Flumequine (R-802)   中文名称: 氟甲喹

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

氟甲喹抑制负责双链DNA断裂反应的真核拓扑异构酶II以及细菌回旋酶，相对于对细菌回旋酶的影响，氟甲喹对拓扑异构酶II的抑制作用较高。氟甲喹对 12 种临床杀鲑鱼菌株的最低抑菌浓度 (MIC) 范围为 0.06 μg/mL 至 32 μg/mL。对于最具耐药性的分离株，氟甲喹抑制 E(max) 值高达 16，这表明外排对耐药表型的重要贡献。氟甲喹累积实验证实，高 E(max) 值与低得多的累积水平相关。细胞测定：将中国仓鼠肺细胞系CHL/IU常规维持在补充有10%胎牛血清的Dulbeccos改良MEM培养基中的单层培养物中，在37°C、5% CO2气氛下。用溶解在 DMSO 中的氟甲喹 (R-802) 处理指数生长的细胞 1 小时。选择剂量范围是为了获得受损和高度受损的细胞。氟甲喹 (R-802) 处理后，将细胞包埋于溶解在盐水中的 1% GP42 琼脂糖中。测定每个剂量的细胞数量和细胞活力。

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针对革兰氏阴性菌（大肠杆菌、肠炎沙门菌、嗜水气单胞菌），氟甲喹（R-802）表现出强效的浓度依赖性抗菌活性，敏感菌株的MIC值为0.06-2 μg/mL [2][3]
- 针对携带gyrA基因突变的氟甲喹耐药大肠杆菌菌株，MIC值升高至8-32 μg/mL，表明耐药性由靶基因突变得介导[3]
- 大鼠肝细胞体外毒性实验显示，氟甲喹（R-802）在浓度高达100 μg/mL时细胞毒性极低，细胞活力＞85%[1]
- 该药物通过稳定DNA旋转酶-DNA和拓扑异构酶IV-DNA切割复合物，阻止DNA链连接，抑制细菌DNA复制和转录[3]

Flumequine（4000 ppm，口服）在给药后 3 小时但在 24 小时内不会在成年小鼠的胃、结肠和膀胱中诱导剂量依赖性 DNA 损伤。大西洋鲑鱼口服含药饲料后，氟甲喹的生物利用度为 44.7%。氟甲喹静脉注射后稳态分布容积为 3.5 L/kg，消除半衰期 (t 1/2) 为 22.8 小时，血浆药物浓度-时间曲线下面积 (AUC) 为 140 μg×小时/mL大西洋鲑鱼的管理。氟甲喹 (100 mg/L) 会降低水生杂草千屈菜 (Lythrum salicaria L) 的根、下胚轴、子叶的平均长度以及次生根的平均数量。氟甲喹（10 mg/kg，口服）导致稳态分布体积静脉内给药后 (Vss) 为 2.41 L/kg（鳕鱼）和 2.15 L/kg（濑鱼）。全身清除率 (Cl) 分别为 0.024 L/h.kg（鳕鱼）和 0.14 L/h.kg（濑鱼），消除半衰期 (t1/2 λ z) 计算为 75 小时（鳕鱼）和 31 小时给予氟甲喹（10 mg/kg，口服）后数小时（濑鱼）。口服氟甲喹后，口服生物利用度 (F) 计算为 65%（鳕鱼）和 41%（濑鱼）。

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在大肠杆菌诱导的尿路感染小鼠模型中，以20和40 mg/kg/天的剂量口服氟甲喹（R-802），连续5天，显著降低肾脏和膀胱中的细菌载量，微生物根除率分别为70%和90%[2]
- 在感染杀鲑气单胞菌的虹鳟鱼（Oncorhynchus mykiss）中，以10 mg/kg/天的剂量口服氟甲喹（R-802），连续7天，死亡率降低80%，并清除脾脏和肾脏中的细菌[5]
- 在小鼠体内，氟甲喹（R-802）组织穿透性良好，在尿路、胃肠道和肝脏中达到治疗浓度[2]

细菌DNA旋转酶活性检测：将纯化的大肠杆菌DNA旋转酶与超螺旋质粒DNA在反应缓冲液中于37°C孵育。加入系列浓度（0.03-16 μg/mL）的氟甲喹（R-802），混合物孵育60分钟。加入SDS和蛋白酶K终止反应，随后在55°C孵育1小时。通过1%琼脂糖凝胶电泳分离DNA产物，溴化乙锭染色。通过测量超螺旋DNA条带强度，定量DNA旋转酶介导的超螺旋松弛抑制效果[3]
- 细菌拓扑异构酶IV活性检测：将分离的金黄色葡萄球菌拓扑异构酶IV与松弛型质粒DNA在反应缓冲液中孵育。加入0.06-32 μg/mL浓度的氟甲喹（R-802），混合物在37°C孵育45分钟。加入终止液终止反应，通过琼脂糖凝胶电泳分析DNA产物，评估DNA解连环反应的抑制情况[3]

中国仓鼠肺细胞系CHL/IU在37°C、5% CO₂环境下使用添加有10%胎牛血清的Dulbecco改良MEM培养基以单层形式常规培养。将指数生长的细胞暴露于溶解在 DMSO 中的氟甲喹 (R-802) 溶液中一小时。选择剂量范围以提取严重受损和未受损的细胞。用氟甲喹 (R-802) 处理后，将细胞包埋在 1% 盐水溶解的 GP42 琼脂糖中。对于每个剂量，都会确定细胞的数量和活力。

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细菌生长抑制检测：将细菌菌株（大肠杆菌、肠炎沙门菌）在Mueller-Hinton肉汤中37°C振荡培养。加入系列浓度（0.015-64 μg/mL）的氟甲喹（R-802），24小时后测量600 nm处的光密度（OD600），监测细菌生长。MIC定义为抑制≥90%细菌生长的最低浓度[2][3]
- 肝细胞毒性检测：分离大鼠肝细胞，以5×10⁴个细胞/孔接种到96孔板中。用10-200 μg/mL的氟甲喹（R-802）处理细胞24和48小时。基于线粒体脱氢酶活性的比色法检测细胞活力[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

59.3

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)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。