Kazia Therapeutics (NASDAQ: KZIA) details board change, cash runway and cancer pipeline

Rhea-AI Filing Summary

Kazia Therapeutics Limited reports board changes, shareholder voting outcomes, and shares an updated corporate overview. Chairman Bryce Carmine will retire effective March 31, 2026, and the board will shrink from four to three directors, with Ebru Davidson joining the Audit, Risk and Governance Committee. The company states his resignation is not due to any disagreement over operations or policies. Shareholders re-elected director Steven Coffey, with 1,050,412,780 votes for and 3,637,588 against.

Kazia also furnishes a detailed investor presentation and fact sheet outlining its oncology pipeline. Lead asset paxalisib, a brain-penetrant dual PI3K/mTOR inhibitor, has been studied in more than 550 patients and is being advanced in glioblastoma, pediatric brain cancers, brain metastases, and triple negative breast cancer, where early Phase 1b data include one complete metabolic response and two partial responses. The company highlights cash and cash equivalents of about US$46 million, no debt, and an expected cash runway into 2029, as well as a preclinical PD-L1 protein degrader (NDL2) and VEGFR3 inhibitor EVT801.

Insights

Biotech equity analyst

Routine governance changes alongside a well-funded, multi-asset oncology pipeline.

Kazia Therapeutics combines a board refresh with an extensive update on its cancer drug portfolio. The chairman’s planned retirement, explicitly not tied to disagreements, looks like normal succession rather than a sign of instability.

The exhibits emphasize a diversified pipeline led by paxalisib, which has FDA Fast Track, Orphan Drug, and Rare Pediatric Disease designations across glioblastoma and pediatric brain tumors. Early signals in triple negative breast cancer, including one complete metabolic response and two partial responses, are encouraging but still preliminary.

From a financing perspective, around US$46 million in cash with no debt and stated runway into 2029 materially reduces near-term funding risk. The mention of a $50 million private placement in Q4 2025 indicates the company has already raised significant capital to support these programs, though ultimate value will depend on future trial readouts and regulatory interactions.

Key Figures

Votes for Coffey re-election: 1,050,412,780 votes Votes against Coffey re-election: 3,637,588 votes Cash and cash equivalents: US$46 million +5 more

8 metrics

Votes for Coffey re-election 1,050,412,780 votes Shareholder resolution to re-elect director Steven Coffey

Votes against Coffey re-election 3,637,588 votes Shareholder resolution to re-elect director Steven Coffey

Cash and cash equivalents US$46 million Stated cash position with runway into 2029

ADS outstanding 11.4 million ADS American Depository Shares outstanding as described in fact sheet

Private placement size $50 million Pricing of private placement of equity securities in Q4 2025

TNBC responses 1 CR, 2 PR Paxalisib in stage IV and metastatic triple negative breast cancer

Paxalisib patients treated Over 550 patients Adult and pediatric patients across Phase 1–3 trials and expanded access

DMG median OS 15.6 months Diffuse midline glioma patients in PNOC Phase 2 trial, from diagnosis

Key Terms

triple negative breast cancer, Rare Pediatric Disease Designation, overall survival, PD-L1 protein degrader, +2 more

6 terms

triple negative breast cancer medical

"Phase 1b clinical study in TNBC ongoing"

Triple negative breast cancer is a type of breast cancer that lacks three common markers used to identify and target the disease, making it more challenging to treat. It tends to grow and spread more quickly than other forms, which can lead to more aggressive outcomes. Its complexity can impact medical research and treatment developments, influencing investor interest in healthcare companies working on new therapies.

Rare Pediatric Disease Designation regulatory

"Paxalisib granted Rare Pediatric Disease Designation by the US FDA"

A rare pediatric disease designation is an official regulatory status given to a drug or therapy that targets a serious or life‑threatening condition primarily affecting children and is uncommon in the population. It matters to investors because the status often brings financial and development perks — such as tax credits, reduced fees, faster review and periods of market protection — which can lower costs, speed approval and improve the commercial outlook; think of it as a VIP pass that makes bringing a scarce, child‑focused treatment to market easier and potentially more profitable.

overall survival medical

"showed clinically meaningful improvement in a prespecified secondary analysis for OS"

Overall survival is the average or median length of time patients remain alive after starting a treatment or entering a clinical study, measured regardless of cause of death. Investors care because it is a clear, hard measure of a therapy’s real-world benefit — like timing how long a new battery actually runs — and strong improvements in overall survival can drive regulatory approval, market adoption and revenue potential.

