{"id":3033,"date":"2026-08-22T21:13:31","date_gmt":"2026-08-22T20:13:31","guid":{"rendered":"https:\/\/seamlessbio.de\/?page_id=3033"},"modified":"2026-08-23T00:18:20","modified_gmt":"2026-08-22T23:18:20","slug":"what-is-mrp2-abcc2","status":"publish","type":"page","link":"https:\/\/seamlessbio.de\/de\/what-is-mrp2-abcc2\/","title":{"rendered":"What is MRP2 (ABCC2)?"},"content":{"rendered":"
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Quick Definition<\/p>\n

What is MRP2 (Multidrug Resistance-Associated Protein 2 \/ ABCC2)?:<\/strong> MRP2 (ABCC2, cMOAT) is an ABC efflux transporter on the canalicular membrane of hepatocytes that exports organic anions, glucuronide and sulfate conjugates, glutathione conjugates, and bile salts into bile. MRP2 inhibition reduces biliary excretion of these substrates, contributing to intrahepatic cholestasis and drug-induced liver injury.<\/p>\n<\/div>\n

Why BSEP and MRP2 are often assessed together<\/h2>\n

BSEP and MRP2 work in concert on the hepatocyte canalicular membrane. Many cholestatic drugs inhibit both simultaneously \u2014 clinical severity of cholestatic DILI correlates with combined BSEP + MRP2 inhibition. Adding MRP2 to the BSEP vesicle panel is practical and cost-effective: identical assay format, similar incubation conditions, and more informative result than BSEP alone.<\/p>\n

MRP2 and Dubin-Johnson syndrome<\/h2>\n

Genetic MRP2 deficiency (Dubin-Johnson syndrome) causes conjugated hyperbilirubinemia without symptoms \u2014 the benign clinical phenotype helps validate MRP2 as a relevant DDI target and explains why some drugs cause drug-induced conjugated hyperbilirubinemia without full cholestatic DILI.<\/p>\n

Key Facts<\/h2>\n