How Race Oncology’s Drug Targets the ‘Undruggable’ MYC Oncogene

A Paradigm Shift in Understanding Bisantrene

Race Oncology Limited has announced a significant scientific breakthrough in the understanding of its lead anticancer drug candidate, (E,E)-bisantrene (RCDS1). Contrary to previous assumptions that it acted similarly to anthracycline chemotherapies like doxorubicin, new research reveals that bisantrene’s primary anticancer activity stems from its ability to bind and stabilise G-quadruplex (G4) DNA and RNA structures. These unique four-stranded configurations are found throughout the human genome and play a crucial role in regulating gene expression, including that of oncogenes such as MYC.

This discovery fundamentally changes the clinical and commercial outlook for bisantrene, positioning it as a targeted agent that modulates cancer-driving genetic mechanisms rather than a conventional chemotherapy with broad DNA damage effects.

Targeting the Master Regulator MYC

The MYC gene is a master regulator implicated in over 70% of human cancers, controlling cell growth, metabolism, and survival pathways. Historically, MYC has been considered “undruggable” due to its protein structure lacking suitable binding sites for small molecule inhibitors. By stabilising G4 structures within the MYC promoter region, bisantrene effectively downregulates MYC expression, thereby suppressing oncogenic signalling and tumour proliferation.

Race Oncology’s data demonstrate a dose-dependent reduction of MYC expression in cancer cell models shortly after treatment with RCDS1, highlighting a promising mechanism to overcome longstanding challenges in targeting this critical oncogene.

Broader Implications of G4 Binding

Beyond MYC, the G4-binding activity of bisantrene inhibits enzymes such as topoisomerase II and telomerase, both vital for cancer cell replication and immortality. Additionally, it indirectly increases levels of m6A RNA methylation, a modification linked to gene expression regulation and cancer progression. These multifaceted effects suggest a broad anticancer potential with the possibility to modulate treatment resistance and enhance efficacy.

Importantly, this mechanism distinguishes bisantrene from traditional anthracyclines, which are often limited by cardiotoxicity. Race Oncology’s proprietary formulation, RC220, aims to leverage these unique properties to deliver safer and more effective cancer therapies.

Clinical and Commercial Pathways Forward

Understanding the precise mechanism of action enables Race Oncology to strategically identify cancer types most likely to respond to bisantrene and rationally design combination therapies. This targeted approach can streamline clinical development, reduce trial risks, and improve patient outcomes.

Moreover, the mechanistic insights facilitate the development of pharmacodynamic biomarkers predictive of treatment response, a factor known to increase the likelihood of regulatory approval. From a commercial perspective, clarity on the drug’s action enhances attractiveness for pharma partnerships, licensing, and potential mergers, all critical for accelerating global patient access.

Next Steps and Industry Engagement

Race Oncology plans to advance additional preclinical studies to further elucidate bisantrene’s G4-binding effects and identify optimal clinical indications and drug combinations. The company also intends to publish these findings in peer-reviewed journals and present at major oncology conferences, including the upcoming European Society of Medical Oncology (ESMO) Annual Conference.

Investors and stakeholders are invited to a webinar hosted by Race’s CEO, Dr Daniel Tillett, to discuss the significance of this discovery and its implications for the company’s clinical and commercial strategy.