ArticleNature communications2026
The disulfonic acid ANDS disrupts ANP32B-p53 interaction to suppress chronic myeloid leukemia.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Eradicating leukemic stem cells (LSCs), a major driver of primary resistance and relapse in chronic myeloid leukemia (CML) following tyrosine kinase inhibitor (TKI) treatment, is critical for achieving a cure. Previously, we identified that ANP32B promotes CML LSCs' survival and leukemogenesis by directly binding and inhibiting p53 activity, suggesting a therapeutic opportunity. Here, we show that 1-amino-8-naphthol-2,4-disulfonic acid (ANDS) binds unacetylated p53 and restores p53 activity by disrupting ANP32B-p53 interaction. Consequently, ANDS inhibits CML cell proliferation, impairs LSC function and prolongs survival in the CML mouse model while sparing normal progenitor cells. Based on notion that ANDS, as a previously-identified CaMKP inhibitor, potentially activates p-CaMKIIγ to accelerate CML progression, we find that ANDS combination with KN93, a p-CaMKIIγ inhibitor, synergistically suppresses both TKI-sensitive and -resistant CML. Thus, we highlight that ANDS alone or in combination with CaMKP inhibitor could become a therapeutic strategy for eradicating LSCs and overcoming TKI-resistance in CML.
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