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Oranor (Noroxin)

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Oranor is used to treat certain types of infections, including infections of the urinary tract and prostate (a male reproductive gland). Oranor is in a class of antibiotics called fluoroquinolones. It works by killing bacteria that cause infections. Antibiotics will not work for colds, flu, or other viral infections.

Other names for this medication:
Ambigram, Danilon, Gyrablock, Loxone, Nolicin, Norbactin, Norflohexal, Norfloxacin, Norilet, Normax, Noroxin, Noroxine, Uroflox, Uroxacin

Similar Products:
Cipro, Levaquin, Quixin, Tequin, Avelox, Ocuflox


Also known as:  Noroxin.


Oranor comes as a tablet to take by mouth. It is usually taken twice a day for 3 to 28 days. The length of treatment depends on the type of infection being treated. Your doctor will tell you how long to take Oranor. Take Oranor at around the same times every day and try to space your doses 12 hours apart. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take Oranor exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.

Take Oranor at least 1 hour before or 2 hours after meals or after drinking milk or eating dairy products.

Swallow the tablets with a full glass of water.

You should begin to feel better during the first few days of your treatment with Oranor. If your symptoms do not improve or if they get worse, call your doctor.

Take Oranor until you finish the prescription, even if you feel better. Do not stop taking Oranor without talking to your doctor unless you experience certain serious side effects listed in the IMPORTANT WARNING or SIDE EFFECT sections. If you stop taking Oranor too soon or if you skip doses, your infection may not be completely treated and the bacteria may become resistant to antibiotics.

Oranor is also sometimes used to treat certain infections of the stomach and intestines. Talk to your doctor about the risks of using this medication for your condition.

This medication may be prescribed for other uses; ask your doctor or pharmacist for more information.


Take exactly as prescribed by your doctor. Do not take in larger or smaller amounts or for longer than recommended. Follow the directions on your prescription label.

Take Oranor with a full glass of water (8 ounces). Drink several extra glasses of fluid each day to prevent crystals from forming in the urine.

Take Oranor on an empty stomach 1 hour before or 2 hours after eating a meal, drinking milk, or eating a dairy product such as yogurt or cheese.

If you are being treated for gonorrhea, your doctor may also have you tested for syphilis, another sexually transmitted disease.

Take this medication for the full prescribed length of time. Your symptoms may improve before the infection is completely cleared. Skipping doses may also increase your risk of further infection that is resistant to antibiotics. Oranor will not treat a viral infection such as the common cold or flu.


If you overdose Generic Oranor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep bottle closed tightly. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Oranor are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Taking norfloxacin increases the risk that you will develop tendinitis (swelling of a fibrous tissue that connects a bone to a muscle) or have a tendon rupture (tearing of a fibrous tissue that connects a bone to a muscle) during your treatment or for up to several months afterward. These problems may affect tendons in your shoulder, your hand, the back of your ankle, or in other parts of your body. Tendinitis or tendon rupture may happen to people of any age, but the risk is highest in people over 60 years of age. Tell your doctor if you have or have ever had a kidney, heart, or lung transplant; kidney disease; a joint or tendon disorder such as rheumatoid arthritis (a condition in which the body attacks its own joints, causing pain, swelling, and loss of function); or if you participate in regular physical activity. Also tell your doctor if you have ever had any tendon problems during or after your treatment with norfloxacin or another quinolone or fluoroquinolone antibiotic. Tell your doctor and pharmacist if you are taking oral or injectable steroids such as dexamethasone (Decadron, Dexpak), methylprednisolone (Medrol), or prednisone (Sterapred). If you experience any of the following symptoms of tendinitis, stop taking norfloxacin, rest, and call your doctor immediately: pain, swelling, tenderness, stiffness, or difficulty in moving a muscle. If you experience any of the following symptoms of tendon rupture, stop taking norfloxacin and get emergency medical treatment: hearing or feeling a snap or pop in a tendon area, bruising after an injury to a tendon area, or inability to move or bear weight on an affected area.

