Difloxin (Difloxin) is a fluoroquinolone (flor-o-KWIN-o-lone) antibiotic that fights bacteria in the body. Difloxin is used to treat different types of bacterial infections. Difloxin is also used to treat people who have been exposed to anthrax or certain types of plague. Fluoroquinolone antibiotics can cause serious or disabling side effects. Difloxin should be used only for infections that cannot be treated with a safer antibiotic. The FDA approved Difloxin in December 1996. This medication may be available under multiple brand names and/or in several different forms.
Other names for this medication:
Levofloxacin,
Levaquin,
Armolev,
Auxxil,
Cravit,
Cravox,
Difloxin,
Elequine,
Glevo,
Iquix,
Leflox,
Lefloxin,
Leflumax,
Lequin,
Levobact,
Levocin,
Levocine,
Levoday,
Levoflox,
Levofloxacina,
Levofloxacino,
Levofloxacinum,
Levomac,
Levomax,
Levoquin,
Levoquinol,
Levores,
Levotac,
Levox,
Levoxa,
Levoxacin,
Levoxin,
Levozine,
Levunid,
Locin,
Lovequin,
Loxin,
Loxof,
Lufi,
Medibiox,
Mosardal,
Nevotek,
Nislev,
Novacilina,
Oftaquix,
Orlev,
Ovel,
Ovelquin,
Proxime,
Quantrum,
Quinobiot,
Quixin,
Recamicina,
Reskuin,
Tamiram,
Tavaloxx,
Tavanic,
Trevox,
Truxa,
Ultraquin,
Uniflox,
Volequin,
Voxin,
Similar Products:
Moxin,
Adecur,
Alprostadil,
Narutis,
Metacycline,
Kefnir,
Forzest,
Efamat,
Klabet,
Noroxine,
Mareen,
Redomex,
Aciclobeta,
Ceftin,
Ulcratex,
Asicot,
Podomexef,
Cleocin,
Gabator,
Lanso,
Elcontrol,
Mebutar,
Zoldicam,
Pents,
Zolen,
Prostol,
Leflumax,
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Itinerant-to-localized electron transition in CaRu1-xSnxO3 and SrRu1-xPbxO3. Insulin resistance is a key component of the insulin resistance syndrome and is a crucially important metabolic abnormality in Type 2 diabetes. The results suggest that some lesion mimic mutations in rice may be involved in disease resistance, and cloning of these genes may provide a clue to developing broad-spectrum resistance to diverse pathogens. Overall, it can be argued that neither the IgE/mast cell axis, nor the IL-5/eosinophil axis, are the cause of airway hyperresponsiveness, but that the T-cell in its own right is the main determining factor in establishing the degree of bronchial hyperresponsiveness. In contrast IL-8, and MIP-2 provoked dramatic polymorphonuclear leukocyte recruitment in both the central nervous nortylin 25 mg system and skin.
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