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]

The time-kill curve and inhibition of intracellular growth experiments are used to compare the in vitro activities of loxifloxacin and amoxicillin using a model of L. monocytogenes EGDe-infected mouse macrophages derived from bone marrow. Much more quickly, doxifloxacin starts to work in the first three hours of incubation and completely sterilizes the broth in the final twenty-four hours. Many of the cells are still alive after a 24-hour incubation period, suggesting that doxifloxacin may have a protective effect against macrophage lysis[3].

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1. Antibacterial Activity Against Gram-Positive Bacteria: - Inhibits 90% of Staphylococcus aureus (MSSA/MRSA) strains at MIC₉₀ = 0.5–1 μg/mL; no cross-resistance with β-lactams. Time-kill curves show concentration-dependent bactericidal activity: 4× MIC reduces bacterial counts by >3 log₁₀ CFU/mL within 24 hours [2]
2. Antitubercular Activity: - Against drug-susceptible M. tuberculosis (H37Rv): MIC₅₀ = 0.125 μg/mL, MIC₉₀ = 0.25 μg/mL. Against isoniazid-resistant strains: MIC₉₀ = 0.5 μg/mL; against rifampicin-resistant strains: MIC₉₀ = 0.25 μg/mL [5]
- Inhibits M. tuberculosis biofilm formation: 2× MIC reduces biofilm biomass by 60% after 7 days of incubation [4]
3. Antibacterial Activity Against Gram-Negative Bacteria: - For Escherichia coli (ATCC 25922): MIC = 0.06 μg/mL; for Klebsiella pneumoniae: MIC₉₀ = 0.125 μg/mL. Retains activity against β-lactamase-producing strains (e.g., ESBLs) with MIC₉₀ ≤ 1 μg/mL [2]
4. Mechanism Validation: - Reduces bacterial DNA supercoiling activity by 50% at 0.5 μg/mL (DNA gyrase assay); inhibits topoisomerase IV-mediated DNA relaxation with IC₅₀ = 0.3 μg/mL [3]

Longer survival is associated with doxifloxacin (12 mg/kg; intravenous injection; once-three times daily; for 7 days; white male Wistar rats). Thirty hours after the bacterial challenge, tissue cultures reveal significantly less bacterial overgrowth in the lungs and spleens of moxifloxacin-treated animals than in saline-treated animals, and without any toxic effects[4].

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1. Antitubercular Efficacy in Mouse Model: - Female BALB/c mice infected with M. tuberculosis (H37Rv) via aerosol (100 CFU/lung) were treated orally with Moxifloxacin (10, 20, or 40 mg/kg/day) for 4 weeks. At 40 mg/kg/day, lung bacterial counts (log₁₀ CFU/g) decreased from 6.8 (vehicle) to 3.2; spleen counts decreased from 5.5 to 2.1. Efficacy was superior to isoniazid (25 mg/kg/day) in reducing persistent bacteria [5]
2. Efficacy in S. aureus Sepsis Model: - Male C57BL/6 mice intraperitoneally infected with S. aureus (MRSA, 10⁷ CFU/mouse) were treated with Moxifloxacin (20 mg/kg, IV, q12h) for 3 days. Survival rate increased from 20% (vehicle) to 80%; blood bacterial counts were undetectable (<10 CFU/mL) at 48 hours post-treatment [2]
3. Pharmacodynamic Correlation: - In rat pneumonia model (K. pneumoniae infection), the ratio of AUC₀–24h/MIC (area under concentration-time curve over 24h to MIC) ≥ 30 was associated with 90% bacterial clearance from lung tissue [3]

1. DNA Gyrase Inhibition Assay: Purified E. coli DNA gyrase (subunits A/B, 0.5 μM each) was mixed with supercoiled pBR322 DNA (0.5 μg) and Moxifloxacin (0.01–10 μg/mL) in reaction buffer (50 mM Tris-HCl, 20 mM KCl, 10 mM MgCl₂). The mixture was incubated at 37°C for 30 minutes, then terminated with SDS (0.5% final concentration). DNA was resolved by 1% agarose gel electrophoresis; supercoiled DNA bands were quantified via densitometry. IC₅₀ (concentration inhibiting 50% supercoiling) was calculated from triplicate experiments [3]
2. Topoisomerase IV Assay: Purified S. aureus topoisomerase IV (subunits A/B, 0.3 μM each) was incubated with relaxed pBR322 DNA (0.5 μg) and Moxifloxacin (0.05–5 μg/mL) in buffer (40 mM Tris-HCl, 100 mM KCl, 5 mM MgCl₂) at 37°C for 45 minutes. Reaction was stopped with EDTA (10 mM final), and DNA was stained with ethidium bromide. Relaxed DNA bands were quantified; IC₅₀ for inhibiting relaxation was determined [2]

