NASDAQ: KZIA | X: @KaziaTx Beyond Inhibition. Reprogramming Cancer Control. 2026 Corporate Overview April 2026 This presentation contains forward - looking statements, which can generally be identified as such by the use

NASDAQ: KZIA | X: @KaziaTx Beyond Inhibition. Reprogramming Cancer Control. 2026 Corporate Overview April 2026

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 describing Kazia's future plans, strategies, intentions, expectations, objectives, goals or prospects, and other statements that are not historical facts, are also forward - looking statements, including, but not limited to, statements regarding: the timing for interim or final results and data related to Kazia's clinical and preclinical trials, or third - party trials evaluating Kazia's product candidates, timing and plans with respect to enrolment of patients in Kazia's clinical and preclinical programs, the potential benefits of paxalisib, NDL2, MSETC, and EVT801, the potential results of combination studies of paxalisib and other collaborations, timing for any regulatory submissions or discussions with regulatory agencies, the potential market opportunity for paxalisib, NDL2, MSETC, and EVT801, and Kazia's strategy and plans with respect to its business and programs. Such statements are based on Kazia's expectations and projections about future events and future trends affecting its business and are subject to certain risks and uncertainties that could cause actual results to differ materially from those anticipated in the forward - looking statements, including risks and uncertainties: associated with clinical and preclinical trials and product development, the risk that interim and preclinical data may not be reflective of final data, related to regulatory approvals, and related to the impact of global economic conditions, including disruptions in the banking industry. These and other risks and uncertainties are described more fully in Kazia's Annual Report, filed on Form 20 - F with the SEC, and in subsequent filings with the SEC. Kazia undertakes no obligation to publicly update any forward - looking statement, whether as a result of new information, future events, or otherwise, except as required under applicable law. You should not place undue reliance on these forward - looking statements, which apply only as of the date of this presentation. Certain information contained in this presentation and statements made orally during this presentation relate to or are based on studies, publications, surveys, and other data obtained from third - party sources and our own internal estimates and research. While we believe these third - party studies, publications, surveys and other data to be reliable as of the date of this presentation, it has not independently verified, and makes no representations as to the adequacy, fairness, accuracy or completeness of, any information obtained from third - party sources. In addition, no independent source has evaluated the reasonableness or accuracy of our internal estimates or research, and no reliance should be made on any information or statements made in this presentation relating to or based on such internal estimates and research. 1 Forward - Looking Statements

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 development, and a commitment to clinical impact 2 Kazia Therapeutics Limited

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

Company Highlights 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 indications, including breast cancer, evaluated to date in >550 adult and pediatric patients across Phase 1 - 3 clinical trials and expanded access programs Advancing NDL2 - a potentially first - in - class protein degrader designed to target intracellular PD - L1 to overcome immune resistance beyond checkpoint blockade Developing EVT801 , an oral, highly selective VEGFR3 inhibitor targeting tumor lymphangiogenesis and metastatic spread, with strong partnering potential Cash & Cash Equivalents: Approximately US$46 million (Runway expected to fund planned operations into 2029, excluding additional or expanded trials) No outstanding debt American Depository Shares Outstanding: Approximately 11.4 million 01 02 03 05 06 Advancing MSETC - a potentially first - in - class SETDB1 inhibitor designed to target SETDB1, a key epigenetic regulator of immune evasion 04 4

A Differentiated, Multi - Layered Approach Paxalisib Transcriptional Reprogramming o Alters gene expression programs that drive tumor growth and immune suppression o Exerts downstream effects on tumor transcriptional programs and immune microenvironment modulation o Activity extends beyond pathway inhibition, toward tumor - state reprogramming Epigenetic Focus & Integration MSETC Chromatin Regulation NDL2 Immune Protein Degradation o Eliminates intracellular PD - L1 and overcomes resistance mechanisms beyond antibody - based therapies o Disrupts immune checkpoint stability and transcriptionally regulated immune resistance pathways o Intersects with epigenetic immune regulation by targeting intracellular PD - L1 protein (rather than blocking receptor interaction) o Restores immune visibility by reactivating suppressed signaling pathways o A chromatin - modifying enzyme implicated in cancer drug resistance, immune evasion, and metastatic progression o Its integration provides a mechanistic anchor that unifies paxalisib and NDL2 under a coherent tumor - state epigenetic strategy Epigenetic Therapeutics Immuno - Oncology Targeted Protein Degradation A strategic expansion to a multi - modal platform targeting stable tumor states 5 Data on file.

Complementary Layers of Cancer Control Paxalisib 6 Brain - penetrant dual PI3K / mTOR inhibitor with epigenetic and immunomodulatory activity PD - L1 Protein Degrader Platform First - in - class optimized PD - L1 protein degrader SETDB1 Inhibitor Platform First - in - class optimized SETDB1 inhibitor Epigenetic Pathway Modulation Reprograms PI3K - driven metastatic and immune - suppressive tumors Immune Responsiveness Reduces immune suppression and improves therapy sensitivity Clinically Validated Asset Shows clinical activity across breast cancer, CNS tumors Multiple US FDA designations granted - Fast Track, Orphan Drug, and Rare Pediatric Disease Strategic Backbone Across Breast & CNS Cancer Relevant in high - unmet - need advanced breast cancer populations beyond TNBC and CNS tumors, including glioblastoma and pediatric brain cancer Evaluated in >550 patients to date Phase 1b clinical study in TNBC ongoing NDL2 (Lead Compound) is First - in - Class PD - L1 Protein Degrader Targets the intracellular PD - L1 protein to overcome the mechanisms of resistance to antibody - based checkpoint inhibitors Epigenetic & Immune Reprogramming of Resistant Tumors Restores immune sensitivity in refractory tumors Development & Value Inflection Path Designed for rapid transition to first - in - human trials and translational milestones prior to clinical proof - of - concept Platform & Combination Potential Applicable across solid tumors and a strong rationale for monotherapy or in combination IND initiating studies commencing 2026 MSETC (Lead Compound) is First - in - Class SETDB1 Inhibitor Targets SETDB1, a key epigenetic regulator that suppresses immune signaling at the chromatin level Releases tumor - intrinsic immune suppression Immune Visibility in Resistant Tumors Reactivates interferon and antigen presentation pathways Designed to convert "immune cold" tumors into immune - responsive states Development & Value Inflection Path Designed for rapid transition to first - in - human trials and translational milestones prior to clinical proof - of - concept Positioned for early partnering or combination - driven clinical strategy Platform & Combination Potential Strong rationale for combination with checkpoint inhibitors and targeted therapies Broad applicability across solid tumors and potential backbone for immuno - oncology regimens IND initiating studies commencing 2026 Differentiated oncology portfolio designed to overcome resistance in aggressive and immunotherapy - refractory cancers

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: vascular endothelial growth factor receptor 3 7

