Moxifloxacin

401.43

401.43

1806241-263-5

U188XYD42P

DTXSID3048491

C62052

J01MA14|J - Antiinfectives for systemic use|S - Sensory organs

82.1

2.9

Solid

1.408±0.06 g/cm3(Predicted)

240 °C

636.4°C at 760 mmHg

338.7ºC

1.633

1.68e-01 g/L

Store in tight, light-resistant container as defined in the USP-NF. This material should be handled and stored per label instructions to ensure product integrity. /Moxifloxacin hydrochloride/

7.26X10-15 mm Hg at 25 deg C (est)

23D -193°

Henry's Law constant = 3.11X10-20 atm-cu m/mol at 25 °C (est)

198.5 Ų [M+H]+ [CCS Type: TW, Method: calibrated with Waters Major Mix]|210.7 Ų [M+Na]+ [CCS Type: TW, Method: calibrated with Waters Major Mix]|202.63 Ų [M-H]-

Slightly yellow to yellow crystalline powder, mp 324-325 °C (decomposes), specific optical rotation: -256 °C at 25 °C/D (c = 0.5 in water) /Moxifloxacin hydrochloride/|Hydroxyl radical reaction rate constant = 1.28X10-10 cu cm/molec-sec at 25 °C (est)|Ozone radical reaction rate constant = 1.75X10-18 cu cm/molec-sec at 25 °C (est)

3

22-40

36/37

Xn

P264, P270, P273, P280, P301+P312, P305+P351+P338, P330, P337+P313, P501

H302

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including moxifloxacin hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Moxifloxacin hydrochloride/

|Warning|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P273, P280, P301+P312, P305+P351+P338, P330, P337+P313, and P501|Aggregated GHS information provided by 25 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Respiratory Protection: Use a NIOSH-approved respirator, if it is determined to be necessary by an industrial hygiene survey involving air monitoring. In the event that a respirator is not required, an approved dust mask should be used. Gloves: Chemically compatible. Eye Protection: Safety glasses or goggles. Protective Clothing: Protect exposed skin. /Moxifloxacin hydrochloride/

This material is assumed to be combustible. /Moxifloxacin hydrochloride/

Water spray, dry chemical, carbon dioxide, or foam as appropriate for surrounding fire and materials. /Moxifloxacin hydrochloride/

Wear approved respiratory protection, chemically compatible gloves and protective clothing. Wipe up spillage or collect spillage using a high efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately labelled container for disposal. Wash spill site. /Moxifloxacin hydrochloride/

Engineering controls such as exhaust ventilation are recommended. /Moxifloxacin hydrochloride/|As with all dry powders it is advisable to ground mechanical equipment in contact with dry material to dissipate the potential buildup of static electricity. /Moxifloxacin hydrochloride/|As a general rule, when handling USP Reference Standards avoid all contact and inhalation of dust, mists, and/or vapors associated with the material. Wash thoroughly after handling. /Moxifloxacin hydrochloride/|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

The major factor in removal of fluoroquinolone antiobiotics such as moxifloxacin, is sorption to sludge. This along with long-term cycling and persistence of these drugs in the sewage treatment plant has made activated sludge a large reservoir of fluoroquinolone antibiotics(1).

Symptoms of overdose include CNS and gastrointestinal effects such as decreased activity, somnolence, tremor, convulsions, vomiting, and diarrhea. The minimal lethal intravenous dose in mice and rats is 100 mg/kg.

Moxifloxacin, like other fluoroquinolones, is associated with a low rate (1% to 3%) of serum enzyme elevations during therapy. These abnormalities are generally mild, asymptomatic and transient, resolving even with continuation of therapy. Moxifloxacin has been linked to rare but occasionally severe and even fatal cases of acute liver injury. The time to onset is typically short (1 day to 3 weeks) and the presentation is often abrupt with nausea, fatigue, abdominal pain and jaundice. The pattern of serum enzyme elevations can be either hepatocellular or cholestatic, cases with the shorter times to onset usually being more hepatocellular. In addition, the onset of illness may occur a few days after the medication is stopped. Many (but not all) cases have prominent allergic manifestations with fever and rash, and the liver injury may occur in the context of a generalized hypersensitivity reaction (Case 1). Autoantibodies are usually not present. Cases with a cholestatic pattern of enzymes may run a prolonged course but are usually self-limiting, although at least one case of chronic cholestasis and vanishing bile duct syndrome leading to liver failure has been published. Most reported cases have been mild with recovery within 4 to 8 weeks of onset.

