Methoprene

310.47

310.47

254-993-2

DTXSID8032627

Clear amber liquid|Pale yellow liquid (technical grade)

2918990090

35.5

5.5

0.9261 g/cm³ @ Temp: 20 °C

<25 °C

100 °C @ Press: 0.05 Torr

Flash point is 96 deg C (Closed cup).

1.462

1.4 mg l -1 (room temperature)

0-6°C

3.15 x l0 -3 Pa (25 °C)

LD50 orally in rats: >34500 mg/kg (Siddall)

Faint fruity odor

Henry's Law constant = 5.71X10-5 atm-cu m/mole at 25 °C (est)

BP: 135-136 °C; water solubility: 6.85 mg/L at 20 °C|BP: 279.9 °C at 97.2 kPa. VP: 0.623 mPa at 20 °C, 1.08 mPa at 25 °C. logP >6. Density: 0.924 at 20 °C, 0.921 at 25 °C. Solubility in water, 6.85 ppm at 20 °C, 0.921 ppm at 25 °C. Soluble in most organic solvents, e.g. in acetone and hexane >500, methanol >450 (all in g/L at 20 °C). Dynamic viscosity: 51.3 mPa/sec at 20 °C, 17.8 mPa/sc at 40 °C; kinematic viscosity: 55.3 sq mm/sec at 20 °C, 19.2 sq mm/sec at 40 °C. Surface tension: 50.1 mN/m /S-Methoprene/|Stable in water, organic solvents and in the presence of dilute alkali and acid|Pale yellow liquid; fruity odor /Technical S-Methoprene/|Hydroxyl radical reaction rate constant = 8.3X10-11 cu cm/molecule-sec at 25 °C (est)|Ozone reaction rate constant = 3.4X10-16 cu cm/molecule-sec at 25 °C (est)

Very slightly corrosive to some metals.

UN30829/PG3

2

36/37/38-51/53

26-36-60-61

JR1685000

Xi,N

Stable under recommended storage conditions.

P261, P264, P271, P273, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P391, P403+P233, P405, P501

H315

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.|Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material; Contaminated packaging: Dispose of as unused product.

USEPA/Office of Pesticide Programs; Reregistration Eligibility Decision Document for Methoprene (March 1991). The RED summarizes the risk assessment conclusions and outlines any risk reduction measures necessary for the pesticide to continue to be registered in the USA.[Available from, as of June 24, 2016: http://www.epa.gov/pesticides/reregistration/status.htm]|USEPA/Office of Pesticide Programs; Pesticide Fact Sheet: June 2001 Update of the March 1991 Methoprene R.E.D. Fact Sheet (June 2001).[Available from, as of June 27, 2016: https://www3.epa.gov/]|U.S. Environmental Protection Agency/Pesticides and Toxic Substances; R.E.D. Facts on Methoprene 738-F-91-104 (March 1991). Includes information on pesticide reregistration, regulatory history, health effects, routes of exposure, environmental hazards and product labeling.[Available from, as of May 17, 2000: http://www.cpa.gov/oppsrrd1/factsheets/0030fact.pdf]

|Warning|H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P273, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 198 companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H315: Causes skin irritation [Warning Skin corrosion/irritation]

Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Impervious clothing. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) 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).

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical, or carbon dioxide.|Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.|Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapor or mist. Normal measures for preventive fire protection.|Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.|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.|Wash contaminated skin with soap and water. Treat eye exposures by irrigating exposed eyes with copious amounts of clean water or saline for at least 15 minutes. Remove contact lenses, if present, prior to irrigation. If irritation persists after irrigation, send patient to a healthcare facility for further medical attention.

Non-irritating to skin and eyes (rabbits).

Methoprene is listed as an ingredient in drops to prevent fleas in dogs(1).

