Metabolism / Metabolites
Two major metabolic pathways for imidacloprid degradation have been identified. The first is oxidative cleavage, producing 6-chloronicotinic acid, which conjugates with glycine to form hippuric acid-type conjugates. These two metabolites together account for the majority of the identified metabolites, approximately 30% of the recovered radiolabeled material. A smaller amount of pyridyl dechlorination occurs, producing 6-hydroxynicotinic acid and its methyl mercaptouric acid derivative, which may be a degradation product of the glutathione conjugate. The 6-methyl mercaptonicotinic acid conjugate with glycine and the glycine conjugate account for 5.6% of the recovered radiolabeled material. The second important biodegradation step begins with hydroxylation at the 4- or 5-position of the imidazolium ring; approximately 16% of the recovered radiolabeled material was identified as a combination of 4-hydroxy and 5-hydroxy imidacloprid. Dehydration yields olefin compounds. These biotransformation products and the unchanged parent compound are excreted in urine and feces, while guanidine compounds are a minor metabolite, excreted only in feces (A623).

Toxicity Summary
Imidacloprid acts on nicotinic acetylcholine receptors; chlorination inhibits the degradation of acetylcholinesterase (L1130). Toxicity Data
LD50: 450 mg/kg (oral, rat) (L1130)
LD50: 131 mg/kg (oral, mouse) (L1130)
LD50: >5000 mg/kg (dermal contact, rat) (L1130)
LD50: 69 mg/m3 (inhalation (aerosol), rat) (L1130)
LD50: 5323 mg/m3 (inhalation (dust), rat) (L1130)

[1]. Imidacloprid, a neonicotinoid insecticide, induces insulin resistance. J Toxicol Sci. 2013;38(5):655-60.

[2]. Insecticide imidacloprid influences cognitive functions and alters learning performance and related gene expression in a rat model. Int J Exp Pathol. 2015 Oct;96(5):332-7.

[3]. Neurobehavioral impairments caused by developmental imidacloprid exposure in zebrafish. Neurotoxicol Teratol. 2015 May-Jun;49:81-90.

[4]. A 90 days oral toxicity of imidacloprid in female rats: morphological, biochemical and histopathological evaluations. Food Chem Toxicol. 2010 May;48(5):1185-90.

[5]. Effect of imidacloprid on antioxidant enzymes and lipid peroxidation in female rats to derive its No Observed Effect Level (NOEL). J Toxicol Sci. 2010 Aug;35(4):577-81.

[6]. Immunotoxic effects of imidacloprid following 28 days of oral exposure in BALB/c mice. Environ Toxicol Pharmacol. 2013 May;35(3):408-18.

2-Imidazolidinyl, 1-[(6-chloro-3-pyridyl)methyl]-N-nitro- has been reported in Streptomyces canus and Ganoderma lucidum, and relevant data are available. Imidacloprid is a neonicotinoid insecticide, belonging to a class of neuroactive insecticides designed to mimic nicotine. Nicotine was discovered and used as an insecticide and rodenticide as early as the 17th century. Its effectiveness as an insecticide spurred the search for insecticidal compounds with less selective effects on mammals, ultimately leading to the discovery of neonicotinoid insecticides. Like nicotine, neonicotinoid insecticides bind to nicotinic acetylcholine receptors on cells. In mammals, nicotinic acetylcholine receptors are distributed in cells of the central and peripheral nervous systems. In insects, however, these receptors are limited to the central nervous system. Low to moderate activation of these receptors causes neural excitation, while high levels of activation overstimulate and block the receptors, leading to paralysis and death. Nicotine acetylcholine receptors are activated by the neurotransmitter acetylcholine. Acetylcholine is broken down by acetylcholinesterase, which terminates signal transduction at these receptors. However, acetylcholinesterase cannot break down neonicotinoid insecticides, and their binding to receptors is irreversible. Because most neonicotinoid insecticides bind much more strongly to receptors on insect neurons than to those on mammalian neurons, they are far more toxic to insects than to mammals. The main reason for the low toxicity of neonicotinoid insecticides to mammals is the lack of charged nitrogen atoms at physiological pH. These uncharged molecules can penetrate the blood-brain barrier in insects, while the blood-brain barrier in mammals filters them out. However, some neonicotinoid insecticide breakdown products are toxic to humans, especially when they are charged. Due to their low toxicity and other excellent properties, neonicotinoid insecticides are among the most widely used insecticides in the world. Most neonicotinoid insecticides are readily soluble in water and decompose slowly in the environment, thus they can be absorbed by plants and provide insect protection during plant growth. Currently, neonicotinoid insecticides are used on crops such as corn, rapeseed, cotton, sorghum, sugar beets, and soybeans. They are also used on the vast majority of fruit and vegetable crops, including apples, cherries, peaches, oranges, berries, leafy greens, tomatoes, and potatoes. Multiple studies have shown that the use of neonicotinoid insecticides is associated with several adverse ecological impacts, including bee colony collapse (CCD) and a decline in bird populations due to reduced insect populations. This has led to the suspension or banning of the use of these insecticides in Europe. See also: imidacloprid (preferred); imidacloprid; moxifloxacin (one of the ingredients); imidacloprid; ivermectin (ingredient).

C9H10CLN5O2

255.66

255.052

105827-78-9

86418

White to off-white solid powder

1.6±0.1 g/cm3

442.3±55.0 °C at 760 mmHg

136-144ºC

221.3±31.5 °C

0.0±1.1 mmHg at 25°C

1.706

-0.43

1

4

3

17

319

0

YWTYJOPNNQFBPC-UHFFFAOYSA-N

InChI=1S/C9H10ClN5O2/c10-8-2-1-7(5-12-8)6-14-4-3-11-9(14)13-15(16)17/h1-2,5H,3-4,6H2,(H,11,13)

N-[1-[(6-chloropyridin-3-yl)methyl]-4,5-dihydroimidazol-2-yl]nitramide

Confidor Admire Imidacloprid

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

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.)