High dosages of flupora mango (0.1–25 µM; 72 h) cause human hepatocytes to express CYP1A1 and CYP3A4 mRNA [1]. The induction of caspase-3/7 in HepG2 cells is time- and dose-dependent, with flupora mango (0.1-25 µM; 72 h) showing significant effects on caspase-3/7 activity, a key indicator of the cell sterilizing process [1].

Fluorophora cockroach, with IC50 values of 800 and 10 nM, respectively, blocks both glutathione-induced chloride ion desensitizing and non-desensitizing currents [2]. With IC50 values of 28 and 35 nM in the calm and active states, respectively, fluorophora inhibits the intercepted GABA uptake [2].

RT-PCR[1]
Cell Types: Human hepat cells
Tested Concentrations: 0.1-25 µM
Incubation Duration: 72 hrs (hours)
Experimental Results: The expression of CYP1A1 and CYP3A4 mRNA was Dramatically increased in a dose-dependent manner.

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Apoptosis analysis[1]
Cell Types: HepG2 Cell
Tested Concentrations: 0.05, 0.1, 0.5, 1, 3.125, 6.25, 12.5, 25, 50 µM
Incubation Duration: 24, 48, 72 hrs (hours)
Experimental Results: Demonstrated time and dose dependence Induces caspase-3/7 activity from 0.1 µM to 6.25 µM, while slowly decreasing from 12.5 µM to 50 µM.