IDENTIFICATION AND USE: Methoprene is a clear amber liquid. It is used for control of many insect pests in public health, stored commodities (including tobacco), food handling, processing and storage establishments, on animals, and on plants (including glasshouse plants). Particular uses include control of mosquito larvae; sciarid flies in mushroom houses; cigarette beetles and tobacco moths in stored tobacco; Pharaoh's ants; leaf miners on glasshouse chrysanthemums; stored product pests in food and tobacco processing plants and warehouses. HUMAN EXPOSURE AND TOXICITY: There are no data available. ANIMAL STUDIES: Non-irritating to skin and eyes (rabbits). In 2 year feeding trials, rats receiving 5000 mg/kg diet and mice receiving 2500 mg/kg diet showed no ill-effects. No teratogenic effects on rats at 1000 mg/kg and on rabbits at 500 mg/kg. No mutagenic effects on rats at 2000 mg/kg. No reproductive adverse effects in 3-generation reproduction studies on rats at 2500 mg/kg diet. Methoprene applied at a concentration of 0.2 ppm did not significantly affect the locomotor activities of mosquitofish or goldfish. This application rate is ten times the suggested rates. Methoprene-membrane interaction and perturbation of cell bioenergetics may underlie the mechanism of toxicity of this compound in non-target organisms. Methoprene induces a weak mutagenic effect in the Drosophila wing spot test. ECOTOXICITY STUDIES: Xenopus laevis embryos (stage 8) were exposed to the test chemicals for 96 hr. Assays were conducted under static renewal (24 hr) conditions and chemical concentrations in water were measured at the beginning and end of the renewal periods. Methoprene exposure did not result in developmental toxicity at concentrations up to 2 mg/L. Applications of amethoprene enhanced the levels of dopamine in the brains of 4-day-old male honey bees.

Exposure to multiple stressors from natural and anthropogenic sources poses risk to sensitive crustacean growth and developmental processes. Applications of synthetic pyrethroids and insect growth regulators near shallow coastal waters may result in harmful mixture effects depending on the salinity regime. The potential for nonadditive effects of a permethrin (0.01-2 ug/L), methoprene (0.03-10 ug/L ), and salinity (10-40 ppt) exposure on male and female Uca pugnax limb regeneration and molting processes was evaluated by employing a central composite rotatable design with multifactorial regression. Crabs underwent single-limb autotomy followed by a molting challenge under 1 of 16 different mixture treatments. During the exposure (21-66 d), individual limb growth, major molt stage duration, abnormal limb regeneration, and respiration were monitored. At 6 d postmolt, changes in body mass, carapace width, and body condition factor were evaluated. Dorsal carapace tissue was collected, and protein and chitin were extracted to determine the composition of newly synthesized exoskeleton. The present results suggest chronic, low-dose exposures to multiple pesticide stressors cause less-than-additive effects on U. pugnax growth processes. Under increasing concentrations of methoprene and permethrin, males had more protein in their exoskeletons and less gain in body mass, carapace width, and body condition compared to females. Females exhibited less gain in carapace width than controls in response to methoprene and permethrin. Females also displayed elevated respiration rates at all stages of molt, suggesting a high metabolic rate. Divergent growth and fitness between the sexes over the long term could influence crustacean population resilience.

