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Trifloxystrobin Sale

(Synonyms: 肟菌酯,CGA 279202) 目录号 : GC34845

A fungicide

Trifloxystrobin Chemical Structure

Cas No.:141517-21-7

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10mM (in 1mL DMSO)
¥446.00
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50mg
¥405.00
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100mg
¥630.00
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产品描述

Trifloxystrobin is a fungicide.1,2 It inhibits the growth of R. solani isolates from sugar beet crops (EC50s = 0.14-823.54 μg/ml).1 Trifloxystrobin (100-1,000 ppm) inhibits mycelial growth of C. gloeosporioides when used in combination with tebuconazole .2 It is toxic to various aquatic species, including R. arenarum, P. santafecinus, E. bicolor, and L. latrans tadpoles (LC50s = 0.22, 0.14, 0.1, and 0.26 mg/L, respectively).3 It also reduces mobility of tadpoles and decreases predation of trifloxystrobin-exposed, but not non-exposed, tadpoles by eels.

1.Arabiat, S., and Khan, M.Sensitivity of Rhizoctonia solani AG-2-2 from sugar beet to fungicidesPlant Dis.100(12)2427-2433(2016) 2.Dev, D., and Narendrappa, T.In vitro evaluation of fungicides against Colletotrichum gloeosporioides (Penz.) Penz and Sacc. causing anthracnose of pomegranate (Punica granatum L.)J. Appl. Nat. Sci.8(4)2268-2272(2017) 3.Junges, C.M., Peltzer, P.M., Lajmanovich, R.C., et al.Toxicity of the fungicide trifloxystrobin on tadpoles and its effect on fish-tadpole interactionChemosphere87(11)1348-1354(2012)

Chemical Properties

Cas No. 141517-21-7 SDF
别名 肟菌酯,CGA 279202
Canonical SMILES C/C(C1=CC(C(F)(F)F)=CC=C1)=N\OCC2=C(C=CC=C2)/C(C(OC)=O)=N\OC
分子式 C20H19F3N2O4 分子量 408.37
溶解度 DMSO : 125 mg/mL (306.09 mM);Water : < 0.1 mg/mL (insoluble) 储存条件 Store at -20°C
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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。
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1 mM 2.4488 mL 12.2438 mL 24.4876 mL
5 mM 0.4898 mL 2.4488 mL 4.8975 mL
10 mM 0.2449 mL 1.2244 mL 2.4488 mL
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Research Update

Trifloxystrobin blocks the growth of Theileria parasites and is a promising drug to treat Buparvaquone resistance

Commun Biol 2022 Nov 15;5(1):1253.PMID:36380082DOI:10.1038/s42003-022-03981-x.

Theileria parasites are responsible for devastating cattle diseases, causing major economic losses across Africa and Asia. Theileria spp. stand apart from other apicomplexa parasites by their ability to transform host leukocytes into immortalized, hyperproliferating, invasive cells that rapidly kill infected animals. The emergence of resistance to the theilericidal drug Buparvaquone raises the need for new anti-Theileria drugs. We developed a microscopy-based screen to reposition drugs from the open-access Medicines for Malaria Venture (MMV) Pathogen Box. We show that Trifloxystrobin (MMV688754) selectively kills lymphocytes or macrophages infected with Theileria annulata or Theileria parva parasites. Trifloxystrobin treatment reduced parasite load in vitro as effectively as Buparvaquone, with similar effects on host gene expression, cell proliferation and cell cycle. Trifloxystrobin also inhibited parasite differentiation to merozoites (merogony). Trifloxystrobin inhibition of parasite survival is independent of the parasite TaPin1 prolyl isomerase pathway. Furthermore, modeling studies predicted that Trifloxystrobin and Buparvaquone could interact distinctly with parasite Cytochrome B and we show that Trifloxystrobin was still effective against Buparvaquone-resistant cells harboring TaCytB mutations. Our study suggests that Trifloxystrobin could provide an effective alternative to Buparvaquone treatment and represents a promising candidate for future drug development against Theileria spp.

Trifloxystrobin-induced mitophagy through mitochondrial damage in human skin keratinocytes

J Toxicol Sci 2016;41(6):731-737.PMID:27853101DOI:10.2131/jts.41.731.

