# EDGAR Filing Document

**Accession Number:** 0001131343
**File Stem:** 0001213900-26-003683
**Filing Date:** 2026-1
**Character Count:** 25315
**Document Hash:** e7b7b214f948de2d03cfee90c8d845f6
**Contains OCR:** False
**Source Format:** 

## Filing Content

## Filing Summary
**0001213900-26-003683.hdr.sgml**: 20260113

**ACCESSION NUMBER**: 0001213900-26-003683

**CONFORMED SUBMISSION TYPE**: 6-K

**PUBLIC DOCUMENT COUNT**: 39

**CONFORMED PERIOD OF REPORT**: 20260113

**FILED AS OF DATE**: 20260113

**DATE AS OF CHANGE**: 20260113

**FILER**: 

**COMPANY DATA:**
- **COMPANY CONFORMED NAME:** ALTERITY THERAPEUTICS LTD
- **CENTRAL INDEX KEY:** 0001131343
- **STANDARD INDUSTRIAL CLASSIFICATION:** PHARMACEUTICAL PREPARATIONS [2834]
- **ORGANIZATION NAME:** 03 Life Sciences
- **EIN:** 000000000
- **STATE OF INCORPORATION:** C3
- **FISCAL YEAR END:** 0630

**FILING VALUES:**
- **FORM TYPE:** 6-K
- **SEC ACT:** 1934 Act
- **SEC FILE NUMBER:** 000-49843
- **FILM NUMBER:** 26528475

**BUSINESS ADDRESS:**
- **ADDRESS IS A NON US LOCATION:** YES
- **STREET 1:** LEVEL 3, 460 BOURKE STREET
- **CITY:** MELBOURNE
- **PROVINCE COUNTRY:** C3
- **BUSINESS PHONE:** 61 3 9349 4906

**MAIL ADDRESS:**
- **ADDRESS IS A NON US LOCATION:** YES
- **STREET 1:** LEVEL 3, 460 BOURKE STREET
- **CITY:** MELBOURNE
- **PROVINCE COUNTRY:** C3

**FORMER COMPANY:**
- **FORMER CONFORMED NAME:** PRANA BIOTECHNOLOGY LTD
- **DATE OF NAME CHANGE:** 20010105

**SECURITIES AND EXCHANGE COMMISSION**

**Washington, D.C. 20549**

**FORM 6-K**

**REPORT OF FOREIGN PRIVATE ISSUER**

**PURSUANT TO RULE 13a-16 OR 15d-163**

**UNDER THE SECURITIES EXCHANGE ACT OF 1934**

**For the month of January 13, 2026**

**Alterity Therapeutics Limited**

(Name of Registrant)

**Level 14, 350 Collins Street, Melbourne, Victoria 3000 Australia**

(Address of Principal Executive Office)

**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 ☐

**This Form 6-K is being incorporated by reference into our Registration Statement on Form S-8 (Files No. [333-251073](http://www.sec.gov/Archives/edgar/data/1131343/000121390020040485/ea130838-s8_alteritytherape.htm), [333-248980](http://www.sec.gov/Archives/edgar/data/1131343/000121390020027969/ea127207-s8_alteritytherap.htm) and [333-228671](http://www.sec.gov/Archives/edgar/data/1131343/000114420418063081/tv508429_s-8.htm)) and our Registration Statements on Form F-3 (Files No. [333-274816](http://www.sec.gov/Archives/edgar/data/1131343/000101376223000033/ea185947-f3_alteritytherape.htm), [333-251647](http://www.sec.gov/Archives/edgar/data/1131343/000121390020044324/ea132148-f3_alteritytherape.htm), [333-231417](http://www.sec.gov/Archives/edgar/data/1131343/000114420419025615/tv521271_f3.htm) and [333-250076](http://www.sec.gov/Archives/edgar/data/1131343/000121390020036934/ea129831-f3_alteritytherap.htm))**

**ALTERITY THERAPEUTICS LIMITED**

**(a development stage enterprise)**

The following exhibits are submitted:

99.1 [Corporate Presentation](ea027267001ex99-1_alterity.htm)

**<u>SIGNATURE</u>**

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.