LD50 Rat oral >34600 mg/kg|LD50 Dog oral >5000 mg/kg|LD50 Rabbit percutaneous 3500 mg/kg|LD50 Non-toxic to adult bees (oral and topical) >1000 ug/l/bee|For more Non-Human Toxicity Values (Complete) data for METHOPRENE (7 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ ...The possible effects of mosquito control treatments of wetlands with Bacillus thuringiensis israelensis /Bti/ (136, applied as Vectobac-G granules) and methoprene (applied as Altosid sand granules) on wetland breeding bird communities /were examined/. Data collected two years before (1980 and 1990) were compared to data collected three years after (1991 and 1993) treatments were applied. Total numbers of species and individuals observed remained relatively constant throughout the study period, but several individual species varied annually, most likely due to changes in water levels and habitat available. ...No effect /was found/ of Bti or methoprene treatments on the bird community or on 19 individual bird species. The few differences that were observed between control and treatment were inconsistent over time and were likely due to chance because of the large number of comparisons that were completed. Despite relatively large reductions of aquatic insects (including mosquitoes) in mid to late summer following both treatment types, it is unlikely that food available to bird species in these wetlands was depressed during the breeding season. Effects of weather and predation were probably more important influences on species and community parameters than was mosquito control treatment during the study period. Because of lower aquatic insect densities in mid to late summer, other parts of the avian life cycle such as late summer survival, dispersal of young birds, or migrating birds may be more affected by mosquito control treatments.|/AQUATIC SPECIES/ ... In these studies, the aqueous stability and developmental toxicity of methoprene and several degradation products (methoprene acid, methoprene epoxide, 7-methoxycitronellal, and 7-methoxycitronellic acid) were examined. Xenopus laevis /clawed toad/ embryos (stage 8) were exposed to the test chemicals for 96 hr. Assays were conducted under static renewal (24 hr) conditions and chemical concentrations in water were measured at the beginning and end of the renewal periods. Methoprene exposure did not result in developmental toxicity at concentrations up to 2 mg/L, which is slightly higher than its water solubility. Methoprene acid, a relatively minor degradation product, produced developmental toxicity when concentrations exceeded 1.25 mg/L. Methoprene epoxide and 7-methoxycitronellal caused developmental toxicity at concentrations of 2.5 mg/L and higher. 7-Methoxycitronellic acid was not developmentally toxic at a test concentration as high as 30 mg/L. The five test chemicals had differential stability in aqueous solution that was in some instances affected by the presence of test organisms. These data indicate that methoprene and its degradation products are not potent development toxicants in X. laevis. This, in combination with the fact that field applications of sustained-release formulations of methoprene result in methoprene concentrations that do not typically exceed 0.01 mg/L, suggests that concerns for methoprene-mediated developmental toxicity to amphibians may be unwarranted.|/AQUATIC SPECIES/ Using subtractive hybridization, ...17 genes that are either up- or down-regulated in the hepatopancreas (Hp) of the lobster, Homarus americanus, by acute exposure to the juvenile hormone analog methoprene /were identified/. The expression of some of the genes obtained from the subtraction libraries was confirmed by real time Q-PCR experiments. These genes encode several different classes of proteins including: structural, enzymatic and regulatory polypeptides. Enzymes represent the predominant genes up-regulated by methoprene. Included in this group are betaine-homocysteine S-methyltransferase (BHMT) and two other enzymes of the methionine cycle. Increased expression of a translation factor (eIF2), as well as of cytosolic (aldose reductase), structural (beta-tubulin, L5A) and plasma membrane (CD42d) proteins was observed. In addition, a major feature of altered gene expression in methoprene treated Hp was increased levels of enzymes associated with protein turnover, including trypsin, ubiquitin conjugating enzyme and ubiquitin carboxyl terminal hydrolase. Down-regulation of the members of the hemocyanin family was observed. Assays confirmed elevated levels of trypsin in the Hp of lobsters after 24 hr exposure to methoprene. ...Findings suggest a wide variety of cellular targets are altered by methoprene.|/AQUATIC SPECIES/ Exposure to multiple stressors from natural and anthropogenic sources poses risk to sensitive crustacean growth and developmental processes. Applications of synthetic pyrethroids and insect growth regulators near shallow coastal waters may result in harmful mixture effects depending on the salinity regime. The potential for nonadditive effects of a permethrin (0.01-2 ug/L), methoprene (0.03-10 ug/L ), and salinity (10-40 ppt) exposure on male and female Uca pugnax limb regeneration and molting processes was evaluated by employing a central composite rotatable design with multifactorial regression. Crabs underwent single-limb autotomy followed by a molting challenge under 1 of 16 different mixture treatments. During the exposure (21-66 days), individual limb growth, major molt stage duration, abnormal limb regeneration, and respiration were monitored. At 6 days postmolt, changes in body mass, carapace width, and body condition factor were evaluated. Dorsal carapace tissue was collected, and protein and chitin were extracted to determine the composition of newly synthesized exoskeleton. The present results suggest chronic, low-dose exposures to multiple pesticide stressors cause less-than-additive effects on U. pugnax growth processes. Under increasing concentrations of methoprene and permethrin, males had more protein in their exoskeletons and less gain in body mass, carapace width, and body condition compared to females. Females exhibited less gain in carapace width than controls in response to methoprene and permethrin. Females also displayed elevated respiration rates at all stages of molt, suggesting a high metabolic rate. Divergent growth and fitness between the sexes over the long term could influence crustacean population resilience.|For more Ecotoxicity Excerpts (Complete) data for METHOPRENE (22 total), please visit the HSDB record page.