Absorption, Distribution and Excretion
This study investigated the tissue distribution, metabolic pathways, and excretion of radiolabeled fipronil in rats. Following a single oral administration of 14C-fipronil (10 mg/kg body weight) to rats, approximately 4% of the drug was excreted in urine and feces 72 hours later. The highest radioactivity levels were observed in adipose tissue and adrenal glands at the end of the experiment. The primary source of radioactivity in the studied tissues (adipose tissue, adrenal glands, liver, kidneys, and testes) was fipronil sulfone. Five metabolites were isolated from urine by liquid chromatography-tandem mass spectrometry (LC-MS/MS). These metabolites were mostly formed by the loss of trifluoromethylsulfinyl groups followed by hydroxylation and/or conjugation with glucuronic acid or sulfuric acid. In conclusion, the retention of the fipronil sulfone metabolite in tissues after fipronil administration raises concerns about the potential toxicity of this insecticide. To investigate the localization of fipronil in canine skin, we applied 14C-labeled fipronil drops to a male beagle at a therapeutic dose of 10 mg/kg. Using autoradiography, we precisely measured radioactivity in the skin and its appendages at different time intervals after administration. Radioactivity was primarily found in the stratum corneum (active epidermis) and pilosebaceous units (mainly located in the sebaceous glands and epithelium). For up to 56 days post-administration, we significantly detected 14C-labeled fipronil in these structures, not only in the administration area (neck) but also in the lumbar region, indicating mechanical displacement of fipronil. No radioactivity was detected in the dermis or subcutaneous tissue, confirming the low transdermal absorption rate of fipronil. In vitro, the absorption of 14C-fipronil through the epidermal membranes of humans, rabbits, and mice was measured in a horizontal glass diffusion cell. ...Using the epidermal membrane as a barrier between the two halves of the diffusion cell, the absorption rates of pure fipronil suspension (200 g/L, prepared with EP60145A (a formulation matrix)) and two aqueous solutions of fipronil at concentrations of 0.2 g/L and 4 g/L (with EP60145A as the matrix) were determined. ...Fipronil at concentrations of 4 g/L and 200 g/L showed higher permeability to the epidermal membranes of rabbits and mice than to humans, while at a concentration of 0.2 g/L, permeability was similar in humans and mice. In different species, drug permeability increased over time. Eight hours later, the percentage of penetration into the rat epidermal membrane was 0.08% for the pure formulation, 0.07% for rabbits, and 0.01% for humans; the percentages of penetration for the 4.0 g/L active ingredient dosage were 0.14%, 0.67%, and 0.07%, respectively; and the percentages for the 0.2 g/L active ingredient dosage were 0.9%, 13.9%, and 0.9%, respectively. At a dosage of 4.0 g/L, fipronil penetrated the skin of all three animal groups more slowly than testosterone or hydrocortisone. These two reference penetrants were chosen because their inherent skin penetration rates differ by two orders of magnitude, with testosterone penetrating faster. Based on the results for these two compounds, fipronil is considered a slow penetrant in the EP 60145A formulation. In a study on the absorption, distribution, metabolism, and excretion of fipronil in ruminants, three lactating goats were administered [phenyl(U)-14C]-fipronil (19.2 mCi/mmol) orally in capsule form twice daily at doses of 0.05, 2, or 10 ppm, respectively, for seven consecutive days prior to feeding. Assuming a daily dry matter intake of 2.0 kg, these doses are approximately equivalent to nominal daily doses of 0.1, 4, and 20 mg, respectively. Milk was collected twice daily. Animals were sacrificed approximately 24 hours after the last administration, and tissues were obtained for analysis. Recovery of the radiolabeled substance in urine, milk, and tissues indicated a minimum absorption rate of approximately 19% at 0.05 ppm, approximately 33% at 2 ppm, and approximately 15% at 10 ppm. Of the administered radiolabeled substance, 18–64% was recovered in feces, 1–5% in milk, and 8–25% in tissues. The total recoveries were similar in the low-dose (83%) and high-dose (77%) groups, but slightly lower in the medium-dose (50%) group. The main reason for the difference in animal recoveries among the low-dose, high-dose, and medium-dose groups was the different excretion rates of the radiolabeled material in feces: 18% at 2 ppm, 64% at 0.05 ppm, and 61% at 10 ppm. The reason for this difference is unclear. Among all tissues, the highest total residual concentrations were found in the omentum and kidney fat (approximately 1.9 ppm at a 10 ppm dose), followed by the liver (0.86 ppm), with much lower concentrations in the kidneys, milk (0.17 ppm), and skeletal muscle. For more complete data on absorption, distribution, and excretion of fipronil (15 items), please visit the HSDB records page.
Metabolisms/Metabolites
Fipronil is effective against early-stage sugarcane borers and termites. This study investigated the residues and metabolism of fipronil (Regent 0.3 G) in sugarcane leaves and juice after application at 75 and 300 g ai/ha. Sugarcane leaf samples were collected at different time intervals. Sugarcane juice samples were collected at harvest. Gas chromatography was used to quantitatively analyze the residues of fipronil and its metabolites. The limits of quantification for fipronil and its metabolites in sugarcane leaves and juice were 0.01 mg/kg. Seven days after application of fipronil at 75 g ai/ha and 300 g ai/ha, the total residues of fipronil and its metabolites in sugarcane leaves were 0.26 mg/kg and 0.66 mg/kg, respectively. No residues were detected at either concentration 60 and 90 days after application. In sugarcane leaves, fipronil was the main component, followed by its metabolites amides, desulfinyl groups, sulfones, and sulfides. No fipronil or its metabolites were detected in sugarcane juice samples after application of both doses at harvest. This study investigated the enantioselective bioaccumulation and elimination of fipronil in the African scarab beetle (Anodonta woodiana, or A. woodiana) and determined its major metabolites: fipronil desulfinyl, fipronil sulfide, and fipronil sulfone. The acute toxicity of the enantiomers and their three metabolites was also studied. During bioaccumulation, fipronil reached equilibrium in A. woodiana after 11 days, with a bioaccumulation factor (BCF) of 0.2. The enantiomeric fraction (EF) values indicated enantioselectivity in bioaccumulation, with higher enrichment of the S-fipronil enantiomer. In A. woodiana, the degradation of fipronil followed a first-order kinetic model, with half-lives of 5.8 days for R-fipronil and 7.6 days for S-fipronil. The EF values gradually decreased from 0.5, indicating preferential degradation of the R-enantiomer. The degradation of single enantiomers was also studied, showing that A. woodiana rapidly converts R-fipronil to S-fipronil. Three metabolites were detected in both the A. woodiana-water system, with higher concentrations of fipronil sulfone and fipronil sulfide. Based on the 72-hour LC50 values, the toxicity of S-fipronil was significantly higher than that of the racemic mixture and R-fipronil. Furthermore, the toxicity of these metabolites was also higher than that of the parent fipronil. These findings suggest that individual enantiomers and their metabolites of chiral pollutants should be considered in risk assessments. Fipronil is a phenylpyrazole insecticide commonly used in residential and agricultural applications. To further understand the potential risks of fipronil to humans, researchers analyzed the urine and serum of adult Long Evans rats administered doses of fipronil (5 and 10 mg/kg body weight) to identify metabolites as potential biomarkers for human biomonitoring studies. The study found seven unique metabolites in treated rat urine, two of which were previously unreported—M4 and M7, which were preliminarily identified as a nitrosamine and an imine, respectively. Fipronil sulfone was confirmed as the major metabolite in rat serum. Subsequently, researchers evaluated the fipronil metabolites identified in the corresponding matrices in matched human urine (n=84) and serum (n=96) samples from volunteers with no known history of pesticide exposure. Although fipronil or its metabolites were not detected in human urine, fipronil sulfone was detected at concentrations ranging from 0.1 to 4 ng/mL in the serum of approximately 25% of the subjects. These results indicate that rats exposed to fipronil produce multiple metabolites, and that fipronil sulfone is a useful biomarker in human serum. Furthermore, humans may be frequently exposed to fipronil, thus requiring more comprehensive characterization. This study used radiolabeled fipronil to investigate its tissue distribution, metabolic pathways, and elimination in rats. Following a single oral administration of 14C-fipronil (10 mg/kg body weight) to rats, approximately 4% of the drug was eliminated from urine and feces 72 hours later. At the end of the experiment, the highest levels of radioactivity were observed in adipose tissue and adrenal glands. The main radioactive substances found in the studied tissues (adipose tissue, adrenal glands, liver, kidneys, and testes) originated from fipronil sulfone. Five additional metabolites were isolated from urine by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Most of these metabolites were formed by the loss of trifluoromethylsulfinyl groups followed by hydroxylation and/or conjugation with glucuronic acid or sulfate. In conclusion, the retention of fipronil sulfone metabolites in tissues after fipronil administration raises concerns about the potential toxicity of this insecticide. For more complete data on the metabolites/metabolites of fipronil (15 in total), please visit the HSDB record page. Organic nitriles are converted to cyanide ions in the liver by cytochrome P450 enzymes. Cyanide ions are rapidly absorbed and distributed throughout the body. Cyanide is primarily metabolized to thiocyanate by thiocyanate oxidase or 3-mercaptopyruvate thiotransferase. Cyanide metabolites are excreted in the urine. (L96)