---

| | |
|:---|:---|
| **Alterity Therapeutics Limited** | **Alterity Therapeutics Limited** |
| By: | /s/ Julian Babarczy |
|  | Julian Babarczy |
|  | Chairman |

---

Date: January 13, 2026

## Exhibit 99.1

**Exhibit 99.1**

![](ex99-1_001.jpg)

January 2026 Corporate Presentation

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Forward looking statements 2 This presentation may contain some statements that may be considered "Forward - Looking Statements", within the meaning of the US Securities Laws. Thus, any forward - looking statement relating to financial projections or other statements relating to the Company's plans, objectives, expectations or intentions involve risks and uncertainties that may cause actual results to differ materially. For a discussion of such risks and uncertainties as they relate to us, please refer to our 2025 Form 20 - F, filed with US Securities and Exchange Commission, in particular Item 3, Section D, titled "Risk Factors.''

![](ex99-1_003.jpg)

Alterity is a late clinical stage biopharmaceutical company dedicated to developing treatments for neurodegenerative diseases Our goal is to slow the course of disease progression We strive to create an alternate future and improve patient quality of life Alterity means the state of being different 3

![](ex99-1_004.jpg)

Investment highlights 4 Positive Phase 2 data in Multiple system atrophy, a Parkinsonian disorder Large market potential in neurodegenerative diseases Highly experienced leadership team in movement disorders Oral administration preferred over competition Robust efficacy on functional endpoint in double - blind study Patient friendly administration Three FDA approvals in neurology Potential to treat Parkinson's disease and related disorders

![](ex99-1_005.jpg)

Promising portfolio in neurodegenerative diseases Program: Drug discovery Indication: Discovery Pre - clinical Phase 1 Natural History Positive topline data Positive topline data Phase 2 Phase 3 Collaboration Multiple system atrophy Open label study Parkinson's disease Neurodegenerative diseases Friedreich's ataxia ATH434 - 201 ATH434 - 202 ATH434 ATH434 Multiple system atrophy Natural history study bioMUSE Multiple system atrophy Double blind study 5

![](ex99-1_006.jpg)

Multiple System Atrophy (MSA): Parkinsonian disorder with no approved treatment 0 Years: 3 6 9 7.5 years median survival after symptom onset Over 50% require wheelchair in 5 years Rapidly progressive Highly debilitating Up to 50,000 patients in U.S. Disease characteristics: • Motor: Parkinsonism, uncoordinated movements, balance problems, falls • Autonomic dysfunction: blood pressure maintenance, bladder control, bowel function • Atrophy and α - synuclein accumulation in multiple brain regions Premotor MSA Clinically probable MSA Death can occur Clinically established MSA Urinary dysfunction REM sleep behavior disorder Orthostatic hypotension Parkinsonism Cerebellar features Multidomain autonomic failure Pyramidal signs 6 Sources: Fanciulli, Wenning. NEJM 2015 \| Wenning, et al. Mov Disorders 2022 \| Coon, et al. Brain 2015 \| Multiple System Atrophy: National Institute of Neurological Disorders and Stroke (nih.gov) Recurrent falls Indwelling catheter Frontal executive dysfunction Unintelligible speech Gastrostomy Tracheostomy Bronchopneumonia Uroseptic fever Sudden death

![](ex99-1_007.jpg)

Targeting the pathology in Parkinsonian disorders

![](ex99-1_008.jpg)

Alpha - synuclein and iron balance vital for normal CNS function Two forms of iron required for cellular function: • Energy production and activity of many enzymes • Neurotransmitter synthesis (e.g., dopamine) • Myelin synthesis α - Synuclein protein: • Present in all neurons • Regulates neurotransmitter release • Facilitates neuronal communication Myelination of axons Fe 2+ Fe 3+ Fe 2+ Reactive Fe 3+ Stable 8

![](ex99-1_009.jpg)