Fifteen males and 5 females, mean age of 34 years, were given moxifloxacin under two conditions separated by a minimum 7-day washout period: alone as a single oral 400 mg dose, and immediately following 10 mg of IM morphine sulfate. Moxifloxacin serum concentrations were determined by a validated HPLC procedure. Pharmacokinetic parameters including Cmax, Tmax, AUC0-infinity, and t1/2 were estimated using noncompartmental methods and analyzed using ANOVA. Results: Moxifloxacin pharmacokinetics were similar between the two treatments. Geometric least square mean Cmax, values for moxifloxacin were 3.4 mg (alone) vs 2.8 mg/L (with morphine) (90% confidence interval (CI) of moxifloxacin alone vs with morphine sulfate was 71%-98%). Corresponding geometric mean AUC0-infinity values were 41.5 and 39.6 mgh/L (90% CI = 87%-104%). Tmax and t1/2 values for moxifloxacin were similar when coadministered with morphine. Conclusion: Moxifloxacin was well tolerated when taken with and without morphine sulfate. Administration of a single IM dose of morphine did not reduce the bioavailability or alter the elimination profile of oral moxifloxacin. Implications: Concurrent administration of morphine and moxifloxacin is unlikely to reduce the efficacy of this quinolone.|Pharmacokinetic interaction (decreased absorption of oral moxifloxacin). Moxifloxacin should be given at least 4 hours before or 8 hours after buffered didanosine (pediatric oral solution admixed with antacid).|Concomitant use of corticosteroids increases the risk of severe tendon disorders (e.g., tendinitis, tendon rupture), especially in geriatric patients older than 60 years of age.|Quinolones, including Avelox, have been reported to enhance the anticoagulant effects of warfarin or its derivatives in the patient population. In addition, infectious disease and its accompanying inflammatory process, age, and general status of the patient are risk factors for increased anticoagulant activity. Therefore the prothrombin time, International Normalized Ratio (INR), or other suitable anticoagulation tests should be closely monitored if a quinolone is administered concomitantly with warfarin or its derivatives.|For more Interactions (Complete) data for Moxifloxacin (17 total), please visit the HSDB record page.

No dosage adjustment is recommended for mild, moderate, or severe hepatic insufficiency (Child-Pugh Classes A, B, or C). However, due to metabolic disturbances associated with hepatic insufficiency, which may lead to QT prolongation, Avelox should be used with caution in these patients.|Use of moxifloxacin should be avoided in patients with known prolongation of the QT interval, in those with uncorrected hypokalemia, ... .|Avoid Avelox in patients with known history of myasthenia gravis.|Concomitant use of corticosteroids increases the risk of severe tendon disorders (e.g., tendinitis, tendon rupture), especially in geriatric patients older than 60 years of age.|For more Populations at Special Risk (Complete) data for Moxifloxacin (7 total), please visit the HSDB record page.

50% bound to serum proteins, independent of drug concentration.

While data specific to moxifloxacin were not located(SRC, 2012), the literature suggests that some pharmaceutically active compounds originating from human and veterinary therapy are not eliminated completely in municipal sewage treatment plants and are therefore discharged into receiving waters(1). Wastewater treatment processes often were not designed to remove them from the effluent(2). Selected organic waste compounds may be degrading to new and more persistent compounds that may be released instead of or in addition to the parent compound(2). Studies have indicated that several polar pharmaceutically active compounds can leach through soils(1).

