Flonicamid
(Synonyms: 氟啶虫酰胺) 目录号 : GC47354
A pyridinecarboxamide insecticide
Cas No.:158062-67-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Flonicamid is a pyridinecarboxamide insecticide.1 It inhibits the brown planthopper (N. lugens) inward-rectifying potassium channel Kir1 (IC50 = 0.64 µM). Flonicamid (100 µg/ml) inhibits aphid (M. persicae) salivation and sap ingestion during feeding on Japanese radish leaves.2 It induces toxicity in the aphid species A. gossypii, R. padi, S. graminum, and L. erysimi (LC50s = 0.64, 0.74, 0.78, and 2.01 µg/ml, respectively) and rats (LD50 = ≥844 mg/kg).3,2 Formulations containing flonicamid have been used for the control of pest insects in agriculture.
1.Ren, M., Niu, J., Hu, B., et al.Block of Kir channels by flonicamid disrupts salivary and renal excretion of insect pestsInsect Biochem. Mol. Biol.9917-26(2018) 2.Morita, M., Ueda, T., Yoneda, T., et al.Flonicamid, a novel insecticide with a rapid inhibitory effect on aphid feedingPest. Manag. Sci.63(10)969-973(2007) 3.Morita, M., Yoneda, T., and Akiyoshi, N.Research and development of a novel insecticide, flonicamidJ. Pestic. Sci.39(3)179-180(2014)
| Cas No. | 158062-67-0 | SDF | |
| 别名 | 氟啶虫酰胺 | ||
| Canonical SMILES | O=C(NCC#N)C1=C(C(F)(F)F)C=CN=C1 | ||
| 分子式 | C9H6F3N3O | 分子量 | 229.2 |
| 溶解度 | DMSO : 100 mg/mL (436.38 mM; Need ultrasonic) | 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.363 mL | 21.815 mL | 43.63 mL |
| 5 mM | 0.8726 mL | 4.363 mL | 8.726 mL |
| 10 mM | 0.4363 mL | 2.1815 mL | 4.363 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。
Flonicamid metabolite 4-trifluoromethylnicotinamide is a chordotonal organ modulator insecticide†
Pest Manag Sci 2022 Nov;78(11):4802-4808.PMID:35904889DOI:10.1002/ps.7101.
Background: The selective aphicide Flonicamid is known to cause symptoms in aphids that are like those of chordotonal organ TRPV channel modulator insecticides such as pymetrozine, pyrifluquinazon and afidopyropen. Flonicamid is classified by the Insecticide Resistance Action Committee as a chordotonal organ modulator with an undefined target site. However, although it has been shown not to act on TRPV channels, Flonicamid's action on chordotonal organs has not been documented in the literature. Results: Flonicamid causes locusts to extend their hindlegs, indicating an action on the femoral chordotonal organ. In fruit flies, it abolishes negative gravitaxis behavior by disrupting transduction and mechanical amplification in antennal chordotonal neurons. Although Flonicamid itself only weakly affects locust chordotonal organs, its major animal metabolite 4-trifluoromethylnicotinamide (TFNA-AM) potently stimulates both locust and fly chordotonal organs. Like pymetrozine, TFNA-AM rapidly increases Ca2+ in antennal chordotonal neurons in wild-type flies, but not iav1 mutants, yet the effect is nonadditive with the TRPV channel agonist. Conclusions: Flonicamid is a pro-insecticide form of TFNA-AM, a potent chordotonal organ modulator. The functional effects of TFNA-AM on chordotonal organs of locusts and flies are indistinguishable from those of the TRPV agonists pymetrozine, pyrifluquinazon and afidopyropen. Because our previous results indicate that TFNA-AM does not act directly on TRPV channels, we conclude that it acts upstream in a pathway that leads to TRPV channel activation. © 2022 Society of Chemical Industry.
Flonicamid and knockdown of inward rectifier potassium channel gene CsKir2B adversely affect the feeding and development of Chilo suppressalis
Pest Manag Sci 2021 Apr;77(4):2045-2053.PMID:33342029DOI:10.1002/ps.6232.
Background: The selective insecticide Flonicamid shows highly insecticidal activities against piercing-sucking insects and has been widely used for the control of Hemipteran insect pests, whereas its effects on Lepidopteran insect pests remain largely unknown. Recently, inward rectifier potassium (Kir) channel has been verified to be a target of Flonicamid, however, functional characterization of Lepidopteran Kir genes is still lacking. Results: Flonicamid shows no insecticidal toxicity against Chilo suppressalis larvae. However, the feeding and growth of larvae were reversibly inhibited by Flonicamid (50-1200 mg L-1 ). Flonicamid treatment also remarkably reduced and delayed the pupation and eclosion of Chilo suppressalis. Additionally, five distinct Kir channel genes (CsKir1, CsKir2A, CsKir2B, CsKir3A and CsKir3B) were cloned from Chilo suppressalis. Expression profiles analysis revealed that CsKir2A was predominately expressed in the hindgut of larvae, whereas CsKir2B had high expressions in the Malpighian tubules and hindgut. RNA interference (RNAi)-mediated knockdown of CsKir2B significantly reduced the growth and increased the mortalities of larvae, whereas silencing of CsKir2A had no obvious effects on Chilo suppressalis. Conclusion: Flonicamid exhibits adverse effects on the growth and development of Chilo suppressalis. CsKir2B might be involved in the feeding behavior of Chilo suppressalis. These results provide valuable information on the effects of Flonicamid on non-target insects as well as the function of insect Kir channels, and are helpful in developing new insecticide targeting insect Kir channels. © 2020 Society of Chemical Industry.
