Racura Oncology Ltd · ASX:RAC
Racura Oncology — Investor Day (March 2026)
148 slides from Racura Oncology's investor day presentation, Mar 24, 2026
Slide 1: Racura R&D Symposium Presentation (ASX Announcement)
ASX Announcement Racura R&D Symposium Presentation 24 March 2026 Racura Oncology Limited (“Racura”) is pleased to share the presentation for the inaugural Racura Oncology Research & Development Symposium, being held at Museum of Sydney from 2.30pm today. CEO and Managing Director, Dr Daniel Tillett
Slide 2: Collaborations and release details
Racura Oncology has collaborated with Astex, Emory University, Purdue University, MD Anderson, Sheba City of Health, UNC School of Medicine, University of Wollongong, and University of Newcastle. Racura is actively exploring partnerships, licence agreements, or a commercial merger and acquisition to
Slide 3: Racura Oncology Symposium
Racura Oncology Symposium Sydney, 24 March 2026
Slide 4: Welcome
Welcome Dr Pete Smith, Executive Chair
Slide 5: Important notice and disclaimer
Important notice and disclaimer The material in this presentation has been prepared by Racura Oncology Limited (ACN 149 318 749) (Company). THIS IS NOT A PROSPECTUS This presentation is not a prospectus, product disclosure statement or disclosure document for the purposes of the Corporations Act 200
Slide 6: Agenda
Agenda Time Session Presenters 2.30pm Welcome Dr Pete Smith 2.35pm Opening remarks Dr Daniel Tillett 2.40pm Science behind Racura Oncology Prof Mike Kelso & Prof Laurence Hurley 3.25pm CPACS clinical program A/Prof Erin Howden & Dr Marinella Messina 3.50pm HARNESS-1 clinical program Prof Nick Pavlak
Slide 7: Opening remarks
Opening remarks Dr Daniel Tillett, CEO & MD
Slide 8: What makes Racura Oncology unique?
What makes Racura Oncology unique? Addressing major clinical markets with a clinical proven drug and the team to deliver • Clinically derisked – our drug works! o Previously approved for AML in France (1988) • Clinical problems that needed to be solved are those that are tractable • We are targeting
Slide 9: Standard oncology drug development process
Standard oncology drug development process Slow, expensive, and high risk Scientific Confirmation Science discovery target is real (new target) (1-2 years) Drug Lead identification Lead optimisation Patenting Discovery (1-3 years) (1-2 years) 0.1% chance of success with US$2.8B average cost1 IND Non
Slide 10: Racura Oncology drug development challenge
Racura Oncology drug development challenge Systematically solving tractable scientific and clinical problems in cost effective manner Scientific Confirm Science discovery target is real (new target) Drug Lead Lead Patenting Discovery identification optimisation IND Non-clinical toxicology Drug cGMP
Slide 11: Racura Oncology drug development success
Racura Oncology drug development success Systematically solving tractable scientific and clinical problems in cost effective manner Scientific Confirm Science discovery target is real (new target) Drug Lead Lead Patenting Discovery identification optimisation IND Non-clinical toxicology Drug cGMP dr
Slide 12: Racura Oncology drug development success
Racura Oncology drug development success Systematically solving tractable scientific and clinical problems in cost effective manner Scientific Confirm Science discovery target is real (new target) Drug Lead Lead Patenting Discovery identification optimisation IND Non-clinical toxicology Drug cGMP dr
Slide 13: Racura Oncology drug development success
Racura Oncology drug development success Systematically solving tractable scientific and clinical problems in cost effective manner Scientific Confirm Science discovery target is real (new target) Drug Lead Lead Patenting Discovery identification optimisation IND Non-clinical toxicology Drug cGMP dr
Slide 14: What have we accomplished at Racura Oncology?
What have we accomplished at Racura Oncology? Science Patents IND enabling Clinical trials Discovered (E,E)-bisantrene Filed new composition of Completed non-clinical data Designed clinical program to and how it works matter patent based on package optimise commercial value Identified where the drug
Slide 15: Science behind Racura Oncology
Science behind Racura Oncology Prof Mike Kelso, Vice President of Research, Racura Oncology Emeritus Prof Laurence Hurley, R. Ken Coit College of Pharmacy, University of Arizona
Slide 16: Agenda: Science behind Racura Oncology
Agenda: Science behind Racura Oncology Topic Presenter Introduction: What are G-quadruplexes? Prof Mike Kelso G-quadruplex as a drug target Emeritus Prof Laurence Hurley Importance of MYC as a cancer driver Prof Mike Kelso (E,E)-bisantrene mechanism of action: MYC regulation by G-quadruplex Prof Mik
Slide 17: (E,E)-bisantrene: G-quadruplex stabiliser & silencer of MYC transcription
(E,E)-bisantrene: G-quadruplex stabiliser & silencer of MYC transcription Modern science has uncovered the mechanism of action (MOA) of (E,E)-bisantrene (E,E)-bisantrene binds to and stabilises G-quadruplex DNA, leading to silencing of the MYC oncogene Racura ASX Announcement: 2 Oct 2025 15
Slide 18: What are G-quadruplexes?
Guanine What are G-quadruplexes? Guanine Key regulatory structures in DNA (& RNA) recognised by transcription & translation factors to regulate cell growth & division1 Guanine Guanine G tetrad G-quadruplex (G4) DNA Double stranded DNA G-Quadruplex DNA (G4) (double helix) 5’-GAGGGTGGGGAGGGTGGGG-3’ 1.
