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Fenvalerate Sale

(Synonyms: 氰戊菊酯) 目录号 : GC46147

A pyrethroid ester insecticide and acaricide

Fenvalerate Chemical Structure

Cas No.:51630-58-1

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25mg
¥450.00
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50mg
¥720.00
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100mg
¥1,170.00
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250mg
¥2,932.00
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产品描述

Fenvalerate is a pyrethroid ester insecticide and acaricide.1,2 It is a slow activator of voltage-gated sodium channel 1.8 (Nav1.8).1 It induces mortality in pyrethroid-susceptible and -resistant strains of M. domestica (LD50s = 0.014-5 μg/fly).3 Fenvalerate also induces mortality in tobacco budworm larvae but is associated with pyrethroid resistance with an increase in LD50 values from 1.01 to 20.85 μg/g over a six-year timeframe.4 It induces mortality in 95.5% of T. macfarlanei spider mites when applied to leaves at a concentration of 0.015%.2 Formulations containing fenvalerate have been used in the control of insects in agriculture.

|1. Choi, J.S., and Soderlund, D.M. Structure-activity relationships for the action of 11 pyrethroid insecticides on rat Nav1.8 sodium channels expressed in Xenopus oocytes. Toxicol. Appl. Pharmacol. 211(3), 233-244 (2006).|2. Jose, V.T., and Shah, A.H. Chemical control of the spider mite, Tetranychus macfarlanei B & P, the pest of cotton. Pesticides 20(12), 19-23 (1986).|3. Pedersen, L.-E.K. The potency of cyclopropane pyrethroid ethers against susceptible and resistant strains of the house fly Musca domestica. Experientia 42(9), 1057-1058 (1986).|4. Martinez-Carrillo, J.L., and Reynolds, H.T. Dosage-mortality studies with pyrethroids and other insecticides on the tobacco budworm (Lepidoptera: Noctuidae) from the Imperial Valley, California. J. Econ. Entomol. 76(5), 983-986 (1983).

Chemical Properties

Cas No. 51630-58-1 SDF
别名 氰戊菊酯
Canonical SMILES O=C(C(C1=CC=C(Cl)C=C1)C(C)C)OC(C#N)C2=CC=CC(OC3=CC=CC=C3)=C2
分子式 C25H22ClNO3 分子量 419.9
溶解度 DMF: 30 mg/ml,DMSO: 1 mg/ml,Ethanol: 5 mg/ml 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.3815 mL 11.9076 mL 23.8152 mL
5 mM 0.4763 mL 2.3815 mL 4.763 mL
10 mM 0.2382 mL 1.1908 mL 2.3815 mL
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Research Update

Do cypermethrin and Fenvalerate disturb the function of the bovine cervix in vitro?

J Endocrinol 2022 May 6;253(3):133-142.PMID:35343441DOI:10.1530/JOE-21-0336.

This study aimed to investigate the effect of pyrethroid insecticides on the regulation of bovine cervical function. Cervical cells or strips obtained from cows during the periovulation period were treated with cypermethrin and Fenvalerate (0.1-10 ng/mL). None of the pyrethroids exerted a cytotoxic effect, whereas only Fenvalerate increased the cervical contraction force and mRNA expression of receptor of oxytocin and prostaglandin (PG) synthases. Both pyrethroids inhibited PG secretion and decreased the amount of diacylglycerol, which is the second messenger involved in oxytocin signal transmission, and Fenvalerate decreased the myosin light-chain kinase level. These findings indicate that Fenvalerate induces greater disruption of cervical function than cypermethrin.

Paternal Fenvalerate exposure transgenerationally impairs cognition and hippocampus in female offspring

Ecotoxicol Environ Saf 2021 Oct 15;223:112565.PMID:34358930DOI:10.1016/j.ecoenv.2021.112565.

