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Fenoxaprop-P-ethyl Sale

(Synonyms: 精恶唑禾草灵) 目录号 : GC30454

Fenoxaprop-P-ethyl是一种杂环氧基苯氧基丙酸类除草剂,

Fenoxaprop-P-ethyl Chemical Structure

Cas No.:71283-80-2

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10mM (in 1mL DMSO)
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500mg
¥446.00
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产品描述

Fenoxaprop-P-ethyl is a post-emergent phenoxy herbicide of the aryloxyphenoxy propionate group.

[1]. Zawahir S, et al. Acute intentional self-poisoning with a herbicide product containing fenoxaprop-P-ethyl, ethoxysulfuron, andisoxadifen ethyl: a prospective observational study. Clin Toxicol (Phila). 2009 Sep;47(8):792-797.

Chemical Properties

Cas No. 71283-80-2 SDF
别名 精恶唑禾草灵
Canonical SMILES C[C@@H](OC1=CC=C(OC2=NC3=CC=C(Cl)C=C3O2)C=C1)C(OCC)=O
分子式 C18H16ClNO5 分子量 361.78
溶解度 DMSO: ≥ 100 mg/mL (276.41 mM) 储存条件 Store at -20°C
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1 mM 2.7641 mL 13.8206 mL 27.6411 mL
5 mM 0.5528 mL 2.7641 mL 5.5282 mL
10 mM 0.2764 mL 1.3821 mL 2.7641 mL
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Research Update

The safener isoxadifen-ethyl confers fenoxaprop-p-ethyl resistance on a biotype of Echinochloa crus-galli

Background: Some herbicides are commercially formulated with safeners to increase crop selectivity. Fenoxaprop-p-ethyl is formulated with the safener isoxadifen-ethyl for Echinochloa crus-galli control in rice. Safeners act on crops by increasing herbicide metabolism, but this effect may also occur in weeds. The objective of this study was to investigate the effect of the safener isoxadifen-ethyl on the resistance to fenoxaprop-p-ethyl in a biotype of E. crus-galli. Results: A screening of 52 biotypes identified lack of control in the biotype SANTPAT-R treated with the recommended dose of 69 g ha-1 of the commercial formulation of fenoxaprop-p-ethyl with the safener isoxadifen-ethyl. While this biotype survived doses greater than 2208 g ha-1 of the formulation fenoxaprop-p-ethyl + isoxadifen-ethyl, it was killed with 69 g ha-1 of fenoxaprop-p-ethyl without the safener. A glutathione-s-transferase (GST) enzymes inhibitor reduced the resistance factor in two dose-response curves. A minor effect of a CytP450 inhibitor was observed. The previous spraying of the safener isoxadifen-ethyl followed by fenoxaprop-p-ethyl induced survival in the resistant but not in the susceptible biotype. The GST1 and GSTF1 genes were up-regulated in the resistant biotype. ACCase gene mutations were not found, and no cross-resistance to other ACCase inhibitors was identified. Conclusion: The safener isoxadifen-ethyl present in the commercial herbicide formulation of fenoxaprop-p-ethyl is associated with resistance in the E. crus-galli SANTPAT-R biotype. This resistance is related with herbicide metabolization mediated by GST pathways. This is the first field-selected weed biotype with herbicide resistance due to safener presence in the sprayed formulation. ? 2022 Society of Chemical Industry.

Degradation of Fenoxaprop-p-Ethyl and Its Metabolite in Soil and Wheat Crops

The dissipation kinetics of fenoxaprop-p-ethyl and its metabolite (fenoxaprop acid) at two application rates under wheat field conditions for two seasons was investigated. Herbicides were extracted by solid liquid extraction, cleaned up, and analyzed by a liquid chromatography-UV detector. Dissipation followed first-order kinetics; in soil, fenoxaprop-p-ethyl dissipated rapidly with an average half-life of 1.45 to 2.30 days, while fenoxaprop acid persisted for more than 30 days. The method was validated in terms of accuracy, linearity, specificity, and precision. Linearity was in the range of 5 to 5,000 ng, with a limit of detection (LOD) of 2 and 1 ng for fenoxaprop-p-ethyl and fenoxaprop acid, respectively. The quantitation limits in soil, grain, and straw were 5, 8, and 10 ng g-1 for fenoxaprop-p-ethyl and 5, 10, and 10 ng g-1 for fenoxaprop acid, respectively. Recovery in soil, grains, and straw ranged from 85.1 to 91.25%, 72.5 to 84.66%, and 77.64 to 82.24% for fenoxaprop-p-ethyl and 80.56 to 86.5%, 78 to 81.88%, and 75.2 to 79.68% for fenoxaprop acid, respectively. At harvest, no detectable residues of fenoxaprop-p-ethyl or acid were observed in soil, wheat grain, and straw samples. Owing to the short persistence under field conditions, fenoxaprop-p-ethyl is safe for use because parent and metabolite residues were below the European Union maximum residue limit and would not pose an adverse effect on the environment and human or animal foods.

