Emamectin Benzoate
Based on 2 publication(s) in Google Scholar
Emamectin Benzoate (MK-244) is an orally active nervoussystem toxicant by binding g-aminobutyric (GABA) receptor in insects. Emamectin Benzoate is one of semi-synthetic derivative of Avermectin (HY-15311) with a broadspectrum of insecticidal and acaricidal activity. Emamectin Benzoate induces ROS-mediated DNA damage and cell apoptosis. Emamectin Benzoate, a mixture of the natural Emamectin B1a benzoate and Emamectin B1b benzoate, has the main component of Emamectin B1a benzoate.
For research use only. We do not sell to patients.
- Purity : 98.83%
- CAS No.: 155569-91-8
- Formula: C49H75NO13.C7H6O2
- Molecular Weight:1008.24(Based on Emamectin B1a Benzoate)
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Storage:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications Citing Use of MedChemExpress (MCE) Emamectin Benzoate
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Biological Activity
Description
IC50 & Target
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Mite |
In Vitro
Emamectin Benzoate (MK-244; 2.5-40 μM; 12 and 24 h) decreases cell viability in a time- and dose-dependent manner[1].
Emamectin Benzoate (2.5-20 μM; 24 hours) induces apoptosis and DNA damage in 16HBE cells. Emamectin Benzoate induces ROS generation in 16HBE cells[1].
Emamectin Benzoate (2.5-20 μM; 12 hours) increases the amounts of cytochrome-c, caspase-3, cas-pase-9, cleaved-PARP, Bax/Bcl-2[1].
Emamectin Benzoate (2.5, 5, 10, 15 μM; 72 h) inhibits cell viability with an IC50 of 3.72 μM in Trichoplusia Tn5B1-4 cell. Emamectin Benzoat induces chromatin condensation in nuclei and cell apoptosis[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human normal bronchial epithelial cell line 16HBE
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Concentration:2.5, 5, 7.5,10,15, 20, 40 μM
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Incubation Time:12 and 24 hours
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Result:Decreased cell viability in a time- and dose-dependent manner wirh IC50s of 11.88 μM and 9.67 μM in 12 and 24 hours, respectively.
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Cell Line:human normal bronchial epithelial cell line 16HBE
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Concentration:2.5, 5, 10, 20 μM
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Incubation Time:24 hours
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Result:Induced apoptosis and caused chromatin shrinkage and nuclear fragmentation.
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Cell Line:human normal bronchial epithelial cell line 16HBE
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Concentration:2.5, 5, 10, 20 μM
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Incubation Time:12 hours
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Result:Increased the amounts of cytochrome-c, caspase-3, cas-pase-9, cleaved-PARP, Bax/Bcl-2.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:10 weeks old Swiss albino male mice (25-30 g)[3]
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Dosage:25, 50, 100 mg/kg
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Administration:Oral; daily; for 14 days
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Result:Caused a marked induction of oxidative damage in liver tissue as demonstrated by an increased level of TBARS and reduced GSH level.
Chemical Information
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CAS No. 155569-91-8
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Appearance Solid
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Molecular Weight 1008.24(Based on Emamectin B1a Benzoate)
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Formula C49H75NO13.C7H6O2
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Color White to off-white
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SMILES
C[C@H]1O[C@@H](O[C@@]2([H])[C@H](C)O[C@@H](O[C@]([C@@H](C)/C=C/C=C3CO[C@@]4([H])[C@]\3(O)[C@H]5C=C(C)[C@H]4O)([H])/C(C)=C/C[C@@H]6C[C@H](OC5=O)C[C@]7(C=C[C@H](C)[C@@H](C(C)C)O7)O6)C[C@@H]2OC)C[C@@H](OC)[C@@H]1NC.C[C@H]8O[C@@H](O[C@@]9([H])[C@H](C)O[C@@H](O[C@]([C@@H](C)/C=C/C=C%10CO[C@@]%11([H])[C@]\%10(O)[C@H]%12C=C(C)[C@H]%11O)([H])/C(C)=C/C[C@@H]%13C[C@H](OC%12=O)C[C@]%14(C=C[C@H](C)[C@@H]([C@H](CC)C)O%14)O%13)C[C@@H]9OC)C[C@@H](OC)[C@@H]8NC.O=C(O)C%15=CC=CC=C%15
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Synonyms
MK-244
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Publications (2)
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Journal Impact Factor
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Most Recent
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Nat Commun
Enhancing tandem mass spectrometry-based metabolite annotation with online chemical labeling. [Abstract]2025 Jul 26;16(1):6911. PMID: 40715063 -
Toxicol Appl Pharmacol
Proteome profiling of emamectin-treated primary rat cortical cells following up to twelve days in vitro exposure. [Abstract]2026 Jun:511:117824. PMID: 42009082
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.08 mg/mL; Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 2.08 mg/mL; Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Genotoxicity/Mutagenicity Study
The bacterial reverse mutation assay detects point mutations that restore amino-acid prototrophy in auxotrophic Salmonella typhimurium or Escherichia coli tester strains; after exposure to a test article, mutagenic activity is read out as an increased number of revertant colonies on minimal agar compared with the vehicle control. The assay uses tester strains with different mutation targets so that base-substitution and frameshift mutagens can be detected, and testing is performed with and without exogenous mammalian metabolic activation because some chemicals require biotransformation to become mutagenic.
Purity & Documentation
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Data Sheet (290 KB)
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SDS (623 KB)
- English - EN (623 KB)
- Français - FR (623 KB)
- Deutsch - DE (623 KB)
- Norwegian - NO (623 KB)
- Español - ES (623 KB)
- Swedish - SV (623 KB)
- Italian - IT (623 KB)
- Korean - KR (623 KB)
- Portuguese - PT (623 KB)
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Handling Instructions (2659 KB)
References
[1]. Chenguang Niu, et al. Toxic effects of the Emamectin Benzoate exposure on cultured human bronchial epithelial (16HBE) cells. Environ Pollut. 2020 Feb;257:113618. [Content Brief]
[2]. Shaorong Luan, et al. Emamectin benzoate induces ROS-mediated DNA damage and apoptosis in Trichoplusia Tn5B1-4 cells. Chem Biol Interact. 2017 Aug 1;273:90-98. [Content Brief]
[3]. Özge Temiz, et al. Biopesticide emamectin benzoate in the liver of male mice: evaluation of oxidative toxicity with stress protein, DNA oxidation, and apoptosis biomarkers. Environ Sci Pollut Res Int. 2020 Jun;27(18):23199-23205. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)