| Size | Price | Stock | Qty |
|---|---|---|---|
| 100mg |
|
||
| 250mg | |||
| Other Sizes |
| Targets |
Abamectin acts primarily as an agonist at two types of ligand-gated chloride channels in invertebrates: the glutamate-gated chloride channels (GluCls) and the GABA-gated chloride channels (GABACls). It binds irreversibly to subunit interfaces of these Cys-loop receptor channels, leading to sustained chloride ion influx, hyperpolarization of nerve and muscle cell membranes, flaccid paralysis, and ultimately death of the target pest. In mammals, GABA receptors are confined to the central nervous system, but the blood-brain barrier largely prevents abamectin from accessing these sites, conferring a favorable safety margin. In vertebrates, avermectins also exert a blocking action on GABA-gated chloride channels, which at lower doses manifests as coarse tremors, while at higher concentrations channel activation suppresses neuronal activity.
|
|---|---|
| ln Vitro |
Avermectin B1 (0 - 80 μM, 12 h) causes ROS-mediated DNA damage and cytotoxicity in murine fibroblasts (MEFs) through ATM/ATR and MAPK [1]. Avermectin B1 (10 μM, 24 h) causes a considerable amount of cytotoxicity by causing ROS overproduction in Chinese mitten crab hemocytes. G.pallida is toxically killed by /mL, 72 h) [2]. In MGC803 cells, avermectin B1 (4 μM, 24 h) inhibits ROS-mediated PI3K/AKT signal fluorescence, hence inducing autophagy and cell fluorescence [4].
In vitro studies have demonstrated potent bioactivity of abamectin against various target organisms. In Sf9 cell assays (derived from Spodoptera frugiperda), abamectin at concentrations of 5–15 μg/mL inhibited cell growth and induced apoptotic cell death in a time- and dose-dependent manner, with proliferation inhibition rates reaching 30.74–39.27% after 72 hours of treatment and maximum apoptosis rates of 24.13–27.29%. In root-knot nematode (Meloidogyne spp.) assays, the most effective formulation exhibited larvicidal activity with an LC₅₀ of 21.66 μg/mL, and egg-hatching inhibition with LC₅₀ values of 12.83–13.57 μg/mL. In mouse embryonic fibroblast (MEF) cells, abamectin reduced cell viability with an IC₅₀ of 45.6 μM after 12-hour exposure. |
| ln Vivo |
Avermectin B1 (powder coating, 0.2 mg/kg single dosage) works wonders against Onchocera microfilariae and Strongyloides equine [5].
In vivo studies confirm abamectin’s efficacy against a range of agricultural pests and parasites. In cucumber plants infected with root-knot nematodes, abamectin formulations achieved general mean reductions in root galls of 23.05–75.23%, reductions in egg masses of 14.46–65.63%, and total population density reductions of 39.24–87.08%. In leaf-dipping assays against second-instar larvae of Spodoptera frugiperda, abamectin exhibited an LC₅₀ of 8.33 mg/L one day post-treatment. In a horse model (pruritic dermatosis), oral administration of abamectin at 0.2 mg/kg as a single dose significantly decreased mean strongyle egg counts at days 14, 28, and 42 post-treatment, and resulted in zero microfilaria counts by day 14. |
| Enzyme Assay |
Radioligand binding assays are the standard method for studying abamectin’s interaction with its receptor targets. Typically, crude membrane homogenates prepared from target tissues (e.g., insect heads or nematode whole bodies) are incubated with tritium-labeled abamectin (³H-abamectin) in binding buffer (e.g., 50 mM Tris-HCl, pH 7.4) at room temperature for 60–120 minutes. Non-specific binding is determined in the presence of excess unlabeled abamectin (10–100 μM). Bound and free radioligands are separated by rapid vacuum filtration through glass fiber filters (e.g., Whatman GF/B), followed by three washes with ice-cold buffer. Filter-bound radioactivity is quantified by liquid scintillation counting. Scatchard analysis yields binding parameters: Kd (dissociation constant, typically ~10–11 nM for GABAA receptors) and Bmax (maximum binding capacity). In resistance studies, the Kd value between susceptible and resistant strains may not differ significantly, but a reduction in Bmax (e.g., a 63.6% decrease) indicates a reduction in receptor number rather than altered affinity.
