Mutations of calreticulin (CALR) are one of the main disease drivers of myeloproliferative neoplasms (MPN), a group of malignant diseases of the bone marrow. In-silico-docking studies, i.e. computer-assisted simulation of the disease mechanism, identified a group of chemicals that block a crucial interaction. It was shown in a cell model that hematoxylin, the most potent of the tested compounds, acts as a novel CALR inhibitor. Mutated CALR cells are selectively killed by using this drug. Thus, a decisive step towards the therapy of this type of blood cancer has been achieved and patients with primary myelofibrosis (PMF), who often develop myeloid leukaemia, could greatly benefit from it.
Hematoxylin binds to mutant calreticulin and disrupts its abnormal interaction with thrombopoietin receptor
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