AcephateAnticholinesterase insecticide CAS# 30560-19-1 |
2D Structure
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Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
Cas No. | 30560-19-1 | SDF | Download SDF |
PubChem ID | 1982 | Appearance | Powder |
Formula | C4H10NO3PS | M.Wt | 183.17 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in water | ||
Chemical Name | N-[methoxy(methylsulfanyl)phosphoryl]acetamide | ||
SMILES | CC(=O)NP(=O)(OC)SC | ||
Standard InChIKey | YASYVMFAVPKPKE-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C4H10NO3PS/c1-4(6)5-9(7,8-2)10-3/h1-3H3,(H,5,6,7) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Anticholinesterase insecticide that produces cholinotoxicity. Displays weak inhibition of rat acetylcholinesterase (AChE) but potently inhibits cockroach AChE. |
Acephate Dilution Calculator
Acephate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 5.4594 mL | 27.297 mL | 54.5941 mL | 109.1882 mL | 136.4852 mL |
5 mM | 1.0919 mL | 5.4594 mL | 10.9188 mL | 21.8376 mL | 27.297 mL |
10 mM | 0.5459 mL | 2.7297 mL | 5.4594 mL | 10.9188 mL | 13.6485 mL |
50 mM | 0.1092 mL | 0.5459 mL | 1.0919 mL | 2.1838 mL | 2.7297 mL |
100 mM | 0.0546 mL | 0.273 mL | 0.5459 mL | 1.0919 mL | 1.3649 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Exploring hazards of acute exposure of Acephate in Drosophila melanogaster and search for l-ascorbic acid mediated defense in it.[Pubmed:27701059]
J Hazard Mater. 2017 Jan 5;321:690-702.
This study reveals protective role of l-ascorbic acid (25, 50 and 100mug/mL) against toxic impacts of acute sub-lethal exposure of Acephate (5mug/mL) in a non-target organism Drosophila melanogaster. Organismal effect was evident from increased impairment in climbing activities (9 folds) of treated individuals who also manifested altered ocular architecture. These anomalies were reduced with l-ascorbic acid (l-AA) supplementation. Acephate induced apoptotic lesions in eye imaginal discs and gut confirmed tissue damage that also reduced with l-AA co-treatment. Reduction in viability of fat body cells ( approximately 41%), neural cells ( approximately 42%) and hemocytes (3 folds) indicates cytotoxic and immunotoxic potential of Acephate, which were significantly mitigated with l-AA co-administration. The sub-cellular toxic impacts of Acephate treatment became obvious from enhancement in activities of antioxidant enzymes (CAT by approximately 1.63 folds, SOD by approximately 1.32 folds), detoxifying enzymes (Cyp450 by approximately 1.99 folds and GST by approximately 1.34 folds), 2.1 times boost in HSP 70 expression, and inhibition of cholinesterase activity (by approximately 0.66 folds). DNA breaks evident through comet assay confirmed Acephate triggered genotoxicity which could also be prevented through co-administration of. L-AA Furthermore, the study proposes the use of Drosophila as a model to screen chemicals for their protective potential against pesticide toxicity.
Acephate exposure during a perinatal life program to type 2 diabetes.[Pubmed:27765684]
Toxicology. 2016 Nov 30;372:12-21.
Acephate has been used extensively as an insecticide in agriculture. Its downstream sequelae are associated with hyperglycemia, lipid metabolism dysfunction, DNA damage, and cancer, which are rapidly growing epidemics and which lead to increased morbidity and mortality rates and soaring health-care costs. Developing interventions will require a comprehensive understanding of which excess insecticides during perinatal life can cause insulin resistance and type 2 diabetes. A Wistar rat animal model suggests that Acephate exposure during pregnancy and lactation causes alterations in maternal glucose metabolism and programs the offspring to be susceptible to type 2 diabetes at adulthood. Therapeutic approaches based on preventive actions to food contaminated with insecticides during pregnancy and lactation could prevent new cases of type 2 diabetes.
Bio-remediation of acephate-Pb(II) compound contaminants by Bacillus subtilis FZUL-33.[Pubmed:27372122]
J Environ Sci (China). 2016 Jul;45:94-9.
Removal of Pb(2+) and biodegradation of organophosphorus have been both widely investigated respectively. However, bio-remediation of both Pb(2+) and organophosphorus still remains largely unexplored. Bacillus subtilis FZUL-33, which was isolated from the sediment of a lake, possesses the capability for both biomineralization of Pb(2+) and biodegradation of Acephate. In the present study, both Pb(2+) and Acephate were simultaneously removed via biodegradation and biomineralization in aqueous solutions. Batch experiments were conducted to study the influence of pH, interaction time and Pb(2+) concentration on the process of removal of Pb(2+). At the temperature of 25 degrees C, the maximum removal of Pb(2+) by B.subtilis FZUL-33 was 381.31+/-11.46mg/g under the conditions of pH5.5, initial Pb(2+) concentration of 1300mg/L, and contact time of 10min. Batch experiments were conducted to study the influence of Acephate on removal of Pb(2+) and the influence of Pb(2+) on biodegradation of Acephate by B.subtilis FZUL-33. In the mixed system of Acephate-Pb(2+), the results show that biodegradation of Acephate by B.subtilis FZUL-33 released PO4(3+), which promotes mineralization of Pb(2+). The process of biodegradation of Acephate was affected slightly when the concentration of Pb(2+) was below 100mg/L. Based on the results, it can be inferred that the B.subtilis FZUL-33 plays a significant role in bio-remediation of organophosphorus-heavy metal compound contamination.
Degradation of acephate by Enterobacter asburiae, Bacillus cereus and Pantoea agglomerans isolated from diamondback moth Plutella xylostella (L), a pest of cruciferous crops.[Pubmed:27498509]
J Environ Biol. 2016 Jul;37(4):611-8.
Acephate-degrading bacterial isolates were isolated from the larval gut of diamondback moth Plutella xylostella, a notorious pest of cruciferous crops worldwide that has developed resistance to insecticides. Partial 16S rRNA gene sequencing identified the isolates as Bacillus cereus (PX-B.C.Or), Enterobacter asburiae (PXE), and Pantoae agglomerans (PX-Pt.ag.Jor). All isolates grew on minimal media (MM) in the presence of Acephate at 100 and 200 ppm, with maximum growth at 200 ppm. LC-MS analyses of spent medium showed that E. asburiae degraded Acephate to methamidophos and O, O-dimethyl phosporamidate and B. cereus O,S-dimethyl to phosphorothioate but P. agglomerans to an unnamed compound. All three isolates used Acephate as a source of carbon and energy for growth; however, P. agglomerans used it also as source of sulphur. Strong evidence revealed that the bacterial communities present in the gut of diamondback moth might aid in Acephate degradation and play a role in the development of insecticide resistance.