PD-L1 protein degrader medical

"NDL2 – a potentially first-in-class protein degrader designed to target intracellular PD-L1"

A PD‑L1 protein degrader is a drug designed to remove a specific protein (PD‑L1) that acts like a brake on the immune system’s ability to attack cancer cells; instead of merely blocking the brake, it aims to take the brake off entirely by degrading the protein. For investors this matters because the approach could produce stronger or longer-lasting anti‑cancer effects than traditional blockers, offering commercial upside if safe and effective, but it also carries typical drug-development and regulatory risks.

Fast Track Designation regulatory

"Paxalisib received Fast Track Designation by the US FDA"

A "fast track designation" is a process that speeds up the review and approval of a product or project, allowing it to reach the market or be completed more quickly than usual. For investors, it can signal that a product may become available sooner, potentially leading to earlier revenue or benefits, and indicating a priority status that might influence company performance and market opportunities.

brain-penetrant medical

"Lead asset paxalisib is an oral, brain-penetrant dual PI3K / mTOR inhibitor"

A brain-penetrant drug or molecule can cross the brain’s natural security gate (the blood–brain barrier) to reach and act on cells inside the brain. For investors, that matters because treatments that reach the brain can address disorders like Alzheimer’s, depression, or brain cancer—opening large markets—but they also carry higher technical risk, stricter safety testing and unique regulatory challenges compared with drugs that act elsewhere in the body.

Form 6-K: How Foreign Companies Report to the SEC →

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION 

WASHINGTON, D.C. 20549

FORM 6-K

REPORT OF FOREIGN PRIVATE ISSUER

PURSUANT TO RULE 13a-16 OR 15d-16

UNDER THE SECURITIES EXCHANGE ACT OF 1934

For the Month of March 2026

Commission File Number: 000-29962

Kazia Therapeutics Limited.

(Exact Name of Registrant as Specified in Its Charter)

Three International Towers Level 24 300 Barangaroo Avenue Sydney NSW 2000

(Address of principal executive offices)

Indicate by check mark whether the registrant files or will file annual reports under cover of Form 20-F or Form 40-F.

Form 20-F  ☒        Form 40-F ☐

INFORMATION CONTAINED IN THIS FORM 6-K REPORT

Departure of Director

This report on Form 6-K (the “Report”) contains information regarding a change to the board of directors (the “Board”) of Kazia Therapeutics Limited (the “Company”). On March 26, 2026, Bryce Carmine, the current Chairman of the Board, notified the Board of his intent to retire. The Board accepted his resignation from the Board and all of its committees, including his roles as Chair of the Board and member of the Remuneration and Nomination Committee and Audit, Risk and Governance Committee, effective March 31, 2026.

Mr. Carmine’s resignation was not the result of any disagreement between him and the Company on any matter relating to the Company’s operations, policies or practices. Effective upon Mr. Carmine’s resignation, Ms. Ebru Davidson was appointed to the Audit, Risk and Governance Committee of the Board and the size of the Company’s Board of Directors was reduced from four to three Directors.

Results of Annual General Meeting

As scheduled, the Company held its Annual General Meeting (the “AGM”) at 9.00 a.m., Sydney time, on March 25, 2026, online at https://kaziatherapeutics.verovoting.com.au. At the AGM, the Company’s shareholders voted on one resolution with respect to the re-election of Steven Coffey as a director of the Company, which is listed below and was described in more detail in the Company’s Notice of Annual General Meeting and accompanying Explanatory Statement, which are available electronically on the “For Investors” section of the Company’s website.

Resolution 1 – Re-election of Steven Coffey as Director

The re-election of Steven Coffey as a director of the Company was approved by the Company’s shareholders. The results of the approval were as follows:

		FOR		AGAINST		ABSTAIN
VOTES		1,050,412,780		3,637,588		1,289,127

Investor Presentation and Fact Sheet

The Company is furnishing with this Report on Form 6-K (i) its corporate presentation, dated March 27, 2026, as Exhibit 99.1 and (ii) its fact sheet, dated March 27, 2026, as Exhibit 99.2.

The information in this Report, including Exhibits 99.1 and 99.2, is being furnished and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, nor shall it be deemed incorporated by reference into any filing under the Securities Act of 1933 or the Exchange Act, except as expressly set forth by specific reference in such a filing.

EXHIBIT INDEX

The following exhibits are furnished as part of this Form 6-K:

Exhibit		Description
99.1		Investor Presentation dated March 27, 2026.
99.2		Fact Sheet dated March 27, 2026.

1

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the Registrant has duly caused this report to be signed on its behalf by the undersigned, thereunto duly authorized.

