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Pharmacological particulars
Pharmacodynamic properties
Florfenicol acts by inhibiting protein synthesis at the ribosomal level and its action is bacteriostatic and time-dependent. Laboratory tests have shown that florfenicol is active against the most commonly isolated bacterial pathogens involved in bovine respiratory disease which include Histophilus somni, Mannheimia haemolytica, Pasteurella multocid and Mycoplasma bovis.
Florfenicol is considered to be a bacteriostatic agent, but in vitro studies demonstrate its bactericidal activity against Histophilus somni, Mannheimia haemolytica and Pasteurella multocida.
For Histophilus somni, Mannheimia haemolytica and Pasteurella multocida the following florfenicol breakpoints have been determined by CLSI (Clinical and Laboratory Standards institute) in 2020 for bovine respiratory pathogens: susceptible ≤ 2 µg/ml, intermediate : 4 µg/ml, resistant : ≥ 8 µg/ml.
Surveillance data of the susceptibility of target field isolates from cattle, collected in 2019 and 2020 across Europe, show consistent efficacy of florfenicol with no finding of resistant isolates. The in vitro Minimum Inhibitory Concentration (MIC) distribution values for these field isolates are presented in the table below.
Range (µg/ml)
MIC50 (µg/ml)
MIC90 (µg/ml)
Histophilus somni (n=29)
Mannheimia haemolytica (n=132)
Pasteurella multocida (n=144)
There are no established breakpoints for Mycoplasma bovis nor have culture techniques been standardized by CLSI.
Resistance to florfenicol is mainly mediated by an efflux system due to a specific (Flo-R) or multidrug transporter (AcrAB-TolC). The genes corresponding to these mechanisms are coded on mobile genetic elements such as plasmids, transposon or genes cassettes. Resistance to florfenicol in the target pathogens has only been reported on rare occasions, and was associated with efflux pump and the presence of the floR gene.Meloxicam is a non-steroidal anti-inflammatory drug (NSAID) of the oxicam class which acts by inhibition of prostaglandin synthesis, thereby exerting anti-inflammatory, anti-exudative, analgesic and antipyretic effects. It reduces leukocyte infiltration into the inflamed tissue. To a minor extent it also inhibits collagen-induced thrombocyte aggregation. Meloxicam also has anti-endotoxic properties, because it has been shown to inhibit production of thromboxane B2 induced by E. coli endotoxin after administration in calves, lactating cows and pigs. The bioavailability of meloxicam in this combination product is lower compared to the use of meloxicam when administered on its own. The impact of this difference on anti-inflammatory effects has not been investigated in field trials. However, a clear antipyretic effect has been demonstrated in the first 48 hours after administration.
Pharmacokinetic particulars
After subcutaneous administration of the product at recommended dose of 1 ml/10 kg bodyweight maximum mean plasma concentration (Cmax) of 4.6 mg/l and 2.0 mg/l occurred 10 hours (h) and 7 h after dosing for florfenicol and meloxicam, respectively. Efficacious plasma levels of florfenicol are maintained above the MIC90 of 1 µg/ml, 0.5 µg/ml and 0.2 µg/ml for 72 h, 120 h and 160 h, respectively.
Florfenicol is largely distributed in the whole body and has a low plasma protein binding (approximately 20%). Meloxicam is extensively bound to plasma proteins (97%) and is distributed in all well-perfused organs.
Florfenicol is mainly excreted via the urine and to a small extent via the faeces with a half-life of about 60 h. Meloxicam excretion is equally divided between urine and faeces, with a half-life of about 23 h.