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Biological Half-Life
Female rabbits, rats, and mice were administered M&B 46,030 (fipronil technical grade) (purity: 95.4% (based on information provided in record number 261658)) by gavage for 14 consecutive days. Two groups of rabbits received doses of 0.4 or 1.2 mg/kg/day, and two groups of rats and two groups of mice received doses of 0.4 or 4.0 mg/kg/day (rabbit study data are available in record number 261658). The major metabolite recovered was M&B 46136. The study authors estimated the elimination half-life of M&B 46136 in rabbit blood and adipose tissue to be 11 days and 10 days, respectively. In rodents, these values were 5 days and 6–7 days, respectively. The brain tissue half-life of the metabolite ranged from 4 days (mice) to 9 days (rats) in the three animal groups. The half-life in the liver was 3 to 5 days. In the thyroid gland of rodents, the half-life was 5 days. For rabbits, the concentration of M&B 46030 in the thyroid gland varied too much to calculate its elimination half-life. Male and female CD rats were administered 4 or 40 mg/kg of fipronil-(U-[(14)C]phenyl) (radiochemical purity >99%) by gavage. The specific activity of the administered formulation was adjusted as needed using unlabeled fipronil (purity 99.4%). …The estimated elimination half-lives for males and females in the 40 mg/kg dose group were 135 hours and 171 hours, respectively, while the estimated elimination half-lives for males and females in the 4 mg/kg dose group were 183 hours and 245 hours, respectively. Two female New Zealand white rabbits, five female Sprague-Dawley rats, and ten female CD1 mice were orally administered 5 mg/kg of M&B 46030-[phenyl-U-(14)C] (radiochemical purity: 98.7%, specific activity: 45.1 μCi/mg). The specific activity of the administered formulation was adjusted to approximately 5.8 to 5.9 μCi/mg using unlabeled M&B 46030 (purity: 99.3%). Urine and feces were collected within 168 hours post-administration. Blood samples were collected from each animal at specified time intervals within 168 hours post-administration. ... Regarding pharmacokinetic parameters, the peak plasma concentrations (Cmax) in rabbits, rats, and mice were 0.31, 0.64, and 0.58 μg/g, respectively. The times to peak concentration (tmax) in rabbits, rats, and mice were 12, 9, and 4 hours post-administration, respectively. The half-lives (t1/2) in rabbits, rats, and mice were 14, 3, and 3 days, respectively. Female rabbits, rats, and mice were administered M&B 46,030 (fipronil technical grade) (purity: 95.4% (based on information provided in record number 261658)) by gavage for 14 consecutive days. Two groups of rabbits received 0.4 or 1.2 mg/kg/day of the test drug, and two groups of rats and two groups of mice received 0.4 or 4.0 mg/kg/day of the test drug, respectively (rabbit study data are available in record number 261658). …For rabbits, the authors estimated the elimination half-lives of M&B 46136 in blood and fat to be 11 days and 10 days, respectively. For rodents, the corresponding values were 5 days and 6 to 7 days, respectively. The brain tissue half-lives in all three animals ranged from 4 days (mice) to 9 days (rats). The liver half-lives of the metabolites were 3 to 5 days. The half-lives in the rodent thyroid gland were 5 days. In rabbits, the concentration of M&B 46030 in the thyroid gland varies too much to calculate the elimination half-life. Pharmacokinetic studies have shown that in male and female rats, the whole blood half-life is 149–200 hours after a single low-dose administration (14) C-fipronil (uniformly labeled on the benzene ring; radiochemical purity >97%)).

