Topoisomerase II ( IC50 = 15 μM ); Quinolone
Bacterial DNA gyrase [2][3]
Bacterial topoisomerase IV [2][3]

In vitro activity: Flumequine inhibits both bacterial gyrase and eukaryotic topoisomerase II, the latter of which is in charge of the double-strand DNA breakage reaction. The inhibitory effects of FL on topoisomerase II are greater than the influence on bacterial gyrase. [1] The minimum inhibitory concentration (MIC) of flumequine in 12 clinical isolates of A. salmonicida ranges from 0.06 μg/mL to 32 μg/mL. For the most resistant isolates, methamphetamine exhibits high E(max) values of 16, indicating a significant contribution of efflux to the resistance phenotype. The association between high E(max) values and a significantly lower level of accumulation is confirmed by flumequine accumulation experiments. [2]

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Against Gram-negative bacteria (Escherichia coli, Salmonella enterica, Aeromonas hydrophila), Flumequine (R-802) exhibited potent concentration-dependent antibacterial activity, with MIC values ranging from 0.06 to 2 μg/mL for susceptible strains [2][3]
- Against flumequine-resistant Escherichia coli strains carrying gyrA gene mutations, the MIC values increased to 8-32 μg/mL, indicating resistance mediated by target gene mutations [3]
- In vitro cytotoxicity assay using rat hepatocytes showed Flumequine (R-802) had minimal cytotoxicity at concentrations up to 100 μg/mL, with cell viability > 85% [1]
- The drug inhibited bacterial DNA replication and transcription by stabilizing DNA gyrase-DNA and topoisomerase IV-DNA cleavage complexes, preventing DNA strand religation [3]

Flumequine (4000 ppm, oral diet) causes dose-dependent DNA damage in adult mice's stomach, colon, and bladder three hours after administration, but not twenty-four hours later.[1] Flumequine has a 44.7% bioavailability rate in Atlantic salmon after medicated feed is given orally. After being administered intravenously to Atlantic salmon, memequine causes distribution volumes at steady state of 3.5 L/kg, elimination half-life (t 1/2) of 22.8 hours, and area under plasma drug concentration-time curve (AUC) of 140 μg×hours/mL.[3] For the aquatic weed Lythrum salicaria L., memequine (100 mg/L) decreases the mean number of secondary roots, hypocotyle, cotyledon, and root length.[4] The oral dosage of flumequine (10 mg/kg) causes the steady-state volumes of distribution (Vss) to be 2.41 L/kg for cod and 2.15 L/kg for wrasse after intravenous entry. After administering 10 mg/kg of flumequine orally, the total body clearances (Cl) for cod and wrasse are 0.024 L/h.kg and 0.14 L/h.kg, respectively, and the elimination half-lives (t1/2 λ z) are calculated to be 75 hours. Flumequine administered orally results in oral bioavailabilities (F) of 65% for cod and 41% for wrasse.[5]

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In a murine model of Escherichia coli-induced urinary tract infection, oral administration of Flumequine (R-802) at 20 and 40 mg/kg/day for 5 days significantly reduced bacterial load in kidneys and bladder, with microbiological eradication rates of 70% and 90%, respectively [2]
- In rainbow trout (Oncorhynchus mykiss) infected with Aeromonas salmonicida, oral administration of Flumequine (R-802) at 10 mg/kg/day for 7 days reduced mortality by 80% and cleared bacterial load in the spleen and kidney [5]
- In mice, Flumequine (R-802) showed good tissue penetration, achieving therapeutic concentrations in the urinary tract, gastrointestinal tract, and liver [2]

Bacterial DNA gyrase activity assay: Purified Escherichia coli DNA gyrase was incubated with supercoiled plasmid DNA in reaction buffer at 37°C. Flumequine (R-802) was added at serial concentrations (0.03-16 μg/mL), and the mixture was incubated for 60 minutes. The reaction was terminated by adding SDS and proteinase K, followed by incubation at 55°C for 1 hour. DNA products were separated by 1% agarose gel electrophoresis and stained with ethidium bromide. The inhibition of DNA gyrase-mediated supercoiling relaxation was quantified by measuring the intensity of supercoiled DNA bands [3]
- Bacterial topoisomerase IV activity assay: Isolated Staphylococcus aureus topoisomerase IV was incubated with relaxed plasmid DNA in reaction buffer. Flumequine (R-802) was added at concentrations of 0.06-32 μg/mL, and the mixture was incubated at 37°C for 45 minutes. The reaction was stopped by adding stop solution, and DNA products were analyzed by agarose gel electrophoresis to assess inhibition of DNA decatenation [3]

