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Moxifloxacin (oral)
Clinical data
Pregnancy
category
Routes of
administration
Oral, IV, local (eyedrops)
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability86 to 92%
Protein binding30 to 50%
MetabolismGlucuronide and sulfate conjugation
Cytochrome P450 system not involved
Elimination half-life12 hours
ExcretionBiliary and renal
Identifiers
CAS Number
PubChem CID
DrugBank
E number{{#property:P628}}
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Chemical and physical data
FormulaC21H24FN3O4
Molar mass401.431 g/mol

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Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [1] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

Moxifloxacin is a synthetic fluoroquinolone antibiotic agent. Bayer AG developed the drug (initially called BAY 12-8039) and it is marketed worldwide (as the hydrochloride) under the brand name Avelox® (in some countries also Avalox®) for oral treatment. Each tablet contains 400 mg. In most countries the drug is also available in parenteral form for intravenous infusion. Moxifloxacin is also sold in an ophthalmic solution (eye drops) under the name Vigamox® for the treatment of conjunctivitis.

Mode of action

Moxifloxacin inhibits bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. Topoisomerases are essential enzymes which play a crucial role in the replication and repair of bacterial DNA. This mechanism is lethal to susceptible bacteria. Moxifloxacin is often referred to as a chemotherapeutic drug because its mode of action has so far not been noted in any natural occurring or semi-synthetic antibiotic.

Distribution

Moxifloxacin is found in high concentrations in body tissues and fluids, such as saliva, nasal and bronchial secretions, sinus mucosa, skin blister fluid, subcutaneous and intraocular tissues. There is good penetration into bone.[1] Pus does not seem to inhibit the drug's potential to reach effective concentrations in infectious foci easily.

Susceptible bacteria

A broad spectrum of bacteria is susceptible including, but not limited to:

Pharmacokinetic behaviour in patients with decreased liver and renal function

Mild, moderate and severe renal dysfunction does not alter half-life, metabolization or excretion significantly. The same is true to for mild to moderate liver impairment (Child-Pugh class A and B). Nothing is known about severe liver impairment (Child-Pugh class C).

Uses

Moxifloxacin can be used to treat respiratory infections including acute sinusitis, acute exacerbations of chronic bronchitis and community-acquired pneumonia as well as skin and skin structure infections. Moxifloxacin is also used for the treatment of complicated intra-abdominal infections, as seen in hospitals. Since moxifloxacin is primarily metabolized and eliminated via the hepatic route, moxifloxacin is not indicated for the treatment of urinary tract infections.

Moxifloxacin is used as a Second-line agent in tuberculosis and may potentially have benefits in reducing treatment duration from its current six month to four months.[2]

In ophthalmology, moxifloxacin is available the form of eye drops, marketed by Alcon as Vigamox®, to treat conjunctival infections caused by susceptible bacteria and to prevent infection following eye surgeries such as LASIK.[3]

Resistance

Resistance to moxifloxacin arises in Mycobacterium tuberculosis if moxifloxacin is used alone instead of in combination with other anti-TB drugs,[4] and this appears to be the explanation for the appearance of moxifloxacin resistance in newly diagnosed TB patients in Baltimore[5] and in Taiwan.[6] Worryingly, the development of resistance can appear in as short a time as seven days.[6] This calls into question the first line use of moxifloxacin and other respiratory quinolones first line for the treatment of community-acquired pneumonia in populations where TB is still endemic.

Dosage

The dosage is 400 mg daily orally or via intravenous infusion (1 hour). The duration of treatment depends on the disease and ranges from 5 days in acute exacerbations of chronic bronchitis to 60 days for post-exposure prophylaxis of anthrax. The bioavailability of moxifloxacin is over 90%[7] and therefore there are no advantages to using intravenous moxifloxacin when the patient is able to swallow tablets. Bioavailability is markedly reduced, however, when taken with sucralfate or aluminum-containing antacids. The intravenous preparation is not licensed for use in the UK.

There is no sufficient clinical data about dosage to patients under 18 years of age. In geriatric patients no dose reductions are necessary.

