Kazia Therapeutics Ltd · NASDAQ:KZIA
Kazia Therapeutics — Investor Presentation (April 2026)
59 slides from Kazia Therapeutics's investor presentation, April 2026
Slide 1: Beyond Inhibition. Reprogramming Cancer Control. 2026 Corporate Overview
Beyond Inhibition. Reprogramming Cancer Control. 2026 Corporate Overview NASDAQ: KZIA | X: @KaziaTx April 2026
Slide 2: Forward-Looking Statements
Forward-Looking Statements This presentation contains forward-looking statements, which can generally be identified as such by the use of words such as “may,” “will,” “estimate,” “future,” “forward,” “anticipate,” “plan,” “expect,” “explore,” “potential” or other similar words. Any statement describ
Slide 3: Kazia Therapeutics Limited
Kazia Therapeutics Limited • Sydney-based clinical-stage oncology company focused on high-need cancers of the central nervous system and select aggressive solid tumors • Founded in 2016, the company is dedicated to advancing transformative therapies by harnessing next-generation science, disciplined
Slide 4: Our mission is to redefine cancer treatment
Our mission is to redefine cancer treatment by moving beyond conventional pathway inhibition toward therapeutic reprogramming of cancer biology by targeting regulatory drivers of growth, immune escape, and relapse to deliver more durable outcomes for patients with the greatest unmet need. 3
Slide 5: Company Highlights
01 Clinical-stage oncology company advancing next-generation differentiated therapies designed to overcome resistance in aggressive and immunotherapy-refractory cancers Lead asset paxalisib is an oral, brain-penetrant dual PI3K / mTOR inhibitor for solid tumor 02 indications, including breast cancer
Slide 6: A Differentiated, Multi-Layered Approach
A Differentiated, Multi-Layered Approach A strategic expansion to a multi-modal platform targeting stable tumor states Paxalisib Transcriptional Reprogramming Epigenetic Focus & Integration o Alters gene expression programs that drive tumor growth and immune suppression o Exerts downstream effects o
Slide 7: Complementary Layers of Cancer Control
Complementary Layers of Cancer Control Differentiated oncology portfolio designed to overcome resistance in aggressive and immunotherapy-refractory cancers Paxalisib PD-L1 Protein Degrader SETDB1 Inhibitor Platform Brain-penetrant dual PI3K / mTOR inhibitor with Platform epigenetic and immunomodulat
Slide 8: Pipeline Overview
Pipeline Overview High-value indications with strong partnering potential *Product candidates (not approved); IDH: Isocitrate dehydrogenase, DIPG: Diffuse Intrinsic Pontine Glioma, AT / RT: Atypical Teratoid Rhabdoid Tumor, CNS: central nervous system, TNBC: triple negative breast cancer, VEGFR3: va
Slide 9: Development Plan At a Glance
Development Plan At a Glance 8
Slide 10: Market Landscape: Growth & Opportunity
Market Landscape: Growth & Opportunity • We believe oncology innovation will drive exponential market growth. • New modalities are expanding therapeutic options for previously resistant cancers. • We believe Kazia’s pipeline is strategically aligned with these high-growth areas. Epigenetic Drugs Imm
Slide 11: Paxalisib
Paxalisib 10
Slide 12: Paxalisib Overview
Paxalisib Overview Brain-penetrant, oral, once daily small molecule dual PI3K / mTOR inhibitor with epigenetic and Asset Overview immunomodulatory activity Origin Discovered by Genentech (GDC-0084); In-licensed by Kazia Therapeutics Development Stage Clinical Advanced Breast Cancer (ABC, Phase 1), G
Slide 13: Developmental History & Milestones