Pathology of Parkinsonian disorders α - synuclein Aggregation PET imaging of α - synuclein pathology (18F - C05 - 05) Parkinson's disease n = 24 n = 13 n = 9 n = 7 \* n = 3 n = 8 \* 0 30000 S. nigra (T) S. nigra (pc) Cerebellum 10000 20000 nmol iron/g of human brain Multiple system atrophy n = 8 n = 8 n = 9 n = 8 n = 11 n = 8 \* n = 9 n = 6 \* n = 10 n = 8 \* 0 30000 10000 20000 nmol iron/g of human brain Putamen (M) Putamen (L) Globus pallidus (M) Globus pallidus (L) S. nigra (T) Healthy Control Increased Brain Iron Patients Healthy controls Parkinson's disease 9 Endo et al., Neuron 2024; Dexter et al. Brain.1991 Multiple System Atrophy

![](ex99-1_010.jpg)

Iron converts native α - SYN into a β - sheet conformation and promotes its aggregation either directly or via increasing levels of oxidative stress. The disturbance of iron homeostasis leads to abnormal iron deposition in the brain and causes neurotoxicity via generation of free radicals and oxidative stress. The close association of iron accumulation with distinct α -synuclein - pathology - related anatomical regions of the two disease subtypes supports the critical involvement of pathological iron in disease progression and further suggests the two disease subtypes as distinct pathological identities in relation to disease pathogenesis. Role of iron and α - synuclein in disease pathogenesis 10 doi 10.3233/JAD - 170601 (2018); doi.org/10.3390/ijms25084269 (2024)

![](ex99-1_011.jpg)

Excess labile iron is the key driver of pathology causing α - synuclein aggregation and oxidative injury Iron imbalance Excess labile iron Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 3+ PCBP Fe 2+ Neuron death and impaired oligodendrocyte function monomer or normal oligomers fibrils α - syn fibrils damage multiple organelles α - syn fibrils impair myelin production in MSA α - Synuclein aggregation Mitochondrial dysfunction ROS damage to cellular components. Lipid peroxidation Increased ROS ROS Fe 2+ 11 PCBP

![](ex99-1_012.jpg)

Fe 3+ Stable Fe 3+ 2+ Fe Reactive Fe 2+ ATH434 mechanism of action: Iron chaperone ATH434 chaperones excess labile (reactive) iron to reduce neuronal injury Sources: Adapted from Yanatori et al., BBA 2020 and Philpott et al., Frontiers Mol Bio. 2023 \| Buffering Fe 2+ in labile iron pool PCBP: Poly(rC) - binding proteins 1 Efflux iron from cell (ferroportin) 2 Increase iron storage (ferritin) Fe 3+ Endosome Mitochondria Ferritin Ferroportin DMT1 ZIP8 ZIP14 Transferrin receptor Labile iron Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ Fe 2+ ATH434 Fe 2+ ATH434 PCBP PCBP 1 Fe 2+ PCBP 2 Tf Fe 3+ Fe 3+ PCBP Fe 2+ Enzyme PCBP ROS Fe 2+ Fe 2+ ATH434 Fe 2+ Fe 2+ 3 Pall, et al. Metallomics, 2024. 12 Chaperone mechanisms: 3

![](ex99-1_013.jpg)

Treatment approach: Address underlying pathology Based on mechanism of action, ATH434 is a potential disease modifying therapy Chaperones excess labile iron in the CNS Reduces α - synuclein aggregation and oxidative injury Preserves neurons and oligodendrocyte cell function Stabilizes or improves patient function 13

![](ex99-1_014.jpg)

ATH434: Small molecule drug candidate Broad treatment potential Potential to treat many neurodegenerative diseases (e.g., Parkinson's, Frederich Ataxia) Orphan & Fast Track designations US FDA Fast Track Designation and Orphan drug designation in U.S. and EU Blood - brain barrier penetrant Acts intracellularly to address underlying pathology Iron chaperone Moderate binding affinity, redistributes excess labile iron in CNS Oral administration Preferred by patients and doctors vs infusions (IV, intrathecal) or injections ATH434 binding to labile iron 14

![](ex99-1_015.jpg)

