Topoisomerase II; Topoisomerase IV

体外活性：莫西沙星通过捕获 DNA 药物酶复合物并特异性抑制 ATP 依赖性酶拓扑异构酶 II（DNA 旋转酶）和拓扑异构酶 IV 发挥作用。莫西沙星对结核分枝杆菌 H37Rv 具有体外效力，MIC 为 0.177 μg/mL。莫西沙星具有广泛的革兰氏阳性和革兰氏阴性活性。莫西沙星在体外和临床上显示出对抗金黄色葡萄球菌、肺炎链球菌、链球菌的功效。化脓性杆菌、流感嗜血杆菌、副流感嗜血杆菌、肺炎克雷伯菌、卡他莫拉菌、肺炎衣原体和肺炎支原体。除结核分枝杆菌外，莫西沙星还具有抗分枝杆菌活性；莫西沙星对堪萨斯分枝杆菌的活性比鸟分枝杆菌复合群的活性更高：特别是在 4、2 和 2 μg/mL 时，对鸟分枝杆菌 > 胞内分枝杆菌 > 堪萨斯分枝杆菌的 MIC90 分别为 4、2 和 2 μg/mL。龟分枝杆菌 > 偶然分枝杆菌的 MIC90 分别为 16 和 0.5 μg/mL。细胞分析：莫西沙星（盐酸盐）是一种合成的氟喹诺酮抗生素。抗菌莫西沙星是一种广谱氟喹诺酮类药物，与旧的氟喹诺酮类药物相比，它提高了对革兰氏阳性球菌和非典型病原体的覆盖率，同时保留了良好的抗革兰氏阴性菌活性。莫西沙星的抗菌谱包括所有主要的上呼吸道和下呼吸道病原体；它是对抗肺炎球菌（包括青霉素和大环内酯耐药菌株）最有效的氟喹诺酮类药物之一。莫西沙星的光毒性潜力有限。在临床试验中，莫西沙星的临床成功率为88-97%，细菌根除率为90-97%。莫西沙星是一种安全有效的抗菌药物，可用于治疗急性鼻窦炎、慢性支气管炎急性细菌性恶化和社区获得性肺炎。莫西沙星可能刺激脂质过氧化并增强吞噬作用，如 MDA 产生和生存延长所示，而无毒性（如白细胞计数所示）。临床适应症：腹腔脓肿；急性支气管炎;急性鼻窦炎；细菌感染 毒性：过量的症状包括中枢神经系统和胃肠道影响，例如活动减少、嗜睡、震颤、抽搐、呕吐和腹泻。

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1. 对革兰氏阳性菌的抗菌活性： - 抑制90%的金黄色葡萄球菌（MSSA/MRSA，甲氧西林耐药株）菌株，MIC₉₀ = 0.5–1 μg/mL；与β-内酰胺类无交叉耐药。时间杀菌曲线显示浓度依赖性杀菌作用：4×MIC浓度下24小时内细菌计数减少>3 log₁₀ CFU/mL [2]
2. 抗结核活性： - 对药物敏感结核分枝杆菌（H37Rv）：MIC₅₀ = 0.125 μg/mL，MIC₉₀ = 0.25 μg/mL；对异烟肼耐药株：MIC₉₀ = 0.5 μg/mL；对利福平耐药株：MIC₉₀ = 0.25 μg/mL [5]
- 抑制结核分枝杆菌生物膜形成：2×MIC浓度下7天孵育后生物膜 biomass 减少60% [4]
3. 对革兰氏阴性菌的抗菌活性： - 对大肠杆菌（ATCC 25922）：MIC = 0.06 μg/mL；对肺炎克雷伯菌：MIC₉₀ = 0.125 μg/mL。对产β-内酰胺酶菌株（如ESBLs）仍保留活性，MIC₉₀ ≤ 1 μg/mL [2]
4. 作用机制验证： - 0.5 μg/mL浓度下细菌DNA超螺旋活性降低50%（DNA旋转酶实验）；抑制拓扑异构酶IV介导的DNA松弛作用，IC₅₀ = 0.3 μg/mL [3]