Development Plan At a Glance 8

Market Landscape: Growth & Opportunity 1. Epigenetic Drugs Market 2. I mmuno - Oncology Market 3. Targeted Protein Degradation Market o Current Market: $15 - 20B o Projected 2034: $80B+ o Growth Driver: Oncology applications o Current Market: $83.34B o Projected 2035 : $409.44B o Growth Driver : Increasing prevalence of cancer and need for innovative therapies, rising success of immunotherapies o 2025 Market: $699.3m o Projected 2033: $3.26B o Growth Driver: Prevalence of chronic disease conditions such as cancer, demand for novel treatments Epigenetic Drugs Immuno - Oncology Targeted Protein Degradation 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. 9

Paxalisib Overview Brain - penetrant, oral, once daily small molecule dual PI3K / mTOR inhibitor with epigenetic and immunomodulatory activity Asset Overview Discovered by Genentech (GDC - 0084); In - licensed by Kazia Therapeutics Origin Clinical Development Stage Advanced Breast Cancer (ABC, Phase 1), Glioblastoma (GBM, Phase 3), Childhood Brain Cancer (Phase 2 / Preclinical) Lead Indications Oral, capsule Formulation Oral once - per - day dual PI3K / mTOR inhibitor in clinical development for ABC; addresses key mechanisms of immunotherapy resistance; as well as ability to cross the blood brain barrier (BBB) as a potential therapy for primary and secondary brain cancers Key Differentiators PI3K / mTOR kinase inhibitor that disrupts core oncogenic signalling driving tumor growth and survival, while also affecting tumor epigenetic regulation, transcriptional state, and the immune microenvironment beyond its core kinase inhibition Mechanism of Action Fast Track and Orphan Drug for GBM; Fast Track for PI3K - altered brain metastases with radiation; and Rare Pediatric Disease and Orphan Drug for select pediatric gliomas, including diffuse intrinsic pontine glioma (DIPG) and atypical teratoid/rhabdoid tumor (AT / RT) FDA Designations Patent protection projected until 2043; coverage in over 40 jurisdictions, including U.S., Europe, Japan, China, and India; three patent families: paxalisib molecule per se (granted), synthesis of paxalisib (granted), and secondary medical uses / combination treatments (pending) IP 11

Paxalisib Developmental History & Milestones Early2000's Genentech develops GDC - 0084 as a potential new therapeutic for glioblastoma 2012 - 2015 Genentech Phase 1 clinical study in 47 patients with advanced, high - grade glioma . Study demonstrated a favorable safety profile and provided efficacy signals 2016 Kazia in - licenses GDC - 0084 from Genentech following deep due diligence which included Phase 1 study and animal data March2018 Kazia commences company - sponsored Phase 2 clinical study of GDC - 0084 as a first line therapy in patients with glioblastoma August2020 Paxalisib granted Breakthrough Designation by the US FDA for glioblastoma January2021 GBM AGILE pivotal study commences recruiting paxalisib arm February2018 GDC - 0084 awarded Orphan Drug Designation by the US FDA in glioblastoma August 2019 GDC - 0084 becomes paxalisib ' with the granting of an International Non - Proprietary Name (INN) by the World Health Organization July2024 GBM AGILE Phase 2/3 trial data showed clinically meaningful improvement in a prespecified secondary analysis for OS in paxalisib - treated, newly diagnosed unmethylated patients with glioblastoma July2022 Paxalisib granted Rare Pediatric Disease Designation by the US FDA for rare childhood brain cancer, AT / RT July2025 ABC - Pax Phase 1 b preliminary results from the first TNBC patient achieved > 50 % reduction in circulating tumor cells July2023 Paxalisib received Fast Track Designation by the US FDA for solid tumor brain metastases with PI3K pathway mutations in combination with radiation therapy June2025 Kazia commences Phase 1b ABC - Pax study of paxalisib in combination with immunotherapy in patients with triple negative breast cancer (TNBC) January2026 Complete metabolic response in a stage IV TNBC patient treated under expanded access, and two partial responses reported in the ongoing Phase 1b study in metastatic TNBC 12 Expanding the clinical footprint of paxalisib into solid tumors beyond CNS

Paxalisib Paxalisib (GDC - 0084) EC: endometrial, OC: ovarian cancer, ROA: route of administration 1. Layman et al 2024 2. Piqray TOS - 358 (Totus Medicines) STX - 478 (Scorpion Therapeutics, acquired by Eli Lilly) OKI - 219 (OnKure Therapeutics) Zovegalisib (RLY - 2608) (Relay Therapeutics) PIKTOR (two drugs, Faeth, acquired by Sensei Bio) Gedatolisib (Celcuity) Alpelisib (Novartis) Paxalisib (Kazia) PI3K PI3K PI3K PI3K PI3K + mTOR PI3K / AKT / mTOR PI3K PI3K / mTOR Targets P1b (Solid tumors) P1/2 (HR+ / HER2, solid tumors) P1a/b (HR+ / HER2 - , HER2+) P3 (HR+ / HER2 - BC) P2 (EC, OC) P1 (HR+ / HER2 - BC) P3 (HR+ / HER2 - BC) Marketed (HER2 - BC) P3 (GBM) P1 (TNBC & HER2 - BC) Development Stage No Grade 3/4 toxicities Low Grades 1 - 2 Limited toxicities Grade 3 AEs with fulvestrant Grade 3 AEs with paclitaxel Grade 4 neutropenia reported in combo with palbociclib 1 Severe Hyper - sensitivity warning 2 Limited toxicities Safety Oral Oral Oral Oral Oral IV IV Oral (QD) ROA Unknown Unknown Yes Unknown Unknown Partial Poor Yes Brain Penetration Designed to be best - in - class PI3K pathway inhibitor with modest mTOR activity Relevant marketed or active clinical PI3K inhibitor programs 13

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, especially in more aggressive and heterogeneous settings, is often broader - Pathway dependence can arise not only from PIK3CA mutations, but also from PTEN loss, upstream signaling, downstream escape, and other network - level mechanisms o Dose de - escalation is critical for epigenetic effect o Enhances immune visibility through viral mimicry pathways and supports synergy with immune checkpoint inhibition o May allow a wider range of tumors where PI3K signaling is functionally relevant, including wild - type disease, to be addressed o May help address resistance mechanisms that can emerge when only one node of the pathway is targeted Kazia believes dual inhibition is necessary for broader biological effects, including functional epigenetic reprogramming and immune reinvigoration. PI3K and mTOR together influence tumor state, immune signaling, and resistance biology. 14

