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December 8, 2025BloodOpen Access

Preclinical activity of investigational menin inhibitor DSP-5336 (Enzomenib)-based combinations against MLL1-rearranged (MLL-r) or mutant-NPM1 AML models

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Authors

WFWarren FiskusCMChristopher P. MillSWSteven L. Warner

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Overview

Preclinical study highlights preclinical anti-AML effects of DSP-5336 using mass cytometry, suggesting promising combination therapies.

Key Points

  • Apoptosis was significantly induced by DSP-5336 in AML cell lines and patient-derived cells, supporting its anti-cancer potential.
  • Mass cytometry analysis confirmed reduced expression of CD11b and key oncogenes after treatment with DSP-5336.
  • Preclinical activity of DSP-5336 was assessed, showcasing synergistic effects with CDK9 inhibitors against resistant AML models.
  • These findings support the potential clinical utility of DSP-5336 in treating MLL1-rearranged AML, highlighting the need for further studies.

Cite This Study

Fiskus et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dcechttps://doi.org/10.1182/blood-2025-1497
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Synergistic targeting of KMT2A-rearranged AML with combined LSD1 and menin inhibitors2025
  2. 2Protein degradation of MYC/GSPT1 combined with menin inhibition overcomes resistance to menin inhibition in KMT2A-rearranged Acute Myeloid Leukemia2025 · 1 citations
  3. 3Therapeutic Implications of Menin Inhibitors in the Treatment of Acute Leukemia: A Critical Review2025 · 7 citations
  4. 4Identifying novel 'druggable’ targets via Npm1A-turboid fusion and mass spectrometry to overcome genetic or adaptive resistance to menin inhibitors in mtNPM1 AML2025
  5. 5DOT1L/menin inhibitors target replication fork plasticity and create novel vulnerability to PARP inhibitor in MLL-rearranged AML2025