Quinolone antibiotic
- Bacterial DNA gyrase (subunit A/B) and topoisomerase IV (subunit A/B):
- For Mycobacterium tuberculosis (H37Rv strain): MIC₉₀ (minimum inhibitory concentration inhibiting 90% growth) = 0.25 μg/mL (DNA gyrase inhibition-driven) [5]
- For Staphylococcus aureus (MSSA): MIC₉₀ = 0.5 μg/mL (topoisomerase IV as primary target) [2]
- For Escherichia coli: Ki = 1.2 μM (DNA gyrase ATPase activity inhibition) [3]

使用时间杀伤曲线和细胞内生长抑制实验来比较洛西沙星和阿莫西林的体外活性，使用来自骨髓的单增李斯特菌EGDe感染的小鼠巨噬细胞模型。更快的是，多西沙星在孵化的前三个小时内开始发挥作用，并在最后的二十四小时内对肉汤进行完全消毒。许多细胞在 24 小时潜伏期后仍然存活，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]

多西沙星（12 mg/kg；静脉注射；每天一次至三次；持续 7 天；白色雄性 Wistar 大鼠）与更长的生存期相关。细菌攻击后 30 小时，组织培养显示，与生理盐水处理的动物相比，莫西沙星处理的动物肺和脾脏中细菌过度生长明显减少，并且没有任何毒性作用[4]。

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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]

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moxifloxacin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程序测定moxifloxacin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moxifloxacin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。moxifloxacin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）。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. 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]

Animal Model: Stenotrophomonas maltophilia infected 144 white male Wistar rats, weighing 300–400 g and maturing between 18 and 22 weeks[4].
Dosage: 12 mg/kg
Administration: Intravenous injection; once per day, twice per day, three times per day; for 7 days
Result: demonstrated a marked reduction in the overgrowth of bacteria in the lungs and spleens without being toxic.

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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]

Absorption, Distribution and Excretion
Moxifloxacin is well absorbed via the gastrointestinal tract. The absolute oral bioavailability is approximately 90%. Food has little effect on absorption. After oral or intravenous administration, approximately 45% of moxifloxacin is excreted unchanged (approximately 20% in urine and approximately 25% in feces). The volume of distribution is 1.7 to 2.7 L/kg. The blood flow rate is 12 ± 2 L/hr. Moxifloxacin binds to serum proteins at a rate of approximately 30-50%, regardless of drug concentration. Moxifloxacin is widely distributed throughout the body, with tissue concentrations typically higher than plasma concentrations. Following oral or intravenous administration of 400 mg moxifloxacin, it can be detected in saliva, nasal and bronchial secretions, sinus mucosa, skin vesicular fluid, subcutaneous tissue, skeletal muscle, and peritoneal tissues and fluids. Following oral or intravenous administration of moxifloxacin, approximately 45% is excreted unchanged (approximately 20% in urine and approximately 25% in feces). Of the total oral dose, 96% ± 4% is excreted unchanged or as known metabolites. The mean (± standard deviation) apparent total clearance and renal clearance are 12 ± 2 L/h and 2.6 ± 0.5 L/h, respectively. Oral moxifloxacin tablets are well absorbed from the gastrointestinal tract. The absolute bioavailability of moxifloxacin is approximately 90%. Concomitant administration with a high-fat meal (i.e., 500 calories of fat) does not affect the absorption of moxifloxacin. Ocular permeability and pharmacokinetics of moxifloxacin have been determined through in vitro and ex vivo studies, as well as animal and human studies, compared to other fluoroquinolones (ofloxacin, ciprofloxacin, gatifloxacin, norfloxacin, levofloxacin, and lomefloxacin). The results consistently demonstrate that moxifloxacin achieves higher maximum concentrations in ocular tissues compared to other fluoroquinolones, significantly exceeding its minimum inhibitory concentrations (MICs) against relevant ocular pathogens. This superior performance is attributed to moxifloxacin's unique structure, which combines high lipophilicity (enhancing corneal permeability) with high water solubility at physiological pH. The latter property creates a high concentration gradient at the tear film/corneal epithelium interface, driving better moxifloxacin penetration into the eye. Furthermore, the higher concentration of moxifloxacin in VIGAMOX (0.5% vs. 0.3%) allows more antibiotic to reach ocular tissues. The series of studies summarized in this report clearly demonstrates that moxifloxacin penetrates ocular tissues more readily than gatifloxacin, ciprofloxacin, ofloxacin, or levofloxacin (with two to three times greater permeability). The sustained enhanced permeability of topical moxifloxacin provides a significant advantage in ophthalmic treatment. For more complete data on absorption, distribution, and excretion of moxifloxacin (6 items in total), please visit the HSDB record page. Metabolites/Metabolites: Approximately 52% of the oral or intravenous dose is metabolized via glucuronide and sulfate conjugates. The cytochrome P450 system is not involved in metabolism. Sulfate conjugates account for 38% of the dose, and glucuronide conjugates account for 14%. Approximately 52% of the oral or intravenous dose of moxifloxacin is metabolized via glucuronide and sulfate conjugates. The cytochrome P450 system is not involved in the metabolism of moxifloxacin and is not affected by moxifloxacin. Sulfate conjugates (M1) account for approximately 38% of the administered dose and are primarily excreted in feces. Approximately 14% of the oral or intravenous dose is converted to glucuronide conjugates (M2), which are excreted only in the urine. The peak plasma concentration of M2 is approximately 40% of the parent drug, while the plasma concentration of M1 is typically less than 10% of that of moxifloxacin.

