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September 2026 Investor Presentation Developing new therapies to treat kidney diseases with unmet clinical needsAuthorised for lodgement by the Board of the Company
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2 Forward looking statements This presentation includes forward-looking statements that are subject to risks and uncertainties. Although we believe that the expectations reflected in the forward looking statements are reasonable at this time, Dimerix can give no assurance that these expectations will prove to be correct. Readers are cautioned not to place undue reliance on forward-looking statements. Actual results could differ materially from those anticipated. Reasons may include risks associated with drug development and manufacture, risks inherent in the regulatory processes, delays in clinical trials, results of clinical trials, contractual risks, risks associated with patent protection, future capital needs or other general risks or factors, including but not limited to those factors outlined in the most recent Dimerix Limited Annual Report.
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3 ~$1.9 billion* 5 commercial licensing partners *total upfront and potential milestone payments + royalties on net sales DMX-200: Phase 3 Global Opportunity 1. Based on ASX releases 05 October 2023, 27 May 2024, 07 January 2025, 01 May 2025 and 16 June 2026; SEA = Southeast Asia, G CC = Gulf Cooperation Council; 2. AS release 10 March 2026; 3. ASX release 28 April 2026; 3. Guruswamy Sangameswaran KD, Baradhi KM. Focal Segmental Glomerulosclerosis (July 2021), online: https://www.ncbi.nlm.nih.gov/books/NBK532272/; 4. ASX release 11 March 2024 and 28 April 2026; 5. ASX releases: 14 December 2015, 21 November 2018, 07 June 2021 and 30 September 2025 FSGS indication is a rare disease that causes scarring of the kidney, leading to irreversible damage3 Orphan drug designations regulatory, marketing exclusivity and pricing benefits in key territories5 5 commercial partners DMX-200 licensed USA, EU, Canada, Australia, NZ, Japan, China, S.Korea, SEA and GCC1 up to $1.9 billion in total development and sales milestone payments plus royalties on net sales1 Phase 3 trial recruitment complete in trial of DMX-200 in focal segmental glomerulosclerosis (FSGS)2 Reduced risk Proteinuria endpoint passed blinded interim (futility) assessment1 Blinded review confirmed ACTION3 statistically powered (>90%) to demonstrate statistical significance of predicted proteinuria treatment effect of DMX-2004
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4 Cycle of damage in glomerular diseases What is FSGS? Focal = some Segmental = sections Glomerulo = of the kidney filtering units Sclerosis = are scarred 3 Pro-inflammatory environment drives sclerosis and fibrosis that is permanent and non-reversable 2 Constant pressure causes inflammation of glomerulus and influx of inflammatory immune cells 1 High blood pressure causes hyperfiltration within filter units (glomeruli) of the kidney1 Fewer kidney cells drive higher blood pressure and further hyperfiltration and inflammation As cells die, glomerular become scarred and protein leaks into the urine (proteinuria) Glomeruli exposed to stress from high blood pressure 1. Lewis, E. J. et al. (2001), New Engl J Medicine 345, 851 –860 DMX-200 Existing blood pressure medication
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5 Interpreting proteinuria as a surrogate endpoint Dip test uPCR g/g Neg <0.13 Trace 0.13 + 0.62 0.88 ++ 1.24 +++ 2.30 ++++ >3.09 normal Minimal uPCR for ACTION3 inclusion proteinuric nephrotic NORMALMICROALBUMINURIAHEAVY ALBUMINURIA Proteinuria is the quantity of protein in the urine A healthy kidney is a good filter and allows little to no protein into the urine1 • When kidneys are damaged, protein can leak into the urine causing proteinuria • Proteinuria represents an important early marker of kidney function2 Inside a healthy kidney Inside a damaged kidney 1.Guruswamy Sangameswaran KD, Baradhi KM. Focal Segmental Glomerulosclerosis (July 2021), online: https://www.ncbi.nlm.nih.gov/books/NBK532272/; 2. Nephcure FSGS living with the disease (2024) at https://nephcure.org/livingwithkidneydisease/ns-and-other-glomerular-diseases/understanding-fsgs/ ; 3. Adapted from graphics pre pared by Renal Unit at the Royal Infirmary of Edinburgh and the University of Edinburgh; 4. PARASOL outcomes 2024, a working group made up of: NephCure, ISGD, NKF, KHI are co -sponsors of the project, FDA and EMA involvement, University of Michigan is data co ordinating center, Industry invited as participants Proteinuria as a predictor of kidney disease3 Proteinuria is typically less variable and easier to measure than eGFR4