|
| Cell Assay |
Cell viability assay [1]
Cell Types: mouse embryonic fibroblasts [3]. (MEF) Cell Tested Concentrations: 0, 0.5, 5, 10, 20, 40, 80 μM Incubation Duration: 12 hrs (hours) Experimental Results: Cell viability diminished, IC50 value was 45.6 μM. Western Blot Analysis [3] Cell Types: MGC803 Cell Tested Concentrations: 0-4 μM Incubation Duration: 24 h Experimental Results: The expression of active caspase-3 and Bax/Bcl-2 increased, and MMP diminished in a dose-dependent manner. A typical in vitro cytotoxicity protocol using Drosophila melanogaster S2 cells is as follows: S2 cells are seeded at a density of 1×10⁵ cells per well in 96-well plates containing Schneider‘s medium supplemented with 15% FBS, penicillin/streptomycin (50 U/mL, 50 μg/mL), and gentamicin (50 μg/mL). Abamectin is added to cultures at a final concentration of 10 μM (with DMSO as vehicle control, DMSO concentration matched to the highest compound concentration). Cultures are maintained for 7 days, with one-quarter of the medium replaced three times per week (every 48–72 hours). Cell viability is assessed daily using the AlamarBlue® assay: 120 μL of medium is removed from each well and replaced with 80 μL of AlamarBlue prediluted 1:10 in Schneider’s medium. After 1.5 hours of incubation at 37°C, fluorescence intensity is measured (excitation 530 nm/emission 590 nm) using a microplate reader. Proliferation inhibition rates and apoptosis induction can be further evaluated by flow cytometry, morphological analysis, and Western blot. The Sf9 cell line (Spodoptera frugiperda) is also commonly used for similar assays. |
| Animal Protocol |
Animal/Disease Models: Horse (with pruritic skin disease) [5]
Doses: 0.2 mg/kg, single dose. Route of Administration: Oral Experimental Results: Mean Strongyloides egg counts were diminished at 14, 28 and 42 days after treatment, and all horses had zero microfilariae counts after 14 days of treatment. Animal/Disease Models: Healthy adult ewes (pharmacokinetic/PK/PK determination) [6] Doses: 0.2 mg/kg Route of Administration: subcutaneous injection (left neck of each sheep) Experimental Results: pharmacokinetic/PK/PK characteristics of abamectin B1 Parameter average Kcl (/day) 0.17 t1 /2cl (day) 4.36 Kab (/day) 0.24 t1/2ab (day) 3.15 Cmax (ng/mL) 6.24 tmax (day) 4.20 AUC (0-27) (ng/day /mL) 80.2 AUC(0-∞) ) (ng/day/mL) 84.7 MRT (day) 8.80 A representative in vivo protocol for efficacy testing in plant systems: Cucumber (Cucumis sativus L.) plants grown in pots containing sterilized soil are inoculated with root-knot nematodes (e.g., Meloidogyne incognita) at a rate of approximately 3,000 eggs and second-stage juveniles per pot. Abamectin formulations (e.g., DIVA 1.8% EW, RIOMECTIN 5% ME, AGRIMEC GOLD 8.4% SC, or ZORO 3.6% EC) are applied as soil drenches at recommended field rates. Treatments are typically applied at planting and repeated once at 30 days post-planting. After approximately 60–90 days of growth, plants are carefully uprooted and root systems are washed free of soil. Parameters evaluated include: number of root galls per root system, egg mass counts, total nematode population density in soil and roots, and plant growth parameters (root dry weight, shoot dry weight, plant height). Efficacy is expressed as percent reduction relative to untreated control. In mammalian models (e.g., rats), abamectin is typically administered orally by gavage at doses ranging from sublethal (e.g., 2 mg/kg for 5 days) to acute toxicity studies (LD₅₀ determination). |
| ADME/Pharmacokinetics |
The pharmacokinetic profile of abamectin varies by species and route of administration. In dairy sheep following subcutaneous administration (0.2 mg/kg), the elimination half-life (t₁/₂) in blood plasma is 1.7 days with a mean residence time (MRT) of 3.7 days; in milk, t₁/₂ is 1.9 days with MRT of 3.8 days. The milk-to-plasma concentration ratio is approximately 0.89, primarily dependent on milk fat content. In lambs suckling treated ewes, mean maximal plasma concentration reaches 1.6 μg/L at 3.3 days, with an elimination half-life of 2.7 days. Abamectin is detectable in ewe plasma and milk for up to 23 days post-administration, but lamb exposure is only about 10% of the maternal exposure, even though only 1.0% of the administered dose is excreted in milk. In another study, the terminal half-life was reported as 28 hours with absolute oral bioavailability of 69.7%. Abamectin undergoes extensive metabolism, is highly lipophilic, and distributes widely into tissues. In agricultural settings, residues on crops dissipate over time; for example, in green beans, abamectin residues follow first-order degradation kinetics.
|
| Toxicity/Toxicokinetics |
The acute oral LD₅₀ of abamectin in rats is 10 mg/kg, classifying it as highly toxic to mammals via the oral route; the dermal LD₅₀ in rats is >2000 mg/kg, indicating low dermal toxicity. In mice, reported oral LD₅₀ values range from 13.5 to 24 mg/kg. Chronic toxicity studies in dogs established a no-effect level (NEL) of 1.5 mg/kg/day (oral, 1 year). Abamectin is not genotoxic, as demonstrated in a variety of standard tests for mutagenicity, clastogenicity, and unscheduled DNA synthesis. While it is generally safe in mammals at therapeutic doses due to the blood-brain barrier, high doses can induce neurotoxic symptoms including ataxia, tremors, mydriasis, depression, recumbency, and coma—reflecting its GABAA agonism. The compound exhibits high oral toxicity to mammals, with some evidence of negative reproductive effects at high doses. It is highly toxic to aquatic organisms and bees, and poses moderate to high toxicity to most fauna and flora. However, its low aqueous solubility and strong binding to soil particles minimize environmental mobility and groundwater contamination risk. Notably, dog breeds with the MDR-1 gene defect are exceptionally sensitive to macrocyclic lactone toxicity.
|
| References |
[1]. Yiran Liang, et al. Abamectin induces cytotoxicity via the ROS, JNK, and ATM/ATR pathways. PLoS One. Environ Sci Pollut Res Int. 2020 Apr;27(12):13726-13734.