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Biological half-life
11.5–15.6 hours (single oral dose)
Mean (± standard deviation) elimination half-life in plasma is 12 ± 1.3 hours

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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 hours)[1]
-Food (high-fat meal) does not affect absorption: Cmax and AUC₀–∞ change 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), allowing for once-daily administration [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]

Hepatotoxicity
Similar to other fluoroquinolones, the incidence of serum enzyme elevations during moxifloxacin treatment is low (1% to 3%). These abnormalities are usually mild, asymptomatic, and transient, and resolve with continued treatment. Moxifloxacin is associated with rare but occasionally severe and even fatal cases of acute liver injury. Onset is usually short (1 day to 3 weeks), with symptoms often appearing suddenly, including nausea, fatigue, abdominal pain, and jaundice. Serum enzyme elevations can be hepatocellular or cholestatic, with shorter-onset cases generally being more hepatocellular. Symptoms may also appear within days of discontinuation of the drug. Many (but not all) cases have significant allergic reactions, such as fever and rash, and liver injury may occur against a background of systemic hypersensitivity (Case 1). Autoantibodies are usually absent. Cases with a cholestatic enzyme pattern may have a longer course but usually resolve spontaneously, although at least one case of chronic cholestasis and disappearance of bile duct syndrome leading to liver failure has been reported. Most reported cases are mild and recover within 4 to 8 weeks of onset.
Probability Score: B (Rare but likely a cause of clinically significant liver damage).
Pregnancy and Lactation Effects
◉ Overview of Lactation Use
There is currently no information regarding the use of moxifloxacin during lactation. Fluoroquinolones have traditionally been avoided due to concerns about adverse effects on the developing joints of infants. However, recent studies suggest the risk is minimal. Calcium in breast milk may prevent the absorption of small amounts of fluoroquinolones in breast 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 observe for adverse reactions such as diarrhea or candidiasis (thrush, diaper rash). However, it is generally recommended to use other medications with more comprehensive safety information.
The risk to a breastfeeding infant from the mother's use of moxifloxacin-containing eye drops 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 blot away excess medication with absorbent tissue.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found as of the revision date.

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Protein binding
50% bound to serum proteins, regardless of drug concentration.

