commercial THI formulations and a DEL+THIA mixture increased serum FT3 and FT4 levels in rats. Further research is needed to determine the effects of endocrine disruptors on humans and the potential health risks of these pesticides to humans, especially children, as these hormones are crucial for growth and development.

---

Non-human toxicity values
Oral LD50 in rats (female): 444 mg/kg
Oral LD50 in rats (male): 836 mg/kg
Dermal LD50 in rats: >2000 mg/kg
Inhalation LC50 in rats (female): 1223 mg/m³/4 hr
For more complete non-human toxicity data on Thiacloprid (9 species), 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 compound with a cyanamide structure, in which the hydrogen atom is replaced by a 1,3-thiazolidin-2-subunit, and the nitrogen atom of this subunit is replaced by a (6-chloropyridin-3-yl)methyl group. It is an exogenous substance, an environmental pollutant, and a neonicotinoid insecticide. Thiacloprid belongs to the thiazolidinedonid, nitrile, and monochloropyridine class of compounds. Its function is similar to that of 2-chloropyridine and cyanamide. There are reports that Thiacloprid exists in Streptomyces canus, and relevant data are 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.

---

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).

View More

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)

---

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).

View More

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

---

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.

---

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