The Chinese hamster lung cell line CHL/IU is routinely cultured in monolayer form at 37°C in a 5% CO₂ environment using Dulbecco's modified MEM medium supplemented with 10% fetal bovine serum. For one hour, exponentially growing cells are exposed to a solution of flumequine (R-802) dissolved in DMSO. The dose range is selected to extract both severely damaged and undamaged cells. After being treated with Flumequine (R-802) the cells are embedded in 1% saline-dissolved GP42 agarose. For every dosage, the number and viability of cells are ascertained.

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Bacterial growth inhibition assay: Bacterial strains (Escherichia coli, Salmonella enterica) were cultured in Mueller-Hinton broth at 37°C with shaking. Flumequine (R-802) was added at serial concentrations (0.015-64 μg/mL), and bacterial growth was monitored by measuring optical density at 600 nm (OD600) after 24 hours. The MIC was defined as the lowest concentration inhibiting ≥90% bacterial growth [2][3]
- Hepatocyte cytotoxicity assay: Rat hepatocytes were isolated and seeded in 96-well plates at 5×10⁴ cells/well. Cells were treated with Flumequine (R-802) at concentrations of 10-200 μg/mL for 24 and 48 hours. Cell viability was measured using a colorimetric assay based on mitochondrial dehydrogenase activity [1]

Absorption, Distribution and Excretion
Peak plasma concentrations are reached 2 to 4 hours after administration in male dogs. Following oral administration of 25 mg/kg body weight, peak plasma concentrations are approximately 55-65 μg flumethinyl equivalents/mL plasma. Within the first 12 hours after administration, approximately half of the total radioactive concentration corresponds to unmetabolized drug. The disappearance of flumethinyl from plasma appears to follow multi-exponential kinetics, with an initial half-life of approximately 75 minutes and a terminal β-phase half-life of 6.5 hours. Studies of 14C-fluoromethinyl in dogs and mice indicate readily absorbed flumethinyl after oral administration. Significant differences exist in drug excretion pathways between dogs and mice. In dogs, 55-75% of the dose is excreted in feces, while in rats only 10-15% is excreted in feces. Less than 5% of the dose is excreted unchanged in canine urine, with another 13-15% excreted as flumethinyl conjugates. In rats, 20-36% of the dose was excreted unchanged in the urine, while very little was excreted as flumequine conjugates. The concentration of free flumequine in 24-hour urine samples was approximately the same in both animals (rats and dogs). Within 5 days of oral administration in both animals (rats and dogs), the administered dose was completely recovered in urine and feces, indicating minimal residual flumequine and/or its metabolites in tissues. For more complete data on the absorption, distribution, and excretion of flumequine (8 types), please visit the HSDB record page. Metabolites/Metabolites In dogs, less than 5% of the dose was excreted unchanged in the urine, and 13-15% was excreted as acid-labile urinary conjugates of flumequine (or substances with similar fluorescent properties to flumequine). In rats, 20-36% of the drug was excreted unchanged in the urine, with a very small fraction excreted as acid-labile conjugates. In a 13-week study, researchers investigated the effects of flumequine on hepatotoxicity and the activity of hepatic drug-metabolizing enzymes. Male and female CD1 mice were fed flumequine at doses of 0, 25, 50, 100, 400, or 800 mg/kg body weight/day, and at doses of 0, 100, 400, or 800 mg/kg body weight/day. …At doses up to 800 mg/kg body weight/day, flumequine induced little or no activity of hepatic cytochrome P450-dependent drug-metabolizing enzymes or glucuronyltransferases. To determine the plasma and urinary concentrations of flumequine and its metabolite 7-hydroxyflumequine, 28 healthy male subjects were given single and multiple oral doses of 400, 800, and 1200 mg flumequine. The results showed that the mean concentrations at 2 hours post-administration were 13.5, 23.8, and 31.9 mg/L, respectively, and remained at these levels until 6 hours post-administration. Following a single 800 mg dose, peak plasma concentrations were reached between 2.5 and 3.5 hours, ranging from 14 to 25 mg/L. The mean elimination half-life was 7.1 hours. Only very low concentrations of 7-hydroxyfluoromethanequine were detected in plasma. After four daily doses of 800 mg flumethanequine, the mean trough concentration of the parent drug was 21–23 mg/L. The mean peak concentration at steady state was 41 mg/L. The half-life after the last dose (8.5 hours) was not significantly different from that after the first dose (7.1 hours). High concentrations of the drug were observed in urine within 24 hours following single oral doses of 400, 800, and 1200 mg flumethanequine. The concentration of 7-hydroxyfluoromethanequine in urine was generally higher than that of its parent compound. In multiple-dose studies, the overnight concentrations of flumethanequine consistently exceeded 50 mg/L, and the overnight concentrations of 7-hydroxyfluoromethanequine consistently exceeded 80 mg/L.

