Quinolone; TOPO IV
Bacterial DNA gyrase [2][3][5]
Bacterial topoisomerase IV [2][3][5]

In vitro activity: Levofloxacin exhibits moderate activity against anaerobes and is active against the majority of aerobic Gram-positive and Gram-negative organisms.[1] Levofloxacin is 2- to 4-fold more active than ciprofloxacin against Staphylococcus aureus, Xanthomonas maltophilia, and Bacteroides fragilis, and two-fold more active than ciprofloxacin against Streptococcus pneumoniae. When it comes to killing coagulase-negative staphylococci and Acinetobacter species, levofloxacin is two to eight times more potent than ciprofloxacin; however, these differences in potency might not have any practical significance. 90% of streptococci are inhibited by levofloxacin at concentrations ranging from 1 mg to 2 mg/mL.[2] Levofloxacin shows bactericidal and inhibitory properties against extracellular or intracellular tubercle bacilli that are two times stronger than those of ofloxacin. [3] Levofloxacin, with a 50% inhibitory concentration of about 80 mg/mL at 48 and 72 hours, has the least inhibitory effect on osteoblastic cell growth. As shown by alizarin red staining and biochemical analysis on day 14, levofloxacin significantly inhibits calcium deposition.[4] In cultured rabbit chondrocytes, levofloxacin inhibits glycosaminoglycan synthesis first, DNA synthesis second, and mitochondrial function at actual arthropathic concentrations; however, these changes are reversible and do not result in the death of the cells.[5]

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Against Gram-negative bacteria (Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae), Levofloxacin [(-)-Ofloxacin] exhibited potent concentration-dependent antibacterial activity, with MIC values ranging from 0.03 to 1 μg/mL for susceptible strains [2][3][5]
- Against Gram-positive bacteria (Staphylococcus aureus, Streptococcus pneumoniae, Enterococcus faecalis), the drug showed significant antibacterial activity, with MIC values of 0.125-4 μg/mL, superior to the racemic ofloxacin against most strains [2][5]
- Levofloxacin [(-)-Ofloxacin] inhibited bacterial DNA replication and transcription by stabilizing DNA gyrase-DNA and topoisomerase IV-DNA cleavage complexes, preventing DNA strand religation [2][3]
- It maintained antibacterial activity against nalidixic acid-resistant Gram-negative bacteria, with MIC values 2-4 times lower than ofloxacin [5]

Levofloxacin is equally as effective as ciprofloxacin, if not more so, in treating systemic infections in mice with pyelonephritis. Mice's serum and tissue contain greater concentrations of levofloxacin than ciprofloxacin.[2]

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In a murine model of Escherichia coli-induced pyelonephritis, oral administration of Levofloxacin [(-)-Ofloxacin] at 10 and 20 mg/kg/day for 3 days significantly reduced bacterial load in kidneys and urine, with cure rates of 75% and 90%, respectively [2]
- In rats infected with Pseudomonas aeruginosa pneumonia, intravenous administration of Levofloxacin [(-)-Ofloxacin] at 5 and 10 mg/kg twice daily for 5 days improved survival rates by 60% and 85%, and reduced lung tissue bacterial counts by 1-2 log10 CFU/g [3]
- The drug showed good tissue penetration in vivo, achieving therapeutic concentrations in kidneys, lungs, skin, and gastrointestinal tract [1]

Bacterial DNA gyrase activity assay: Purified Escherichia coli DNA gyrase was incubated with supercoiled plasmid DNA in reaction buffer at 37°C. Levofloxacin [(-)-Ofloxacin] was added at serial concentrations (0.015-8 μg/mL), and the mixture was incubated for 60 minutes. The reaction was terminated by adding SDS and proteinase K, followed by incubation at 55°C for 1 hour. DNA products were separated by 1% agarose gel electrophoresis and stained with ethidium bromide. The inhibition of DNA gyrase-mediated supercoiling relaxation was quantified by measuring the intensity of supercoiled DNA bands [2][3]
- Bacterial topoisomerase IV activity assay: Isolated Staphylococcus aureus topoisomerase IV was incubated with relaxed plasmid DNA in reaction buffer. Levofloxacin [(-)-Ofloxacin] was added at concentrations of 0.03-16 μg/mL, and the mixture was incubated at 37°C for 45 minutes. The reaction was stopped by adding stop solution, and DNA products were analyzed by agarose gel electrophoresis to assess inhibition of DNA decatenation [2][5]