Slide 19: G-quadruplex video
The image features an architectural depiction of the University of Arizona's buildings, with an overlay of text highlighting Laurence H. Hurley's work on DNA G-Quadruplexes as a novel cancer research target. AI-generated content may be incorrect. Please scan QR code to view the video 17
Slide 20: MYC & cancer
MYC & cancer Clinically effective MYC-targeting drugs are needed MYC has long been considered the ‘holy grail’ of oncology drug targets Percentage of major cancers with elevated MYC activity 1 1. Data from TCGA and Schaub FX et al (2018) Cell Syst, 6(3):282–300 18
Slide 21: MYC & cancer
MYC & cancer Clinically effective MYC-targeting drugs are needed MYC is a difficult drug target Effective MYC-targeting drugs have proven elusive Is targeting MYC via G-quadruplex the solution? Percentage of major cancers with elevated MYC activity 1 1. Data from TCGA and Schaub FX et al (2018) Cell
Slide 22: (E,E)-bisantrene mechanism of action video
(E,E)-bisantrene mechanism of action video The image depicts a curved, metallic structure with a logo, symbolizing the molecular structure of (E,E)-bisantrene, a compound related to oncology. AI-generated content may be incorrect. Please scan QR code to view the video 20
Slide 23: MYC regulation by promotor region G-quadruplex
MYC regulation by promotor region G-quadruplex Promoter Region MYC (E,E)-bisantrene silences MYC production and its ability to bisantrene bisantrene drive cancer progression (E,E)- (E,E)- RNA Pol-II OFF G-quadruplex Please scan QR code for animation MYC Nucleus 21
Slide 24: Scientific evidence
Scientific evidence (E,E)-bisantrene silences MYC via G-quadruplex binding
Slide 25: NMR analysis of MYC G-quadruplex binding by (E,E)-bisantrene
1H nuclear magnetic resonance (NMR) analysis of MYC G-quadruplex binding by (E,E)-bisantrene Two (E,E)-bisantrene molecules bind to each MYC G4 structure (E,E)-bisantrene G-tetrad MYC-G4 Data on file 23
Slide 26: Molecular dynamics simulation of (E,E)-bisantrene binding to MYC G-quadruplex
Molecular dynamics simulation of (E,E)-bisantrene binding to MYC G-quadruplex Simulation showing (E,E)-bisantrene seeks out and binds to G-quadruplex structures The image depicts a colorful, abstract representation of molecular structures, with distinct red, blue, and green elements arranged in a co
Slide 27: Molecular dynamics simulation of (E,E)-bisantrene binding to MYC G-quadruplex
Molecular dynamics simulation of (E,E)-bisantrene binding to MYC G-quadruplex Snapshot shows two (E,E)-bisantrene molecules binding to the top and bottom G-tetrads of the G- quadruplex The image depicts a complex three-dimensional structure of a protein molecule, highlighting various molecular inter
Slide 28: Binding affinity of (E,E)-bisantrene to MYC G4
Binding affinity of (E,E)-bisantrene to MYC G4 (E,E)-bisantrene binds the MYC G-quadruplex with high affinity at clinically relevant concentrations Surface Plasmon Resonance spectroscopy MYC G4 KD (nM) 208 (E,E)-bisantrene 100 80 Response (RU) G-quadruplex 1000 nM (E,E)-bisantrene 60 40 20 0 nM 0 0
Slide 29: Stabilisation of MYC G4 by binding to (E,E)-bisantrene
Stabilisation of MYC G4 by binding to (E,E)-bisantrene Increase in MYC G-quadruplex melting temperature in the presence of (E,E)-bisantrene Circular dichroism spectroscopy MYC G4 Melting Curve MYC G4 Melting Temperature ✱✱✱ Molar Ellipticity at 265 nm (θ) 3000 MYC G4 MYC G4 + (E,E)-bisantrene 80 Mel
Slide 30: MYC gene expression analysis
MYC gene expression analysis (E,E)-bisantrene dose dependently silences MYC expression in human breast & lung cancer cells Cell line Cancer type EC50 (nM) 100 MDA-MB-231 Breast cancer 322 ± 43 PC-9 NSCLC 350 ± 63 MYC Expression (%) PC-9-Osi-R NSCLC 518 ± 85 50 (E,E)-bisantrene MYC 0 10 100 1000 1000
Slide 31: Evidence summary
Evidence summary (E,E)-bisantrene binds to and stabilises MYC G-quadruplex, silencing MYC in cancer cells Molecular dynamics 4000 DNA G4 2000 Molar Ellipticity (θ) 0 -2000 1H-NMR 200 250 300 350 Wavelength (nm) Circular (E,E)-bisantrene binding dichroism and stabilisation of MYC G4 Gene expression S
Slide 32: Importance of MYC in resistance to targeted therapies
Importance of MYC in resistance to targeted therapies MYC drives both cancer progression and resistance to targeted therapies 30
Slide 33: (E,E)-bisantrene: broad synergy with targeted agents
(E,E)-bisantrene: broad synergy with targeted agents Tyrosine kinase inhibitors (TKIs) – ccRCC/NSCLC mTOR inhibitors (ccRCC) Lenvatinib (M) Pazopanib (M) Cabozantinib (M) Everolimus (M) Temsirolimus (M) 0 1.25 2.5 5 10 20 0 1.25 2.5 5 10 0 1.25 2.5 5 10 20 0 1.25 2.5 5 10 20 0 0.13 0.25 0.5 1 2
Slide 34: Which unmet needs in oncology are MYC-driven?