Risk Assessment of Flonicamid Resistance in Musca domestica (Diptera: Muscidae): Resistance Monitoring, Inheritance, and Cross-Resistance Potential
J Med Entomol 2021 Jul 16;58(4):1779-1787.PMID:33758935DOI:10.1093/jme/tjab036.
Flonicamid is a chordotonal modulator and novel systemic insecticide that has been used frequently for controlling a broad range of insect pests. The risk of Flonicamid resistance was assessed through laboratory selection and determining inheritance pattern and cross-resistance potential to five insecticides in house fly, Musca domestica L. Very low to high Flonicamid resistance in M. domestica populations was found compared with the susceptible strain (SS). A flonicamid-selected (Flonica-RS) M. domestica strain developed 57.73-fold resistance to Flonicamid screened for 20 generations compared with the SS. Overlapping 95% fiducial limits of LC50 of the F1 and F1ǂ, and dominance values (0.87 for F1 and 0.92 for F1ǂ) revealed an autosomal and incomplete dominant Flonicamid resistance. The monogenic model of resistance inheritance suggested a polygenic Flonicamid resistance. The Flonica-RS strain displayed negative cross-resistance between Flonicamid and sulfoxaflor (0.10-fold) or clothianidin (0.50-fold), and very low cross-resistance between Flonicamid and flubendiamide (4.71-fold), spinetoram (4.68-fold), or thiamethoxam (2.02-fold) in comparison with the field population. The estimated realized heritability (h2) value of Flonicamid resistance was 0.02. With selection mortality 40-90%, the generations required for a 10-fold increase in LC50 of Flonicamid were 94-258 at h2 (0.02) and slope (3.29). Flonicamid resistance was inherited as autosomal, incomplete dominant, and polygenic in the Flonica-RS. Negative or very low cross-resistance between Flonicamid and sulfoxaflor, clothianidin, flubendiamide, spinetoram, and thiamethoxam means that these insecticides can be used as alternatives for controlling M. domestica. These data can be useful in devising the management for M. domestica.
Biotransformation of insecticide Flonicamid by Aminobacter sp. CGMCC 1.17253 via nitrile hydratase catalysed hydration pathway
J Appl Microbiol 2021 May;130(5):1571-1581.PMID:33030814DOI:10.1111/jam.14880.
Aims: This study evaluates Flonicamid biotransformation ability of Aminobacter sp. CGMCC 1.17253 and the enzyme catalytic mechanism involved. Methods and results: Flonicamid transformed by resting cells of Aminobacter sp. CGMCC 1.17253 was carried out. Aminobacter sp. CGMCC 1.17253 converts Flonicamid into N-(4-trifluoromethylnicotinoyl) glycinamide (TFNG-AM). Aminobacter sp. CGMCC 1.17253 transforms 31·1% of the Flonicamid in a 200 mg l-1 conversion solution in 96 h. Aminobacter sp. CGMCC 1.17253 was inoculated in soil, and 72·1% of Flonicamid with a concentration of 0·21 μmol g-1 was transformed in 9 days. The recombinant Escherichia coli expressing Aminobacter sp. CGMCC 1.17253 nitrile hydratase (NHase) and purified NHase were tested for the Flonicamid transformation ability, both of them acquired the ability to transform Flonicamid into TFNG-AM. Conclusions: Aminobacter sp. CGMCC 1.17253 transforms Flonicamid into TFNG-AM via hydration pathway mediated by cobalt-containing NHase. Significance and impact of the study: This is the first report that bacteria of genus Aminobacter has flonicamid-transforming ability. This study enhances our understanding of flonicamid-degrading mechanism. Aminobacter sp. CGMCC 1.17253 has the potential for bioremediation of Flonicamid pollution.
Biotransformation of Flonicamid and sulfoxaflor by multifunctional bacterium Ensifer meliloti CGMCC 7333
J Environ Sci Health B 2021;56(2):122-131.PMID:33283619DOI:10.1080/03601234.2020.1852854.
Flonicamid is a novel, selective, systemic pyridinecarboxamide insecticide that effectively controls hemipterous pests. Sulfoxaflor, a sulfoximine insecticide, effectively controls many sap-feeding insect pests. Ensifer meliloti CGMCC 7333 transforms Flonicamid into N-(4-trifluoromethylnicotinoyl) glycinamide (TFNG-AM). Resting cells of E. meliloti CGMCC 7333 (optical density at 600 nm [OD600] = 5) transformed 67.20% of the Flonicamid in a 200-mg/L solution within 96 h. E. meliloti CGMCC 7333 transforms sulfoxaflor into N-(methyl(oxido){1-[6-(trifluoromethyl) pyridin-3-yl] ethyl}-k4-sulfanylidene) urea (X11719474). E. meliloti CGMCC 7333 resting cells (OD600 = 5) transformed 89.36% of the sulfoxaflor in a 200 mg/L solution within 96 h. On inoculating 2 mL of E. meliloti CGMCC 7333 (OD600 = 10) into soil containing 80 mg/kg Flonicamid, 91.1% of the Flonicamid was transformed within 9 d (half-life 2.6 d). On inoculating 2 mL of E. meliloti CGMCC 7333 (OD600 = 10) into soil containing 80 mg/kg sulfoxaflor, 83.9% of the sulfoxaflor was transformed within 9 d (half-life 3.4 d). Recombinant Escherichia coli harboring the E. meliloti CGMCC 7333 nitrile hydratase (NHase)-encoding gene and NHase both showed the ability to transform Flonicamid or sulfoxaflor into their corresponding amides, TFNG-AM and X11719474, respectively. These findings may help develop a bioremediation agent for the elimination of Flonicamid and sulfoxaflor contamination.