Accumulated evidence of ATH434 efficacy 15 Sources: Bradbury et al, Am Acad. Neurol 2024; Finkelstein, Acta Neuropath Comm 2017; Beauchamp et al, Neurotherapeutics 2022; 1 Heras - Garvin et al, Mov Disord. 2021; 2 Finkelstein et al, J Park Dis 2022 Clinical observations Preserve neurons / function α - Synuclein Midbrain iron incl. s. nigra Model Target disease Improved motor performance n/a Monkey MPTP Parkinson's disease Improved motor performance Mouse MPTP Parkinson's disease Improved motor performance Mouse A53T Parkinson's disease Improved motor performance Mouse tau knockout Parkinson's disease Improved motor performance PLP - α - syn MSA 1 Improved motor performance PLP - α - syn MSA 2 Stable ATH434 consistently improved motor performance by reducing α - synuclein aggregation and preserving neurons

![](ex99-1_016.jpg)

ATH434 clinical development program in MSA

![](ex99-1_017.jpg)

Diligent approach to de - risk development program 17 • Observational study in individuals with MSA • Designed to de - risk clinical development program • Identify biomarkers to improve accuracy of patient selection Phase 2 ATH434 - 201 ATH434 - 202 Randomized double - blind placebo - controlled trial Results : clinically meaningful efficacy on MSA rating scale, measures of orthostatic hypotension, disease severity Natural History Study Open label trial in advanced MSA patients Results: showed improved neurological symptoms in more advanced patients and favorable safety bioMUSE

![](ex99-1_018.jpg)

BioMUSE natural history study informs and de - risks clinical development program N=21 Patient criteria: Clinically Probable MSA Biomarkers: • MRI: iron, volume, glial pathology • Fluid: NfL, aggregated α - synuclein • Digital: Wearable movement sensors Clinical: UMSARS 1, autonomic function, motor function global measures Objective: Track clinical and biomarker endpoints over observation period 12 months of observation bioMUSE BioMUSE natural history study allowed us to optimize patient selection in our Phase 2 trials 18 \*Biomarkers of progression in Multiple System Atrophy (bioMUSE).; 1NfL: Neurofilament light chain

![](ex99-1_019.jpg)

BioMUSE natural history study results bioMUSE Identified "iron signature" of early MSA Differentiated MSA from Parkinson's disease (PD) Revised selection criteria in ATH434-201 and ATH434 - 202 protocols to exclude PD patients Improved precision of volume measurements Novel strategies for measuring brain iron in individual regions State of the art methods enabled precise measurements of brain iron and volume with MRI Optimized patient selection in Phase 2 trials Advanced MRI methods α - synuclein SAA in CSF Precision biomarker assessment Structural mapping Iron content in pallidum 19 Sources: Presentations/Posters on file, including Claassen et al, MDS Conference 2021 and 2022.

![](ex99-1_020.jpg)

ATH434 - 201: Randomized, double - blind, placebo - controlled study 20 N=77 Study design: Endpoints: Patient criteria: • Clinical diagnosis of MSA • Motor symptoms ≤4 years • No severe impairment • Elevated brain iron on MRI • Elevated plasma NfL Placebo twice daily 50 mg twice daily Key clinical endpoint: modified UMSARS Part 1 75 mg twice daily ATH434 ATH434 - 201 MRI - Magnetic Resonance Imaging; UMSARS - Unified MSA Rating Scale (UMSARS) Scale – measures activities of daily living CGI - S - Clinical Global Impression - Severity scale; OHSA - Orthostatic Hypotension Symptom Assessment Additional secondary endpoints: CGI - S, OHSA, Wearable Sensors, Safety ATH434 12 months treatment Key biomarker endpoint: brain iron content by MRI

![](ex99-1_021.jpg)

Importance of the U nified MSA R ating S cale Part I (UMSARS I) 21 ATH434 - 201 Speech Walking Swallowing Falling Handwriting Orthostatic symptoms Cutting food Urinary function Dressing Bowel function Hygiene Sexual function ^ Validated rating scale to assess MSA disease severity Rates functional impairment in domains affected in MSA Rated from 0 to 48 higher scores worse ^ Modified version of UMSARS I excludes sexual function item UMSARS Part I Items: UMSARS is the FDA endorsed clinical endpoint to support approval for the treatment of MSA