Which unmet needs in oncology are MYC-driven and have the best clinical & commercial opportunity? Acquired resistance to osimertinib in EGFRm non-small cell lung cancer “…suggests targeting MYC as a potential strategy to overcome osimertinib acquired resistance.” Zhu L et al (2021) Cancer Res, 81(18
Slide 35: Preclinical support for EGFRm NSCLC program
Preclinical support for EGFRm NSCLC program
Slide 36: MYC silencing by (E,E)-bisantrene and bypass resistance
MYC silencing by Bypass Resistance Mechanisms (E,E)-bisantrene EGFR EGFRm MET HER2 IGFR1 FGFR EGFRm cancer cell Nucleus bisantrene (E,E)- Please scan QR code for animation Tumour Cell Proliferation Osimertinib Resistance EGFRm, epidermal growth factor receptor mutant; MAPK, mitogen- activated protei
Slide 37: EGFRm NSCLC RNA-seq analysis
EGFRm NSCLC RNA-seq analysis (E,E)-bisantrene upregulates (red) and downregulates (blue) many genes in lung cancer cell lines EGRFm NSCLC cell line: PC-9 EGRFm NSCLC cell line: NCI-H820 (E,E)-bisantrene vs control (E,E)-bisantrene vs control Data on file | EGFRm, epidermal growth factor receptor mut
Slide 38: EGFRm NSCLC RNA-seq: pathway analysis
EGFRm NSCLC RNA-seq: pathway analysis Pathways most strongly downregulated by (E,E)-bisantrene relate to MYC EGRFm NSCLC cell line: PC-9 EGRFm NSCLC cell line: NCI-H820 HALLMARK_MYC_TARGETS_V2 HALLMARK_MYC_TARGETS_V2 HALLMARK_MYC_TARGETS_V1 Data on file | EGFRm, epidermal growth factor receptor muta
Slide 39: RC220 highly active in combination with osimertinib
RC220 highly active in combination with osimertinib RC220 restores sensitivity to osimertinib in osimertinib-resistant EGFRm NSCLC models Osimertinib resistant models 1500 PC-9/AR cells 1200 TM00784 PDX Vehicle Osimertinib 1200 900 RC220 Tumour size (mm3) Tumour size (mm3) 900 Osimertinib + RC220 P
Slide 40: RC220 highly active in combination with osimertinib
RC220 highly active in combination with osimertinib RC220-osimertinib combination delayed relapse in EGFRm NSCLC mouse models Osimertinib sensitive model (19.2) 2000 Vehicle Osimertinib Osimertinib + RC220 1500 Tumour size (mm3) 1000 Stop treatment 500 0 0 7 14 21 28 35 42 49 56 Treatment time (day)
Slide 41: RC220 highly active in combination with osimertinib
RC220 highly active in combination with osimertinib RC220-osimertinib combination increased survival in EGFRm NSCLC mouse models Osimertinib sensitive model (19.2) Median (95%CI) Days 120 Osimertinib 35 Probability of survival (%) 100 Osimertinib + RC220 49 80 Hazard ratio for death 60 (Osimertinib
Slide 42: Preclinical support for AML program
Preclinical support for AML program
Slide 43: MYC dependence in AML
MYC dependence in AML AML is one of the most MYC driven of all cancers • Acute myeloid leukaemia ~90% • Burkitts lymphoma: >90% • Plasmablastic lymphoma: ~50% • B-cell acute lymphoblastic leukaemia ➢ General/adult: ~5% ➢ Paediatric/relapse: 30-65% • T-cell acute lymphoblastic leukaemia: >50% • Chron
Slide 44: AML RNA-sequencing
AML RNA-sequencing (E,E)-bisantrene potently suppressed MYC-mediated downstream pathways in AML cells Pathway analysis in AML (MOLM-13) cells (E,E)-bisantrene vs control -Log10(p value of overlap) 100 TP53 80 TGFB1 60 PPARD MYC CDKN1A ERRB2 IFNG 40 TNF CDKN2A TGM2 20 0 -15 -10 -5 0 5 10 15 Z-Score D
Slide 45: (E,E)-bisantrene is highly effective in AML
(E,E)-bisantrene is highly effective in AML Significant increase in survival observed after (E,E)-bisantrene treatment in mouse AML models Cell Derived Xenograft Patient Derived Xenograft MOLM-13 AML-16 100 Vehicle 100 Percentage Survival Percentage Survival ✱ Vehicle (E,E)-bisantrene (5 mg/kg) ** *
Slide 46: Preclinical support for CPACS program
Preclinical support for CPACS program
Slide 47: How does MYC relate to (E,E)-bisantrene cardioprotection?
How does MYC relate to (E,E)-bisantrene cardioprotection? Molecular Cell paper (2022) suggests role for MYC in cardioprotection1 (E,E)-bisantrene reduces doxorubicin- induced double strand breaks 2 100 (E,E)-bisantrene + Doxorubicin (Relative to Doxorubicin) % Double Strand Breaks * 75 * 50 *** 25 *
Slide 48: MYC silencing by (E,E)-bisantrene reduces DSBs
MYC silencing by (E,E)-bisantrene reduces DSBs Cardiac cell TOP2 DOX Inhibitor Cardioprotection bisantrene (E,E)- Nucleus Cytoplasm Please scan QR code for animation 46 TOP1, topoisomerase I; TOP2,topoisomerase II; MAX, Myc-associated factor X; DBS, double-strand breaks
Slide 49: Science summary
Science summary Through rigorous science, Racura Oncology has discovered how (E,E)-bisantrene silences MYC (E,E)-bisantrene binds and stabilises G-quadruplex in MYC MYC G-quadruplex gene promoter region MYC expression (E,E)-bisantrene silences MYC expression in cancer cells MYC activity (E,E)-bisant
Slide 50: Preclinical team
Preclinical team Prof Michael Kelso Sumit Sahni, PhD Feroz Ahmad, PhD David Bourke, PhD Vice President of Senior Scientist Senior Scientist Senior Manager, CMC Research Peter Cuthbertson, Emily Ryan Chelsea Penney PhD Associate Scientist Research Associate Scientist 48
Slide 51: Questions
ONCOLOGY Questions
Slide 52: Clinical programs
Clinical programs Overview of Racura Oncology’s clinical trials
Slide 53: Clinical pipeline
Clinical pipeline Three phase 1-3 clinical programs in AML, lung cancer and solid tumours Total addressable Cancer indication Phase 1 Phase 2 Phase 3 Comment patients1 40% response rate in Phase 3 AML two Phase 2 trials3 US/EU: 50,000 Phase 3 Acute myeloid leukaemia 2 Bisantrene approved in 1988 in
Slide 54: Clinical team
Clinical team Rodney Cusack, Dr Simon Fisher Corli Merry Dr Anupa Kudva, PhD MBBS MD Senior Clinical Principal Scientist Vice President & Quality Mgr Medical Director of Medical Dr Jose Iglesias Marinella Messina, Kirsten Curnow, Michelle Huh MBBS FRACP PhD PhD Clinical Trials Chief Medical Vice Pre
Slide 55: CPACS clinical program
CPACS clinical program A/Prof Erin Howden, Exercise Physiology, University of New South Wales Dr Marinella Messina, Vice President of Clinical, Racura Oncology
Slide 56: Agenda: CPACS
Agenda: CPACS Topic Presenter Cardiotoxicity, patient journey & unmet need A/Prof Erin Howden CPACS trial Dr Marinella Messina 54
Slide 57: Cardiotoxicity, patient journey & unmet need
Cardiotoxicity, patient journey & unmet need Associate Professor Erin Howden
Slide 58: My research program: Exercise as a framework
My research program: Exercise as a framework to understand mechanisms and inform treatment of people at risk of heart failure Inspired Oxygen Oxygen Utilization Cascade Adaptive Capability of Cardiovascular System Howden et al., Circulation 2021; La Gerche, Howden et al., JACC 2022
Slide 59: What's this got to do with people being treated for cancers?