Paxalisib Paxalisib Mechanism of Action Paxalisib Dual Inhibition PI3K AKT mTOR Growth factor receptor Metastasis Inflammation Immune re - invigoration Cancer immune visibility Primary tumor burden + PARP Inhibition + Immunotherapy 15 PI3K oral inhibitor clinically proven to cross the blood - brain barrier IC 50 (nM) mTORC 1 / 2 p110 p110 p110 p110 70 3 10 46 2 Paxalisib > 1 ,000 2.5 89 565 820 Idela lis ib > 9,100 290 250 1200 5 Alpelis ib 4 ,600 116 262 166 52 Buparlis ib 1 ,200 0 .1 1 .0 9.1 0 .3 Taselis ib 580 3 75 33 3 Pictilis ib Comparative Potency vs. Other PI3K Inhibitors Note: Lower IC 50 implies more potent activity Source: HF Zhao et al. (2017) Molecular Cancer . 16:100

Paxalisib Clinical & Translational Manifestations In clinical settings, there is evidence that paxalisib's downstream epigenetic effects manifest as: Paxalisib is positioned as a backbone therapy within the emerging category of functional epigenetic reprogramming therapeutics. Reduction of Aggressive Circulating Tumor Cell (CTC) and CTC - Cluster Phenotypes Enhanced Activity When Combined with Immune Checkpoint Inhibition Modulation of Immune Exhaustion Markers Observable impact on metastatic biology Combination - enabling potential Evidence of tumor microenvironment (TME) reprogramming T IO 16 Pax

Paxalisib Cutting - edge preclinical program to evaluate paxalisib in combination with immuno - therapies for advanced breast cancer Paxalisib alone and in combination with other targeted agents is active in preclinical models of DIPG and AT / RT. US FDA has awarded Orphan Drug Disease and Rare Pediatric Disease Designations in DIPG and AT / RT. If paxalisib were to be approved, Kazia could be entitled to receive a pediatric priority review voucher which are tradeable and have historically commanded prices in excess of USD $100 million. Licensing & Collaborations Opportunistic partnering and strategic collaborations continue to add value Licensing Key Collaborations Summary To develop, manufacture, and commercialize paxalisib as a potential treatment for intractable epilepsy in focal cortical dysplasia type 2 (FCD T2) and tuberous sclerosis complex (TSC) disease To develop and commercialize paxalisib in Greater China, Hong Kong, Macau, and Taiwan Territories and Responsibilities US$1.5m US$11m, comprising US$7m in cash and a US$4m equity investment Upfront Payment Potential milestone payments of up to US$19m upon the achievement of development and regulatory milestones Contingent milestone payments of up to US$281m in GBM + further milestones payable in indications beyond GBM Milestone Payments A percentage of sub - licensing revenues and royalties on net sales of products incorporating paxalisib Mid - teen percentage royalties on commercial sales Royalties on Net Sales 17

Paxalisib: Advanced Breast Cancer Paxalisib Potential in Breast Cancer 1. Cancer.org 2024 2. Data Bridge Market Research Paxalisib inhibits PI3K / mTOR, a central oncogenic pathway driving cell survival and proliferation, resistance to endocrine, HER2 - targeted, and cytotoxic therapies, and immune suppression within the tumor microenvironment (TME). PI3K / mTOR signaling is frequently dysregulated in breast cancer and associated with tumor proliferation, disease progression, and therapeutic resistance. Brain metastases develop in ~25 - 46% of patients with metastatic TNBC over the disease course, with ~10 - 15% present at initial metastatic diagnosis. PI3K / mTOR in Breast Cancer Paxalisib Opportunity Breast Cancer >300,000 new cases of invasive BC in the US Triple Negative Breast Cancer Rare, fast - growing, and aggressive form of breast cancer Accounts for approximately 10 - 15% of all breast cancer 5 - year survival rate of 3 - 5% Predicted market growth of $1.5B by 2030 18 The most diagnosed cancer and leading cause of death in women

Paxalisib: Advanced Breast Cancer Current Treatment Landscape * Potential future regimen, depending on Keynote B49 readout ( NCT04895358 ); CPS = Combined Positive Score; wt = wildtype; NS = not statistically significant 1. BC subtypes and distribution: (7% unknown subtype) Cancer.org ; 2. Treatment: NCCN Guidelines Version 4.2025, simplified and with focus on preferred regimens; 3. https://www.pdl1portal.com/tnbc/ ; 4. Pavese et al. 2022 ; 5. Keytruda.com ; 6. Khosravi - Shani et al 2017 ; 7. Gacia - Saenz et al 2025 ; Bardia et al 2024 ; 8. Baselga et al 2012 ; 9. Jacobson 2022 ; 10. Wu et al 2020 ; 11. Yardley et al 2013 HR+ / HER2 - PD - L1 CPS <10 PD - L1 CPS > 10 mPFS: 9.7 v 5.6 months ORR 53% (17% CR, 35% PR) 5 mPFS 15.0 vs 3.0 months in patients with brain metstases 9 mPFS 5.6 vs 2.9 months; No OS benefit 7 mOS: 9 - 12 months 6 mPFS 27.6 vs 14.5 months ORR: 42.1 vs 34.7% (NS) 10 BRCA m mPFS: 4.8 vs 1.7 months ORR: 31% 7 mPFS 5.6 vs 2.9 months; No OS benefit 7 mPFS 7.8 vs 3.2 months 11 BRCA wt 9% 70% 4% 10% 1 38% 3 62% 20% 4 80% PD - L1 CPS > 1 * Pembro + chemo TBD Chemo PARPi Sacituzumab govitecan Pembrolizumab + chemo PARPi or platinum Aromatase inhibitor + CDK4/6 inhibitor Everolimus + endocrine therapy HR+ / HER2+ HR - / HER2+ Pertuzumab + trastuzumab + docetaxel or paclitaxel mPFS:18.5 vs 12.4 months 8 Fam - trastuzumab deruxtecan - nxki HR - / HER2 - (TNBC) BRCA wt Modest results for HER2 - subtypes, despite checkpoint and PARP inhibitors BRCA m Subtypes Stratification 1 st line 2 nd line 19

Paxalisib: Advanced Breast Cancer Consistent & Statistically Significant Signals PARP Inhibitor Checkpoint Inhibitor o Reduced tumor volume o Lung metastases o Lymph node metastases o Liver inflammation o Lung inflammation o Liver and spleen EMH o No observed toxicity o Reduced tumor volume o Lung metastases o Lymph node metastases o Liver inflammation o Lung inflammation o Liver and spleen EMH o No observed toxicity 4T1 Mouse Model o Standard model for TNBC o Immunotherapy resistant model o Highly tumorigenic and invasive Preclinical studies combining paxalisib with either checkpoint inhibitor or PARP inhibitor resulted in highly consistent and statistically significant signals of efficacy. Tumor * PD1: pembrolizumab or "pembro" 20 Tumor approx. 100mm 3

