Trifluoperazine induces ferroptosis in acute myeloid leukemia by suppressing the Nrf2/SLC7A11/GPX4 axis.
An old antipsychotic drug kills leukemia cells in the lab by triggering a different death pathway, suggesting new treatment possibilities.
Xu J et al. demonstrated that trifluoperazine, a repurposed antipsychotic agent, induces ferroptosis in acute myeloid leukemia cells by suppressing the Nrf2/SLC7A11/GPX4 antioxidant axis in preclinical studies. These findings identify a novel mechanism for AML cell death and suggest potential for drug repurposing strategies targeting ferroptosis pathways in hematologic malignancies.
What the study was
- Study design
- Preclinical experimental study (in vitro/cell line, likely with in vivo component)
- Population
- AML cell lines
- Category
- Drug Development
- Maturity
- Exploratory
- Journal
- European journal of pharmacology
Why it surfaced
Drug repurposing for AML is an active and clinically relevant area; ferroptosis pathway targeting is a novel mechanism; however, purely preclinical evidence limits score (non-human study cap: max 5).
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