In HepG2 cells, Trovafloxacin (20 μM; 24 hours; ) and tumor necrosis factor (TNF; 4 ng/mL) incubation induces apoptosis and increases leakage of lactate dehydrogenase (LDH)[1]. Trovafloxacin (20 μM; 24 hours; HepG2 cells) and TNF (4 ng/mL) incubation increases expression of early NF-κB-related factors A20 and IκBα[1]. Trovafloxacin prolongs TNF-induced activation of MAPKs and IKKα/β activation in HepG2[1]. Trovafloxacin is a potent TO-PRO-3 uptake inhibitor by apoptotic cells. Trovafloxacin also inhibits ATP release from apoptotic cells. Trovafloxacin is equally active against both penicillin-susceptible and -resistant pneumococci, with MICs of 0.06-0.25 mg/mL reported for more than 700 isolates. The MICs of Trovafloxacin at which 90% of isolates are inhibited for 55 isolates of pneumococci is 0.125 μg/mL[3].

In male C57BL/6 J mice, TNF-induced p65 nuclear translocation disrupted by Trovafloxacin (150 mg/kg; oral administration). Trovafloxacin treatment increases expression of early NF-κB-related factors A20 and IκBα[1]. Trovafloxacin increased serum levels of alanine amino transferases (ALT) and pro-inflammatory cytokines when administered in combination with lipopolysaccharide (LPS) or TNF to mice induces severe liver toxicity associated with vast apoptotic areas in the liver[1].