A Korea University research team has discovered that pitavastatin, a widely used lipid-lowering drug, can directly inhibit the Mcl-1 protein—an essential survival factor for therapy-resistant triple-negative breast cancer (TNBC). By blocking Mcl-1–dependent mitochondrial protection, pitavastatin eliminates cancer stem-like cells, suppresses metastasis, and restores paclitaxel sensitivity in preclinical models. This repurposed drug may offer a safer, faster-to-deploy therapeutic strategy for patients with aggressive or chemotherapy-refractory TNBC.

Cells have a remarkable housekeeping system: proteins that are no longer needed, defective, or potentially harmful are labeled with a molecular “tag” and dismantled in the cellular recycling machinery. This process, known as the ubiquitin-proteasome system, is crucial for health and survival. Now, an international team of scientists led by CeMM, AITHYRA and the Max Planck Institute of Molecular Physiology in Dortmund has identified a new class of small molecules that harness this natural system to accelerate the removal of an immune-modulating enzyme called IDO1. The findings, published in Nature Chemistry (DOI: 10.1038/s41557-025-02021-5), introduce a new concept in drug discovery that could transform how we target difficult proteins in cancer and beyond.