Fidaxomicin (Tiacumicin B) is a semisynthetic macrolide antibiotic used to treat Clostridium difficile-associated diarrhea in adults. Fidaxomicin has minimal systemic absorption and has not been linked to serum enzyme elevations during therapy or to instances of clinically apparent, acute liver injury.

Fidaxomicin acts as a RNA polymerase inhibitor by binding to the DNA template–RNA polymerase (RNAP) complex prior to the formation of the open RNAP-DNA complex in which transcription is initiated. Therefore it will inhibit protein synthesis. As a result, apoptosis is triggered in susceptible organisms such as C. difficile. [1]

The minimum inhibitory concentration for 90% of organisms for fidaxomicin against C. difficile is 0.9978 to 2 μg/mL. Fidaxomicin is not systemically absorbed as shown by a plasma concentrations below the lower limit of quantification after single-dose or multiple-dose. In contrast, fecal concentrations of fidaxomicin are much higher and are concentration-dependent. Cmax = 2 hours; Tmax = 5.2 ng/mL; AUC = 14 ng?hr/mL. Fidaxomicin is hydrolyzed by gastric acid or intestinal microsomes into a less active metabolite (OP-1118). The cytochrome enzyme system are not involved in the metabolism of fidaxomicin. [1]