[2]. Nicola Sasanelli, et al. Abamectin Efficacy on the Potato Cyst Nematode Globodera pallida. Plants (Basel). 2019 Dec 19;9(1):12. [3]. Yi Huang, et al. Cytotoxicity induced by abamectin exposure in haemocytes of Chinese mitten crab, Eriocheir sinensis. Environ Toxicol Pharmacol. 2020 Jul;77:103384. [4]. Shanshan Zhu, et al. Abamectin induces apoptosis and autophagy by inhibiting reactive oxygen species-mediated PI3K/AKT signaling in MGC803 cells. J Biochem Mol Toxicol. 2019 Jul;33(7):e22336. [5]. Mogg TD, et al. Efficacy of avermectin B1 given orally against equine intestinal strongyles and Onchocera microfilaria. Aust Vet J. 1990 Nov;67(11):399-401. [6]. Peyami Sari, et al. Pharmacokinetics of Abamectin/Levamisole Combination in a Medium Chain Mono and Diglyceride-Based Vehicle and an In Vitro Release and In Vitro In Vivo Correlation Study for Levamisole. AAPS PharmSciTech. 2017 May;18(4):1254-1260. |
| Molecular Formula |
C95H142O28
|
|---|---|
| Molecular Weight |
1732.15
|
| Exact Mass |
1730.9688
|
| CAS # |
71751-41-2
|
| PubChem CID |
6435890
|
| Appearance |
White to off-white solid powder
|
| Density |
1.2±0.1 g/cm3
|
| Boiling Point |
940.9±65.0 °C at 760 mmHg
|
| Melting Point |
150-155°C
|
| Flash Point |
268.1±27.8 °C
|
| Vapour Pressure |
0.0±0.6 mmHg at 25°C
|
| Index of Refraction |
1.571
|
| LogP |
6.51
|
| Hydrogen Bond Donor Count |
6
|
| Hydrogen Bond Acceptor Count |
28
|
| Rotatable Bond Count |
15
|
| Heavy Atom Count |
123
|
| Complexity |
3430
|
| Defined Atom Stereocenter Count |
38
|
| SMILES |
C[C@@H](CC)[C@]1([H])[C@@H](C)C=C[C@@]2(O[C@@]3([H])C[C@]([H])(OC([C@@]4([H])[C@@](/C(CO5)=C/C=C/[C@H](C)[C@H](O[C@@]6([H])C[C@H](OC)[C@@H](O[C@]7([H])O[C@@H](C)[C@H](O)[C@@H](OC)C7)[C@H](C)O6)/C(C)=C/C3)(O)[C@@]5([H])[C@H](O)C(C)=C4)=O)C2)O1.C[C@H]8C=C[C@@]9(O[C@@]%10([H])C[C@]([H])(OC([C@@]%11([H])[C@@](/C(CO%12)=C/C=C/[C@H](C)[C@H](O[C@@]%13([H])C[C@H](OC)[C@@H](O[C@]%14([H])O[C@@H](C)[C@H](O)[C@@H](OC)C%14)[C@H](C)O%13)/C(C)=C/C%10)(O)[C@@]%12([H])[C@H](O)C(C)=C%11)=O)C9)O[C@@H]8C(C)C
|
| Chemical Name |
Avermectin B(sub 1)
|
| Synonyms |
Abamectin AgrimekAvidAvid ECAffirmAgri-MekEPA Pesticide Chemical Code 122804MK 0936MK 936VertimecZephyrHSDB 6941Avomec
|
| HS Tariff Code |
2934.99.9001
|
| 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)
|
| Solubility (In Vitro) |
DMSO : ~250 mg/mL (~286.34 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (2.38 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 (2.38 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. 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 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.08 mg/mL (2.38 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.5773 mL | 2.8866 mL | 5.7732 mL | |
| 5 mM | 0.1155 mL | 0.5773 mL | 1.1546 mL | |
| 10 mM | 0.0577 mL | 0.2887 mL | 0.5773 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.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT02533336 | TERMINATED | Drug: abamectin and fenpyroximate | Malaria | National Institute for Medical Research, Tanzania | 2015-11-09 | Phase 3 |
| NCT01869205 | COMPLETED | Device: Endobronchial valve | Pulmonary Emphysema | Asan Medical Center | 2013-03 | Phase 3 |
|
|
|
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