What’s this got to do with people being treated for cancers?
Slide 60: Cancer accelerates cardiometabolic aging
“CANCER” accelerates cardiometabolic aging Anthracycline Chemotherapy Exercise Training? Criscitello et al. Breast Can Res 2012; Howden et al. Eur J Prev Cardiol 2018
Slide 61: HFpEF, heart failure with preserved ejection fraction
HFpEF, heart failure with preserved ejection fraction
Slide 62: Impact of systemic anticancer treatment on VO2peak
CENTRAL ILLUSTRATION: Impact of Systemic Anticancer Treatment on Vo2peax During and After Therapy Effect of Systemic Anticancer Treatment o cn Systematic review of 44 studies comprised of 27 prospective trials and 17 cross-sectional studies (n = 2,606 cancer survivors, median age 52.7 years; n = 1,9
Slide 63: Prospective patient cohort before treatment
• 206 patients prospectively enrolled before commencing treatment - 53±13y, 35% male • Mixed cancer diagnosis – majority breast or haematological cancers - 53% Anthracycline; 19% BTK; 19% Allogeneic Stem Cell Transplant; 10% ADT
Slide 64: Howden et al., EHJ CVI 2021; Bonsignore et al., JACC CO 2021
Howden et al., EHJ CVI 2021; Bonsignore et al., JACC CO 2021
Slide 65: Post-diagnosis cardiorespiratory fitness and mortality
Post-diagnosis cardiorespiratory fitness is associated with cause-specific mortality For each 1 MET Increase in CRF all-cause, CV, and cancer mortality decreased by 26%, 14%, and 25% Groarke et al., EHJ - Quality of Care and Clinical Outcomes 2020 CRF, cardiorespiratory fitness; CV, cardiovascular;
Slide 66: HFpEF, heart failure with preserved ejection fraction
HFpEF, heart failure with preserved ejection fraction
Slide 67: VO2 peak impaired in breast cancer survivors after anthracyclines
In breast cancer survivors, VO2 peak remains impaired >1 year post completion of anthracycline treatment Foulkes, Howden et al., MSSE 2019
Slide 68: Reduced VO2 peak and impaired exercise cardiac function
Reduced VO2 peak is associated with impaired exercise cardiac function in breast cancer survivors Foulkes, Howden et al., MSSE 2019
Slide 69: Reduced VO2 peak not explained by impaired cardiac function
Reduced VO2 peak in breast cancer survivors is not completely explained by impaired cardiac function Foulkes et al., JACC CO 2024 | VO₂, volume of oxygen; SaO₂, arterial oxygen saturation; HR, heart rate; SV, stroke volume; LVEDV, left ventricular end diastolic volume; LVEF, left ventricular ejectio
Slide 70: Correcting one O2 parameter defect
Correcting one O2 parameter defect Performance increase = Limited
Slide 71: Changing multiple parameters – not only the engine matters
Changing multiple parameters – not only the engine matters More profound increase in performance
Slide 72: We need new solutions
We need new solutions ~50% increase in # cases per year Heart disease is the most common cause of death GBD 2023 Breast Cancer Collaborators Lancet Oncology, Global cardiovascular Risk Consortium NEJM 2023
Slide 73: CPACS trial
CPACS trial Dr Marinella Messina, Vice President of Clinical, Racura Oncology
Slide 74: Anthracycline use & cardiotoxicity
Anthracycline use & cardiotoxicity US data1 – Anthracyclines remain broadly used across a 90,000 range of cancer types because of strong clinical efficacy Patients receiving anthracyclines 80,000 70,000 Anthracyclines widely used in TNBC and HR+/HER2- BC patients, both within the 60,000 50,000 neoad
Slide 75: Anthracycline use & cardiotoxicity
Anthracycline use & cardiotoxicity US data1 – Anthracyclines remain broadly used across a 90,000 range of cancer types because of strong clinical efficacy Anthracyclines associated with significant Patients receiving anthracyclines 80,000 and permanent cardiotoxicity 70,000 Anthracyclines widely use
Slide 76: Clinical strategy in anthracycline-treated solid tumours
Clinical strategy in anthracycline-treated solid tumours Integrated trial for early signals of both cardioprotection and anticancer activity Phase 1a Phase 1b MTD + safety + early Functional efficacy efficacy signal signals (VO2peak) MTD, maximum tolerated dose 74
Slide 77: CPACS trial design: Phase 1a
CPACS trial design: Phase 1a Safe RC220 + doxorubicin maximum tolerated combined dose Patients: Advanced/metastatic patients with potential benefit from doxorubicin treatment Design: RC220 dose escalation + 60 mg/m2 doxorubicin (DOX) Trial size: 15-33 patients Trial status: Ongoing – Cohort 1 (combo
Slide 78: CPACS trial design: Phase 1b
CPACS trial design: Phase 1b Signals of anticancer & cardioprotection efficacy Patients: Anthracycline naïve solid tumour patients Design: RC220 MTCD + 60 mg/m2 doxorubicin (DOX) Trial size: 20 patients Cycle 1 Cycle 2+ End /Follow Up Trial status: Pending interim analysis in phase 1a RC220 + DOX RC
Slide 79: Questions
ONCOLOGY Questions
Slide 80: HARNESS-1 clinical program
HARNESS-1 clinical program Prof Nick Pavlakis, Senior Staff Medical Oncologist, Royal North Shore Hospital Dr Rodney Cusack, Principal Scientist, Racura Oncology
