Tebufenozide
(Synonyms: 虫酰肼) 目录号 : GC48135
An insecticide and ecdysone receptor agonist
Cas No.:112410-23-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Tebufenozide is an insecticide that acts as a non-steroidal agonist of the insect ecdysone receptor (EcR; IC50 = 0.85 nM in a cell-free preparation of C. suppressalis integument).1 It induces a premature molt and is lethal to S. litura third instar larva (LD50 = 0.33 µM per larva).1,2 It also inhibits p-glycoprotein activity in LLC-PK1 porcine kidney epithelial cells transfected with human MDR1, the gene for p-glycoprotein (IC50 = 21.5 µM).3 Tebufenozide has low toxicity in mammals, birds, and most aquatic species, but it dose-dependently decreases colony formation and induces apoptosis and cell cycle arrest in HeLa cells when used at concentrations ranging from 50 to 200 µg/ml.4,5
1.Minakuchi, C., Nakagawa, Y., Kamimura, M., et al.Binding affinity of nonsteroidal ecdysone agonists against the ecdysone receptor complex determines the strength of their molting hormonal activityEur. J. Biochem.270(20)4095-4104(2003) 2.Yokoi, T., Minami, S., Nakagawa, Y., et al.Structure-activity relationship of imidazothiadiazole analogs for the binding to the ecdysone receptor of insect cellsPestic. Biochem. Physiol.12040-50(2015) 3.Miyata, K.-i., Nakagawa, Y., Kimura, Y., et al.Structure-activity relationships of dibenzoylhydrazines for the inhibition of P-glycoprotein-mediated quinidine transportBioorg. Med. Chem.24(14)3184-3191(2016) 4.Xu, W., Wang, B., Yang, M., et al.Tebufenozide induces G1/S cell cycle arrest and apoptosis in human cellsEnviron. Toxicol. Pharmacol.4989-96(2017) 5.Abass, K.M.An investigation into the formation of tebufenozide's toxic aromatic amine metabolites in human in vitro hepatic microsomesPestic. Biochem. Physiol.13373-78(2016)
| Cas No. | 112410-23-8 | SDF | |
| 别名 | 虫酰肼 | ||
| Canonical SMILES | CCC1=CC=C(C(NN(C(C)(C)C)C(C2=CC(C)=CC(C)=C2)=O)=O)C=C1 | ||
| 分子式 | C22H28N2O2 | 分子量 | 352.5 |
| 溶解度 | DMSO : 125 mg/mL (354.64 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 | 2.8369 mL | 14.1844 mL | 28.3688 mL |
| 5 mM | 0.5674 mL | 2.8369 mL | 5.6738 mL |
| 10 mM | 0.2837 mL | 1.4184 mL | 2.8369 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。
Tebufenozide has limited direct effects on simulated aquatic communities
Ecotoxicology 2022 Oct;31(8):1231-1240.PMID:36083423DOI:10.1007/s10646-022-02582-y.
The use of insecticides to control undesirable pest species in forestry has undergone a shift from broad spectrum to narrow spectrum insecticides to reduce the risk of effects on non-target species. However, there is still risk of direct effects on non-target species as some insecticides function as hormone mimics, or through indirect pathways as the insecticide is broken down in the environment. Tebufenozide, an ecdysone hormone mimic, is the active ingredient in insecticides used in a variety of large scale pest control programs. An oft cited reason for the safety of Tebufenozide is that it is rapidly broken down in the environment by microbes. We investigated the potential non-target effects of two Tebufenozide formulations used in Canada, Mimic 240LV and Limit 240, on aquatic communities using an outdoor mesocosm experiment. We focus on direct effects on amphibian larvae (wood frog, Rana sylvaticus), zooplankton communities, and effects on biofilm and phytoplanktonic microbial communities that could arise from either direct toxicity, or from breaking down the insecticide as a nutrient and/or carbon source. There was limited evidence for direct effects on amphibian larvae or zooplankton communities. There were small but non-significant shifts in biofilm microbial communities responsible for nutrient cycling. Beta diversity in the plankton community was slightly higher among tanks treated with insecticide indicating a community dispersion/disbiosis effect. Overall, we found limited evidence of negative effects, however, subtle changes to microbial communities did occur and could indicate changes to ecosystem function.
Tebufenozide induces G1/S cell cycle arrest and apoptosis in human cells
Environ Toxicol Pharmacol 2017 Jan;49:89-96.PMID:27960113DOI:10.1016/j.etap.2016.12.002.
