116255-48-2
Chemical Structure
Bromuconazole
- CAS No.: 116255-48-2
- Formula:C13H12BrCl2N3O
- Molecular Weight:377.06
IUPAC Name: 1-((4-bromo-2-(2,4-dichlorophenyl)tetrahydrofuran-2-yl)methyl)-1H-1,2,4-triazole
InChIKey: HJJVPARKXDDIQD-UHFFFAOYSA-N
SMILES: ClC1=CC=C(C(Cl)=C1)C2(OCC(Br)C2)CN3N=CN=C3
Biological Activity: Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability. Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process. Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction[1][2][3][4][5][6][7].
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Bromuconazole | Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability. Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process. Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction. | |||||||||||||||||||||
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- [1]. Rjiba-Touati K, et al. Genotoxic damage and apoptosis in rat glioma (F98) cell line following exposure to bromuconazole. Neurotoxicology. 2023;94:108-116. [Content Brief]
- [2]. Rjiba-Touati K, et al. Bromuconazole fungicide induces cell cycle arrest and apoptotic cell death in cultured human colon carcinoma cells (HCT116) via oxidative stress process. Biomarkers. 2022;27(7):659-670. [Content Brief]
- [3]. Abdelhadya DH, et al. Bromuconazole-induced hepatotoxicity is accompanied by upregulation of PXR/CYP3A1 and downregulation of CAR/CYP2B1 gene expression. Toxicol Mech Methods. 2017;27(7):544-550. [Content Brief]
- [4]. Kim M, et al. Bromuconazole impairs implantation process through cellular stress response in human trophoblast and endometrial cells. Pestic Biochem Physiol. 2025;214:106632. [Content Brief]
- [5]. Huang Y, et al. Bromuconazole exposure induces cardiac dysfunction by upregulating the expression LEF1. Sci Total Environ. 2024;933:173113. [Content Brief]
- [6]. Rjiba-Touati K, et al. Bromuconazole caused genotoxicity and hepatic and renal damage via oxidative stress process in Wistar rats. Environ Sci Pollut Res Int. 2022;29(10):14111-14120. [Content Brief]
- [7]. Qin Z, et al. Bromuconazole exposure induces cardiotoxicity and lipid transport disorder in larval zebrafish. Comp Biochem Physiol C Toxicol Pharmacol. 2022;262:109451. [Content Brief]
Keywords
