Racura Oncology Presents MYC Silencing Data at AACR Cancer Conference
Racura Oncology presents MYC silencing data at global cancer conference
Racura Oncology (ASX: RAC) presented preclinical mechanism of action data at the 2026 American Association of Cancer Research (AACR) Annual Meeting in San Diego (17-22 April 2026). The data demonstrates how (E,E)-bisantrene binds to and stabilises G-quadruplex (G4) structures in the c-MYC gene promoter region, leading to silencing of MYC gene expression—a key cancer driver described as a “master cell growth regulator.”
Dr Sumit Sahni, Racura Oncology Senior Scientist, delivered the poster presentation titled “(E,E)-bisantrene silences c-MYC expression by stabilizing its promotor region G-quadruplex.” The company states that the presentation data supports its current and planned clinical trials across multiple oncology indications.
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What is MYC and why does silencing it matter for cancer treatment?
The c-MYC gene regulates cell growth and division. When overactive, it drives cancer progression across multiple tumour types, making it a critical target in oncology research. MYC has historically been considered “undruggable” due to its structure and cellular function.
G-quadruplex (G4) structures are non-canonical DNA and RNA secondary structures that play key roles in gene regulation. These structures form in specific sequences of genetic material and influence whether genes are switched on or off. (E,E)-bisantrene stabilises the G4 structure located in the c-MYC promoter region, effectively “turning off” MYC expression by preventing the gene from being read and translated into proteins that drive cancer cell growth.
If (E,E)-bisantrene can reliably silence MYC, it addresses a mechanism relevant across multiple cancer types, supporting Racura’s multi-indication clinical strategy.
Key preclinical findings from the AACR presentation
The research team employed multiple experimental methods to characterise how (E,E)-bisantrene interacts with the c-MYC G4 structure. Techniques included circular dichroism spectroscopy, surface plasmon resonance, nuclear magnetic resonance, molecular dynamics simulations, qPCR gene expression analysis, and RNA-sequencing with pathway analysis.
Binding affinity studies revealed that (E,E)-bisantrene binds to c-MYC G4 with a dissociation constant (Kd) of 208 nM and shows approximately 1.5-fold selectivity over a mutant double-stranded DNA sequence. Nuclear magnetic resonance spectroscopy determined a 2:1 binding stoichiometry (two molecules of (E,E)-bisantrene to one c-MYC G4 structure).
Gene expression experiments demonstrated that treatment of breast (MDA-MB-231) and lung (PC-9, PC-9-Osimertinib-resistant) cancer cells dose-dependently suppressed c-MYC expression within two hours. The half maximal effective concentrations (EC50) were 322.5 nM for MDA-MB-231 cells, 349.9 nM for PC-9 cells, and 518.1 nM for PC-9-Osimertinib-resistant cells.
RNA-sequencing analysis showed that gene set enrichment analysis identified the most strongly downregulated pathways as related to c-MYC. The transcriptomic profile produced by (E,E)-bisantrene was similar to that of CX-5461 (Pidnarulex), a known G4-binding comparator currently under investigation.
| Measurement | Result |
|---|---|
| Binding affinity (Kd) to c-MYC G4 | 208 nM |
| Selectivity vs mutant dsDNA | ~1.5-fold |
| Binding stoichiometry | 2:1 |
| EC50 (MDA-MB-231 breast cancer) | 322.5 nM |
| EC50 (PC-9 lung cancer) | 349.9 nM |
| EC50 (PC-9-Osimertinib-resistant) | 518.1 nM |
These findings provide mechanistic validation for the clinical programmes currently underway, demonstrating that (E,E)-bisantrene engages its intended target at therapeutically relevant concentrations.
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How the data supports Racura’s clinical pipeline
Racura describes the presentation data as supporting “current and planned clinical trials” across its development programmes. The company is advancing clinical programmes with its proprietary formulation of (E,E)-bisantrene (RC220):
- Phase 3 programme in acute myeloid leukaemia (AML)
- Phase 1a/b programme in mutant EGFR non-small cell lung cancer (EGFRm NSCLC) — in combination with osimertinib (Australia New Zealand Clinical Trial Registration #2626000325303)
- Phase 1a/b programme in combination with doxorubicin for solid tumours — aims to deliver cardioprotection and enhanced anticancer activity (ClinicalTrials.gov ID: NCT06815575)
Racura’s composition of matter intellectual property filings provide 20 years of patent protection over (E,E)-bisantrene. The mechanism of action data de-risks the scientific thesis across all three clinical programmes simultaneously, as MYC dysregulation is implicated in multiple cancer types.
Management commentary
Dr Sumit Sahni, Racura Oncology Senior Scientist
“It was a privilege to be chosen to present Racura’s mechanism of action data at the leading annual international cancer conference, AACR. I sincerely thank my preclinical team colleagues and our valued collaborators for their outstanding work that has uncovered the primary mechanism by which (E,E)-bisantrene exerts its anticancer activity. The strong interest and positive reception this work received at the conference is very encouraging.”
The preclinical work was conducted in collaboration with Astex, Emory University, Purdue University, MD Anderson, Sheba City of Health, UNC School of Medicine, University of Wollongong, and University of Newcastle. These partnerships have enabled Racura to generate comprehensive data characterising the drug’s mechanism of action and supporting its clinical development strategy.
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