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Interactions
15 men and 5 women (mean age 34 years) took moxifloxacin in two settings with a washout period of at least 7 days between the two settings: oral administration of 400 mg alone, and administration immediately after intramuscular injection of 10 mg morphine sulfate. Serum moxifloxacin concentrations were determined using a validated high-performance liquid chromatography method. Pharmacokinetic parameters, including Cmax, Tmax, AUC0-∞, and t1/2, were estimated using a non-compartmental model and analyzed using analysis of variance (ANOVA). Results: The pharmacokinetic parameters of moxifloxacin were similar under both treatment regimens. The geometric least squares mean Cmax of moxifloxacin was 3.4 mg/L (monotherapy) and 2.8 mg/L (combined with morphine) (90% confidence interval (CI) for moxifloxacin monotherapy and combined with morphine sulfate was 71%-98%). The corresponding geometric mean AUC0-∞ was 41.5 mg·h/L and 39.6 mg·h/L (90% CI = 87%-104%). The Tmax and t1/2 values of moxifloxacin combined with morphine were similar. Conclusion: Moxifloxacin monotherapy or combined with morphine sulfate was well tolerated. A single intramuscular injection of morphine did not reduce the bioavailability of oral moxifloxacin or alter its elimination curve. Conclusion: Concomitant use of morphine and moxifloxacin is unlikely to reduce the efficacy of this quinolone drug.
Pharmacokinetic interactions (reduced absorption of oral moxifloxacin). Moxifloxacin should be taken at least 4 hours before or at least 8 hours after taking buffered didanoxin (pediatric oral solution mixed with an antacid).
Concomitant use of corticosteroids increases the risk of serious tendinopathy (e.g., tendinitis, tendon rupture), especially in elderly patients over 60 years of age.
Quinolone drugs (including aviroxa) have been reported to enhance the anticoagulant effect of warfarin or its derivatives in the patient population. Furthermore, infectious diseases and their associated inflammatory processes, patient age, and general condition are risk factors for enhanced anticoagulant activity. Therefore, if quinolones are used concomitantly with warfarin or its derivatives, prothrombin time, international normalized ratio (INR), or other appropriate anticoagulant tests should be closely monitored.
For more complete data on interactions of moxifloxacin (17 in total), please visit the HSDB records page.

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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 0.1–100 μg/plate in Ames assay (Salmonella typhimurium TA98, TA100 strains) [3]
2. In vivo toxicity: - In a 4-week oral toxicity study in rats (100, 300, 600 mg/kg/day): no deaths; mild elevation of liver enzymes (ALT/AST) was observed in the 600 mg/kg/day dose group (returned to normal after 2 weeks) [3]
- Cardiac safety: In a canine telemetry study, no QT interval prolongation was observed at the therapeutic dose (20 mg/kg/day); QT was only observed 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 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 less than 5% [1]
- Avoid use in combination with antacids containing Mg²⁺/Al³⁺: the Cmax of moxifloxacin decreases by 40% (chelation effect) [1]

[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.

Therapeutic Uses

Anti-infective Drug
Moxifloxacin hydrochloride eye drops are used to treat conjunctivitis caused by moxifloxacin-sensitive Corynebacterium spp., Micrococcus luteus, Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus hemolyticus, Staphylococcus hominis, Staphylococcus warwickii, Streptococcus pneumoniae, Streptococcus viridans, Acinetobacter loborrhea, Haemophilus influenzae, Haemophilus parainfluenzae, or Chlamydia trachomatis. /US Product Label Includes/
Moxifloxacin is used to treat acute bacterial sinusitis caused by moxifloxacin-sensitive Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis; acute bacterial exacerbations of chronic bronchitis caused by susceptible Streptococcus pneumoniae, Haemophilus influenzae, Haemophilus parainfluenzae, Klebsiella pneumoniae, Staphylococcus aureus (oxacillin-sensitive [methicillin-sensitive] strains), or Moraxella catarrhalis; and community-acquired pneumonia (CAP) caused by susceptible Streptococcus pneumoniae (including multidrug-resistant strains), Staphylococcus aureus (oxacillin-sensitive strains), Klebsiella pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Chlamydia pneumoniae (formerly known as Chlamydia pneumoniae), or Moraxella catarrhalis. /US Product Label Includes/
Moxifloxacin is used to treat uncomplicated skin and soft tissue infections caused by susceptible Staphylococcus aureus (oxacillin-sensitive strains) or Streptococcus pyogenes (group A beta-hemolytic streptococci), and complicated skin and soft tissue infections caused by susceptible Staphylococcus aureus (oxacillin-sensitive strains), Escherichia coli, Klebsiella pneumoniae, or Enterobacter cloacae. /US Product Label Includes/
For more complete data on the therapeutic uses of moxifloxacin (12 types), please visit the HSDB record page.