Paxalisib Developmental History & Milestones Expanding the clinical footprint of paxalisib into solid tumors beyond CNS 2012-2015 August 2019 July 2023 June 2025 January 2026 GDC-0084 becomes Paxalisib received Fast Kazia commences Phase Genentech Phase 1 February2018 Complete metabolic ‘paxalisib’
Slide 14: Paxalisib (GDC-0084)
Paxalisib Paxalisib (GDC-0084) Designed to be best-in-class PI3K pathway inhibitor with modest mTOR activity Relevant marketed or active clinical PI3K inhibitor programs Paxalisib Alpelisib Gedatolisib PIKTOR Zovegalisib OKI-219 STX-478 TOS-358 (Kazia) (Novartis) (Celcuity) (two drugs, (RLY-2608) (O
Slide 15: Pan-PI3K & mTOR Inhibition Advantage
Paxalisib Pan-PI3K & mTOR Inhibition Advantage Paxalisib is a comprehensive pathway and biology modulator, not simply a broader PI3K inhibitor. o Not built around a mutation-defined strategy – Narrows the addressable biology to tumors where a specific mutation is the dominant driver – Cancer biology
Slide 16: Paxalisib Mechanism of Action
Paxalisib Paxalisib Mechanism of Action PI3K oral inhibitor clinically proven to cross the blood-brain barrier Growth factor receptor Comparative Potency vs. Other PI3K Inhibitors IC 50 (nM) p110 p1 1 0 p1 1 0 p1 1 0 mTORC PI3K α β γ δ 1/ 2 Paxalisib 2 46 10 3 70 Paxalisib Idelalisib 820 565 89 2.5
Slide 17: Clinical & Translational Manifestations
Paxalisib Clinical & Translational Manifestations In clinical settings, there is evidence that paxalisib’s downstream epigenetic effects manifest as: Pax IO T Reduction of Aggressive Enhanced Activity When Modulation of Immune Circulating Tumor Cell (CTC) Combined with Immune Exhaustion Markers and
Slide 18: Licensing & Collaborations
Paxalisib Licensing & Collaborations Opportunistic partnering and strategic collaborations continue to add value Licensing Key Collaborations Summary To develop, manufacture, and commercialize To develop and paxalisib as a potential Cutting-edge preclinical program to Territories and commercialize p
Slide 19: Paxalisib Potential in Breast Cancer
Paxalisib: Advanced Breast Cancer Paxalisib Potential in Breast Cancer The most diagnosed cancer and leading cause of death in women PI3K / mTOR in Breast Cancer Paxalisib Opportunity Breast Cancer PI3K / mTOR signaling is Paxalisib inhibits PI3K / mTOR, a • >300,000 new cases of invasive frequently
Slide 20: Current Treatment Landscape
Paxalisib: Advanced Breast Cancer Current Treatment Landscape Modest results for HER2- subtypes, despite checkpoint and PARP inhibitors 10%1 70% 4% 9% Subtypes HR- / HER2- HR+ / HER2- HR- / HER2+ HR+ / HER2+ (TNBC) 62% 38%3 Stratification PD-L1 PD-L1 CPS <10 CPS >10 80% 20%4 BRCA wt BRCA m Pembroliz
Slide 21: Consistent & Statistically Significant Signals
Paxalisib: Advanced Breast Cancer Consistent & Statistically Significant Signals Preclinical studies combining paxalisib with either checkpoint inhibitor or PARP inhibitor resulted in highly consistent and statistically significant signals of efficacy. Tumor 4T1 Mouse Model o Standard model for TNBC
Slide 22: Kazia-Sponsored Clinical Phase 1b Study Overview
Paxalisib: Advanced Breast Cancer Kazia-Sponsored Clinical Phase 1b Study Overview Multi-center, open-label, randomized trial Inclusion Criteria Treatment Endpoints Arm A Primary Paxalisib plus Olaparib (28-Day Cycle) • HER2-negative stage IV (metastatic) BC • Safety and tolerability of • Confirmed
Slide 23: Early Clinical Trial Epigenetic Effects
Paxalisib: Advanced Breast Cancer Early Clinical Trial Epigenetic Effects Combination regimen results in >50% reduction in CTCs First-in-human data reflects mechanistic synergy consistent with the preclinical data. Circulating Tumor Cells (CTCs) Patient One Results at Day 21 • Cancer cells that deta
