What Makes This New Breast Cancer Drug Different from Others

Scientists at Oregon Health & Science University created a molecule called SU212 that represents a fundamental shift in how researchers approach triple-negative breast cancer treatment.

Unlike conventional therapies that target rapidly dividing cells, this new drug attacks the energy production system that cancer cells depend on for survival.

The breakthrough was published in Cell Reports Medicine and tested using a humanized mouse model designed to closely simulate human biological responses.

The research team led by Dr. Sanjay Malhotra, co-director of the Center for Experimental Therapeutics at OHSU Knight Cancer Institute, demonstrated that SU212 successfully suppressed both tumor growth and metastasis in laboratory trials.

This achievement offers unprecedented hope for patients facing one of the most aggressive and treatment-resistant forms of breast cancer.

Triple-negative breast cancer currently lacks targeted therapies because it does not respond to hormone treatments or HER2-targeted drugs that work for other breast cancer types.

Why Is Triple-Negative Breast Cancer So Difficult to Treat

Triple negative breast cancer earned its name because tumor cells test negative for estrogen receptors, progesterone receptors, and HER2 protein, the three most common targets for breast cancer medications.

This absence of targetable markers leaves chemotherapy as the primary treatment option, which often proves inadequate for long-term disease control.

Approximately 15 percent of all breast cancer diagnoses fall into this category, affecting around 40,000 women annually in the United States alone.

The disease demonstrates particularly aggressive behavior with a high recurrence rate within the first three years following initial diagnosis.

Survival statistics reflect this severity, with overall five-year survival rates at 77 percent across all stages but dropping dramatically to just 12 percent for metastatic cases.

Patients with triple-negative breast cancer face higher rates of distant recurrence, particularly in visceral organs like the lungs, liver, and brain, compared to other breast cancer subtypes.

Did you know?
Triple negative breast cancer accounts for 15 percent of all breast cancers but has a five-year survival rate of only 12 percent when it spreads to distant organs, making it one of the deadliest forms of the disease.

How Does SU212 Attack Cancer Cells Differently

SU212 works by binding to and degrading the enzyme enolase 1 (ENO1), which plays a critical role in how cancer cells produce energy.

Traditional cancer drugs typically interfere with DNA replication or cell division mechanisms, affecting both cancerous and healthy rapidly dividing cells throughout the body.

This new approach specifically targets the metabolic pathway that cancer cells exploit to fuel their abnormal growth, potentially causing fewer side effects in normal tissues.

The molecule was initially developed during Dr. Malhotra's tenure at the National Cancer Institute in Bethesda, Maryland, and was further refined at Stanford University before arriving at OHSU in 2020.

In humanized mouse models, SU212 demonstrated the ability to suppress tumor growth and prevent metastatic spread by forcing cancer cells to degrade the ENO1 enzyme.

This metabolic disruption essentially starves cancer cells of the energy they need to proliferate and spread to other organs.

What Role Does ENO1 Play in Cancer Progression

Enolase 1 is a glycolytic enzyme that catalyzes the conversion of 2-phosphoglycerate to phosphoenolpyruvate, one of the final steps in glucose breakdown to produce cellular energy.

Cancer cells overexpress ENO1 compared with normal cells, enabling them to meet the high energy demands required for rapid, uncontrolled growth.

This overexpression correlates with increased glycolytic flux, enhanced tumor progression, and worse overall survival rates across multiple cancer types.

Research shows that ENO1 also serves functions beyond glucose metabolism, acting as a plasminogen receptor that can promote inflammatory responses supporting tumor development.

The enzyme helps cancer cells consume glucose at elevated rates by increasing the expression of glucose transporters on cell membranes.

Metabolic intermediates produced by this glucose consumption promote the biosynthesis of nucleotides, amino acids, and triglycerides, which are essential for cancer cell proliferation.

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Could This Treatment Help Diabetic Cancer Patients

Dr. Malhotra noted that SU212 may prove especially valuable for cancer patients who also suffer from diabetes, a metabolic disease characterized by high blood sugar levels.

Since the molecule targets how cells process glucose, it could potentially address both the cancer's energy metabolism and help regulate glucose levels in diabetic patients.

This dual benefit represents a unique advantage over conventional chemotherapy agents that often complicate diabetes management through side effects and drug interactions.

Beyond triple-negative breast cancer, researchers expect SU212 could treat other malignancies influenced by enolase one overexpression, including glioma, pancreatic cancer, and thyroid carcinoma.

Each of these cancer types exhibits elevated ENO1 levels, which contribute to aggressive growth and treatment resistance.

A drug that effectively inhibits enolase one across multiple cancer types could transform treatment protocols for some of the most challenging oncological conditions.

When Will Human Clinical Trials Begin

The research team's next priority is to move SU212 from laboratory studies into human clinical trials, a process that requires substantial funding, rigorous safety testing, and FDA regulatory approval.

OHSU's Center for Experimental Therapeutics, which Dr. Malhotra co-directs, focuses specifically on accelerating the translation of laboratory discoveries into treatments available to patients in hospitals and clinics.

This institutional commitment to rapid clinical application positions the SU212 project favorably for advancement through the drug development pipeline.

While no specific timeline has been announced for trial initiation, the successful humanized mouse model results provide strong justification for proceeding to human testing.

Humanized mouse models offer more accurate predictions of human responses compared to standard animal models, potentially reducing the risk of unexpected outcomes in early-phase clinical trials.

As research teams work to secure funding and complete regulatory requirements, patients and oncologists await this potentially transformative treatment option for one of breast cancer's most lethal forms.

The development of SU212 represents more than a single drug candidate; it signals a paradigm shift toward metabolic targeting in cancer therapy.

As scientists continue unraveling the complex relationship between cellular metabolism and cancer progression, treatments like SU212 may pave the way for an entirely new class of precision medicines that attack tumors where they are most vulnerable.