Bacterial growth inhibition assay: Bacterial strains (Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus) were cultured in Mueller-Hinton broth at 37°C with shaking. Levofloxacin [(-)-Ofloxacin] was added at serial concentrations (0.0075-32 μg/mL), and bacterial growth was monitored by measuring optical density at 600 nm (OD600) after 24 hours. The MIC was defined as the lowest concentration inhibiting ≥90% bacterial growth [2][3][5]
- Resistant strain susceptibility assay: Nalidixic acid-resistant Escherichia coli strains were cultured in the presence of Levofloxacin [(-)-Ofloxacin] (0.125-8 μg/mL) and ofloxacin (0.25-16 μg/mL) for 24 hours. Bacterial colony counts were performed to compare the antibacterial activity of the two drugs [5]

Matured male Albino mice
10.7 mg/kg
Intraperitoneal injection; 10.7 mg/kg, once daily for 10 days or 3 weeks.

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Pyelonephritis mouse model: Female BALB/c mice were intraurethrally inoculated with a pathogenic strain of Escherichia coli. Levofloxacin [(-)-Ofloxacin] was dissolved in sterile water and administered orally via gavage at 10 or 20 mg/kg/day for 3 days. Mice were euthanized, and kidneys and urine samples were collected to quantify bacterial load via colony counting [2]
- Pneumonia rat model: Male Wistar rats were intratracheally inoculated with Pseudomonas aeruginosa. The drug was dissolved in saline and administered intravenously at 5 or 10 mg/kg twice daily for 5 days. Survival rates were recorded, and lung tissues were collected for bacterial count and histopathological analysis [3]
- Tendon toxicity evaluation model: Male Sprague-Dawley rats were administered Levofloxacin [(-)-Ofloxacin] orally at 100, 200, 400 mg/kg/day for 14 days. Achilles tendons were harvested, and histological changes (collagen fiber disruption, inflammation) were observed under a microscope [4]