The impairments of maternal Fenvalerate exposure have been well documented in previous study, but little was known about the effects of paternal Fenvalerate exposure. The current study aimed to assess the effects of paternal Fenvalerate exposure on spatial cognition and hippocampus across generations. Adult male mice (F0) were orally administered with Fenvalerate (0, 2 or 20 mg/kg) for 5 weeks. F0 males were mated with untreated-females to generate F1 generation. F1 males were mated with F1 control females to generate F2 generation. For F1 and F2 adult offspring, spatial learning and memory were detected by Morris water maze. Results showed that spatial learning and memory were impaired in F1 females but not F1 males derived from F0 males exposed to 20 mg/kg FEN. Furthermore, significant impairment of spatial learning and memory were found in F2 females but not F2 males derived from F0 males exposed to 20 mg/kg FEN. As expected, histopathology showed that neural density in hippocampal CA3 region was reduced in F1 and F2 females but not F1 and F2 males derived from F0 males exposed to 20 mg/kg FEN. Mechanistically, hippocampal thyroid hormone receptor alpha1 (TRα1) was down-regulated in F1 and F2 females derived from F0 males exposed to 20 mg/kg FEN. Correspondingly, hippocampal brain-derived neurotrophic factor, tropomyosin receptor kinase B and p75 neurotrophin receptor, three downstream genes of TR signaling, were down-regulated in F1 and F2 females. Taken together, the present study firstly found that paternal Fenvalerate exposure transgenerationally impaired spatial cognition in a gender-dependent manner. Hippocampal TR signaling may, at least partially, contribute to the process of cognitive impairment induced by paternal Fenvalerate exposure. Further exploration in the mode of action of Fenvalerate is critically important to promote human health and environmental safety.

Chemistry and fate of Fenvalerate and esfenvalerate

Rev Environ Contam Toxicol 2003;176:137-54.PMID:12442505DOI:10.1007/978-1-4899-7283-5_3.

Fenvalerate is listed under Class IV of the U.S. Food and Drug Administration (USFDA) Surveillance Index Classification, indicating a low hazard potential to humans from both exposure and toxicological standpoints; thus, minimal monitoring is required (Reed 1981; Eisler 1992). To date, monitoring efforts have been of limited value in evaluating concentrations of Fenvalerate and its subsequent risk to the environment. Few regulations currently exist for protection of sensitive natural resources against Fenvalerate or esfenvalerate, although current application rates may be lethal to many nontarget species, including bees, fish, and aquatic invertebrates. Additional monitoring is recommended to measure residues in the environment and evaluate risks associated with use. It is clear that both Fenvalerate and esfenvalerate are considerably less harmful to the environment and most nontarget organisms than most other insecticides. They are considerably less persistent and more selective in their toxicity, except for their high degree of toxicity to fish and aquatic invertebrates. However, they are moderately persistent in soils and, because of low water solubilities, high octanol-water partition coefficients (Kow), and moderate persistence, both Fenvalerate and esfenvalerate have been identified as having the potential to accumulate in aquatic sediments and biota (Nowell et al. 1999). Numerous studies of Fenvalerate dynamics in soils indicate that it is relatively immobile and readily degraded. In almost all cases, the degradation products formed are less toxic than the parent insecticide. However, some degradation products from Fenvalerate may demonstrate elevated toxicity, and more research into and increased monitoring of abiotic degradation may be warranted. Results from environmental monitoring are minimal at best and do not adequately support research done in the laboratory. These results are critical for accurately determining the risk these insecticides pose to the environment. The pyrethroids are poised to fill the gap left in the insecticide market with the impending suspension of many of the organophosphates and possibly at least some carbamates. One agent, chlorpyrifos, has already been heavily restricted by the U.S. Environmental Protection Agency (USEPA), and one manufacturer has ceased production. The environmental risk posed by both Fenvalerate and esfenvalerate can change significantly with increased application, and current information is not sufficient to adequately assess the risk that a dramatic rise in use would pose. Future efforts should focus on increased environmental monitoring and research on esfenvalerate fate with increased and repeated application. Pyrethroids, including Fenvalerate and esfenvalerate, have also recently been linked to endocrine disruption (Garey and Wolff 1998; Go et al. 1999). Endocrine disruption is an emerging field, and more research is essential in documenting and managing these types of effects. Research into the bioavailability and dynamics of esfenvalerate at the sediment-water interface is also of key importance. Current information indicates that resuspension or desorption from soils should be minimal, but this is not equivalent to the fraction of sediment-sorbed esfenvalerate that may be bioavailable to sensitive aquatic species. In terms of risk, Fenvalerate and esfenvalerate are significant improvements over many of their predecessors, but it is clear that more information is needed to fully support this conclusion.