Methoprene's production may result in its release to the environment through various waste streams; its use as an insecticide(1) will result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 5300(SRC), determined from a structure estimation method(2), indicates that methoprene is expected to be immobile in soil(SRC). Volatilization of methoprene from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.7X10-5 atm-cu m/mole(SRC), using a fragment constant estimation method(2). However, adsorption to soil is expected to attenuate volatilization(SRC). Methoprene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.4X10-4 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). The biodegradation half-life of methoprene was approximately 10 days at a surface treatment rate of 1 kg/ha in sandy and silty loam soils(3). Methoprene is rapidly photodegraded on inert surfaces, such as soil, forming methoxycitronellal(4).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 5300(SRC), determined from a structure estimation method(2), indicates that methoprene is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 5.7X10-5 atm-cu m/mole(SRC), developed using a fragment constant estimation method(2). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 32 hours and 15 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 278 days if adsorption is considered(4). Methoprene is stable to hydrolysis under environmental conditions (pH 5 to 9)(5). According to a classification scheme(6), an estimated BCF of 2000(SRC), from its log Kow of 5.5(7) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism(SRC). Methoprene is rapidly degraded in both sterile and nonsterile pond water exposed to sunlight (>80% of applied methoprene is degraded within 13 days)(8). Degradation is somewhat less rapid under sterile conditions than under nonsterile conditions indicating that, although photolysis may be the main degradation route, microbial metabolism contributes to methoprene degradation(9). The biodegradation half-life in the pond water was about 30 hr at 0.001 ppm and 40 hr at 0.01 ppm(9).|AQUATIC FATE: The stability of methoprene in water was studied. An emulsifiable concentrate (E.C.) persisted for 134 days at 4.5 °C and for 49 days at 20 °C in both fresh and salt water. The slow release flowable liquid degraded at 20 °C at about the same rate as did the E.C. formulation at 4.5 °C.|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), methoprene, which has an estimated vapor pressure of 2.4X10-4 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase methoprene is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals and ozone(SRC); the half-lives for these reactions in air are estimated to be 4.6 hours and 48 minutes(SRC), calculated from rate constants of 8.3X10-11 and 3.4X10-16 cu cm/molecule-sec at 25 °C, respectively(SRC), that were derived using a structure estimation method(2). Methoprene contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of methoprene with photochemically-produced hydroxyl radicals has been estimated as 8.3X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 4.6 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the vapor-phase reaction of methoprene with ozone has been estimated as 3.4X10-16 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 48 minutes at an atmospheric concentration of 7X10+11 ozone molecules per cu cm(2). Methoprene is not expected to hydrolyze under environmental conditions (pH 5 to 9)(3). Methoprene is rapidly degraded in both sterile and nonsterile pond water exposed to sunlight (>80% of applied methoprene is degraded within 13 days)(4). Photodegradation products include methoxycitronellic acid, (2E)-4,5-epoxy-11-methoxy-3,7,11-trimethyl-2-dodecenoate, and 8-methoxy-4,8-dimethyl-2-nonanone(4). Methoprene is rapidly photodegraded on inert surfaces, forming methoxycitronellal(4).

An estimated BCF of 2000 was calculated in fish for methoprene(SRC), using a log Kow of 5.5(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism(SRC). Uncharacterized methoprene residues accumulated in edible tissues of bluegill sunfish and crayfish at maximum bioconcentration factors of 457 and 75, respectively(4).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of methoprene can be estimated to be 5300(SRC). According to a classification scheme(2), this estimated Koc value suggests that methoprene is expected to be immobile in soil.

The Henry's Law constant for methoprene is estimated as 5.7X10-5 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that methoprene is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 32 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 15 days(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The volatilization half-life from a model pond is about 278 days when adsorption is considered(3). Methoprene's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Methoprene is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.4X10-4 mm Hg(SRC), determined from a fragment constant method(1).

SURFACE WATER: Methoprene was not detected in samples from five sites collected in 1996 and 1997 along the Mississippi river in the state of Mississippi(1). Methoprene was detected in Canadian surface water at respective concentrations of 0.1 and 0.65 ug/L in one of 37 samples collected in Hamilton Harbor and one of 14 samples collected from Ottawa Stream; samples were collected in 2003(2).

Occupational exposure to methoprene may occur through inhalation and dermal contact with this compound at workplaces where methoprene is produced or used. Use data indicate that the general population may be exposed to methoprene via dermal contact with consumer products containing methoprene. (SRC)