Absorption, Distribution and Excretion
Levofloxacin is rapidly and almost completely absorbed after oral administration, with an oral bioavailability of approximately 99%. Due to its near-complete absorption, intravenous and oral formulations of levofloxacin can be used interchangeably. The time to peak concentration (Tmax) is typically reached 1–2 hours after administration, and the peak plasma concentration (Cmax) is directly proportional to the dose—a 500 mg intravenous infusion results in a peak plasma concentration of 6.2 ± 1.0 µg/mL within 60 minutes; while a 750 mg intravenous infusion results in a peak plasma concentration of 11.5 ± 4.0 µg/mL within 90 minutes. Co-administration with food prolongs the time to peak concentration by approximately 1 hour and slightly decreases the peak plasma concentration, but these changes may not be clinically significant. Systemic absorption is approximately 50% lower after inhalation than after oral administration. Most of the administered levofloxacin is excreted unchanged in the urine. Following a single oral dose of levofloxacin, approximately 87% of the drug is excreted unchanged in the urine within 48 hours, and less than 4% is excreted in the feces within 72 hours. Levofloxacin is widely distributed in the body, with a mean volume of distribution of 1.09–1.26 L/kg (approximately 89–112 L) after oral administration. Drug concentrations in many tissues and body fluids may be higher than in plasma. Levofloxacin is known to penetrate well into skin tissues, body fluids (e.g., blisters), lung tissue, and prostate tissue. The mean apparent systemic clearance of levofloxacin ranges from 8.64–13.56 L/h, and the renal clearance ranges from 5.76–8.52 L/h. The relatively similarity of these ranges suggests low non-renal clearance. Following a single or multiple doses of 500 mg or 750 mg levofloxacin, its mean volume of distribution is typically 74 to 112 L, indicating its widespread distribution throughout the body. In healthy subjects, levofloxacin reaches peak concentrations in skin tissue and vesicular fluid approximately 3 hours after administration. Following once-daily oral administration of 750 mg and 500 mg levofloxacin in healthy subjects, the AUC ratio in skin tissue biopsy to plasma was approximately 2, and the AUC ratio in vesicular fluid to plasma was approximately 1. Levofloxacin also penetrates well into lung tissue. After a single oral 500 mg dose, lung tissue concentrations are typically 2–5 times higher than plasma concentrations within 24 hours, ranging from approximately 2.4 to 11.3 μg/g. The pharmacokinetics of levofloxacin are linear and predictable after single and multiple oral or intravenous administrations. Steady-state plasma concentrations are reached within 48 hours after a once-daily oral administration of 500 mg or 750 mg. Following multiple once-daily oral dosing regimens, the mean peak and trough plasma concentrations (± standard deviation) were approximately 5.7±1.4 and 0.5±0.2 μg/mL in the 500 mg dose group, and approximately 8.6±1.9 and 1.1±0.4 μg/mL in the 750 mg dose group, respectively. Following multiple once-daily intravenous dosing regimens, the mean peak and trough plasma concentrations (± standard deviation) were approximately 6.4±0.8 and 0.6±0.2 μg/mL in the 500 mg dose group, and approximately 12.1±4.1 and 1.3±0.71 μg/mL in the 750 mg dose group, respectively. When levaquin is administered orally at 500 mg, food intake prolongs the time to peak concentration by approximately 1 hour and reduces peak concentration by approximately 14% (tablets) and approximately 25% (oral solution). Therefore, levofloxacin tablets can be taken regardless of food intake. It is recommended that levofloxacin oral solution be taken 1 hour before or 2 hours after a meal. After oral administration, levofloxacin is rapidly and almost completely absorbed. Peak plasma concentrations are usually reached 1 to 2 hours after oral administration. The absolute bioavailability of 500 mg and 750 mg levofloxacin tablets is approximately 99%, indicating that levofloxacin is completely absorbed orally. In healthy volunteers, after a single intravenous injection of levofloxacin, the mean peak plasma concentration was 6.2 ± 1.0 μg/mL 60 minutes after a 500 mg intravenous infusion and 11.5 ± 4.0 μg/mL 90 minutes after a 750 mg intravenous infusion. Levofloxacin is primarily excreted unchanged in the urine. The mean terminal plasma elimination half-life after a single or multiple oral or intravenous injections of levofloxacin is approximately 6 to 8 hours. The mean apparent total clearance and renal clearance were approximately 144–226 mL/min and 96–142 mL/min, respectively. The renal clearance exceeded the glomerular filtration rate, suggesting that levofloxacin is secreted in the renal tubules in addition to glomerular filtration. Concomitant administration of cimetidine or probenecid reduced levofloxacin renal clearance by approximately 24% and 35%, respectively, indicating that levofloxacin secretion occurs in the proximal tubules of the kidney. No levofloxacin crystals were found in freshly collected urine samples from subjects treated with levofloxacin. For more complete data on the absorption, distribution, and excretion of levofloxacin (6 items), please visit the HSDB record page. Metabolites/Metabolites Only two metabolites were identified in humans: desmethyllevofloxacin and levofloxacin-N-oxide, neither of which appeared to have any relevant pharmacological activity. Following oral administration, less than 5% of the administered dose is recovered in urine, indicating minimal metabolism of levofloxacin in the human body. The specific enzymes responsible for the demethylation and oxidation of levofloxacin have not been identified. Levofloxacin is stereochemically stable in plasma and urine and is not metabolized to its enantiomer, D-ofloxacin. Levofloxacin has limited metabolism in the human body and is primarily excreted unchanged in urine. Approximately 87% of the administered dose is recovered unchanged in urine within 48 hours after oral administration, while less than 4% is recovered in feces within 72 hours. The demethylated and N-oxide metabolites recovered in urine are less than 5% of the administered dose, and these are the only metabolites found in the human body. These metabolites have virtually no associated pharmacological activity. Levofloxacin is primarily excreted unchanged (87%); metabolism of levofloxacin in the human body is limited. After oral administration, levofloxacin is rapidly and almost completely absorbed. It is distributed throughout the body, particularly in the skin and lungs. Levofloxacin is stereochemically stable in plasma and urine and is not metabolized to its enantiomer, D-ofloxacin. Levofloxacin is metabolized to a limited extent in the human body and is primarily excreted unchanged in the urine. After oral administration, approximately 87% of the administered dose is excreted unchanged in the urine within 48 hours, while less than 4% is excreted in the feces within 72 hours. Less than 5% of the administered dose is excreted in the urine as demethylated and N-oxide metabolites, which are currently the only metabolites found in the human body. These metabolites have virtually no associated pharmacological activity. Levofloxacin is primarily excreted unchanged in the urine (L1009).
Elimination route: Primarily excreted unchanged in the urine.
Half-life: 6-8 hours
Biological half-life
The mean terminal elimination half-life of levofloxacin is 6-8 hours.
The mean plasma terminal elimination half-life of levofloxacin after a single or multiple oral or intravenous injection is approximately 6 to 8 hours.
This study employed an open-label crossover design to investigate the pharmacokinetics of oral levofloxacin and its penetration into inflammatory fluid in 6 healthy male subjects (aged 18-45 years). Subjects received either 500 mg of the drug every 12 hours for 5 times, or 500 mg of the drug every 24 hours for 3 times. ...The mean plasma terminal elimination half-life for the two dosing regimens was 7.9 hours and 8 hours, respectively, and the half-life in inflammatory fluid was also the same. ...
Under non-fasting conditions, the absorption, distribution, and excretion of radioactive substances in albino and colored rats were investigated after a single oral dose of 20 mg kg(-1) of (14)C-levofloxacin. ...24 hours after administration, the uveal concentration reached its maximum (C(max)) of 26.33 ± 0.75 μg eq. g(-1), and then slowly decreased, with a terminal half-life of 468.1 hours (19.5 days).

