Bifenthrin suppresses A. gambiae as well as C. quinquefasciatus, whose respective LD50 values are 0.15 and 0.16 ng/mg[1]. Filter paper treated with benthrin and subjected to C. Only doses of 0.5% and 0.125%, respectively, of quinquefasciatus and A gambiae tarsi can result in 100% mortality [1].

Absorption, Distribution and Excretion
Male and female rats were administered single oral doses of (14)C-labeled bifenthrin (labeled in the acid or alcohol fraction, respectively) at doses of 4 and 35 mg/kg. (14)C was rapidly excreted in feces and urine at rates of 66-83% and 13-25%, respectively. The highest residual levels were found in fat, slightly above 1 ppm after low-dose administration, and 8 ppm and 16 ppm in fat in male and female rats after high-dose administration, respectively. Residual levels in other organs were generally below 0.2 ppm after low-dose administration and below 1 ppm after high-dose administration. Tissue residues were assessed after rats were orally administered (0.5 mg/kg/day) of (14)C-bifenthrin for 70 days. The average peak concentrations of (14)C were: fat 9.6 ppm, skin 1.7 ppm, liver 0.4 ppm, kidney 0.3 ppm, ovary 1.7 ppm, sciatic nerve 3.2 ppm, whole blood 0.06 ppm, and plasma 0.06 ppm. Analysis continued for 85 days after drug withdrawal (cleanup period). Based on the clearance rate of 14C, the half-lives of each organ were estimated as follows: fat 51 days, skin 50 days, liver 19 days, kidney 28 days, and ovary and sciatic nerve 40 days. Fat analysis showed that the parent compound accounted for the vast majority (65-85%) of the 14C residues in fat. Pyrethroid compounds can be absorbed through intact skin when applied topically. /Pyrethroids/ ... This article describes the pharmacokinetics of bifenthrin in rats after oral, inhalation, and intravenous administration. In addition, the acute toxicity of pyrethroid compounds via oral and inhalation routes is also described. Male rats were divided into groups and administered bifenthrin via gavage at a dose of 3.1 mg/kg (dissolved in 1 mL/kg corn oil, i.e., the lower limit of the critical acute oral dose, BMDL), and via inhalation at an equivalent dose (0.018 mg/L), for 4 hours. Plasma and brain tissue concentrations of bifenthrin were measured at 2, 4, 6, 8, and 12 hours after administration. The maximum plasma concentrations of bifenthrin were 361 ng/mL (0.853 μM, oral) and 232 ng/mL (0.548 μM, inhalation), respectively; the maximum brain tissue concentrations were 83 ng/g and 73 ng/g, respectively. After gavage administration, the area under the concentration-time curve (AUC) values in plasma and brain tissue were 1969 h ng/mL and 763 h ng/mL, respectively; after inhalation administration, the AUC values in plasma and brain tissue were 1584 h ng/mL and 619 h ng/mL, respectively. Following intravenous administration, the apparent terminal half-lives (t1/2) in plasma and brain tissue were 13.4 h and 11.1 h, respectively, with AUC0-∞ values of 454 h ng/mL and 1566 h ng/mL, respectively. Plasma clearance was 37 mL/min/kg. Peak concentrations in plasma and brain tissue were generally slightly higher (approximately 14%) after oral administration. Inhalation administration avoids the first-pass effect in the liver and therefore does not increase drug exposure in plasma or brain tissue. The elimination half-life is comparable to other pyrethroid insecticides, indicating low bioaccumulation potential. …This study evaluated the oral distribution and bioavailability of bifenthrin in adult male Long-Evans rats. In the distribution study, rats were administered bifenthrin (0.3 or 3 mg/kg) orally by gavage and sacrificed in batches (0.25 h to 21 days). Blood, liver, brain, and adipose tissue were collected. In the bioavailability study, rats were cannulated via the jugular vein and administered bifenthrin orally (0.3 or 3 mg/kg) or intravenously (0.3 mg/kg). Blood samples were collected in batches (0.25 to 24 hours later). Tissue samples were extracted, and the bifenthrin content was analyzed by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Peak