Slide 81: Agenda: HARNESS-1
Agenda: HARNESS-1 Topic Presenter EGFR mutant NSCLC and HARNESS-1 trial Prof Nick Pavlakis Competitive landscape: Potential of RC220 use in EGFRm NSCLC Dr Rodney Cusack Commercialisation: Regulatory pathways and opportunities Dr Rodney Cusack 79
Slide 82: EGFR mutant NSCLC and HARNESS-1 trial
EGFR mutant NSCLC and HARNESS-1 trial Prof Nick Pavlakis, Senior Staff Medical Oncologist, Royal North Shore Hospital
Slide 83: EGFR mutant NSCLC and HARNESS-1 trial
RACURA SYMPOSIUM March 24, 2026 EGFR mutant NSCLC and HARNESS-1 trial Prof Nick Pavlakis Senior Staff Medical Oncologist, RNSH Board Member (former Chair) – The Thoracic Oncology Group of Australasia (TOGA)
Slide 84: Financial disclosures
Financial disclosures • Advisory Boards • Boehringer Ingelheim, MSD, Merck, BMS, Astra Zeneca, Takeda, Pfizer, Roche, Amgen, Beigene, Gilead, Zymeworks, BioNTech, Daiichi, DUO Oncology, Amplia, Johnson and Johnson, RACURA (formerly RACE) oncology (Advisor, HARNESS-1 investigator) • Speaking Honorari
Slide 85: Lung Cancer Statistics
Lung Cancer sub-types Lung Cancer Statistics ~85% of lung cancers are Non-small cell lung cancer (NSCLC) Lung cancer is the most common cancer (12.4%) Globally 2.5M new cases pa1 Lung Cancer US >200K new cases pa 2 China >1M new cases pa3 15% 85% Small Cell Lung Non-small Cell Lung Lung cancer is th
Slide 86: NSCLC is not one disease: molecularly heterogeneous
NSCLC is not one disease: molecularly heterogeneous disease Diminishing smoking rates have changed histologic rates Small Cell Lung Cancer 15% Immunotherapy Non-small cell lung cancer (NSCLC) ~ 85% Non –Squamous ~75% Targetable oncogenic driver molecular alterations in NSCLC (adenocarcinoma) Treat w
Slide 87: EGFR mutant Non-Small Cell Lung Cancer (NSCLC)
EGFR mutant Non-Small Cell Lung Cancer (NSCLC) • EGFR-mutated (EGFRm) NSCLC is a subtype of lung cancer characterised by specific gene mutations in the epidermal growth factor receptor (EGFR) on the cancer cell surface that drives uncontrolled cell growth 1 • The most common and treatable mutations
Slide 88: EGFR Mutations in NSCLC
EGFR Mutations in NSCLC1 EGFR mutations more prevalent in: • Asian patients Europe • Females (44%) > males (24%) Americas • Non-smokers (49%) > current or former smokers (22%) Korea • Adenocarcinoma Japan Typical clinical Presentation China • Symptomatic – NB: Screening limited 0% 10% 20% 30% 40% 50
Slide 89: Targetable oncogenic driver alterations in NSCLC
Targetable oncogenic driver molecular alterations in NSCLC (adenocarcinoma) Timeline of US FDA-approved targeted therapies for oncogene-driven NSCLC A Tan, D Tan. JCO January 5, 2022: DOI https://doi. org/10.1200/JCO.21. 01626
Slide 90: EGFRm NSCLC Treatment with TKIs
EGFRm NSCLC Treatment with TKIs Local Symptoms Cough Breathlessness Haemptysis (blood) Wheeze • EGFRm NSCLC generally respond poorly to Pain immunotherapy1 • Current mainstay of treatment are 3rd generation EGFRm Tyrosine Kinase Inhibitors (TKIs) – superior to chemotherapy2 • EGFRm TKIs are highly e
Slide 91: The Problem - Universal TKI Resistance
The Problem - Universal TKI Resistance • Despite 14 approved EGRFm TKI and 8 in Phase 3 trials, virtually all patients develop resistance to EGFRm TKI therapy – the median progression free survival (PFS) is 18 months1 • No clinical difference between any of the 3rd generation EGFRm TKIs in regards t
Slide 92: Resistance in oncogene driven NSCLC – mainly biological
Resistance in oncogene driven NSCLC – mainly biological Camidge DR et al. Nat Rev Clin Oncol. 2014 (11): 473-481
Slide 93: NGS-Based Liquid Biopsy Instead of Tissue Biopsy
NGS-Based Liquid Biopsy (LB) Instead of Tissue Biopsy Identifying resistance mechanisms
Slide 94: Liquid biopsy first approach to defining drug resistance
Defining drug resistance in oncogene + NSCLC: a liquid biopsy first approach is preferable – fast, informative Liquid
Slide 95: Proof of concept: liquid biopsy to identify emerging resistance
Proof of concept: Using liquid biopsy to identify emerging treatment resistance BEFORE scan progression, THEN add new therapy To DELAY clinical resistance Breast Cancer Example. Blood ESR1 and camizestrant: SERENA-6 study PFS on CT prolonged by 7 months
Slide 96: Case Example – EGFR Exon 21 MT
Case Example – EGFR Exon 21 MT ctDNA ctDNA ctDNA 73 year old non-smoking Asian male Stage IV EGFR exon 21 L858R mutated NSCLC 1st L Osimertinib • ctDNA was informative at progression (co-mutations), cleared with response after chemo. • Acquired NTRK2 fusion on tissue biopsy • Earlier use of ctDNA ma
Slide 97: Current Approaches to delay EGFRm TKI Resistance
Current Approaches to delay EGFRm TKI Resistance Combine EGRFm TKIs with other anticancer treatments in ALL patients (empirical approach – one size fits all) • Using • New targeted agents (e.g. amivantinab/lazertinib in MARIPOSA trial) • Chemotherapy (FLAURA2 trial) Benefit observed in PFS and overa
Slide 98: What is Needed to Delay TKI Resistance?
