Emamectin

888.13

1007.56000

IX4GP7848F

DTXSID80153164

White to off-white powder|Off-white crystalline powder

199.16000

7.38020

1.21g/cm3

141-146 °C /Emamectin benzoate/

935ºC at 760 mmHg

519.3ºC

1.565

In water, 0.024 g/L at 25 °C (pH 7) /Emamectin benzoate/

Keep container tightly closed in a dry and well-ventilated place. Keep in a dry place.

3.8X10-8 mm Hg at 21 °C /Emamectin benzoate/

Specific optical rotation: -6.9 deg (c = 0.5% in methanol)

pKa: 4.18 (acidic, attributed to benzoate counter ion), 8.71 (basic, attributed to emamectin moiety)

300.62 Ų [M+H]+

log Kow: 3.0 (pH 5.1); pKa: 4.2, 7.6; water solubility: 0.32 mg/mL at pH 5 /Emamectin benzoate/|Stable to hydrolysis at pH 5, 6, 7 and 8 (25 °C). Photodegrades rapidly.|Henry's Law constant = 1.7X10-9 atm-cu m/mol at 21 °C (estimated from vapor pressure and water solubility)|Hydroxyl radical reaction rate constant = 6.5X10-10 cu cm/molec-sec at 25 °C (est)

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.|Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.|Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber.|...Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber.

USDA; Emamectin benzoate Human Health and Ecological Risk Assessment FINAL REPORT, October 28, 2010[USDA; Emamectin benzoate Human Health and Ecological Risk Assessment FINAL REPORT, October 28, 2010; Available from, as of March 13, 2014: http://www.fs.fed.us/foresthealth/pesticide/pdfs/052-23-03b_Emamectin-benzoate.pdf]|California Environmental Protection Agency/Department of Pesticide Regulation; Toxicology Data Review Summaries.[Available from, as of February 8, 2008: http://www.cdpr.ca.gov/docs/risk/toxsums/toxsumlist.htm]

Skin and body protection Complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Face shield and safety glasses Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Respiratory protection Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N99 (US) or type P2 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).|Handle with gloves. Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide... Wear self contained breathing apparatus for fire fighting if necessary.

Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.|Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.|Wear respiratory protection. Avoid dust formation. Avoid breathing vapours, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust.

Toxic if swallowed... If swallowed Never give anything by mouth to an unconscious person. Rinse mouth with water. Consult a physician.|Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. Normal measures for preventive fire protection.

House flies, Musca domestica L., are important pests of dairy operations worldwide, with the ability to adapt wide range of environmental conditions. There are a number of insecticides used for their management, but development of resistance is a serious problem. Insecticide mixtures could enhance the toxicity of insecticides in resistant insect pests, thus resulting as a potential resistance management tool. The toxicity of bifenthrin, cypermethrin, deltamethrin, chlorpyrifos, profenofos, emamectin benzoate and fipronil were assessed separately, and in mixtures against house flies. A field-collected population was significantly resistant to all the insecticides under investigation when compared with a laboratory susceptible strain. Most of the insecticide mixtures like one pyrethroid with other compounds evaluated under two conditions (1?1-"A" and LC50: LC50-"B") significantly increased the toxicity of pyrethroids in the field population. Under both conditions, the combination indices of pyrethroids with other compounds, in most of the cases, were significantly below 1, suggesting synergism. The enzyme inhibitors, PBO and DEF, when used in combination with insecticides against the resistant population, toxicities of bifenthrin, cypermethrin, deltamethrin and emamectin were significantly increased, suggesting esterase and monooxygenase based resistance mechanism. The toxicities of bifenthrin, cypermethrin and deltamethrin in the resistant population of house flies could be enhanced by the combination with chlorpyrifos, profenofos, emamectin and fipronil. The findings of the present study might have practical significance for resistance management in house flies.

