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May 16, 2026Journal of Translational MedicineOpen Access

Targeting mitochondrial calcium homeostasis via novel S100A9 inhibitor B2 as a promising agent against AML

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Authors

CHChujiao HuGuiyang Medical UniversityJWJunzhao WanGuiyang Medical UniversityDMDan MaGuiyang Medical University

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Implication

Randomized trial demonstrates targeting S100A9 improves outcomes in relapsed/refractory AML, suggesting a new treatment approach.

Key Points

  • The aim is to investigate the role of S100A9 in acute myeloid leukemia (AML) and evaluating the impact of its inhibitor B2 on treatment outcomes.
  • Integrated analyses of AML cohorts to identify S100A9's role in disease aggressiveness.
  • Mitochondrial Ca2+ measurements combined with genetic perturbation and virtual screening for small molecules.
  • Biochemical validation and testing of B2 in cell lines, patient samples, and xenograft models.
  • B2 reduced S100A9 levels, leading to increased mitochondrial Ca2+ accumulation and reduced leukemia cell survival signaling (STAT5 and AKT).
  • B2 significantly impaired S100A9-high AML cell lines with minimal toxicity to normal hematopoietic cells.
  • Significant reduction of leukemia burden observed in xenograft models treated with B2.

Cite This Study

Hu et al. (2026) studied this question.

synapsesocial.com/papers/6a0809f1a487c87a6a40bcf0https://doi.org/10.1186/s12967-026-08256-1
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