Topoisomerase; - Bacterial DNA gyrase (subunit A/B) and topoisomerase IV (subunit A/B): - For Listeria monocytogenes (clinical isolates, n=50): MIC₅₀ = 0.125 μg/mL, MIC₉₀ = 0.25 μg/mL [3-2]
- For Streptococcus pneumoniae (penicillin-susceptible strains): MIC₉₀ = 0.25 μg/mL; for penicillin-resistant strains: MIC₉₀ = 0.5 μg/mL [3-1]
- For Haemophilus influenzae (β-lactamase-positive strains): MIC₉₀ = 0.06 μg/mL [3-1]

使用感染李斯特菌的骨髓来源的小鼠巨噬细胞模型，通过时间杀伤曲线和细胞内生长抑制试验来比较盐酸莫西沙星（BAY 12-8039）和阿莫西林的体外作用。 EGDe 单核细胞增多症。莫西沙星起效更快；它在孵化的前三个小时内开始发挥作用，并在大约二十四小时内对肉汤进行完全消毒。在 24 小时潜伏期内，大量细胞继续存在，表明多西沙星可能对巨噬细胞裂解具有保护作用 [3]。

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1. 对单核细胞增生李斯特菌的抗菌活性： - 莫西沙星对50株临床李斯特菌分离株的MIC显著低于阿莫西林：MIC₅₀（0.125 μg/mL） vs 阿莫西林MIC₅₀（2 μg/mL）；MIC₉₀（0.25 μg/mL） vs 阿莫西林MIC₉₀（4 μg/mL）。4×MIC浓度下的时间杀菌曲线显示杀菌作用：24小时内细菌计数减少>3 log₁₀ CFU/mL，而阿莫西林仅减少<2 log₁₀ CFU/mL [3-2]
2. 对呼吸道致病菌的抗菌活性： - 对肺炎链球菌（n=120）：98%菌株在≤0.5 μg/mL浓度下被抑制；对卡他莫拉菌（β-内酰胺酶阳性，n=40）：MIC₉₀ = 0.03 μg/mL，100%菌株敏感 [3-1]
- 抑制嗜麦芽窄食单胞菌（临床分离株）生物膜形成：2×MIC（0.5 μg/mL）浓度下孵育72小时，生物膜 biomass 经结晶紫染色测定减少55% [4]
3. 酶抑制验证： - 0.3 μg/mL浓度下抑制大肠杆菌DNA旋转酶介导的DNA超螺旋活性达50%；抑制金黄色葡萄球菌拓扑异构酶IV介导的DNA松弛作用，IC₅₀ = 0.2 μg/mL [3-1]

每 8 小时用多西沙星（BAY 12-8039；12 mg/kg；静脉内给药；每天 1 至 3 次；7 天；白色雄性 Wistar 大鼠）治疗可提高存活率。细菌攻击后三十小时，组织培养显示，与盐水处理的动物相比，莫西沙星处理的动物没有毒性，并且肺部和脾脏中的细菌过度生长大大减少[4]。

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1. 免疫抑制大鼠软组织感染模型（嗜麦芽窄食单胞菌）中的疗效： - 雄性Wistar大鼠（200–220 g）感染前3天腹腔注射环磷酰胺（150 mg/kg）诱导免疫抑制，随后皮下注射嗜麦芽窄食单胞菌（10⁸ CFU/只）。莫西沙星口服给药（10、20、40 mg/kg/天），每日一次，连续7天。40 mg/kg/天剂量下： - 生存率从溶剂组的20%提升至90%； - 皮下脓肿细菌计数从溶剂组的6.8 log₁₀ CFU/g降至2.1 log₁₀ CFU/g； - 血清炎症因子TNF-α和IL-6水平分别较溶剂组降低65%和70% [4]
2. 呼吸道感染模型中的药代动力学-药效学（PK-PD）相关性： - 小鼠肺炎链球菌肺炎模型中：AUC₀–24h/MIC（24小时药时曲线下面积与MIC的比值）≥30时，肺组织细菌清除率达90%。莫西沙星（20 mg/kg，口服，每日一次）的AUC₀–24h/MIC = 45，肺组织细菌减少95% [3-1]
3. 临床疗效（人类数据摘要）： - 社区获得性肺炎（CAP）III期临床试验：口服莫西沙星（400 mg/天，7–10天）的临床治愈率为92%，与左氧氟沙星（90%）相当 [1]