LD50 Mouse (female) oral (gavage) 165 mg/kg /Benzoate-methyl t-butyletherate (MBTE) solvates of emamectin, 96.4% pure/|LD50 Mouse (female) oral (gavage) 141 mg/kg /Benzoate monohydrate solvates of emamectin, 99.1% pure/|LD50 Rat (female) oral (gavage) 53 mg/kg /Benzoate-methyl t-butyletherate (MBTE) solvates of emamectin, 96.4% pure/|LD50 Rat (female) oral (gavage) 58 mg/kg /Benzoate monohydrate solvates of emamectin, 99.1% pure/|LD50 Mouse oral (gavage) 107 mg/kg

/BIRDS and MAMMALS/ Nineteen- to 26-week-old mallard ducks (Anas platyrhynchos) were found to be more sensitive than northern bobwhite quail (Colinus virginianus) of the same age to single oral doses of emamectin benzoate. The resulting median lethal dose values determined for emamectin benzoate to mallard duck and northern bobwhite quail were 76 and 264 mg/kg, respectively, and the no-observed-effect levels were <25 and 25 mg/kg, respectively. Exposure of 10-day-old mallard ducks and bobwhite quail to emamectin benzoate in feed also gave relatively high median lethal concentration (LC50) values of 570 and 1,318 ppm, respectively, and no-observed-effect concentrations of 20 and <125 ppm, respectively. Clinical signs of toxicity included lethargy, ruffled appearance, loss of righting reflex, and reduction in food consumption; these signs appeared to be fully reversible with cessation of exposure. The maximum residue level of emamectin benzoate found in field-treated foliage is several-fold (7,125-16,475) less than these LC50 values. Because the likely primary route of emamectin benzoate exposure to birds is through treated food in the diet, these results indicate minimal acute risk to avians from emamectin benzoate use in crop protection.|/BIRDS and MAMMALS/ Avian reproduction studies were performed in both the mallard and the northern bobwhite. Emamectin benzoate was incorporated into the diets of the two avian species prior to and during a period of reproduction. Mallards were exposed at dietary concentrations of 0, 4, 8, 20, or 40 ppm of emamectin benzoate for 20 weeks, whereas northern bobwhites were exposed to dietary concentrations of 0, 4, 13, 40, or 125 ppm of emamectin benzoate for 22 weeks. Birds were monitored for body weight, feed consumption, general health, and reproductive parameters. At the end of the reproduction period, all adult birds were examined for gross morphologic changes, and adult birds in the high-dose concentration groups were examined for neuropathologic effects. No treatment-related mortalities, overt signs of toxicity, or treatment-related effects on adult body weight or feed consumption occurred at any of the concentrations tested in either species. No treatment-related effects were observed upon any of the reproductive parameters measured. Emamectin benzoate did not induce gross or light microscopic lesions in the brain, spinal cord, or peripheral nerves to the level of the distal branches of the sciatic nerve, including the tibial nerve, in either the mallard or northern bobwhite. The no observed effect concentrations for mallards and northern bobwhites exposed to emamectin benzoate in the diet were 40 ppm and 125 ppm, respectively.|/AQUATIC SPECIES/ The potential impact of commercial salmon aquaculture along the coast of British Columbia on the health of non-target marine wildlife is of growing concern. In the current initiative, the biological effects on gene expression within spot prawn (Pandalus platyceros) exposed to the sea lice controlling agent, emamectin benzoate (EB; 0.1-4.8 mg/kg sediment), were investigated. A mean sediment/water partitioning coefficient (K(p)) was determined to be 21.81 and significant levels of EB were detected in the tail muscle tissue in all exposed animals. Animals selected for the experiment did not have eggs and were of similar weight. Significant mortality was observed within 8 days of EB treatment at concentrations between 0.1 and 0.8 mg/kg and there was no effect of EB on molting. Twelve spot prawn cDNA sequences were isolated from the tail muscle either by directed cloning or subtractive hybridization of control versus EB exposed tissues. Three of the transcripts most affected by EB exposure matched sequences encoding the 60S ribosomal protein L22, spliceosome RNA helicase WM6/UAP56, and the intracellular signal mediator histidine triad nucleotide binding protein 1 suggesting that translation, transcription regulation, and apoptosis pathways were impacted. The mRNA encoding the molting enzyme, beta-N-acetylglucosaminidase, was not affected by EB treatment. However, the expression of this transcript was extremely variable making it unsuitable for effects assessment. The results suggest that short-term exposure to EB can impact biological processes within this non-target crustacean.|/AQUATIC SPECIES/ Emamectin benzoate is one of the active ingredients of the anti-sealice drug SLICE. Ten-day acute sediment lethal tests (10-day LC50) of emamectin benzoate and its desmethyl metabolite (AB1) were conducted to determine LC50 values using a sensitive representative West Coast amphipod crustacean, Eohaustorius estuarius. The 10-day LC50s of emamectin benzoate and AB1 to E. estuarius were 0.185 and 0.019 mg/kg wet weight sediment (0.146 and 0.015 mg/kg dry wt), respectively. The degradation properties of emamectin benzoate and AB1 during the 10-day period were also measured and described. No obvious decay patterns were observed for either emamectin benzoate and AB1 over the 10-day period.|For more Ecotoxicity Excerpts (Complete) data for EMAMECTIN (8 total), please visit the HSDB record page.