Trifloxystrobin is a strobilurin class fungicide, the mode of action of which is to block the mitochondrial electron transport chain and inhibit energy production in fungi. Although adverse effects have been reported by occupational or environmental exposure of fungicides, the pathophysiological mechanism in human cells remains poorly understood. In the present study, we investigated the impact of Trifloxystrobin on exposed skin at the cellular organelle level using HaCaT, the human skin keratinocyte cell line. Cells were treated with Trifloxystrobin for 48 hr and Trifloxystrobin showed detrimental effects on mitochondria evidenced by altered mitochondrial membrane potential and morphology. To identify autophagic degradation of the damaged mitochondria, confocal imaging and Western blotting were performed. Trifloxystrobin induced autophagy-related proteins in HaCaT cells. The mitochondrial reactive oxygen species scavenger mitoTEMPO was applied to further explore the mechanism of trifloxystrobin-mediated mitophagy in human skin cells. PINK1 and Parkin were overexpressed by Trifloxystrobin, and mitoTEMPO alleviated the effects on mitophagy induction. Taken together, our findings indicated that mitochondrial damage and mitophagy may play a role in trifloxystrobin-induced toxicity in human keratinocytes and this could be suggested as a mechanism of cutaneous diseases developed by exposure.

Residues and dissipation of Trifloxystrobin and its metabolite in tomatoes and soil

Environ Monit Assess 2014 Nov;186(11):7793-9.PMID:25086714DOI:10.1007/s10661-014-3967-3.

A simple residue analytical method using the quick, easy, cheap, effective, rugged, and safe (QuEChERS) procedure for the determination of Trifloxystrobin and its metabolite Trifloxystrobin acid (CGA321113) in tomato and soil was developed using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). The limits of detection were 0.0005 mg/kg for Trifloxystrobin and 0.001 mg/kg for Trifloxystrobin acid, respectively. The average recoveries in tomato and soil ranged from 73-99 % for Trifloxystrobin and 75-109 % for Trifloxystrobin acid, with relative standard deviations below 15 %. The method was then used to study the dissipation and residues in tomato and soil. The dissipation half-lives of Trifloxystrobin in tomato were 2.9 days (Beijing) and 5.4 days (Shandong), while in soil were 1.9 days (Beijing) and 3.0 days (Shandong), respectively. The final results showed that the major residue compound was Trifloxystrobin in tomato whereas it was its metabolite, Trifloxystrobin acid, in soil. The final residues of total Trifloxystrobin (including Trifloxystrobin acid) were below the EU maximum residue limit of 0.5 mg kg(-1) in tomato 3 days after the treatment.

Peer review of the pesticide risk assessment of the active substance Trifloxystrobin

EFSA J 2017 Oct 20;15(10):e04989.PMID:32625286DOI:10.2903/j.efsa.2017.4989.

The conclusions of EFSA following the peer review of the initial risk assessments carried out by the competent authorities of the rapporteur Member State, the United Kingdom, and co-rapporteur Member State, Greece, for the pesticide active substance Trifloxystrobin are reported. The context of the peer review was that required by Commission Implementing Regulation (EU) No 844/2012. The conclusions were reached on the basis of the evaluation of the representative uses of Trifloxystrobin as a fungicide on apple, pear, quince, grapes and strawberry. The reliable end points, appropriate for use in regulatory risk assessment are presented. Missing information identified as being required by the regulatory framework is listed. Concerns are identified.

Trifloxystrobin induces tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in HaCaT, human keratinocyte cells

Drug Chem Toxicol 2017 Jan;40(1):67-73.PMID:27149887DOI:10.1080/01480545.2016.1174871.

As the outermost layer of the body, the skin plays an important role in exposure to pesticides, which could have negative impacts on human health. Trifloxystrobin is a widely used fungicide of the strobilurin class, however, there is little information regarding the skin contact-associated toxic mechanism. Therefore, the present study was performed in order to identify the skin toxicity mechanism of Trifloxystrobin using HaCaT (keratinocyte of human skin) cells. Following 24 or 48 h treatment, cell viability, and subsequent Annexin V-FITC/propidium iodide assay, TUNEL assay and Western blotting were performed to investigate the cell death mechanism of Trifloxystrobin. Exposure to Trifloxystrobin resulted in diminished viability of HaCaT cells in both a time- and concentration-dependent manner. The cell death was derived through apoptotic pathways in the HaCaT cells. Furthermore, we explored the effect of Trifloxystrobin on TRAIL-mediated extrinsic apoptosis using siRNA transfection. Knockdown of death receptor 5 suppressed trifloxystrobin-provoked apoptosis. These results indicate that Trifloxystrobin induces TRAIL-mediated apoptosis and has an inhibitory effect in keratinocytes that can interfere with the barrier function and integrity of the skin. This could be proposed as a mechanism of skin toxicity by Trifloxystrobin and considered in the management of pesticide exposure.