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6 phase 3 clinical trial 1. ASX release 11 March 2024, Predictive Power statistical model using industry standard as set by the independent renal biostat istician consultant for Dimerix, b linded interim Phase 3 analysis data does not guarantee a statistically significant outcome at the end of the trial; 2. ASX release 28 April 2026; 3. number and % of eligible patients who have completed 2 years treatment and elected to enter the OLE as at 16 June 2026; ARB = angiotensin receptor blocker; uPCR = urinary proteinuria; eGFR = estimated glomerular filtration rate (kidney function); A randomised, double-blind, multi-centre, placebo-controlled study of renal outcomes of DMX-200 in patients with FSGS receiving an ARB (n=≥286) ARB + DMX-200 ARB + placebo Planned blinded statistical powering review2 Phase 3 Trial Timeline Final analysis: Primary = uPCR Secondary = eGFR2 @104 weeks Background • Patients recruited, then screened and stabilised on background medications • Patients randomised to receive drug or placebo • DXB remains blinded at all times during study Open Label Extension DMX-200 75/81 (93%)3 patients enrolled in open label extension study to date ACTION3 Study End European Renal Association Posters 2025 Successful interim analysis1 (using statistical measure) 72 patients @ 35 weeks (% change in uPCR) demonstrated DMX-200 was performing better than placebo at that point in time1 ACTION3 remains appropriately statistically powered (>90%) to demonstrate a treatment effect for proteinuria primary endpoint2
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7 adult patient recruitment by territory Trial designed for potential approval globally Recruitment completed (adult population)1 1. ASX release 15 December 2025; 2. Final numbers of adult patients, ASX release 10 March 2026; paediatric patients will continue to recruit, and will not impact final analysis timelines 333 Adult patients recruited, randomised and dosed (target ≥286)2 Latin America Asia Pacific US / Europe
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8 AT-1 / ETA antagonist Novartis atrasentan (ETA antagonist) Inflammatory modulator APOL1 inhibitor TRPC inhibitor Phase 2 Phase 3 Preclinical/Phase 1 Boeringer Ingelheim BI 764198 Other River3Renal R3R01 (ABCA1 Stimulator) Akebia praliciguat (sGC Stimulator) Vertex Pharma VX-147 targets small FSGS cohort Dimerix DMX-200 (CCR2 Inhibitor) Travere sparsentan (AT1/ETA dual antagonist) Source: Company information and clinicaltrials.gov Competitive/complementary trial landscape in FSGS Low competition in inflammatory treatment options, large unmet medical need DMX-200 is the only inflammatory modulator in development specifically for FSGS DMX-200 has potential for use in conjunction with other drugs in development if approved Visterra/Otsuka VIS-171 (IL-2 Modulator) Certa Tx OCX-063 (GPR68 Inhibitor) Vera Tx Atacicept (BAFF/APRIL Inhibitor) Hansoh HS-10390 (AT1/ERA dual antagonist) Evergreen EG-102 (Undisclosed MoA) Walden Bioscience WAL0921 (suPARInhibitor) Sanofi Frexalimab(CD40L), SAR442970 (OX40/TNFα), or Rilzabrutinib(BTKi) Delta4 Repositioned Clopidogrel (P2Y12 Inhibitor) Programs presumed on hold (no recent updates) Basket study including of patients with IgAN, FSGS, MCD, Alport syndrome and/or DKD FSGS specific studies Approved
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9 Summary of licensing deals for DMX-200 to date 1. Based on US conversions & further terms outlined in ASX Announcement on 01 May 2025; 2. Based on US conversions & further terms outlined in ASX Announcement on 16 June 2026; ; 3. Based on Euro conversions & further terms outlined in ASX Announcement on 5 October 2023; 4. Based on J apanese ¥ Yen conversions & further terms outlined in ASX Announcement on 7 January 2025 ; 5. Based on US dollar conversions & further terms outlined in ASX Anno uncement on 27 May 2024 Dimerix has successfully partnered DMX-200 across multiple key markets EU, CA, AU, NZ AU$10.8 milllion3 Upfront Up to AU$219 million3 Milestones Escalating mid-teen-20% Royalties 3 GCC, Iraq AU$0.5 million5 Upfront Up to AU$120 million5 Milestones Starting at 30% Royalties 5 Japan AU$7.2 million4 Upfront + 1st milestone Up to AU$100 million4 Milestones Between 15-20% Royalties 4Licensing deals collectively valued up to ~AU$1.9 billion in total upfront and potential milestone fees plus royalties1-5 >AU$80 million in total upfront payments1-5 China,S.Korea.SEA AU$14.1 million2 Upfront Up to AU$467 million2 Milestones Between 10-15% Royalties 2 United States AU$48 million1 Upfront Up to AU$892 million1 Milestones Escalating low- teen-low twenties% Royalties 1
