Race Oncology Cracks the Code on Bisantrene’s Anticancer Mechanism

Race Oncology (ASX: RAC) has delivered a scientific breakthrough that could reshape how its lead drug candidate, (E,E)-bisantrene (also known as RCDS1), is understood and used in cancer treatment. The company has discovered that the molecule works by binding to G-quadruplex (G4) DNA and RNA structures, rather than behaving like traditional chemotherapies such as doxorubicin.

The finding is not just academic — it has significant clinical and commercial implications.

G4 structures are unique three-dimensional configurations found throughout the genome and are critical in regulating the expression of cancer-driving genes such as MYC. By binding to these G4 regions, RCDS1 reduces the activity of MYC and other oncogenes, while also disrupting the function of key enzymes such as topoisomerase 2 and telomerase. This multifaceted mechanism gives RCDS1 a potentially powerful role in inhibiting cancer growth and overcoming resistance.

Race CEO Dr Daniel Tillett described the discovery as transformative.

“The discovery that (E,E)-bisantrene acts primarily through G4-DNA and RNA binding, and not as a doxorubicin-like agent, fundamentally changes our thinking on how best to use this drug in the clinic,” Tillett said. “Bisantrene continues to surprise, and we look forward to building on this mechanism of action discovery in our future clinical and commercial plans.”

This insight allows Race to better target cancers most likely to respond to RCDS1 and identify drug combinations with the highest potential for synergy. It also improves the ability to design biomarker-driven clinical trials, which are preferred by regulators and can increase the chance of successful drug approval.

Importantly, Race now positions RCDS1 not merely as a reimagined chemotherapy but as a novel targeted therapy in the emerging field of G4-DNA binding drugs. There are only a handful of such compounds currently in development worldwide, and none are yet approved.

The company’s work shows that RCDS1 downregulates MYC expression in a dose-dependent manner in various cancer cells. Given that MYC is overexpressed or dysregulated in over 70 percent of human cancers, this could open doors across multiple oncology indications.

Additionally, G4 binding has downstream effects on RNA modification systems, particularly increasing levels of m6A, a regulatory marker whose loss is associated with cancer aggressiveness. By indirectly boosting m6A through MYC downregulation and G4-RNA binding, RCDS1 may mimic the effects of inhibiting certain cancer-promoting enzymes without needing to target them directly.

Race will now pursue additional preclinical studies and refine its clinical strategy for RCDS1. The company is also exploring publication of the discovery in peer reviewed journals and presentations at upcoming scientific conferences.

With a more detailed understanding of how RCDS1 functions, Race can now engage with potential pharma partners from a position of greater scientific clarity — a major tick in the box for commercial discussions.