Paxalisib: Advanced Breast Cancer Kazia - Sponsored Clinical Phase 1b Study Overview Multi - center, open - label, randomized trial Inclusion Criteria Endpoints Treatment Arm B Recurrent, unresectable or metastatic TNBC Confirmed that tumors express PD - L1 with a combined positive score (CPS) 10 Meet all current prescribing criteria for commencing pembrolizumab therapy Total enrollment: 12 Paxalisib 15mg QD + olaparib 300 mg BID, n=6 Paxalisib 30mg QD + olaparib 300 mg BID, n=6 Paxalisib plus Olaparib (28 - Day Cycle) Primary Safety and tolerability of paxalisib in combination with either olaparib or pembro / chemotherapy Determine recommended Phase 2 dose (RP2D) Secondary Progression and response rates To assess the utility of novel liquid biopsy assessments Arm A HER2 - negative stage IV (metastatic) BC Confirmed gBRCAm (BRCA1, BRCA2 or both) Prior treatment with chemotherapy in the metastatic setting Meet all current prescribing criteria for commencing olaparib therapy Total enrollment: 12 Paxalisib 30mg QD + pembrolizumab 200mg + clinician's choice of IV chemotherapy QW3, n=6 Paxalisib plus Pembrolizumab / Chemotherapy (21 - Day Cycle) Paxalisib 15mg QD + pembrolizumab 200mg + clinician's choice of IV chemotherapy QW3, n=6 Trial ID: ACTRN12624001340527 SABCS 2025 poster presentation. 21

Paxalisib: Advanced Breast Cancer Early Clinical Trial Epigenetic Effects First - in - human data reflects mechanistic synergy consistent with the preclinical data. Combination regimen results in >50% reduction in CTCs Patient Profile 61 - year - old woman with metastatic triple - negative breast cancer localized to the left upper lobe of the lung Regimen Paxalisib + pembrolizumab + standard chemotherapy Patient One Results at Day 21 End of Cycle 1 >50% reduction in total circulating tumor cells count Comparable reduction in CTC clusters (these aggregates are associated with heightened metastatic potential) Reduction in the mesenchymal phenotype of the remaining CTCs; this phenotype is one of the hallmarks of aggressive metastatic seeding cancer cells Such results are not typically seen with chemotherapy or immunotherapy therapies Cancer cells that detach from a primary tumor or metastatic site and enter the bloodstream Cellular drivers of metastasis, capable of seeding new tumors in distant organs Clusters possess significantly higher metastatic potential than single CTCs (enhanced survival, immune evasion, and colonization capacity) CTCs are generally resistant to current therapies Reductions in CTC burden indicate potential disruption to the metastatic process itself. Circulating Tumor Cells (CTCs) Trial ID: ACTRN12624001340527 Kazia Press Release 10 July 2025 SABCS 2025 poster presentation. 22

Generally well tolerated at 30mg daily Majority of adverse events assessed as unlikely related to paxalisib All paxalisib - related events were mild to moderate to date Paxalisib: Advanced Breast Cancer Early Evidence of Tumor Regression 1 CR in mTNBC patient treated under expanded access, and 2 PRs in ongoing study Safety Preliminary Clinical Responses 1 expanded access TNBC patient achieved a confirmed complete metabolic response following re - treatment with pembrolizumab / chemotherapy plus paxalisib (under an expanded access protocol) 2/2 evaluable TNBC trial patients achieved confirmed partial responses (iRECIST) Responses reported in patients with visceral and multi - organ metastases Median treatment duration at data cut - off: ~6.1 months Trial ID: ACTRN12624001340527 Kazia Press Release 27 January 2026 23

Paxalisib: Glioblastoma (GBM) Paxalisib Potential in Glioblastoma Data on file. Market research performed 2021. Glioblastoma Multiforme Treatment Market Size Report, 2034 PI3K / mTOR signaling pathway is a central regulator of cell growth and is hyperactivated in approximately ~85% to 90% of glioblastoma cases. PI3K / mTOR in Glioblastoma Lung 14 million cancer cases per annum Breast Colon Prostate Stomach Glioblastoma Multiforme 133,000 cases per annum worldwide 5 - year survival of 3 - 5% $3.6B market size (2024) The most aggressive malignant brain cancer 24 Unlike other PI3K inhibitors approved for peripheral cancers, paxalisib crosses the blood - brain barrier overcoming a major obstacle in CNS drug delivery. Paxalisib Opportunity

Paxalisib: Glioblastoma (GBM) NDU: Newly Diagnosed Unmethylated, OS: Overall Survival GBM - AGILE (Phase 2/3) (NCT03970447 ) Phase 2 (NCT03522298 ) Adaptive, multi - arm randomized Open - label, single arm Study Type Newly diagnosed unmethylated GBM and recurrent GBM Newly diagnosed unmethylated GBM Patient Population Mixed: subgroup analyses Enriched for unmethylated MGMT Status Concurrent SOC control Historical SOC Comparator OS SoC OS Paxalisib OS Primary Endpoint 11.9 months* 15.54 months* (n=46) (n=54) in prespecified secondary in prespecified secondary 15.7 months (n=30) mOS analysis in NDU analysis in NDU GBM GBM Paxalisib demonstrated a ~3.8 month improvement in median Overall Survival 15.5 months vs. 11.9 (SoC) in a prespecified secondary analysis in newly diagnosed unmethylated GMB (GBM - AGILE) and 15.7 months in the Phase 2 trial Represents a strong OS signal reported in this GBM population Designations granted: Orphan Drug, Fast Track, and Rare Pediatric Disease *GBM - AGILE; Prespecified secondary analysis of median Overall Survival Paxalisib in Newly Diagnosed Unmethylated GBM Patients Consistent median overall survival data Overall Summary 25

Paxalisib: Glioblastoma (GBM) US FDA Type C Meeting December 2024 October 2025 FDA follow - up next steps: o Meeting anticipated for 1H 2026 o Anticipated outcome: Update from FDA discussion regarding paxalisib commercial and development path forward in GBM 26 202 6 Paxalisib in GBM commercial and development path forward Kazia plans to request follow - up meeting with the FDA to: o Discuss overall survival (OS) findings in NDU GBM patients treated with paxalisib o Seek agency feedback on a potential commercial and development pathway aligned with the FDA Oncology Center of Excellence's Project FrontRunner initiative Kazia Press Release 27 October 2025 FDA position: o Data on OS would generally not be appropriate for accelerated approval but could be considered to support a traditional / standard approval o Secondary endpoint OS data from the GBM - AGILE study may be supportive and informative for designing and executing a pivotal registrational study in pursuit of a standard approval Kazia position & next steps: o Aligned with the FDA on key aspects of the design of a proposed registrational / pivotal Phase 3 study in NDU GBM patients o To finalize the protocol for the pivotal Phase 3 study and discuss with a number of global contract research organizations (CROs) with experience in the neuro - oncology drug development space Kazia Press Release 31 December 2024

