Authors: Stefan Balabanov, Artur Gontarewicz, Gunhild Keller, Laura Raddrizzani, Melanie Braig, Roberta Bosotti, Jürgen Moll, Edgar Jost, Christine Barett, Imke Rohe, Carsten Bokemeyer, Tessa L. Holyoake, Tim H. Brümmendorf
DOI: 10.1371/journal.pone.0019164
Abstract Summary
Danusertib, a dual-action inhibitor targeting both aurora and ABL kinases, shows promise against imatinib-resistant chronic myeloid leukemia, including the challenging T315I mutation. Resistance to Danusertib develops less frequently than to imatinib and occurs through a different mechanism—overexpression of the Abcg2 drug efflux pump rather than kinase mutations. Combining both drugs significantly reduces resistance emergence, suggesting a potential strategy for more durable CML control.
Why Brain? 🧠
Danusertib shows promise against drug-resistant leukemia by targeting multiple pathways. Unlike standard therapy, resistance develops through drug efflux rather than mutations, suggesting combination treatments could prevent resistance and improve outcomes.
The image is AI-generated for illustrative purposes only. Courtesy of Midjourney.
