| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg |
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| 100mg |
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| 250mg | |||
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| Targets |
Fluopyram's primary molecular target is succinate dehydrogenase (SDH), also known as Complex II of the mitochondrial electron transport chain. SDH is a key enzyme in the tricarboxylic acid (TCA) cycle and the respiratory chain. It catalyzes the oxidation of succinate to fumarate and the reduction of ubiquinone to ubiquinol, a reaction that is coupled to the production of ATP. By binding to the ubiquinone-binding site of the enzyme, Fluopyram inhibits SDH activity, thereby blocking the flow of electrons in the respiratory chain and disrupting the production of ATP. This energy depletion leads to the death of the fungal cell. Fluopyram's selectivity for fungal SDH over mammalian SDH is the basis for its safety in mammals. It is a potent inhibitor of fungal SDH and is effective at very low concentrations. In addition to its primary target, Fluopyram has been shown to activate the constitutive androstane receptor (CAR) and the pregnane X receptor (PXR), which are nuclear receptors involved in the regulation of drug metabolism. It can also increase the levels of caspase-3, TNF-α, and NF-κB, indicating potential effects on apoptosis and inflammation at higher concentrations. However, its primary mechanism of action is SDH inhibition.
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| ln Vitro |
In vitro studies have characterized Fluopyram's activity as a potent inhibitor of succinate dehydrogenase. Its activity is typically measured using enzyme inhibition assays. In these assays, SDH is isolated from fungal cells (e.g., from Botrytis cinerea), and its activity is measured by monitoring the reduction of a artificial electron acceptor (e.g., 2,6-dichlorophenolindophenol, DCPIP) in the presence of succinate. Fluopyram is added to the reaction at various concentrations, and the inhibition of SDH activity is measured. The IC50 value, which is the concentration required to inhibit 50% of the enzyme activity, is determined from the dose-response curve. In vitro studies have confirmed that Fluopyram is a potent inhibitor of SDH. In addition to enzyme assays, in vitro mycelial growth inhibition assays are performed. In these assays, fungal mycelia are grown on agar plates containing various concentrations of Fluopyram, and the radial growth of the mycelia is measured. The EC50 value, which is the concentration that inhibits 50% of mycelial growth, is determined. These in vitro studies confirm that Fluopyram's antifungal activity is due to its inhibition of SDH.
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| ln Vivo |
In vivo studies have demonstrated Fluopyram's efficacy as a fungicide and nematicide in agricultural settings. In field trials, Fluopyram has been shown to effectively control fungal diseases in a variety of crops, including grapes, vegetables, and cereals. Its efficacy is typically measured by assessing disease severity on treated plants compared to untreated controls. For example, in vineyards, Fluopyram is used to control Botrytis cinerea (gray mold), and its effectiveness is measured by the reduction in the incidence of infected berries. In addition to its fungicidal activity, Fluopyram has nematicidal properties and is used to control plant-parasitic nematodes. In vivo studies have shown that Fluopyram can reduce nematode populations in soil and protect plant roots from damage. The compound is applied to crops as a foliar spray or as a seed treatment. Its systemic properties allow it to be taken up by the plant and provide protection against pathogens. These in vivo studies are crucial for demonstrating the practical utility of Fluopyram in agriculture.
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| Enzyme Assay |
The in vitro enzyme assay for Fluopyram is a standard succinate dehydrogenase (SDH) inhibition assay. In this assay, SDH is typically isolated from a fungal source, such as Botrytis cinerea or a related plant pathogen. The enzyme is incubated with its substrate, succinate, and an artificial electron acceptor, such as 2,6-dichlorophenolindophenol (DCPIP) or a tetrazolium salt. The reduction of the electron acceptor is measured spectrophotometrically, as it is coupled to the oxidation of succinate by SDH. Fluopyram is added to the reaction at various concentrations. The inhibition of the enzyme activity is calculated by comparing the rate of reduction in the presence of the inhibitor to the rate in its absence. The IC50 is determined from the dose-response curve. This assay is a direct measure of Fluopyram's potency at its molecular target. It is used to confirm the compound's mechanism of action and to compare its potency to that of other SDHI fungicides. This is a standard biochemical assay for characterizing SDH inhibitors.
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| Cell Assay |
In vitro cell-based assays for Fluopyram are typically performed using fungal cultures to measure its antifungal activity. The most common assay is the mycelial growth inhibition assay. In this assay, fungal spores or mycelial plugs are placed on the surface of agar plates containing a growth medium and various concentrations of Fluopyram. The plates are incubated under conditions optimal for fungal growth, and the diameter of the fungal colonies is measured after a set period (e.g., 3-7 days). The percent inhibition of mycelial growth is calculated relative to control plates without the compound. The EC50, which is the effective concentration that inhibits 50% of mycelial growth, is determined. Another cell-based assay is the spore germination inhibition assay, where fungal spores are incubated in liquid medium with Fluopyram, and the germination rate is measured microscopically. These cell-based assays are used to determine the potency of Fluopyram against specific fungal pathogens and to screen for resistance. They are standard assays in agricultural research.