Toxicity Summary
Identification and Uses: Fipronil is a solid. Fipronil is a pyrazole acaricide and insecticide used to control insects, ticks, lice, and mites on pets. Human Studies: Most exposure cases (89%) resulted in mild, transient health effects. The most common symptoms were neurological (50%), such as headache, dizziness, and paresthesia, followed by ocular symptoms (44%), gastrointestinal symptoms (28%), respiratory symptoms (27%), and skin symptoms (21%). Exposure was usually due to accidental spraying/splashing/overflow of the product or inadequate ventilation of the handling area before re-entry. In vitro cytogenetic tests were performed on fipronil using human lymphocyte cultures. No increase in chromosomal aberrations was reported at any dose level. However, in the basic comet assay, fipronil induced DNA damage in human peripheral blood lymphocytes in vitro. Animal Studies: No skin irritation was observed in rabbits. In studies on female rats, some animals showed peak clinical symptoms of toxicity two days after administration, and death occurred four days after administration. At the end of the observation period on day 7 after administration, some toxic symptoms and weight loss were still observed. Because these results suggested potential bioaccumulation of the test substance, a five-day cumulative dosing study was conducted, dividing four female rats into groups and administering 75 mg/kg body weight of fipronil orally daily for five days. Neurotoxic clinical symptoms were observed after two administrations, and three of the four rats died after three or four administrations. In the only surviving rat in the study, abnormal behavioral responses persisted until six days after the last administration, by which time its weight had recovered to most of its pre-treatment level. Researchers administered commercially available fipronil-containing products orally to pregnant Wistar rats from day 6 to day 20 of gestation at doses of 0.1, 1.0, or 10.0 mg/kg/day. Fipronil caused disordered aggressive behavior in female rats; at the lowest dose, aggression against male intruders decreased, while at the highest dose, aggression increased, but neither dose interfered with the overall activity of female rats in open field experiments. Histopathological analysis revealed no abnormalities. In pregnant rats, fipronil interfered with the development of the reproductive system in neonatal females, manifested as delayed vaginal opening and altered estrous cycles, but had no significant effect on fertility. In this study, CHO-K1 cells were used to evaluate the agonist and antagonist activities of fipronil and its metabolite fipronil sulfone using an in vitro reporter gene assay. Regarding estrogenic and anti-estrogenic activities, neither fipronil nor fipronil sulfone showed agonist activity, but both exhibited similar antagonist activity via estrogen receptor α (ERα). In thyroid hormone receptor (TR) activity assays, only fipronil sulfone showed anti-thyroid hormone activity. Exposing Salmonella Typhimurium strains TA98, TA100, TA1535, TA1537, and TA1538 to the photodegradation product of fipronil (desulfinylfipronil) yielded negative results regardless of metabolic activation. Ecotoxicity studies showed that exposure to fipronil in red-legged partridges (Alectoris rufa) altered blood biochemical parameters and sex hormone levels, and reduced cellular immune responses, antioxidant levels, and carotenoid staining capacity. The fertilization rate of red-legged partridges in the exposed group was reduced, the eggs laid had lower antioxidant content, and the cellular immune response in offspring was also weakened. Fipronil was administered as an equal mixture of two enantiomers. After 7 days of subchronic exposure, juvenile Pimephales promelas exhibited enantioselective toxicity, with the racemic mixture and the (+) enantiomer showing higher toxicity than the (-) enantiomer. It is noteworthy that although the racemic mixture contains 50% (+) enantiomers and 50% (-) enantiomers with lower toxicity, the difference in toxicity between the two is not significant. Fipronil regulates enzyme biomarkers in honeybees (Apis mellifera). Fipronil blocks chloride ions through GABA-regulated chloride channels, thereby disrupting the activity of the central nervous system (CNS). (T10) Organic nitriles can decompose into cyanide ions both in vivo and in vitro. Therefore, the main toxic mechanism of organic nitriles is the production of toxic cyanide ions, or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth electron transport chain complex (located on the mitochondrial membrane of eukaryotic cells). It forms a complex with the ferric atom in this enzyme. The binding of cyanide to this cytochrome prevents electrons from being transferred from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted, and cells can no longer perform aerobic respiration to produce ATP for energy. Tissues that rely primarily on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide can also exert toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydrocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinate dehydrogenase, and copper/zinc superoxide dismutase. Cyanide binds to the iron ions in methemoglobin to form inactive cyanogenic methemoglobin. (L97)