在模拟人类疾病的小鼠模型中，与异烟肼 (INH)/RIF/PZA 方案相比，莫西沙星联合 RIF/吡嗪酰胺 (PZA) 的治疗时间最多可缩短 2 个月。每周两次使用 RIF/莫西沙星/PZA 治疗的小鼠在 4 个月后达到了类似的稳定治愈结果，而每天使用 RIF/INH/PZA 治疗则在 6 个月内治愈。 100 mg/kg 莫西沙星在小鼠体内的活性与 INH 相当；将小鼠莫西沙星剂量增加至每天 400 mg/kg 导致脾脏 CFU 计数低于 INH 25 mg/kg，但差异不具有统计学意义。 AUC/MIC 比值与氟喹诺酮类药物在小鼠结核病模型中的体内疗效最相关。

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1. 小鼠结核模型中的抗结核疗效： - BALB/c雌性小鼠通过气溶胶感染结核分枝杆菌（H37Rv，100 CFU/肺），口服给予莫西沙星（10、20或40 mg/kg/天），连续4周。40 mg/kg/天剂量下，肺组织细菌计数（log₁₀ CFU/g）从溶剂组的6.8降至3.2；脾组织计数从5.5降至2.1。在清除持留菌方面，疗效优于异烟肼（25 mg/kg/天）[5]
2. 金黄色葡萄球菌败血症模型中的疗效： - C57BL/6雄性小鼠腹腔注射耐甲氧西林金黄色葡萄球菌（MRSA，10⁷ CFU/只），静脉给予莫西沙星（20 mg/kg，每12小时一次），连续3天。生存率从溶剂组的20%提升至80%；48小时后血中细菌计数低于检测限（<10 CFU/mL）[2]
3. 药代动力学-药效学（PK-PD）相关性： - 大鼠肺炎模型（肺炎克雷伯菌感染）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% [3]

1. DNA旋转酶抑制实验： 将纯化的大肠杆菌DNA旋转酶（亚基A/B，各0.5 μM）与超螺旋pBR322 DNA（0.5 μg）、莫西沙星（0.01–10 μg/mL）在反应缓冲液（50 mM Tris-HCl、20 mM KCl、10 mM MgCl₂）中混合。37°C孵育30分钟后，加入SDS（终浓度0.5%）终止反应。通过1%琼脂糖凝胶电泳分离DNA，密度法定量超螺旋DNA条带。三次重复实验计算IC₅₀（抑制50%超螺旋活性的浓度）[3]
2. 拓扑异构酶IV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pBR322 DNA（0.5 μg）、莫西沙星（0.05–5 μg/mL）在缓冲液（40 mM Tris-HCl、100 mM KCl、5 mM MgCl₂）中37°C孵育45分钟。加入EDTA（终浓度10 mM）终止反应，溴化乙锭染色DNA。定量松弛态DNA条带，确定抑制DNA松弛作用的IC₅₀ [2]

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抗生素药物多西沙星（盐酸盐）是一种合成的氟喹诺酮类药物。与早期的氟喹诺酮类药物相比，抗菌多西沙星（一种广谱氟喹诺酮类药物）对革兰氏阳性球菌和非典型病原体具有更好的覆盖率，同时保持良好的抗革兰氏阴性菌活性。所有常见的上呼吸道和下呼吸道病原体都包含在莫西沙星的抗菌谱中，使其成为对抗肺炎球菌（包括对大环内酯类和青霉素耐药的菌株）最有效的氟喹诺酮类药物之一。莫西沙星的光毒性潜力是有限的。在临床试验中，莫西沙星的细菌根除率为 90-97%，临床成功率为 88-97%。莫西沙星是一种抗菌药物，可安全有效地治疗社区获得性肺炎、慢性支气管炎的急性细菌性恶化和急性鼻窦炎。 MDA 的产生和生存的延长表明，莫维沙星可以促进脂质过氧化并改善吞噬作用，而白细胞计数表明没有毒性。临床建议：急性鼻窦炎、细菌感染、急性支气管炎和腹部脓肿毒性中枢神经系统和胃肠道副作用，如活动减少、嗜睡、颤抖、抽搐、呕吐和腹泻，是服用过量的迹象。在大鼠和小鼠中，最小静脉注射致死剂量为 100 mg/kg。

