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
... In this study, the tissue distribution, the metabolic fate, and the elimination of fipronil was investigated in rats using radiolabeled fipronil. When a single oral dose of (14)C-fipronil (10 mg/kg b.w.) was given to rats, the proportion of dose eliminated in urine and feces 72 hr after dosing was ca 4% for each route. At the end of the experiment the highest levels of radioactivity were found in adipose tissue and adrenals. The main part of the radioactivity present in investigated tissues (adipose tissue, adrenals, liver, kidney, testes) was due to fipronil-sulfone. Five additional metabolites, isolated from urine were characterized by LC-MS/MS. Most of them are formed by the loss of the trifluoromethylsulphinyl group and subsequent hydroxylation and/or conjugation to glucuronic acid or sulfate. In conclusion, the retention of the metabolite fipronil sulfone in tissues following fipronil administration raises the question of the potential toxicity of this insecticide.
To investigate the localization of fipronil in dog skin, (14)C-fipronil was topically applied to a male beagle dog (spot-on administration) at the therapeutic dose of 10 mg/kg. By means of autohistoradiography, the radioactivity was precisely detected in the skin and appendages at various intervals after application. Radioactivity was predominantly observed within the stratum corneum, the viable epidermis, and in the pilo-sebaceous units (mainly in the sebaceous glands and epithelial layers). (14)C-fipronil was significantly detected in these structures up to 56 days post-treatment, in the application zone (neck) but also in the lumbar zone, thus indicating the mechanical displacement of fipronil. No radioactivity was detected in either the dermal or the hypodermal layers, confirming the low percutaneous passage of fipronil.
Absorption of (14)C-fipronil through epidermal membranes of humans, rabbits, and rats was measured in vitro in horizontal glass diffusion cells. ... The epidermal membranes were set up as a barrier between the two halves of the diffusion cells, and the absorption rates of a neat suspension of fipronil (200 g/L) as a formulation in EP60145A (a formulation base) and of two aqueous dilutions of the formulation containing 0.2 and 4 g/L of fipronil suspended in EP 60145A were determined ... . Fipronil at doses of 4 and 200 g/L penetrated rabbit and rat epidermal membranes to a greater extent than those of humans, whereas at 0.2 g/L the extent of penetration was similar through human and rat skin. The extent of penetration increased with time across species. The % of the applied dose that had penetrated the different membranes after 8 hr was 0.08% through rat epidermal membranes, 0.07% through rabbit membranes, and 0.01% through human membranes for the neat formulation; 0.14, 0.67, and 0.07% of the dose of 4.0 g/L active ingredient; and 0.9, 13.9, and 0.9% of the dose of 0.2 g/L active ingredient, respectively. At the dose of 4.0 g/L, fipronil penetrated the skin of all three species more slowly than either testosterone or hydrocortisone. These two reference permeants were selected because their intrinsic rates of dermal penetration differ by two orders of magnitude, that of testosterone being faster. On the basis of the results for these two compounds, fipronil was considered to be a slow penetrant when applied as a formulation in EP 60145A.
In a study of the absorption, distribution, metabolism, and excretion of fipronil in ruminants, [phenyl(U)-14C]-fipronil (19.2 mCi/mmol) was administered orally by capsule twice daily before feeding to three lactating goats at a dose of 0.05, 2, or 10 ppm for 7 days; assuming a daily intake of 2.0 kg dry matter, these doses are approx equivalent to nominal daily doses of 0.1, 4, and 20 mg, respectively. Milk was collected twice daily. The animals were killed about 24 hr after admin of the final dose and tissues obtained for analysis. The recovery of radiolabel in urine, milk, and tissues indicated that the min absorption of test material was about 19% at 0.05 ppm, 33% at 2 ppm, and 15% at 10 ppm. Of the administered radiolabel, 18-64% was recovered in feces, 1-5% in the milk, and 8-25% in the tissues. Total recovery was similar at the low (83%) and high doses (77%) but was somewhat lower at the intermediate dose (50%). The greatest contributor to the difference in recovery between the animals at the low and high doses and those at the intermediate dose was the amount of radiolabel excreted in the feces: 18% of the total radiolabel administered at 2 ppm, 64% at 0.05 ppm, and 61% at 10 ppm. The reason for this difference is not clear. The greatest total tissue residues were observed in omental and renal fat (about 1.9 ppm at the 10 ppm dose), followed by liver (0.86 ppm) and much lower concns in kidney, milk (0.17 ppm), and skeletal muscle.