![](ex99-1_022.jpg)

Populations and key endpoints 22 All patients in Imaging and Clinical analysis populations were randomized and treated Imaging analysis population Clinical analysis population 71 61 6 no post baseline UMSARS I 5 neg. CSF α - syn SAA 10 d/c before week 26 1 completed week 26 w/o MRI Population Change from BL to week 52 Endpoint Imaging Iron content in s. nigra by MRI Biomarker (Primary) Clinical Change in Modified UMSARS Part I Clinical (Key secondary) 77 Randomized ATH434 - 201

![](ex99-1_023.jpg)

ATH434 - 201 ATH434 - 201 Placebo 75 mg twice daily 50 mg twice daily N=24 N=25 N=22 63.9 (6.7) 63.1 (6.1) 61.3 (6.6) Age (y) 62.5% 52.0% 63.6% Gender (% male) 2.3 (0.9) 2.6 (0.8) 2.5 (0.8) Duration of motor symptoms (y) 14.4 (4.4) 15.2 (5.4) 16.9 (3.9) Modified UMSARS I 48.9 (16.8) 47.8 (18.4) 57.6 (14.2) Motor score of Parkinson plus scale 1 32.3 (9.0) 31.1 (9.1) 34.9 (12.5) Plasma NfL (pg/mL) 96% 92% 91% CSF aggregating α - syn SAA (+) 15.0 (12.2) 13.8 (13.2) 13.5 (9.8) OH symptom assessment 70.8% 60.0% 59.1% Clinical phenotype: MSA - P (%) 29.2% 4.0% 4.5% Severe orthostatic hypotension 23 Baseline characteristics ATH434 - 201 1 Payan et al. PlosOne 2011 Groups balanced at baseline except for severe orthostatic hypotension - a predictor of rapid disease progression Clinical Analysis Population

![](ex99-1_024.jpg)

Clinically significant efficacy on modified UMSARS Part I Change from baseline to week 52 ATH434 - 201 worsening Modified UMSARS I Relative treatment effect Difference vs. placebo LS mean (SE) Placebo N=22 48% - 3.8 (1.6) ATH434 50 mg N=25 30% - 2.4 (1.7) ATH434 75 mg N=24 Relative Treatment Effect Change ATH434 - Change Placebo Change Placebo 14 16 26 24 22 20 18 \* P=0.02 for 50 mg 0 13 26 39 52 P=0.16 for 75 mg 35% P - value 0.11 - 2.8 (1.7) ATH434 75 mg N=24 Effect of ATH434 with Baseline OH change as covariate given imbalance of severe OH at baseline Clinical Analysis Population 24

![](ex99-1_025.jpg)

Efficacy on Clinical Global Impression of Severity (CGI - S) scale Change from baseline to week 52 Clinical Analysis Population 25 1.5 1.0 \* p=0.009 0.5 0.0 worsening Change in CGI - S (week 52 - Baseline) ATH434 - 201 50 mg Placebo • CGI - S • 7 - point scale, ranging from 1 to 7 • higher score indicates a worse outcome • Assesses total picture over prior 28 days • illness severity, impact of illness on function, level of distress and any other aspects of impairment ATH434 - 201 ATH434 - 201 75 mg LS mean (SE)

![](ex99-1_026.jpg)

Orthostatic Hypotension Symptom Assessment (OHSA) Change from baseline to week 52 10 5 - 5 0 Change In OHSA (week S2 BL) • Assesses symptoms of low blood pressure when going from sitting to standing (e.g., dizziness / feeling faint / lightheadedness) • Patient reported outcome p=0.08 worsening mean (SE) p=0.14 ATH434 50 mg ATH434 75 mg Placebo ATH434 - 201 Clinical Analysis Population 26 Kaufmann, et al. Clin Auton Res 2012..

