Researchers at the University of Alberta have uncovered promising evidence about zelenirstat, a novel drug developed by Pacylex Pharmaceuticals, demonstrating its potential to interrupt critical metabolic processes in triple-negative breast cancer (TNBC) cells. The findings, set to be presented at the American Association for Cancer Research (AACR) Annual Meeting, suggest the drug could provide a significant breakthrough in treating one of the most challenging forms of breast cancer.
The study reveals that zelenirstat effectively reduces complex I formation and oxidative phosphorylation within the mitochondria of TNBC cells. By disrupting these fundamental energy production mechanisms, the drug shows potential to impede cancer cell growth and survival. Critically, the research also demonstrated that zelenirstat can reduce the growth of TNBC stem cells, which could have profound implications for preventing cancer metastasis.
Dr. Luc Berthiaume, Chief Scientific Officer at Pacylex, emphasized the significance of these findings. Previous research had already shown zelenirstat's ability to disrupt growth signaling and energy production in acute myeloid leukemia cells. These new studies extend that understanding to aggressive breast cancer cells, highlighting the drug's potential versatility in cancer treatment.
The research is particularly significant because mitochondrial oxidative phosphorylation plays a crucial role in cancer stem cell survival and metastasis. These two processes are primarily responsible for cancer-related mortality and treatment resistance. By targeting these fundamental cellular mechanisms, zelenirstat offers a potentially innovative approach to cancer therapy.
Pacylex has already completed a Phase 1 multiple ascending dose study demonstrating zelenirstat's safety and tolerability. The drug has received both Orphan Drug Designation and Fast Track Designation from the FDA for acute myeloid leukemia treatment, underscoring its promising therapeutic potential.
While further research and clinical trials are needed, these findings represent a significant step forward in understanding how targeted molecular interventions might interrupt cancer cell metabolism. The potential to reduce cancer stem cell growth and metastasis could ultimately translate into more effective treatment strategies for patients battling aggressive cancers.