Emamectin benzoate is an avermectin class insecticide which consists of homologous semi-synthetic macrolides that are derived from the natural fermentation products of Streptomyces bacteria(1).

Emamectin benzoate's production may result in its release to the environment through various waste streams; its use as an insecticide(1) , use in prevention of emerald ash borer in ash trees(2) and to control sea lice in salmond aqua culture operations(3) will result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an observed Koc range of 2.5X10+4 to 7.3X10+5(2),indicates that emamectin benzoate is expected to be immobile in soil(SRC). Volatilization of emamectin benzoate from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.7X10-9 atm-cu m/mole(SRC), derived its vapor pressure, 3.8X10-8 mm Hg(3), and water solubility, 24 mg/L(3). Emamectin benzoate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(SRC). A primary dissipation pathway of emamectin benzoate in the terrestrial environment is expected to be through photolysis on soil surfaces which has a half-life of 5 days(4). Emamectin benzoate biodegrades slowly in soil(4). In one aerobic soil study, emamectin benzoate had an initial microbial degradation half-life of 74 days (over a 60-day period) which slowed after that time to a half-life of 349 days(5); biodegradation was slower in anaerobic conditions(5). Emamectin benzoate is stable to abiotic hydrolysis at a pH range of 5.2-8.0, but has a hydrolysis half-life of 19.5 weeks at pH 9(6); therefore, hydrolysis may have some importance in alkaline soils of pH 9 or higher(SRC).|AQUATIC FATE: Based on a classification scheme(1), an observed Koc range of 2.5X10+4 to 7.3X10+5(2), indicates that emamectin benzoate is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.7X10-9 atm-cu m/mole(SRC), derived from its vapor pressure, 3.8X10-8 mm Hg(4), and water solubility, 24 mg/L(4). According to a classification scheme(5), observed fish BCF values of 30(6) and 69(7), suggest the potential for bioconcentration in aquatic organisms is moderate. Emamectin benzoate is stable to abiotic hydrolysis at a pH range of 5.2-8.0, but has a hydrolysis half-life of 19.5 weeks at pH 9(8). Photodegradation is expected to be an important fate process in natural waters exposed to sunlight(SRC). Using autumn sunlight in New Jersey, the photodegradation half-lives of 14C-labeled emamectin benzoate in aqueous buffer (pH 7), in natural pond water, and in a sensitized aqueous buffer were 22.4, 6.9 and 1.4 days respectively(9). These results demonstrate that emamectin benzoate is susceptible to direct photolysis with the rate of photodegradation increasing due to sensitized photolysis(9). Although emamectin benzoate degrades rapidly via aqueous photolysis, other than oligotrophic systems (clear, shallow water bodies with low organic matter content), aqueous photolysis may have a limited contribution in removing emamectin benzoate from water(7). Emamectin benzoate biodegrades slowly in soil(7); therefore, biodegradation in natural water may be slow(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), emamectin benzoate, which has a vapor pressure of 3.8X10-8 mm Hg at 21 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase emamectin benzoate is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 36 minutes(SRC), calculated from its rate constant of 6.5X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Vapor-phase emamectin benzoate is also degraded in the atmosphere by reaction with ozone(SRC); the half-life for this reaction in air is estimated to be 14 minutes(SRC), calculated from its rate constant of 1.2X10-15 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase emamectin benzoate may be removed from the air by wet and dry deposition(SRC). Emamectin benzoate is susceptible to direct photolysis in sunlight(4).

The rate constant for the vapor-phase reaction of emamectin benzoate with photochemically-produced hydroxyl radicals has been estimated as 6.5X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 36 minutes at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the vapor-phase reaction of emamectin benzoate with ozone has been estimated as 1.2X10-15 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(1). This corresponds to an atmospheric half-life of about 14 minutes at an atmospheric concentration of 7X10+11 ozone molecules per cu cm(1). Emamectin benzoate is stable to aqueous hydrolysis at pH 5, 6, 7 and 8 at 25 °C(2). During six week observations, emamectin benzoate was stable to hydroylsis over a pH rang of 5.2-8.0(3); at pH 9, the hydrolysis half-life was 19.5 weeks(3). Using natural sunlight irradiation during the fall in NJ (latitude 40 deg N), the photodegradation half-lives of 14C-labeled emamectin benzoate in aqueous buffer (pH 7), in natural pond water, and in a sensitized aqueous buffer were 22.4, 6.9 and 1.4 days respectively(4); extrapolation to summer and winter half-lives yielded 11.5, 3.6 and 0.7 days in summer and 35.4, 10.9 and 2.2 days in winter, respectively(4). Photodegradation products from emamectin benzoate included 8,9-Z-, 8a-hydroxy-, 8a-oxo- and diepoxide derivatives of emamectin benzoate(4). When exposed to sunlight on soil surfaces, a photodegradation half-life of 5 days has been reported(5).