concentrations of bifenthrin in blood and liver were reached 1–2 hours after oral administration, with concentrations of approximately 90 ng/mL (or g) and 1000 ng/mL (or g) in blood and liver, respectively, at the 0.3 mg/kg dose. Bifenthrin was rapidly cleared from both blood and liver. Peak concentrations in brain tissue were reached at 4–6 hours, and were lower than blood concentrations at both doses (12 ng/g and 143 ng/g, respectively). Peak concentrations of bifenthrin in adipose tissue were reached at 8 hours (157 ng/g) and 24 hours (1145 ng/g) after administration in the 0.3 mg/kg and 3 mg/kg dose groups, respectively, and persisted for 21 days after oral administration. Following intravenous administration, blood concentrations of bifenthrin exhibited a biexponential decline, with a distribution half-life of 0.2 hours and an elimination half-life of 8 hours. The bioavailability of bifenthrin is approximately 30%. These in vivo distribution and kinetic data for bifenthrin may help reduce uncertainties in the risk assessment of this pyrethroid insecticide. Metabolism/Metabolites Male and female rats were treated with single oral doses of 4 and 35 mg/kg, respectively, of bifenthrin labeled in the acid or alcohol moiety. 14C is rapidly excreted in feces and urine, with excretion rates of 66-83% and 13-25% in feces and urine, respectively. The main fecal metabolites have intact ester bonds and are hydroxylated at the acid or alcohol moiety, such as hydroxymethyl bifenthrin, 4'-hydroxybifenthrin, and 3'- or 4'-hydroxymethyl bifenthrin. Ester cleavage products derived from monohydroxylated and dihydroxylated parent compounds were also detected. On the other hand, urinary metabolites are mainly ester bond cleavage products, such as 4'-OH-BPacid (4'-hydroxy-2-methyl-3-phenylbenzoic acid), BPacid (2-methyl-3-phenylbenzoic acid), 4'-OH-BPalcohol (4'-hydroxy-2-methyl-3-phenylbenzyl alcohol), dimethoxy-BPacid, 4'-methoxy-BPacid, dimethoxy-BPalcohol, BPacid, and TFPacid. [3-(2-chloro-3,3,3-trifluoro-1-propenyl-2,2-dimethylcyclopropanecarboxylic acid], cis- and trans-hydroxymethyl TFPacid. The main metabolic pathway is thought to be ester bond hydrolysis, oxidation of the acid moiety at the 3'- and 4'-positions of the methyl and phenyl groups, and O-methylation. Conjugation reactions are also thought to occur; however, details are not yet available.
Primary alcohol esters of trans-substituted acids decompose most rapidly because they undergo rapid hydrolysis and oxidative attack. For all secondary alcohol esters and primary alcohols of cis-substituted cyclopropanecarboxylic acids, oxidative attack... Dominant. /Pyrethroids/
Pyrethroids are reportedly inactivated in the gastrointestinal tract after ingestion. In animals, pyrethroids are rapidly metabolized into water-soluble, inactive compounds. /Pyrethroids/
Bifenthrin is a pyrethroid insecticide that exhibits estrogenic activity in fish. However, bifenthrin has been documented to have anti-estrogenic activity in vitro, in ER-CALUX (estrogen receptor) cell lines. We investigated whether the formation of metabolites was the cause of this contradiction. We used Menidia Beryllina (inland silverfish) was exposed to 10 ng/L bifenthrin, 10 ng/L 4-hydroxybifenthrin, and a mixture of 10 ng/L bifenthrin and 25 μg/L synergist ether (PBO) (a P450 inhibitor). The levels of estrogen-mediated proteins (chorionic gonadotropin) in larvae of the metabolite-exposed group were significantly higher than those in the bifenthrin/PBO-exposed group, while the levels in the bifenthrin monotherapy group were intermediate (not significantly different from either group). This indicates that metabolites are the main source of estrogenic activity of bifenthrin in vivo. Synthetic pyrethroids are typically metabolized in mammals via ester hydrolysis, oxidation, and conjugation, and do not accumulate in tissues. In the environment, synthetic pyrethroids degrade relatively rapidly in soil and plants. Ester hydrolysis and oxidation at different sites on the molecule are the main degradation processes. /Pyrethroid/