Moxifloxacin is excreted in the breast milk of rats. Moxifloxacin may also be excreted in human milk. Because of the potential for serious adverse reactions in infants who are nursing from mothers taking Avelox, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.

For the treatment of sinus and lung infections such as sinusitis, pneumonia, and secondary infections in chronic bronchitis. Also for the treatment of bacterial conjunctivitis (pinkeye).|FDA Label

Moxifloxacin is a fourth generation fluoroquinolone with expanded activity against gram-positive bacteria as well as atypical pathogens. Moxifloxacin has been linked to mild ALT elevations during therapy and to rare instances of idiosyncratic acute liver injury with symptoms and jaundice.

Antiinfective Agents

Anti-Infective Agents|Moxifloxacin hydrochloride ophthalmic solution is used for the treatment of conjunctivitis caused by susceptible strains of Corynebacterium spp., Micrococcus luteus, Staphylococcus aureus, S. epidermidis, S. haemolyticus, S. hominis, S. warneri, Streptococcus pneumoniae, viridans streptococci, Acinetobacter lwoffii, Haemophilus influenzae, H. parainfluenzae, or Chlamydia trachomatis. /Included in US product label/|Moxifloxacin is used for the treatment of acute bacterial sinusitis caused by susceptible Streptococcus pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis; acute bacterial exacerbations of chronic bronchitis caused by susceptible S. pneumoniae, H. influenzae, H. parainfluenzae, Klebsiella pneumoniae, Staphylococcus aureus (oxacillin-susceptible [methicillin-susceptible] strains), or M. catarrhalis; and community-acquired pneumonia (CAP) caused by susceptible S. pneumoniae (including multidrug-resistant strains), S. aureus (oxacillin-susceptible strains), K. pneumoniae, H. influenzae, Mycoplasma pneumoniae, Chlamydophila pneumoniae (formerly Chlamydia pneumoniae), or M. catarrhalis. /Included in US product label/|Moxifloxacin is used for the treatment of uncomplicated skin and skin structure infections caused by susceptible S. aureus (oxacillin-susceptible strains) or Streptococcus pyogenes (group A beta-hemolytic streptococci) and for the treatment of complicated skin and skin structure infections caused by susceptible S. aureus (oxacillin-susceptible strains), Escherichia coli, K. pneumoniae, or Enterobacter cloacae. /Included in US product label/|For more Therapeutic Uses (Complete) data for Moxifloxacin (12 total), please visit the HSDB record page.

/BOXED WARNING/ WARNING: Fluoroquinolones, including Avelox, are associated with an increased risk of tendinitis and tendon rupture in all ages. This risk is further increased in older patients usually over 60 years of age, in patients taking corticosteroid drugs, and in patients with kidney, heart or lung transplants.|/BOXED WARNING/ WARNING: Fluoroquinolones, including Avelox, may exacerbate muscle weakness in persons with myasthenia gravis. Avoid Avelox in patients with known history of myasthenia gravis.|Serious and occasionally fatal hypersensitivity and/or anaphylactic reactions reported in patients receiving fluoroquinolones, including moxifloxacin. Although generally reported after multiple doses, these reactions may occur with first dose. Some reactions have been accompanied by cardiovascular collapse, loss of consciousness, tingling, edema (pharyngeal or facial), dyspnea, urticaria, or pruritus. In addition, other possible severe and potentially fatal reactions (may be hypersensitivity reactions or of unknown etiology) have been reported, most frequently after multiple doses. These include fever, rash or severe dermatologic reactions (e.g., toxic epidermal necrolysis, Stevens-Johnson syndrome), vasculitis, arthralgia, myalgia, serum sickness, allergic pneumonitis, interstitial nephritis, acute renal insufficiency or failure, hepatitis, jaundice, acute hepatic necrosis or failure, anemia (including hemolytic and aplastic), thrombocytopenia (including thrombotic thrombocytopenic purpura), leukopenia, agranulocytosis, pancytopenia, and/or other hematologic effects. Discontinue moxifloxacin at first appearance of rash, jaundice, or any other sign of hypersensitivity. Institute appropriate therapy as indicated (e.g., epinephrine, corticosteroids, and maintenance of an adequate airway and oxygen).|Sensory or sensorimotor axonal polyneuropathy affecting small and/or large axons resulting in paresthesias, hypoesthesias, dysesthesias, and weakness have been reported with fluoroquinolones.|For more Drug Warnings (Complete) data for Moxifloxacin (22 total), please visit the HSDB record page.