Paxalisib: Childhood Brain Cancer Paxalisib Potential in Childhood Brain Cancer 1. NCI: Childhood Brain and Other Nervous System Cancer 2. NIH: PI3K Pathway in Pediatric Brain Tumors 3. Strategic Market Research: Pediatric Brain Tumor Market Report Childhood Brain Cancer The most common malignancy of childhood Represents about one third of childhood cancer deaths 5 - year survival rates below 20% in pediatric high - grade gliomas (particularly DMGs) Predicted market growth of $3.5B by 2030 Given the frequent dysregulation of the PI3K / mTOR pathway in pediatric brain tumors and limited effective therapies, paxalisib's ability to cross the blood - brain barrier and combine with multiple treatment modalities presents a compelling therapeutic opportunity. PI3K / mTOR signaling pathway is a central regulator of cell growth and is hyperactivated in approximately ~65% to 70% of pediatric high - grade brain tumors, including DMGs and atypical teratoid / rhabdoid tumors (AT / RT). 27 High unmet need especially in patients with diffuse midline gliomas (DMGs) PI3K / mTOR in Childhood Brain Cancer Paxalisib Opportunity

Paxalisib: Childhood Brain Cancer Paxalisib in Childhood Brain Cancer Preclinical Research Phase 1 monotherapy clinical trial at St. Jude Children's Research Hospital completed ( NCT03696355 ) PNOC022, Phase 2 clinical trial in combination with ONC201, ongoing ( NCT05009992 ) Orphan Drug Designation (ODD) and Rare Pediatric Disease Designation (RPDD) granted by FDA in Aug 2020 Clinical Trials Regulatory Interaction ODD and RPDD granted by FDA in June and July 2022, respectively Kazia is actively pursuing three forms of childhood brain cancer: Advanced Childhood Cancer (PI3K / mTOR activated) Atypical Teratoid / Rhabdoid Tumors (AT / RT) Diffuse Midline Gliomas (DMG, DIPG) Research proposals under discussion Positive preclinical data as monotherapy and in combination (AACR 2022, 2023, 2024) Positive preclinical data in combination with ONC201 Regulatory strategy under discussion Phase 2 clinical trial in combination with chemotherapy for treatment of high - risk malignancies commenced 2024 ( ACTRN12623000096651 ) PNOC035, Phase 2 clinical trial evaluating paxalisib safety and efficacy Awaiting site initiation and first patient enrolled ( NCT07447076 ) PNOC: Pediatric Neuro - Oncology Consortium 28

Paxalisib: Childhood Brain Cancer Paxalisib in Diffuse Midline Gliomas (DMG) Overall Survival - Cohort 2 (post RT) Median OS 15.6 months [CI 95%; 12.0, 22.4] Trial ID: NCT05009992 1. Hargrave, D., Bartels, U. & Bouffet, E. Diffuse brainstem glioma in children: critical review of clinical trials. Lancet Oncol 7, 241 - 8 (2006) 29 Central imaging review analysis of PFS ongoing 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 patients with biopsy - proven DMG were enrolled in the PNOC Phase 2 study between November 2021 and June 2023 (median age 9 years [range 3 - 37], n=41, female [60%]) o Updated Median OS from time of diagnosis was 15.6 months (Confidence interval (CI) 12.0, 22.4) o Cohort 3 enrolled 30 recurrent patients (in conjunction with radiation therapy) had median OS 8.7 months [CI 95% 8.5, NA] o Most common grade 3 and above treatment - related adverse events were decreased neutrophil count (n=4); mucositis (n=3); and colitis, drug reaction with eosinophilia and systemic symptoms, decreased lymphocyte count, hyperglycemia, and hypokalemia (n=2) o Next Steps: Further PK and biomarker analyses ongoing for subsequent cohorts; anticipate further update 2026

Paxalisib: Brain Metastases Paxalisib in Brain Metastasis Trial ID: NCT0419298 1 Interim analysis showed encouraging clinical activity of paxalisib in combination with radiation therapy. August 2022 July 2023 February 2024 30 Data from first stage presented at 2022 Annual Conference on CNS Clinical Trials and Brain Metastases , Toronto, Canada All 9 patients evaluated for efficacy exhibited a clinical response , according to RANO - BM criteria, with breast cancer representing the most common primary tumor Fast Track Designation granted by US FDA for paxalisib in combination with radiation therapy in patients with solid tumor brain metastases and PI3K pathway mutations Announced early conclusion , based on Stage 2 positive safety data and promising clinical response findings observed to date. Full clinical study report pending MSKCC - sponsored Phase 1 trial Preliminary data presented at two 2024 scientific congresses: American Society for Radiation Oncology Annual Meeting (ASCO) & Society for Neuro - Oncology Annual Meeting (SNO)

Paxalisib: Brain Metastases Paxalisib in Brain Metastasis Trial ID: NCT0419298 1 RANO - BM: Response assessment in neuro - oncology brain metastases, WBRT: whole - brain radiation therapy, SRS: stereotactic radiosurgery 1. Zhou et al. 2021, Kim et al. 2020 Response signal seen for concurrent paxalisib and brain RT MSKCC - sponsored Phase 1 trial Interim analysis showed encouraging clinical activity of paxalisib in combination with radiation therapy. 31 Primary objective of identifying the maximum tolerated dose (MTD) was met: Concurrent daily administration of paxalisib with brain radiotherapy was generally well - tolerated at a maximum dose of 45mg per day in advanced solid tumor patients with brain metastases and PI3K pathway mutations Over two - thirds of the patients at MTD achieved intracranial response compared to historical response rates (20 - 40%) 1 for WBRT alone Future goals include: Extending the duration of PI3K inhibition, neoadjuvant, adjuvant, and maintenance (ideally with complementary systemic therapy options) Integrating PI3K inhibition with CNS tumor types with relevant pathway driver mutations and potentially SRS Overall Summary

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 proliferation & migration in TNBC cell model) o Overcoming metastasis and drug resistance in combination with immunotherapy (epigenetic reprogramming of dormant cancer cells and improved cancer immune visibility) o Generally well tolerated (evaluated in 550 adult and pediatric patients across Phase 1 - 3 clinical trials and expanded access programs) Clinical and Translational Epigenetic Data Demonstrate That Paxalisib: o Reduces CTC and CTC - clusters as well as aggressive mesenchymal phenotypes (observable impact on metastatic biology) o Enhances activity when combined with immune checkpoint inhibition (combination - enabling potential) o Modulates immune exhaustion markers (evidence of tumor microenvironment reprogramming) On Strategy o Positioned as a backbone therapy within the emerging category of functional epigenetic reprogramming therapeutics Next Steps o Advanced Breast Cancer : 1) Provide additional preclinical data and updates from the QIMR collaboration throughout the year and 2) ongoing updates from Phase 1b advanced breast cancer clinical study (ACTRN12624001340527) throughout 2026 o Glioblastoma : 1) Anticipated follow - up FDA Type C meeting to discuss commercial and development path forward, 2) finalize Phase 3 approval protocol, assess costs / timelines, and select strategic CRO partner, and 3) updates from ongoing GBM trials o Pediatric & Brain Metastasis Programs : 1) PNOC team to complete PK / biomarker data analysis and provide update, 2) complete analysis and close out MSKCC Phase 2 clinical brain metastasis study, 3) data release / updates from other brain met trials, and 4) initiate enrollment for PNOC035 AT / RT study Paxalisib 32

