Size | Price | Stock | Qty |
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50mg |
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100mg |
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Other Sizes |
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ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Most organophosphate compounds are ... absorbed from skin, conjunctiva, gastrointestinal tract, & lung. /Organophosphate compounds/ The rate of dermal absorption /of organophosphorus pesticides/ may be ... influenced by the solvent used. /Organophosphorus pesticides/ Many of the organophosphorus insecticides are excreted in the milk ... /Organophosphorus insecticides/ Following their absorption, most organophosphorus cmpd are excreted almost entirely as hydrolysis products in the urine. /Anticholinesterase agents/ For more Absorption, Distribution and Excretion (Complete) data for PHENTHOATE (6 total), please visit the HSDB record page. Metabolism / Metabolites ELSAN DEGRADED RAPIDLY IN /CABBAGE SEEDLING, STRAWBERRY & APPLE FRUIT/ ... & WAS HYDROLYZED TO NON-TOXIC DERIVATIVES. MAIN METABOLITES ... WERE ELSAN CARBOXY DERIVATIVES, MANDELIC ACID & BIS(CARBETHOXYBENZYL)DISULFIDE. MAJOR URINARY METABOLITES /OF PHENTHOATE IN MICE/ @ DOSAGE OF 30 MG/KG WERE THE O-DEMETHYLATED ACID (25.8%), THE O-DEMETHYLATED OXON ACID (18.4%) & DIMETHYL PHOSPHORODITHIONATE (16.9%). INITIAL PRODUCT OF P-S CLEAVAGE ... WAS FURTHER METABOLIZED INTO CORRESPONDING SULFIDE, MANDELIC ACID, & S-METHYLATED DERIV. In plants, there is oxidation to the thiophosphate, followed by hydrolysis. Identified metabolites are phosphoric acid, dimethyl and monomethyl phosphate. Five metabolites were detected in the plasma and urine of a patient following ingestion of the organophosphate insecticide, phenthoate. Intact phenthoate was detected only in gastric lavage fluid. After methylation of acidic extracts of plasma and urine, phenthoate acid, demethyl phenthoate, demethyl phenthoate oxon acid, demethyl phenthoate S-isomer, and demethyl phenthoate acid S-isomer were identified with synthesized phenthoate analogues by gas chromatography and gas chromatograph-mass spectrometry. The main metabolites were phenthoate acid and demethyl phenthoate oxon acid. Although demethyl phenthoate oxon acid was a significant metabolite, no phenthoate oxon, phenthoate oxon acid or demethyl phenthoate oxon were detected. If the oxon was formed in the patient, it may have been rapidly degraded by carboxylesterase or glutathione transferase to demethyl phenthoate oxon acid. For more Metabolism/Metabolites (Complete) data for PHENTHOATE (7 total), please visit the HSDB record page. |
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Toxicity/Toxicokinetics |
Toxicity Data
LC50 (rat) = 59 mg/m3/4h Interactions Phenthoate ... was rapidly hydrolyzed by rat liver and plasma carboxylesterases to the corresponding non-toxic metabolite, phenthoate acid. A partially purified enzyme isolated from rat liver microsomes was 7-fold more effective in hydrolyzed phenthoate than the microsomal fraction. O,S,S-Trimethyl phosphorodithioate (TMPDT) and O,O,S-trimethyl phosphorothioate (TMPT), 2 impurities present in technical formulations of phenthoate, were examined for their inhibiting effects on the esterase degradation of (phenyl-14)C-phenthoate in vitro. Incubation of (14)C-phenthoate with rat liver and plasma carboxylesterases in the presence of these impurities greatly diminished the amount of phenthoate acid formed. TMPDT was superior in its inhibitory action against rat liver carboxylesterase to that of TMPT. TMPDT was equipotent in inhibiting crude rat liver and plasma carboxylesterases than rat liver carboxylesterases. The in vitro metabolism of phenthoate (O,O-dimethyl S-(alpha-(carboethoxy)benzyl)phosphorodithioate) was followed in rats after oral administration of a nontoxic dose of 100 mg/kg. The same metabolic study was conducted following coadministration of 0.5% O,S,S-trimethyl phosphorodithioate (OSS-Me). When administered alone, phenthoate was metabolized principally by carboethoxy ester hydrolysis and cleavage of the P-O and C-S bonds, resulting in at least 6 metabolites. The primary urinary metabolite excreted was phenthoate acid. Coadministration of 0.5% OSS-Me did not alter the types of metabolites excreted. However, a reduction of the carboxylesterase-catalyzed product (phenthoate acid) was observed, indicating that the enzyme responsible for the major pathway of phenthoate detoxication was inhibited. The levels of total lipids, free fatty acids, cholesterol, and lipase activity were studied in selected tissues of Channa punctatus Bloch during individual and combined exposures of carbaryl and phenthoate. The total lipid levels decreased with elevated levels of free fatty acids and lipase activity during all exposures, suggesting increased lipid hydrolysis to derive energy as an attempt to face the pesticide toxic stress. The cholesterol levels showed an elevated trend. ... The effect produced by carbaryl + phenthoate treatment remained higher than either of the pesticides alone, suggesting the manifestation of an additive effect. Some phenothiazines may antagonize & some may potentiate the toxic anticholinesterase effects of ... /organophosphorus insecticides/. /Organophosphate cholinesterase inhibitors/ For more Interactions (Complete) data for PHENTHOATE (7 total), please visit the HSDB record page. Non-Human Toxicity Values LD50 MOUSE ORAL 350-400 MG/KG /TECHNICAL PRODUCT/ LD50 RAT ORAL 300-400 MG/KG /TECHNICAL PRODUCT/ LD50 Rat oral 77.7 mg/kg LD50 Rat oral 118 mg/kg For more Non-Human Toxicity Values (Complete) data for PHENTHOATE (10 total), please visit the HSDB record page. |
References | |
Additional Infomation |
Phenthoate is an organic thiophosphate that is ethyl mandelate in which the hydroxy group has been replaced by a (dimethoxyphosphorothioyl)sulfanediyl group. It has a role as an EC 3.1.1.7 (acetylcholinesterase) inhibitor, an acaricide and an agrochemical. It is an organic thiophosphate, an organothiophosphate insecticide and an ethyl ester.