Moxifloxacin is a quinolone/fluoroquinolone antibiotic. Moxifloxacin can be used to treat infections caused by the following bacteria: Aerobic Gram-positive microorganisms: Corynebacterium species, Micrococcus luteus, Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus haemolyticus, Staphylococcus hominis, Staphylococcus warneri, Streptococcus pneumoniae, and Streptococcus viridans group. Aerobic Gram-negative microorganisms: Acinetobacter lwoffii, Haemophilus influenzae, and Haemophilus parainfluenzae. Other microorganisms: Chlamydia trachomatis.
Moxifloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. Moxifloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria.

Compounds that inhibit the activity of DNA TOPOISOMERASE II. Included in this category are a variety of ANTINEOPLASTIC AGENTS which target the eukaryotic form of topoisomerase II and ANTIBACTERIAL AGENTS which target the prokaryotic form of topoisomerase II. (See all compounds classified as Topoisomerase II Inhibitors.)|Substances that inhibit the growth or reproduction of BACTERIA. (See all compounds classified as Anti-Bacterial Agents.)

Well absorbed from the gastrointestinal tract. Absolute oral bioavailability is approximately 90%. Food has little effect on absorption.|Approximately 45% of an oral or intravenous dose of moxifloxacin is excreted as unchanged drug (~20% in urine and ~25% in feces).|1.7 to 2.7 L/kg|12 +/- 2 L/hr|Moxifloxacin is approximately 30-50% bound to serum proteins, independent of drug concentration. The volume of distribution of moxifloxacin ranges from 1.7 to 2.7 L/kg. Moxifloxacin is widely distributed throughout the body, with tissue concentrations often exceeding plasma concentrations. Moxifloxacin has been detected in the saliva, nasal and bronchial secretions, mucosa of the sinuses, skin blister fluid, subcutaneous tissue, skeletal muscle, and abdominal tissues and fluids following oral or intravenous administration of 400 mg.|Approximately 45% of an oral or intravenous dose of moxifloxacin is excreted as unchanged drug (~20% in urine and ~25% in feces). A total of 96% + or - 4% of an oral dose is excreted as either unchanged drug or known metabolites. The mean (+ or - SD) apparent total body clearance and renal clearance are 12 + or - 2 L/hr and 2.6 + or - 0.5 L/hr, respectively.|Moxifloxacin, given as an oral tablet, is well absorbed from the gastrointestinal tract. The absolute bioavailability of moxifloxacin is approximately 90 percent. Co-administration with a high fat meal (that is, 500 calories from fat) does not affect the absorption of moxifloxacin.|The ocular penetration and pharmacokinetics of moxifloxacin in comparison to other fluoroquinolones (ofloxacin, ciprofloxacin, gatifloxacin, norfloxacin, levofloxacin, and lomefloxacin) have been determined by in vitro and ex vivo techniques, as well as in animal and human studies. ... The results consistently demonstrate higher maximum concentrations for moxifloxacin relative to the other fluoroquinolones in ocular tissues with levels well above its minimum inhibitory concentrations for relevant ocular pathogens. This superior performance is due to the unique structure of moxifloxacin that combines high lipophilicity for enhanced corneal penetration with high aqueous solubility at physiological pH. The latter property creates a high concentration gradient at the tear film/corneal epithelial interface providing a driving force for better ocular penetration for moxifloxacin. In addition, the higher concentration of moxifloxacin in VIGAMOX (i.e., 0.5% vs. 0.3%) allows more antibiotic to be available to ocular tissues. It is clear from the array of studies summarized in this report that moxifloxacin penetrates ocular tissues better (two- to three-fold) than gatifloxacin, ciprofloxacin, ofloxacin, or levofloxacin. This consistent, enhanced penetration of topical moxifloxacin offers powerful advantages for ophthalmic therapy.|For more Absorption, Distribution and Excretion (Complete) data for Moxifloxacin (6 total), please visit the HSDB record page.