	Kazia Therapeutics Limited.
	By:	/s/ John Friend
	Name:	John Friend
	Title:	Chief Executive Officer
Date: March 31, 2026

2

Exhibit 99.1

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

1 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, 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, 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. Forward-Looking Statements

2 Kazia Therapeutics Limited is a 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.

3 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.

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 04 05 4

Our Approach 5 A New Approach to Cancer o Cancer progression, metastasis, and treatment resistance are increasingly understood not as single-gene problems, but as failures of regulatory control. o Transcriptional programs, chromatin states, and immune checkpoints adapt dynamically to evade therapy. o The next wave of oncology innovation is shifting beyond simple inhibition toward therapies that reprogram cancer biology. Epigenetic Therapeutics Immuno-Oncology Targeted Protein Degradation We believe Kazia is positioned at the intersection of three of the fastest-growing and strategically important areas in oncology.

Complementary Layers of Cancer Control Paxalisib Brain-penetrant dual PI3K / mTOR inhibitor with epigenetic and immunomodulatory activity PD-L1 Protein Degrader Platform First-in-class optimized PD-L1 protein degrader Epigenetic Pathway Modulation – Inhibits PI3K-driven epigenetic regulators – Reprograms metastatic and immune-suppressive tumor states Enhances Immune Responsiveness – Reduces tumor-driven immune suppression – Improves sensitivity to immunotherapy and other targeted therapeutics Clinically Validated Asset – Evidence of clinical activity across CNS, breast cancer, and other solid tumors – Fast Track, Orphan Drug, and Rare Pediatric Disease designations from US FDA Strategic Backbone Across CNS & Breast Cancer – Demonstrated relevance in high-unmet-need CNS tumors, including glioblastoma – Expanding applicability into large breast cancer populations beyond TNBC – Shared biological drivers enable multi-indication development and commercial scale Safety and tolerability evaluated in >550 patients to date Phase 1b clinical study in TNBC ongoing NDL2 (Lead Compound) is First-in-Class PD-L1 Protein Degrader – Target intracellular PD-L1 protein rather than transiently block receptor–ligand interaction – Designed to overcome mechanisms of resistance to antibody- based checkpoint inhibitors Epigenetic & Immune Reprograming of Resistant Tumors – Targets tumor-intrinsic immune evasion not reached by existing immunotherapies – Potential to restore immune sensitivity in refractory tumors Platform & Combination Potential – Potential broad applicability across solid tumors and rationale for combination with pathway inhibitors and cytotoxics – Potential backbone for next-generation immuno-oncology regimens Clear Development & Value Inflection Path – Designed for rapid transition to first-in-human trials – Multiple preclinical and translational milestones prior to clinical proof-of-concept IND initiating studies commencing 2026 Kazia is building a differentiated oncology portfolio aligned with the current shift in oncology, designed to overcome resistance in aggressive and immunotherapy-refractory cancers. 6

Pipeline Overview 7 High-value indications with strong partnering potential

Development Plan At a Glance 8

Market Landscape: Growth & Opportunity 9 1. Epigenetic Drugs Market 2. Immuno-Oncology Market 3. Targeted Protein Degradation Market o Current Market: $15–20B o Projected 2034: $80B+ o Growth Driver: Oncology applications Immuno-Oncology 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 Targeted Protein Degradation 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 • 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.

10 Paxalisib

Paxalisib Overview 11 Asset Overview Brain-penetrant, oral, once daily small molecule dual PI3K / mTOR inhibitor with epigenetic and immunomodulatory activity Origin Discovered by Genentech (GDC-0084); In-licensed by Kazia Therapeutics Development Stage Clinical Lead Indications Advanced Breast Cancer (ABC, Phase 1), Glioblastoma (GBM, Phase 3), Childhood Brain Cancer (Phase 2 / Preclinical) Formulation Oral, capsule Key Differentiators 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 Mechanism of Action 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 FDA Designations 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) IP Full IP portfolio comprising three families of patents: compound, process, and secondary with major jurisdictions including U.S., Europe, Japan, China, and India