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| Animal Protocol |
In vivo animal experiments for Fluopyram are primarily conducted to assess its toxicological profile and environmental fate, rather than its efficacy as a fungicide (which is studied in plants). Standard toxicological studies are conducted in rodents (rats and mice) and sometimes in dogs to determine its acute and chronic toxicity. In a typical acute toxicity study, a single dose of Fluopyram is administered to animals by oral gavage, and the animals are observed for 14 days to determine the LD50 (lethal dose for 50% of the population). In a subchronic toxicity study, animals are administered Fluopyram daily for 28 or 90 days, and various parameters are measured, including body weight, food consumption, hematology, clinical chemistry, and histopathology of major organs. These studies are required for the registration of Fluopyram as a pesticide to ensure its safety for human health and the environment. They provide data on its potential for toxicity, carcinogenicity, and reproductive and developmental toxicity.
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| ADME/Pharmacokinetics |
The pharmacokinetic (PK) properties of Fluopyram are important for understanding its behavior in the environment and in mammals. After administration, Fluopyram is absorbed and distributed throughout the body. It is metabolized in the liver by cytochrome P450 enzymes. The primary metabolic pathway involves hydroxylation and oxidation. The metabolites are excreted primarily in the urine and feces. Fluopyram has a molecular weight of 396.7 g/mol and a molecular formula of C16H11ClF6N2O, indicating it is a relatively lipophilic molecule. Its logP is not provided, but its structure suggests it has moderate lipophilicity, which influences its absorption and distribution. For research use, Fluopyram is available as a PESTANAL analytical standard for residue testing. Its stability is ensured by storing it under recommended conditions. Understanding its PK is crucial for assessing its potential for bioaccumulation and its persistence in the environment.
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| Toxicity/Toxicokinetics |
Fluopyram is considered to have low acute toxicity to mammals. However, like all pesticides, it can be harmful if ingested, inhaled, or absorbed through the skin in large amounts. It is classified as Aquatic Chronic 2, indicating it is hazardous to aquatic life with long-lasting effects. In toxicological studies, Fluopyram has been shown to activate CAR and PXR nuclear receptors, which are involved in the regulation of drug metabolism. It can also increase the levels of caspase-3, TNF-α, and NF-κB, indicating potential effects on apoptosis and inflammation at higher concentrations. The safety of Fluopyram for humans is ensured by the establishment of maximum residue limits (MRLs) in food products. For agricultural workers, appropriate safety measures, including the use of personal protective equipment (PPE), are recommended to minimize exposure. As a pesticide, its use is regulated by government agencies to protect human health and the environment.
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| References | |
| Additional Infomation |
Fluopyram belongs to the benzamide class of compounds, formed by the condensation of the carboxyl group of 2-(trifluoromethyl)benzoic acid with the amino group of 2-[3-chloro-5-(trifluoromethyl)pyridin-2-yl]ethylamine. It is a fungicide used for foliar spraying and seed treatment to control gray mold, powdery mildew, and other diseases. It is an EC 1.3.5.1 [succinate dehydrogenase (quinone)] inhibitor and antifungal pesticide. It belongs to the benzamide class, organochlorine compounds, pyridine compounds, and (trifluoromethyl)benzene compounds, and is also a benzamide fungicide.
Fluopyram is a commercial fungicide and nematicide developed by Bayer Crop Science. It is registered for agricultural use in many countries and is used to protect a wide range of crops from fungal diseases and nematode damage. It is particularly effective against Botrytis spp. (gray mold), Sclerotinia spp., Monilia spp., powdery mildews, and leaf spot diseases. It is applied as a foliar spray or as a seed treatment. In China, Fluopyram is registered for various crops and is valued for its dual fungicidal and nematicidal activity. Its mechanism of action as an inhibitor of succinate dehydrogenase (SDH) places it in the SDHI class of fungicides. This class of fungicides is widely used in agriculture, and resistance management strategies are important to maintain their efficacy. Fluopyram is also available as an analytical standard (PESTANAL) for residue testing. It is not a therapeutic drug and is not approved for any medical use. Its use is strictly regulated to ensure food safety and environmental protection. |
| Molecular Formula |
C16H11N2OF6CL
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|---|---|
| Molecular Weight |
396.71474
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| Exact Mass |
396.046
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| CAS # |
658066-35-4
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| PubChem CID |
11158353
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| Appearance |
White to off-white solid powder
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| LogP |
5.136
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
8
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
26
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| Complexity |
484
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
KVDJTXBXMWJJEF-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C16H11ClF6N2O/c17-12-7-9(15(18,19)20)8-25-13(12)5-6-24-14(26)10-3-1-2-4-11(10)16(21,22)23/h1-4,7-8H,5-6H2,(H,24,26)
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| Chemical Name |
N-[2-[3-chloro-5-(trifluoromethyl)pyridin-2-yl]ethyl]-2-(trifluoromethyl)benzamide
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~125 mg/mL (~315.09 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.24 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (5.24 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.5207 mL | 12.6037 mL | 25.2073 mL | |
| 5 mM | 0.5041 mL | 2.5207 mL | 5.0415 mL | |
| 10 mM | 0.2521 mL | 1.2604 mL | 2.5207 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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