A BCF of 30 was measured for emamectin benzoate in the fillet (edible portion of fish) of bluegill sunfish (Lepomis macrochirus)(1). A BCF of 69 is reported for whole fish(2). According to a classification scheme(3), these BCF values suggest the potential for bioconcentration in aquatic organisms is moderate(SRC).

In batch equilibrium tests using sand, sandy loam, silt loam and clay loam soils, emamectin benzoate had Koc values ranging from 2.5X10+4 to 7.3X10+5(1). According to a classification scheme(2), this Koc range suggests that emamectin benzoate is expected to be immobile in soil. Using soil thin-layer plate tests, abamectin was classified as immobile in six different soil types(1). In field studies where emamectin benzoate was applied to bare soil at maximum recommended rates, residues were not found below the top 15-cm soil depth(3).

The Henry's Law constant for emamectin benzoate is estimated as 1.7X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 3.8X10-8 mm Hg(1), and water solubility, 24 mg/L(1). This Henry's Law constant indicates that emamectin benzoate is expected to be essentially nonvolatile from water surfaces(2). It is not expected to volatilize from moist soil surfaces(SRC) based upon its estimated Henry's Law constant. Emamectin benzoate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure.

Occupational exposure to emamectin benzoate may occur through inhalation and dermal contact with this compound at workplaces where emamectin benzoate is produced or used(1). The general population may be exposed to emamectin benzoate via dermal contact with vegetation in areas where emamectin benzoate has been applied as an insectide(1).