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Biological half-life
Rats orally administered 0.5 (14)C-bifenthrin was administered at mg/kg/day for 70 days, and tissue residues were then assessed. …After discontinuation, the analysis was extended to 85 days (purification period). Based on the (14)C-purification status, the half-lives of various tissues were estimated as follows: fat 51 days, skin 50 days, liver 19 days, kidney 28 days, ovary and sciatic nerve 40 days. …After intravenous administration, the apparent terminal half-lives (t1/2) in plasma and brain tissue were 13.4 hours and 11.1 hours, respectively. …After intravenous administration, the concentration of bifenthrin in the blood showed a bi-exponential decrease, with a distribution half-life of 0.2 hours and an elimination half-life of 8 hours.

Toxicity Summary
Identification and Uses: Bifenthrin is a light brown, viscous, oily substance. It is registered for the control of a wide range of insects, including aphids, worms, ants, midges, moths, beetles, grasshoppers, mites, midges, spiders, ticks, wasps, maggots, thrips, caterpillars, flies, fleas, and other pests, and is suitable for use in home, public health, agricultural, and industrial environments. Human Exposure and Toxicity: Nervous system effects include dizziness, headache, tingling and numbness, muscle spasms, and tremors. Skin effects include rash, hives, blisters, ulcers, and itching. Respiratory symptoms include shortness of breath, asthma, respiratory distress, respiratory irritation, cough, difficulty breathing, sinus problems, and chest pain. Most gastrointestinal symptoms are nausea and vomiting; a few cases have experienced abdominal pain and diarrhea. Eye symptoms include red, painful, and swollen eyes, itchy and watery eyes, and blurred vision. Cardiovascular symptoms such as hypertension, arrhythmia, and heart attack have occurred in a few cases. Even within “acceptable” limits, exposure to bifenthrin increases the risk and frequency of inflammatory responses and diseases such as asthma. Animal studies: Non-irritating to skin; virtually non-irritating to eyes (rabbit); no skin sensitization (guinea pig). Bifenthrin technical grade, active ingredient 88.35%, cis 98%, trans 2%. Concentrations of 200, 100, 50, 12, and 0 ppm were added to the diet of 50 rats per group (per sex per dose) for 2 years. No carcinogenic effects have been reported. Adverse reactions included tremor, abrasion, hair loss, tail lacerations, decreased weight gain (females only), and 12% erythrocyte reduction (males only). All adverse reactions were observed at a concentration of 200 ppm. Bifenthrin technical grade 89.7% was encapsulated in gelatin capsules at nominal concentrations of 0, 0.75, 1.50, 3.0, and 5.0 mg/kg/day and administered to four beagle dogs per group (one group per sex) for 52 consecutive weeks. At doses of 3.0 and 5.0 mg/kg/day, intermittent delayed tremor appeared at week 29. The active ingredient of bifenthrin technical grade was 88.35%, with 98% of the cis isomer and 2% of the trans isomer. Rats were fed bifenthrin at 100, 60, 30, and 0 ppm in their diet, respectively, from 8 weeks before mating in the F0 generation to weaning in the F2b generation; each dose group consisted of 25 rats, half male and half female. No effects on fertility or reproduction were observed; other effects included lactational tremor and reduced ovarian weight in adult rats. Bifenthrin was not teratogenic in rats (≥2 mg/kg/day) and rabbits (8 mg/kg/day). In the highest dose group (9 mg/kg/day), tremors were observed in 6 out of 40 tested juvenile mice (4 males, day 10; 2 females, day 28). Bifenthrin did not show mutagenicity in the Ames test and did not cause chromosomal aberrations in Chinese hamster ovary (CHO) cells. Ecotoxicity studies: Based on available data, bifenthrin exhibits mild acute toxicity to birds. At the highest tested concentration in birds, bifenthrin did not show adverse effects on reproduction. Mammalian toxicity data indicate that the compound has moderate acute toxicity to small mammals. Rainbow trout showed different responses to acute toxicity of bifenthrin compared to hardhead trout, and different biotransformation rates of bifenthrin in the liver. Bifenthrin exhibits high acute and chronic toxicity to freshwater fish and aquatic amphibians, and extremely high toxicity to freshwater aquatic invertebrates. Bifenthrin is also classified as having extremely high acute toxicity to estuarine/marine fish and invertebrates.