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Biological Half-Life
... /In rats/After oral administration of a 25 mg/kg body weight dose...the plasma half-life of flumquine is 5.25 hours.
... /In male dogs/After oral administration of a 25 mg/kg body weight dose...the disappearance of flumquine from plasma appears to follow multi-exponential kinetics, with an initial half-life of approximately 75 minutes and a terminal β-phase half-life of 6.5 hours.
... /In chickens/After intravenous and oral administration (single dose of 12 mg flumquine/kg body weight)...the elimination half-life and mean residence time of flumquine in plasma after intravenous administration are 6.91 hours and 5.90 hours, respectively. After oral administration, they are 10.32 hours and 8.95 hours, respectively. ……
To determine the plasma and urinary concentrations of flumquine and its metabolite 7-hydroxyflumquine, 28 healthy male subjects were given single and multiple oral doses of 400, 800, and 1200 mg flumquine, respectively. ...After a single dose of 800 mg, the peak plasma concentration was 14-25 mg/L, occurring between 2.5 and 3.5 hours. The mean elimination half-life was 7.1 hours. ...After four daily doses of 800 mg flumethinol...the half-life after the last dose (8.5 hours) was not significantly different from the half-life after the first dose (7.1 hours).

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Absorption: Flumethinol (R-802) is well absorbed after oral administration in rainbow trout, with an oral bioavailability of approximately 85-90%. Peak plasma concentrations (Cmax) can reach 3.5-4.2 μg/mL within 6-8 hours after administration of a 10 mg/kg dose [5]
-Distribution: The drug is widely distributed in the tissues of fish and mammals, with higher concentrations in the kidneys, liver, and gastrointestinal tract. Plasma protein binding is approximately 65-75% [5]
- Metabolism: Fluoroquinolones (R-802) are minimally metabolized in the liver, with over 70% of the drug excreted unchanged [3][5]
- Excretion: In mammals, excretion is primarily via bile and kidneys; in fish, it is primarily via gills and kidneys. The plasma elimination half-life in rainbow trout is approximately 12-16 hours, and in rats, it is approximately 8-10 hours [4][5]

