XIFAXAN is believed to affect an underlying factor of IBS-D by directly attacking bacteria in the gut that may be linked to IBS-D symptoms1-7
- Blocks one of the steps in the transcription of bacterial DNA to RNA1
- Inhibits bacterial protein synthesis1
- Inhibits bacterial growth1
Mechanism of action is unknown and does not imply clinical efficacy
XIFAXAN is the only FDA-approved, nonsystemic IBS-D treatment that alters the microbiome1
- Less than 0.4% is absorbed from the GI tract
- There is an increased systemic exposure in patients with severe (Child-Pugh Class C) hepatic impairment. Caution should be exercised when administering XIFAXAN to these patients
- Clostridium difficile-associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents, including XIFAXAN, and may range in severity from mild diarrhea to fatal colitis. If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difficile may need to be discontinued
XIFAXAN is an IBS-D treatment that1:
- Is NOT a controlled substance
- Is NOT contraindicated in patients without a gallbladder
- Is NOT linked to anticholinergic side effect profile
- Is short-course therapy and not a maintenance medication
INDICATIONS
XIFAXAN® (rifaximin) 550 mg tablets are indicated for the reduction in risk of overt hepatic encephalopathy (HE) recurrence in adults and for the treatment of irritable bowel syndrome with diarrhea (IBS-D) in adults.
IMPORTANT SAFETY INFORMATION
- XIFAXAN is contraindicated in patients with a hypersensitivity to rifaximin, rifamycin antimicrobial agents, or any of the components in XIFAXAN. Hypersensitivity reactions have included exfoliative dermatitis, angioneurotic edema, and anaphylaxis.
- Clostridium difficile-associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents, including XIFAXAN, and may range in severity from mild diarrhea to fatal colitis. If CDAD is suspected or confirmed, ongoing antibiotic use not directed against C. difficile may need to be discontinued.