Tebufenozide is a non-steroidal insect growth regulator and is extensively used to control pests, although it is considered to be safe for mammals and environmentally friendly. However, previous studies have found that Tebufenozide is cytotoxic to man, although the exact mechanism remains elusive. This study will investigate the apoptotic molecular mechanisms which result from tebufenozide-induced DNA damage in HeLa cells. Our results demonstrate that Tebufenozide could trigger arrest in G1/S phase related to a downregulation of cyclin E and cyclin-dependent kinase (CDK) 2 protein. In addition, Western blotting showed apoptosis was associated with the upregulation of p53, Bax and cleaved-PARP, as well as downregulation of Bcl-2 and PARP. Tebufenozide also regulated changes in mitochondrial permeability and reduced mitochondrial number and intracellular ATP production. Briefly, these results suggest that tebufenozide- induces cell cycle arrest and apoptosis through activating p53 protein in a Bax- and Bcl-2-triggered mitochondrial pathway. This work provides some scientific context for the safe use of Tebufenozide in agriculture.
Tebufenozide resistance is associated with sex-linked inheritance in Plutella xylostella
Insect Sci 2015 Apr;22(2):235-42.PMID:25813528DOI:10.1111/1744-7917.12081.
The diamondback moth (DBM), Plutella xylostella (L.), is a major pest of cruciferous crops. Tebufenozide, a novel nonsteroidal ecdysone agonist, exhibits good efficacy and has played an increasingly important role in the control of Lepidopteran pests in China. For its resistance management, the genetic basis of Tebufenozide resistance was studied using a laboratory selected resistant strain of DBM (resistant ratio, RR = 268). A series of crosses with laboratory susceptible and resistant strains revealed that Tebufenozide resistance in this pest was partially biased toward female heredity, with a large difference in RR for F1 (RR = 29) and rF1 progeny (RR = 147). The dominance calculated for these 2 cross progeny was -0.788 and 0.09, respectively. Further analysis showed that the susceptible male and female larvae were similar in their sensitivity to Tebufenozide, but the resistant female larvae showed significantly higher resistance than the resistant male larvae. The heredity of Tebufenozide resistance in DBM might be linked with the W sex chromosome, which suggested that DBM has the ability to develop high levels of resistance to Tebufenozide. This is the first report of sex-linked inheritance of Tebufenozide resistance in P. xylostella (L.).
Cytotoxic effects of Tebufenozide in vitro bioassays
Ecotoxicol Environ Saf 2016 Jul;129:180-8.PMID:27043174DOI:10.1016/j.ecoenv.2016.03.025.
Tebufenozide is considered an environmentally friendly pesticide due to its specificity on target insects, but the effects on human are well studied. Studies on the toxicity of Tebufenozide at molecular and cellular level is poorly understood. The present study reveals non-selective cytotoxic effects of Tebufenozide, and the apoptotic mechanism induced by Tebufenozide on HeLa and Tn5B1-4 cells. We demonstrate that the viability of HeLa and Tn5B1-4 cells is inhibited by Tebufenozide in a time- and concentration-dependent manner. Intracellular biochemical assays showed that tebufenozide-induced apoptosis of two cell lines concurrent with a decrease in the mitochondrial membrane potential and an increase reactive oxygen species generation, the release of cytochrome-c into the cytosol and a marked activation of caspase-3. These results indicate that a mitochondrial-dependent intrinsic pathway contributes to Tebufenozide induced apoptosis in HeLa and Tn5B1-4 cells and suggests potential threats to ecosystems and human health.
Tebufenozide disrupts ovarian development and function in silkmoths
Insect Biochem Mol Biol 2013 Dec;43(12):1087-99.PMID:24121094DOI:10.1016/j.ibmb.2013.09.002.
Adult development and production of up to 400 eggs within the pupal case of female silkmoths are both dependent on 20-hydroxyecdysone (20E), the steroid hormone of insects. When adult development was initiated with Tebufenozide, the non-steroidal ecdysteroid agonist, instead of 20E, full development of all epidermal tissues like the wing was witnessed, but ovarian growth and egg formation was minimal. Administration of Tebufenozide to female pharate adults caused disruption of the follicular epithelium, produced nurse cell damage, and inhibited oogenesis. Reduced ability to synthesize RNA and protein accompanied these Tebufenozide induced morphological disturbances of the follicles. In vivo accumulation of vitellogenin (Vg) from the hemolymph was reduced in Tebufenozide treated female ovaries as well as their ability to accumulate Vg in vitro. Determination of protein staining intensity and antibody reactivity of Vg pointed out that hemolymph Vg level remained fairly constant all through adult development whether induced by 20E or Tebufenozide. Measurement of hemolymph volumes and hemolymph Vg levels of control and experimental animals allowed us to conclude that egg development involves the uptake of all the hemolymph proteins and not Vg alone. The loss of hemolymph that accompanies egg maturation was considerably reduced in Tebufenozide initiated female pharate adults. 20E could not overcome ovarian growth inhibitory effects of Tebufenozide. Dual mechanisms, one involving ecdysteroid antagonist action at the beginning of development, and the other unrelated to that function during heightened egg formation, are needed explain the biphasic inhibitory actions of Tebufenozide on silkmoth ovaries.