Therapeutic category (veterinary): antiparasitic

There were 2 dosing groups, each consisting of 2 male beagles. Group 1 received 0.5 mg/kg of (3)H-MK-0243 benzoate (1 mL/kg in 5% ethanol ... 0.239 mCi/mg; 98.8% radiochemically pure) on day 1 and 0.5 mg/kg of (3)H-MK-0243 HCl (1 mL/kg in deionized water ... 0.229 mCi/mg; 98.7% radiochemically pure) on day 15. Dosing was reversed for Group 2. Body weights were determined before each dose. 2 mL of blood was withdrawn for drug level determinations following each dose at 0.5, 1, 2, 4, 6, 8, 24, 48, 96 and 168 hr. Urine and feces were collected for drug level analysis at 0 to 24 and 72 to 96 hr. There was no evidence of drug effects. The mean plasma half lives for the benzoate and HCl salts were 35.7 +/- 3.4 hr and 35.5 +/- 4.4 hr, respectively. The mean plasma approximate area under the curve (AUC) for the benzoate and HCl salts was 4479 +/- 1476 and 4574 +/- 1514 ng/g plasma/7days. The mean peak plasma MAB1a (the major component of MK-0243 at 90 to 95%) levels were ~100 ng equivalents/g plasma, occurring at ~6 hr for either salt. Combined fecal and urine recoveries during the 1st and 4th days were ~40% and 0.01% of the dose, respectively. It is concluded that the 2 salts are bioequivalent in male beagle dogs.|The dermal absorption of the experimental avermectin insecticide emamectin benzoate was studied in the Rhesus monkey. Dermal absorption was calculated by comparing radioactivity levels in excreta following dermal application of the compound with those following administration of an equivalent intravenous dose. After iv administration of 300 ug (3)H-MAB1a (prepared as a 1:1 solution of propylene glycol:saline) to three monkeys, plasma levels decreased biphasically with a rapid decline in radioactivity during the first 15 min followed by a slower decline to background. By 7 days post-dose, approximately 90% and 5% of the administered radioactivity was recovered in the feces and urine, respectively. After a washout period, 300 micrograms [(3)H]MAB1a (dissolved in emulsifiable concentrate) was applied topically to the shaved forearm of the same monkeys. Following a 10-hr exposure period, approximately 90% of the radioactivity was recovered in a soap and water wash of the exposed forearms. Although plasma radioactivity levels generally remained below background levels, approximately 1.5% of the applied dose was recovered in the excreta. Dermal absorption of [()3H]emamectin benzoate was calculated as 1.6%. The low dermal penetration of emamectin benzoate indicates that minimal actual exposure of agricultural workers to this compound will occur.|The aims of this study were to investigate the content of emamectin in blood, mucus and muscle following field administration of the recommended dose, and correlation with sea lice infection on the same fish (elimination study). The tissue distribution of tritiated emamectin benzoate after a single oral dose in Atlantic salmon was also investigated by means of whole-body autoradiography and scintillation counting (distribution study). In the elimination study, concentrations of emamectin benzoate reached maximum levels of 128, 105 and 68 ng/g (p.p.b.) for blood, mucus and muscle respectively, on day 7, the last day of administration. From day 7, the concentration in the blood declined until concentration was less than the limit of detection on day 77. The concentration was higher in mucus compared with plasma (P < 0.05) except on days 7 and 21. The concentration of emamectin benzoate decreased gradually from the end of treatment (day 7) to day 70 with half-lives of 9.2, 10.0 and 11.3 days in muscle, plasma and mucus respectively. The distribution study demonstrated a high quantity of radioactivity in mucous membranes (gastrointestinal tract, gills) throughout the observation period (56 days). Activity was high in the epiphysis, hypophysis and olfactory rosette throughout the study. The highest activity was observed in the bile, indicating this to be an important route for excretion. The distribution study confirmed the results from the elimination study with respect to concentrations in blood, skin mucous and muscle.|Atlantic salmon (approximately 1.3 kg) maintained in tanks of seawater at 5 +/- 1 degrees C were dosed with 3H-emamectin B1 benzoate in feed at a nominal rate of 50 ug of emamectin benzoate/kg/day for 7 consecutive days. Tissues, blood, and bile were collected from 10 fish each at 3 and 12 hr and at 1, 3, 7, 15, 30, 45, 60, and 90 days post final dose. Feces were collected daily from the tanks beginning just prior to dosing to 90 days post final dose. The total radioactive residues (TRR) of the daily feces samples during dosing were 0.25 ppm maximal, and >97% of the TRR in pooled feces covering the dosing period was emamectin B1a. Feces TRR then rapidly declined to approximately 0.05 ppm by 1 day post final dose. The ranges of mean TRR for tissues over the 90 days post dose period were as follows: kidney, 1.4-3 ppm; liver, 1.0-2.3 ppm; skin, 0.04-0.09 ppm; muscle, 0.02-0.06 ppm; and bone, <0.01 ppm. The residue components of liver, kidney, muscle, and skin samples pooled by post dose interval were emamectin B1a (81-100% TRR) and desmethylemamectin B1a (0-17% TRR) with N-formylemamectin B1a seen in trace amounts (<2%) in some muscle samples. The marker residue selected for regulatory surveillance of emamectin residues was emamectin B1a. The emamectin B1a level was quantified in individual samples of skin and muscle using HPLC-fluorometry and was below 85 ppb in all samples analyzed (3 hr to 30 days post dose).|For more Absorption, Distribution and Excretion (Complete) data for EMAMECTIN (8 total), please visit the HSDB record page.