PD - L1 Protein Degrader Platform 33

PD - L1 Protein Degrader Platform Platform Overview Lead candidate, NDL2, is an optimized bicyclic peptide PD - L1 degrader designed to target intracellular PD - L1, thereby restoring anti - tumor immune responses even in cases of immune evasion or checkpoint inhibitor resistance Asset Overview Developed by QIMR Berghofer Origin Preclinical; IND expected in 18 months Development Stage Breast cancer and non - small cell lung cancer (NSCLC) in early stage and metastatic settings Lead Indications Intravenous infusion Formulation First in Class: As the science surrounding PD - L1 degraders is novel (<5yrs), there are no PD - L1 degraders in clinical studies at this time Key Differentiators Target intracellular PD - L1 protein pools Recruits cellular degradation machinery Targets intracellular PD - L1 protein species that cannot be targeted by standard checkpoint inhibitors Mechanism of Action N / A FDA Designations Initial composition of matter IP filed in 2021 IP 34 Complementing paxalisib's transcriptional and epigenetic effects, Kazia's NDL2 program addresses immune resistance at the post - translational regulatory level

PD - L1 Protein Degrader Platform Asare - Werehene et al., Front. Immunol., 2025, DOI: 10.3389/fimmu.2025.1543529; Liu et al., Biochemical Pharmacology, 2024, DOI: 10.1016/j.bcp.2023.115984 Healthy Cell PD - L1 expressed on cell surface (sPD - L1) Binds to PD - 1 on cell surface Prevents autoimmunity Limits tissue damage by suppressing overactive immune response s c Cancer Cell PD - L1 translocates into the nucleus (nPD - L1) nPD - L1 has been shown to induce transcription of genes leading to angio - genesis, tumori - genesis, drug resistance, and tumor recurrence Surface PD - L1 mediates immune evasion nPD - L1 s c IMP Distinct distributions of PD - L1 (cell surface, cytosol, nucleus) have different functions on tumor progress. Intracellular PD - L1 has been implicated in immunotherapy resistance, metastatic progression, and immune suppression independent of canonical PD - 1 / PD - L1 extracellular signaling. Targeting nPD - L1 could provide a therapeutic benefit , including in patients who are resistant to existing anti - PD - 1 / L1 therapies. Current Anti - PD - 1 / L1 Therapy Landscape Limited by intracellular PD - L1 35

PD - L1 Protein Degrader Platform Targeted Protein Degradation (TPD) therapies opened a new frontier for treating cancer by exploiting naturally occurring protein degradation pathways to disrupt critical cellular processes. 36 NDL2 is an optimized bicyclic peptide PD - L1 degrader Designed to target intracellular PD - L1 Formation of a ternary complex (intracellular PD - L1 : NDL2 : E3 ligase) which leads to proteasomal degradation Restoring anti - tumor immune responses Even in cases of immune evasion or checkpoint inhibitor resistance NDL2: First - In - Class PD - L1 Degrader Targeting intracellular PD - L1

PD - L1 Protein Degrader Platform Sullivan et al., PLoS ONE 2023, doi.org/10.1371/journal.pone.0286724 PD - (L)1 mAbs NDL2 Peptide Degrader of PD - L1 Block the PD - 1:PD - L1 interaction at the cell surface; Fc effector function varies by isotype / engineering Targeted protein degradation via intracellular E3 ubiquitin proteasome system Primary Mechanism IV / SC IV Route of Administration (ROA) Surface protein Intracellular PD - L1 Pools Addressed Commonly cited global commercial checkpoint inhibitors include: Pembrolizumab, Nivolumab, Cemiplimab, Atezolizumab, Durvalumab, and Avelumab Academic programs in early preclinical development (no clinical programs nor industry programs identified) Competitors / Development Stage 37 Key Differentiator NDL2 distinguishes itself as a modality facing minimal competitive challenges

PD - L1 Protein Degrader Platform Preclinical & Translational Manifestations Across multiple preclinical models and patient - derived samples, NDL2 demonstrated : Data generated collectively supports intracellular PD - L1 as a mechanistically distinct and therapeutically actionable driver of immune evasion, disease progression, and metastasis. Suppressed metastatic spread in aggressive tumor models Targeted resistance mechanisms enriched in immunotherapy - refractory disease T Enhanced activity of anti - PD - 1 therapy in combination Anti - PD - 1 NDL2 T Reduced tumor growth as monotherapy NDL2 38

PD - L1 Protein Degrader Platform Gold Standard model for TNBC Immunocompetent BALB/c mice Highly tumorigenic and invasive Intermitted dosing Tumor Inoculation NDL2 IP injection Day - 10 Tumors approx . 100 mm 3 Harvest 0 1 2 3 4 5 6 7 8 +/ - antiPD1 IP injection 1x10 5 4T1 cells right mammary gland BALB/c mice 0 2 4 6 10 8 Tumour volume NDL2 - D NDL2 - D+ PD1 a b c d e f 0 2 4 6 8 10 Days of treatment a; *p<0.05, b/c; *p<0.05, d; **p<0.01, e; *p<0.05, f; **p<0.01 versus Vehicle, Two - way Anova, Dunnett's post test 49% 73% NDL2 reduces primary tumor volume by 49% as a monotherapy NDL2 reduces primary tumor volume by 73% in combination with anti - PD1 Efficacy in 4T1 Mouse Model NDL2 monotherapy and anti - PD1 combination reduces primary tumor burden with intermittent dosing Vehicle PD1 NDL2 NDL2 + PD1 Tumor Volume (Fold change versus Day 0) 39

PD - L1 Protein Degrader Platform Method : FFPE sections from Control (vehicle), anti - PD 1 , NDL 2 or NDL 2 + anti - PD 1 ( 10 mg/kg) tumors were stained using the BondRX automatic FFPE staining platform and the change in expression characterized with high resolution digital pathology . Significant differences are calculated as one - way ANOVA Kruskal - Wallis test comparison to vehicle control (N = 3 - 5 mice per group) . Control PD1 NDL2 Combo 15 10 5 0 20 %CD8 + TIL Population ns ns Increases in CD8 + T Cell Proliferation Control PD1 NDL2 Combo 0 5 10 15 %CD8 + TIL Population ns ns 40 Increase in CD8 + T Cell Infiltration Efficacy in 4T1 Mouse Model (Cont.) NDL2 and anti - PD1 combination therapy reduces T cell exhaustion