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10 DMX-200 - geographic diversification of fee revenue Collectively, five commercial agreements valued up to A$1.9 billion across upfront + milestone fees:1 Based on ASX releases 05 October 2023, 27 May 2024, 07 January 2025, 01 May 2025 and 16 June 2026 On signing Short Term Potential Longer Term Potential Diversified revenue & risk sharing with licensing partners Upfront fees Milestone Payments Milestone Payments Royalties A$81 million + A$237 million + A$1.56 billion 10 – 30 % = In licensing fees Between now and commercial launch Post commercial launch Post commercial launch Upfront and development milestones collectively A$318 million
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DMX-652 in Acute Kidney Injury
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12 DMX-652: Phase 2 in acute kidney injury A complementary, clinical-stage pipeline addition 1. Dimerix internal analysis; Mission Therapeutics MTX -652 development file; 2. Zarbock et al, Intensive Care Med 2023; Vervoort et al, Ann Thorac Surg 2023; 3. Dimerix internal market analysis consensus figure based on meta-analysis of 21 market reports (2026) ; Includes China and Japan markets, label expansion into sep sis-associated AKI (SA-AKI) and contrast-associated AKI Large value potential • Secured a Phase 2 ready asset, which is already FDA cleared & manufactured • Substantial work to date undertaken by originator means significant early risk already removed1 First and best in class • First-in-class USP30 target that promotes renewal of mitochondria • DMX-652 targets one of the emerging key drivers of kidney injury and reduces both cellular energy failure and inflammation Leverages existing expertise • Dimerix team are experts in kidney disease; capable of identifying high value assets • Experienced in-house team with proven track record of advancing high value assets through clinical development and into commercialisation Large and growing market • No approved therapy for high-risk acute kidney injury patients and growing demand for new therapies2 • US$3.5 Billion in 2026 • est. US$7.5 Billion by 2036 Strategic value • Dimerix has significant optionality over the development and commercialisation direction of DMX-652, as the outright asset owner • DMX-652 has the potential to be used for a variety of other indications, many of which may also have large markets and unmet medical needs
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13 A first-in-class, oral, once-daily USP30 inhibitor for the prevention of acute kidney injury in high-risk patients undergoing cardiac surgery Introducing DMX-652 Small molecule New chemical entity; oral capsule formulation; GMP- grade API available to support Phase 2 clinical trial Once-daily dosing Convenient dosing schedule to provide pre-operative and post operative USP30 inhibition Well tolerated Phase 1 multi-part study completed in 109 healthy volunteers, (85 volunteers administered DMX-652) no serious adverse events and wide therapeutic margin Phase 2 ready IND open, approved protocol and established global medical advisory board Key value proposition with encouraging safety profile
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14 What is AKI associated with cardiac surgery ~26% of patients undergoing cardiac surgery suffer kidney injury; increases to 30-50% in high-risk patients Mitochondria = “batteries” for the kidney cell The kidney has the second-highest mitochondrial content and oxygen consumption in the body to fuel intense energy demands Cardiac Surgery1 Cardiopulmonary bypass starves the kidney of oxygen (ischaemia) and causes oxidative stress in kidney cells Kidney starved of oxygen Ischaemia2 Healthy mitochondria Currently no approved disease-modifying therapies Reperfusion: restores blood flow to kidney3 kidney damage caused by a massive influx of reactive oxygen species (ROS) that leads to cell death Mitochondria rupture Sudden decline in kidney function (hours) AKI Drives ICU stays, dialysis, mortality and/or progression to Chronic Kidney Disease Damaged mitochondria causes rupture of the mitochondrial membrane Source: Scurt FG et al, Kidney360 2024; Zarbock A et al, Intensive Care Med 2023; KDIGO clinical practice guidelines for AKI