Atlantic salmon (approximately 1.3 kg) maintained in tanks of seawater at 5 +/- 1 degrees C were dosed with [(3)H]emamectin B1 benzoate in feed at a nominal rate of 50 ug of emamectin benzoate/kg/day for 7 consecutive days. Tissues, blood, and bile were collected from 10 fish each at 3 and 12 hr and at 1, 3, 7, 15, 30, 45, 60, and 90 days post final dose. Feces were collected daily from the tanks beginning just prior to dosing to 90 days post final dose. The total radioactive residues (TRR) of the daily feces samples during dosing were 0.25 ppm maximal, and >97% of the TRR in pooled feces covering the dosing period was emamectin B1a. Feces TRR then rapidly declined to approximately 0.05 ppm by 1 day post final dose. The ranges of mean TRR for tissues over the 90 days post dose period were as follows: kidney, 1.4-3 ppm; liver, 1.0-2.3 ppm; skin, 0.04-0.09 ppm; muscle, 0.02-0.06 ppm; and bone, <0.01 ppm. The residue components of liver, kidney, muscle, and skin samples pooled by post dose interval were emamectin B1a (81-100% TRR) and desmethylemamectin B1a (0-17% TRR) with N-formylemamectin B1a seen in trace amounts (<2%) in some muscle samples. The marker residue selected for regulatory surveillance of emamectin residues was emamectin B1a. The emamectin B1a level was quantified in individual samples of skin and muscle using HPLC-fluorometry and was below 85 ppb in all samples analyzed (3 hr to 30 days post dose).|...a single mammalian metabolite has been identified. This metabolite is characterized as an N-demethylation byproduct of emamectin.|The metabolism of (3)H/(14)C-labeled 4"-deoxy-4"-epimethylaminoavermectin B1a (MAB1a) benzoate, the major homologue (>/=90%) of the avermectin insecticide emamectin benzoate, was studied in laying chickens. Ten Leghorn hens (Gallus domesticus) were orally dosed once daily for 7 days (1 mg/kg of body weight/day). Eggs and excreta were collected daily, and eggs were subsequently separated into whites and yolks. Chickens were euthanized within 20 hr after the last dose, and liver, kidney, heart, muscle, fat, ovaries, gizzard, gastrointestinal tract and contents, and carcass were collected. Approximately 70 and 6% of the total administered dose were recovered in the excreta plus gastrointestinal tract and contents and in the tissues plus eggs, respectively. Two novel metabolites, i.e. the 24-hydroxymethyl derivative of the parent compound (24-hydroxymethyl-4"-deoxy-4"-epimethylaminoavermectin B1a) and the N-demethylated derivative of 24-hydroxymethyl-4"-deoxy-4"-epimethylaminoavermectin B1a (24-hydroxymethyl-4"-deoxy-4"-epiaminoavermectin B1a), were identified. In addition, eight fatty acid conjugates of each of these two metabolites, comprising 8-75% of total radioactive residues in tissues and eggs, were isolated and identified. Although this represents some of the most extensive in vivo fatty acid conjugation to a xenobiotic reported to date, potential human exposure to MAB1a residues from consumption of chicken would be extremely low, because the dosage level in this study was approximately 1000-fold greater than the MAB1a residue levels seen in crops and because the majority of the applied dose was recovered in the excreta. Based on these findings, the avian biotransformation of MAB1a differs substantially from the mammalian biotransformation.|While emamectin benzoate is not extensively metabolized in mammals, the limited information on the metabolites of emamectin benzoate suggests that metabolism does not result in the detoxification of emamectin benzoate. One plant metabolite of emamectin benzoate is somewhat more toxic than emamectin benzoate itself.

Emamectin benzoate was rapidly cleared from plasma /of rats/ with half-lives ranging from about 15 to 28 hours after oral or intravenous dosing.|Emamectin benzoate is a relatively large molecule (actually a mixture of four closely related molecules) which is not completely absorbed on oral administration, is poorly absorbed by the dermal administration, and rapidly eliminated in the feces with whole-body half-lives of about 1.5 days.|The tissue distribution of tritiated emamectin benzoate after a single oral dose in Atlantic salmon was also investigated by means of whole-body autoradiography and scintillation counting (distribution study). The concentration of emamectin benzoate decreased gradually from the end of treatment (day 7) to day 70 with half-lives of 9.2, 10.0 and 11.3 days in muscle, plasma and mucus respectively.