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Absorption: Levofloxacin [(-)-ofloxacin] is rapidly and well absorbed after oral administration, with an oral bioavailability of 95-100%. After administration of 500 mg, the peak plasma concentration (Cmax) can reach 2.8-3.2 μg/mL within 1-2 hours [1]
-Distribution: The drug is widely distributed in tissues and fluids throughout the body, with higher concentrations in the kidneys, lungs, prostate, and bones. The plasma protein binding rate is approximately 20-30% [1]
- Metabolism: Levofloxacin [(-)-ofloxacin] is minimally metabolized by the liver, with over 80% of the drug excreted unchanged [1]
- Excretion: Primarily excreted via the kidneys, with 70-80% of the administered dose excreted in the urine within 24 hours. The plasma elimination half-life is approximately 6-8 hours [1]

Toxicity Summary
Levofloxacin inhibits bacterial type II topoisomerase, topoisomerase IV, and DNA gyrase. Like other fluoroquinolones, levofloxacin inhibits the A subunits of DNA gyrase, both encoded by the gyrA gene. This leads to strand breaks, supercoiling, and rejoining on bacterial chromosomes; DNA replication and transcription are inhibited. Hepatotoxicity
Short-term studies have shown mild elevations in serum ALT and AST levels in 2% to 5% of patients taking levofloxacin. These abnormalities are usually asymptomatic and transient, rarely requiring dose adjustments. Due to the widespread use of levofloxacin, at least 50 cases of clinically significant liver injury have been reported, most of which are case reports. The clinical presentation and course are similar to those of other fluoroquinolones, suggesting this injury is likely a common effect of this class of drugs. The incubation period is usually short (1 to 3 weeks) and the onset is rapid, presenting as hepatocellular or mixed injury, jaundice, and in some cases, liver failure. Cholestatic hepatitis can also occur. Immune allergic reactions, such as fever, rash, and eosinophilia, are common but not particularly prominent. Autoantibodies are rare. Liver injury is usually self-limiting, but there have been several cases of acute liver failure associated with fluoroquinolones, as well as some cases of persistent jaundice, cholestasis, and bile duct disappearance syndrome. Like ciprofloxacin, levofloxacin is also associated with hypersensitivity reactions, including rare Stevens-Johnson syndrome and toxic epidermal necrolysis, which may be accompanied by liver injury. Although levofloxacin-induced liver injury is rare, fluoroquinolones are generally one of the most common causes of clinically significant liver injury, including fatal cases, chronic liver injury, and bile duct reduction.
Probability Score: A (Etiology of Clinically Significant Liver Injury Established).

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Effects during pregnancy and lactation
◉ Overview of medication use during lactation
Levofloxacin is the S-enantiomer of the fluoroquinolone drug ofloxacin. There is currently no clinical information regarding the use of levofloxacin during lactation. However, the drug concentration in breast milk appears to be far lower than the infant's dosage, and no adverse effects are expected on breastfed infants. Fluoroquinolones such as levofloxacin have traditionally been avoided due to concerns about potential adverse effects on the infant's developing joints. However, recent studies suggest the risk is minimal. Calcium in cow's milk may hinder the absorption of small amounts of fluoroquinolones in breast milk, but there is currently insufficient data to confirm or refute this claim. Lactating women can use levofloxacin, but close monitoring of the infant's gut microbiota is necessary, for example, for changes in diarrhea or candidiasis (thrush, diaper rash). Avoiding breastfeeding for 4 to 6 hours after taking the medication can reduce the amount of levofloxacin the infant is exposed to through breast milk. The risk to breastfed infants from maternal use of eye drops containing levofloxacin is negligible.
◉ 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
Levofloxacin has a protein binding rate of 24-38% in plasma, primarily binding to albumin. Protein binding is independent of plasma concentration.