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15 DMX-652 aims to enable the body's natural quality-control system to remove damaged mitochondria (a process called mitophagy) before they trigger kidney cell death Source: Tang C et al, Nat Rev Nephrol 2021; Bhatia D, Choi ME, J Life Sci 2019; Mission Therapeutics MTX -652 preclinical package (2024) How DMX-652 works – unique, novel mechanism • USP30 opposes Ub tagging, removing the ‘eat me’ tag • Damaged mitochondria are not effectively removed • Drives inflammation and cell death Sudden decline in kidney function (hours) Acute Kidney Injury (AKI) Kidney tubule cell USP30 removes damaged mitochondria ‘eat me’ tag • Ubiquitin-specific protease 30 (USP30) enzyme expressed on mitochondria • USP30 regulates Ubiquitin (Ub) accumulation to remove damaged mitochondria whilst also preventing premature clearance of healthy mitochondria Healthy kidney Maintain kidney function Kidney tubule cell Ub Ub USP30 regulates Ub which “tags” damaged mitochondria • DMX-652 blocks USP30, enabling normal ubiquitination • selective degradation of damaged mitochondria, leaving only healthy mitochondria DMX-652 targets USP30 Kidney tubule cell Ub UbUbUb Ub Damaged mitochondria can now be “tagged” & removed Aims to: • Preserve kidney function • Reduced AKI severity and incidence • Prevent dialysis • Shorter ICU and hospital stays • Reduced risk of progression to CKD Ub Ub Ub Ub Ub Ub UbUb
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16 DMX-652 Pre-clinical data demonstrates efficacy signal 0 5 10 15 20 25 30 35 40 Vehicle DMX-652 % Fibrosis 0 10 20 30 40 50 60 70 80 90 100 Vehicle DMX-652 Tubular atrophy (%) uIRI - Unilateral renal ischemia -reperfusion model, UUO - Unilateral ureteral obstruction model. Bars = mean ± error; values, ****<0.0001, ***<0.001. Mission Therapeutics unpublished data ******* DMX-652 reduces scarring (fibrosis) • The UUO model predicts acute to chronic kidney disease progression. • DMX-652 significantly reduces the scarring that drives chronic disease DMX-652 reduces kidney damage • The uIRI model replicates the processes of cardiac surgery that cause AKI • DMX-652 significantly reduces the number of kidney tubules damaged when blood is restricted
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17 A multicentre, double-blind, randomised, placebo-controlled study evaluating the safety and efficacy of DMX-652 in patients at high risk of AKI following cardiac surgery (n=160) Source: Mission Therapeutics MTX -652 Phase 2 protocol (FDA Study-May-Proceed, 2023); Dimerix MTX-652 development plan (2026); MAKE 30 & MAKE 90 = Major Adverse Kidney Events occurring at 30 or 90 days Proposed phase 2 clinical trial design 160 patients · 28 days on drug · 90-day follow-up · ~25 sites in US / EU / Australia Primary endpoint Secondary endpoints AKI incidence by 7 days post-surgery Screening/randomisation • Patients identified as high-risk for AKI • Stabilised on background medication pre-surgery • Standard peri-operative and post- operative care continues throughout Treatment phase Placebo N=80 DMX-652 N=80 Follow up Day 0 Day of surgery Day 7 Day 28 Day 90 Safety and tolerability PK MAKE30 MAKE90
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18 With no approved disease-modifying therapies, severe consequences for patients, surgeons, and health systems Consequences of CS-AKI2: • Prolonged intensive care and hospital length of stay • Higher rates of renal replacement therapy (dialysis) • Increased short- and long-term mortality • Substantially elevated risk of progression to chronic kidney disease and end-stage renal disease “CS-AKI is a predictable, frequent and devastating complication of cardiac surgery. Effective preventive therapies are a critical unmet need.” Consensus position, 2024 ADQI Conference 1. Alshaikh HN et al, Ann Thorac Surg 2018; Zarbock A et al, Intensive Care Med 2023; 2. Scurt FG et al, Kidney360 2024; Lau D et al, J Thorac Cardiovasc Surg 2021 Significant unmet need in AKI 0 No approved therapies for the prevention of cardiac surgery- associated AKI 1 in 4 Cardiac surgery patients develop AKI after on-pump surgery1 30-50% AKI rate in high-risk patients (e.g. age, diabetes, low cardiac function, prior kidney disease)1
