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Renor (Norfloxacin)

Renor is a white to pale yellow crystalline powder with a molecular weight of 319.34 and a melting point of about 221°C. It is freely soluble in glacial acetic acid, and very slightly soluble in ethanol, methanol and water. Renor is available in 400-mg tablets. Each tablet contains the following inactive ingredients: cellulose, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, magnesium stearate, and titanium dioxide. Renor, a fluoroquinolone, differs from non-fluorinated quinolones by having a fluorine atom at the 6 position and a piperazine moiety at the 7 position.

Other names for this medication:
Norfloxacin, Noroxin, Ambigram, Baccidal, Barazan, Bexinor, Chibroxin, Chibroxine, Danilon, Epinor, Firin, Flox, Floxatral, Grenis, Janacin, Lexinor, Loxone, Microxin, Nalion, Noflo, Nolicin, Noprose, Noracin, Norax, Norbactin, Norflohexal, Norilet, Normax, Noroxine, Norsol, Norzen, Nufloxib, Oranor, Renor, Respexil, Senro, Shinun, Trizolin, Uritracin, Uroxacin, Utinor, Zoroxin,

Similar Products:
Dazomet, Cefadroxil, Remex, Sofovir, Hycid, Nizoral, Amoklavin, Klimicin, Sovaldi, Spiron, Ranitic, Telaprevir, Daclin, Zosec, Metrosa, Flunil, Moxifloxacin, Novidat, Clindasome, Podomexef, Aldozone, Zevin, Protoner, Topilex, Cotrimstada, Lanpro, Allerfex, Kovar, Lutamidal, Gantin, Orlev, Amolin, Cryofaxol, Kifluzol, Acimox, Allupol, Strattera, Clinfol, Amoksiklav, Amovet, Flagicure, Prolic, Geloderm, Prospera, Spectrem, Aurene,

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Caspase-1 and -3 are sequentially activated in motor neuron death in Cu,Zn superoxide dismutase-mediated familial amyotrophic lateral sclerosis. Tumor angiogenesis factor with possible implications for glioblastoma multiforme. STUDIES ON THE METABOLISM OF I-131-LABELLED L-THYROXIN IN HYPERTHYROIDISM DURING AND AFTER TREATMENT The mechanism of respiratory burst was studied by modulating membrane surfaces with lipophilic ions in guinea-pig polymorphonuclear leukocytes and their subcellular membranes.

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Green waste compost as an amendment during induced phytoextraction of mercury-contaminated soil. To explore the escape pathway of the antagonist CP-376395 in the binding pocket of CRF1R, molecular dynamics (MD) simulations, dynamical network analysis, random acceleration molecular dynamics (RAMD) simulations and adaptive biasing force (ABF) calculations were performed on the crystal structure of CRF1R in complex with CP-376395. The therapeutic use of a corticosteroid-antibiotic-enzyme ointment in common foot lesions. Mutation of a SRY/Sox-binding site in one of the regions did not impair in vivo testis-specific expression of the reporter gene.

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