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The Apical sodium-dependent bile acid transporter (ASBT), also known as the ileal bile acid transporter (IBAT), is a transmembrane protein encoded by the SLC10A2 gene that is essential for the enterohepatic circulation of bile acids [9, 10]. Located on the apical membrane of enterocytes in the terminal ileum, ASBT mediates the sodium-dependent reabsorption of bile acids from the intestinal lumen, returning them to the liver via the portal vein [9]. This process is crucial for maintaining the bile acid pool and regulating cholesterol levels, as bile acids are the primary catabolic product of cholesterol [10]. Pharmacological modulation of this system, either through direct binding of bile acids by sequestrants or through the inhibition of ASBT, is used to treat conditions such as hypercholesterolemia, chronic constipation, and cholestatic liver diseases [6, 7, 8]. By increasing the fecal excretion of bile acids, these therapies reduce the systemic bile acid burden and stimulate the liver to convert more cholesterol into new bile acids, thereby lowering LDL cholesterol levels [10]. Recent clinical advances have focused on ASBT inhibitors like odevixibat and maralixibat for the treatment of severe pruritus associated with rare cholestatic disorders such as Alagille syndrome and progressive familial intrahepatic cholestasis [1, 2].
Inhibition of the apical sodium-dependent bile acid transporter (ASBT) or direct sequestration of bile acids in the gut to prevent reabsorption and promote fecal excretion.
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