Spiromesifen
(Synonyms: 螺甲螨酯) 目录号 : GC48093
An insecticide and acaricide
Cas No.:283594-90-1
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Spiromesifen is an insecticide and acaricide that reduces lipid biosynthesis via inhibition of acetyl-CoA carboxylase.1,2 It inhibits chitinase from Egyptian cotton leafworm (S. littoralis) larvae (IC50s = 0.60 and 0.72 μM for enzyme isolated from lab and field strains, respectively).3 It induces toxicity in whitefly (T. vaporariorum) nymphs (LC50 = 0.61 mg/L), spider mite (T. cinnabarinus) eggs (LC50 = 0.16 mg/kg), and second instar larvae of S. littoralis lab and field strains (LC50s = 0.44 and 0.68 ppm, respectively, at 72 hours post-application).1,2,3 Spiromesifen (600 mg/kg) also induces 50, 60, and 70% mortality in the Lepidoptera pests H. armigera, O. nubilalis, and P. xylostella, respectively, and induces 100% mortality in M. separata when used at a dose of 100 mg/kg.2 It induces toxicity in D. magna (EC50 = >0.092 mg a.s./L) and the fish species O. mykiss and L. macrochirus (LC50s = 0.016 and >0.034 mg a.s./L, respectively) but not rats (LD50 = >2,000 mg/kg).4 Spiromesifen also inhibits the human GST isozyme GSTA1-1 (IC50 = 12.1 μM).5
1.Karatolos, N., Williamson, M.S., Denholm, I., et al.Resistance to spiromesifen in Trialeurodes vaporariorum is associated with a single amino acid replacement in its target enzyme acetyl-coenzyme A carboxylaseInsect Mol. Biol.21(3)327-334(2012) 2.Liu, Z., Lei, Q., Li, Y., et al.Design, synthesis, structure, and acaricidal/insecticidal activity of novel spirocyclic tetronic acid derivatives containing an oxalyl moietyJ. Agric. Food Chem.59(23)12543-12549(2011) 3.Ismail, S.M., and Morshedy, M.Evaluation of some environmentally safe cemicals against Spodoptera littoralisAlexandria Sci. Exch. J.30(1)121-127(2009) 4.Authority, E.F.S.Conclusion on the peer review of the pesticide risk assessment of the active substance spiromesifenEFSA J.10(10)2879(2012) 5.Chronopoulou, E.G., Papageorgiou, A.C., Markoglou, A., et al.Inhibition of human glutathione transferases by pesticides: Development of a simple analytical assay for the quantification of pesticides in waterJ. Mol. Catal. B: Enzymatic8143-51(2012)
| Cas No. | 283594-90-1 | SDF | |
| 别名 | 螺甲螨酯 | ||
| Canonical SMILES | CC1=C(C2=C(OC(CC(C)(C)C)=O)C3(CCCC3)OC2=O)C(C)=CC(C)=C1 | ||
| 分子式 | C23H30O4 | 分子量 | 370.5 |
| 溶解度 | DMSO : 125 mg/mL (337.40 mM; ultrasonic and warming and heat to 60°C) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 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。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.6991 mL | 13.4953 mL | 26.9906 mL |
| 5 mM | 0.5398 mL | 2.6991 mL | 5.3981 mL |
| 10 mM | 0.2699 mL | 1.3495 mL | 2.6991 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Spiromesifen induces histopathological and cytotoxic changes in the midgut of the honeybee Apis mellifera (Hymenoptera: Apidae)
Chemosphere 2021 May;270:129439.PMID:33395581DOI:10.1016/j.chemosphere.2020.129439.
The honeybee Apis mellifera is an important pollinator that, similarly to other bees, undergoes colony losses due to several problems, including the use of pesticides in the agriculture. In addition to direct mortality, pesticides cause side-effects in some non-target organs, such as the midgut, which is the main organ for digestion and absorption. Spiromesifen is a pesticide used to control mites and whiteflies, which can be ingested by bees feeding on contaminated floral resources. This study evaluated the histopathological and cytological effects of the ingestion of Spiromesifen on the midgut of A. mellifera workers. The bees were exposed per os to the field recommended dose of Spiromesifen, and the midgut was analyzed after 24h and 48h of exposure to the pesticide. The midgut has a single layer of digestive cells, with spherical nucleus, nests of regenerative cells and layers of peritrophic matrix in the lumen. Bees treated with Spiromesifen presented histological and cytological changes in the midgut, including disorganization of the epithelial architecture, release of cell fragments to the lumen, accumulation of mitochondria in the apical cytoplasm, alteration of the basal labyrinth, changes in the rough endoplasmic reticulum and cell degeneration. The occurrence of damage in the digestive cells of the A. mellifera midgut indicates that Spiromesifen does not cause mortality in honeybees, but its side-effects can damage the midgut, which may affect the longevity and behavior of this pollinator.
Spiromesifen and spirotetramat resistance in field populations of Bemisia tabaci Gennadius in Spain
Pest Manag Sci 2019 Jan;75(1):45-52.PMID:30009510DOI:10.1002/ps.5144.