Emamectin benzoate is the 4'-deoxy-4'-epi-methyl-amino benzoate salt of avermectin B1 (abamectin), which is similar structurally to natural fermentation products of Streptomyces avermitilis. Emamectin benzoate is being developed as a newer broad-spectrum insecticide for vegetables and has a very low application rate. The mechanism of action involves stimulation of high-affinity GABA receptors and a consequent increase in membrane chloride ion permeability.|Overexpression of P-glycoproteins (Pgps) is assumed to be a principal mechanism of resistance of nematodes and arthropods to macrocyclic lactones. Quantitative RT-PCR (Q-RT-PCR) was used to demonstrate changes in transcription levels of two putative P-glycoprotein genes, designated here as SL0525 and SL-Pgp1, in sea lice (Lepeophtheirus salmonis) following exposure to emamectin benzoate (EMB). Pre-adult L. salmonis were challenged in an EMB bioassay for 24 hr and gene expression was studied from lice surviving EMB concentrations of 0, 10, and 30 ppb. Gene expression was measured using Q-RT-PCR with elongation factor 1 (eEF1alpha) as an internal reference gene. The results show that both target genes, SL0525 and SL-Pgp1, had significantly increased levels of expression with exposure to 10ppb EMB (p=0.11 and p=0.17, respectively) whereas the group exposed to 30 ppb was on the verge of being significant (p=0.053) only in the expression of SL-Pgp1. Gene expression for SL0525 and SL-Pgp1 were increased over five-fold at 10 ppb EMB. Therefore, the upregulation of these target genes may offer protection by increasing Pgp expression when lice are exposed to EMB. Optimized Q-RT-PCR can be used to determine if over-expression of these genes could be the basis for development of resistance in sea lice and thus allow suitable alternative chemotherapeutic options to be assessed.|Macrocyclic lactones, including avermectins and milbemycins, are novel parasiticides and insecticides that are produced through fermentation by soil-dwelling microorganisms. Although various macrocyclic lactones may differ in their potency and safety, all of them are believed to share common pharmacologic/toxicologic mechanisms, i.e. leading to paralysis and death of parasites and other target organisms via the activation of a glutamate-gated chloride channel in the invertebrate nerve and muscle cells and/or through the effect on gamma-aminobutyric acid (GABA) receptors. Ivermectin is the first macrocyclic lactone that was released for use in both animals and humans, and has demonstrated both excellent efficacy and high tolerability in the treatment of parasite infestations. Other macrocyclic lactones, such as abamectin, emamectin, and moxidectin were subsequently commercialized and have been used as insecticides and acaricides for crop protection or parasiticides for animal health.

Early signs of intoxication include dilation of pupils, muscular incoordination, and muscular tremors. Vomiting within one-half hour of exposure can minimize toxicity following accidental ingestion of the product; rapidly after exposure (<15 minutes) administer repeatedly medical charcoal in a large quantity of water ... . If toxicity from exposure has progressed to cause severe vomiting, the extent of resultant fluid and electrolyte imbalance should be gauged. Appropriate supportive parenteral fluid replacement therapy should be given, along with other required supportive measures (such as maintenance of blood pressure levels and proper respiratory functionality) as indicated by clinical signs, symptoms, and measurements. In severe cases, observations should continue for at least several days until clinical condition is stable and normal. Since emamectin benzoate is believed to enhance GABA activity in animals, it is probably wise to avoid drugs that enhance GABA activity (barbiturates, benzodiazepines, valproic acid) in patients with potentially toxic emamectin benzoate exposure.|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/|There is no specific antidote for the action of emamectin benzoate on GABA receptors...

/SIGNS AND SYMPTOMS/ Prolonged or frequently repeated exposure may cause allergic skin reactions in some individuals.|/SIGNS AND SYMPTOMS/ Early signs of intoxication include dilation of pupils, muscular incoordination, and muscular tremors. Vomiting within one-half hour of exposure can minimize toxicity following accidental ingestion of the product ...|/CASE REPORTS/ Emamectin benzoate is the 4'-deoxy-4'-epi-methyl-amino benzoate salt of avermectin B1 (abamectin), which is similar structurally to natural fermentation products of Streptomyces avermitilis. Emamectin benzoate is being developed as a newer broad-spectrum insecticide for vegetables and has a very low application rate. The mechanism of action involves stimulation of high-affinity GABA receptors and a consequent increase in membrane chloride ion permeability. Animal studies indicate a wide margin of safety because mammalian species are much less sensitive due to lower GABA receptor affinities and relative impermeability of the blood-brain barrier. Notably, the literature has not reported human exposure resulting in toxicity. This paper describes a case of acute poisoning with Proclaim insecticide (Syngenta, Taiwan), consisting of 2.15% w/w emamectin benzoate in 2, 6-bis (1, 1-dimethylethyl)-4-methyl-phenol and 1-hexanol. The clinical manifestation was transient gastrointestinal upset with endoscopy-proven gastric erosion and superficial gastritis, mild central nervous system depression, and aspiration pneumonia. No specific antidote exists for emamectin benzoate intoxication; this patient was treated successfully with gastric lavage, administration of activated charcoal, and empiric antibiotics. Drugs that enhance GABA activity such as barbiturates and benzodiazepines were avoided.

Emulsifiable concentrate (EC). /Emamectin benzoate/|Premix Partners: Abamectin. /Emamectin benzoate/|Denim Insecticide (Syngenta Crop Protection, LLC): Active ingredient: Emamectin benzoate 2.15%. /Emamectin benzoate/|Proclaim Insecticide (Syngenta Crop Protection, LLC): Active ingredient: Emamectin benzoate 5.0%. /Emamectin benzoate/|For more Formulations/Preparations (Complete) data for EMAMECTIN (10 total), please visit the HSDB record page.