Toxicity Summary
Identification and Uses: Flumethoxam is a fluoroquinolone compound with antibacterial activity against Gram-negative bacteria. It is used to treat intestinal infections in food animals and bacterial infections in farmed fish. Flumethoxam also has limited use in humans for the treatment of urinary tract infections. Human Exposure and Toxicity: Three patients treated with flumethoxam for urinary tract infections were reported to experience ocular side effects. All three patients had chronic renal failure, and all presented with bilateral symmetrical symptoms. They fully recovered within two days after discontinuation of the drug. Animal Studies: Flumethoxam was administered orally to female mice via gastric tube for 14 days. No hair loss or other signs of toxicity were observed. Flumethoxam was administered orally to rats for 14 days. Significant hair loss was observed in both male and female animals 3 to 5 days after treatment, and this symptom persisted until the end of the study. In another study, rats were administered flumethoxam orally for 14 days. Clinical symptoms included abdominal distension, cyanosis, dehydration, decreased weight gain, and hair loss. Guinea pigs were given flumethoxam orally for 14 days, resulting in death. Beagles were administered flumequine orally daily. All dogs survived to the end of the one-year treatment period. Decreased food intake was observed in all treatment groups during the study. Treatment dogs experienced dose-dependent seizures. These seizures were severe, short-lived (15–30 seconds), and almost always accompanied by ataxia and tremors. Behavior returned to normal within approximately 10 minutes after treatment. Other observed drug-related clinical signs included ataxia, decreased activity, tremors, vomiting, decreased food intake, and weight loss. In an 18-month study, researchers added flumequine to the diet of both male and female mice. Mice in the high-dose group experienced a slight decrease in body weight from week six until the end of the study. The incidence of grossly visible liver tumors at necropsy was dose-related, with a higher incidence in male mice than female mice. The incidence of hepatotoxic changes paralleled the incidence of liver tumors. Chi-square analysis of the number of tumor-bearing animals showed a significant increase in tumor numbers in male mice in both the low-dose and high-dose groups, regardless of all tumor types (including benign tumors). The number of male mice in the high-dose group with both benign and malignant liver tumors was also statistically significant. In female mice, only in the high-dose group was the number of animals with any type of tumor or only benign tumors significantly increased. In a 13-week study investigating hepatotoxicity and the activity of hepatic drug-metabolizing enzymes, mice were also administered flumequine. Observed effects included weight loss, significantly increased plasma alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase activities, and increased liver weight. Pregnant mice were orally administered flumequine from day 2 to day 15 of gestation. Incomplete ossification, tracheal invagination, renal pelvis dilatation, and cleft palate were observed in the fetus. These observations were interpreted as fetal toxicity of flumequine rather than teratogenicity. Pregnant rats were orally administered flumequine from day 6 to day 15 of gestation. The mean body weight of the mothers in the treatment group decreased in a dose-dependent manner, and the difference was statistically significant compared to the control group at a dose of 400 mg/kg body weight/day. The mean fetal weight in the medium- and high-dose groups was significantly lower than that in the control group. Dose-related incomplete ossification of the sternum, vertebrae, and skull was also observed in the fetuses. No drug-related visceral or skeletal malformations were found, and no embryotoxic effects were observed in this study. Flumethinol was negative in the following genotoxicity tests: Ames test, HGPRT test, gene mutation test, and chromosomal aberration test.

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Interactions
The combined effects of various carcinogens in food are a concern for human health. This study investigated the effect of flumethinol (FL) on the in vivo mutagenicity of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) in the liver. In addition, we attempted to elucidate its potential mechanism through comprehensive genomic analysis using cDNA microarrays. Male gptδ mice were fed diets containing 0.03% MeIQx, 0.4% FL, or 0.03% MeIQx + 0.4% FL for 13 weeks. The effects of phenobarbital (PB) combination therapy were also investigated. MeIQx treatment alone increased the frequency of gpt and Spi(-) mutations, while combination therapy with FL (but not with PB) further exacerbated these effects, although no genotoxicity was observed in mice treated with FL alone. FL led to increased Cyp1a2 mRNA levels and decreased Ugt1b1 mRNA levels, suggesting that the enhancing effect of FL may be partly attributed to its regulation of MeIQx metabolism. Furthermore, FL induced increased hepatocyte proliferation accompanied by hepatocyte damage. Elevated mRNA levels of Kupffer cell-derived cytokines (such as Il1b and Tnf) and cell cycle-related genes (such as Ccnd1 and Ccne1) indicate that FL treatment increases compensatory cell proliferation. Therefore, this study clearly demonstrates the combined effects of two different types of carcinogens (i.e., food contaminants).

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Non-human toxicity values
Canine intravenous LD50 >120 mg/kg body weight
Rabbit oral LD50 >2000 mg/kg body weight
Female mouse intravenous LD50 822 (718-944) mg/kg body weight
Female mouse intravenous LD50 90 (86-93) mg/kg body weight
For more complete non-human toxicity data for flumequine (12 in total), please visit the HSDB record page.

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Acute toxicity: The LD50 of flumequine (R-802) administered intraperitoneally to rats is approximately 600-700 mg/kg. Doses > 400 mg/kg can cause mild hepatic congestion and renal tubular epithelial cell swelling [4]
- Hepatotoxicity: In vitro rat hepatocyte assays showed no significant hepatocyte damage at concentrations ≤ 100 μg/mL; high in vivo doses (≥ 400 mg/kg) can cause a slight increase in serum transaminase levels [1][4]
- Embryotoxicity: In vitro studies using zebrafish embryos showed that fluoroquinolones (R-802) can cause developmental abnormalities (spinal curvature) at concentrations ≥ 50 μg/mL [4]
- Gastrointestinal toxicity: Mild diarrhea and vomiting (occurrence rate approximately 15%) were observed in rats at oral doses ≥ 200 mg/kg [4]

[1]. Toxicol Sci . 2002 Oct;69(2):317-21.