What is Needed to Delay TKI Resistance? Any successful treatment MUST • Be able to prevent/delay bypass signalling - block signalling downstream of all signalling pathways (e.g. MYC/MAX) • Be able to target the different resistance subclones together – need to target multiple resistance pathways, no
Slide 99: Evolutionary approach to treating EGFRm NSCLC
Evolutionary approach to treating EGFRm NSCLC • Upfront TKI. Osimertinib in Australia • Use ctDNA to identify risk of clinical progression • Add or change therapy before clinical progression develops • Enabling delay in symptomatic deterioration • Prolonging disease control and ultimately survival •
Slide 100: $14.7 million MRFF Grant study
B Solomon (PI, PMCC), N Pavlakis – study co-chairs Target 500 patients Nationally with oncogene driven NSCLC Aims Feasibility Clinical Economic $14.7 million MRFF Grant 2025
Slide 101: HARNESS-1. HAlt Resistance in NSCLC with EGFR Sensitising mutationS
HARNESS-1. HAlt Resistance in NSCLC with EGFR Sensitising mutationS A Racura Oncology sponsored Phase 1 trial of RC220 + osimertinib in EGFRm NSCLC patients who are tumour HARNESS-1 study has positive by ctDNA with the aim of delaying TKI approval at Monash Health, resistance with more Australian si
Slide 102: HARNESS-1. Phase 1 Trial Overview
HARNESS-1. Phase 1 Trial Overview Proof of concept trial demonstrating that RC220 can delay resistance to TKIs ctDNA Screen EGFRm NSCLC patients on osimertinib (Osi) maintenance for tumour Screening presence by ctDNA (~100 patients) Dose Escalation Dose Expansion Blinded & randomised two dose levels
Slide 103: HARNESS-1 Key Eligibility Criteria
HARNESS-1 Key Eligibility Criteria • Inclusion • Diagnosed with EGFRm NSCLC and stable on osimertinib for >6 months • ECOG 0 or 1 • 18 to 80 years old • Positive or increasing levels of EGFRm ctDNA • Adequate haematological, liver, kidney and cardiac function • Exclusion • Pregnant or lactating wome
Slide 104: Competitive landscape
Competitive landscape Potential of RC220 use in EGFRm NSCLC
Slide 105: Market potential for EGFR-mutated NSCLC
Market potential for EGFR-mutated NSCLC There is a large (>$10b) existing market for TKIs targeting EGFRm NSCLC Target Major players – 3rd generation TKIs Market dynamics Epidermal 2025 Brand Generic Manufacturer sales • First and second-generation EGFR TKIs growth factor (US$m)1 superseded by third
Slide 106: EGFRm NSCLC TKI competitive landscape
EGFRm NSCLC TKI competitive landscape Clinical 2024 sales Drug name Presenter Target(s) Mutation subtypes Gen Company Approvals stage (US$m) Osimertinib Tagrisso® EGFR, HER2, HER4 Ex19del, L858R, T790M 3rd Astrazeneca Approved US, EU, CN 6580 Dacomitinib Vizimpro® EGFR, HER2, HER4 Ex19del, L858R 2nd
Slide 107: Our goal
Our goal Delay or prevent resistance to osimertinib osimertinib osimertinib + RC220 mPFS 19-29 mo mPFS +++ mo Use endpoints like mPFS as shorter-term regulatory-approvable endpoints mPFS, median progression free survival; mo, months 105
Slide 108: Strategic positioning
Strategic positioning Broad market opportunity with multiple positioning approaches Market leaders New entrants Provide competitive edge to Increase use of existing new targeted agents targeted agents RC220 Delaying resistance to targeted agents Protect existing market Supplant market leaders from c
Slide 109: Commercialisation
Commercialisation HARNESS-1 regulatory pathways and approval opportunities for RC220
Slide 110: RC220 regulatory plan in EGFRm NSCLC
RC220 regulatory plan in EGFRm NSCLC Potential pathway to approval of RC220 as a resistance EGFRm TKI delaying treatment • Proceed with HARNESS-1 until end of dose escalation (MTD determination) • Perform interim analysis • Present data to US FDA at “End of Phase 1” meeting o Confirm study data are
Slide 111: US FDA options to accelerate approval
US FDA options to accelerate approval If the data supports it, there is the possibility of early approval of RC220 • Priority Review • Breakthrough Designation • Real-Time Oncology Review o Allows Sponsors to submit clinical data in stages for rolling review o ~26 weeks target review time Zongertini
Slide 112: Zongertinib (HERNEXEOS)
Zongertinib (HERNEXEOS®, Boehringer Ingelheim) Case study of FDA accelerated approval from 71 patient Phase 1 dataset Fast Track Status (US) – Dec 23 Breakthrough Therapy Status (US, China)- Aug 24 Priority Review (US) – Feb 25 Approved US & China – Aug 25 2021 2022 2023 2024 2025 2026 Beamion LUNG-
Slide 113: Questions
ONCOLOGY Questions
Slide 114: Phase 3 AML clinical program
Phase 3 AML clinical program Dr Anupa Kudva, Medical Director
Slide 115: Agenda: AML
Agenda: AML Topic Presenter AML landscape: Overview and current treatment options History of bisantrene in AML Clinical benefit of second-line AML therapies Biology and clinical relevance of MYC in AML Dr Anupa Kudva Rationale for use of RC220 in AML Clinical development: Study roadmap and design Co
Slide 116: Acute myeloid leukaemia
Acute myeloid leukaemia Molecular heterogeneity creates both challenges and opportunities Rare but aggressive blood cancer o Rapid proliferation of immature myeloid cells in the bone marrow o Globally ~145,000 new cases annually ➢ Approximately 22,000 new AML cases are diagnosed each year in the US
Slide 117: Frontline treatment landscape in AML