![](ex99-1_027.jpg)

0 - 50 - 100 worsening ATH434 - 201 Step count worsening 0 - 1000 - 2000 - 3000 Change In steps/day p = 0.04 \* p = 0.10 Total time walking Change In bouts/day Total standing time Pendant Wearable movement sensor ATH434 - 201 50 mg ATH434 - 201 75 mg Placebo Change In minutes/day 0 - 10 - 20 - 40 - 30 p = 0.13 p = 0.15 worsening Bouts of walking 0 - 20 - 40 - 80 - 60 Change In minutes/day worsening Clinical Analysis Population 27 ATH434 preserved walking in outpatient setting Change from baseline to week 52

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28 1 - Reporting one or more event 2 - None related to Study Drug ATH434 - 201 • Similar rates of AEs in ATH434 and placebo participants • No severe or serious AEs related to study drug • No hematologic side effects ATH434 - 201 75 mg N=26 ATH434 - 201 50 mg N=25 Placebo twice daily N=26 N (%) of subjects 1 25 (96.2%) 21 (84.0%) 24 (92.3%) Any Adverse Event (AE) 7 (26.9%) 10 (40.0%) 14 (53.8%) UTI 8 (30.8%) 7 (28.0%) 8 (30.8%) Fall 4 (15.4%) 6 (24.0%) 1 (3.8%) Covid - 19 5 (19.2%) 1 (4.0%) 2 (7.7%) Fatigue 2 (7.7%) 3 (12.0%) 1 (3.8%) Back pain 6 (23.1%) 3 (12.0%) 8 (30.8%) Severe AEs 2 7 (26.9%) 5 (20.0%) 10 (38.5%) Serious AEs 2 Adverse Events

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Neuroimaging Endpoints 29 \* MSA Atrophy Index: composite z - score of putamen, GP, cerebellum and brainstem vs. healthy age - matched population Change in Iron Content by MRI ATH434 demonstrated target engagement on reducing iron on MRI • Reduced/stabilized iron content in Pallidum (GP) > Putamen • Reduced iron content in s. nigra at 50 mg dose but not 75 mg (primary endpoint) Iron content, No observable difference, Compared to placebo: ^p = 0.03, ¶ p = 0.08 0.0000 - 0.1000 - 0.2000 - 0.3000 - 0.4000 - 0.5000 - 0.6000 worsening Z - score ATH434 - 201 50 mg ATH434 - 201 75 mg Placebo Change in Brain Volume \* 26 weeks 52 weeks ATH434 showed trends in preserving brain volume ATH434 - 201 75 mg 50 mg Region Week 52 Week 26 Week 52 Week 26 ¶ Pallidum Putamen S. nigra

![](ex99-1_030.jpg)

ATH434 - 202: Open label study in advanced MSA Key objective was to assess efficacy and safety of ATH434 75 mg dose for comparison to 75 mg dose in 201 double - blind study ATH434 - 201 ATH434 - 202 75mg BID 75 mg BID Parameter N=24 N=10 63.9 (6.7) 64.5 (7.5) Age (yr) 2.3 (0.9) 3.9 (1.8) Duration of motor symptoms (yr) 14.4 (4.4) 19.2 (5.3) Modified UMSARS I 1 48.9 (16.8) 57.5 (20.4) Motor score of Parkinson Plus Scale2 32.3 (9.0) 42.1 (14.1) Plasma NfL (pg/mL) 15.0 (12.2) 16.7 (14.8) OH Symptom Assessment 29.2% 40.0% Severe Orthostatic Hypotension Mean (SD) Single arm, open - label Design Advanced MSA (n=10) Population ATH434 75 mg BID x 12 months Treatment Iron, volume Brain MRI Biomarkers UMSARS I, clinical/patient global impressions of change Clinical Measures ATH434 - 202 30 1 MSA affected areas by MSA - atrophy index. Trujillo, P. et al Annals of Clin and Trans Neuro, 2025

![](ex99-1_031.jpg)