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19 Source: Company information and clinicaltrials.gov Competitive/complementary trial landscape in AKI Mitophagy modulator Tissue damage signalling Cellular ischaemia Phase 2 Phase 3 Phase 1 Inflammatory modulator Arch Biopartners LSALT peptide Dimerix DMX-652 USP30 Inhibitor UnicyciveTherapeutics UNI-494 Mitochondrial K-ATP channel PAUSED DEVELOPMENT AM-Pharma Ilofotasealfa Alkaline phosphatase EnnovaBio ENN0403 Protein kinase inhibitor Haemodynamic DMX-652's differentiated mechanism of action supports complementary use and the potential for superior or additive outcomes River2Renal R2R01 RXFP1 agonist
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20 Strategic fit: shared renal capabilities, shared regulatory/clinical infrastructure, shared small-molecule know-how DMX-200 and DMX-652: complementary growth pillars 1. ASX release 10 March 2026; 2. ASX releases March 2024 and April 2026; 3. ASX releases 05 October 2023, 27 May 2024, 07 January 2025; 01 May 2025 and 16 June 2026; 4. ASX release 17 July 2026 1Focal Segmental Glomerulosclerosis (FSGS) rare kidney disease 1 Acute kidney injury associated with cardiac surgery 2CCR2 inhibitor that modulates inflammatory pathways involved in kidney damage 2 USP30 inhibitor designed to enhance mitophagy and mitochondrial quality control in damaged cells 3existing in-house infrastructure and global network 3 Can leverage existing expertise in clinical, regulatory, manufacturing, nephrology networks, know-how, and commercial relationships 4 4 provides a new growth engine, with an open IND, FDA clearance to proceed to Phase 2, and completed Phase 1 safety studies more advanced, near-commercialisation asset with Phase 3 fully recruited and commercial partnering activity Shared kidney disease focus Different Mechanisms of Action Shared Development Infrastructure Balanced Risk and Timing DMX-200 DMX-652
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21 Disciplined, stage-gated capital deployment focused on the clinical value inflection1 Key potential value inflection points Asset acquisition Patents assigned; Phase 2 ethics submission; Clinical site initiation First patient dosed in Phase 2 50% recruitment; Phase 2 interim / futility Phase 2 readout Preparation for Phase 3 DMX-652 H2 2026 H1 2027 H2 2027 H1 2028 H2 2028 Paediatric recruitment completion; first patient completes open label extension study ACTION3 Phase 3 FSGS readout NDA dossier submission DMX-200 Two clinically differentiated assets in renal disease, addressing two separate high unmet need indications with independent timelines; building a steady cadence of value-creating milestones Potential for additional licensing partners in available territories 1. Based on current anticipated activities timeline Phase 3 IDMC safety review
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22 Corporate overview 1. As at 3 September 2026; 2. Past 90 trading days liquidity as at 5 August 2026; 3. Shareholder register as at 3 September 2026; 3. ASX release 28 August 2026; 4. ASX release 3 September 2026 Ticker Symbol ASX: DXB Cash Balance (Jun26)* $16.2 million Market Capitalisation1 $174 million Share price1 $0.29 Total ordinary shares on issue1 600,396,776 Average Daily Liquidity by value for past 90 trading days2 $0.85 million S H A R E P R I C E S U B S T A N T I A L S H A R E H O L D E R S 3 Position Holder Name Holding % IC 1 Mr P Meurs 91,090,374 15.3% TOTAL (TOP 5) Shareholders 155,204,214 25.9% *excluding ~$48.1million: • AU$14.1 million Everest upfront payment received; 3 and • $34 million available loan facility 4
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W E L L P O S I T I O N E D TO D E L I V E R AGA I N ST ST R AT E G I C P L A N Dimerix HQ 425 Smith St, Fitzroy 3065 Victoria, Australia T. +61 1300 813 321 E. investor@dimerix.com (ASX:DXB) A biopharmaceutical company developing innovative new therapies in areas with unmet medical needs, with a core focus on kidney diseases. ESG Statement Dimerix is committed to integrating Environmental, Social and Governance (ESG) considerations across the development cycle of its programs, processes and decision making. The Dimerix commitment to improve its ESG performance demonstrate a strong, well-informed management attitude and a values led culture that is both alert and responsive to the challenges and opportunities of doing business responsibly and sustainably.
