MTE #15: Ileal Bile Acid Transporter Inhibitors for Cholestatic Liver Disease—Therapeutic Promise for Symptoms and Disease Modification? (Ticketed)

Nov 07 2026
Convention Center: Room 1A
12:45 PM - 1:30 PM
Ticketed event Ticketed Event
CE Credits CE Credits

Description

Ileal bile acid transporter (IBAT) inhibitors have emerged as a novel and increasingly relevant therapeutic class in the management of cholestatic liver diseases. Initially developed to address cholestatic pruritus through interruption of enterohepatic bile acid circulation, these agents have demonstrated meaningful symptomatic benefit across multiple cholestatic conditions. However, growing clinical experience and evolving mechanistic insights have raised important questions regarding their potential role beyond symptom control. Presented by the Cholestatic Autoimmune Liver Disease Special Interest Group, experts in this session provide a focused review of IBAT inhibitors, including their mechanism of action, clinical trial data, and current use in cholestatic liver diseases. Presenters highlight the distinction between symptomatic management and the emerging hypothesis that IBAT inhibition may influence disease biology, inflammation, and progression.

Objectives

  • Describe the current clinical utilization of ileal bile acid transporter (IBAT) inhibitors in cholestatic liver diseases, including approved and emerging indications, patient selection, safety considerations, and their role in the management of cholestatic pruritus.
  • Discuss the proposed mechanistic pathways through which IBAT inhibitors may exert disease-modifying effects in cholestatic liver disease, including modulation of enterohepatic bile acid circulation; farnesoid X receptorfibroblast growth factor 19 signaling; hepatic bile acid load; bile duct injury; ductular reaction; and downstream fibrogenic processes.
  • Evaluate emerging evidence and knowledge gaps regarding the immunologic and inflammatory effects of bile acid modulation, including potential impacts of IBAT inhibition on immune activation; gut-liver crosstalk; and autoimmune pathways relevant to cholestatic autoimmune liver diseases.