| Indication | For treatment of adults with mild to moderate infections caused by susceptible strains of Haemophilus influenzae, Streptococcus pneumoniae, or Moraxella catarrhalis. |
| Pharmacodynamics | Grepafloxacin has in vitro activity against a wide range of gram-positive and gram-negative aerobic microorganisms, as well as some atypical microorganisms. |
| Mechanism of action | Grepafloxacin exerts its antibacterial activity by inhibiting bacterial topoisomerase II (DNA gyrase) and topoisomerase IV, essential enzymes for duplication, transcription, and repair of bacterial DNA. |
| Absorption | Rapidly and extensively absorbed following oral administration. The absolute bioavailability is approximately 70%. |
| Volume of distribution | Not Available |
| Protein binding | 50% |
| Metabolism | Primarily hepatic via CYP1A2 and CYP3A4. The major metabolite is a glucuronide conjugate; minor metabolites include sulfate conjugates and oxidative metabolites. The oxidative metabolites are formed mainly by the cytochrome P450 enzyme CYP1A2, while the cytochrome P450 enzyme CYP3A4 plays a minor role. The nonconjugated metabolites have little antimicrobial activity compared with the parent drug, and the conjugated metabolites have no antimicrobial activity |
| Route of elimination | Not Available |
| Half life | 15 ± 3 hours |
| Clearance | Not Available |
| Toxicity | Withdrawn from the US market in 1999 due to associations with QTc prolongation and adverse cardiovascular events. |