Racura Oncology Ltd · ASX:RAC
Racura Oncology — Race Oncology — Technical Presentation (October 2025)
20 slides from Racura Oncology's technical presentation, October 2025
Slide 1: At the Heart of Cancer Care: Anticancer MOA Webinar
O c t o b e r 2 0 2 5 A T T H E H E A R T O F C A N C E R AT THE C A R E HEART OF CANCER CARE Dr Daniel Tillett – CEO Dr Pete Smith – Exec Chair Anticancer MOA Webinar 0 ASX: RAC | RACE ONCOLOGY LIMITED | ABN 61 149 318 749 11
Slide 2: Important Notice and Disclaimer
Important Notice and Disclaimer A T T H E The material in this presentation has been prepared by Race Oncology Limited (ACN 149 318 749) (Company). H E A R T THIS IS NOT A PROSPECTUS This presentation is not a prospectus, product disclosure statement or disclosure document for the purposes of the Co
Slide 3: How does (E,E)-bisantrene work?
How does (E,E)-bisantrene work? A T T H E • In our DNA & RNA there exist special folded structures called G-quadruplexes H E A R T (G4) O F • G4 structures act like switches that control many of the important genes that C A N C E R cause or allow cancer to grow • (E,E)-bisantrene binds to and stabil
Slide 4: What are G-quadruplexes?
What are G-quadruplexes? A T T H E • Key regulatory structures which bind to specific transcription and H E A R T translation factors to regulate cell growth and division in DNA & RNA O F • Stabilised by Hoogsteen hydrogen base pairing between G bases to form a C A N C E R planar array that is furth
Slide 5: Discovery of the G4 Mechanism of Action
A T T H E H E A R T O F C A N C E R C A R E Discovery of the G4 Mechanism of Action 555
Slide 6: The many anticancer effects of bisantrene
The many anticancer effects of bisantrene A T T H E H E A R T • (E,E)-bisantrene has a large number of seemingly unrelated anticancer activities O F • Inhibits DNA replication & RNA transcription C A N C E R • Inhibits angiogenesis • Inhibits telomerase and cell division (G4-binding) C A R E • Inhib
Slide 7: First clue – not an anthracycline
First clue – not an anthracycline A T T H E H E A R T • Cluster analysis of the anticancer responses O F of 195 drugs across 102 cancer cell lines C A N C E R • RCDS1 grouped with an unrelated group of drugs including G4 binders C A R E 7
Slide 8: Second clue – downregulates MYC
Second clue – downregulates MYC A T T H E H E A R T O F 150 C A N C E R MYC Expression (%) EC50: 322.5 + 42.6 nM C A R E 100 50 0 10 100 1000 10000 RCDS1 RCDS1 (nM) 8
Slide 9: Third clue – G4 in RNA increase m6A levels
Third clue – G4 in RNA increase m6A levels A T T H E H E A R T • Bisantrene has been previously described to inhibit FTO and increase O F global levels of m6A in RNA C A N C E R • METTL14/METLL3 complex bind to RNA G4s leading to increased m6A in C A R E adjacent adenine present in the linker region
Slide 10: Eureka – (E,E)-bisantrene acts via G4-binding
Eureka – (E,E)-bisantrene acts via G4-binding A T T H E H E A R T • In early 2025 realised all anticancer activities of (E,E)-bisantrene can be explained by it O F acting as G4-DNA & RNA stabilising drug C A N C E R • Bisantrene known to be a G4-binder since C A R E 2010 – little attention paid to t
Slide 11: Model of (E,E)-bisantrene bound to the G4 structure in c-myc promoter
Model of (E,E)-bisantrene bound the G4 structure found in c-myc gene promoter region A T T H E H E A R T O F C A N C E R C A R E 11
Slide 12: MYC – the 'undruggable' cancer target
A T T H E H E A R T O F C A N C E R C A R E Chemistry MYC – the& Discovery ‘undruggable’ cancer target 12 12
Slide 13: MYC - background
MYC - background A T T H E • MYC discovered in 1982 H E A R T • It is still considered to be ‘undruggable’ O F C A N C E R • No direct inhibitors in pharma pipelines • Much of the protein is unstructured and difficult to target C A R E MYC/MAX • MYC regulates expression of 2,000-4,000 genes heterodi
Slide 14: MYC & cancer
MYC & cancer A T T H E % of major cancers with elevated MYC • MYC is a ‘holy grail’ target in oncology H E A R T activity • ~70% of all malignancies have increased O F MYC activity C A N C E R • >1m new cases of cancer with elevated MYC C A R E activity annually in the US • Implicated in all the ‘Ha
Slide 15: What are the causes of MYC upregulation?
What are the causes of MYC upregulation? A T T H E H E A R T • 30-40% of MYC upregulation is due to other signalling pathways being activated/mutated e.g. WNT, Notch, O F growth factors C A N C E R • 28–35% gene amplification or chromosomal alterations C A R E • 10–20%, epigenetic deregulation • 15–
Slide 16: MYC drives all of the 'Hallmarks of Cancer'
MYC drives all of the ‘Hallmarks of Cancer’ A T T H E H E A R T O F C A N C E R C A R E 16
Slide 17: Commercial significance
17 A T T H E H E A R T O F C A N C E R C A R E Commercial significance
Slide 18: Why does any of this matter for investors?
Why does any of this matter for investors? A T T H E H E A R T Knowing the MOA of a drug... O F C A N C E R • Makes it much simpler to identify the cancer type(s) and/or drug combinations that will work C A R E best • Reduces risk by highlighting potential toxicities arising from off- and on-target
Slide 19: Questions
A T T H E H E A R T O F C A N C E R C A R E Questions Race Oncology 19 A T T H E H E A R T O F C A N C E R C A R E 19
Slide 20: Contact
A T T H E H E A R T O F C A N C E R C A R E Contact P E T E S M IT H Executive Chair JA N E L O W E Investor & Media Relations +61 2 8051 3043 +61 411 117 774 peter.smith@raceoncology.com jane.lowe@irdepartment.com.au www.raceoncology.com Authorised for release by the Board ASX: RAC | RACE ONCOLOGY
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