Taking norfloxacin may worsen muscle weakness in people with myasthenia gravis (a disorder of the nervous system that causes muscle weakness) and cause severe difficulty breathing or death. Tell your doctor if you have myasthenia gravis. Your doctor may tell you not to take norfloxacin. If you have myasthenia gravis and your doctor tells you that you should take norfloxacin, call your doctor immediately if you experience muscle weakness or difficulty breathing during your treatment.

Talk to your doctor about the risks of taking norfloxacin.

oranor tabletas 400 mg precio

An E. coli isolate from wastewater, which possessed at least two distinct fluoroquinolone resistance mechanisms, inactivated ciprofloxacin and norfloxacin by N-acetylation.

oranor norfloxacino tabletas 400 mg

Minimal inhibitory concentrations (MICs) of the 4-quinolones ciprofloxacin, enoxacin, norfloxacin, ofloxacin, pefloxacin, difloxacin, A-56620, and CI-934 are consistent world-wide, with allowances for differences in acquired resistance. MICs of these drugs for Enterobacteriaceae correlate with those of nalidixic acid, but resistance to the quinolones is rare if a breakpoint of greater than 2 mg/L is accepted. Most intestinal pathogens are sensitive. Acinetobacter, Pseudomonas aeruginosa, and other Pseudomonas species except Pseudomonas maltophilia are usually sensitive. Ciprofloxacin is generally the most active of the 4-quinolones against these organisms. All of the new agents have antistaphylococcal activity, but that of norfloxacin and ofloxacin is borderline. Against streptococci, including enterococci and pneumococci, the drugs' activity is moderate or poor. Haemophilus influenzae and Branhamella catarrhalis are very sensitive. Gonococci and meningococci are also highly sensitive to the new agents, but activity against Chlamydia trachomatis and the mycoplasmas is borderline. The organisms associated with nonspecific vaginal infection are not very sensitive. Anaerobes except Bacteroides ureolyticus and Clostridium perfringens are mostly resistant.

oranor y alcohol

Laboratory-derived fluoroquinolone-resistant mutants were obtained by serial passage of Streptococcus sanguis and Streptococcus anginosus isolates on agar containing increasing concentrations of old and new fluoroquinolones, ofloxacin and DU-6859a, respectively. Sequencing of an S. sanguis isolate exposed to DU-6859a showed that resistance was associated with two mutations in the quinolone resistance determining region (QRDR) of the gyrA gene (Ser83-->Phe; Glu87-->Lys), and with a mutation in the parC gene (Ser79-->Ile). However, different mutations in the gyrA gene (Ser83-->Tyr) and parC gene (Ser79-->Phe) were found in a S. sanguis isolate exposed to ofloxacin. A fluoroquinolone-resistant isolate, QR-95101, from a dental infection, had a single mutation in the gyrA gene (Ser83-->Phe) and in the parC gene (Ser79-->Phe). Two fluoroquinolone-resistant mutants, QS-701OFm and QS-701DUm, were obtained from S. anginosus QS-701, by exposure to ofloxacin and DU-6859a, respectively. These mutants showed a common substitution at codon 83 (Ser-->Phe) in the gyrA gene but had different substitutions at codon 87 (QS-701OFm, Glu-->Gln; QS-701DUm, Glu-->Lys). They also had different substitutions at codons 79 and 135 in the parC gene (QS-701OFm, Ser79-->Leu but no change at Glu135; QS-701DUm, Ser79-->Ile and Glu135-->Gln). The resistance levels of the DU-6859a-selected resistant S. sanguis mutant QS-951DUm to DU-6859a, ofloxacin, ciprofloxacin and norfloxacin were higher than those of the ofloxacin-selected resistant mutant QS-951OFm. However, ampicillin susceptibilities of these mutants were not different from the parental strains. In S. anginosus, the DU-6859a-selected fluoroquinolone-resistant mutant QS-701DUm was resistant to all the fluoroquinolones tested, while the ofloxacin-selected mutant QS-701OFm was resistant to three fluoroquinolones, but not DU-6859a. The results indicate that different fluoroquinolones select distinct mutations in the QRDR of the gyrA and parC genes in oral streptococci. The gyrA or parC mutation in oral streptococci may determine the levels of fluoroquinolone resistance.

