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During the 25th Congress of the European Hematology Association (EHA), the MPN Hub spoke to Haifa Kathrin Al-Ali, University Hospital Halle (Saale), Halle (Saale), DE. We asked: Why should we target murine double minute 2 (MDM2) with the small molecule inhibitor KRT-232 in patients with myelofibrosis (MF)?
Approximately 50% of patients with MF discontinue treatment with Janus kinase (JAK) inhibitors within 3 years. Resistance to JAK inhibitors, such as ruxolitinib, is the primary reason for treatment termination, after which, patient prognosis is poor. Novel therapeutic approaches are therefore critical to improve patient survival in this setting. As a negative modulator of p53, MDM2 overexpression has been associated with malignancy.
KRT-232 is a potent, selective and, importantly, orally available MDM2 inhibitor, which may be successful in targeting malignant stem cells and hematopoietic cells. This interview provides insight into the phase IIa trial investigating KRT-232 for the treatment of patients with MF who have been previously treated with a JAK inhibitor.
Why should we target MDM2 with small molecule inhibitor KRT-232 in patients with MF?
Update from MANIFEST phase II study: CPI-0610 + ruxolitinib in patients with myelofibrosis and naïve to JAK inhibitor treatment
Bromodomain and extraterminal domain (BET) proteins are transcriptional regulators of oncogenic pathways that drive...
Novel agents to treat MF with suboptimal response to ruxolitinib: Combining ruxolitinib with navitoclax or KRT-232
Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway dysregulation is central to the pathogenesis of...
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