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24 Commercial manufacturing sites established in USA3 DMX-200 – inflammatory modulator A CCR2 inhibitor working synergistically alongside the current standard of care (AT1R blocker): G protein-coupled receptor (GPCR) 1. ASX release and investor presentation 29Jul20 and ASX release 11Mar24 BID: bis in die/ twice a day
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25 1. Ayoub MA, et al. (2015) PLoS One; doi.org/10:e0119803; 2. ASX presentation 27 October 2020; 3. Liu Y. et al (2024) Role of MCP-1 as an inflammatory biomarker in nephropathy, Front. Immunol., Sec. Inflammation doi.org/10.3389/fimmu.2023.1303076; CCR2: C -C chemokine receptor type 2; AT1R: Angiotensin II type 1 receptor; MCP1: Monocyte chemoattractant protein -1 (also known as CCL2, the ligand for CCR2); BRET: Bioluminescence Resonance Energy Transfer Assay ; PCR = protein creatinine ratio; *P<0.05 vs sham STNx rats ; † P<0.05 vs vehicle STNx rats; • CCR2 activation promotes recruitment of inflammatory monocytes to the kidney • Monocytes promote sclerosis and fibrosis of the kidney • Podocytes are the essential filter cells of the kidney DMX-200 inhibits CCR21 DMX-200 reduces inflammatory cells1,2,3 DMX-200 preserves podocytes1 Simultaneous inhibition of CCR2 and AT1R preserves the number of essential filter cells (podocytes) in the kidney1 Sham Vehicle DMX-200 ARB DMX-200 +ARB Podocytes, n/gcs 20 15 10 5 0 * * * † Sham Vehicle DMX-200 ARB DMX-200 +ARB Macrophages, n/area 200 150 100 50 0 * † † † Simultaneous inhibition of CCR2 and AT1R reduces recruitment of monocytes to the kidney1 in-vivo1 in-vitro Complex of CCR2 and AT1R increases aberrant signaling when both receptors activated1 MCP-1 & Angiotensin II present Only MCP-1 present Angiotensin II present No ligand DMX-200: unique pharmacology DMX-200 +ARB Sham Vehicle DMX-200 ARB 400 300 200 100 0 500 Proteinuria (mg/24hours) * Simultaneous inhibition of CCR2 and AT1R reduces proteinuria an important early marker of kidney function1
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26 “Any reduction in proteinuria could yield years of preserved native kidney function and delay the onset of kidney failure and its attendant morbidity and mortality” Kidney survival study – Troost et al, August 20202 DMX-200: Phase 2 met primary endpoint PCR = protein creatinine ratio; ARB = angiotensin receptor blocker; 1. Trachtman, et al., 2018. J Amer Soc Nephrology 29(11): 2745-2754; 2. Troost JP et al (August 2020); doi.org/10.1053/j.ajkd.2020.04.014; 3. Repeated measures mixed model analysis per protocol; top line data was reported as grouped analysis on 29 July 2020, study not designed for statistical significance; Clinically encouraging outcomes achieved for patients,1,2 with no safety concerns noted3 E F F I C A C Y • 86% of patients demonstrated reduced proteinuria when administered DMX-200 compared to when administered placebo • DMX-200 reduced inflammatory biomarker by 39% vs placebo S A F E T Y • No safety concerns noted – reduced development risk Average reduction of 17% in proteinuria after 16 weeks treatment on DMX-200 versus placebo3
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27 DMX-200 Phase 2 effect on inflammatory biomarker1 uMCR = Urinary MCP-1 creatine ratio; PCR = protein creatinine ratio; *placebo adjusted difference 1. ASX presentation 27 October 2020; 2. Liu Y. et al (2024) Role of MCP-1 as an inflammatory biomarker in nephropathy, Front. Immunol., Sec. Inflammation doi.org/10.3389/fimmu.2023.1303076 Average baseline MCP-1 versus average baseline proteinuria MCP-1 levels reduced when on DMX- 200 treatment 0 5 10 15 0.0 0.5 1.0 1.5 Time uMCR normalised uMCR normalised to baseline v time N=7, GeoMean On active On placebo (weeks) -37%* -39%* 50% 0% -50% high MCP-1 correlates to high proteinuria Change in MCP-1 over time on DMX-200 versus placebo • 16 weeks treatment with DMX-200 vs placebo reduced inflammatory biomarker by 39%: ▪ DMX-200 blocks receptor responsible for inflammation ▪ Translates to reduced inflammation and subsequent fibrosis (scarring) in the kidney2 Unlike other CCR2 antagonists investigated to date, treatment with DMX-200 reduces the urine concentration of the pro-inflammatory ligand of CCR2 called MCP-12
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28 DMX-200 intellectual property portfolio Exclusivity 7/10 years Orphan exclusivity from marketing approval date in many territories1 + Paediatric exclusivity period extension1 Portfolio 2 Exp.2042 (if granted) Method of Use & Formulation Global application3 1. DMX-200 is a “New Chemical Entity: an active moiety not previously approved, which can attract exclusivity periods in various territories; 2. Granted patents US9,314,450, US10,058,555, US10,525,038, US11,382,896, US12,083,102, CN2012800046165, CA2,821,985, EP12734251.7, HK 1404477.8 , IL227414, JP2013-547780, SA2013/5897, AU2012206945; 3. Patent applications: PCT/AU2022/050013, PCT/AU2022/050249 and PCT/AU2024/050416; 4. US Provisio nal Application 63/887,984 Portfolio 3 Exp.2042 (if granted) Formulation Global application3 Portfolio 5 Exp.2045/6 (if granted) Method of Use Provisional application4 Trademarks Various trademarks Global applications Portfolio 1 Exp.2032 (2033 in US) Method of Use Granted in key territories2 Portfolio 4 Exp.2044 (if granted) Method of Use & Formulation Global application3 DMX-200