/EXPL THER/ The effects of methoprene, a juvenile hormone analogue (JHA), on Trypanosoma cruzi bloodstream trypomastigotes (Tulahuen strain, Tul 2 stock) were studied. It was observed that 150 uM of methoprene in in vitro experiments cause cellular death of T. cruzi. In contrast, methoprene was not able to clear bloodstream trypomastigotes in in vivo experiments, but it was observed a decrease of parasitemia levels of infected mice treated with 200 ug of methoprene/mouse/day during 5 days. According to these results and the low toxicity of methoprene, we suggest that this compound will serve as an effective agent to sterilize blood for transfusions.|/EXPL THER/ Drug therapy for the treatment of African sleeping sickness is limited by toxicity and resistance and in the last 50 years only one new drug has been introduced for the treatment of the human disease. We report that the juvenile hormone analog, methoprene, and several structurally related isoprenoid compounds kill Trypanosoma brucei in culture. Of the other isoprenoids tested, juvenile hormone III and mammalian retinoid X receptor ligands were the most potent trypanocides. Both the procyclic forms and the bloodstream trypomastigotes are killed by these compounds with LD50 values of 5-30 uM. Of the two methoprene stereoisomers, the EE form was the most active, suggesting that a protein target may be involved in mediating effects of these analogues against the parasite. Methoprene was not, however, able to clear trypanosomes from the blood of infected mice. Methoprene acid, the immediate downstream metabolite of methoprene, is not an effective anti-trypanosomal agent, suggesting that in the mice methoprene is converted to an inactive compound. Since methoprene and its analogues have low and well characterized toxicity in mammals these studies stress the importance of further exploring these isoprenoids as lead compounds for the treatment of African sleeping sickness.

When (14)C methoprene was administered orally to rats, slightly less than 20% was excreted within 5 days in the urine and a similar amount in feces and almost 40% was excreted as (14)C02. About 17% was retained in the body. Highest concentrations were in liver (84.5 ppm), kidneys (29 ppm), lungs (26 ppm), fat (36.5 ppm), and the adrenal cortex (12-13 ppm). About 12 labeled compounds were detected in the urine but no unchanged methoprene was observed.|Distribution and elimination of (14)C given to chickens as methoprene (14)C (isopropyl (2E,4E)-11-methoxy-3,7,11-trimethyl-2,4-dodecadienate 5 (14)C were investigated. When about 4 mg of methoprene was given in a single oral dose to colostomized chickens, elimination of (14)C was greatest in exhaled air; however, when 105 or 107 mg of methoprene was given, elimination of (14)C was greatest in urine. Up to 19% of the (14)C from a single dose of methoprene was eliminated over a 14 day period in the eggs of laying hens, and (14)C was detected in all tissues and organs examined.|When the metabolic fate of methoprene (isopropyl (2E,4E)-11-methoxy-3,7,11-trimethyl- 2,4-dodecadienoate) was studied in a guinea pig, a steer, and a cow, a rather large percentage of the radiolabel was incorporated in the tissues and respired by the animals. In the urine and feces, a small amount of radiolabel was metabolized into free primary metabolites, somewhat more was incorporated into simple glucuronides, and a considerable quantity of radiolabel was found in polar compounds, possibly complex conjugates or polar biochemicals. No methoprene was found in the urine, but approximately 40% of the radiolabel in feces was contributed by unmetabolized methoprene. The formation of conjugates and the metabolism of methoprene was more extensive in the steer than in the guinea pig.|Treatment of Leghorn chickens with a single oral dose of (5-14C)methoprene (isopropyl (2E,4E)-11-methoxy-3,7,11-trimethyl-2,4-dodecadienoate) resulted in residual radioactivity in tissues and eggs. The chemical nature of the residual radiolabel in tissue (muscle, fat, liver), eggs, and excrement was thoroughly examined at several doses (0.6 to 77 mg/kg). Although a high initial dose (59 mg/kg) resulted in methoprene residues in muscle (0.01 ppm), fat (2.13 ppm), and egg yolk (8.03 ppm), these residues of methoprene represented only 39 and 2% of the total (14)C label in fat and egg yolk, respectively. Radiolabeled natural products from extensive degradation of methoprene were by far the most important 14C residues in tissues and eggs, particularly at the lower dose of 0.6 mg/kg where (14)C cholesterol and normal (14)C fatty acids (as triglyceride) contributed 8 and 71% of the total radiolabel in egg yolk. Novel minor metabolites of methoprene were observed in lipid depots, resulting from saturation of the dienoate system. These minor metabolites were conjugated to glycerol and/or cholesterol. radioactivity were found in the bile, liver, skin, fetus, and udder. In all species, approximately 40 percent of the radioactivity in the feces was due to unchanged methoprene. No methoprene was found in the urine.|For more Absorption, Distribution and Excretion (Complete) data for METHOPRENE (6 total), please visit the HSDB record page.

