Fenhexamid
(Synonyms: 环酰菌胺,KBR 2738) 目录号 : GC49563
A fungicide
Cas No.:126833-17-8
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
Fenhexamid is a fungicide.1,2 It inhibits germ-tube elongation and mycelial growth of several strains of the plant pathogenic fungus B. cinerea (EC50s = 0.13-8.3 and 0.03-16.5 µM, respectively).1 Fenhexamid inhibits 3-ketoreductase (IC50 = 3 µM for the B. cinerea enzyme), is an estrogen receptor α (ERα) agonist (EC50 = 9 µM in a yeast reporter assay), and inhibits the androgenic effect of dihydrotestosterone in MDA-kb2 cells (IC20 = 2.02 µM).1,3,4 It increases the proliferation and migration of BG1 ovarian cancer cells when used at a concentration of 10 µM.5 In field studies, fenhexamid applied at 842 g AI/ha provides 27.3 and 13.9% disease control for lettuce drop caused by S. minor or S. sclerotiorum, respectively.2 Formulations containing fenhexamid have been used as fungicides in agriculture.
1.Debieu, D., Bach, J., Montesinos, E., et al.Role of sterol 3-ketoreductase sensitivity in susceptibility to the fungicide fenhexamid in Botrytis cinerea and other phytopathogenic fungiPest. Manag. Sci.69(5)642-651(2013) 2.Matheron, M.E., and Porchas, M.Activity of boscalid, fenhexamid, fluazinam, fludioxonil, and vinclozolin on growth of Sclerotinia minor and S. sclerotiorum and development of lettuce dropPlant Dis.88(6)665-668(2004) 3.Teng, Y., Manavalan, T.T., Hu, C., et al.Endocrine disruptors fludioxonil and fenhexamid stimulate miR-21 expression in breast cancer cellsToxicol. Sci.131(1)71-83(2013) 4.Orton, F., Rosivatz, E., Scholze, M., et al.Widely used pesticides with previously unknown endocrine activity revealed as in vitro antiandrogensEnviron. Health Perspect.119(6)794-800(2011) 5.Go, R.-E., Kim, C.-W., and Choi, K.-C.Effect of fenhexamid and cyprodinil on the expression of cell cycle- and metastasis-related genes via an estrogen receptor-dependent pathway in cellular and xenografted ovarian cancer modelsToxicol. Appl. Pharmacol.289(1)48-57(2015)
| Cas No. | 126833-17-8 | SDF | Download SDF |
| 别名 | 环酰菌胺,KBR 2738 | ||
| Canonical SMILES | O=C(C1(CCCCC1)C)NC2=C(Cl)C(Cl)=C(C=C2)O | ||
| 分子式 | C14H17Cl2NO2 | 分子量 | 302.2 |
| 溶解度 | DMF: 5 mg/ml,DMSO: 3 mg/ml,Ethanol: slightly soluble | 储存条件 | -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 | 3.3091 mL | 16.5453 mL | 33.0907 mL |
| 5 mM | 0.6618 mL | 3.3091 mL | 6.6181 mL |
| 10 mM | 0.3309 mL | 1.6545 mL | 3.3091 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。
The role of Fenhexamid on the proliferation of ovarian cancer BG-1 cells
Int J Clin Exp Pathol 2018 Apr 1;11(4):2025-2031.PMID:31938309doi
To study the influence of Fenhexamid in pesticide residue to the human ovarian cancer BG-1 cell proliferation. Detecting the effectiveness of 17β-estradiol, Fenhexamid and Fulvestrant to BG-1 cell proliferation by MTT, and detecting the expression levels of cyclin D1 and cyclin E by Western blot. Fenhexamid can promote BG-1 cell proliferation for its estrogen-like effect. On the other hand, it can help to improve the expression levels of cyclin D1 and cyclin E in BG-1 cells which is regulated by ER-dependent pathway. And 17β-estradiol is also regulated by the same way. The existence of Fenhexamid can promote ovarian cancer cell proliferation, so for patients with ovarian cancer, Fenhexamid in pesticide residue may make medical conditions worse.
The role of Fenhexamid on the proliferation of ovarian cancer BG-1 cells [Retraction]
Int J Clin Exp Pathol 2020 Mar 1;13(3):634.PMID:32269705doi
[This retracts the article on p. 2025 in vol. 11, PMID: 31938309.].
Endocrine disruptors fludioxonil and Fenhexamid stimulate miR-21 expression in breast cancer cells
Toxicol Sci 2013 Jan;131(1):71-83.PMID:23052036DOI:10.1093/toxsci/kfs290.
