17th March 2017

Mode of action

TARGAXAN® is a broad spectrum antibiotic with low potential for clinically relevant resistance 1-4

Rifaximin-α inhibits bacterial RNA synthesis by irreversibly binding to the beta-subunit of the DNA-dependent RNA polymerase enzyme. 1 The gene encoding the bacterial DNA-dependent RNA polymerase is carried on chromosomal DNA, 3 meaning that to develop resistance to rifaximin-α, a mutation is required in the bacterial chromosomal DNA 3,4

Rifaximin-α acts locally in the gut, therefore no dose adjustment in hepatic insufficiency is required 1

  • The pyridoimidazole ring makes TARGAXAN® virtually non-absorbable. 5 Therefore, bacteria outside the gastrointestinal tract are not exposed to appreciable selective pressure 6 , which means that rifaximin-α has a low potential to induce resistance.

  • Some cases of development of Clostridium difficile strains resistant to rifaximin-α have been documented, however the incidence has been low in the studies published to date. 7,8
  • In studies with repeated, high doses of rifaximin-α in healthy volunteers and Inflammatory Bowel Disease patients, strains resistant to rifaximin-α developed, but were unstable and did not colonise the gastrointestinal tract or replace rifaximin-α-sensitive strains. When treatment was discontinued, resistant strains disappeared rapidly 1

UKE-HEP-XIF-2000014   DOP: June 2020


  1. TARGAXAN® 550 Summary of Product Characteristics. Available from: https://www.medicines.org.uk/emc/medicine/27427
  2. Scarpignato C, Pelosini I. Digestion. 2006;73 Suppl 1:13–27
  3. Jiang ZD & DuPont HL. Chemotherapy 2005;51 Suppl 1:67-72
  4. Pons MJ et al. Microbial Drug Resist 2012;18(4):376-9
  5. Adachi JA et al. Clin Inf Dis 2006;42:541-47
  6. Bass NM, et al. N Engl J Med 2010;362(12):1071-81
  7. Marchese A et al. Chemotherapy 2000;46:253–66
  8. Hecht DW et al. Antimicrob Agents Chemother 2007;51(8):2716–19