About 4 mg (14)C methoprene was administered orally to colostomized chickens. (14)C02 was the main (14)C product detected. When large doses were given, elimination was greatest in urine and (14)C was also found in the eggs and all tissues and organs examined ... . In addition to natural (14)C cholesterol and (14)C fatty acid triglycerides, there were metabolites conjugated to glycerol and/or cholesterol. Urine ... and ... feces contained compounds ... and each had undergone considerable isomerization. About 19% of the (14)C appeared in the eggs. Most of this was associated with egg proteins. The egg yolks also had radiolabeled fatty acid glycerides and cholesterol. Blood contained radiolabeled cholesterol and traces of cholesteryl esters. Tissue residues were similar to those found in eggs.|A Hereford steer received a single oral dose of 5-(14)C-methoprene and sacrificed 2 weeks later. No primary metabolites were observed in fat, muscle, liver, lung, blood and bile. However, the majority of the tissue radioactivity was present as (14)C cholesterol. About 72% of the activity in bile appeared in cholesterol, cholic acid, and deoxycholic acid. Protein and cholesteryl esters of fatty acids also contained some radioactivity.|When administered to a lactating cow, 5-(14)C-methoprene gave rise to randomly labeled acetate. This was incorporated into milk fat which was degraded to saturated and mono and di- enoic fatty acids. Labeled lactose, lactalbumin, casein, and free and esterified cholesterol was also observed ... . Similar qualitative results were observed in urine of a guinea pig orally dosed with methoprene. Quantitative differences were observed.|Studies with housefly microsomal enzymes showed that the Beta-esterases present did not appreciably hydrolyze methoprene whereas other analogs were metabolized. Microsomal oxidase activity against juvenile hormone analogs was greater in resistant fly strains. ... Branched chain esters of methoprene analogs did not show significant difference in hydrolysis by housefly microsomal esterases. Methoprene was effective at 0.1 ug/pupa while others were ineffective at 10 ug/pupa.|For more Metabolism/Metabolites (Complete) data for METHOPRENE (15 total), please visit the HSDB record page.

The degradation of methoprene by unidentified pond organisms was studied. The half-life in the pond water was about 30 h at 0.001 ppm and 40 h at 0.01 ppm.|In wheat, the half-life of methoprene was estimated to be 3 to 7 weeks, depending on moisture content. The only metabolite observed was the free acid.