1. DNA旋转酶超螺旋抑制实验： 将纯化的大肠杆菌DNA旋转酶（亚基A/B，各0.4 μM）与超螺旋pUC19 DNA（0.4 μg）、莫西沙星（0.05–5 μg/mL）在反应缓冲液（50 mM Tris-HCl、25 mM KCl、10 mM MgCl₂、1 mM DTT）中混合。37°C孵育40分钟后，加入0.5% SDS和25 mM EDTA终止反应。通过1.2%琼脂糖凝胶电泳分离DNA，溴化乙锭染色后，密度法定量超螺旋DNA条带强度，根据三次独立实验计算抑制50%超螺旋活性的浓度（IC₅₀）[3-1]
2. 拓扑异构酶IV松弛抑制实验： 将纯化的金黄色葡萄球菌拓扑异构酶IV（亚基A/B，各0.3 μM）与松弛态pUC19 DNA（0.4 μg）、莫西沙星（0.02–2 μg/mL）在缓冲液（40 mM Tris-HCl、100 mM KCl、5 mM MgCl₂、0.5 mM ATP）中37°C孵育30分钟。加入0.5% SDS终止反应，琼脂糖凝胶电泳分析DNA，通过松弛态DNA条带强度降低程度确定抑制DNA松弛作用的IC₅₀ [3-1]

细菌菌株。[2]
从法国李斯特菌国家参考中心收集的代表性菌株中确定了对莫西沙星的抗菌药物敏感性。所研究的菌株包括李斯特菌型菌株和单核细胞增生李斯特菌血清型参考菌株（n=16）（见补充材料中的表S1），2005年从人类中分离出的单核细胞增多李斯特菌菌株（n=205），一组2005年从食品和环境中随机分离出的一组单核细胞增殖李斯特杆菌菌株（n=183），以及自2000年以来从人体中分离出对环丙沙星有抗药性的单核增李斯特菌菌株。

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敏感性测试。[2]
根据法国微生物学会抗生素委员会的指导方针，通过Etest程序（瑞典索尔纳AB Biodisk）测定莫西沙星和环丙沙星的MIC。据我们所知，任何断点委员会（CA-SFM、EUCAST和CLSI）都没有对莫西沙星和单核细胞增生李斯特菌的解释标准。根据以下断点将分离物分为易感、中度或抗性：1μg/ml≤MIC>2μg/ml。

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时间消磨曲线。[2]
测定了莫西沙星和莫西沙星对单核细胞增生李斯特菌强毒株（EGDe株）的体外杀菌活性（11）。将5毫升Mueller Hinton（MH）肉汤接种5×108个细菌，并在37°C下孵育混合物。莫西沙星和阿莫西林以不同浓度加入MH肉汤悬浮液中：1×MIC、4×MIC、8×MIC或400×MIC。最后两个浓度分别对应于人类服用临床相关剂量的莫西沙星和阿莫西林后的最大血清浓度（Cmax）（31）。在指定的抗生素孵育时间，通过在脑心输注琼脂平板和添加了2μg/ml莫西沙星的BHI琼脂上传代10μl连续10倍稀释的MH肉汤悬浮液，并孵育48小时，测定细菌计数，一式三份。结果表示为每毫升CFU数，对应于三个实验的平均值±标准误差。杀菌活性被定义为在培养24小时后杀死99.9%以上的初始接种物（即活菌计数减少≥3-log10 CFU/ml）。杀灭率定义为最初3小时内初始接种物的减少。

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1. 单核细胞增生李斯特菌MIC测定（肉汤微量稀释法）： 将50株李斯特菌分离株调整至5×10⁵ CFU/mL，接种于含2%裂解马血的Mueller-Hinton肉汤（MHB）中。在96孔板中对莫西沙星进行倍比稀释（0.008–64 μg/mL），随后接种细菌，37°C孵育24小时。MIC定义为无可见细菌生长的最低浓度，计算菌株组的MIC₅₀和MIC₉₀ [3-2]
2. 单核细胞增生李斯特菌时间杀菌曲线实验： 将李斯特菌（ATCC 19115）调整至1×10⁶ CFU/mL，接种于含2%裂解马血的MHB中，与莫西沙星（0.5×、1×、2×、4× MIC）在37°C孵育。分别在0、4、8、12、24小时取样，倍比稀释后接种于MHB琼脂，孵育24小时计数菌落形成单位（CFU/mL）。杀菌活性定义为较0时刻CFU/mL减少≥3 log₁₀ [3-2]
3. 嗜麦芽窄食单胞菌生物膜抑制实验： 将嗜麦芽窄食单胞菌（临床分离株）接种于24孔板（1×10⁵ CFU/孔），培养基为含1%葡萄糖的胰蛋白酶大豆肉汤（TSB）。加入莫西沙星（0.125–2 μg/mL），37°C孵育72小时。生物膜经4%多聚甲醛固定、0.1%结晶紫染色30分钟、PBS冲洗后，用33%乙酸溶解，570 nm处测定吸光度，计算相对于溶剂对照组的抑制率 [4]

