indication

For the treatment of urinary tract infection

pharmacology

Norfloxacin is a quinolone/fluoroquinolone antibiotic. Norfloxacin 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.

mechanism of action

The bactericidal action of Norfloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination. Norfloxacin is a broad-spectrum antibiotic that is active against both gram-positive and gram-negative bacterias. The fluorine atom at the 6 position increases potency against gram-negative organisms, and the piperazine moiety at the 7 position is responsible for anti-pseudomonal activity

biotransformation

Via liver and kidney

absorption

Rapid

half life

3-4 hours

route of elimination

Norfloxacin is eliminated through metabolism, biliary excretion, and renal excretion. Renal excretion occurs by both glomerular filtration and tubular secretion as evidenced by the high rate of renal clearance (approximately 275 mL/min).

drug interactions

Acenocoumarol: The quinolone antibiotic, norfloxacin, may increase the anticoagulant effect of acenocoumarol.

Aluminium: Formation of non-absorbable complexes

Aminophylline: Norfloxacin may increase the effect of aminophylline.

Anisindione: The quinolone antibiotic, norfloxacin, may increase the anticoagulant effect of anisindione.

Artemether: Additive QTc-prolongation may occur. Concomitant therapy should be avoided.

Caffeine: Norfloxacin may increase the effect and toxicity of caffeine.

Calcium: Formation of non-absorbable complexes

Calcium Acetate: Calcium salts such as calcium acetate may decrease the absorption of quinolone antibiotics such as norfloxacin. Of concern only with oral administration of both agents. Interactions can be minimized by administering oral quinolone at least 2 hours before, or 6 hours after, the dose of an oral calcium supplement. Monitor for decreased therapeutic effects of oral quinolones if administered with oral calcium supplements.

Clozapine: Ciprofloxacin may increase clozapine serum levels

Cyclosporine: Norfloxacin may increase the effect and toxicity of cyclosporine.

Dicumarol: The quinolone antibiotic, norfloxacin, may increase the anticoagulant effect of dicumarol.

Dyphylline: Norfloxacin may increase the effect of dyphylline.

Foscarnet: Increased risk of convulsions

Iron: Formation of non-absorbable complexes

Iron Dextran: Formation of non-absorbable complexes

Lumefantrine: Additive QTc-prolongation may occur. Concomitant therapy should be avoided.

Magnesium: Formation of non-absorbable complexes

Magnesium oxide: Formation of non-absorbable complexes

Oxtriphylline: Norfloxacin may increase the effect of oxtriphylline.

Sucralfate: Formation of non-absorbable complexes

Tacrine: The metabolism of Tacrine, a CYP1A2 substrate, may be reduced by strong CYP1A2 inhibitors such as Norfloxacin. Consider modifying therapy to avoid Tacrine toxicity. Monitor the efficacy and toxicity of Tacrine if Norfloxacin is initiated, discontinued or if the dose is changed.

Tacrolimus: Additive QTc-prolongation may occur increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution.

Tamsulosin: Norfloxacin, a CYP3A4 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Norfloxacin is initiated, discontinued, or dose changed.

Theophylline: Norfloxacin may increase the effect of theophylline.

Thiothixene: May cause additive QTc-prolonging effects. Increased risk of ventricular arrhythmias. The strong CYP1A2 inhibitor, Norfloxacin, may also decrease the metabolism and clearance of Thiothixene, a CYP1A2 substrate. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of both agents if concomitant therapy is initiated, discontinued or dose changed. Thorough risk:benefit assessment is required prior to co-administration.

Tizanidine: Norfloxacin may decrease the metabolism and clearance of Tizanidine. Consider alternate therapy or use caution during co-administration.

Tolterodine: Norfloxacin may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity.

Toremifene: Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Consider alternate therapy. A thorough risk:benefit assessment is required prior to co-administration.

Tramadol: Norfloxacin may increase Tramadol toxicity by decreasing Tramadol metabolism and clearance.

Trazodone: The CYP3A4 inhibitor, Norfloxacin, may increase Trazodone efficacy/toxicity by decreasing Trazodone metabolism and clearance. Monitor for changes in Trazodone efficacy/toxicity if Norfloxacin is initiated, discontinued or dose changed.

Trimipramine: Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution.

Voriconazole: Additive QTc prolongation may occur. Consider alternate therapy or monitor for QTc prolongation as this can lead to Torsade de Pointes (TdP).

Vorinostat: Additive QTc prolongation may occur. Consider alternate therapy or monitor for QTc prolongation as this can lead to Torsade de Pointes (TdP).

Warfarin: The quinolone antibiotic, norfloxacin, may increase the anticoagulant effect of warfarin.

Zinc: Formation of non-absorbable complexes

Ziprasidone: Additive QTc-prolonging effects may increase the risk of severe arrhythmias. Concomitant therapy is contraindicated.

Zuclopenthixol: Additive QTc prolongation may occur. Consider alternate therapy or use caution and monitor for QTc prolongation as this can lead to Torsade de Pointes (TdP).