Environmentally relevant concentrations of Fenvalerate induces immunotoxicity and reduces pathogen resistance in Chinese rare minnow (Gobiocypris rarus)

Sci Total Environ 2022 Sep 10;838(Pt 3):156347.PMID:35671856DOI:10.1016/j.scitotenv.2022.156347.

Fenvalerate is a broadly used type II pyrethroid with a potential toxic effect in fish. However, information on the immunotoxicity of Fenvalerate in fish is scarce. Here, to discover the immunotoxicity of Fenvalerate and its underlying mechanism in fish, adult Chinese rare minnow was exposed to Fenvalerate at 0, 0.3, 1, and 3 μg/L for 28 days and then subjected to Pseudomonas fluorescens (P. fluorescens) challenge. Fenvalerate induced significant pathological changes, with disintegration of cell boundaries in the intestine, epithelial hyperplasia in gills, and vacuolation of hepatocytes at 3 μg/L treatment. Additionally, the pathological characteristics were more serious during P. fluorescens infection after Fenvalerate exposure. A significant increase in neutrophil counts was observed after 3 μg/L Fenvalerate exposure for 28 days (p < 0.05), whereas significantly increased monocyte and neutrophil counts and greatly decreased lymphocyte counts were detected at 24 h post-injection (hpi) with P. fluorescens (p < 0.05). Furthermore, obvious decreases in LYS, IgM, ALP, and C3 levels were detected in plasma after 3 μg/L Fenvalerate exposure for 28 days, which was consistent with the results at 24 and 48 hpi. Notably, fish exposed to Fenvalerate suppressed the transcription of TLR-NF-κB signaling pathway-relevant genes in response to P. fluorescens, accompanied by high mortalities and bacterial loads. Therefore, our results demonstrate that Fenvalerate at environmentally relevant concentrations caused immunotoxicity in fish. This study highlights the importance of considering the combined effects of chemicals and pathogens to refine our ability to predict the effects of environmental contaminants on aquatic organisms.

Fenvalerate decreases semen quality in puberty rat through germ cell apoptosis

Andrologia 2018 Nov;50(9):e13079.PMID:29968265DOI:10.1111/and.13079.

Fenvalerate, a widely used synthetic pyrethroid insecticide, may adversely affect semen quality in males, but the possible mechanism remains unclear. In our study, forty male SD rats were randomly divided into one control group and three treatment groups administered with Fenvalerate (0.02, 1 and 50 mg kg-1 day-1 ) by gavage from post-natal day 28 (PND 28) to PND 88. Semen quality parameters were measured by computer-assisted sperm analysis, histological changes in testes were observed by hematoxylin-eosin (HE) staining, germ cell apoptosis was measured by TdT-mediated dUTP Nick-End Labeling (TUNEL) and caspases protein levels were measured by western blotting. Results showed that the increased body weight, the relative testis weight, the sperm concentration and the sperm motility were all significantly reduced in the 50 mg kg-1 day-1 Fenvalerate group. Increased inner diameter of seminiferous tubules and disturbed array of spermatogenic cells in testicular were observed in Fenvalerate exposure groups. Meanwhile, TUNEL-positive germ cells significantly increased in 1 and 50 mg kg-1 day-1 Fenvalerate exposure groups, and the expression of caspase-8 and caspase-3 in rat testes were also significantly up-regulated. Taken together, our results indicate that Fenvalerate has an adverse effect on semen quality, which may be related to germ cell apoptosis.