oranor suspension

The mechanisms underlying the bactericidal power of fluoroquinolones against intracellular parasites in host macrophages remain poorly understood. We have analyzed the effect of norfloxacin, a fluoroquinolone antibiotic, on the production of reactive oxygen intermediates (O(2)(*-) and H(2)O(2)) and NADPH oxidase activity in mouse macrophages. The generation of anion superoxide (O(2)(*-)) was found to be significantly greater in macrophages incubated with norfloxacin than in untreated controls. This enhancing effect of norfloxacin was dose-dependent and reached maximal values within 10 min after its addition. The O(2)(*-) generated was mainly intracellular, as determined by the use of specific dyes, such as lucigenin and luminol, and able to diffuse freely through the cell membrane. Also, the production of H(2)O(2) was increased in macrophages in response to norfloxacin. The positive effect of norfloxacin was associated to an enhanced mobilization of NADPH oxidase subunits p47(phox) and p67(phox) from the cytosol to the plasma membrane in phagocytic cells. The effect of the antibiotic persisted in vivo for several hours. These data support the notion that norfloxacin inhibits mycobacterial growth within phagocytic cells by enhancing intracellular production of O(2)(*-) and other reactive oxygen species.

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Fifty distinct strains of mycobacteria were investigated to determine their in-vitro susceptibility to five new fluoroquinolones (norfloxacin, pefloxacin, ofloxacin, enoxacin and ciprofloxacin). Ofloxacin and ciprofloxacin were found to be the most active, with minimum inhibitory concentrations (MIC) of 1.25 mg/l or less to all strains of Mycobacterium tuberculosis, M. bovis, M. xenopi, M. kansasii and BCG tested. All agents showed little activity against M. malmoense and M. avium-intracellulare complex with MIC values of greater than 2.5 mg/l.

oranor 500 mg

In patients at high risk for disseminated candida infections, suppression of bacterial flora and the more common candida pathogens may permit some less pathogenic, but natively resistant candida species, such as C. krusei, to emerge as systemic pathogens.

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Despite the identification of many genes and pathways involved in the persistence phenomenon of bacteria, the relative importance of these genes in a single organism remains unclear. Here, using Escherichia coli as a model, we generated mutants of 21 known candidate persister genes and compared the relative importance of these mutants in persistence to various antibiotics (ampicillin, gentamicin, norfloxacin, and trimethoprim) at different times. We found that oxyR, dnaK, sucB, relA, rpoS, clpB, mqsR, and recA were prominent persister genes involved in persistence to multiple antibiotics. These genes map to the following pathways: antioxidative defense pathway (oxyR), global regulators (dnaK, clpB, and rpoS), energy production (sucB), stringent response (relA), toxin-antitoxin (TA) module (mqsR), and SOS response (recA). Among the TA modules, the ranking order was mqsR, lon, relE, tisAB, hipA, and dinJ. Intriguingly, rpoS deletion caused a defect in persistence to gentamicin but increased persistence to ampicillin and norfloxacin. Mutants demonstrated dramatic differences in persistence to different antibiotics at different time points: some mutants (oxyR, dnaK, phoU, lon, recA, mqsR, and tisAB) displayed defect in persistence from early time points, while other mutants (relE, smpB, glpD, umuD, and tnaA) showed defect only at later time points. These results indicate that varying hierarchy and importance of persister genes exist and that persister genes can be divided into those involved in shallow persistence and those involved in deep persistence. Our findings suggest that the persistence phenomenon is a dynamic process with different persister genes playing roles of variable significance at different times. These findings have implications for improved understanding of persistence phenomenon and developing new drugs targeting persisters for more effective cure of persistent infections.

