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The disulfonic acid ANDS disrupts ANP32B-p53 interaction to suppress chronic myeloid leukemia

Yu-Sheng Wei1, Fei-Yu Jin1, Hong-Hui Zeng1

  • 1Institute of Aging & Tissue Regeneration, State Key Laboratory of Systems Medicine for Cancer, Ren-Ji Hospital, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.

Nature Communications
|June 10, 2026
PubMed

Insights

A novel compound, ANDS, targets leukemic stem cells in chronic myeloid leukemia (CML) by restoring p53 activity. This approach shows promise for eradicating CML and overcoming resistance to tyrosine kinase inhibitors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Leukemic stem cells (LSCs) drive resistance and relapse in chronic myeloid leukemia (CML) after tyrosine kinase inhibitor (TKI) therapy.
  • ANP32B protein promotes CML LSC survival by inhibiting p53 activity, presenting a therapeutic target.

Purpose of the Study:

  • To investigate the therapeutic potential of 1-amino-8-naphthol-2,4-disulfonic acid (ANDS) in eradicating CML LSCs.
  • To explore the synergistic effects of ANDS with p-CaMKIIγ inhibitors in TKI-resistant CML.

Main Methods:

  • Investigated ANDS binding to unacetylated p53 and its effect on the ANP32B-p53 interaction.
  • Assessed ANDS efficacy in inhibiting CML cell proliferation and LSC function in a CML mouse model.
  • Evaluated the combination therapy of ANDS with KN93 (a p-CaMKIIγ inhibitor) in TKI-sensitive and -resistant CML models.

Main Results:

  • ANDS restores p53 activity by disrupting the ANP32B-p53 complex, inhibiting CML cell proliferation and LSC function.
  • ANDS treatment prolonged survival in a CML mouse model without affecting normal progenitor cells.
  • Combination therapy with KN93 synergistically suppressed both TKI-sensitive and -resistant CML.

Conclusions:

  • ANDS represents a potential therapeutic strategy for eradicating CML LSCs by restoring p53 activity.
  • The combination of ANDS with CaMKP inhibitors offers a promising approach to overcome TKI resistance in CML.

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