Paxalisib Developmental History & Milestones 12 Early 2000'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 March 2018 Kazia commences company- sponsored Phase 2 clinical study of GDC-0084 as a first line therapy in patients with glioblastoma August 2020 Paxalisib granted Breakthrough Designation by the US FDA for glioblastoma January 2021 GBM AGILE pivotal study commences recruiting paxalisib arm February 2018 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 July 2024 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 July 2022 Paxalisib granted Rare Pediatric Disease Designation by the US FDA for rare childhood brain cancer, AT / RT July 2025 ABC-Pax Phase 1b preliminary results from the first TNBC patient achieved >50% reduction in circulating tumor cells July 2023 Paxalisib received Fast Track Designation by the US FDA for solid tumor brain metastases with PI3K pathway mutations in combination with radiation therapy June 2025 Kazia commences Phase 1b ABC-Pax study of paxalisib in combination with immunotherapy in patients with triple negative breast cancer (TNBC) January 2026 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 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. GlobalData 3. Piqray Five PI3K inhibitors have been approved by the US FDA. Chronic lymphocytic leukemia Follicular lymphoma Follicular lymphoma Chronic lymphocytic leukemia Follicular lymphoma Follicular lymphoma Breast cancer Paxalisib (Kazia) PIKTOR (two drugs, Faeth, acquired by Sensei Bio) Zovegalisib (RLY-2608) (Relay Therapeutics) Alpelisib (Novartis) Gedatolisib (Celcuity) WXFL- 10030390 (Jiatan)2 Targets PI3K / mTOR PI3Kα + mTOR PI3Kα PI3Kα PI3K / AKT / mTOR PI3K / mTOR Development Stage P3 (GBM) P1 (TNBC & HER2- BC) P2 (EC, OC) P1(HR+ / HER2-BC) P3 (HR+ / HER2- BC) Marketed (HER2- BC) P3 (HR+ / HER2- BC) P2 in China (solid tumors) Safety Limited toxicities Grade 3 AEs with paclitaxel Grade 3 AEs with fulvestrant Severe Hyper- sensitivity warning3 Grade 4 neutropenia reported in combo with palbociclib1 Unknown ROA Oral (QD) Oral Oral IV IV Oral Brain Penetration Yes Unknown Unknown Poor Partial Unknown Designed to be best-in-class PI3K pathway inhibitor with modest mTOR activity 13 Relevant marketed or active clinical P13K inhibitor programs

Paxalisib Unlocking the Potential of PI3K / mTOR Pathway Inhibition 14 Brain penetrant PI3K / mTOR inhibitor with epigenetic and immunomodulatory activity While traditionally classified as a kinase inhibitor, emerging clinical and translational data support a broader and more differentiated mechanism of action. Traditional View New Evidence Core Signalling Inhibition - PI3K / mTOR Axis • Disrupts key oncogenic networks controlling tumor growth, survival, metabolism, and protein translation Downstream Epigenetic Modulation (EZH2 Axis) • Alters epigenetic regulators including EZH2 • Reshapes chromatin accessibility and transcriptional programs linked to metastasis and therapeutic resistance Transcriptional Reprogramming & Cellular State Shifts • Suppresses metastatic and resistance markers • Shifts tumor biology away from mesenchymal, invasive states toward less aggressive phenotypes Tumor Immune Microenvironment Modulation • Reduces inflammatory and immune exhaustion signatures • Enhances immune visibility through viral mimicry pathways and supports synergy with immune checkpoint inhibition

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 PI3K oral inhibitor clinically proven to cross the blood-brain barrier IC50 (nM) p110 α p110 β p110 γ p110 δ mTORC 1/ 2 Paxalisib 2 46 10 3 70 Idelalisib 820 565 89 2.5 >1,000 Alpelisib 5 1200 250 290 >9,100 Buparlisib 52 166 262 116 4,600 Pilaralisib 39 383 23 36 >15,00 0 Taselisib 0.3 9.1 1.0 0.1 1,200 Pictilisib 3 33 75 3 580 Comparative Potency vs. Other PI3K Inhibitors Note: lower IC50 implies more potent activity Source: HF Zhao et al. (2017) Molecular Cancer. 16:100 15

Paxalisib Clinical & Translational Manifestations 16 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 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. Opportunistic partnering and strategic collaborations continue to add value Licensing & Collaborations 17 Licensing Key Collaborations Summary Territories and Responsibilities To develop and commercialize paxalisib in Greater China, Hong Kong, Macau, and Taiwan 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 Upfront Payment US$11m, comprising US$7m in cash and a US$4m equity investment US$1.5m Milestone Payments Contingent milestone payments of up to US$281m in GBM + further milestones payable in indications beyond GBM Potential milestone payments of up to US$19m upon the achievement of development and regulatory milestones Royalties on Net Sales Mid-teen percentage royalties on commercial sales A percentage of sub- licensing revenues and royalties on net sales of products incorporating paxalisib

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). P13K / 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. 18 P13K / 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 The most commonly diagnosed cancer and leading cause of death cancer in women