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Interactions
This study employed a novel two-stage analytical approach, utilizing a standardized water column toxicity test, to characterize and quantify the interactions between type I and type II pyrethroids and the water flea (Hyalella azteca). In six experiments, we tested all possible binary combinations of bifenthrin, permethrin, cypermethrin, and lambda-cyhalothrin. All mixtures underwent 4-day lethality analysis, with two mixtures (permethrin-bifenthrin and permethrin-cyhalothrin) also undergoing 10-day subchronic lethality testing and sublethal effects on swimming and growth. Interactions between mixtures were first analyzed using regression analysis, then compared with concentration-additive (CA) and independent-action (IA) models to further characterize the mixture responses. Of the six mixtures tested, two mixtures (including cypermethrin-bifenthrin and cypermethrin-permethrin) exhibited significant negative interactions (antagonistic effects), but these were observed only at the 4-day acute lethality endpoint. In both cases, the mixtures' responses fell between the CA and IA models. All other mixtures showed an additive effect on 4-day lethality, and bifenthrin-permethrin and deltamethrin-permethrin also showed additive effects on 10-day subchronic lethality and sublethal response.
The synergist enhances the insecticidal activity of pyrethroids by inhibiting the hydrolytic enzymes responsible for pyrethroid metabolism in arthropods. When synergist is used in combination with pyrethroids, the latter's insecticidal activity can be increased by 2-12 times.
When 1000 ppm pyrethroids and 10000 ppm synergist are added to feed, enlargement, marginalization, and cytoplasmic inclusions in rat hepatocytes are noticeable within just 8 days, but do not reach their maximum value. These changes are dose-proportional and similar to the effects of DDT. The effects of the two compounds have an additive effect. /Pyrethroids/
This study investigated three carbamate insecticides (methamidophos, methomyl, and pyraclostrobin) and one pyrethroid insecticide (bifenthrin), including pure chemicals and commercial formulations, to reveal the potential toxic effects of additives and solvents in commercial formulations and to evaluate cellular stress responses as a defense mechanism. The toxic effects on A549 cells derived from human lung cancer were assessed by measuring the following parameters: (1) the threshold concentration (LOEC) leading to reduced growth rate; (2) the sublethal concentration (SC) that inhibits cell growth but does not kill cells; and (3) the expression levels of several stress proteins (such as HSP27, HSP72/73, HSP90, GRP78, and GRP94). LOECs were observed at lower concentrations when using commercial formulations (such as Dicarzol (methamidophos), Lannate20 (methomyl), and Talstar or Kiros EV (bifenthrin)) compared to the pure active molecules. The presence of propylene glycol and propylene glycol monomethyl ether in Talstar and Kiros, respectively, is not the cause of the high toxicity of these commercially available formulations, nor does it enhance the toxicity of bifenthrin. When cells were exposed to a mixture of four different commercially available formulations, an additive rather than synergistic adverse reaction was observed… All insecticides upregulated GRP78 expression, with the commercially available formulations triggering the stress response more effectively. This suggests that the insecticides and additives in the commercially available formulations disrupt endoplasmic reticulum function. Conversely, all insecticides downregulated HSP72/73 expression. This appears to be related to a reduction in protein synthesis in the cytosol, which is due to the endoplasmic reticulum's unfolded protein response. In fact, tunicamycin, known to inhibit N-linked glycosylation in the endoplasmic reticulum, was found to induce a similar negative correlation between GRP78 overexpression and HSP72/73 low expression. The highest concentration of commercially available bifenthrin increased GRP94 expression and decreased HSP27 expression. Methomyl and Lanat 20 only induced low expression of HSP90.