For more Absorption, Distribution and Excretion (Complete) data for Fipronil (15 total), please visit the HSDB record page.

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Metabolism / Metabolites
Fipronil gives effective control of early shoot borer and termites in sugarcane. The persistence and metabolism of fipronil in sugarcane leaves and juice were studied following application of fipronil (Regent 0.3 G) at 75 and 300 g a.i./ha. Samples of sugarcane leaves were collected at various time intervals. Samples of sugarcane juice were collected at harvest. Residues of fipronil and its metabolites were quantified by gas liquid chromatograph. The limit of quantification of fipronil and its metabolites was 0.01 mg/kg for sugarcane leaves and juice. Total residues of fipronil and its metabolites in sugarcane leaves after 7 days of its application at 75 and 300 g a.i./ha were 0.26 and 0.66 mg/kg, respectively. Residues could not be detected after 60 and 90 following fipronil application at either concentration. In sugarcane leaves, fipronil was found to be the main constituent, followed by its metabolites amide, desulfinyl, sulfone and sulfide. Samples of sugarcane juice did not reveal the presence of fipronil or its metabolites following its application at both the dosages at harvest.
The enantioselective bioaccumulation and elimination of fipronil in Anodonta woodiana (A. woodiana) were studied and the main metabolites fipronil desulfinyl, fipronil sulfide and fipronil sulfone were determined. The acute toxicity of the enantiomers of fipronil and the three metabolites were also investigated. In the bioaccumulation process, fipronil in A. woodiana reached equilibrium after 11 days with BCF value of 0.2, and the enantiomeric fraction (EF) values showed that the bioaccumulation was enantioselective with enantioenrichment of S-fipronil. The degradation of fipronil in A. woodiana fitted first-order kinetics model with half-lives of the enantiomers were 5.8 d for R-fipronil and 7.6 d for S-fipronil, and the EF values decreasing from 0.5 gradually indicating the R-enantiomer was preferentially degraded. The degradation of single enantiomers was also performed and the results revealed a fast conversion of R-fipronil to S-fipronil by A. woodiana. The three metabolites were all detected in A. woodiana-water system, in which fipronil sulfone and fipronil sulfide had higher concentration levels. According to the 72-hr LC50 values, S-fipronil was much more toxic than the racemate and R-fipronil. Moreover, the metabolites were more toxic than the parent fipronil. The results suggested the individual enantiomers of chiral pollutants and the metabolites should be considered in the risk assessments.
Fipronil is a phenylpyrazole insecticide commonly used in residential and agricultural applications. To understand more about the potential risks for human exposure associated with fipronil, urine and serum from dosed Long Evans adult rats (5 and 10 mg/kg bw) were analyzed to identify metabolites as potential biomarkers for use in human biomonitoring studies. Urine from treated rats was found to contain seven unique metabolites, two of which had not been previously reported-M4 and M7 which were putatively identified as a nitroso compound and an imine, respectively. Fipronil sulfone was confirmed to be the primary metabolite in rat serum. The fipronil metabolites identified in the respective matrices were then evaluated in matched human urine (n=84) and serum (n=96) samples from volunteers with no known pesticide exposures. Although no fipronil or metabolites were detected in human urine, fipronilsulfone was present in the serum of approximately 25% of the individuals at concentrations ranging from 0.1 to 4 ng/mL. These results indicate that many fipronil metabolites are produced following exposures in rats and that fipronil sulfone is a useful biomarker in human serum. Furthermore, human exposure to fipronil may occur regularly and require more extensive characterization.
... In this study, the tissue distribution, the metabolic fate, and the elimination of fipronil was investigated in rats using radiolabeled fipronil. When a single oral dose of (14)C-fipronil (10 mg/kg b.w.) was given to rats, the proportion of dose eliminated in urine and feces 72 hr after dosing was ca 4% for each route. At the end of the experiment the highest levels of radioactivity were found in adipose tissue and adrenals. The main part of the radioactivity present in investigated tissues (adipose tissue, adrenals, liver, kidney, testes) was due to fipronil-sulfone. Five additional metabolites, isolated from urine were characterized by LC-MS/MS. Most of them are formed by the loss of the trifluoromethylsulphinyl group and subsequent hydroxylation and/or conjugation to glucuronic acid or sulfate. In conclusion, the retention of the metabolite fipronil sulfone in tissues following fipronil administration raises the question of the potential toxicity of this insecticide.