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Toxicity data
LD50: 640 mg/kg (oral, rat)

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Interactions
Warfarin: Potential pharmacological interaction (prolonged prothrombin time). Monitor prothrombin time or other appropriate coagulation tests and monitor for bleeding.
Theophylline: Pharmacokinetic interactions are unlikely. However, some quinolones have pharmacokinetic interactions with other drugs (prolonged theophylline half-life and increased risk of theophylline-related adverse reactions). Closely monitor serum theophylline concentrations and adjust the theophylline dose accordingly; note that adverse theophylline reactions (e.g., seizures) may occur regardless of whether theophylline concentrations are elevated. Sucralfate: Pharmacokinetic interactions may exist (decreased levofloxacin absorption); no pharmacokinetic interactions occur if administered 2 hours apart. Levofloxacin should be administered at least 2 hours before or after sucralfate. Probenecid: Pharmacokinetic interactions may exist (increased AUC and half-life of levofloxacin). Clinically insignificant; no dose adjustment is required. For more complete data on interactions of levofloxacin (16 in total), please visit the HSDB record page. Tendon toxicity: Oral administration of levofloxacin [(-)-ofloxacin] at a dose ≥200 mg/kg/day for 14 days caused mild to moderate histological changes in the Achilles tendon of rats, including collagen fiber disorder and focal inflammation. No tendon rupture was observed [4]
- Gastrointestinal toxicity: Mild and reversible side effects included nausea (3-5%), diarrhea (2-4%), and abdominal discomfort (1-3%) [1]
- Central nervous system (CNS) toxicity: Rare adverse reactions included headache (2-3%), dizziness (1-2%), and insomnia (<1%); seizures were extremely rare [1]

[1]. Drugs . 1994 Apr;47(4):677-700.

[2]. Antimicrob Agents Chemother . 1992 Apr;36(4):860-6.

[3]. Antimicrob Agents Chemother . 1994 May;38(5):1161-4.

[4]. J Orthop Res . 2000 Sep;18(5):721-7.

[5]. Antimicrob Agents Chemother . 1995 Sep;39(9):1979-83.

Therapeutic Uses

Antibacterial agents; anti-infective agents, urinary system; nucleic acid synthesis inhibitors. Levofloxacin is used to treat acute bacterial sinusitis caused by susceptible Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis. /US product label includes/
Levofloxacin is used to treat community-acquired pneumonia caused by susceptible Staphylococcus aureus (oxacillin-sensitive strains), Streptococcus pneumoniae (including penicillin-resistant strains (penicillin MIC ≥ 2 μg/mL)), Haemophilus influenzae, Haemophilus parainfluenzae, Klebsiella pneumoniae, Legionella pneumophila, Moraxella catarrhalis, Chlamydia pneumoniae (formerly known as Chlamydia pneumoniae), or Mycoplasma pneumoniae. /US product label includes/
Levofloxacin is used to treat mild to moderate complicated urinary tract infections caused by susceptible Enterococcus faecalis, Enterobacter cloacae, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, or Pseudomonas aeruginosa. Pseudomonas aeruginosa infection and acute pyelonephritis caused by susceptible Escherichia coli, including cases complicated by bacteremia. /US product label contains/
For more complete data on the therapeutic uses of levofloxacin (of 23), please visit the HSDB record page.

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Drug Warning
/Black Box Warning/ Warning: Fluoroquinolones, including levofloxacin, increase the risk of tendinitis and tendon rupture in people of all ages. The risk is further increased in older patients (usually over 60 years of age), patients taking corticosteroids, and patients who have received kidney, heart, or lung transplants.
/Black Box Warning/ Warning: Fluoroquinolones, including levofloxacin, may worsen muscle weakness in patients with myasthenia gravis. Levofloxacin should be avoided in patients with a known history of myasthenia gravis. Rarely reported adverse events, including serious and even fatal ones, have occurred in patients receiving fluoroquinolones (including levofloxacin). Some events are caused by hypersensitivity reactions, while others are of unknown etiology. These adverse events can be severe and usually occur after multiple doses. Clinical manifestations may include one or more of the following: 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 renal insufficiency; hepatitis; jaundice; acute liver necrosis or renal failure; anemia (including hemolytic anemia and aplastic anemia); thrombocytopenia (including thrombotic thrombocytopenic purpura); leukopenia; agranulocytosis; pancytopenia; and/or other hematological abnormalities. If rash, jaundice, or any other signs of an allergic reaction occur, the medication should be discontinued immediately and supportive care should be initiated. Post-marketing reports indicate serious hepatotoxicity (including acute hepatitis and death) in patients treated with levofloxacin. In clinical trials involving over 7,000 patients, no evidence of drug-related serious hepatotoxicity was found. Serious hepatotoxicity typically occurs within 14 days of treatment initiation, with most cases occurring within 6 days. Most cases of serious hepatotoxicity are unrelated to allergic reactions. Most fatal hepatotoxicity reports occurred in patients 65 years of age or older, and most were unrelated to allergic reactions. Levofloxacin should be discontinued immediately if a patient develops signs and symptoms of hepatitis. For more complete data on drug warnings for levofloxacin (19 in total), please visit the HSDB records page.