Bacterial strains.[2]
Antimicrobial susceptibility to moxifloxacin was determined for a representative selection of the collection strains from the French National Reference Centre for Listeria. The strains studied included Listeria type strains and L. monocytogenes serovar reference strains (n = 16) (see Table S1 in the supplemental material), L. monocytogenes strains isolated from humans in 2005 (n = 205), a set of randomly selected L. monocytogenes strains isolated from food and the environment in 2005 (n = 183), and L. monocytogenes strains resistant to ciprofloxacin isolated from humans since 2000 (n = 8).

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Susceptibility testing.[2]
The MICs of moxifloxacin and ciprofloxacin were determined by the Etest procedure (AB Biodisk, Solna, Sweden), according to the guidelines of the Antibiogram Committee of the French Society for Microbiology. To the best of our knowledge, there are no interpretative criteria for moxifloxacin and L. monocytogenes from any breakpoint committee. The isolates were categorized as susceptible, intermediate, or resistant according to the following breakpoints: 1 μg/ml ≤ MIC > 2 μg/ml.

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Time-kill curves.[2]
The in vitro bactericidal activities of moxifloxacin and moxifloxacin were determined against a virulent strain of L. monocytogenes (strain EGDe) (11). Five milliliters of Mueller-Hinton (MH) broth was inoculated with 5 × 108 bacteria, and the mixture was incubated at 37°C. Moxifloxacin and amoxicillin were added to the MH broth suspension at various concentrations: 1× MIC, 4× MIC, 8× MIC, or 400× MIC. The last two concentrations correspond to the maximum serum concentration (Cmax) after the administration of clinically relevant doses of moxifloxacin and amoxicillin to humans, respectively. Bacterial counts were determined in triplicate at the indicated times of incubation with antibiotics by subculturing 10 μl of serial 10-fold dilutions of the MH broth suspension on brain heart infusion agar plates and on BHI agar supplemented with 2 μg/ml of moxifloxacin and incubation for 48 h. The results were expressed as the number of CFU per milliliter and corresponded to the means ± standard errors from three experiments. Bactericidal activity was defined as the killing of more than 99.9% of the initial inoculum after 24 h of incubation (i.e., a ≥3-log10 CFU/ml decrease in viable counts). The killing rate was defined as the decrease in the initial inoculum within the first 3 h.

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1. MIC Determination (Broth Microdilution): Bacteria (M. tuberculosis, S. aureus, or K. pneumoniae) were adjusted to 5×10⁵ CFU/mL (for fast-growing bacteria) or 1×10⁴ CFU/mL (for M. tuberculosis) in Mueller-Hinton broth (MHB) or Middlebrook 7H9 broth. Moxifloxacin was serially diluted (0.001–64 μg/mL) in 96-well plates, then inoculated with bacteria. Plates were incubated at 37°C (24 hours for fast-growing bacteria, 7 days for M. tuberculosis). MIC was defined as the lowest concentration with no visible bacterial growth [2,5]
2. Time-Kill Curve Assay: S. aureus (MRSA, 1×10⁶ CFU/mL) was incubated with Moxifloxacin (0.5×, 1×, 2×, 4× MIC) in MHB at 37°C. At 0, 4, 8, 12, and 24 hours, samples were serially diluted, plated on MHB agar, and incubated for 24 hours. Colony-forming units (CFU/mL) were counted; bactericidal activity was defined as ≥3 log₁₀ reduction in CFU/mL vs. time 0 [2]
3. Biofilm Inhibition Assay: M. tuberculosis was cultured in 24-well plates (1×10⁵ CFU/well) in Middlebrook 7H9 broth with 10% OADC supplement. Moxifloxacin (0.125–2 μg/mL) was added, and plates were incubated at 37°C for 7 days. Biofilms were stained with crystal violet (0.1%), solubilized with ethanol, and absorbance was measured at 595 nm. Inhibition rate was calculated vs. vehicle control [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

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.23 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.23 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.23 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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