Claudia Einer, Ditte Emilie Munk, Eok Park, Banu Akdogan, Judith Nagel, Josef Lichtmannegger, Carola Eberhagen, Tamara Rieder, Mikkel H Vendelbo, Bernhard Michalke, Ralf Wimmer, Andreas Blutke, Annette Feuchtinger, Philip Dershwitz, Ana A DiSpirito, Tawhidul Islam, Rui E Castro, Byong-Keol Min, TaeWon Kim, Seoyoung Choi, Dasol Kim, Chunwon Jung, Hongjae Lee, Dongsik Park, Weonbin Im, So-Young Eun, You-Hee Cho, Jeremy D Semrau, Cecília M P Rodrigues, Simon Hohenester, Thomas Damgaard Sandahl, Alan A DiSpirito, Hans Zischka
BACKGROUND: Excess copper causes hepatocyte death in hereditary Wilson disease (WD). Current WD treatments by copper-binding chelators may gradually reduce copper overload; they fail, however, to bring hepatic copper close to normal physiological levels. Consequently, lifelong daily dose regimens are required to hinder disease progression. This may result in severe issues due to non-adherence or unwanted drug reactions, but also in drug switching and ultimate treatment failures. STUDY AIMS: To comparatively test bacteria-derived copper binding agents - methanobactins (MBs) - for efficient liver copper depletion in WD rats, as well as their safety and effect duration...
March 24, 2023: Gastroenterology