For more Metabolism/Metabolites (Complete) data for Fipronil (15 total), please visit the HSDB record page.
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)

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Biological Half-Life
Female rabbits, rats and mice were dosed orally by gavage with M&B 46,030 (fipronil technical) (purity: 95.4% (based upon information provided under record no. 261658)) for 14 days. Two groups of rabbits received 0.4 or 1.2 mg/kg/day and two groups each of rats and mice were dosed with 0.4 or 4.0 mg/kg/day of the test material (study data for the rabbits is presented in record no. 261658). ... The predominant metabolite which was recovered was M&B 46136. ... For the rabbit, the study authors estimated the elimination half-lives for M&B 46136 to be 11 and 10 days for blood and fat, respectively. For the rodents, the values were 5 and 6 to 7 days, respectively. The brain half-lives ranged from 4 (mouse) to 9 days (rat) for the 3 species. The liver half-life values for the metabolite ranged between 3 and 5 days. The half-life in the thyroid of the rodents was 5 days. For the rabbit, the concentrations of M&B 46030 in the thyroid were too variable to calculate an elimination half-life.
Male and female CD rats were dosed orally by gavage with 4 or 40 mg/kg of Fipronil- (U-[(14)C] phenyl) (radiochemical purity > 99%). The specific activities of the dosing preparations were adjusted as required using unlabeled Fipronil (purity 99.4%). ... Elimination t1/2 estimates were 135 and 171 hours for 40 mg/kg males and females, compared to 183 and 245 hours for 4 mg/kg males and females.
Two female New Zealand white rabbits, 5 female Sprague-Dawley rats and 10 female CD1 mice were dosed orally with 5 mg/kg of M&B 46030- [phenyl-U-(14)C] (radiochemical purity: 98.7%, specific activity: 45.1 uCi/mg). The specific activity of the dosing preparations was adjusted to approximately 5.8 to 5.9 uCi/mg, using unlabeled M&B 46030 (purity: 99.3%). Urine and feces were collected up to 168 hours post-dose. Blood was drawn from each animal at specified intervals up to 168 hours post-dose. ... For the pharmacokinetic parameters, the Cmax values in the blood were 0.31, 0.64 and 0.58 ug/g for the rabbit, rat, and mouse, respectively. The tmax times were 12, 9 and 4 hours post-dose for the rabbit, rat, and mouse, respectively. The reported t1/2 times were 14, 3, and 3 days for the rabbit, rat and mouse, respectively.
Female rabbits, rats and mice were dosed orally by gavage with M&B 46,030 (fipronil technical) (purity: 95.4% (based upon information provided under record no. 261658)) for 14 days. Two groups of rabbits received 0.4 or 1.2 mg/kg/day and two groups each of rats and mice were dosed with 0.4 or 4.0 mg/kg/day of the test material (study data for the rabbits is presented in record no. 261658). ... For the rabbit, the study authors estimated the elimination half-lives for M&B 46136 to be 11 and 10 days for blood and fat, respectively. For the rodents, the values were 5 and 6 to 7 days, respectively. The brain half-lives ranged from 4 (mouse) to 9 days (rat) for the 3 species. The liver half-life values for the metabolite ranged between 3 and 5 days. The half-life in the thyroid of the rodents was 5 days. For the rabbit, the concentrations of M&B 46030 in the thyroid were too variable to calculate an elimination half-life.
Pharmacokinetic investigations showed that the whole-blood half-life at the single low dose was 149-200 hr in male and female rats /administered (14)C-fipronil (labelled uniformly at the phenyl ring; radiochemical purity, >97%)/... .