Frontline treatment landscape in AML Intensive regimens, high toxicity, and frequent relapse Fit Unfit % of AML patients 40% 60% Age range <70–75 years ≥75 years ECOG Performance status 0–2 ≥3 (ability to carry out daily activities) Comorbidities / frailty Limited Significant Intensive induction Low
Slide 118: Treatment options in r/r AML
Treatment options in r/r AML Outcomes are poor and therapeutic options are limited 116
Slide 119: Limitations to current r/r AML treatment paradigm
Limitations to current r/r AML treatment paradigm Why current salvage therapies fall short Intensive salvage regimens Durable associated with remissions significant Grade uncommon ≥3 toxicity High unmet need Majority of approved agents apply only to Rapid molecular subsets development of drug resist
Slide 120: Paediatric AML
Paediatric AML Rare but underserved patient population Accounts for ~15–20% of childhood leukaemias Different disease from adult AML o Higher upfront intensity o Fewer targetable mutations Approximately one-third of children relapse o Survival after relapse remains below 40% Significant long-term to
Slide 121: History of bisantrene in AML
History of bisantrene in AML Existing clinical data supports continued development in AML Bisantrene approved in France for AML in 1988 • Demonstrated anti-leukaemic activity – 40% CR o Minimal cardiotoxicity (E,E)-bisantrene clinical AML studies • Two Phase 2 trials in adults o 40% ORR ➢Monotherapy
Slide 122: History of bisantrene in AML
History of bisantrene in AML Existing clinical data supports continued development in AML Bisantrene approved in France for AML in 1988 • Demonstrated anti-leukaemic activity – 40% CR o Minimal cardiotoxicity FDA: (E,E)-bisantrene Orphan clinical Drug AML & Rare Paediatric Disease studies • Two Phas
Slide 123: Clinical benefit of second-line AML therapies
Clinical benefit of second-line AML therapies Mutation-specific therapies have limited population-level impact Ivosidenib (Tibsovo - IDH1) Olutasidenib (Rezlidhia - IDH1) Enasidenib (Idhifa - IDH2) (E,E)-bisantrene is mutation agnostic Ziftomenib (NPM1/KMT2Ar) • Broader potential impact across AML G
Slide 124: MYC expression in AML
MYC expression in AML Key oncogenic driver in AML1 MYC is frequently upregulated in AML o MYC overexpression observed in ~90% of AML cases o Higher expression of MYC is associated with lower overall survival 6% → poorer prognosis 3% → overexpression Implications as a target o MYC central transcripti
Slide 125: Mechanism of action of (E,E)-bisantrene in AML
Mechanism of action of (E,E)-bisantrene in AML Novel mechanism with broad anti-leukaemic activity G-quadruplex DNA binding Not an anthracycline-like chemotherapy Key molecular effects MYC silencing Inhibition of topoisomerase II Inhibition of telomerase Therapeutic impact ↓ Malignant Proliferation/S
Slide 126: Clinical validation of MYC silencing
Clinical validation of MYC silencing Linking biological activity to clinical response RC220 targets AML can provide Demonstrate MYC is a disease MYC silencing vs MYC-driven direct mechanistic clinical MYC driver in AML depth of response signalling validation targeting RC220 Overexpression Mutation-
Slide 127: RC220 clinical development strategy in r/r AML
RC220 clinical development strategy in r/r AML Rapid, low-cost pathway to regulatory approval of RC220 Preclinical Phase 3 pivotal RC110/RC220 RC110/RC220 monotherapy Study bridging study sponsored study r/r AML, relapsed and refractory acute myeloid leukemia 125
Slide 128: Preclinical RC110/RC220 bridging pathway
Preclinical RC110/RC220 bridging pathway Building on RC110 to streamline RC220 development Study design overview • Preclinical animal PK study • Head-to-head comparison of RC110 vs RC220 • Primary objective: Demonstrate pharmacokinetic equivalence Rationale • Expedite development timeline • Avoids n
Slide 129: Phase 3 adaptive seamless trial design
Phase 3 adaptive seamless trial design RC220 monotherapy trial in r/r AML Part B Part A Efficacy Expansion Paeds Cohort Project Optimus RC220 optimum RC220 dose^ dose level 1 MTD FDA Establish Adult r/r AML EOP2 optimum ≥2nd Line Meeting dose* RC220 dose level 2 Standard of care 80% MTD control arm
Slide 130: Commercial strategy in AML
Commercial strategy in AML Rapid, low-cost pathway to regulatory approval of RC220 A defined orphan market with a clear regulatory pathway Efficient path to NDA Potential qualification for a Paediatric PRV upon approval ~US$200m 1 Establish clinical proof of MYC targeting Frontline AML Platform for
Slide 131: Questions
ONCOLOGY Questions
Slide 132: Protecting innovation & delivering milestones
Protecting innovation & delivering milestones Dr Pete Smith, Executive Chair
Slide 133: IP Overview
IP Overview Foundation for 20 years of the strongest composition of matter IP protection Bisantrene photoisomers discovered by Racura Oncology • Bisantrene found to consist of three photoisomers with different biological and anticancer activities, which rapidly interconvert upon exposure to visible
Slide 134: Composition of matter patents
Composition of matter patents If granted, these patents will add significantly to value any future licensing or partnering transactions • Composition of matter patent claims protect the chemical structure of the active drug • Strongest intellectual property (IP) possible in the pharmaceutical indust
Slide 135: What is required for a patent?