Contraindications

  • Known hypersensitivity to moxifloxacin,other quinolones, or any other ingredient of the preparation.
  • Patients with history of tendon disorder related to quinolone treatment
  • Documented QT prolongation

Pregnancy and lactation

  • Pregnancy : Moxifloxacin has been assigned to class C.
  • Lactation : Moxifloxacin is found in high concentration in the milk of breastfeeding mothers. Either the drug or the breastfeeding should be discontinued.

Side effects

Possible side effects include gastrointestinal tract disturbances (nausea, vomiting, anorexia, bloating, abdominal pain, diarrhea, and pseudomembranous colitis caused by Clostridium difficile), skin reactions (also Stevens-Johnson syndrome), rhabdomyolysis, and serious heart problems (prolonged QT interval and torsades de pointes). Development of resistance has been noticed as well as rare cases of hepatotoxicity and seizures. Tendon rupture (including rupture of the Achilles tendon) can also occur.

Moxifloxacin may have a much higher attack rate of Clostridium difficile than other respiratory quinolones, such as levofloxacin.[8]

Interactions

Antacids containing aluminium or magnesium ions inhibit the absorption of moxifloxacin. Drugs that prolong the QT interval (e.g. pimozide) may have an additive effect on QT prolongation and lead to increased risk of ventricular arrhythmias. The INR (International Normalised Ratio) may be increased or decreased in patients treated with warfarin. A precautionary measure would be to monitor the INR more closely and, if necessary, adjust the anticoagulant dose as necessary.

Unlike ciprofloxacin, moxifloxacin has no interactions with warfarin or theophylline.

Trade names

Topical use: US:

  • Vigamox® 0.5% ophthalmic preparation (marketed by Alcon)


Systemic use:

  • US: Avelox® (marketed by Bayer)
  • UK: Avelox® (marketed by Bayer, no intravenous preparation available)

References

  1. Malincarne L, Ghebregzabher M, Moretti M; et al. (2006). "Penetration of moxifloxacin into bone in patients undergoing total knee arthroplasty". J Antimicrob Chemother. 57 (5): 950&ndash, 4. doi:10.1093/jac/dkl091.
  2. Nuermberger EL, Yoshimatsu T, Tyagi S; et al. (2004). "Moxifloxacin-containing regimens of reduced duration produce a stable cure in murine tuberculosis". Am J Resp Crit Care Med. 170: 1131&ndash, 34. doi:10.1164/rccm.200407-885OC.
  3. Kim, Terrance (2003-09). "Refractive surgery prophylaxis; new options in fluoroquinolones spark a fresh, and ongoing, body of research to be evaluated". Ophthamology Management. Retrieved 2007-03-26. Check date values in: |date= (help)
  4. Ginsburg AS, Sun R, Calamita H; et al. (2005). "Emergence of fluoroquinolone resistance in Mycobacterium tuberculosis during contrinuously dosed mocifloxacin monotherapy in a mouse model". Antimicrob Agents Chemother. 49 (9): 3977&ndash, 79. doi:10.1128/AAC.49.9.3977-3979.2005.
  5. Ginsburg AS, Hooper N, Parrish N; et al. (2003). "Fluoroquinolone resistance in patients with newly diagnosed tuberculosis". Clin Infect Dis. 37: 1448&ndash, 52. doi:10.1086/379328. PMID 14614666.
  6. 6.0 6.1 Wang J-Y, Hsueh P-R, Jan I-S; et al. (2006). "Empirical treatment with a fluoroquinolone delays the treatment for tuberculosis and is associated with a poor prognosis in endemic areas". Thorax. 61: 903&ndash, 8. doi:10.1136/thx.2005.056887.
  7. Ballow C, Lettieri J, Agarwal V; et al. (1997). "Absolute bioavailability of moxifloxacin". doi:10.1016/S0149-2918(00)88306-X.
  8. von Baum M, Sigge A, Bommer M; et al. (2006). "Moxifloxacin prophylaxis in neutropenic patients". J Antimicrob Chemother. 58 (4): 891&ndash, 94. doi:10.1093/jac/dkl320.

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