OHSU Researchers Engineer SU212 Molecule to Disrupt Enzyme Pathways in Aggressive Triple-Negative Breast Cancer

OHSU scientists develop SU212 to disable a key enzyme in triple-negative breast cancer, shrinking tumors and slowing spread in breakthrough study.

By: AXL Media

Published: Mar 11, 2026, 11:42 AM EDT

Source: Information for this report was sourced from Oregon Health & Science University

Molecular Intervention in High-Risk Oncology

The OHSU Knight Cancer Institute has announced a significant advancement in the treatment of triple-negative breast cancer, a subtype known for its aggressive nature and lack of targeted therapies. Researchers have engineered an experimental molecule called SU212 that effectively neutralizes the enolase 1 (ENO1) enzyme, a biological catalyst that cancer cells exploit to sustain rapid growth. According to Sanjay V. Malhotra, Ph.D., senior author of the study published in Cell Reports Medicine, this discovery represents a critical step for a patient population that currently has very few effective pharmacological options. By disabling the metabolic engines of these tumors, the research offers a potential pathway for treating the roughly 15 percent of breast cancer cases that fall into this high-risk category.

Degradation of the ENO1 Metabolic Engine

The therapeutic mechanism of SU212 involves a process of targeted protein degradation. The molecule attaches itself to the ENO1 enzyme, which is typically found in abnormally high concentrations within malignant cells compared to healthy tissue. Once bound, SU212 causes the enzyme to physically break down, depriving the cancer cells of a primary regulator of glucose metabolism. Without the ability to efficiently convert glucose into energy, the tumors in humanized mouse models demonstrated a marked decrease in growth and a diminished capacity for metastasis. This strategy differs from traditional inhibitors by completely removing the offending enzyme from the cellular environment.

Implications for Patients with Metabolic Comorbidities

The link between cancer progression and glucose regulation suggests that this new treatment strategy could be particularly beneficial for specific patient demographics. Malhotra noted that because the ENO1 enzyme is central to how cells process sugar, the effectiveness of SU212 may have unique relevance for cancer patients who also manage metabolic disorders like diabetes. By disrupting the metabolic pathways that tumors use to thrive in high-sugar environments, the molecule addresses a critical intersection between chronic disease and oncology. This multifaceted approach aims to treat the cancer while acknowledging the broader physiological context of the patient.