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Non-human toxicity values
Oral LD50 in rats: 375 mg/kg
Oral LD50 in rats: 54.5 mg/kg
Oral LD50 in quail: 1800 mg/kg
Oral LD50 in ducks: >4450 mg/kg
Dermal LD50 in rabbits: >2000 mg/kg

[1]. Bifenthrin: a useful pyrethroid insecticide for treatment of mosquito nets. J Med Entomol. 2002 May;39(3):526-33.

[2]. Structure-activity relationships for the action of 11 pyrethroid insecticides on rat Na v 1.8 sodium channels expressed in Xenopus oocytes. Toxicol Appl Pharmacol. 2006 Mar 15;211(3):233-44.

Bifenthrin is a grayish-white to light brown waxy solid with a slightly sweet taste and a very faint odor. It is a broad-spectrum insecticide. Bifenthrin is a carboxylic acid ester formed by the condensation of cis-3-(2-chloro-3,3,3-trifluoropropenyl)-2,2-dimethylcyclopropanecarboxylic acid with [(2-methyl-1,1'-biphenyl)-3-yl]methanol. It is a pyrethroid insecticide and a pyrethroid acaricide. It is an organochlorine compound, an organofluorine compound, and a cyclopropane carboxylic acid ester. Functionally, it is related to cis-chrysanthemic acid. Bifenthrin is currently being investigated in the clinical trial NCT01560247 (European Observational Registry Study of Percutaneous Reperfusion Therapy for Ischemic Stroke).
See also: ...See more...