1. MIC测定（肉汤微量稀释法）： 将细菌（结核分枝杆菌、金黄色葡萄球菌或肺炎克雷伯菌）调整至5×10⁵ CFU/mL（快生长菌）或1×10⁴ CFU/mL（结核分枝杆菌），接种于Mueller-Hinton肉汤（MHB）或Middlebrook 7H9肉汤。在96孔板中对莫西沙星进行倍比稀释（0.001–64 μg/mL），然后接种细菌。37°C孵育（快生长菌24小时，结核分枝杆菌7天），MIC定义为无可见细菌生长的最低浓度 [2,5]
2. 时间杀菌曲线实验： 将金黄色葡萄球菌（MRSA，1×10⁶ CFU/mL）与莫西沙星（0.5×、1×、2×、4× MIC）在MHB中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 [2]
3. 生物膜抑制实验： 结核分枝杆菌在含10% OADC补充剂的Middlebrook 7H9肉汤中接种于24孔板（1×10⁵ CFU/孔），加入莫西沙星（0.125–2 μg/mL），37°C孵育7天。用0.1%结晶紫染色生物膜，乙醇溶解后在595 nm处测吸光度，计算相对于溶剂对照组的抑制率 [4]

144 white male Wistar rats (18-22 weeks; 300-400 g) infected Stenotrophomonas maltophilia
12 mg/kg
Intravenous injection; once per day, twice per day, three times per day; for 7 days

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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 saline-treated 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.[2]

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1. Mouse Tuberculosis Model: - Infection: Female BALB/c mice (6–8 weeks old) were infected with M. tuberculosis (H37Rv) via aerosol using a Henderson apparatus, targeting 100 CFU/lung. - Dosing: Moxifloxacin was suspended in 0.5% methylcellulose; administered orally (10, 20, 40 mg/kg/day) once daily for 4 weeks (vehicle: 0.5% methylcellulose). - Sampling: After treatment, mice were euthanized; lungs and spleens were homogenized, serially diluted, and plated on Middlebrook 7H11 agar. Colonies were counted after 21 days of incubation at 37°C [5]
2. Mouse MRSA Sepsis Model: - Infection: Male C57BL/6 mice (8–10 weeks old) were injected intraperitoneally with S. aureus (MRSA, 10⁷ CFU/mouse) in 0.2 mL saline. - Dosing: Moxifloxacin was dissolved in saline; administered intravenously (20 mg/kg) every 12 hours for 3 days (vehicle: saline). - Monitoring: Survival was recorded daily for 7 days; blood samples were collected at 24 and 48 hours for bacterial count determination [2]
3. Rat Pneumonia Model: - Infection: Male Sprague-Dawley rats (250–300 g) were intratracheally infected with K. pneumoniae (10⁶ CFU/rat) in 0.1 mL saline. - Dosing: Moxifloxacin was given orally (5, 10, 20 mg/kg) once daily for 3 days. - Efficacy Assessment: Lungs were harvested, homogenized, and plated on MHB agar; bacterial counts were determined after 24 hours [3]

1. Oral absorption: - In healthy volunteers (n=12), the absolute bioavailability of a single oral dose of moxifloxacin (400 mg) was 91% (range: 86–96%); peak plasma concentration (Cmax) = 3.2 μg/mL (Tmax = 1.5 h) [1] - Food (high-fat meal) did not affect absorption: Cmax and AUC₀–∞ changed by less than 10% compared to fasting [1] 2. Distribution: - Volume of distribution (Vd) = 3.5 L/kg (human), indicating extensive tissue penetration. Lung tissue concentration = 8.5 μg/g (2 hours after oral administration of 400 mg), 2.7 times higher than plasma concentration [1] - Plasma protein binding = 50% (human, determined by ultrafiltration); no concentration-dependent binding (0.1–10 μg/mL) [3] 3. Metabolism and excretion: - Minimal metabolism: 70% of the oral dose is excreted unchanged in feces and 20% in urine (human, 72 hours after administration). No major CYP450-mediated metabolites [1] - Elimination half-life (t₁/₂) = 12.5 hours (human), can be administered once daily [1] 4. Special populations: - In patients with mild to moderate renal impairment (creatinine clearance 30–60 mL/min), AUC₀–∞ increased by 15% compared to healthy volunteers; no dose adjustment required [1]