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29 Completed in healthy volunteers: strong safety & pharmacokinetic foundation to support Phase 2 clinical trial Source: Mission Therapeutics MTX -652 Phase 1 Clinical Study Report (MTX652_001), 2024; FDA Pre -IND meeting minutes DMX-652 Phase 1 study met primary endpoint 85 Healthy volunteers received DMX-652; across 5 study sites 0 No serious adverse events (SAE) reported in any cohort Up to 200mg Single dose well tolerated; maximum tolerated dose not reached 100mg Once daily x 14 days; multiple ascending dose; well tolerated • No serious adverse events • Almost all TEAEs of mild severity • No ECG signal: no QT/QTc prolongation • Well tolerated in elderly subjects • Wide therapeutic margin in non-clinical tox studies Safety • Rapid oral absorption; no effect of food or formulation • Once-daily dosing profile supported • Clean DDI profile: not a CYP450 inducer/inhibitor • Modelled 100mg loading / 50mg daily achieves ~80% target occupancy • Phase 2 dose selected using validated PK modelling Pharmacokinetics & Drug/Drug Interactions (DDI)
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30 Unlike competing programs targeting specific inflammatory or fibrotic pathways, DMX-652 acts on a downstream, convergent driver of kidney injury — making it applicable across causes of AKI Only USP30 inhibitor in clinical development for CS-AKI No other mitophagy modulators are in clinical development for cardiac surgery-associated AKI 1 Targets a ‘cause-neutral’ pathway Mitochondrial dysfunction drives AKI regardless of cause — making DMX-652 mechanistically broad and complementary to existing care Damage-sensing mechanism USP30 inhibition selectively amplifies mitophagy only where mitochondria are already damaged — avoiding the indiscriminate effects of broader pathway activators Tang C et al, Nat Rev Nephrol 2021; Dimerix competitive landscape analysis (2026); clinicaltrials.gov searches; CS -AKI = cardiac surgery related acute kidney injury DMX-652: first-in-class, best-in-class potential 3 Expansion potential beyond CS-AKI Same mitophagy mechanism applicable to a large range of other diseases, including other AKI causes, kidney transplant, cardiac disease, and lung disease 42
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31 With no approved disease-modifying therapies, severe consequences for patients, surgeons, and health systems Consequences of CS-AKI2: • Prolonged intensive care and hospital length of stay • Higher rates of renal replacement therapy (dialysis) • Increased short- and long-term mortality • Substantially elevated risk of progression to chronic kidney disease and end-stage renal disease “CS-AKI is a predictable, frequent and devastating complication of cardiac surgery. Effective preventive therapies are a critical unmet need.” Consensus position, 2024 ADQI Conference 1. Alshaikh HN et al, Ann Thorac Surg 2018; Zarbock A et al, Intensive Care Med 2023; 2. Scurt FG et al, Kidney360 2024; Lau D et al, J Thorac Cardiovasc Surg 2021 DMX-652 - significant unmet need in AKI 0 No approved therapies for the prevention of cardiac surgery- associated AKI 1 in 4 Cardiac surgery patients develop AKI after on-pump surgery1 30-50% AKI rate in high-risk patients (e.g. age, diabetes, low cardiac function, prior kidney disease)1
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32 DMX-652 Intellectual property DMX-652 The acquisition secures owned composition-of-matter IP, plus exclusive freedom-to-operate rights and regulatory exclusivity A C Q U I R E D · A S S I G N E D T O D I M E R I X Composition-of-matter patent family Directly covers DMX-652 (originally MTX-652) — a novel USP30-inhibitor compound; this is the core, 100% owned patent underpinning the asset Granted in initial territories (incl. Japan) · US Notice of Allowance received 2041 Anticipated patent expiry 19 Territories filed worldwide US · EU · Japan · China LICENSED · EXCLUSIVE RIGH T S Freedom-to-operate patents An exclusive licence to specific USP30-inhibitor patent families secures DMX-652's freedom to operate — granted broadly across the US, Europe and Asia. Licensed patents: PCT/GB2016/050851 · PCT/GB2019/050608 REGULATORY EXCLUSIVITY New Chemical Entity exclusivity ≥5 yrs US data exclusivity (NCE), from marketing approval up to 7 / 10 yrs US / EU, with orphan drug designation Acquired (assigned to Dimerix): composition-of-matter family PCT/EP2021/064897, anticipated expiry 2041. Licensed (exclusive, f reedom to operate): PCT/GB2016/050851 & PCT/GB2019/050608. Regulatory exclusivity anticipated on marketing approval; orphan drug designation not yet granted. DMX -652 was previously known as MTX-652 at Mission Therapeutics