PD - L1 Protein Degrader Platform Body Weight 90 100 110 120 % Change in body weight (versus Day 0) ns ns ns * ns, not significant (verus Vehicle), One - way ANOVA, Dunnett's post test No toxicity observed for NDL2 Normal body weight Normal liver weight for treatment duration Safety in 4T1 Mouse Model NDL2 shows no evidence of toxicity Liver Weight 1.5 1.0 0.5 0.0 2.0 Liver weight (g) ns; not significant (versus Vehicle), One - way Anova, Dunnett's post test ns ns ns 41

PD - L1 Protein Degrader Platform 42 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 - associated form of PD - L1, preserving PD - L1 essential for normal immune regulation Recent Preclinical and Translational Data Demonstrate That NDL2: o Reduces tumor growth as monotherapy o Enhances the activity of anti - PD - 1 therapy o Targets resistance mechanisms enriched in immunotherapy - refractory disease o Preserves normal immune checkpoint function at the cell surface and therefore avoids toxicity associated with anti - PD - L1 agents On Strategy o NDL2 is reshaping cancer cell behavior by altering the functional protein landscape rather than simply blocking extracellular signaling o NDL2 represents a complementary modality to epigenetic and transcriptional reprogramming, extending Kazia's strategy into targeted protein degradation Next Steps o Initiate IND enabling studies o Integrate a clinical liquid biopsy to enable patient stratification, real - time monitoring, and personalized treatment optimization o Launch PD - L1 degrader and NDL2 awareness campaign through abstracts, manuscripts, videos, and medical congress presentations

SETDB1 Inhibitor Platform 43

SETDB1 Inhibitor Platform 44 Platform Overview Lead candidate, MSETC is an optimized, bicyclic peptide designed to target SETDB1, a key epigenetic regulator of immune evasion. By inhibiting SETDB1, MSETC could restore anti - tumor immune responses, including in tumors resistant to checkpoint inhibitors. Asset Overview Developed by QIMR Berghofer Origin Preclinical; IND expected in 18 months Development Stage Solid tumors with low immunogenicity ("immune cold", e.g. TNBC, NSCLC, CRC) Lead Indications Intravenous infusion Formulation First - in - class SETDB1 inhibitor (chromatin - level immune regulator); targets immune evasion; potential to convert "immune cold" tumors into responsive tumors; combination - ready with immunotherapy and targeted agents; intracellular / nuclear mechanism not addressed by antibody therapies Key Differentiators SETDB1 is a histone methyltransferase implicated in immune resistance and immune evasion that silences genes involved in immune recognition and interferon signaling through chromatin modification; designed to suppress immune signaling pathways, increase tumor visibility to the immune system, and potentially reverse resistance to checkpoint inhibitors Mechanism of Action N / A FDA Designations Initial composition of matter IP filed in 2022 IP Complementing paxalisib's transcriptional modulation and NDL2's protein degradation

SETDB1 Inhibitor Platform SETDB1: Making Cancer Visible to the Immune System Why is This a Big Opportunity ? Why Isn't Everyone Doing This? Access through leading research from QIMR Berghofer First - in - class optimized approach to targeting SETDB1 Complements Kazia's existing focus on reprogramming cancer behavior Why Kazia? What is SETDB1? Why Does This Matter? A protein that cancer cells use to hide from the immune system Turns off signals that would normally alert the body to attack the tumor, acting like an internal "off switch" Many cancers become resistant to immunotherapy because they can no longer be "seen" by the immune system. By targeting SETDB1, we aim to: o Turn those signals back on o Make tumors more visible o Help existing therapies work again Targets a major global unmet need : aggressive, treatment - resistant cancers Novel first - in - class therapeutic and companion biomarker platform with lead indications in NSCLC , CRC , and metastatic breast cancer (TNBC) Many patients still do not respond or develop resistance to immunotherapy SETDB1 works inside the cell nucleus , making it difficult to target It has only recently been recognized as a key driver of immune resistance New technologies (like advanced peptides) are now making this possible 45

SETDB1 Inhibitor Platform MSETC: First - In - Class Bicyclic Peptide Inhibitor Target SETDB1, a key regulator of tumor immune evasion SETDB1 is a key regulator of tumor immune evasion, driving resistance to immunotherapy in solid cancers Overexpressed in aggressive solid tumors Novel biology identified using an AI - integrated epigenetic drug discovery engine Translational obervations: Selective enrichment of the nuclear SETDB1 complex in I/O - resistant and metastatic patients Companion biomarker: A liquid biopsy - based nSETDB1 biomarker Targeting nuclear SETDB1 Drug Development MSETC, first - in - class therapeutic Potent and selective bicycle - based peptide therapeutic Lead candidate generation and extensive optimization using AI - integrated epigenetic drug discovery engine Optimized IV delivery Structural breakthrough : First co - crystal structure of MSETC bound to the nuclear SETDB 1 - ATF 7 IP - importin complex MSETC large scale manufacturing capability Mechanism of Action MSETC disrupts the nuclear SETDB1 complex Selective complex disruption: MSETC disrupts the nuclear SETDB1 complex, a key driver of immunotherapy resistance, metastasis, and recurrence Disease - specific targeting: Complex is absent in healthy cells Preserves normal function: Does not inhibit SETDB1 catalytic activity, maintaining essential immune function Pharmacokinetics & Safety PK & safety package established Comprehensive PK and safety package established Benchmarking suggests superior characteristics relative to current clinical - stage epigenetic therapies Biological Activity Dual targeting therapeutic Targets metastatic initiating tumor cells Reverses terminal immune exhaustion In vivo MSETC efficacy: o Inhibits primary tumor burden and metastases with monotherapy and in combination with immunotherapy o Blinded pathology analysis shows no evidence of autoimmunity Epigenetic Reprogramming Drives immune visibility and anti - metastatic activity Increases interferon (IFN) signaling Induces viral mimicry Upregulates MHC Class I & II expression Promotes tumor - specific neoantigen presentation Induces durable immune memory Disruption of metastatic initiating tumor cells Preclinical / translational data on file.