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oranor con alcohol 2015-12-11

Twenty-eight trials conducted on women with uncomplicated cystitis were reviewed comparing various treatment times or various antibiotics administered as single-dose or 3-day courses. With all antibiotics, a single-dose was less efficient than a Cotrim 240 Mg 3-day or greater than or equal to 5-day treatment in eradicating bacteriuria. The difference was more pronounced with beta-lactams than with trimethoprim/sulfonamide combinations. With the latter antibacterial agent, no benefits were achieved by increasing treatment times to greater than or equal to 5 days. Beta-lactam antibiotics were more effective when administered for greater than or equal to 5 days than when given as a 3-day course. Short-term treatment was more effective with trimethoprim/sulfonamide than with beta-lactams. Adverse reactions did not increase with treatment time when penicillins or norfloxacin was used, which was the case with oral cephalosporins. With trimethoprim/sulfonamide combinations, adverse reactions increased markedly when treatment was given for greater than 3 days. In conclusion, single-dose treatment is less efficient than treatment for greater than or equal to 3 days, beta-lactams should be administered for greater than or equal to 5 days, the optimal treatment time with trimethoprim/sulfonamide combinations seems to be 3 days, and considerable differences exist among various antibiotics.

oranor 500 mg 2017-03-05

This study was performed to assess the corneal penetration of three topically applied fluoroquinolones (levofloxacin, norfloxacin and lomefloxacin) in corneal buttons obtained from patients undergoing Cipro Drug Card penetrating keratoplasty.

oranor 200 mg 2015-01-02

Silver nanoparticles are known to have antimicrobial properties and have been used extensively in medicine, although the mechanism(s) of action have not yet been clearly established. In the present study, the findings suggest a novel mechanism for the antibacterial effect of silver nanoparticles on Escherichia coli, namely, the induction of a bacterial apoptosis-like response. We propose a possible mechanism for the bacterial apoptosis-like response that includes the following: accumulation of reactive oxygen species (ROS) (detected with H2DCFDA staining), increased intracellular calcium levels (detected with Fura-2 AM), phosphatidylserine exposure in the outer membrane (detected with Annexin V) which is the hallmarks of early apoptosis, disruption of the membrane potential [detected with DiBAC4(3)], activation of a bacterial caspase-like protein (detected by FITC-VAD-FMK staining) and DNA degradation ( Dosis Sanprima Syrup detected with TUNEL assay) which is the hallmarks of late apoptosis in bacterial cells treated with silver nanoparticles. We also performed RecA expression assay with western blotting and observed activation of SOS response to repair the damaged DNA. To summarize, silver nanoparticles are involved in the apoptosis-like response in E. coli and the novel mechanisms which were identified in this study, suggest that silver nanoparticles may be an effective antimicrobial agent with far lower propensity for inducing microbial resistance than antibiotics.

oranor norfloxacino 400 mg 2017-10-20

Cholera is an infectious transmissible disease characterized by the development of secretory diarrhea and that presents in epidemic and endemic forms. In Latin-America we are currently seen what could be the eight pandemic in cholera history, due to Vibrio cholerae 0:1 El Tor, Inaba serotype, infection. In the present preliminary study we analyze 300 patients with a clinical picture suggesting cholerae. In 250 cases, Vibrio cholerae 0:1 strains were isolated. The identification was made using mainly the following test and procedures: 1) growth in TCBS (saccharose fermentation), 2) Reactivity with sodium desoxycholate, 3) Oxidase-cytochrome test and 4) agglutination with polyvalent antisera. All isolated Vibrio cholerae strains 0:1 were sensitive to tetracycline, trimethoprim-sulfamethoxazole, norfloxacin, ciprofloxacin and gentamicin, but Cifran Ct 600 Mg Use were resistant to ampicillin. This report summarizes the main features of Vibrio cholerae 0:1 El Tor, Inaba serotype, isolated in Colombian cholera epidemic.

oranor suspension 2016-07-16

A case of a patient with schistosomiasis haematobium history, from Mozambique, is presented. This patient was admitted in the Institute of Terramycin Brand Name Tropical Medicine for having urination troubles and purulent urethral secretion. Serotype B Haemophilus influenzae, biotype i.v. of the urethra, was isolated. The strain was sensitive to ampicillin, chloramphenicol, ceftraxione, and norfloxacin, and resistant to tetracycline and erythromycin. The patient got better after receiving treatment with norfloxacin. A comment is made on the role of this microorganism as a sexual transmission pathogen.

