Screening reactive compounds finds a cell death type linked to GPX4 as a weak point in aging cells

Senescent cells appear to depend on GPX4 to avoid ferroptosis, making GPX4 inhibition a preclinical senolytic vulnerability.

An electrophilic-compound screen of 10,480 compounds, activity-based protein profiling, functional assays, and melanoma, prostate, and ovarian cancer models identified GPX4-dependent ferroptosis in senescent cells.

The evidence comes from screening, cellular assays, and cancer models rather than human clinical testing of GPX4 inhibitors as senolytics.