Toxicity Summary
IDENTIFICATION AND USE: Fipronil is a solid. Fipronil is a pyrazole acaricide and insecticide that may be used for insect, tick, lice, and mite control on pets. HUMAN STUDIES: Most cases of exposure (89%) had mild, temporary health effects. Neurological symptoms (50%) such as headache, dizziness, and paresthesia were the most common, followed by ocular (44%), gastrointestinal (28%), respiratory (27%), and dermal (21%) symptoms. Exposures usually occurred from inadvertent spray/splash/spill of products or inadequate ventilation of the treated area before re-entry. Fipronil was tested in an in vitro cytogenetics assay using human lymphocyte cultures. No increase in chromosome aberrations was reported at any dose level. However, in an alkaline comet assay fipronil induced DNA damage in human peripheral blood lymphocytes in vitro. ANIMAL STUDIES: No skin irritation was observed in rabbits. In studies with female rats, the clinical signs of toxicity did not reach their peak until 2 days after treatment in some animals, and deaths did not occur until 4 days after treatment. Some signs of toxicity and body-weight loss were still evident when the observation period ended at day 7 after treatment. Since these findings suggested that bioaccumulation of the test material could occur, a 5-day study with cumulative treatment was performed in which groups of 4 female rats were given fipronil at 75 mg/kg bw/day orally for up to 5 days. Clinical signs of neurotoxicity were seen after administration of 2 doses, and 3 of 4 rats died after admin of 3 or 4 doses. In the only rat that survived the study, abnormal behavioral responses persisted until 6 days after administration of the final dose, at which time it had regained most of its pretreatment weight. A commercial product that contains fipronil was administered orally to pregnant Wistar rats at dosages of 0.1, 1.0, or 10.0 mg/kg/day from the 6th to the 20th day of gestation. The fipronil caused a disturbance of the maternal aggressive behavior; the aggression against a male intruder decreased at the lowest dose, but increased at the highest dose, without interfering with the general activity of the dams in the open field test at either dose. The histopathological analysis revealed no abnormalities. In pregnant rats fipronil interfered with development of neonatal female reproductive system as evidenced by delay in vaginal opening and estrus cycle alterations without apparent significant effects on fertility. The agonistic and antagonistic activities of fipronil and its metabolite, fipronil sulfone were evaluated by in vitro reporter gene assays using CHO-K1 cells. For estrogenic and antiestrogenic activities, both fipronil and fipronil sulfone showed no agonistic activities but exhibited the similarly antagonistic activities via estrogen receptor alpha (ERalpha). In the thyroid hormone receptor (TR) assay, only fipronil sulfone showed anti-thyroid hormone activity. Salmonella typhimurium strains TA98, TA100, TA1535, TA1537, and TA1538 were exposed to a photodegradation product (desulfinyl fipronil) of fipronil with or without metabolic activation with negative result. ECOTOXICITY STUDIES: Fipronil exposure in red-legged partridge (Alectoris rufa) altered blood biochemistry and sexual hormone levels and reduced cellular immune response, antioxidant levels, and carotenoid-based coloration. Exposed pairs also had reduced egg fecundation rate and produced eggs with fewer antioxidants and offspring that had reduced cellular immune response. Fipronil is applied as an equal mixture of two enantiomers. Enantioselective toxicity was observed in larval fathead minnows (Pimephales promelas) after the 7-d subchronic exposure, with increased toxicity of the racemate and (+) enantiomer observed compared with the (-) enantiomer. Curiously, toxicities of the racemate and (+) enantiomer were not significantly different, even though the racemate contains 50% of the (+) enantiomer and 50% of the less toxic (-) enantiomer. Fipronil modulated enzyme biomarkers in the honeybee Apis mellifera.