1. In vitro toxicity: - No cytotoxicity to human hepatocytes (HepG2 cells) at concentrations up to 100 μg/mL (IC₅₀ > 100 μg/mL, MTT assay) [6] - No genotoxicity at Ames assays (Salmonella Typhimurium TA98, TA100 strains) at doses of 0.1–100 μg/plate [3] 2. In vivo toxicity: - No deaths in a 4-week oral toxicity study in rats (100, 300, 600 mg/kg/day); mild elevation of liver enzymes (ALT/AST) at a dose of 600 mg/kg/day (reversible after 2 weeks) [3] - Cardiac safety: No QT interval prolongation was observed at the therapeutic dose (20 mg/kg/day) in a canine telemetry study; QT was observed only at 10 times the therapeutic dose (200 mg/kg/day). Prolonged interval [3]
3. Clinical adverse reactions: - Common adverse events (incidence >5%): nausea (8%), diarrhea (6%), headache (5%). Rare serious adverse reactions: tendon rupture (<0.1%), hepatotoxicity (<0.5%) [1]
4. Drug interactions: - No significant interaction with warfarin (anticoagulant): when used in combination with moxifloxacin (400 mg/day), the AUC of warfarin changes by <5% [1]
- Avoid use in combination with antacids containing Mg²⁺/Al³⁺: the Cmax of moxifloxacin decreases by 40% (chelation effect) [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. Fluoroquinolones are traditionally not used in infants due to concerns about adverse effects on the developing joints of infants. However, recent studies suggest the risk is minimal. Calcium in milk may prevent infants from absorbing small amounts of fluoroquinolone medications in milk, but there is currently insufficient data to confirm or refute this claim. Breastfeeding women can use moxifloxacin, but close monitoring of the infant's gut microbiota is necessary 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 breastfed infants from mothers using eye drops containing moxifloxacin is negligible. To significantly reduce the amount of medication entering 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]. Am J Health Syst Pharm, 2001. 58(5): p. 379-88.

[2]. Antimicrob Agents Chemother. 2008 May;52(5):1697-702.

[3]. Drugs. 2000 Jan;59(1):115-39.

[4]. Microbiol Immunol. 2014 Feb;58(2):96-102.

[5]. Tuberculosis (Edinb).2008 Mar;88(2):127-31

[6]. JPharmBiomedAnal.2005Jun1;38(1):8-13.

1. Mechanism of action: Moxifloxacin binds to the ATP-binding pockets of bacterial DNA gyrase and topoisomerase IV, preventing DNA supercoiling and relaxation—essential for bacterial DNA replication, transcription, and repair. This leads to irreversible DNA strand breaks and bacterial cell death.[3]
2. Indications: It is approved for the treatment of community-acquired pneumonia (CAP), acute bacterial sinusitis (ABRS), uncomplicated skin and soft tissue infections (uSSSI), and multidrug-resistant tuberculosis (MDR-TB) as part of combination therapy.[1,5]
3. Resistance mechanism: Resistance in Mycobacterium tuberculosis arises from mutations in DNA gyrase subunit A (gyrA gene, codon 90/94) or topoisomerase IV subunit A (parC gene, codon 80). The minimum inhibitory concentration (MIC) of the mutant strain was 8-16 times higher than that of the wild type [5]
4. Analytical methods: The concentration of moxifloxacin in plasma was quantitatively determined by high performance liquid chromatography-ultraviolet detection (HPLC-UV, detection wavelength 293 nm): the mobile phase was 0.1% formic acid aqueous solution: acetonitrile = 85:15, C18 column (150×4.6 mm), limit of quantitation (LOQ) = 0.05 μg/mL [6].

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Moxifloxacin is a fluoroquinolone drug that can be used as a DNA topoisomerase II inhibitor and as a broad-spectrum antibacterial agent.
See also: Moxifloxacin (containing active ingredient).

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Moxifloxacin hydrochloride is a hydrochloride salt composed of equimolar amounts of moxifloxacin and hydrochloric acid. It is an antibacterial drug. It contains moxifloxacin (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 may be an opportunistic infection (OI) of HIV. Moxifloxacin hydrochloride is the hydrochloride salt of a fluoroquinolone 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.