Methoprene (isopropyl (2E,4E)-11-methoxy-3,7,11-trimethyl-2,4-dodecadienoate) is an insect juvenile hormone agonist that blocks metamorphosis in some insects. Recent evidence suggests that a metabolite, methoprene acid, activates vertebrate retinoid X receptors (RXRs), and may interfere with retinoic acid-regulated developmental processes. Methoprene, methoxy-methoprene acid, and two major breakdown products were tested for their ability to interfere with retinoid-regulated pathways when using transfected cells. The CV-1 cells were transiently transfected with genes encoding RXRs and response elements attached to luciferase reporters, and retinoic acid-sensitive F9 cells were stably transfected with retinoic acid receptor (RAR)/RXR response elements attached a lacZ reporter (Sil-REM/beta-gal-NEO). Experiments confirmed that methoxy-methopreneacid acted as a ligand for RXRs and was capable of activating transcription through RAR/RXR response elements. However, neither methoprenenor the breakdown products, 7-methoxycitronellal and 7-methoxycitronellic acid, activated transcription in transfected CV-1 or F9 cells.Methoprene and methoxy-methoprene acid may interfere with the conversion of all-trans-retinol and all-trans-retinaldehyde to all-trans-retinoic acid in the F9-derived cell line. Methoprene was as effective as the retinol dehydrogenase inhibitor citral in blocking the retinol-induced transcription of RAR/RXR-regulated reporter genes, whereas methoxy-methoprene acid blocked transcription stimulated by retinaldehyde.|In holometabolous insects such as mosquito, Aedes aegypti, midgut undergoes remodeling during metamorphosis. Insect metamorphosis is regulated by several hormones including juvenile hormone (JH) and 20-hydroxyecdysone (20E). The cellular and molecular events that occur during midgut remodeling were investigated by studying nuclear stained whole mounts and cross-sections of midguts and by monitoring the mRNA levels of genes involved in 20E action in methoprene-treated and untreated Ae. aegypti. We used JH analog, methoprene, to mimic JH action. In Ae. aegypti larvae, the programmed cell death (PCD) of larval midgut cells and the proliferation and differentiation of imaginal cells were initiated at about 36 hr after ecdysis to the 4th instar larval stage (AEFL) and were completed by 12 hr after ecdysis to the pupal stage (AEPS). In methoprene-treated larvae, the proliferation and differentiation of imaginal cells was initiated at 36h AEFL, but the PCD was initiated only after ecdysis to the pupal stage. However, the terminal events that occur for completion of PCD during pupal stage were blocked. As a result, the pupae developed from methoprene-treated larvae contained two midgut epithelial layers until they died during the pupal stage. Quantitative PCR analyses showed that methoprene affected midgut remodeling by modulating the expression of ecdysone receptor B, ultraspiracle A, broad complex, E93, ftz-f1, dronc and drice, the genes that are shown to play key roles in 20E action and PCD. Thus, JH analog, methoprene acts on Ae. aegypti by interfering with the expression of genes involved in 20E action resulting in a block in midgut remodeling and death during pupal stage.|... Here, a major malaria vector, Anopheles gambiae Giles, was used as a model insect to study the action of methoprene on female reproduction. Ecdysteroid titers and expression profiles of ecdysone-regulated genes were determined before and after a blood meal. An ecdysteroid peak was detected at 12 hr post blood meal (PBM). The maximum expression of ecdysone-regulated genes, such as ecdysone receptor (EcR), hormone receptor 3 (HR3) and vitellogenin (Vg) gene, coincided with the ecdysteroid peak. Interestingly, topical application of methoprene at 6 hr PBM delayed ovarian development and egg maturation by suppressing the expression of ecdysone-regulated genes in female mosquitoes. The data suggest that ecdysteroid titers are correlated with Vg synthesis, and methoprene affects vitellogenesis by modulating ecdysteroid action in A. gambiae.|Insect growth regulator (juvenile hormone mimic), preventing metamorphosis to viable adults when applied to larval stages.

Wash contaminated skin with soap and water. Treat eye exposures by irrigating exposed eyes with copious amounts of clean water or saline for at least 15 minutes. Remove contact lenses, if present, prior to irrigation. If irritation persists after irrigation, send patient to a healthcare facility for further medical attention.|If a very large amount of methoprene has been ingested, consider GI decontamination ... .|/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 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 TKO. Use 0.9% saline (NS) or lactated Ringer's (LR) 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 (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

Altosid

Sergeant's Fipronil + Methoprene Spray for Dogs and Cats (Sergeant's Pet Care Products, Inc.): Active ingredient: Methoprene 0.27%; Fipronil 0.29%.|Sergeant's Fipronil + Cyphenothrin + Methoprene BOV Spray for Dogs (Sergeant's Pet Care Products, Inc.): Active ingredient: Methoprene 0.27%; Cyphenothrin 0.1%; and Fipronil 0.29%.|Methoprene Technical (Wellmark International): Active ingredient: Methoprene 90.0%.|Apex 5E (Wellmark International): Active ingredient: Methoprene 67.0%.|For more Formulations/Preparations (Complete) data for METHOPRENE (11 total), please visit the HSDB record page.

The WHO Recommended Classification of Pesticides by Hazard identifies methoprene as unlikely to present an acute hazard in normal use; Main Use: insect growth regulator.|Listed as an ingredient in drops to prevent fleas in dogs

