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December 8, 2025BloodOpen Access

EB2023 primes mitochondria for BCL2 dependence and induces pyroptotic cell death via AMPK signaling and the unfolded protein response

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Authors

MDMichael DavidsonSCSovira ChaudhryBRBenjamin Reisman

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Overview

Experimental treatment with EB2023 demonstrated anti-cancer activity and altered cell death pathways in AML, suggesting new therapeutic strategies.

Key Points

  • To evaluate the effects of EB2023 on cell death mechanisms and its potential synergy with BCL2 inhibitors in AML.
  • Assessment of EB2023's anti-cancer activity in AML cell lines and mouse models.
  • Analysis of cellular effects through RNA-sequencing and Seahorse XF technology.
  • Investigation of metabolic responses and cell death pathways including pyroptosis and UPR.
  • EB2023 showed broad anti-proliferative effects with IC50 values of 5-91 nM in various cancer cell lines.
  • The combination of EB2023 with venetoclax enhanced apoptosis in primary human AML samples.
  • Significant increase in survival in AML mouse models when treated with EB2023 compared to controls.

Cite This Study

Davidson et al. (2025) studied this question.

synapsesocial.com/papers/69362f3a4fa91c937236d442https://doi.org/10.1182/blood-2025-637
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