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December 8, 2025BloodOpen Access

TP53 activation by the natural quassinoid brusatol enhances venetoclax efficacy and overcomes resistance in myeloid leukemias

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Authors

SKShin‐ichiro KawaguchiNTNorihito TakayamaHHHiroko Hayakawa

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Overview

In vitro and in vivo analysis revealed brusatol improves venetoclax's efficacy in AML, suggesting it may help overcome drug resistance.

Key Points

  • Brusatol induced apoptosis in AML cell lines, synergizing with venetoclax to improve therapeutic outcomes.
  • MOLM-14 cells showed the highest sensitivity, with venetoclax having effective IC50 values in combination therapy.
  • Genetic analysis confirmed that TP53 activation is a key mechanism by which brusatol enhances apoptosis in resistant leukemias.
  • The findings support further clinical testing of brusatol with venetoclax in AML patients facing drug resistance.

Cite This Study

Kawaguchi et al. (2025) studied this question.

synapsesocial.com/papers/69362f604fa91c937236dcd9https://doi.org/10.1182/blood-2025-1491
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Also Consider

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

  1. 1Synergistic antitumor effects and mechanisms of KPT-330 combined with venetoclax in Acute Myeloid Leukemia2025
  2. 2Pitavastatin counteracts venetoclax resistance mechanisms in acute myeloid leukemia2025 · 1 citations
  3. 3LSD1 inhibition enhances venetoclax efficacy in Acute Myeloid Leukemia via metabolic rewiring2025
  4. 4Overcoming venetoclax resistance through heme-mediated NOXA/cyclin D1/Mcl-1 axis with a novel artemisinin conjugate.2025 · 2 citations
  5. 5The novel agent VP79s synergistically enhances venetoclax activity in multiple myeloma cells2026