In order for grain handlers and traders to reliably estimate residues of grain protectants in the field, antibody-based rapid tests were developed for carbaryl (1-naphthyl methylcarbamate) and methoprene [isopropyl (E,E)-(RS)-11-methoxy-3,7,11-trimethyldodeca-2,4-dienoate]. To complement the rapid analysis, a simple and rapid extraction technique was developed. In these tests, a pesticide-containing methanol extract of the grain sample and an enzyme-labeled component are added to precoated strips. After a brief incubation, the strips are washed and a substrate/chromogen for the enzyme is added. The color developed is stopped by acidification and the results are read either by eye or in a portable field photometer. The overall test time is under 20 minutes. For carbaryl, the test had a limit of detection of 4.5 ppb (1.1 ppm in grain), while the methoprene test had a limit of detection of 4 ppb (1 ppm in grain) based on the lower datum point, which is 15% inhibition, in the standard curves. Both assays can be used as a screening test for carbaryl and methoprene in animal feed grains.|The invasion and subsequent spread of the mosquito-borne West Nile virus in the United States has resulted in increased use of methoprene. With the increased need for sensitive detection and monitoring of methoprene in the environment, an analytical LC/ESI-MS/MS method has been developed for the analysis of methoprene and two analogues, kinoprene and hydroprene, in water. To improve the ionization efficiency of the nonpolar analytes, a derivatization step with the Cookson-type reagent 4-phenyl-1,2,4-triazoline-3,5-dione (PTAD) was used. Derivatization improved the limit of detection 100-fold. For tandem MS analyses, limits of detection in environmental water samples (S/N = 3) are about 6 pg/mL for methoprene and 20 pg/mL for kinoprene and hydroprene, resulting in limits of quantification (S/N = 10) of 20 pg/mL for methoprene and 60 pg/mL for hydroprene and kinoprene extracted from 10 mL of water. This method was applied to measure methoprene concentrations in water samples from a treated site.|We studied the determination of methoprene in foods by high-performance liquid chromatography (HPLC). The sample was extracted with acetonitrile and the extract was salted out by adding sodium chloride, allowing the acetonitrile layer to separate. The acetonitrile solution was washed with hexane saturated with acetonitrile, cleaned up on a Florisil column and determined by HPLC. The recovery of methoprene from spiked samples was 74.6-82.8%. In an evaluation of this method by 6 analytical laboratories, mean recoveries from spiked samples ranged from 79.4% to 84.6%. Repeatability relative standard deviation values were 2.3-8.8% and reproducibility relative standard deviation values were 8.8-23.6%. The detection limits were 0.001-0.02 ug/g and below the detection limit of the Notified Analytical Method.|A method was developed for the quantitative determination of alachlor, benalaxyl, clomazone, diflubenzuron, dimethomorph, diphenamid, ethofumesate, metalaxyl, methoprene, metobromuron and piperonyl butoxide on tobacco. The pesticides were extracted with water and methanol from five different types of tobacco. The extracts were purified by partition on an extraction cartridge containing diatomaceous earth. The purified extracts were analyzed by reversed-phase high-performance liquid chromatography connected to an atmospheric pressure ionization-electrospray-triple quadrupole mass spectrometer operating in the positive ion mode. Two different transitions and their relative intensities were monitored for unambiguous identification. All pesticides presented overall recovery rates between 35% and 110%. The trueness is near 100% and the interday precision is below 15%. The limits of quantifications are equal or below the guidance residue levels proposed by the Agrochemical Advisory Committee of CORESTA, an association of organizations having scientific research relative to tobacco.|For more Analytic Laboratory Methods (Complete) data for METHOPRENE (8 total), please visit the HSDB record page.

A method was validated and applied for the analysis of the insect growth regulator methoprene [Isopropyl (2E,4E)-11-methoxy-3,7,11-trimethyldodeca-2,4-dienoate], its metabolite methoprene acid, the insecticide permethrin [3-(2,2-dichloro-ethenyl)-2,2-dimethylcyclopropanecarboxylic acid(3-phenoxyphenyl)methylester], and two of its metabolites, m-phenoxybenzyl alcohol and m-phenoxybenzoic acid, in rat plasma and urine using solid-phase extraction and reversed-phase high performance liquid chromatography. The analytes were separated using gradient of 55-100% acetonitrile in water (pH 4.0) at a flow rate ranging between 0.6 and 1.0 mL/min over a period of 20 min, and UV detection at 210 and 254 nm. The retention times ranged from 7.3 to 18.4 min. The limits of detection ranged between 50 and 100 ng/ml, while limits of quantitation were 100-150 ng/mL. Average percentage recovery of five spiked plasma samples was 83.6 +/- 3.9, 80.1 +/- 5.4, 82.1 +/- 4.4, 83.7 +/- 3.9 and 83.1 +/- 4.7, and from urine 79.3 +/- 4.3, 82.0 +/- 5.4, 80.7 +/- 4.2, 78.9 +/- 5.7 and 83.9 +/- 4.5 for methoprene, methoprene acid, permethrin, m-phenoxybenzyl alcohol and m-phenoxybenzoic acid, respectively. The method was linear and reproducible over the range of 100-1000 ng/mL. This method was applied to analyze the above chemicals and metabolites following their combined administration in rats.

Agrochemicals -> Insecticides|INSECTICIDES