On May 6, 2026 Racura Oncology, an Australian Phase 3 stage clinical biopharmaceutical company, reported the discovery of the primary mechanism of action (MOA) of its lead oncology asset, (E,E)-bisantrene. Bisantrene has a long clinical history of activity across a range of cancer indications, but its mechanism of action has been unknown.

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Preclinical studies undertaken by Racura and collaborators identified that (E,E)-bisantrene exerts its anticancer activity by binding to and stabilizing G-quadruplex (G4) DNA and RNA structures, key regulatory elements involved in controlling oncogene expression.

At the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, Racura presented new preclinical data demonstrating that (E,E)-bisantrene directly binds and stabilizes G4 DNA structures within the c-MYC gene promoter region, resulting in potent suppression of c-MYC expression and broad cytotoxic activity in a wide range of cancer models.[1][2]

The MYC protein functions as a master regulator of gene expression, governing thousands of genes involved in cell growth, differentiation, survival, metabolic reprogramming, chemotherapy resistance, and immune surveillance.[3] Crucially, MYC is the most commonly deregulated oncogene across human cancers, and has often been referred to as the ‘holy grail’ of targets due to its prevalence across many cancer indications. The promoter region of the c-MYC gene contains G4 DNA structures, which can suppress MYC expression when stabilized by drug binding.[4]

Race Oncology CEO and Managing Director, Dr Daniel Tillett said, "The discovery that (E,E)-bisantrene acts primarily by binding to G4-DNA structures leading to the inhibition of c-MYC expression fundamentally changes our thinking on how to best use this drug in the clinic.

This body of work significantly advances our understanding of (E,E)-bisantrene and highlights its potential as a best-in-class therapy targeting a central driver of cancer, MYC dysregulation."

(Press release, Racura Oncology, MAY 6, 2026, View Source [SID1234665239])