Flumequine

Flumequine inhibits eukaryotic topoisomerase II, which is responsible for the double-strand DNA breakage reaction as well as bacterial gyrase, inhibitory effects of FL on topoisomerase II are high relative to the influence on bacterial gyrase. ^[1] Flumequine has minimum inhibitory concentration (MIC) ranging from 0.06 μg/mL to 32 μg/mL in 12 clinical A. salmonicida isolates. Flumequine enhibits high E(max) values of 16 for the most resistant isolates, which indicates an important contribution of efflux to the resistance phenotype. Flumequine accumulation experiments confirmes that high E(max) values are associated with a much lower level of accumulation. ^[2]

Flumequine (4000 ppm, oral diet) induces dose-dependent DNA damage in the stomach, colon, and urinary bladder of adult mice at 3 hours but not at 24 hours after its administration. ^[1] Flumequine shows the bioavailability of 44.7% following oral administration of medicated feed in Atlantic salmon. Flumequine results in the volumes of distribution at steady state of 3.5 L/kg, elimination half-life (t _1/2) of 22.8 hours and area under plasma drug concentration-time curve (AUC) of 140 μg×hours/mL following intravenous administration in Atlantic salmon. ^[3] Flumequine (100 mg/L) reduces the mean length of root, hypocotyle, cotyledon and the mean number of secondary roots in aquatic weed Lythrum salicaria L. ^[4] Flumequine (10 mg/kg, oral) results in the volumes of distribution at steady-state (Vss) of 2.41 L/kg (cod) and 2.15 L/kg (wrasse) following intravenous administration. Total body clearances (Cl) are 0.024 L/h.kg (cod) and 0.14 L/h.kg (wrasse) and the elimination half-lives (t1/2 λ z) are calculated to be 75 hours (cod) and 31 hours (wrasse) after Flumequine (10 mg/kg, oral) administration. The oral bioavailabilities (F) are calculated to be 65% (cod) and 41% (wrasse) following oral administration of Flumequine. ^[5]