Approximately 52% or oral or intravenous dose is metabolized via glucuronide and sulphate conjugation. The cytochrome P450 system is not involved in metabolism. The sulphate conjugate accounts for 38% of the dose, and the glucuronide conjugate accounts for 14% of the dose.|Approximately 52% of an oral or intravenous dose of moxifloxacin is metabolized via glucuronide and sulfate conjugation. The cytochrome P450 system is not involved in moxifloxacin metabolism, and is not affected by moxifloxacin. The sulfate conjugate (M1) accounts for approximately 38% of the dose, and is eliminated primarily in the feces. Approximately 14% of an oral or intravenous dose is converted to a glucuronide conjugate (M2), which is excreted exclusively in the urine. Peak plasma concentrations of M2 are approximately 40% those of the parent drug, while plasma concentrations of M1 are generally less than 10% those of moxifloxacin.

11.5-15.6 hours (single dose, oral)|The mean (+ or - SD) elimination half-life from plasma is 12 + or - 1.3 hours

The bactericidal action of moxifloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV. DNA gyrase is an essential enzyme that is involved in the replication, transcription and repair of bacterial DNA. Topoisomerase IV is an enzyme known to play a key role in the partitioning of the chromosomal DNA during bacterial cell division.|The fluoroquinolone antibiotic moxifloxacin has been associated with the acquired long QT syndrome and is used as a positive control in the evaluation of the QT-interval prolonging potential of new drugs. In common with other QT-prolonging agents, moxifloxacin is known to inhibit the hERG potassium K+ channel, but at present there is little mechanistic information available on this action. This study was conducted in order to characterise the inhibition of hERG current (I(hERG)) by moxifloxacin, and to determine the role in drug binding of the S6 aromatic amino-acid residues Tyr652 and Phe656. hERG currents were studied using whole-cell patch clamp (at room temperature and at 35-37 degrees C) in an HEK293 cell line stably expressing hERG channels. Moxifloxacin reversibly inhibited currents in a dose-dependent manner. We investigated the effects of different voltage commands to elicit hERG currents on moxifloxacin potency. Using a 'step-ramp' protocol, the IC50 was 65 uM at room temperature and 29 microM at 35 degrees C. When a ventricular action potential waveform was used to elicit currents, the IC50 was 114 microM. Block of hERG by moxifloxacin was found to be voltage-dependent, occurred rapidly and was independent of stimulation frequency. Mutagenesis of the S6 helix residue Phe656 to Ala failed to eliminate or reduce the moxifloxacin-mediated block whereas mutation of Tyr652 to Ala reduced moxifloxacin block by approximately 66%. Our data demonstrate that moxifloxacin blocks the hERG channel with a preference for the activated channel state. The Tyr652 but not Phe656 S6 residue is involved in moxifloxacin block of hERG, concordant with an interaction in the channel inner cavity.|The bactericidal action of moxifloxacin results from inhibition of the topoisomerase II (DNA gyrase) and topoisomerase IV required for bacterial DNA replication, transcription, repair, and recombination. It appears that the C8-methoxy moiety contributes to enhanced activity and lower selection of resistant mutants of Gram-positive bacteria compared to the C8-H moiety. The presence of the bulky bicycloamine substituent at the C-7 position prevents active efflux, associated with the NorA or pmrA genes seen in certain Gram-positive bacteria.|Torsade de pointes (TdP) is increasingly recognized as a complication of drug therapy. The most common cause of drug-induced QT prolongation is inhibition of the rapidly activating component of the delayed potassium current (I(Kr)). Moxifloxacin, a widely used fluoroquinolone, is a weak I(Kr) inhibitor and has been associated with QT prolongation.|Fluoroquinolones prolong the QT interval by blocking voltage-gated potassium channels, especially the rapid component of the delayed rectifier potassium current I(Kr), expressed by HERG (the human ether-a-go-go-related gene). According to the available case reports and clinical studies, moxifloxacin carries the greatest risk of QT prolongation from all available quinolones in clinical practice and it should be used with caution in patients with predisposing factors for Torsades de pointes (TdP).