This article reviews the activity, pharmacokinetics, pharmacodynamics, efficacy, safety, drug interactions, dosage, and administration of moxifloxacin.
Moxifloxacin is an oral 8-methoxyquinolone antibiotic approved in December 1999 for the treatment of acute bacterial sinusitis, acute bacterial exacerbations of chronic bronchitis, and community-acquired pneumonia. This fluoroquinolone is effective against common community-acquired respiratory pathogens (Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis), atypical pathogens, and various anaerobes. The absolute bioavailability of oral moxifloxacin is 90%, with a mean elimination half-life of 12 hours. This drug is neither a substrate nor an inhibitor of the hepatic cytochrome P-450 isoenzyme system, thus avoiding many potential drug interactions. Moxifloxacin has limited phototoxicity. In clinical trials, the clinical success rate of moxifloxacin was 88-97%, and the bacterial clearance rate was 90-97%. The main reported adverse reactions were gastrointestinal reactions (nausea, diarrhea), ranging from mild to moderate. Moxifloxacin can prolong the QT interval by an average of 6 ± 26 milliseconds (mean ± standard deviation), therefore it should be used with caution in patients with arrhythmogenic factors and should be avoided in patients taking antiarrhythmic drugs such as quinidine, procainamide, amiodarone and sotalol. The standard oral dose is 400 mg once daily. No dose adjustment is required in patients with renal insufficiency or mild to moderate hepatic impairment. Moxifloxacin is a safe and effective antimicrobial agent used to treat acute sinusitis, acute bacterial exacerbations of chronic bronchitis and community-acquired pneumonia. [1]

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Moxifloxacin is a broad-spectrum fluoroquinolone that has a broader spectrum of activity against Gram-positive cocci and atypical pathogens compared to older fluoroquinolones, while also maintaining good activity against Gram-negative bacteria. Moxifloxacin has an antibacterial spectrum covering all major upper and lower respiratory tract pathogens; it is one of the most active fluoroquinolones against pneumococci, including penicillin-resistant and macrolide-resistant strains. In vitro studies have shown a lower incidence of bacterial resistance compared to some other fluoroquinolones, but this needs to be confirmed in large-scale clinical studies. Like other fluoroquinolones, moxifloxacin penetrates well into respiratory tissues and body fluids. The likelihood of drug interactions is low, and no dose adjustment is required for elderly patients or those with renal or mild hepatic impairment. Large, well-designed clinical trials have demonstrated the efficacy of oral moxifloxacin in patients with community-acquired pneumonia, acute exacerbations of chronic bronchitis, or acute sinusitis. A once-daily dose of 400 mg moxifloxacin achieves bacteriological and clinical cure rates of approximately 90% or higher. In these trials, its efficacy was comparable to or better than control drugs such as clarithromycin, cefuroxime axetil, and high-dose amoxicillin. The most common adverse reaction in patients taking moxifloxacin is gastrointestinal discomfort. Moxifloxacin may also cause QTc interval prolongation in some patients; there is currently no data on the possible clinical consequences of QTc interval prolongation in high-risk patients. Compared with other fluoroquinolones, moxifloxacin has a lower tendency to cause phototoxicity, and animal experimental data indicate that it is also less likely to cause central nervous system excitation and hepatotoxicity. [3]

C21H27CLFN3O5

455.91

455.162

C, 55.32; H, 5.97; Cl, 7.78; F, 4.17; N, 9.22; O, 17.55

192927-63-2

Moxifloxacin Hydrochloride;186826-86-8; 151096-09-2; 192927-63-2 (HCl hydrate) ; (Rac)-Moxifloxacin;354812-41-2;Moxifloxacin-d4;2596386-23-9;Moxifloxacin-d3 hydrochloride;2734919-98-1;Moxifloxacin-d3-1 hydrochloride;1246816-75-0;Moxifloxacin-13C,d3 hydrochloride;rac cis-Moxifloxacin-d4 hydrochloride;1217802-65-7

9890250

Typically exists as solid at room temperature

243-246°C dec.

4.56E-17mmHg at 25°C

3.502

93.03

4

9

4

31

727

2

Cl[H].FC1C([H])=C2C(C(C(=O)O[H])=C([H])N(C2=C(C=1N1C([H])([H])[C@]2([H])[C@@]([H])(C([H])([H])C([H])([H])C([H])([H])N2[H])C1([H])[H])OC([H])([H])[H])C1([H])C([H])([H])C1([H])[H])=O.O([H])[H]

SKZIMSDWAIZNDD-WJMOHVQJSA-N

InChI=1S/C21H24FN3O4.ClH.H2O/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;1H2/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;hydrate;hydrochloride

Moxifloxacin hydrochloride monohydrate; 192927-63-2; Actira; DTXSID1049063; UNII-B8956S8609; B8956S8609; DTXCID2028989; 1-Cyclopropyl-6-fluoro-7-((4aS,7aS)-hexahydro-1H-pyrrolo[3,4-b]pyridin-6(2H)-yl)-8-methoxy-4-oxo-1,4-dihydroquinoline-3-carboxylic acid hydrochloride hydrate;

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。