Phenthoate is a synthetic organic thiophosphate compound and organophosphate acetylcholinesterase inhibitor that is used as a pesticide. It is characterized as a colorless crystalline solid with an aromatic odor, and exposure occurs by inhalation, ingestion, or contact. Mechanism of Action Cholinesterase inhibitor. The cardiovascular actions of anticholinesterase agents are complex, since they reflect both ganglionic and postganglionic effects of accumulated ACh on the heart and blood vessels. The predominant effect on the heart from the peripheral action of accumulated ACh is bradycardia, resulting in a fall in cardiac output. Higher doses usually cause a fall in blood pressure, often as a consequence of effects of anticholinesterase agents on the medullary vasomotor centers of the CNS. /Anticholinesterase agents/ Organophosphorus derivatives act by combining with and inactivating the enzyme acetylcholinesterase. ... The inactivation of cholinesterase by cholinesterase inhibitor pesticides allows the accumulation of large amounts of acetylcholine, with resultant widespread effects that may be ... separated into 4 categories: (1) Potentiation of postganglionic parasympathetic activity. ... (2) Persistent depolarization of skeletal muscle ... (3) Initial stimulation following depression of cells of central nervous system ... (4) Variable ganglionic stimulation or blockade ... /Cholinesterase inhibitor pesticides/ The main feature of the toxic mechanism of organophosphorus pesticides is inhibition of the esterase enzyme activity, in particular of cholinesterase, which plays an important physiological part. Organophosphorus pesticides can also indirectly interact with the biochemical receptors of acetylcholine. /Organophosphorus pesticides/ For more Mechanism of Action (Complete) data for PHENTHOATE (7 total), please visit the HSDB record page. |
Molecular Formula |
C12H17O4PS2
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Molecular Weight |
320.36
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Exact Mass |
320.03
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CAS # |
2597-03-7
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PubChem CID |
17435
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Appearance |
Colorless to light yellow liquid
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Density |
1.3±0.1 g/cm3
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Boiling Point |
379.5±52.0 °C at 760 mmHg
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Melting Point |
156ºC
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Flash Point |
183.3±30.7 °C
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Vapour Pressure |
0.0±0.9 mmHg at 25°C
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Index of Refraction |
1.564
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LogP |
3.96
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Hydrogen Bond Donor Count |
0
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Hydrogen Bond Acceptor Count |
6
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Rotatable Bond Count |
8
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Heavy Atom Count |
19
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Complexity |
324
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Defined Atom Stereocenter Count |
0
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SMILES |
CCOC(=O)C(C1=CC=CC=C1)SP(=S)(OC)OC
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InChi Key |
XAMUDJHXFNRLCY-UHFFFAOYSA-N
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InChi Code |
InChI=1S/C12H17O4PS2/c1-4-16-12(13)11(10-8-6-5-7-9-10)19-17(18,14-2)15-3/h5-9,11H,4H2,1-3H3
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Chemical Name |
ethyl 2-dimethoxyphosphinothioylsulfanyl-2-phenylacetate
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Synonyms |
Dimephenthioate; Phenthoate; Phenthoate
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HS Tariff Code |
2934.99.9001
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
DMSO : ~250 mg/mL (~780.37 mM)
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Solubility (In Vivo) |
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 Formulations
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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)] Oral Formulations
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  (Please use freshly prepared in vivo formulations for optimal results.) |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 3.1215 mL | 15.6074 mL | 31.2149 mL | |
5 mM | 0.6243 mL | 3.1215 mL | 6.2430 mL | |
10 mM | 0.3121 mL | 1.5607 mL | 3.1215 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.