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Drug Warning
/Black Box Warning/ Warning: Fluoroquinolones, including avixacin, are associated with an increased risk of tendinitis and tendon rupture in all age groups. This risk is further increased in older patients (typically over 60 years of age), patients taking corticosteroids, and patients who have received a kidney, heart, or lung transplant. /Warning (Black Box)/ Warning: Fluoroquinolones (including moxifloxacin) may worsen muscle weakness in patients with myasthenia gravis. Patients with a known history of myasthenia gravis should avoid using moxifloxacin. Severe and potentially fatal hypersensitivity reactions and/or anaphylactic shock have been reported in patients treated with fluoroquinolones (including moxifloxacin). While these reactions usually occur after multiple doses, they can also occur with the first dose. Some reactions are accompanied by cardiovascular failure, loss of consciousness, tingling, edema (in the throat or face), dyspnea, urticaria, or pruritus. In addition, other serious and potentially fatal reactions (possibly hypersensitivity reactions or of unknown cause) have been reported, most often after multiple doses. These adverse reactions include fever, rash, or severe skin reactions (e.g., toxic epidermal necrolysis, Stevens-Johnson syndrome), vasculitis, arthralgia, myalgia, serum sickness, anaphylactic pneumonitis, interstitial nephritis, acute renal failure or insufficiency, hepatitis, jaundice, acute liver necrosis or insufficiency, anemia (including hemolytic anemia and aplastic anemia), thrombocytopenia (including thrombotic thrombocytopenic purpura), leukopenia, agranulocytosis, pancytopenia, and/or other hematologic adverse reactions. Moxifloxacin should be discontinued immediately upon the onset of rash, jaundice, or any other signs of an allergic reaction. Appropriate treatment should be administered as indicated (e.g., adrenaline, corticosteroids, and maintaining adequate airway patency and oxygenation). Fluoroquinolone use has been reported to cause sensory or sensorimotor axonal polyneuropathy affecting small and/or large axons, leading to paresthesia, hypoesthesia, sensory disturbances, and muscle weakness. For more complete data on drug warnings for moxifloxacin (22 total), please visit the HSDB records page.

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Pharmacodynamics
Moxifloxacin is a quinolone/fluoroquinolone antibiotic. Moxifloxacin can be used to treat infections caused by the following bacteria: Aerobic Gram-positive bacteria: Corynebacterium spp., Micrococcus luteus, Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus haemolyticus, Staphylococcus hominis, Staphylococcus wartii, Streptococcus pneumoniae, and viridans streptococci. Aerobic Gram-negative bacteria: Acinetobacter loborrhea, Haemophilus influenzae, and Haemophilus parainfluenzae. Other microorganisms: Chlamydia trachomatis. Moxifloxacin is a bactericidal agent whose mechanism of action is to bind to an enzyme called DNA gyrase, which blocks bacterial DNA replication. DNA gyrase unwinds the DNA double helix, allowing one DNA double helix to be replicated into two. Notably, this drug has an affinity for bacterial DNA gyrase that is 100 times higher than that for mammalian DNA gyrase. Moxifloxacin is a broad-spectrum antibiotic effective against both Gram-positive and Gram-negative bacteria.

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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 has been 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: Drug resistance in Mycobacterium tuberculosis is caused by 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]

C21H24FN3O4

401.43

401.18

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

151096-09-2

Moxifloxacin Hydrochloride;186826-86-8;(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

152946

White to yellow solid powder

1.4±0.1 g/cm3

636.4±55.0 °C at 760 mmHg

193-195 °C(lit.)

338.7±31.5 °C

0.0±2.0 mmHg at 25°C

1.633

1.6

83.8

2

8

4

29

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

FABPRXSRWADJSP-MEDUHNTESA-N

InChI=1S/C21H24FN3O4/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)/t11-,16+/m0/s1

1-Cyclopropyl-6-fluoro-1,4-dihydro-8-methoxy-7-((4aS,7aS)-octahydro-6H-pyrrolo(3,4-b)pyridin-6-yl)-4-oxo-3-quinolinecarboxylic acid

Avelox;Avalox;Avelon;Vigamox;Moxeza;BAY12-8039;BAY12-8039;BAY 12-8039

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)

DMSO : ~31.25 mg/mL (~77.85 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (6.23 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (6.23 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (6.23 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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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。