Fenhexamid and fludioxonil are antifungal agents used in agricultural applications, which are present at measurable amounts in fruits and vegetables. Fenhexamid and fludioxonil showed endocrine disruptor activity as antiandrogens in an androgen receptor reporter assay in engineered human breast cancer cells. Little is known about how environmental chemicals regulate microRNA (miRNA) expression. This study examined the effect of Fenhexamid and fludioxonil on the expression of the oncomiR miR-21 in MCF-7, T47D, and MDA-MB-231 human breast cancer cells and downstream targets of miR-21 in MCF-7 cells. Fenhexamid and fludioxonil stimulated miR-21 expression in a concentration-dependent manner and reduced the expression of miR-21 target Pdcd4 protein. Antisense to miR-21 blocked the increase in Pdcd4 protein by Fenhexamid and fludioxonil. Fenhexamid and fludioxonil reduced miR-125b and miR-181a, demonstrating specificity of miRNA regulation. Induction of miR-21 was inhibited by the estrogen receptor antagonist fulvestrant, by androgen receptor antagonist bicalutamide, by actinomycin D and cycloheximide, and by inhibitors of the mitogen-activated protein kinases and phosphoinositide 3-kinase pathways. Fenhexamid activation was inhibited by the arylhydrocarbon receptor antagonist α-napthoflavone. Fenhexamid and fludioxonil did not affect dihydrotestosterone-induced miR-21 expression. Fludioxonil, but not Fenhexamid, inhibited MCF-7 cell viability, and both inhibited estradiol-induced cell proliferation and reduced cell motility. Together these data indicate that Fenhexamid and fludioxonil use similar and distinct mechanisms to increase miR-21 expression with downstream antiestrogenic activity.
Fenhexamid induces cancer growth and survival via estrogen receptor-dependent and PI3K-dependent pathways in breast cancer models
Food Chem Toxicol 2021 Mar;149:112000.PMID:33484789DOI:10.1016/j.fct.2021.112000.
Fenhexamid (Fen), a fungicide used to treat gray mold of fruits and vegetables, is reported to function as an endocrine disrupting chemical via the estrogen receptors (ER), despite low-toxicity of the pesticide. In this study, we elucidated that the disrupting effects of Fen are exerted via the ER and phosphatidylinositol 3-kinase (PI3K) pathways in breast cancer models. The WST assay, live cell monitoring, cell cycle analysis, colony formation assay, apoptotic analysis by JC-1 dyeing, and Western blot analysis were applied in ER positive MCF-7 and ER negative MDA-MB-231 breast cancer cells, after exposure to 17β-estradiol (E2), Fen, ICI 182,780 (ICI; an ER antagonist) and/or Pictilisib (Pic; a PI3K inhibitor). Exposure to E2 and Fen induced the cell growth and survival ability of MCF-7 cells by increasing the S-phase cells and regulating the cell cycle-related proteins (Cyclin D1 and E1, p21 and p27). In addition, E2 and Fen treatment resulted in elevated levels of the survival-related proteins (Survivin and PCNA), and inhibited apoptosis by increasing the mitochondrial membrane potential and regulating the apoptosis-related proteins (BAX, BCL-2, and Caspase-9). These changes were reversed to the same level as the control group when exposed to their respective inhibitors, thereby indicating that the changes are exerted via the ER and PI3K pathways. In particular, co-treatment with these inhibitors induced greater inhibition than single treatment. Conversely, no alterations were observed in the ER-negative MDA-MB-231 breast cancer cells. Taken together, these results indicate that Fen promotes the growth of breast cancer cells via the ER and/or PI3K pathways, similar to the E2 mechanism. Although a relatively safe pesticide, Fen possibly exerts its influence as an endocrine disrupting chemical in ER-positive breast cancer cells via the ER and PI3K pathways.
A fungicide, Fenhexamid, is involved in the migration and angiogenesis in breast cancer cells expressing estrogen receptors
Life Sci 2022 Sep 15;305:120754.PMID:35780843DOI:10.1016/j.lfs.2022.120754.
Fenhexamid (Fen) is used to eradicate gray mold of fruits and vegetables leading to greater detection of its residual concentration in wine than other fungicides. Here, we further investigated the malign influence of Fen on the migration and angiogenesis via regulation of the estrogen receptor (ER) and phosphoinositide 3-kinase (PI3K) pathways in breast cancer models. ER-positive MCF-7 and ER-negative MDA-MB-231 breast cancer cells were exposed to 17β-estradiol (E2, 10-9 M), Fen (10-5 M and 10-7 M), ICI 182,780 (ICI; an ER antagonist, 10-8 M) or/and Pictilisib (Pic; a PI3K inhibitor, 10-7 M), and subsequently subjected to migration assay, live cell motility monitoring, trans-chamber assay, immunofluorescence, angiogenesis assay, tumor spheroid formation, and Western blot analysis. In MCF-7 cells, E2 and Fen induced cell migration by regulating the cell migration-related proteins. Although expressions of N-cadherin and Vimentin remained unchanged E2 and Fen induced the decrease of E-cadherin and Occludin in the immunofluorescence assay and Western blot analysis. In addition, Fen increased vessel formation in HUVEC cells. Furthermore, Fen treatment induced the formation of larger and denser tumor spheroids in MCF-7 cells. Western blot further confirmed the increased expressions of vascular endothelial growth factor (VEGF) and sex-determining region Y-box 2 (SOX2) after exposure to Fen. We conclude that Fen plays an important role as an endocrine-disrupting chemical in breast cancer migration and metastasis through the regulation of ER and PI3K signaling pathways.