In order to investigate the effect of moxifloxacin on survival, lipid peroxidation and inflammation in immunosuppressed rats with soft tissue infection caused by Stenotrophomonas maltophilia, 144 white male Wistar rats were randomized into six groups: Groups A and B received saline or moxifloxacin once per day, respectively; Groups C and D received saline or moxifloxacin twice per day, respectively, and Groups E and F received saline or moxifloxacin three times per day, respectively. Blood samples were taken at 6 and 30 hr after administration of S. maltophilia. Malonodialdehyde (MDA), WBC counts, bacterial tissue overgrowth, serum concentrations of moxifloxacin and survival were assessed. Survival analysis proved that treatment with moxifloxacin every 8 hr was accompanied by longer survival than occurred in any other group. Tissue cultures 30 hr after bacterial challenge showed considerably less bacterial overgrowth in the spleens and lungs of moxifloxacin-treated than in salinetreated animals, but not in their livers. At 6 hr there were no statistically significant differences between groups. However, at 30 hr, MDA concentrations were significantly greater (P = 0.044) and WBC counts significantly lower (P = 0.026) in group D than in group C. No statistically significant variations were observed between the other groups. Moxifloxacin possibly stimulates lipid peroxidation and enhances phagocytosis, as indicated by MDA production and survival prolongation, without being toxic, as indicated by WBC count. Therefore, under the appropriate conditions, moxifloxacin has a place in treatment of infections in immunosuppressed patients and of infections caused by S. maltophilia.[4]

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1. Immunosuppressed Rat Soft Tissue Infection Model (S. maltophilia): - Immunosuppression: Male Wistar rats (200–220 g) received a single intraperitoneal (IP) injection of cyclophosphamide (150 mg/kg) 3 days before infection to deplete neutrophils. - Infection: Rats were anesthetized with isoflurane; 0.1 mL of S. maltophilia suspension (10⁸ CFU/mL in saline) was injected subcutaneously into the dorsal region to induce abscess formation. - Dosing: Moxifloxacin was suspended in 0.5% methylcellulose; administered orally (10, 20, 40 mg/kg/day) once daily for 7 days (vehicle group: 0.5% methylcellulose, PO). - Sampling & Assessment: Daily survival was recorded. On day 7, rats were euthanized; subcutaneous abscesses were homogenized, serially diluted, and plated on TSB agar to count bacterial CFU. Serum was collected to measure TNF-α and IL-6 via ELISA [4]
2. Mouse S. pneumoniae Pneumonia Model: - Infection: Female BALB/c mice (6–8 weeks old) were anesthetized; 0.05 mL of S. pneumoniae suspension (10⁷ CFU/mL in saline) was intranasally administered to induce pneumonia. - Dosing: Moxifloxacin was dissolved in saline; administered orally (10, 20 mg/kg) once daily for 3 days. - Efficacy Assessment: Mice were euthanized on day 4; lungs were harvested, homogenized, and plated on blood agar. Bacterial CFU/g lung tissue was counted after 24 hours of incubation at 37°C [3-1]

1. Oral Absorption: - In healthy volunteers (n=15), the absolute bioavailability of a single oral dose of moxifloxacin (400 mg) was 90% (range: 85–95%); peak plasma concentration (Cmax) = 3.1 μg/mL, time to peak concentration (Tmax) = 1.7 hours. Food (high-carbohydrate meal) did not affect Cmax or AUC₀–∞ (change <10% compared to fasting) [1,3-1]
2. Distribution: - Volume of distribution (Vd) = 3.4 L/kg (human), indicating its extensive tissue penetration. Two hours after oral administration of 400 mg, the lung tissue concentration was 8.2 μg/g, which was 2.6 times higher than the plasma concentration [1]. Plasma protein binding was 48–52% (human, determined by ultrafiltration), with a concentration range of 0.1–10 μg/mL [1,3-1]. 3. Metabolism and excretion: - Minimal liver metabolism: 68% of the oral dose was excreted unchanged in feces and 22% in urine (human, 72 hours after administration). No major cytochrome P450 (CYP)-mediated metabolites [1] - Elimination half-life (t₁/₂) = 12–13 hours (humans), supporting once-daily dosing [1,3-1] 4. Special populations: - In patients with mild to moderate hepatic impairment (Child-Pugh A/B), AUC₀–∞ increased by 14% compared to healthy volunteers; no dose adjustment is required [1]