Paxalisib: Advanced Breast Cancer Current Treatment Landscape 19 * 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+ HR- / HER2+ HR+ / HER2- PD-L1 CPS <10 PD-L1 CPS >10 mPFS:18.5 vs 12.4 months8 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 metstases9 mPFS 5.6 vs 2.9 months; No OS benefit7 mOS: 9-12 months6 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 benefit7 mPFS 7.8 vs 3.2 months11 BRCA wt 70% 9% 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 Pertuzumab + trastuzumab + docetaxel or paclitaxel Fam-trastuzumab deruxtecan-nxki HR- / HER2- (TNBC) BRCA wt Modest results for HER2- subtypes, despite checkpoint and PARP inhibitors BRCA m Subtypes Stratification 1st line 2nd line

Paxalisib: Advanced Breast Cancer Consistent & Statistically Significant Signals 20 * αPD1: pembrolizumab or "pembro" Checkpoint Inhibitor PARP 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 Tumor approx. 100mm 3

Paxalisib: Advanced Breast Cancer Paxalisib in Triple Negative Breast Cancer 21 "In treatment -resistant preclinical models of breast cancer, paxalisib (4T1 mouse model, TNBC) has shown encouraging results in inhibiting both the primary tumor burden and metastasis by reinvigorating the immune system within the tumor microenvironment" – Professor Sudha Rao, Group Leader, QIMR Berghofer Combination Paxalisib + KEYTRUDA® (pembrolizumab) data in TNBC preclinical models Combination Paxalisib + LYNPARZA® (olaparib) data in advanced breast cancer preclinical models Paxalisib influence on immune system (example, T cells, B cells, NK cells) and within the tumor and its micro - environment Intellectual Property (IP) o Leading transcriptional biology and epigenetics expert, Professor Rao identified an entirely novel effect of PI3K inhibition: – Immune modulator of the tumor and the surrounding microenvironment – Administration of PI3K inhibitors such as paxalisib, at doses and frequencies different to those conventionally used, appears to activate or reinvigorate the immune system in the tumor, making it more susceptive to immunotherapy o Preliminary data from our collaboration was presented at San Antonio Breast Cancer Symposium in 2024 and 2025

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 15mg QD + pembrolizumab 200mg + clinician's choice of IV chemotherapy QW3, n=6 Paxalisib 30mg QD + pembrolizumab 200mg + clinician's choice of IV chemotherapy QW3, n=6 Paxalisib plus Pembrolizumab / Chemotherapy (21 -Day Cycle) 22 Trial ID: ACTRN12624001340527 SABCS 2025 poster presentation.

Paxalisib: Advanced Breast Cancer Early Clinical Trial Epigenetic Effects Trial ID: ACTRN12624001340527 Kazia Press Release 10 July 2025 SABCS 2025 poster presentation. 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) 23

24 Trial ID: ACTRN12624001340527 Kazia Press Release 27 January 2026 • 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 1 CR in mTNBC patient treated under expanded access, and 2 PRs in ongoing study Paxalisib: Advanced Breast Cancer Early Evidence of Tumor Regression Safety Preliminary Clinical Responses • 1 expanded access patient achieved a confirmed complete metabolic response following re-treatment with pembrolizumab / chemotherapy plus paxalisib (under an expanded access protocol) • 2/2 evaluable 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

Paxalisib: Glioblastoma (GBM) Paxalisib Potential in Glioblastoma 25 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.. P13K / 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 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) Paxalisib in Newly Diagnosed Unmethylated GBM Patients 26 NDU: Newly Diagnosed Unmethylated, OS: Overall Survival Consistent median overall survival data Phase 2 (NCT03522298) GBM-AGILE (Phase 2/3) (NCT03970447) Study Type Open-label, single arm Adaptive, multi-arm randomized Patient Population Newly diagnosed unmethylated GBM Newly diagnosed unmethylated GBM and recurrent GBM MGMT Status Enriched for unmethylated Mixed: subgroup analyses Comparator Historical SOC Concurrent SOC control Primary Endpoint OS OS Paxalisib OS SoC mOS 15.7 months (n=30) 15.54 months* (n=54) in prespecified secondary analysis in NDU GBM 11.9 months* (n=46) in prespecified secondary analysis in NDU 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 Overall Summary

27 Paxalisib: Glioblastoma (GBM) US FDA Type C Meeting 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 December 2024 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 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 2026 Paxalisib in GBM commercial and development path forward Kazia Press Release 27 October 2025 Kazia Press Release 31 December 2024