Slide 24: Early Evidence of Tumor Regression
Paxalisib: Advanced Breast Cancer Early Evidence of Tumor Regression 1 CR in mTNBC patient treated under expanded access, and 2 PRs in ongoing study Preliminary Clinical Responses Safety • 1 expanded access TNBC patient achieved a • Generally well tolerated at 30mg daily confirmed complete metabolic
Slide 25: Paxalisib Potential in Glioblastoma
Paxalisib: Glioblastoma (GBM) Paxalisib Potential in Glioblastoma The most aggressive malignant brain cancer PI3K / mTOR in Glioblastoma Lung PI3K / mTOR signaling pathway is Breast a central regulator of cell growth and is hyperactivated in 14 million cancer approximately ~85% to 90% of cases per g
Slide 26: Paxalisib in Newly Diagnosed Unmethylated GBM Patients
Paxalisib: Glioblastoma (GBM) Paxalisib in Newly Diagnosed Unmethylated GBM Patients Consistent median overall survival data Phase 2 GBM-AGILE (Phase 2/3) (NCT03522298) (NCT03970447) Overall Summary Paxalisib demonstrated a ~3.8 month Study Type Open-label, single arm Adaptive, multi-arm randomized
Slide 27: US FDA Type C Meeting
Paxalisib: Glioblastoma (GBM) US FDA Type C Meeting Paxalisib in GBM commercial and development path forward FDA position: Kazia plans to request FDA follow-up next steps: December 2024 2026 October 2025 o Data on OS would generally not be follow-up meeting with the o Meeting anticipated for 1H 2026
Slide 28: Paxalisib Potential in Childhood Brain Cancer
Paxalisib: Childhood Brain Cancer Paxalisib Potential in Childhood Brain Cancer High unmet need especially in patients with diffuse midline gliomas (DMGs) PI3K / mTOR in Childhood Brain Cancer Paxalisib Opportunity Childhood Brain Cancer PI3K / mTOR signaling pathway is Given the frequent dysregulat
Slide 29: Paxalisib in Childhood Brain Cancer
Paxalisib: Childhood Brain Cancer Paxalisib in Childhood Brain Cancer Kazia is actively pursuing three forms of childhood brain cancer: Diffuse Midline Gliomas Atypical Teratoid / Advanced Childhood Cancer (DMG, DIPG) Rhabdoid Tumors (AT / RT) (PI3K / mTOR activated) Positive preclinical data as Pos
Slide 30: Paxalisib in Diffuse Midline Gliomas (DMG)
Paxalisib: Childhood Brain Cancer Paxalisib in Diffuse Midline Gliomas (DMG) PNOC-sponsored Phase 2 trial in combination with ONC201 In spite of research that has helped improve treatment for DIPG patients, the prognosis remains poor with the median survival range being from 8-11 months.1 o 68 patie
Slide 31: Paxalisib in Brain Metastasis
Paxalisib: Brain Metastases Paxalisib in Brain Metastasis MSKCC-sponsored Phase 1 trial Interim analysis showed encouraging clinical activity of paxalisib in combination with radiation therapy. August 2022 July 2023 February 2024 Data from first stage presented at 2022 Fast Track Designation granted
Slide 32: Paxalisib in Brain Metastasis
Paxalisib: Brain Metastases Paxalisib in Brain Metastasis MSKCC-sponsored Phase 1 trial Interim analysis showed encouraging clinical activity of paxalisib in combination with radiation therapy. Response signal seen for concurrent Overall Summary paxalisib and brain RT Primary objective of identifyin
Slide 33: Summary & Next Steps
Paxalisib Summary & Next Steps Summary o Brain-penetrant dual pan-PI3K / mTOR inhibitor in development (Only 2% of small-molecule drugs are brain-penetrant) o Designed to be best-in-class pan-PI3K pathway inhibitor with modest mTOR activity (dual targeting required to inhibit cancer cell proliferati
Slide 34: PD-L1 Protein Degrader Platform
PD-L1 Protein Degrader Platform 33
Slide 35: Platform Overview
