What is the mechanism of action for Moxifloxacin?

Moxifloxacin works primarily by inhibiting topoisomerase II (also known as DNA gyrase) and topoisomerase IV. These enzymes are crucial for bacterial DNA replication, transcription, repair, and recombination. By inhibiting topoisomerase II, moxifloxacin prevents the unwinding of DNA, which is necessary for replication, and by inhibiting topoisomerase IV, it disrupts the separation of replicated DNA strands. This inhibition leads to the accumulation of DNA breaks and ultimately results in bacterial cell death.

In contrast, other mechanisms of action involve different targets within the bacterial cell. Inhibition of bacterial cell wall synthesis, for example, is the primary mechanism of action for beta-lactam antibiotics, while inhibition of RNA polymerase is the target for rifamycins. Diminished protein synthesis is associated with antibiotics like tetracycline and macrolides. Thus, moxifloxacin's unique mechanism, affecting DNA gyrase, is key to its effectiveness as a fluoroquinolone antibiotic.