Paxalisib: Childhood Brain Cancer Paxalisib Potential in Childhood Brain Cancer 28 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).. High unmet need especially in patients with diffuse midline gliomas (DMGs) P13K / mTOR in Childhood Brain Cancer Paxalisib Opportunity

Paxalisib: Childhood Brain Cancer Paxalisib in Childhood Brain Cancer 29 Kazia is actively pursuing three forms of childhood brain cancer: Diffuse Midline Gliomas (DMG, DIPG) Atypical Teratoid / Rhabdoid Tumors (AT / RT) Advanced Childhood Cancer (PI3K / mTOR activated) Preclinical Research Positive preclinical data in combination with ONC201 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 Positive preclinical data as monotherapy and in combination (AACR 2022, 2023, 2024) ODD and RPDD granted by FDA in June and July 2022, respectively Research proposals under discussion 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

Paxalisib: Childhood Brain Cancer Paxalisib in Diffuse Midline Gliomas (DMG) 30 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) 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 Overall Survival - Cohort 2 (post RT) Median OS 15.6 months [CI 95%; 12.0, 22.4] Central imaging review analysis of PFS ongoing PNOC-sponsored Phase 2 trial in combination with ONC201 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 31 Trial ID: NCT04192981 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 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 32 Trial ID: NCT04192981 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 Interim analysis showed encouraging clinical activity of paxalisib in combination with radiation therapy. MSKCC-sponsored Phase 1 trial 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 33 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

34 PD-L1 Protein Degrader Platform

PD-L1 Protein Degrader Platform Platform Overview 35 Asset 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 Origin Developed by Professor Sudha Rao (QIMR-Berghofer) in 2020 Development Stage Preclinical; IND expected in 12-18 months Lead Indications Breast cancer and non-small cell lung cancer (NSCLC) in early stage and metastatic settings Formulation Intravenous infusion Key Differentiators 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 Mechanism of Action Target intracellular PD-L1 protein pools Recruits cellular degradation machinery Targets intracellular PD-L1 protein species that cannot be targeted by standard checkpoint inhibitors FDA Designations N / A IP Initial composition of matter IP filed in 2021 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 Current Anti-PD-1 / L1 Therapy Landscape 36 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 IMPα c 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. Limited by intracellular PD-L1

PD-L1 Protein Degrader Platform NDL2: First-In-Class PD-L1 Degrader 37 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 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 Targeting intracellular PD-L1

PD-L1 Protein Degrader Platform Key Differentiator 38 Sullivan et al., PLoS ONE 2023, doi.org/10.1371/journal.pone.0286724 NDL2 Peptide Degrader of PD-L1 PD-(L)1 mAbs Primary Mechanism Targeted protein degradation via intracellular E3 ubiquitin proteasome system Block the PD-1:PD-L1 interaction at the cell surface; Fc effector function varies by isotype / engineering Route of Administration (ROA) IV IV / SC PD-L1 Pools Addressed Intracellular Surface protein Competitors / Development Stage Academic programs in early preclinical development (no clinical programs nor industry programs identified) Commonly cited global commercial checkpoint inhibitors include: Pembrolizumab, Nivolumab, Cemiplimab, Atezolizumab, Durvalumab, and Avelumab NDL2 distinguishes itself as a modality facing minimal competitive challenges

PD-L1 Protein Degrader Platform Preclinical & Translational Manifestations 39 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. Reduced tumor growth as monotherapy Enhanced activity of anti-PD-1 therapy in combination Suppressed metastatic spread in aggressive tumor models Targeted resistance mechanisms enriched in immunotherapy- refractory disease T Anti -PD-1 NDL2 T NDL2

PD-L1 Protein Degrader Platform Efficacy in 4T1 Mouse Model 40 • Gold Standard model for TNBC • Immunocompetent BALB/c mice • Highly tumorigenic and invasive Intermitted dosing 0 Tumor Inoculation NDL2 IP injection Day -10 Tumors approx. 100mm3 1 2 3 4 5 6 Harvest 7 8 +/- antiPD1 IP injection 1x105 4T1 cells right mammary gland BALB/c mice 0 2 4 6 8 10 0 2 4 6 8 10 Days of treatment Tumour volume (Fold change versus Day 0) Vehicle αPD1 NDL2-D NDL2-D+αPD1 a b c d e f 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 NDL2 monotherapy and anti-PD1 combination reduces primary tumor burden with intermittent dosing NDL2 NDL2 + αPD1 Tumor Volume