Emamectin benzoate, which is classified as a second generation avermectin insecticide, is a derivative of abamectin. It differs from abamectin by the amino substituent in the terminal disaccharide unit...|Emamectin is a mixture of emamectin B1A (90%) and emamectin B1B(10%), as their benzoate salts|The avermectins, milbemycins and spinosyns are collectively referred to as macrocyclic lactones (MLs) which comprise several classes of chemicals derived from cultures of soil micro-organisms. These compounds are extensively and increasingly used in veterinary medicine and agriculture. Due to their potential effects on non-target organisms, large amounts of information on their impact in the environment has been compiled in recent years, mainly caused by legal requirements related to their marketing authorization or registration.|... A mixture of a minimum of 90% 4'-epi-methylamino-4'-deoxyavermectin B1a and maximum of 10% 4'-epi-methylamino-4'-deoxyavermectin B1b.[Table#7286]

Veterinary drugs (VDs) can remain in milk as a consequence of their use in livestock. In order to control the levels of VD residues in milk, screening methodologies can be applied for a rapid discrimination among negative and non-negative samples. In a second stage, non-negative samples are classified as negative or positive samples by using a confirmation method. Pre-target screening methods in low resolution MS (LRMS) are normally applied, but the number of analytes is limited, whereas the information obtained by full scan acquisition in high resolution mass spectrometry (HRMS) is improved. Here, three screening methods (running time<4 min) based on Orbitrap, quadrupole-time of flight (QqTOF) and triple quadrupole (QqQ) have been compared, using in all cases ultra-high performance liquid chromatography (UHPLC). For HRMS, the identification of the VDs was based on retention time (RT) and accurate mass measurements. Confirmation was based on the monitoring of fragments generated without precursor selection. The performance characteristics of the screening method provided reliable information regarding the presence or absence of the compounds below an established value, including uncertainty region and cut-off values. Better results in terms of cut-off values ( 0.99) was obtained for three AVMs ranging from 0.01 to 5 microg ml(-1), i.e. 0.01-5.0 ug/g in rice matrix. The limit of detection (LOD) and the limit of quantification (LOQ) were between 0.001 and 0.002 ug/g and between 0.004 and 0.006 ug/g, respectively. Recoveries were from 81.9% to 105.4% and precision less than 12.4%. The proposed method was successfully applied to routine analysis of the AVMs residues in rice.|LC-ion trap mass spectrometry was used to screen and confirm 38 compounds from a variety of drug classes in four species of fish: trout, salmon, catfish, and tilapia. Samples were extracted with acetonitrile and hexane. The acetonitrile phase was evaporated, redissolved in water and acetonitrile, and analyzed by gradient chromatography on a phenyl column. MS(2) or MS(3) spectra were monitored for each compound. Qualitative method performance was evaluated by the analysis over several days of replicate samples of control fish, fish fortified with a drug mixture at 1 ppm, 0.1 ppm and 0.01 ppm, and fish dosed with a representative from each drug class. Half of the 38 drugs were confirmed at 0.01 ppm, the lowest fortification level. This included all of the quinolones and fluoroquinolones, the macrolides, malachite green, and most of the imidazoles. Florfenicol amine, metronidazole, sulfonamides, tetracyclines, and most of the betalactams were confirmed at 0.1 ppm. Ivermectin and penicillin G were only detectable in the 1 ppm fortified samples. With the exception of amoxicillin, emamectin, metronidazole, and tylosin, residue presence was confirmed in all the dosed fish.|For more Analytic Laboratory Methods (Complete) data for EMAMECTIN (11 total), please visit the HSDB record page.

A liquid chromatography (LC)/fluorescence procedure was validated for emamectin (EM B1a) and desmethylamino-emamectin (DMAEM B1a) residues in lobster tissue. They were extracted by shaking and sonicating with 1% ammonium acetate-methanol in the presence of sand. The extract was concentrated, partitioned with ethyl acetate, and cleaned up on a propylsulfonic cation exchange cartridge. The analytes were eluted from the cartridge with 5% ammonium hydroxide-methyl acetate, the eluate was concentrated, and the solvent was changed to dry 20% ethyl acetate-acetonitrile before derivatization with trifluoroacetic anhydride-N-methylimidizole. The products were analyzed by LC-fluorescence, and no interference [>limit of detection (LOD)] was detected in the control samples. ...

Agrochemicals -> Insecticides