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Mechanism of Action
Bifenthrin is a relatively stable type I pyrethroid that induces tremors and impairs motor function in rodents, and is therefore widely used. We investigated whether nanomolar concentrations of bifenthrin altered synchronous Ca2+ oscillations (SCO), essential for activity-dependent dendritic development. Primary mouse cortical neurons were cultured in vitro for 8 or 9 days (DIV), loaded with the Ca2+ indicator Fluo-4, and imaged using a Tetra fluorescence imaging plate reader. Acute exposure to bifenthrin rapidly increased the frequency of SCO by 2.7-fold (EC50 = 58 nM) and decreased the amplitude of SCO by 36%. The alteration of SCO characteristics was independent of modification of voltage-gated sodium channels, as 100 nM bifenthrin had no effect on whole-cell Na+ currents or neuronal resting membrane potentials. The L-type Ca2+ channel blocker nifedipine failed to improve bifenthrin-induced SCO activity. Conversely, the metabolite glutamate receptor (mGluR) 5 antagonist MPEP [2-methyl-6-(phenylethynyl)pyridine] restored the bifenthrin-induced increase in SCO frequency to normal without altering baseline SCO activity, indicating that bifenthrin-enhanced mGluR5 signaling is independent of Na+ channel modification. Competitive [AP-5; (-)-2-amino-5-phosphatric acid] and non-competitive N-methyl-D-aspartate antagonists (dizoczepine or MK-801 [(5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cycloheptene-5,10-imine maleate]) both partially reduced the basal and bifenthrin-induced increase in SCO frequency. Bifenthrin-modified SCO rapidly enhanced the phosphorylation of cAMP response element-binding protein (CREB). Subacute (48-hour) exposure to bifenthrin starting from day 2 of culture enhanced neurite growth and persistently increased SCO frequency while decreasing SCO amplitude. Bifenthrin-stimulated neurite growth and CREB phosphorylation were dependent on mGluR5 activity, as MPEP restored both responses to normal. These data collectively reveal a novel mechanism by which bifenthrin effectively alters Ca2+ dynamics and Ca2+-dependent signaling in cortical neurons, thereby exerting long-term effects on activity-driven neuronal plasticity. Bifenthrin is a pyrethroid insecticide with estrogenic activity in fish. However, it has been documented that bifenthrin exhibits anti-estrogenic activity in vitro, particularly in ER-CALUX (estrogen receptor) cell lines. We investigated whether the formation of metabolites contributes to this paradox. We exposed inland silverfish (Menidia beryllina) to solutions of 10 ng/L bifenthrin, 10 ng/L 4-hydroxybifenthrin, and a mixture of 10 ng/L bifenthrin and 25 μg/L synergist ether (PBO, a P450 inhibitor). In the metabolite-exposed group, the level of estrogen-mediated protein (pro-chorionic gonadotropin) in juvenile mice was significantly higher than that in the bifenthrin/PBO-exposed group, while the level in the bifenthrin monotherapy group was intermediate (not significantly different from either group). This indicates that the metabolite is the main contributor to the estrogenic activity of bifenthrin in vivo. Voltage-gated sodium channels are important targets for the neurotoxicity of pyrethroid insecticides in mammals. This study investigated the mechanism of action of bifenthrin on natural sodium channels in neonatal rat cortical neurons, which are the main sites of its toxic effects. Bifenthrin induces a significant late current that persists at the end of the depolarization pulse; a slowly decaying tail current follows repolarization; and a significant change in resting state (25.3% at 10 μM). No significant bifenthrin-induced effect was observed at the peak current. Bifenthrin also induces a concentration-dependent hyperpolarization shift in steady-state activation and inactivation, and slows recovery after channel inactivation. Repeated depolarization enhances the potency of bifenthrin, with higher frequency depolarization showing a more pronounced effect. After repeated activation with a 10 Hz depolarization pulse train, the inhibition rate of channel modification was approximately 64%. These results indicate that bifenthrin can bind to and modify sodium channels in both closed and open states, behaving intermediately between type I and type II sodium channels.
…Since dopaminergic signaling significantly affects the release of gonadotropin-releasing hormone (GnRH2) in fish, this study aimed to determine the effects of bifenthrin exposure on dopaminergic signaling in juvenile rainbow trout (Oncorhynchus mykiss) (RT) after 96 hours and 2 weeks. Our results showed that plasma 17β-estradiol (E2) levels increased after 96 hours and 2 weeks of exposure to 1.5 ppb (3.55 pM) bifenthrin, dopamine receptor 2A (DR2A) expression decreased, and the relative expression of vitellogenin mRNA significantly increased at 2 weeks. In rat brain tissue exposed to 1.5 ppb (3.55 pM) bifenthrin, DR2A mRNA expression decreased by 426-fold at 96 hours and by 269-fold at 2 weeks. At 96 hours, elevated tyrosine hydroxylase transcription levels indicated increased dopamine production in rat brain tissue exposed to 1.5 ppb (3.55 pM) bifenthrin. Relative GnRH2 expression was significantly elevated at 96 hours but significantly decreased after 2 weeks of exposure, suggesting possible activation of feedback loops. These results suggest that the estrogen-like effects of bifenthrin may be partly attributable to changes in signaling within dopaminergic pathways, but may also involve other feedback pathways. For more complete data on the mechanisms of action associated with bifenthrin (9 in total), please visit the HSDB record page.

C23H22CLF3O2

422.87

422.126

82657-04-3

6442842

White to off-white solid powder

1.3±0.1 g/cm3

453.2±45.0 °C at 760 mmHg

68-71°C

136.5±17.9 °C

0.0±1.1 mmHg at 25°C

1.564

7.3

0

5

6

29

622

2

CC1=C(C=CC=C1C2=CC=CC=C2)COC(=O)[C@@H]3[C@@H](C3(C)C)/C=C(/C(F)(F)F)\Cl

OMFRMAHOUUJSGP-IRHGGOMRSA-N

InChI=1S/C23H22ClF3O2/c1-14-16(10-7-11-17(14)15-8-5-4-6-9-15)13-29-21(28)20-18(22(20,2)3)12-19(24)23(25,26)27/h4-12,18,20H,13H2,1-3H3/b19-12-/t18-,20-/m0/s1

(2-methyl-3-phenylphenyl)methyl (1R,3R)-3-[(Z)-2-chloro-3,3,3-trifluoroprop-1-enyl]-2,2-dimethylcyclopropane-1-carboxylate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

DMSO: 100 mg/mL (236.48 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.91 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 25.0 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: ≥ 2.5 mg/mL (5.91 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 25.0 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.)