PD-L1 Protein Degrader Platform 41 Method: FFPE sections from Control (vehicle), anti-PD1, NDL2 or NDL2 + anti-PD1 (10mg/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 0 5 10 15 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 ✱ 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 42 Body Weight Vehicle aPD1 NDL2 NDL2+aPD1 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 NDL2 shows no evidence of toxicity Safety in 4T1 Mouse Model Liver Weight Vehicle αPD1 NDL2-D NDL2-D+αPD1 0.0 0.5 1.0 1.5 2.0 Liver weight (g) ns; not significant (versus Vehicle), One-way Anova, Dunnett's post test ns ns ns

PD-L1 Protein Degrader Platform Summary & Next Steps 43 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

44 EVT801

EVT801 45 Overview Asset Overview A highly selective, potential first-in-class small molecule Vascular Endothelial Growth Factor Receptor-3 (VEGFR3) inhibitor, primarily inhibiting lymphangiogenesis Origin Discovered by Sanofi; Early development by Evotec SE; In-licensed by Kazia in 2021 Development Stage Phase 1 completed Lead Indications Potentially high-grade serous ovarian cancer (HGSOC) Formulation Oral, capsule Key Differentiators 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 Mechanism of Action 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 FDA Designations N / A IP Composition-of-matter to 2032 / 2033 in most jurisdictions (excluding PTE)

EVT801 EVT801 Selectively Inhibits VEGFR3 46 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

EVT801 A Differentiated Anti-Tumor Approach 47 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

EVT801 Phase 1 Dose-Finding Trial Completed 48 Design Monotherapy dose escalation N=26 Dose cohort 3 EVT801 monotherapy Dose cohort 2 EVT801 monotherapy Dose cohort 1 EVT801 monotherapy • 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 Léon Bérard, Lyon PI : Dr Philippe Cassier Trial ID: KZA 0801-101, NCT05114668 MTD: Maximum Tolerated Dose; RP2D: Recommended Phase 2 Dose *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 49 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 Potential for combination use with immuno-oncology therapies 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 4 5 Kazia has initiated a regional and / or global partnership search for EVT801.

50 Corporate Highlights

Near-Term Milestones & Anticipated Catalysts 51 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 platform 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 awareness, NDL2 IND-initiating studies Pricing of $50m private placement of equity securities Q4 2025 Q2 2026 Q3 2026 Q4 2026

Investment Drivers 52 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. Our strategy is aligned with where both science and capital are moving in oncology. • 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 integrated approach allows us to:

Leadership 53 Management 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

www.kaziatherapeutics.com ir@kaziatherapeutics.com

Exhibit 99.2

Kazia Therapeutics Limited ("Kazia") is a 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. 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. Financial Insights Cash & Cash Equivalents: ~ US$46 million (Runway expected to fund planned operations into 2029, excluding additional or expanded trials) Debt: No outstanding debt Ticker: KZIA (NASDAQ) American Depository Shares Outstanding: ~ 11.4 million Key Investment Highlights • Portfolio/Pipeline: The portfolio includes two clinical-stage small- molecule programs: (1) paxalisib, a brain-penetrant dual inhibitor of the PI3K/AKT/mTOR pathway, a critical signaling route that helps cancer cells grow and multiply, licensed from Genentech, and (2) EVT801, a selective vascular endothelial growth factor receptor 3 (VEGFR3) inhibitor discovered by Sanofi and licensed from Evotec SE. Additionally, Kazia has an exclusive collaboration and in-licensing agreement with QIMR Berghofer for a first-in-class PD-L1 protein degrader platform (lead compound NDL2), alongside worldwide rights to combination IP that covers pairing PI3K inhibitors with other cancer therapies including immunotherapies and PARP inhibitors. • Partnerships and Collaborations: Simcere (Greater China), Sovargen (select neurology), QIMR Berghofer (first-in-class PD- L1 degrader platform, research collaborations), Pacific Pediatric Neuro-Oncology Consortium, Memorial Sloan Kettering Cancer Center, Johns Hopkins Medicine, and Dana-Farber Cancer Institute. • Proven Leadership: Dr. John Friend, CEO, and Jeffrey Kraws, Head of Corporate Strategy & Development, bring clinical, operational, and market expertise to support current and future phases of development. • Intellectual Property: Kazia and its partners maintain a global intellectual property portfolio supporting development and durable competitive positioning. Beyond Inhibition. Reprogramming Cancer Control. Disclaimer: This Fact Sheet may contain certain "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. All statements, other than statements of historical facts, contained in this Fact Sheet, including statements regarding our expectations of our financial results for the six months ended December 31, 2025, clinical trial results, strategy, future operations, future financial position, prospects, plans and objectives of management are forward-looking statements. These forward-looking statements involve a number of risks, uncertainties (many of which are beyond Kazia's control), or other assumptions that may cause actual results or performance to be materially different from those expressed or implied by these forward-looking statements, including risks related to clinical trial delays, failure to achieve desired endpoints, regulatory setbacks or delays, financing risks, our dependence on certain partners and collaborators and clinical data variability, and other risks including the risks detailed in the filings we make with the Securities and Exchange Commission from time to time, including under the heading "Risk Factors" in our most recent Annual Report of Form 20-F. There can be no assurance that the future developments affecting Kazia Therapeutics will be those that we have anticipated. Except as required by law, Kazia Therapeutics does not undertake any obligation to update or revise any forward-looking statements whether as a result of new information, future events or otherwise. Furthermore, this Fact Sheet is intended to be used solely for informational purposes and does not constitute an offer, or solicitation of an offer, to sell any securities at any time. Some of the information contained in this Fact Sheet may be derived from industry sources. While we believe that such information is accurate and that the sources from which it has been obtained are reliable, we cannot guarantee the accuracy of such information, as we have not independently verified such information.

