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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Curr Opin Gastroenterol. 2017 May;33(3):149–157. doi: 10.1097/MOG.0000000000000352

Figure 1.

Figure 1

Current and emerging therapies for primary sclerosing cholangitis that modulate bile acid synthesis, detoxification, secretion and reabsorption. AE2, Cl−/HCO3− anion exchanger 2; ASBT, apical sodium-bile acid transporter; ASBT–, apical sodium-bile acid transporter inhibitor; BA, bile acids; BSEP, bile salt export pump; CaCl, Ca2+-dependent chloride channel; CB, conjugated bilirubin; CFTR, cystic fibrosis transmembrane conductance regulator; FGF19, fibroblast growth factor 19; FGFR4, fibroblast growth factor receptor 4; FXR, farsenoid X receptor; MDR2/3, multidrug resistance 2/3; MRP2, multidrug resistance-associated protein 2; MRP3, multidrug resistance-associated protein 3; MRP4, multidrug resistance-associated protein 4; NTCP, sodium/taurocholate cotransporting polypeptide; norUDCA, 24-norUrsodeoxycholic acid; OCA, obetichoic acid; OSTα/β, organic solute transporter α/β; PC, phosphatidylcholine; PSC, primary sclerosing cholangitis; RXR, retinoid X receptor; SULT2A1, sulfotransferase family 2A member 1; UDCA, ursodeoxycholic acid; UGT1A1, uridine diphosphate-glucoronosyltransferase family 1 member A1. Modified from [5].