Fipronil blocks the passage of chloride ions through the GABA-regulated chloride channel, disrupting CNS activity. (T10) Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)

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Interactions
Use of pesticides or insecticides can be highly toxic to aquatic life forms due to leaching and agricultural runoff, rains or flood. Fipronil(FP) is a GABA receptor inhibitor, while buprofezin (BPFN) is an insect growth regulator. Presently, we exposed groups of aquaria acclimated carp fish (Cyprinus carpio) for 96 hr to sub-lethal concentrations of fipronil (400 ug/L; 9.15 x 10(-7) mol/L) and buprofezin (BPFN, 100 mg/L; 1.072 x 10(-6) mol/L) singly or in combination. The extent of damage was assessed at biochemical, hematological, molecular biological and histopathological level. Results obtained in treated fish were compared statistically with those of control non-treated fish and also among treatment groups. Significance level was p<0.05. Compared to control, serum total protein and globulin concentrations decreased significantly (p<0.0001) in fish treated with FP; while albumin concentration remained unaltered with all treatments. Glucose concentration decreased significantly (p<0.002) in fish treated with FP. In contrast, combined FP+BPFN treatment and BPFN treatment caused insignificant elevation of glucose concentration. Hematological assessment demonstrated significant decrease in red blood cell and thrombocyte counts, hemoglobin concentration and hematocrit percent; while white blood cell count showed an increase in all treatment groups (p<0.0001). Blood smears from pesticide treated fish revealed aberrant erythrocyte morphologies which included necrosis, micronuclear formation and hyperchromatosis. DNA laddering assay carried out on whole blood demonstrated excessive smear formation in combined FP+BPFN and BPFN treatment groups but no smear formation was noticeable in FP treated fish. Compared to control, whole blood DNA content increased significantly in the combined FP+BPFN and BPFN treatment groups (p<0.001 and p<0.009). With all treatments histopathological changes observed in the gills were: epithelial uplifting and necrosis of lamellae, lamellar atrophy, disruption of cartilaginous core, fusion and disorganization of lamellae and telangiectasia. In liver these were: karyorrhexis, hepatocellular hypertrophy, nuclear hypertrophy, melanomacrophage aggregates and central vein contraction, while in the kidney: deterioration of glomerulus and dilatation of Bowman's space, dilatation of renal tubules, thyroidisation, altered tubular lumen, nuclear hypertrophy, cellular atrophy, and cellular necrosis were the outcome. Our study revealed that FP and BPFN produce highly toxic effects on fish when given in combination or singly. To our knowledge, this is the first report on toxicity caused by FP and BPFN in single and combined state.
The effects of fipronil and fluoride co-exposure were investigated on antioxidant status of buffalo calves. A total of 24 healthy male buffalo calves divided into 4 groups were treated for 98 consecutive days. Group I, receiving no treatment, served as the control. Animals of groups II and III were orally administered with fipronil at the dosage of 0.5 mg/kg/day and sodium fluoride (NaF) at the dosage of 6.67 mg/kg/day, respectively, for 98 days. Group IV was coadministered with fipronil and NaF at the same dosages as groups II and III. Administration of fipronil alone produced significant elevation in lipid peroxidation (LPO) and decrease in the levels of nonenzymatic antioxidant glutathione (GSH). However, it did not produce any significant effect on the activities of enzymatic antioxidants including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD). NaF exposure led to enhanced oxidative stress as shown by significant increase in the LPO and SOD activities while GPx and CAT activities and GSH levels were significantly decreased. Co-exposure to fipronil and NaF showed additive effects on LPO, GPx activity, and GSH levels.
Fipronil is a relatively new insecticide of the phenpyrazole group. Fipronil-induced effects on antioxidant system and oxidative stress biomarkers are yet to be studied in vivo. The present study was undertaken to evaluate fipronil-induced alterations in the blood biochemical markers and tissue antioxidant enzymes after oral exposure in mice and to explore possible protective effect of pre-treatment of antioxidant vitamins against these alterations. Mice were divided into eight groups containing control, test and amelioration groups. Mice in the test groups were exposed to different doses of fipronil, i.e., 2.5, 5 and 10 mg/kg bw, respectively for 28 days. Mice in the amelioration groups were treated with vitamin E or vitamin C (each at 100 mg/kg) 2 hr prior to high dose (10 mg/kg) of fipronil. Fipronil exposure at three doses caused significant increase in the blood biochemical markers, lipid peroxidation and prominent histopathological alterations; while level of antioxidant enzymes was severely decreased both in kidney and brain tissues. Prior administration of vitamin E or vitamin C in the fipronil exposed mice led to decrease in lipid peroxidation and significant increase in activities of antioxidants, viz., glutathione, total thiol, superoxide dismutase and catalase. Vitamin E and vitamin C administration in fipronil exposed mice also improved histological architecture of the kidney and brain when compared with fipronil alone treated groups. Thus, results of the present study demonstrated that in vivo fipronil exposure induces oxidative stress and pre-treatment with vitamin E or C can protect mice against this oxidative insult.

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Non-Human Toxicity Values
LD50 Rat oral 100 mg/kg
LD50 Mouse ip 32 mg/kg
LD50 Rat oral 97 mg/kg.
LD50 Rat (male) oral (administered in corn oil) 92 mg/kg bw /Technical-grade fipronil; purity, 93-96.7%/
For more Non-Human Toxicity Values (Complete) data for Fipronil (13 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
VET: Ectoparasiticide.
VET: Fipronil is a broad-spectrum pesticide with activity 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.)