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Interactions
The use of pesticides or insecticides can be highly toxic to aquatic organisms due to leaching and agricultural runoff, rainfall, or flooding. Fipronil (FP) is a GABA receptor inhibitor, while thiamethoxam (BPFN) is an insect growth regulator. This study exposed aquarium-adapted carp (Cyprinus carpio) to sublethal concentrations of fipronil (400 μg/L; 9.15 × 10⁻⁷ mol/L) and thiamethoxam (BPFN, 100 mg/L; 1.072 × 10⁻⁶ mol/L) for 96 hours, either alone or in combination. The extent of damage was assessed biochemically, hematologically, molecularly, and histopathologically. Results from the treated groups were statistically compared with those from the untreated control group, and comparisons were made between each treatment group. A significance level of p < 0.05 was considered. Compared to the control group, the serum total protein and globulin concentrations were significantly lower in the fipronil-treated group (p < 0.0001); however, albumin concentration remained unchanged in all treatment groups. Glucose concentration was significantly lower in the fipronil-treated group (p < 0.002). In contrast, the increase in blood glucose concentration was not significant in the FP+BPFN combined treatment group and the BPFN monotherapy group. Hematological assessment showed that red blood cell count, platelet count, hemoglobin concentration, and hematocrit were significantly decreased in all treatment groups, while white blood cell count was significantly increased (p<0.0001). Blood smears of fish in the pesticide-treated groups showed abnormal red blood cell morphology, including necrosis, micronucleus formation, and increased chromatin. Whole blood DNA fragmentation analysis showed that a large number of DNA fragments were observed in both the FP+BPFN combined treatment group and the BPFN monotherapy group, while no DNA fragmentation was observed in the FP monotherapy group. Compared with the control group, the whole blood DNA content was significantly increased in the FP+BPFN combined treatment group and the BPFN monotherapy group (p<0.001 and p<0.009, respectively). The following changes were observed in gill histopathology in all treatment groups: gill epithelial cell elevation and gill filament necrosis, gill filament atrophy, cartilaginous core destruction, gill filament fusion and disorder, and capillary dilation. Liver histopathological changes included: nuclear fragmentation, hepatocyte hypertrophy, nuclear hypertrophy, melanocyte-macrophage aggregation, and central venous constriction. Kidney histopathological changes included: glomerular degeneration and Bowman's capsule dilation, renal tubular dilation, thyroidization, renal tubular lumen alteration, nuclear hypertrophy, cell atrophy, and cell necrosis. Our study indicates that the combined or individual use of fipronil and BPFN is highly toxic to fish. To our knowledge, this is the first report on the toxicity of fipronil (FP) and fluoride (BPFN) alone and in combination. This study investigated the effects of combined exposure to fipronil and fluoride on the antioxidant status of buffalo calves. Twenty-four healthy male buffalo calves were randomly divided into four groups and treated for 98 consecutive days. Group I (Group I) received no treatment and served as the control group. Groups II and III received oral fipronil at a dose of 0.5 mg/kg/day and oral sodium fluoride (NaF) at a dose of 6.67 mg/kg/day, respectively, for 98 days. Group 4 received oral administration of fipronil and sodium fluoride at the same doses as Groups 2 and 3. Fipronil alone significantly increased lipid peroxidation (LPO) levels and decreased the level of the non-enzymatic antioxidant glutathione (GSH). However, it did not significantly affect the activity of enzymatic antioxidants, including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD). Sodium fluoride (NaF) exposure led to enhanced oxidative stress, manifested by significantly increased LPO and SOD activities, while GPx and CAT activities and glutathione (GSH) levels were significantly decreased. Combined exposure to fipronil and NaF showed an additive effect on LPO, GPx activity, and GSH levels. Fipronil is a relatively new benzylpyrazole insecticide. The effects of fipronil on the in vivo antioxidant system and oxidative stress biomarkers remain to be investigated. This study aimed to evaluate changes in blood biochemical markers and tissue antioxidant enzymes in mice after oral administration of fipronil, and to explore the potential protective effect of pre-administration of antioxidant vitamins against these changes. Mice were divided into eight groups, including a control group, an experimental group, and a modified group. Mice in the experimental group received different doses (2.5, 5, and 10 mg/kg body weight) of fipronil for 28 days. Mice in the modified group were given vitamin E or vitamin C (100 mg/kg each) two hours before receiving high-dose (10 mg/kg) fipronil treatment. All three doses of fipronil treatment resulted in significant increases in blood biochemical markers and lipid peroxidation levels, and caused significant histopathological changes; simultaneously, antioxidant enzyme levels in kidney and brain tissues were significantly decreased. Pre-administration of vitamin E or vitamin C in fipronil-treated mice reduced lipid peroxidation levels and significantly increased the activity of antioxidant enzymes (such as glutathione, total thiols, superoxide dismutase, and catalase). Compared with fipronil treatment alone, concurrent administration of vitamin E and vitamin C to mice treated with fipronil improved the tissue structure of kidney and brain tissue. Therefore, the results of this study indicate that in vivo exposure to fipronil induces oxidative stress, and pretreatment with vitamin E or C can protect mice from this oxidative damage.