ATH434 - 201 ATH434 - 202 75mg BID 75 mg BID Change over 12 Months N=24 N=10 5.6 (5.6) 3.5 (4.7) Modified UMSARS I 21% 30% Clinical global impression of change (% stable) 26.4% 30% Patient global impression of change (% stable) - 0.42 (0.29) - 0.44 (0.14) Brain volume 1 Mean (SD) ATH434 - 202: Key data at 75 mg dose Comparison to double blind study at 12 mo • No serious AEs related to study drug • AEs consistent with underlying disease ATH434 - 202 The 75 mg dose demonstrated comparable efficacy to that observed in the double - blind study 31 1 In MSA affected areas by MSA - atrophy index. Trujillo, P. et al. Annals of Clin and Trans Neuro, 2025

![](ex99-1_032.jpg)

ATH434 Phase 2 summary Double - blind trial: ATH434 demonstrated clinically significant efficacy in slowing disease progression in MSA • Both dose levels efficacious on UMSARS I and important secondary endpoints • Efficacy signal at 75 mg strengthens when accounting for baseline differences in severe OH, a predictor of rapid progression • Demonstrated target engagement with reduced iron accumulation in MSA affected brain regions • No safety signals and was well - tolerated 32 Open - label trial: Similar efficacy in advanced MSA as observed in double - blind study • Data consistent on key efficacy endpoints • Biomarkers demonstrated target engagement and similar effect on brain volume • Comparable safety to double - blind study

![](ex99-1_033.jpg)

Commercial assessment & corporate overview

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Approach to commercial assessment Conducted by independent marketing research and forecasting group • Conduct secondary market research Assess unmet needs and competitive landscape • Develop target product profile based on Phase 2 clinical data • Qualitative research Conduct In - depth interviews and Focus groups with general neurologists, movement disorder neurologists and autonomic specialists to identify decision - making behavior and key drivers and barriers to adoption leveraging the target product profile • Develop physician screener and discussion guide for Quantitative Research Exploratory Research • Conduct ~30 - minute online survey among 100 neurologists (~50% general, ~50% specialists) to determine their awareness, interest, market demand and likelihood of product adoption • Assess the Target Product Profile to better understand its viability, differentiation opportunities and potential barriers to adoption • Rigorous methods used to ensure data quality and integrity Quantitative Research • Develop forecast assumptions based on qualitative and quantitative findings. • Build a financial valuation of ATH434 in treatment of MSA Opportunity Analysis and Forecast 34

![](ex99-1_035.jpg)

Key attributes of ATH434 drive significant commercial opportunity in MSA 35 USD $2.4 Billion Potential worldwide annual peak sales for ATH434 in MSA Severely debilitating illness with no approved treatment ripe for new entrants Critical need for a tolerable, disease modifying therapy Importance of inhibiting α -synuclein aggregation to address the underlying pathology of disease Slowing disease progression is key driver of physician interest Stabilizing orthostatic hypotension ^ , one of the most challenging symptoms in MSA, strongly positions ATH434 ^Orthostatic hypertension is the drop in blood pressure on standing; Global peak sales number in U.S. Dollars; Independent market research survey conducted in 2025. Peak sales estimate based on U.S. prevalence of ~19,000 Over 70% of neurologists were "extremely likely" or "very likely' to prescribe ATH434 based on its profile

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Key Objectives for 2026 36 Finalize Regulatory Strategy • Align with the U.S. FDA on pivotal Phase 3 clinical trial protocol • Conduct meetings related to non - clinical data and chemistry/manufacturing • End of Phase 2 meeting mid - year Build for Scalable Growth • Expand intellectual property protection • Evaluate additional high - value indications to grow the pipeline • Strengthen the team to enhance organizational capabilities Deepen External Reach • Publish Phase 2 results in peer - reviewed journal • Deliver poster and presentations at key medical and advocacy meetings • Expand global IR, PR and BD outreach The Foundation is Set • Robust efficacy in Phase 2 study in MSA, a rapidly progressive rare disease with no approved treatment • Commercial assessment demonstrated significant opportunity: USD $2.4B potential peak sales • Moving into Phase 3 program led by an accomplished team with multiple FDA approvals in neurology • Cash Balance of A$54.5M as of 30 September

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ASX: ATH NASDAQ: ATHE