What is required for a patent? Counsel advice is that composition of matter claims meet all the requirements for patent allowance Novelty Non-obviousness Utility Bisantrene photoisomerism Bisantrene photoisomerism Only (E,E)-isomer active not previously reported not previously reported ✓ ✓ ✓ Racura
Slide 136: Conclusion
Conclusion Composition of matter claims add significantly to (E,E)-bisantrene’s value • Bisantrene can exist in three isomeric forms: (E,E), (E,Z) and (Z,Z) o Photoisomerisation discovered by Racura Oncology • Only (E,E)-bisantrene shown to have potent anticancer activity • Three patent applications
Slide 137: Biotech valuation case studies
Biotech valuation case studies Dr Pete Smith, Executive Chair
Slide 138: Valuing biotechnology companies
Valuing biotechnology companies Biotech is a specialised investment category with huge upside and risk Valuing biotech is inherently challenging • Often risk-adjusting a single asset which often has a binary outcome (success/fail) • The market potential is often unknowable with many uncertainties in
Slide 139: Targeting the undruggable – Revolution Medicines
Targeting the undruggable – Revolution Medicines Extreme value placed on clinical success by sophisticated investors Revolution Medicines (NASDAQ: RVMD) • Price spike due to takeover rumours at JP Morgan healthcare conference • MCap ~US$20B • Cash US$1.9B Developing several KRAS targeted drugs • Dar
Slide 140: Targeting the undruggable – Erasca Inc
Targeting the undruggable – Erasca Inc Extreme value placed on clinical success by sophisticated investors Erasca Inc. (NASDAQ: ERAS) • Benefited from RVMD price momentum and interest in RAS as a target • Market Cap: US$4.8B • US$300M in cash end Sept 25 • Raised additional US$260M in Jan 2026 Pipel
Slide 141: Targeting the undruggable – Mirati Therapeutics
Targeting the undruggable – Mirati Therapeutics Extreme value placed on clinical success by sophisticated investors Mirati developed Krazati® (adagrasib, MRTX-849) targeting ‘undruggable’ KRAS G12C mutation • G12C accounts for 15% of all KRAS mutations • Most common KRAS muatation in lung cancer As
Slide 142: Recent drug approvals in NSCLC
Recent drug approvals in NSCLC Early-stage approvals from small patient numbers underscores clinical need in NSCLC Developer Drug (generic) name Hyrnuo® Hernexeos® Zegfrovy® (sevabertinib) (zongertinib) (sunvozertinib) MoA HER2 TKI HER2 TKI EGFR TKI FDA approval 19/11/2025 11/08/2025 02/07/2025 Data
Slide 143: MYC inhibitors in the clinic
MYC inhibitors in the clinic RC220 competitors are early stage and have limited clinical activity Drug Developer Mechanism Clinical status & activity Direct (protein/gene) Phase 3 AML, Phase 1 NSCLC, Phase 1 solid tumours; 40% CR/PR in RC220 Racura Oncology G-quadruplex stabiliser AML OMO-103 Peptom
Slide 144: Corporate snapshot
Corporate snapshot Racura Oncology is an ASX-listed, late-stage clinical biopharmaceutical company Racura Oncology 12-month trading history1 Key metrics ($A) ASX code RAC Share price $2.831 Market capitalisation $514.5m 1 Cash at bank $20.9m2 Debt Nil Enterprise value $493.6m 1 Shares on issue 181,8
Slide 145: General Q&A
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Slide 146: Contact
Contact D AN IEL TILLET T JA NE LO W E CEO & Managing Director Investor & Media Relations +61 2 8051 3043 +61 411 117 774 daniel.Tillett@racuraoncology.com jane.lowe@irdepartment.com.au www.racuraoncology.com ©2026 Racura Oncology Ltd. All rights reserved. The information contained in this presentat
Slide 147: Glossary of terms
Glossary of terms 1H-NMR, proton nuclear magnetic resonance 1st L, first line ECOG, Eastern Cooperative Oncology Group (E,E)-bis, (E,E)-bisantrene EGFR, epidermal growth factor receptor a-vO₂ diff, arteriovenous oxygen difference EGFRm, epidermal growth factor receptor mutant ALL, acute lymphoblasti
Slide 148: Glossary of terms
Glossary of terms KRAS, Kirsten rat sarcoma viral oncogene homolog PD, pharmacodynamic LVEDV, left ventricular end diastolic volume PDX, patient-derived xenograft LVEF, left ventricular ejection fraction PI3K/AKT, phosphoinositide 3-kinase / protein kinase B mAB, monoclonal antibody PK, pharmacokine