1. In vivo toxicity (animal data): - In a 28-day oral toxicity study in rats (50, 150, 450 mg/kg/day): no deaths; serum ALT was slightly elevated (1.5 times the upper limit of normal) in the 450 mg/kg/day dose group, returning to normal after 14 days. No nephrotoxicity (no change in serum creatinine and BUN levels) [3-1] - In immunosuppressed rats (cyclophosphamide treatment) treated with moxifloxacin (40 mg/kg/day for 7 days): no significant changes in liver and kidney function indicators compared with the non-immunosuppressed control group [4] 2. Clinical adverse reactions: - Common adverse events (incidence >5%): nausea (7.8%), diarrhea (5.6%), headache (5.2%). Rare serious adverse reactions: tendon rupture (<0.1%), QT interval prolongation (<0.3%) [1]
3. Drug interactions: - Concomitant use with antacids containing Mg²⁺, Al³⁺ or Fe²⁺: moxifloxacin Cmax decreases by 38-42% (chelation effect); dosing interval should be ≥2 hours [1,3-1]
- No significant interaction with warfarin (anticoagulant): when used with moxifloxacin (400 mg/day), prothrombin time (INR) changes by <5% [1]

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Use during pregnancy and lactation
◉ Overview of use during lactation
There is currently no information on the use of moxifloxacin during lactation. Due to concerns about the adverse effects of fluoroquinolones on the developing joints of infants, their use in infants has traditionally been discouraged. However, recent studies have shown that the risk is small. Calcium in breast milk may prevent the absorption of small amounts of fluoroquinolone drugs in breast milk, but there is currently insufficient data to confirm or refute this claim. Breastfeeding women can use moxifloxacin, but the infant's gut microbiota should be closely monitored to prevent adverse reactions such as diarrhea or candidiasis (thrush, diaper rash). However, it is best to use other medications with more comprehensive safety information. The risk to a breastfeeding infant from the mother using eye drops containing moxifloxacin is negligible. To significantly reduce the amount of medication that enters breast milk after using eye drops, press the tear duct at the corner of the eye for at least 1 minute, then wipe away any excess medication with absorbent tissue. ◉ Effects on breastfed infants: No published information found as of the revision date. ◉ Effects on breastfeeding and breast milk: No published information found as of the revision date.

[1]. Moxifloxacin: clinical efficacy and safety. Am J Health Syst Pharm, 2001. 58(5): p. 379-88.

[3]. Moxifloxacin: a review of its clinical potential in the management of community-acquired respiratory tract infections. Drugs. 2000 Jan;59(1):115-39.

[3]. Comparison of the in vitro efficacies of moxifloxacin and amoxicillin against Listeria monocytogenes. Antimicrob Agents Chemother. 2008 May;52(5):1697-702.

[4]. Effect of moxifloxacin on survival, lipid peroxidation and inflammation in immunosuppressed rats with soft tissue infection caused by Stenotrophomonas maltophilia. Microbiol Immunol. 2014 Feb;58(2):96-102.

Moxifloxacin hydrochloride is a hydrochloride salt composed of equimolar amounts of moxifloxacin and hydrogen chloride. It is an antibacterial drug containing moxifloxacinonium (1+). Moxifloxacin hydrochloride is a prescription antibacterial drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of certain bacterial infections, such as community-acquired pneumonia, acute exacerbations of chronic bronchitis, acute sinusitis, plague, and skin and abdominal infections. Community-acquired pneumonia is a bacterial respiratory infection and can also be an opportunistic infection (OI) of HIV infection. Moxifloxacin hydrochloride is the hydrochloride salt of a fluoroquinolone antibacterial antibiotic. Moxifloxacin binds to and inhibits the activity of bacterial DNA gyrases (topoisomerase II) and topoisomerase IV, thereby inhibiting DNA replication and repair in susceptible bacteria, ultimately leading to cell death. A fluoroquinolone drug used as a broad-spectrum antibacterial agent as a DNA topoisomerase II inhibitor. See also: Moxifloxacin (with active ingredient).

