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EHA 2025 | The disease-modifying potential of mutCALR-targeted therapies: assessing INCA33989 in ET and MF
In this video, Ruben Mesa, MD, Levine Cancer Institute, Atrium Health Wake Forest Baptist Comprehensive Cancer Center, Winston Salem, NC, briefly discusses the disease-modifying potential of INCA33989, a novel monoclonal antibody targeting mutant calreticulin (mutCALR), in patients with essential thrombocythemia (ET) and myelofibrosis (MF). Although investigations with this agent are still in early stages, Dr Mesa is hopeful that it will provide a deeper clinical benefit to patients than the currently available therapies. This interview took place at the 30th Congress of the European Hematology Association (EHA) in Milan, Italy.
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Transcript
We’re very excited to have the CALR-specific therapy presented here at EHA as one of the late-breaking abstracts, sharing both the safety and efficacy as well as the dose-finding that we are finding with the drug. We’re very hopeful that this is going to represent disease-modifying therapy both for myelofibrosis and for ET. The study is early in its conduct so it’s early to say that we’ve proven that yet, but based on the mechanism of action we hope that first it will achieve the benefits that we typically have seen – control of counts, decreasing splenomegaly, improving symptoms – but we hope that there really will be a deeper benefit with this much more specific and targeted therapy for CALR-mutated patients with ET and myelofibrosis...
We’re very excited to have the CALR-specific therapy presented here at EHA as one of the late-breaking abstracts, sharing both the safety and efficacy as well as the dose-finding that we are finding with the drug. We’re very hopeful that this is going to represent disease-modifying therapy both for myelofibrosis and for ET. The study is early in its conduct so it’s early to say that we’ve proven that yet, but based on the mechanism of action we hope that first it will achieve the benefits that we typically have seen – control of counts, decreasing splenomegaly, improving symptoms – but we hope that there really will be a deeper benefit with this much more specific and targeted therapy for CALR-mutated patients with ET and myelofibrosis.
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