Absorption, Distribution and Excretion
Most (88%) of the oral dose is eliminated within 48 hours. In wild oats, the primary absorption occurs via germinating coleoptiles. Absorption is extremely low in the early seedling stages. ... The absorption and transport of labeled carbon (14) in dihydronaphthenic acid from the roots and coleoptiles of wild oats (Avena fatua L), wheat (Triticum aestivum L var. Selkirk), barley (Hordeum vulgare L var. Trail), and flax (Linum usitatissimum L var. Bolley) were studied and concluded to be similar in their absorption and transport patterns.

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Metabolism/Metabolites
Mouse liver microsomes metabolize cis- and trans-(14)C=O-dihydronaphthyl acid in an NADPH-dependent response, producing (14)CO2 primarily in the absence of glutathione (GSH), and (14)CO2 and S-(diisopropylcarbamoyl)-GSH in the presence of GSH. In rats, administration of either isomer resulted in the excretion of S-diisopropylcarbamoyl derivatives of thiouric acid (62%), cysteine (7%), and thioglycolic acid (1.5%), in addition to (14)CO2 (20%). This pathway appears to involve sulfoxide formation, a non-enzymatic reaction of sulfoxide with glutathione, and the formation of thiouric acid.
Rats orally administered various mutagens and carcinogens containing halogenated allyl or halogenated propyl substituents excreted small amounts of 2-haloacrylic acids, such as 2-chloroacrylic acid and 2,3-dichloroacrylic acid, in their urine. These acrylic acids are derived from dihydronaphthoic acid.
The metabolic pathway of dihydronaphthoic acid isomers involves the generation of 2-chloropropenal and 2,3-dichloro-2-propen-1-sulfonic acid via their sulfoxides in the mouse liver microsomal oxidase system. The activity of these acids and liver oxidases in mice and rats was investigated.
The metabolites of dicarboxylate, tricarboxylate, and sulfonate esters were identified and quantified as chloropropenal and chloroallyl thiol, respectively, by headspace analysis using high-performance liquid chromatography (HPLC) and gas chromatography (GLC). Quantitative analysis showed that thiocarbamates are metabolically activated to chloropropenal under the action of a mixed-function oxidase system alone, while the intermediate S-oxidation product is detoxified and converted to chloroallyl thiol when the glutathione/glutathione-S-transferase system is present simultaneously. HPLC co-chromatography identified the major mixed-function oxidase metabolites of the three compounds in mouse microsomes as the corresponding sulfoxides. The study concluded that the formation of mutagenic chloropropenal mainly involves the sulfonation of dihydropyridine acid, followed by σ-rearrangement-1,2-elimination and S-methylene hydroxylation of trihydropyridine acid and sulfoxide sulfate, finally catalyzing the degradation of its α-hydroxy intermediate. The glutathione-S-transferase-catalyzed binding reaction with glutathione diverts the sulfonation intermediate from the activation pathway involved in chloropropenal formation to the detoxification pathway releasing chloroallyl thiosulfate. Thiocarbamates are normally absorbed through the skin, mucous membranes, respiratory tract, and digestive tract. They are rapidly excreted, primarily through exhaled air and urine. The metabolism of thiocarbamates in mammals mainly follows two pathways. One is through sulfonation and binding with glutathione. The binding product is subsequently cleaved into cysteine derivatives, which are metabolized into thiouric acid compounds. The second pathway involves the oxidation of sulfur to sulfoxides, followed by the oxidation of sulfoxides to sulfones, or hydroxylation into compounds that enter the carbon metabolism pool.

Toxicity Summary
Metabolites of benzoates, dibenzoates, and sulfates appear to be mutagenic or carcinogenic. In particular, 2-chloroallyl is a major source of mutagenicity in these herbicides. These metabolites can bind to or damage DNA, leading to base pair substitutions. Benzoates have been shown to be carcinogenic in mice. Some thiocarbamate herbicides (such as EPTC, molinet, pemblatt, and cyclic esters) share a common mechanism of toxicity: inhibition of acetylcholinesterase. Acetylcholinesterase inhibitors suppress the activity of acetylcholinesterase. Due to the crucial role of acetylcholinesterase, 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 relaxation of muscles or organs. The 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.
Interactions
Field trials were conducted in 1979 and 1980 to determine the effects of pendimethalin alone and in combination with aldicarb on the population development of the beet aphid. Sporangium numbers were measured before pesticide treatment in March, after the emergence of white female aphids in July, and at harvest in October; egg and larval densities were measured in March and October. Compared with the control group, sporangium production increased threefold after pendimethalin treatment in July 1979, 1.5 times in July 1980, and two times at harvest in 1980. At all sampling dates, the lichenin/aldicarb combination treatment minimized cyst formation. From March to October 1979, the number of eggs and larvae per 100 ml of soil increased threefold in untreated plots, fivefold in lichenin-treated plots, 1.8 times with aldicarb alone, and only 1.1 times in lichenin/aldicarb combination treatments. In 1980, the number of eggs and larvae per 100 ml of soil decreased by 31% in the untreated control group, but remained unchanged in lichenin-treated plots. However, the lichenin/aldicarb combination treatment reduced the number of eggs and larvae by 52%. Therefore, diallate enhances the killing effect of the nematicide aldicarb against beet cyst nematodes.

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Non-human toxicity values
Oral LD50 in rats: 395 mg/kg
Oral LD50 in dogs: 510 mg/kg
Dermal LD50 in rabbits: 2000-2500 mg/kg

[1].Evaluation of diallate and triallate herbicides for genotoxic effects in a battery of in vitro and short-term in vivo tests. Mutat Res. 1984 Jun;136(3):173-83.

Used as a herbicide. Dimethylamine is a tertiary amine. Dimethylamine is a thiocarbamate herbicide used to control weeds between crops and grasses. It can be applied to the soil before sowing or to the growing crop. It is suitable for alfalfa, white clover, barley, corn, flax, soybeans, lentils, peas, potatoes, red clover, sugar beets, and sweet clover. Thiocarbamate herbicides are primarily used in agriculture as insecticides, herbicides, and fungicides. They are also used as biocides for industrial or other commercial purposes, as well as in household products. Some thiocarbamate herbicides are also used for vector control in public health. Most thiocarbamate herbicides are liquids or solids with low melting points.

C10H17CL2NOS

270.22

269.041

2303-16-4

5284376

BROWN LIQUID
Oily liquid

1.18g/cm3

306ºC at 760mmHg

25-30ºC

>100 °C

0.000791mmHg at 25°C

1.52

4.277

0

2

5

15

234

0

CC(C)N(C(C)C)C(=O)SC/C(=C/Cl)/Cl

SPANOECCGNXGNR-UITAMQMPSA-N

InChI=1S/C10H17Cl2NOS/c1-7(2)13(8(3)4)10(14)15-6-9(12)5-11/h5,7-8H,6H2,1-4H3/b9-5-

S-[(Z)-2,3-dichloroprop-2-enyl] N,N-di(propan-2-yl)carbamothioate

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)

Typically soluble in DMSO (e.g. 10 mM)

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.)