PD-L1 Protein Degrader Platform Platform Overview Complementing paxalisib’s transcriptional and epigenetic effects, Kazia’s NDL2 program addresses immune resistance at the post-translational regulatory level Lead candidate, NDL2, is an optimized bicyclic peptide PD-L1 degrader designed to target int
Slide 36: Current Anti-PD-1 / L1 Therapy Landscape
PD-L1 Protein Degrader Platform Current Anti-PD-1 / L1 Therapy Landscape Limited by intracellular PD-L1 Targeting nPD-L1 could Distinct distributions of Intracellular PD-L1 has been implicated provide a therapeutic PD-L1 (cell surface, in immunotherapy resistance, benefit, including in cytosol, nucl
Slide 37: NDL2: First-In-Class PD-L1 Degrader
PD-L1 Protein Degrader Platform NDL2: First-In-Class PD-L1 Degrader Targeting intracellular PD-L1 Targeted Protein Degradation (TPD) therapies opened a new frontier for treating cancer by exploiting naturally occurring protein degradation pathways to disrupt critical cellular processes. NDL2 is an o
Slide 38: Key Differentiator
PD-L1 Protein Degrader Platform Key Differentiator NDL2 distinguishes itself as a modality facing minimal competitive challenges NDL2 Peptide Degrader of PD-L1 PD-(L)1 mAbs Targeted protein degradation via Block the PD-1:PD-L1 interaction at the cell surface; Primary Mechanism intracellular E3 ubiqu
Slide 39: Preclinical & Translational Manifestations
PD-L1 Protein Degrader Platform Preclinical & Translational Manifestations Across multiple preclinical models and patient-derived samples, NDL2 demonstrated: Anti -PD-1 NDL2 NDL2 T T Reduced tumor growth Enhanced activity of Suppressed metastatic Targeted resistance as monotherapy anti-PD-1 therapy
Slide 40: Efficacy in 4T1 Mouse Model
PD-L1 Protein Degrader Platform Efficacy in 4T1 Mouse Model NDL2 monotherapy and anti-PD1 combination reduces primary tumor burden with intermittent dosing Intermitted dosing 10 Vehicle (Fold change versus Day 0) αPD1 8 NDL2 NDL2-D 1x105 4T1 cells Tumor volume NDL2 IP injection Harvest NDL2 + αPD1 V
Slide 41: Efficacy in 4T1 Mouse Model (Cont.)
PD-L1 Protein Degrader Platform Efficacy in 4T1 Mouse Model (Cont.) NDL2 and anti-PD1 combination therapy reduces T cell exhaustion Increase in CD8+ T Cell Infiltration Increases in CD8+ T Cell Proliferation ✱ ✱✱ ns ns ns 15 20 ns %CD8+ TIL Population %CD8+ TIL Population 15 10 10 5 5 0 0 Control PD
Slide 42: Safety in 4T1 Mouse Model
PD-L1 Protein Degrader Platform Safety in 4T1 Mouse Model NDL2 shows no evidence of toxicity Body Weight Liver Weight 2.0 120 ns % Change in body weight ns ns Liver weight (g) 1.5 ns ns (versus Day 0) ns 110 1.0 100 0.5 0.0 90 1 1 -D e D PD l ic L2 αP h 1 e 1 +α L2 D Ve D l D ic N -D P aP D h +a N V
Slide 43: Summary & Next Steps
PD-L1 Protein Degrader Platform Summary & Next Steps Innovation Breakthrough o Selectively targets cancer intracellular enriched PD-L1 protein o Amongst the first therapeutics to address metastasis-seeding cancer cells resistant to traditional immunotherapy o Precisely degrades the resistance-associ
Slide 44: SETDB1 Inhibitor Platform
SETDB1 Inhibitor Platform 43
Slide 45: Platform Overview
SETDB1 Inhibitor Platform Platform Overview Complementing paxalisib’s transcriptional modulation and NDL2’s protein degradation Lead candidate, MSETC is an optimized, bicyclic peptide designed to target SETDB1, a key epigenetic Asset Overview regulator of immune evasion. By inhibiting SETDB1, MSETC
Slide 46: SETDB1: Making Cancer Visible to the Immune System
SETDB1 Inhibitor Platform SETDB1: Making Cancer Visible to the Immune System • A protein that cancer cells use to hide from the immune system What is SETDB1? • Turns off signals that would normally alert the body to attack the tumor, acting like an internal “off switch” • Many cancers become resista