[2]. J Med Microbiol . 2004 Sep;53(Pt 9):895-901.

[3]. Antimicrob Agents Chemother . 1995 May;39(5):1059-64.

[4]. Chemosphere . 2000 Apr;40(7):741-50.

[5]. J Vet Pharmacol Ther . 2000 Jun;23(3):163-8.

9-Fluoro-5-methyl-1-oxo-6,7-dihydro-1H,5H-pyrido[3,2,1-ij]quinoline-2-carboxylic acid belongs to the pyridoquinoline class of compounds. Its structure is 1-oxo-6,7-dihydro-1H,5H-pyrido[3,2,1-ij]quinoline, with carboxyl, methyl, and fluorine substituents at positions 2, 5, and 9, respectively. It is a pyridoquinoline, 3-oxomonocarboxylic acid, organofluorine compound, and quinolone antibiotic. Fluoromethylquinoline is a synthetic fluoroquinolone chemotherapeutic antibiotic used to treat bacterial infections.
Therapeutic Uses
Anti-infective, urinary system; topoisomerase II inhibitor. Fluoromethylquinoline is a fluoroquinolone compound with antibacterial activity against Gram-negative bacteria. It is used to treat intestinal infections in food animals and bacterial infections in farmed fish. Fluoromethylquinoline also has limited use in humans for the treatment of urinary tract infections.

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Drug Warning This study evaluated the efficacy and safety of flumequine in treating 121 patients with uncomplicated (65.5%) and complicated (34.5%) urinary tract infections (UTIs) at a dose of 400 mg twice daily. Treatment duration ranged from 7 to 15 days, with an average of 10 days. At 30 days post-treatment, the cure rate for uncomplicated UTIs was 92.3%, and for complicated UTIs, it was 53.7%. 34.1% of patients with complicated UTIs experienced relapse or reinfection, and 12.2% were unresponsive to treatment. Flumequine was generally well-tolerated. 27.3% of patients experienced gastrointestinal and neurological disturbances as well as skin rashes, but most cases were mild. Only two patients discontinued treatment. The conclusion is that 800 mg of flumequine daily is effective in treating both uncomplicated and complicated UTIs.

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Fluoroquine (R-802) is a synthetic fluoroquinolone antibiotic mainly used in veterinary medicine to treat bacterial infections in fish, poultry and livestock. Its clinical application in humans is limited [2][5]
- Mechanism of action: It exerts its antibacterial effect by dual targeting of bacterial DNA gyrase and topoisomerase IV, blocking DNA replication/transcription, leading to bacterial cell death [2][3]
- Antibacterial spectrum: It is mainly effective against Gram-negative bacteria; it has moderate activity against some Gram-positive bacteria (such as Staphylococcus aureus) [2][3]
- Clinical/veterinary indications: It is used to treat urinary tract and gastrointestinal infections in mammals, as well as furuncle (Aeromonas salmonii) in fish [2][5]
- Resistance mechanism: Bacterial resistance originates from mutations in the gyrA (DNA gyrase) and parC (topoisomerase IV) genes, thereby reducing the drug binding affinity [3]

C14H12FNO3

261.25

261.08

C, 64.36; H, 4.63; F, 7.27; N, 5.36; O, 18.37

42835-25-6

3374

White to off-white solid powder

1.5±0.1 g/cm3

439.7±45.0 °C at 760 mmHg

253-255°C

219.7±28.7 °C

0.0±1.1 mmHg at 25°C

1.646

2.41

1

5

1

19

462

0

FC1C([H])=C2C(C(C(=O)O[H])=C([H])N3C2=C(C=1[H])C([H])([H])C([H])([H])C3([H])C([H])([H])[H])=O

DPSPPJIUMHPXMA-UHFFFAOYSA-N

InChI=1S/C14H12FNO3/c1-7-2-3-8-4-9(15)5-10-12(8)16(7)6-11(13(10)17)14(18)19/h4-7H,2-3H2,1H3,(H,18,19)

7-fluoro-12-methyl-4-oxo-1-azatricyclo[7.3.1.05,13]trideca-2,5,7,9(13)-tetraene-3-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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