Researchers at Oregon Health & Science University have developed the molecule SU212, which targets the enzyme enolase 1 (ENO1), which is crucial for the growth of triple-negative breast cancer.[1][3] This form of cancer accounts for up to 15% of all breast cancers and is highly aggressive without effective targeted therapies.[1][3] SU212 binds ENO1 at a non-orthosteric site, leading to its degradation and limiting the glycolytic activity of cancer cells.[2][3] In humanized mouse models, including syngeneic, genetic, and patient-derived xenografts, the molecule shrank tumors, suppressed metastasis, and reduced glucose uptake.[1][3] The study was published in Cell Reports Medicine on November 7, 2025.[1][3] In the SU212 diabetic mouse model, it demonstrated antitumor efficacy, improved fatty liver disease, and lowered blood sugar levels.[3] The molecule exhibits a favorable pharmacokinetic profile with minimal toxicity and no effect on key biological systems.[3] ENO1 is overexpressed in cancer cells and promotes the Warburg effect, characteristic of cancer metabolism.[3]