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33 Previous experience: • Senior pharmaceutical executive with a demonstrated record of achievement and leadership over more than 30 years within the pharmaceutical and biotechnology industries • Significant accomplishments in capital raising initiatives, pipeline development and licensing ✓ BSc − Chemistry ✓ MBA − Business Previous experience: • Experienced in product development, commercial strategy development & execution • Successfully commercialized pharmaceutical products globally ✓ BSc (Hons) − Pharmacology ✓ PhD − Pharmaceutics ✓ MBA − Business ✓ M.IP.Law − Intellectual Property Law Previous experience: • Extensive biotech drug development & commercial manufacturing experience • Responsible for successful global commercialization programs & NDA registrations ✓ BSc (Hons) − Chemistry ✓ MBA − Business Previous experience: • Experienced executive in pharmaceutical operations • Background in small molecules development and analytical development ✓ BSc (Hons) − Chemistry ✓ PhD – Industrial Chemistry Previous experience: • Experienced technology and governance professional with a focus in operations, risk management, assurance, and AI • Provides advisory services to a family office with multiple Australian biotech investments ✓ BEng (Hons) − Chemical Engineering ✓ BCom − Commerce (Faulding)(1) 1. Acquired by Pfizer in 2015; 2. Acquired by Pfizer in 2009 (2) (1) Dimerix board
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34 Dimerix management Previous experience: • Experienced in product development, commercial strategy development & execution • Successfully commercialised multiple pharmaceutical products ✓ BSc (Hons) − Pharmacology ✓ PhD − Pharmaceutics ✓ MBA − Business ✓ M.IP.Law − Intellectual Property Law (1) 1. Acquired by Pfizer in 2009; Previous experience: • Experienced finance and governance executive with extensive experience of both ASX and NASDAQ-listed companies. • Brings more than 30 years’ international finance leadership experience across Australia, US, Canada, the UK and Hong Kong. ✓ BSc (Hons) – Business Studies ✓ MAICD ✓ Chartered Accountant Previous experience: • 35 years international experience in drug development, commercialization and corporate leadership • Planning, Financing, Pre-clinical, Clinical Development, Regulatory Approval, Product Launch, Pharmacovigilance, and Medical Affairs ✓ B.Pharm (Hons) - Pharmacy ✓ MBBS - Medicine and Surgery Previous experience: • Experienced pharmaceutical executive in project management, clinical development and research translation • BD and strategic alliance leader • Led multidisciplinary R&D&C teams for 13 years ✓ BSc (Hons) – Genetics ✓ PhD – Molecular Immunology ✓ MBA – Business & Leadership
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35 Medical Advisory Board Professor of Clinical Trials and Personalized Medicine: University Medical Center Groningen, the Netherlands. He specializes in the research of novel treatment approaches to slow the onset of diabetic cardiovascular and renal disease. Hiddo has been instrumental in interactions between industry, researchers and regulatory agencies in the validation of surrogate endpoints for renal trials. Professor of Medicine & Molecular & Cellular Pharmacology: University of Miami. Chief of the Katz Family Division of Nephrology and Hypertension. She has an extensive history of translational excellence for patients with renal disease and has uncovered novel pathogenetic mechanisms and therapeutic approaches for glomerular disorders. Mayer Professor of Renal Medicine: Department of Cardiovascular Sciences; University of Leicester and Nephrologist. Jonathan is the IgA nephropathy Rare Disease Group lead for the UK National Registry of Rare Kidney Diseases (RaDaR) and a member of the steering committee for the International IgA Nephropathy Network. An attending physician and Director of the Kidney and Blood Pressure Center in the Division of Nephrology at Tufts Medical Center. Lesley’s major research interest is in the estimation and measurement of glomerular filtration rate (GFR) and in defining alternative endpoints for CKD progression trials based on GFR decline and changes in albuminuria. Renal Physician and Head of the Renal Clinical trials at the Royal North Shore hospital, Sydney, Australia. Muh Geot’s main areas of research are in understanding the mechanisms of kidney fibrosis, biomarkers research, and identifying strategies in delaying progressive kidney disease including glomerular diseases. Graduated from Haverford College and the University of Pennsylvania School of Medicine. He has been a practicing pediatric nephrologist for 35 years. Has been the PI of NIDDK and industry sponsored clinical trials in glomerular disease and am a Co-Investigator in the NEPTUNE and CureGN observational cohort studies. Assistant Professor in the Division of Nephrology at the University of Michigan. Interest in observational studies in glomerular disease, including NEPTUNE and CureGN. Lead on PARASOL program to define FSGS endpoints with by applying statistical methods for clinical outcome definition and prediction of kidney disease progression.