SETDB1 Inhibitor Platform 47 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 current therapies Emerging Preclinical Rationale Supports SETDB1 Targeting o Reactivates interferon and antigen presentation pathways o Increases tumor visibility to the immune system o Sensitizes tumors to checkpoint inhibition in resistant settings o Targets mechanisms not addressed by current immunotherapies On Strategy o Extends Kazia's cancer reprogramming approach to chromatin - level control of tumor behavior o Complements paxalisib's transcriptional modulation and NDL2's protein degradation o Enables a multi - layered strategy addressing immune evasion across distinct biological levels Next Steps o Advance IND - enabling studies and candidate characterization o Build awareness and value through continued generation and dissemination of preclinical and translational data supporting the SETDB1 platform and MSETC o Define optimal combination strategies with checkpoint inhibitors and targeted therapies o Generate translational data to support patient selection and biomarker - driven development o Evaluate early partnering opportunities aligned with development milestones

EVT801 49 Overview A highly selective, potential first - in - class small molecule Vascular Endothelial Growth Factor Receptor - 3 (VEGFR3) inhibitor, primarily inhibiting lymphangiogenesis Asset Overview Discovered by Sanofi; Early development by Evotec SE; In - licensed by Kazia in 2021 Origin Phase 1 completed Development Stage Potentially high - grade serous ovarian cancer (HGSOC) Lead Indications Oral, capsule Formulation Selective VEGFR3 inhibitor in clinical development; distinct from broader VEGF / VEGFR inhibitors that target multiple VEGF receptors, with the potential for a more favorable safety profile and reduced resistance due to hypoxia Key Differentiators By inhibiting VEGFR - 3, EVT801 restricts lymphangiogenesis (the formation of new lymphatic vessels), stabilizes tumor vasculature, reduces hypoxia, and thereby limits tumor escape and metastatic spread Mechanism of Action N / A FDA Designations Composition - of - matter to 2032 / 2033 in most jurisdictions (excluding PTE) IP

EVT801 EVT801 Selectively Inhibits VEGFR3 Cell Survival (Lymph) - angiogenesis T - Cell Migration Avastin (bevacizumab) VEGFR1 VEGFR2 VEGFR3 VEGF - A VEGF - B VEGF - C VEGF - D VEGF - E Angiogenesis Vasculogenesis T - Cell Migration Signal Modulation LUCENTIS (ranibizumab) SUTENT (sunitinib) NEXAVAR (sorafenib) INLYTA (axitinib) VOTRIENT (pazopanib) EVT801 50

EVT801 A Differentiated Anti - Tumor Approach Tumor Killing Direct effect on VEGFR3 - expressing tumor cells (typically from endothelial origin, e.g. sarcoma) Increase in anti - tumor immune activity No impact on T - cells viability Increased infiltration of effector T - cells Reduction in immunosuppressive myeloid cells Inhibition of tumor escape and metastasis Stabilization of tumor vasculature Inhibition of (lymph) - angiogenesis Avoidance of hypoxia decreases potential for metastatic spread 3 2 1 51

EVT801 Phase 1 Dose - Finding Trial Completed Dose cohort 3 EVT801 monotherapy Dose cohort 2 EVT801 monotherapy Dose cohort 1 EVT801 monotherapy Design Monotherapy dose escalation N=26 6 cohorts Single - patient cohorts initially; expand to 3+3 when toxicity is encountered Mixed population of advanced solid tumors Doses from 50mg QD to 500mg BID Target population: Histologically - confirmed advanced or metastatic solid tumors, unresponsive to standard treatment, or for whom no standard treatment is available or appropriate Sponsor: Kazia Therapeutics Limited Product : EVT801 EudraCT Number: 2021 - 002483 - 47 Clinical Sites (France only): IUCT - Oncopole, Toulouse PI : Dr Gomez - Roca Centre L on B rard, Lyon PI : Dr Philippe Cassier Trial ID: KZA 0801 - 101, NCT05114668 MTD: Maximum Tolerated Dose; RP2D: Recommended Phase 2 Dose 52 Human active dose prediction based on predicted human clearance of 2.5 mL / min / kg: 375 mg BID Patients with 11 different cancer types were enrolled, with heavily pretreated advanced ovarian cancer being the most prevalent indication (11 patients) MTD has been reached at 500mg BID The recommended dose for Phase 2 is 400mg BID* in continuous monotherapy administration Overall Summary Study Background

EVT801 Summary & Next Steps Well - understood mechanism (anti - angiogenesis) with unique differentiating feature (high VEGFR3 selectivity) Strong preclinical data package, with observed activity in multiple tumors and favourable toxicology Phase 1 completed demonstrating encouraging safety and tolerability profile to date o Clinical and biomarker data presented at AACR Ovarian Cancer Research Symposium September 2024 o Primary and secondary objectives successfully met, with MTD and RP2D identified o Encouraging signal of activity observed in high - grade serous ovarian cancer (HGSOC) as well as strong VEGFR3 biomarker expression Next clinical trial under discussion with scientific thought leaders o Consolidate safety data at RP2D and our hypotheses on EVT801 mode of action o Validate HGSOC as indication of choice for clinical trial Phase 2 as monotherapy or in combination with standard - of - care (ex. PARPi) 1 2 3 Potential for combination use with immuno - oncology therapies 4 5 53 Kazia has initiated a regional and / or global partnership search for EVT801.

Corporate Highlights 54

Near - Term Milestones & Anticipated Catalysts Q1 2026 Complete metabolic response in stage IV TNBC expanded access patient and 2 partial responses in metastatic TNBC Phase 1b study Advancement of NDL2 PD - L1 degrader and MSETC SETDB1 inhibitor platforms toward IND - enabling studies Anticipated update from FDA discussion regarding paxalisib commercial and development path forward Readouts from neuro - oncology focused clinical trials in patients with GBM and brain metastases Clinical efficacy and biomarker data from ongoing Phase 1b breast cancer study Update of paxalisib pre - clinical development into additional breast cancer subtypes Publication / Presentation of translational data supporting therapeutic reprogramming strategy for paxalisib Milestone Anticipated Catalyst PD - L1 protein degrader platform update PD - L1 degrader and SETDB1 inhibitor awareness, NDL2 and MSETC IND - initiating studies Pricing of $50m private placement of equity securities Q4 2025 Q2 2026 Q3 2026 Q4 2026 Acquisition of SETDB1 inhibitor platform 55

Investment Drivers Kazia is helping to redefine oncology development by advancing a cohesive therapeutic approach aimed at reprogramming tumor biology. Resistance biology is well documented and combination strategies are actively sought by strategic partners . Build a portfolio that is greater than the sum of its parts Align with clear pharma appetite for epigenetic modulation, immune - sensitization, and targeted degradation assets Generate early clinical and translational proof - of - concept data that is highly attractive for strategic partnering Participate meaningfully in multiple large oncology markets without overextending development resources Our clinical and translational focus is advanced breast cancer and other immunotherapy - challenged solid tumors that represent multi - billion - dollar markets with high unmet need . Our assets are designed to remain relevant across tumor heterogeneity and evolving treatment landscapes. Our strategy is aligned with where both science and capital are moving in oncology. Our integrated approach allows us to: 56

Leadership Managemen t Dr. John Friend Chief Executive Officer Jeffrey J. Kraws Head of Corporate Strategy & Development Jeffrey Bonacorda VP Finance & Controller Robert Apple Chairman Steven Coffey Non - Executive Director Ebru Davidson Non - Executive Director Board of Directors Elissa Hansen Corporate Secretary Dr. Sudha Rao Chief Scientific Officer 57

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