Q4 2025 Pricing of $50 million private placement of equity securities Q1 2026 Clinical trial update; Complete metabolic response in stage IV TNBC expanded access patient and 2 partial responses in metastatic TNBC Phase 1b study Q1 2026 PD-L1 protein degrader platform update Q2 2026 Update from FDA discussion regarding paxalisib commercial and development path forward in GBM Q2 2026 Advancement of NDL2 PD-L1 degrader program toward IND-enabling studies 2H 2026 Readouts from neuro-oncology focused clinical trials in patients with GBM and brain metastases 2H 2026 Clinical efficacy and biomarker data from ongoing Phase 1b breast cancer study 2H 2026 Provide update of paxalisib pre-clinical development into additional breast cancer subtypes 2H 2026 Publication/Presentation of translational data supporting therapeutic reprogramming strategy for paxalisib Pipeline Snapshot ir@kaziatherapeutics.com Milestones & Anticipated Catalysts MARCH 2026 | Rev 02 www.kaziatherapeutics.com

FAQ

What board changes did Kazia Therapeutics (KZIA) report in March 2026?

Kazia Therapeutics reported that Chairman Bryce Carmine will retire effective March 31, 2026. His resignation, which the company states is not due to any disagreement, reduces the board from four to three directors and adds Ebru Davidson to the Audit, Risk and Governance Committee.

How did Kazia Therapeutics (KZIA) shareholders vote on Steven Coffey’s re-election?

Shareholders approved the re-election of Steven Coffey as a director. The resolution received 1,050,412,780 votes for, 3,637,588 votes against, and 1,289,127 abstentions, indicating strong support for his continued role on Kazia’s board of directors.

What are the key assets in Kazia Therapeutics’ (KZIA) oncology pipeline?

Kazia’s key assets are paxalisib, a brain-penetrant dual PI3K/mTOR inhibitor in multiple CNS and breast cancer trials, EVT801, a selective VEGFR3 inhibitor with Phase 1 completed, and NDL2, a first-in-class PD-L1 protein degrader platform currently in preclinical development with IND-enabling studies planned.

What financial position does Kazia Therapeutics (KZIA) highlight in its March 2026 materials?

Kazia highlights approximately US$46 million in cash and cash equivalents, no outstanding debt, and about 11.4 million American Depository Shares outstanding. Management states this cash position is expected to fund planned operations into 2029, excluding additional or expanded clinical trials.

What clinical results for paxalisib in triple negative breast cancer did Kazia (KZIA) share?

Kazia reports early Phase 1b data in metastatic triple negative breast cancer, including a complete metabolic response in a stage IV patient treated under expanded access and two partial responses in the ongoing study. These findings are early and come from a small number of evaluable patients.

Which regulatory designations has paxalisib received according to Kazia Therapeutics (KZIA)?

Paxalisib has received Fast Track and Orphan Drug designations for glioblastoma, Fast Track for PI3K-altered brain metastases with radiation, and Rare Pediatric Disease and Orphan Drug designations for pediatric gliomas, including diffuse intrinsic pontine glioma and atypical teratoid/rhabdoid tumor.

Filing Exhibits & Attachments

2 documents

Press Releases

• EX-99.1 INVESTOR PRESENTATION DATED MARCH 27, 2026 82.4 KB
• EX-99.2 FACT SHEET DATED MARCH 27, 2026 7.0 KB