Background: Spiromesifen and spirotetramat are novel insecticides belonging to the chemical class of tetronic and tetramic acid derivatives. Both compounds have proven very effective against field populations of Bemisia tabaci around the world. However, several growers have recently reported control failures in Spain. Therefore, we studied the resistance level to these insecticides in field populations reporting control failures. In addition, we further selected a spiromesifen-resistant strain to study the mechanisms involved and the cross-resistance pattern. Results: All the new field populations collected were significantly more resistant to Spiromesifen than the susceptible population, confirming the presence of resistance. Several populations showing high levels of resistance to Spiromesifen (>10 000-fold), exhibited cross-resistance to spirotetramat, but resistance ratios were much lower (130-fold). The Spiromesifen laboratory-selected strain was very resistant to Spiromesifen (LC50 > 30 000 mg L-1 ) and spirotetramat (LC50 = 368.1 mg L-1 ), but lacks any cross-resistance to other insecticides, thus providing options for resistance management. None of the synergists tested significantly restored the susceptibility of B. tabaci to either Spiromesifen or spirotetramat. Conclusion: This is the first report of resistance to Spiromesifen and spirotetramat in B. tabaci, and such high levels of resistance have not been reported before in any field collected pest. Our results suggest that enhanced detoxification does not critically contribute to resistance to ketoenols in B. tabaci. The obvious lack of a metabolic resistance mechanism either suggests a target-site resistance mechanism or a metabolic mechanism insensitive to the synergists tested. © 2018 Society of Chemical Industry.
Spiromesifen conferred abnormal development in zebrafish embryos by inducing embryonic cytotoxicity via causing oxidative stress
Aquat Toxicol 2022 Nov;252:106324.PMID:36244087DOI:10.1016/j.aquatox.2022.106324.
Spiromesifen (SPF) is widely used in agriculture to protect against herbivorous mites, whose residues may be harmful to the environment. However, the toxicity assessment of SPF is insufficient. Here, we investigated the toxicological effects of SPF using zebrafish embryos as an animal model. The results showed that SPF exposure solutions at 10, 20, 30, and 40 μM caused cytotoxicity in zebrafish embryos such as reactive oxygen species (ROS) accumulation, mitochondrial membrane potential decrease, cell division arrest, and apoptosis, which further led to developmental toxicity in zebrafish embryos including delayed hatching, decreased survival rate and spontaneous curling rate, and severe morphological deformities. SPF also induced apoptosis via changes in the expressions of apoptosis-related marker genes, caused immunotoxicity by reducing the number of macrophages and the activity of AKP/ALP and increasing inflammatory factors, and disturbed endogenous antioxidant systems via changes SOD, CAT, and GST activities as well as MDA and GSH contents. Therefore, the potential mechanism that caused embryonic developmental toxicity appeared to be related to the generation of oxidative stress by an elevation in ROS and changes in apoptosis-, immune-, antioxidant-related markers. The antioxidant system and inflammatory response simultaneously participated in and resisted the threat of SPF to prevent tissue damage. Taken together, Spiromesifen induced oxidative stress to contribute to developmental toxicity in zebrafish embryos by inducing embryonic cytotoxicity. Our study provides new insight into the toxicity assessment of SPF to non-target organisms.
Residual characteristics and safety assessment of the insecticides Spiromesifen and chromafenozide in lettuce and perilla
Sci Rep 2022 Mar 18;12(1):4675.PMID:35304538DOI:10.1038/s41598-022-08532-2.
This study was performed to investigate the residual characteristics, safety assessment, and pre-harvest interval (PHI) of Spiromesifen and chromafenozide in lettuce (Latuca sativa L.) and perilla (Perilla frutescens (L.) Britton) leaves. Samples were harvested periodically, extracted using QuEChERS method, and analyzed by LC-MS/MS. Average recoveries of Spiromesifen and its metabolite BSN2060-enol and chromafenozide were ranged from 80.6 to 107.9%, with relative standard deviation < 10%. Spiromesifen and cromafenozide initial residues in lettuce were dissipated to 81.45 and 95.52% after 7 days, with half-lives of 2.89 and 1.69 days respectively. Values in perilla leaves were 76.68 and 61.27% after the same period, with half-lives of 4.25 and 6.30 days, respectively. Risk assessment results showed that %ADI (acceptable daily intake) of Spiromesifen and chromafenozide was 6.83 and 0.56, in lettuce and 4.60 and 0.25% in perilla leaves, respectively. Theoretical maximum daily intakes of Spiromesifen and chromafenozide were 67.49 and 3.43%, respectively, indicating that residues of both compounds pose no considerable health risks to consumers. This study provides data for setting maximum residue limits and PHIs for the safe use of Spiromesifen and chromafenozide in lettuce and perilla.
Spiromesifen contributes vascular developmental toxicity via disrupting endothelial cell proliferation and migration in zebrafish embryos
Pestic Biochem Physiol 2022 Nov;188:105242.PMID:36464354DOI:10.1016/j.pestbp.2022.105242.
Spiromesifen (SPF) is a specific contact pesticide, which has been widely used to control the growth of sucking insects like mites and whiteflies on crops. Although its residues in crops and effects on organisms has been extensively reported, its impact on the vasculature is still not being reported. In the present study, using human umbilical vein endothelial cells (HUVECs) and zebrafish embryos, we investigated the effects of SPF on blood vessel development and its mechanism of action. SPF exposure triggered abnormal blood vessel development, including vascular deletions and malformations, inhibition of CCV remodeling, and decrease of SIV areas. SPF exposure also obstructed the migration of endothelial cell from caudal hematopoietic tissue in zebrafish embryos. SPF damaged cytoskeleton, caused cell cycle arrest, inhibited the viability and migration of HUVECs. In addition, SPF also inhibited the expression of the VEGF/VEGFR pathway-related genes (hif1a, vegfa, flt1, and kdrl), cell cycle-related genes (ccnd1, ccne1, cdk2, and pcna), and Rho/ROCK pathway-related genes (itgb1, rho, rock, mlc-1, and vim-1). Taken together, SPF may inhibit the proliferation and migration of vascular endothelial cells through disturbing cytoskeleton via the Rho/ ROCK pathway, resulting in vascular malformation. Our study contributes to potential insight into the mechanism of SPF toxicity in angiocardiopathy.