oranor tabletas 400 mg 2015-06-20

Pseudomonas aeruginosa carries several multidrug efflux operons, including mexEF-oprN, that contribute to its resistance to multiple antibiotics. mvaT affects the expression of several P. aeruginosa genes. In this study, we show that the mvaT mutant PAODeltamvaT is more resistant than its parent PAO1 strain to chloramphenicol and norfloxacin but more sensitive to imipenem; yet Amobiotic Amoxicillin 500 Mg both were less resistant to chloramphenicol, norfloxacin, and imipenem than 'typical'nfxC-type mutants. Neither strain carries the deletion described for nfxC-type mutants in mexT, the mexEF-oprN regulatory gene. Expression of mexEF-oprN is increased by five- to sixfold in PAODeltamvaT, while the expression of oprD is reduced by approximately twofold. mvaT mutation had no effect on the expression of other multidrug resistance operons, although it increased the expression of several ATP-binding cassette transporter genes. We show that mvaT mutation does not affect mexEF-oprN expression through mexT or mexS. We also explored several other potential mechanisms.

oranor norfloxacino tabletas 400 mg 2015-09-13

Bacterial drug resistance is emerging as one of the most significant challenges to Dimopen Amoxicilina 500 Mg Dosis human health. Antimicrobial peptides (AMPs), which are produced by many tissues and cell types of invertebrates, insects, and humans, as part of their innate immune system, have attracted considerable interest as alternative antibiotics. Interest in novel mimics of AMPs has increased greatly over the last few years. This report details a new AMP mimic, based on phenylene ethynylene, with improved antimicrobial activity and selectivity. Screening against a large set of bacterial and other organisms demonstrates broad spectrum antimicrobial activity including activity against antibiotic resistant bacterial like methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococci (VRE) as well as activity against yeast (Candida albicans) and fungus (Stachybotrys chartarum). Bacterial resistance development studies using Staphylococcus aureus show a rapid increase in MIC for conventional antibiotics, ciprofloxacin and norfloxacin. In sharp contrast, no change in MIC was observed for the AMP mimic. Cytotoxicity experiments show that the AMP mimic acts preferentially on microbes as opposed to mammalian red blood cells, 3T3 fibroblasts, and HEPG2 cells. In vivo experiments determined the maximum tolerated dose (MTD) to be 10 mg/kg suggesting a therapeutic window is available. These studies indicate that nonpeptidic amphiphilic AMP mimics could be developed as potential new treatments for antibiotic-resistant bacterial infections.

oranor tabletas 400 mg precio 2016-05-13

We describe the characteristics of seven unusual isolates of vancomycin-resistant enterococci (VRE) carrying both the vanC1 and vanA genes that were detected during a 3-month survey carried out to investigate the occurrence of faecal carriage of VRE. The isolates were identified as Enterococcus gallinarum and showed high-level resistance to both vancomycin and teicoplanin (minimum inhibitory concentrations >256 microg/mL and 64-96 microg/mL, respectively). All seven isolates were also resistant to chloramphenicol, erythromycin and high levels of gentamicin, and showed intermediate susceptibility to both quinolones tested (ciprofloxacin and norfloxacin). Susceptibility to fosfomycin, rifampicin and tetracycline varied among isolates. High-level resistance to gentamicin was associated with the aac(6')-aph(2'') gene, and resistance to erythromycin was associated with the erm(B) gene. The seven vanA-carrying E. gallinarum isolates had similar pulsed-field gel electrophoresis (PFGE) profiles. The emergence of multiple antimicrobial Metronidazol 800 Mg resistance, including high-level resistance to glycopeptides, among E. gallinarum points out the need to increase awareness for detection and proper characterisation of these microorganisms, as they may represent potential reservoirs of transmissible, clinically significant resistance genes in nosocomial settings.