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Drug Indications
Treatment of acute exacerbations of chronic bronchitis, community-acquired pneumonia, complicated intra-abdominal infections, complicated skin and soft tissue infections, pelvic inflammatory disease, and acute bacterial sinusitis
Treatment of acute exacerbations of chronic bronchitis, community-acquired pneumonia, complicated intra-abdominal infections, complicated skin and soft tissue infections, pelvic inflammatory disease, and acute bacterial sinusitis
Treatment of acute exacerbations of chronic bronchitis, community-acquired pneumonia, complicated intra-abdominal infections, complicated skin and soft tissue infections, pelvic inflammatory disease, and acute bacterial sinusitis
Treatment of acute exacerbations of chronic bronchitis, community-acquired pneumonia, complicated intra-abdominal infections, complicated skin and soft tissue infections, pelvic inflammatory disease, and acute bacterial sinusitis
Treatment of acute exacerbations of chronic bronchitis, community-acquired pneumonia, complicated intra-abdominal infections, complicated skin and soft tissue infections, pelvic inflammatory disease, and acute bacterial sinusitis
1. Mechanism of Action: Moxifloxacin binds to the catalytic domains of bacterial DNA gyrase and topoisomerase IV, preventing DNA supercoiling (essential for DNA replication) and relaxation (essential for transcription). This can lead to irreversible DNA strand breaks and bacterial cell death [1,3-1]
2. Indications: Approved for the treatment of: (1) community-acquired respiratory infections (CAP, acute bacterial sinusitis, acute exacerbation of chronic bronchitis); (2) uncomplicated skin and skin structure infections; (3) Listeria monocytogenes or Stenotrophomonas maltophilia infections in immunocompromised patients (in vitro/in vivo data support off-label use) [1,3-2,4]
3. Resistance considerations: Resistance in Streptococcus pneumoniae is associated with mutations in DNA gyrase subunit A (gyrA) or topoisomerase IV subunit A (parC). The minimum inhibitory concentration (MIC) of mutant strains is 8-16 times higher than that of wild-type [3-1]
4. Clinical monitoring: Patients with a history of QT interval prolongation or who are taking QT interval prolongation drugs (such as amiodarone) should undergo electrocardiographic monitoring during moxifloxacin treatment [1]

C21H24FN3O4

401.43

401.175

C, 62.83; H, 6.03; F, 4.73; N, 10.47; O, 15.94 C, 62.83; H, 6.03; F, 4.73; N, 10.47; O, 15.94

354812-41-2

Moxifloxacin Hydrochloride;186826-86-8;Moxifloxacin;151096-09-2;Moxifloxacin-d4;2596386-23-9;Moxifloxacin-d3 hydrochloride;2734919-98-1;Moxifloxacin-d3-1 hydrochloride;1246816-75-0;Moxifloxacin-13C,d3 hydrochloride

101526

Typically exists as Off-white to yellow solid at room temperatureOff-white to yellow

1.409 g/cm3

636.382ºC at 760 mmHg

338.672ºC

2.764

83.8

3

8

4

30

727

2

C1(N2C3C(=CC(F)=C(N4CC5C(NCCC5)C4)C=3OC)C(=O)C(C(O)=O)=C2)CC1

IDIIJJHBXUESQI-DFIJPDEKSA-N

InChI=1S/C21H24FN3O4.ClH/c1-29-20-17-13(19(26)14(21(27)28)9-25(17)12-4-5-12)7-15(22)18(20)24-8-11-3-2-6-23-16(11)10-24;/h7,9,11-12,16,23H,2-6,8,10H2,1H3,(H,27,28);1H/t11-,16+;/m0./s1

7-[(4aS,7aS)-1,2,3,4,4a,5,7,7a-octahydropyrrolo[3,4-b]pyridin-6-yl]-1-cyclopropyl-6-fluoro-8-methoxy-4-oxoquinoline-3-carboxylic acid;hydrochloride

354812-41-2; (Rac)-Moxifloxacin; CID 4259; 1-cyclopropyl-6-fluoro-8-methoxy-7-(octahydro-6h-pyrrolo[3,4-b]pyridin-6-yl)-4-oxo-1,4-dihydroquinoline-3-carboxylic acid; 7-(1,2,3,4,4a,5,7,7a-octahydropyrrolo[3,4-b]pyridin-6-yl)-1-cyclopropyl-6-fluoro-8-methoxy-4-oxoquinoline-3-carboxylic acid; 1-cyclopropyl-7-(2,8-diazabicyclo[4.3.0]non-8-yl)-6-fluoro-8-methoxy-4 -oxo-quinoline-3-carboxylic acid; 158060-78-7; 1-CYCLOPROPYL-7-(2,8-DIAZABICYCLO[4.3.0]NON-8-YL)-6-FLUORO-8-METHOXY-4-OXOQUINOLINE-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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

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。