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Pharmacodynamics
Levofloxacin has a bactericidal effect; its antibacterial mechanism is through inhibition of bacterial DNA replication. Compared to other antibiotics, its duration of action is relatively long, therefore it can be taken once or twice daily. Levofloxacin is associated with QTc interval prolongation; therefore, it should be used with caution in patients with other risk factors for QTc prolongation (e.g., hypokalemia, concomitant medication). Levofloxacin has been shown to be active against a variety of aerobic Gram-positive and Gram-negative bacteria in vitro, and may also have some activity against certain anaerobes and other pathogens (e.g., Chlamydia and Legionella). Levofloxacin resistance may occur, usually due to mutations in DNA gyrase or topoisomerase IV, or alterations in drug efflux pathways. Cross-resistance may exist between levofloxacin and other fluoroquinolones, but due to significant differences in chemical structure and mechanism of action, cross-resistance between levofloxacin and other antibiotic classes (e.g., macrolides) is unlikely. Because antimicrobial susceptibility patterns vary geographically, local susceptibility testing results should be consulted before use to ensure adequate antimicrobial coverage against relevant pathogens. Levofloxacin [(-)-ofloxacin] is the levorotatory isomer of ofloxacin, a second-generation fluoroquinolone antibiotic with enhanced antibacterial activity compared to racemic mixtures [2][5]
- Mechanism of action: It exerts its antibacterial effect by dual targeting of bacterial DNA gyrase and topoisomerase IV, blocking DNA replication/transcription, ultimately leading to bacterial death [2][3][5]
- Clinical indications: Approved for the treatment of respiratory tract infections, urinary tract infections, skin/soft tissue infections, and infections caused by susceptible Gram-negative and Gram-positive bacteria [1]
- Therapeutic advantages: It has higher antibacterial efficacy, longer half-life, and better tissue penetration compared to ofloxacin. Ofloxacin can be administered once daily in some indications [1][5]
- Resistance mechanism: Bacterial resistance mainly originates from gyrA (DNA Mutations in the gyrase and parC (topoisomerase IV) genes reduce drug binding affinity [3][5]

C18H20FN3O4

361.37

361.143

C, 59.83; H, 5.58; F, 5.26; N, 11.63; O, 17.71

100986-85-4

138199-71-0； 177325-13-2；872606-49-0

149096

Off-white to light yellow solid powder

1.5±0.1 g/cm3

571.5±50.0 °C at 760 mmHg

218ºC

299.4±30.1 °C

0.0±1.7 mmHg at 25°C

1.670

0.84

1

8

2

26

634

1

FC1C([H])=C2C(C(C(=O)O[H])=C([H])N3C2=C(C=1N1C([H])([H])C([H])([H])N(C([H])([H])[H])C([H])([H])C1([H])[H])OC([H])([H])[C@]3([H])C([H])([H])[H])=O

GSDSWSVVBLHKDQ-JTQLQIEISA-N

InChI=1S/C18H20FN3O4/c1-10-9-26-17-14-11(16(23)12(18(24)25)8-22(10)14)7-13(19)15(17)21-5-3-20(2)4-6-21/h7-8,10H,3-6,9H2,1-2H3,(H,24,25)/t10-/m0/s1

(2S)-7-fluoro-2-methyl-6-(4-methylpiperazin-1-yl)-10-oxo-4-oxa-1-azatricyclo[7.3.1.05,13]trideca-5(13),6,8,11-tetraene-11-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 1 mg/mL (2.77 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 10.0 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of 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: ≥ 1 mg/mL (2.77 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 10.0 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: ≥ 1 mg/mL (2.77 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 10.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 10 mg/mL (27.67 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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