Acetylcholinesterase (AChE) and the nervous system of insects. Furathiocarb is a carbamate insecticide that targets insect nervous systems by inhibiting acetylcholinesterase.

Furathiocarb is a carbamate insecticide that targets insect nervous systems by inhibiting acetylcholinesterase, an enzyme essential for nerve function. It induces significant proliferation of MHCII-positive B cells and Th1 cytokines.

Furathiocarb is used in agriculture to control a broad range of insects. It is also used in contact allergy studies due to its ability to induce immune responses, including B cell proliferation and Th1 cytokine production.

In vitro assays for carbamates measure the compound's ability to inhibit acetylcholinesterase activity. This is typically done using a colorimetric assay that measures the hydrolysis of a substrate.

Cellular assays for Furathiocarb involve treating immune cells with the compound and measuring its effects on B cell proliferation and cytokine production.

In vivo animal models for Furathiocarb include efficacy studies on target pest species and contact allergy models to study its immunotoxic effects.

Absorption, Distribution and Excretion
Information on the distribution of carbamate insecticides in various organs and tissues of mammals after inhalation or oral exposure is scarce. Residues have been reported in the liver, kidneys, brain, fat, and muscle. In rats, the half-life of carbamate insecticides is approximately 3–8 hours. Urinary excretion of carbamate insecticides in humans also appears to be rapid, and their metabolic pathways in humans are similar to those in rats. /Carbamate Insecticides/
This study investigated the pharmacokinetics of Furathiocarb in male Sprague-Dawley rats following transdermal administration. Furathiocarb and its metabolites (furanone, 3-hydroxyfuranone, and 3-ketofuranone) were analyzed using high-performance liquid chromatography (HPLC) and post-column derivatization. Furadan and 3-hydroxyfuradan, but not Furathiocarb, were detected in plasma and urine. Another potential metabolite, 3-ketofuradan, was not detected in any samples. Plasma concentrations of furadan were higher than those of 3-hydroxyfuradan, but the opposite was true in urine. At a dose of 1500 mg/kg, the area under the plasma concentration-time curve, time to peak concentration (Tmax), and peak plasma concentration (Cmax) of furadan and 3-hydroxyfuradan were 2.4–8.0 mg equivalents/ml, 12 hours, and 0.1–0.4 mg equivalents/ml, respectively. Only the half-life (T1/2, 28 hours) of 3-hydroxyfuradan was calculated. Both metabolites were excreted in a dose-dependent manner and did not reach saturation. Metabolism/Metabolites in rats involves rapid and complete hydrolysis, followed by oxidation and conjugation reactions. Excretion is primarily via the kidneys. The first step in carbamate metabolism is hydrolysis to carbamic acid, which decomposes to carbon dioxide (CO2) and the corresponding amine. The hydrolysis mechanisms of N-methyl and N-dimethyl derivatives differ. The hydrolysis pathway of N-methylcarbamates involves isocyanate intermediates, while the hydrolysis of N-dimethylcarbamates yields products that add to hydroxyl ions, producing alcohols and N-dimethyl-substituted acids. Esterases hydrolyze N-methylcarbamates at a faster rate in mammals than in plants and insects. In addition to hydrolysis, oxidation reactions occur, including aromatic ring hydroxylation, O-dealkylation, N-methyl hydroxylation, N-dealkylation, aliphatic side chain oxidation, and sulfoxide formation to generate the corresponding sulfones. Oxidation reactions are associated with mixed-function oxidases (MFOs). In mammals, conjugation reactions produce O- and N-glucuronides, sulfates, and mercaptouric acid derivatives. Glycosides and phosphates are more common conjugation products in plants. /Carbamate Pesticides/
This study investigated the pharmacokinetics of Furathiocarb in male Sprague-Dawley rats after transdermal administration. Furathiocarb and its metabolites (carbofuran, 3-hydroxycarbofuran, and 3-ketocarbofuran) were analyzed using high-performance liquid chromatography (HPLC) and post-column derivatization. Furadan and 3-hydroxycarbofuran, but not Furathiocarb, were detected in plasma and urine. Another potential metabolite, 3-ketocarbofuran, was not detected in any samples. ...
Carbamate pesticides are enzymatically hydrolyzed in the liver; degradation products are excreted via the kidneys and liver. (L793)

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Biological half-life
The half-life in rats is approximately 3-8 hours. /Carbamate pesticides/

Toxicity Summary
Furathiocarb 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 contractions.

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Toxicity Data
LC50 (Rat) = 214 mg/m3/4h
Non-human Toxicity Values
LD50 (Rat, oral): 53 mg/kg
LD50 (Mouse, oral): 327 mg/kg
LD50 (Rat, dermal): >2,000 mg/kg
LC50 (Rat, inhalation): 0.214 mg/L air/4 hours

Anal. Chem., 80, 9450 (2008)

Furathiocarb is a carbamate, belonging to the 1-benzofuran class of compounds. It is an EC 3.1.1.7 (acetylcholinesterase) inhibitor, a carbamate insecticide, and an agricultural chemical. Furathiocarb is a carbamate insecticide. Carbamate insecticides are derived from carbamic acid, and their insecticidal mechanism 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. Because Sevin has relatively low oral and dermal toxicity to mammals and a broad spectrum of control, it is widely used in lawns and gardens. Most carbamate insecticides are highly toxic to hymenoptera, so precautions must be taken to prevent contact with insects such as bees or parasitic wasps. Some carbamate insecticides can be transported within plants, making them effective systemic treatments. (L795)

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Mechanism of Action
Carbamate pesticides are effective because they inhibit acetylcholinesterase (AChE) in the nervous system. They also inhibit other esterases. The carbamylation of this enzyme is unstable, and AChE regenerates relatively quickly compared to phosphorylases. Therefore, in terms of human exposure, carbamate pesticides are less dangerous than organophosphate pesticides. The ratio of lethal dose to minimum toxicity is much greater in carbamates than in organophosphates. /Carbamate Pesticides/

C18H26N2O5S

382.47

382.156

65907-30-4

47759

Yellow, viscous liquid.

1.208g/cm3

460ºC

1.551

4.262

0

6

8

26

502

0

CCCCOC(=O)N(C)SN(C)C(=O)OC1=CC=CC2=C1OC(C)(C)C2

HAWJXYBZNNRMNO-UHFFFAOYSA-N

InChI=1S/C18H26N2O5S/c1-6-7-11-23-16(21)19(4)26-20(5)17(22)24-14-10-8-9-13-12-18(2,3)25-15(13)14/h8-10H,6-7,11-12H2,1-5H3

(2,2-dimethyl-3H-1-benzofuran-7-yl) N-[butoxycarbonyl(methyl)amino]sulfanyl-N-methylcarbamate

CGA 73102; Deltanet; Promet; Promet 666SCO; 2,4-Dimethyl-5-oxo-6-oxa-3-thia-2,4-diazadecanoic Acid 2,3-Dihydro-2,2-dimethyl-7-benzofuranyl Ester

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.)