Absorption, Distribution and Excretion
In rats, after administration of carbonyl-labeled [14C]pyrimicamb via gavage or intraperitoneal injection, over 50% of the dose was excreted as 14CO2 within 5 hours, and 15% was excreted in the urine; at sacrifice 8 days after administration, virtually no residue was detected. Administration of pirimicamb up to four times daily in rats did not result in drug accumulation in adipose tissue. In dogs, the recovery rate of cyclic-14C-labeled pirimicamb was 86-94%, with 79-88% excreted in the urine and 6-7% in the feces; the recovery rate after 1 day was 74-86%. In dogs, the recovery rate of the carbonyl-labeled dose was 15-26%, primarily excreted in the urine; the unrecovered portion was considered to be rapidly excreted as 14CO2. In lactating cows, after administration of imidacloprid, 96% of the dose appeared in the urine, 4% in the feces, and <0.3% in the milk.
Mechanism of action: A selective systemic insecticide with contact, stomach poison, and respiratory action. It is absorbed through the roots and transported through the xylem. It can penetrate leaves, but its transport range is limited.
Metabolism/Metabolites
The main metabolites of imidacloprid in the urine of rats, dogs, and cattle are similar, produced by oxidation and hydrolysis mechanisms. The main component is hydroxypyrimidine, with modification of the alkyl component of the heterocyclic moiety. In the given dose, 2-dimethylamino-5,6-dimethyl-4-hydroxypyrimidine accounts for 10-16.3%, 2-methylamino-5,6-dimethyl-4-hydroxypyrimidine accounts for 20.5-41%, 2-amino-5,6-dimethyl-4-hydroxypyrimidine accounts for 12.9-21%, and 2-dimethylamino-6-hydroxymethyl-5-methyl-4-hydroxypyrimidine accounts for 1.8-5.7%. The main metabolites are excreted in an unbound form. ...During the metabolism of imidacloprid in mammals, the carbamate ester undergoes partial hydrolysis, followed by demethylation with the dimethylamino group attached to the heterocyclic moiety, generating the following major metabolites, which are excreted in urine: 2-dimethylamino-5,6-dimethyl-4-hydroxypyrimidine (DDHP), 2-methylamino-5,6-dimethyl-4-hydroxypyrimidine (MDHP), and 2-amino-5,6-dimethyl-4-hydroxypyrimidine (ADHP). These metabolites were detected in all urine samples from seven workers who had used imidacloprid. The concentrations of 2-methylamino-5,6-dimethyl-4-hydroxypyrimidine and 2-amino-5,6-dimethyl-4-hydroxypyrimidine were significantly higher than that of 2-dimethylamino-5,6-dimethyl-4-hydroxypyrimidine, indicating that the human body has a considerably strong demethylation capacity. No metabolites were detected in the urine samples of the control group. The pyrimidine compounds studied are sensitive and specific biomarkers for monitoring imidacloprid exposure. Carbamates are enzymatically hydrolyzed in the liver; the degradation products are excreted via the kidneys and liver. (L793)

Toxicity Summary
Pirimicard is a cholinesterase, or acetylcholinesterase (AChE) inhibitor. Carbamate compounds carbamate the enzyme's active site, forming an unstable complex with cholinesterase. This inhibition is reversible. Cholinesterase inhibitors suppress the activity of acetylcholinesterase. Because acetylcholinesterase plays a vital physiological role, chemicals that interfere with its activity are potent neurotoxins, causing excessive salivation and lacrimation even at low doses. High-dose exposure typically results in symptoms such as headache, salivation, nausea, vomiting, abdominal pain, and diarrhea. Acetylcholinesterase breaks down the neurotransmitter acetylcholine, which is released at the neuromuscular junction, causing muscle or organ relaxation. Inhibition of acetylcholinesterase results in the accumulation and sustained action of acetylcholine, leading to continuous nerve impulse transmission and an inability to stop muscle contraction.

---

Toxicity Data
LC50 (Rat) = 300 mg/m3/6hInteractions
Use of thiram in an isotoxic mixture significantly enhanced and prolonged the neurochemical effects of imidacloprid in rats.Non-human Toxicity Values
LD50 Rats (female) Oral 68-221 mg/kg
LD50 Mice (female) Oral 107 mg/kg
LD50 Dogs Oral 100-200 mg/kg
LD50 Rats (female) Dermal >500 mg/kg

For more complete non-human toxicity data, please refer to PIRIMICARB (8 in total), please visit the HSDB record page.

[1]. Effect of Oral Exposure to the Acaricide Pirimicarb, a New Varroacide Candidate, on Apis Mellifera Feeding Rate. Pest Manag Sci. 2018 Aug;74(8):1790-1797.

According to the U.S. Environmental Protection Agency (EPA), imidacloprid may be carcinogenic. Imidacloprid is an aminopyrimidine compound with the structure N,N,4,5-tetramethylpyrimidine-2-amine, substituted at the 4-position with a (dimethylcarbamoyl)oxy group. It is an EC 3.1.1.7 (acetylcholinesterase) inhibitor, carbamate insecticide, agricultural chemical, environmental pollutant, exogenous substance, and pesticide. It is a carbamate, aminopyrimidine, and tertiary amine compound. Its structure is similar to dimethylcarbamic acid. Imidacloprid is a synthetic aminopyrimidine and tertiary amine compound derived from dimethylcarbamic acid. It is a carbamate acetylcholinesterase inhibitor used as an insecticide. It is a colorless or white solid and can be absorbed through inhalation, ingestion, or contact. Imidacloprid is a carbamate insecticide. Carbamate insecticides are derived from carbamic acid and their insecticidal action is similar to that of organophosphate insecticides. They are widely used in homes, gardens, and agriculture. The first carbamate insecticide, Sevin, was introduced in 1956, and its global usage exceeds that of all other carbamate insecticides combined. Due to its relatively low oral and dermal toxicity to mammals and its broad spectrum of application, Sevin is widely used in lawns and gardens. Most carbamate insecticides are highly toxic to hymenopteran insects, therefore precautions must be taken to prevent contact with them by insects such as bees or parasitic wasps. Some carbamate insecticides can be transported within plants, making them effective systemic treatments. (L795)

---

Mechanism of Action
Cholinesterase inhibitor.

C11H18N4O2

238.28622

238.142

23103-98-2

Pirimicarb-d6;1015854-66-6

31645

Colorless solid

1.1±0.1 g/cm3

373.4±52.0 °C at 760 mmHg

90.5°C

179.6±30.7 °C

0.0±0.8 mmHg at 25°C

1.549

1.7

0

5

3

17

270

0

CC1=C(C)N=C(N=C1OC(=O)N(C)C)N(C)C

YFGYUFNIOHWBOB-UHFFFAOYSA-N

InChI=1S/C11H18N4O2/c1-7-8(2)12-10(14(3)4)13-9(7)17-11(16)15(5)6/h1-6H3

[2-(dimethylamino)-5,6-dimethylpyrimidin-4-yl] N,N-dimethylcarbamate

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.

---

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.)