Fenoxaprop-P-ethyl resistance conferred by cytochrome P450s and target site mutation in Alopecurus japonicus

Background: Alopecurus japonicus is a serious grass weed species in wheat fields in eastern Asia, and has evolved strong resistance to acetyl-CoA carboxylase (ACCase)-inhibiting herbicides. Although target-site resistance (TSR) to ACCase inhibitors in A. japonicus has been reported, non-target site resistance (NTSR) has not. This study investigated both TSR and NTSR in a fenoxaprop-P-ethyl-resistant A. japonicus population (AHFD-3), which was collected in Feidong County, Anhui Province, China.
Results: We found that AHFD-3 exhibited high resistance to fenoxaprop-P-ethyl and low resistance to flucarbazone-sodium. The sensitivity of AHFD-3 to fenoxaprop-P-ethyl increased significantly after treatment with cytochrome P450 (P450) inhibitors; however, such synergies between P450 inhibitors and fenoxaprop-P-ethyl were not found in two control populations. Sequences of the entire carboxyltransferase domain of A. japonicus ACCase were obtained, and AHFD-3 plants showed an Asp-2078-Gly substitution in the ACCase. With the derived cleaved amplified polymorphic sequence (dCAPS) method, we found that 85.4% of the plants of AHFD-3 carried this mutation. The P450 content in AHFD-3 plants was significantly higher than those of the two control populations after treatment with fenoxaprop-P-ethyl. Ten partial sequences of P450 genes in A. japonicus were cloned. Three P450 genes were up-regulated 12 h after fenoxaprop-P-ethyl treatment, which were all from the P450 subfamily CYP72A. Moreover, a P450 gene from the P450 family CYP81 was up-regulated after fenoxaprop-P-ethyl treatment in all populations studied.
Conclusion: Fenoxaprop-P-ethyl resistance in AHFD-3 plants was conferred by up-regulation of cytochrome P450s in the CYP72A subfamily and target site mutation of the ACCase gene. ? 2018 Society of Chemical Industry.

Identification of essential genes involved in metabolism-based resistance mechanism to fenoxaprop-P-ethyl in Polypogon fugax

Background: Metabolic resistance is a worldwide concern for weed control but has not yet been well-characterized at the genetic level. Previously, we have identified an Asia minor bluegrass (Polypogon fugax Nees ex Steud.) population AHHY exhibiting cytochrome P450 (P450)-involved metabolic resistance to fenoxaprop-P-ethyl. In this study, we aimed to confirm the metabolic fenoxaprop-P-ethyl resistance in AHHY and uncover the potential herbicide metabolism-related genes in this economically damaging weed species.
Results: Liquid chromatography-tandem mass spectrometry (LC-MS/MS) assays indicated the metabolic rates of fenoxaprop-P-ethyl were significantly faster in resistant (R, AHHY) than in susceptible (S, SDTS) plants. The amount of phytotoxic fenoxaprop-P peaked at 12 h after herbicide treatment (HAT) and started to decrease at 24 HAT in both biotypes. R and S plants at 24 HAT were sampled to conduct isoform-sequencing (Iso-Seq) and RNA-sequencing (RNA-Seq). A reference transcriptome containing 24 972 full-length isoforms was obtained, of which 24 329 unigenes were successfully annotated. Transcriptomic profiling identified 28 detoxifying enzyme genes constitutively and/or herbicide-induced up-regulated in R than in S plants. Real-time quantitative polymerase chain reaction (RT-qPCR) confirmed 17 genes were consistently up-regulated in R and its F1 generation plants. They were selected as potential fenoxaprop-P-ethyl metabolism-related genes, including ten P450s, one glutathione-S-transferase, one UDP-glucosyltransferase, and five adenosine triphosphate (ATP)-binding cassette transporters.
Conclusion: This study revealed that the enhanced rates of fenoxaprop-P-ethyl metabolism in P. fugax were very likely driven by the herbicide metabolism-related genes. The transcriptome data generated by Iso-Seq combined with RNA-Seq will provide abundant gene resources for understanding the molecular mechanisms of resistance in P. fugax.

Fenoxaprop-P-ethyl and mesosulfuron-methyl resistance status of shortawn foxtail (Alopecurus aequalis Sobol.) in eastern China

Resistance to the acetyl-coenzyme A carboxylase (ACCase)- and acetolactate synthase (ALS)- inhibiting herbicides in shortawn foxtail (Alopecurus aequalis) has been reported in wheat fields of eastern China. To better understand the distribution of the resistant populations and the occurrence of the target-site mutations, 74 populations collected from Anhui, Jiangsu and Shandong province were surveyed, and the ACCase and ALS gene fragments, encompassing all the documented mutant codon positions, were amplified and sequenced. Plants from 37 and 34 populations survived fenoxaprop-P-ethyl and mesosulfuron-methyl treatment at 62.1 g a.i. ha-1 and 9 g a.i. ha-1 respectively, with different survival rates. Twenty-seven populations exhibited multiple resistance to fenoxaprop-P-ethyl and mesosulfuron-methyl. Whole-plant dose-response experiments showed that the resistance index ranged from 6.2 to 167.8 for fenoxaprop-P-ethyl, and from 7.8 to 139.5 for mesosulfuron-methyl. Four ACCase (I1781L, I2041N, I2041T and D2078G) and four ALS (P197R, P197S, P197T and W574 L) resistance mutations were detected respectively. Individuals containing two amino acid substitutions were also found. D2078G and W574 L were predominant ACCase and ALS gene mutations respectively. This study has shown that fenoxaprop-P-ethyl and mesosulfuron-methyl resistance was prevalent in A. aequalis in eastern China, and target site mutations in the ACCase and ALS gene were one of the most common mechanisms.