In the event of acute overdose ... adequate hydration /should be/ maintained. ECG monitoring is recommended due to the possibility of QT interval prolongation. The patient should be carefully observed and given supportive treatment. The administration of activated charcoal as soon as possible after oral overdose may prevent excessive increase of systemic moxifloxacin exposure. About 3% and 9% of the dose of moxifloxacin, as well as about 2% and 4.5% of its glucuronide metabolite are removed by continuous ambulatory peritoneal dialysis and hemodialysis, respectively.|Emergency and supportive measures: Maintain an open airway and assist ventilation if necessary. Treat coma, seizures, hypotension, anaphylaxis, and hemolysis if they occur. replace fluid losses resulting from gastroenteritis with IV crystalloids. ... /Antibacterial agents/|Decontamination: Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. /Antibacterial agents/|Enhanced elimination: Most antibiotics are excreted unchanged in the urine, so maintenance of adequate urine flow is important. The role of forced diuresis is unclear. Hemodialysis is not usually indicated, except perhaps in patients with renal dysfunction and a high level of a toxic agent. ... /Antibacterial agents/|For more Antidote and Emergency Treatment (Complete) data for Moxifloxacin (7 total), please visit the HSDB record page.

/HUMAN EXPOSURE STUDIES/ ... Nine men and 9 women participated in a double-blind, randomized, placebo-controlled, crossover study. Each participant received single oral doses (400 mg and 800 mg) of moxifloxacin or placebo. At the time of expected moxifloxacin maximum concentration, several electrocardiographic recordings were obtained at rest and during the course of a submaximal exercise test. QT interval and the corresponding RR interval value were measured within a wide range of RR intervals in each subject. ANOVA showed that both moxifloxacin doses increased mean QT intervals compared with placebo. The mean QT interval duration at RR = 1000 ms was 379 +/- 24 ms during placebo, 394 +/- 33 ms during moxifloxacin 400 mg (P < .05), and 396 +/- 28 ms during moxifloxacin 800 mg (P < .05). Moxifloxacin-induced QT interval prolongation remained significant at all tested heart rates. The increase in QT interval duration relative to placebo remained between 2.3% +/- 2.8% and 4.5% + 3.8% across the range of RR intervals tested. Moxifloxacin prolongs QT interval duration. The amplitude of this effect is small, and the risk of moxifloxacin-induced torsades de pointes is expected to be minimal when the drug is administered at the recommended dose of 400 mg/d. However, moxifloxacin should not be used in patients with predisposing factors of torsades de pointes such as electrolyte disturbances and bradycardia or during coadministration of proarrhythmic drugs.|/CASE REPORTS/ Torsade de pointes (TdP) is increasingly recognized as a complication of drug therapy. The most common cause of drug-induced QT prolongation is inhibition of the rapidly activating component of the delayed potassium current (I(Kr)). Moxifloxacin, a widely used fluoroquinolone, is a weak I(Kr) inhibitor and has been associated with QT prolongation. ... /The authors/ report a case of marked QT prolongation (618 ms) and TdP associated with moxifloxacin use. Although it is difficult to predict which patients are at risk from TdP, careful assessment of the risk/benefit ratio is important before prescribing drugs known to cause QT prolongation.|/CASE REPORTS/ An 87-year-old woman was admitted to the hospital for pneumonia, and antibiotic therapy with intravenous moxifloxacin 400 mg/day was initiated. The patient was noted to have significant QTc interval prolongation 2 hours after administration of moxifloxacin and developed torsade de pointes 8-10 hours after moxifloxacin administration. She was converted back to normal sinus rhythm after a precordial thump. Moxifloxacin was discontinued, and the woman's QTc interval subsequently returned to baseline.Torsade de pointes is a life-threatening arrhythmia that has previously been associated with the use of fluoroquinolones. ... According to the Naranjo probability scale, the episode in this case was probably related to administration of intravenous moxifloxacin.|/CASE REPORTS/ Torsade de pointes occuring due to a long QT interval is a rare but potentially fatal arrhythmia. Acquired long QT develops most commonly because of drugs that prolong ventricular repolarization. It has been reported that fluoroquinolone antimicrobials prolong the corrected QT interval but rarely cause torsade de pointes. A patient with torsade de pointes risk factors (female sex, advanced age, extreme bradycardia and renal failure) who developed the condition on the fourth day of 400 mg/day of oral moxifloxacin treatment is presented. After the moxifloxacin was stopped, the corrected QT interval normalized and a permanent cardiac pacemaker was implanted. During 11 months of follow-up, arrhythmia did not recur.|For more Human Toxicity Excerpts (Complete) data for Moxifloxacin (11 total), please visit the HSDB record page.