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Non-human toxicity values
Oral LD50 in rats: 100 mg/kg
Intraperitoneal LD50 in mice: 32 mg/kg
Oral LD50 in rats: 97 mg/kg
Oral LD50 in male rats (soluble in corn oil): 92 mg/kg body weight / Technical grade fipronil; purity: 93-96.7%/
For more complete non-human toxicity data for fipronil (13 in total), please visit the HSDB record page.

[1]. Fipronil induces CYP isoforms and cytotoxicity in human hepatocytes. Chem Biol Interact. 2006 Dec 15;164(3):200-14.

[2]. Glutamate-activated chloride channels: Unique fipronil targets present in insects but not in mammals. Pestic Biochem Physiol. 2010 Jun 1;97(2):149-152.

Therapeutic Uses
Veterinary: External parasite killer. Veterinary: Fipronil is a broad-spectrum insecticide active against fleas, ticks, mites, and lice.

C12H4CL2F6N4OS

437.1414

435.938

120068-37-3

Fipronil-13C6

3352

White to off-white solid powder

1.9±0.1 g/cm3

510.1±50.0 °C at 760 mmHg

200-201°C

262.3±30.1 °C

0.0±1.3 mmHg at 25°C

1.618

4.76

1

11

2

26

599

0

ZOCSXAVNDGMNBV-UHFFFAOYSA-N

InChI=1S/C12H4Cl2F6N4OS/c13-5-1-4(11(15,16)17)2-6(14)8(5)24-10(22)9(7(3-21)23-24)26(25)12(18,19)20/h1-2H,22H2

5-amino-1-[2,6-dichloro-4-(trifluoromethyl)phenyl]-4-(trifluoromethylsulfinyl)pyrazole-3-carbonitrile

MB-46030 HSDB-7051MB46030 HSDB7051MB 46030 HSDB 7051 Fipronil

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~250 mg/mL (~571.89 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (4.76 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.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (4.76 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)