Slide 47: MSETC: First-In-Class Bicyclic Peptide Inhibitor
SETDB1 Inhibitor Platform MSETC: First-In-Class Bicyclic Peptide Inhibitor Targeting nuclear SETDB1 Target Drug Development Mechanism of Action SETDB1, a key regulator of tumor MSETC, first-in-class therapeutic MSETC disrupts the nuclear SETDB1 immune evasion complex • SETDB1 is a key regulator of t
Slide 48: Summary & Next Steps
SETDB1 Inhibitor Platform Summary & Next Steps Innovation Breakthrough o Targets SETDB1, a chromatin-level regulator that suppresses tumor immune recognition o Addresses immune evasion at its earliest control layer o Represents a novel approach to restoring immune signaling in tumors resistant to cu
Slide 49: EVT801
EVTS8OI ESSKAZIA
Slide 50: EVT801 Overview
EVT801 Overview A highly selective, potential first-in-class small molecule Vascular Endothelial Growth Factor Receptor-3 (VEGFR3) Asset Overview inhibitor, primarily inhibiting lymphangiogenesis Origin Discovered by Sanofi; Early development by Evotec SE; In-licensed by Kazia in 2021 Development St
Slide 51: EVT801 Selectively Inhibits VEGFR3
EVT801 EVT801 Selectively Inhibits VEGFR3 Avastin® LUCENTIS® (bevacizumab) (ranibizumab) VEGF-B VEGF-A VEGF-D VEGF-E VEGF-C SUTENT® EVT801 (sunitinib) VEGFR1 VEGFR2 VEGFR3 NEXAVAR® (sorafenib) INLYTA® Signal Cell Survival Angiogenesis (axitinib) Modulation VOTRIENT® (Lymph)- Vasculogenesis angiogene
Slide 52: A Differentiated Anti-Tumor Approach
EVT801 A Differentiated Anti-Tumor Approach Inhibition of tumor escape and metastasis • Stabilization of tumor vasculature 1 • Inhibition of (lymph)-angiogenesis • Avoidance of hypoxia decreases potential for metastatic spread Increase in anti-tumor immune activity • No impact on T-cells viability 2
Slide 53: Phase 1 Dose-Finding Trial Completed
EVT801 Phase 1 Dose-Finding Trial Completed Study Background Design Overall Summary Monotherapy dose escalation Target population: N=26 Patients with 11 different cancer types Histologically-confirmed advanced were enrolled, with heavily pretreated or metastatic solid tumors, advanced ovarian cancer
Slide 54: Summary & Next Steps
EVT801 Summary & Next Steps Kazia has initiated a regional and / or global partnership search for EVT801. 1 Well-understood mechanism (anti-angiogenesis) with unique differentiating feature (high VEGFR3 selectivity) 2 Strong preclinical data package, with observed activity in multiple tumors and fav
Slide 55: Corporate Highlights
Corporate Highlights 54
Slide 56: Near-Term Milestones & Anticipated Catalysts
Near-Term Milestones & Anticipated Catalysts Q4 Q1 Q2 Q3 Q4 2025 2026 2026 2026 2026 Complete metabolic Readouts from neuro-oncology focused clinical trials in patients Pricing of $50m private response in stage IV TNBC Acquisition of SETDB1 with GBM and brain metastases placement of equity expanded
Slide 57: Investment Drivers
Investment Drivers Kazia is helping to redefine oncology development by advancing a cohesive therapeutic approach aimed at reprogramming tumor biology. Our strategy is aligned with where both science and capital are moving in oncology. Our clinical and translational focus is Our integrated approach
Slide 58: Management
Leadership Management Dr. John Friend Dr. Sudha Rao Jeffrey J. Kraws Jeffrey Bonacorda Elissa Hansen Chief Executive Officer Chief Scientific Officer Head of Corporate VP Finance & Controller Corporate Secretary Strategy & Development Board of Directors Robert Apple Steven Coffey Ebru Davidson Chair
Slide 59: www.kaziatherapeutics.com ir@kaziatherapeutics.com
www.kaziatherapeutics.com ir@kaziatherapeutics.com
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