1-cyclopropyl--7-(2,8-diazabicyclo(4.3.0)non-8-yl)-6-fluoro-8-methoxy-1,4-dihydro-4-oxo-3-quinolinecarboxylic acid

Table: Moxifloxacin Hydrochloride Preparations [Table#7982]|Ophthalmic: Solution: 0.5% (of moxifloxacin) Vigamox (Alcon). /Moxifloxacin hydrochloride/|Moxeza|Vigamox

A simple and rapid HPLC method with UV detection was developed for the separation of ciprofloxacin, levofloxacin and moxifloxacin. Chromatography was carried out using a BDS Hypersil C18 (100 x 4.6 mm, 2.4 microm) HPLC column and an isocratic mobile phase consisting of MeOH/25 mM phosphate buffer 28/72 (v/v) at pH 3 and flow rate 1 ml.min-1 . The effect of mobile phase variables such as methanol content, pH and buffer concentration on the chromatographic behavior of the three fluoroquinolones was investigated. The retention behavior on a sub 3 microm C18 column was also compared with that on three different calixarene-bonded and on monolithic stationary phases. The results indicate that some differences exist between these three types of stationary phases, particularly in the effect of buffer concentration on the retention mechanism of the three used FQs on calixarene-bonded stationary phases.

HPLC determination in serum.|A high performance liquid chromatographic method for determination of moxifloxacin in human saliva was developed. The method involved deproteinisation of the sample with perchloric acid and analysis of the supernatant using a reversed-phase C18 column (150 mm) and fluorescence detection at an excitation wavelength of 290 nm and an emission wavelength of 460 nm. The assay was specific for moxifloxacin and linear from 0.25 to 10.0 ug/mL. The relative standard deviation of intra- and inter-day assays was lower than 10%. The average recovery of moxifloxacin from saliva was 101%. Due to its simplicity, the assay can be used for pharmacokinetic studies of moxifloxacin.|Penetration of levofloxacin and moxifloxacin into cancellous and cortical bone was studied using high-performance liquid chromatography (HPLC).|The aim of this study was to develop a high-performance liquid chromatographic (HPLC) assay for the determination of moxifloxacin in human plasma and lung tissue. The assay was based on HPLC with a Supelcosil ABZ+ column and ultraviolet detection set at a wavelength of 296 nm. The extraction procedure was characterized by a fully automated liquid-solid extraction using an OASIS column for the solid phase. The assay has been found to be linear and validated over the concentration range 3.2 to 0.025 microg/mL for moxifloxacin in plasma and from 16 to 0.25 microg/g for moxifloxacin in lung tissue.|For more Clinical Laboratory Methods (Complete) data for Moxifloxacin (7 total), please visit the HSDB record page.

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