Announcement PDF May 2026 Corporate Presentation 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.’’ 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 Redefining Neurodegenerative Disease Therapy A Potential First-in-Class, Disease-Modifying Therapy for Multiple System Atrophy (MSA) 4 MSA is a rare, rapidly progressive disease (up to 50,000 U.S. patients) Independent assessment supports ~$US2.4B global peak sales opportunity in MSA End-of-Phase 2 FDA meeting planned for mid-2026 to align on Phase 3 design Veteran development team with 3 FDA approvals in Neurology area Up to 48% slowing of disease progression v. placebo (p<0.05) on FDA-endorsed endpoint* Favorable safety profile with no drug-related serious adverse events *modified Unified MSA Rating Scale Part 1 (mUMSARS) Compelling Phase 2 Efficacy on FDA-Endorsed Endpoint Unmet Need with Significant Commercial Potential Pivotal Advancement in 2026 with Clear Regulatory Path Differentiated, Disease- Modifying Approach for MSA Oral iron chaperone ATH434 targets excess reactive iron and α-synucleinopathies Blood brain barrier penetrant small molecule Program: Discovery / Pre-clinical Phase 1 Natural History Phase 2 Phase 3 Collaboration Multiple system atrophy Double blind study Multiple system atrophy Open label study in advanced MSA Multiple system atrophy Natural history study Parkinson’s disease Friedreich’s ataxia Drug discovery Broad opportunity for ATH434 in neurodegenerative disease 5 Planned 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 Multidomain autonomic failure Pyramidal signs Parkinsonism Cerebellar features Recurrent falls Indwelling catheter Frontal executive dysfunction Tracheostomy Bronchopneumonia Urosepsis Unintelligible speech Gastrostomy 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) Sudden death Targeting the pathology in Parkinsonian disorders 8 Targeting key players in MSA pathology Alpha-synuclein and iron balance in health and disease Two forms of iron required for cellular function • Neurotransmitter synthesis (e.g., dopamine) • Myelin synthesis (allows fast signal transmission) α-Synuclein protein • Present in all neurons • Enables neuronal communication Fe2+ Fe3+ Fe2+ Reactive Fe3+ Stable In disease: α-Synuclein aggregates in neurons in MSA impairing communication and leading to dysfunction In disease: Excess reactive iron drives α-synuclein aggregation and oxidative injury Pathology of Parkinsonian disorders 9 Dexter et al. Brain.1991 Parkinson’s disease n = 24 n = 13 n = 9 n = 7 * n = 3 n = 8 * 0 10000 20000 30000 S. nigra (T) S. nigra (pc) Cerebellum nmol iron/g of human brain n = 8 n = 8 n = 9 n = 8 n = 11 n = 8 * n = 9 n = 6 * n = 10 n = 8 * 0 10000 20000 30000 nmol iron/g of human brain Putamen (M) Putamen (L) Globus pallidus (M) Globus pallidus (L) S. nigra (T) Increased Brain Iron in Areas of Pathology Patients Healthy controls Multiple System Atrophy Parkinson’s disease 10 Excess labile iron is a key driver of pathology causing α-synuclein aggregation and oxidative injury Iron imbalance Excess labile iron Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe3+ PCBP Fe2+ 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 Fe2+ PCBP PCBP: Poly(rC)-binding proteins Fe3+ Stable Fe3+ Fe2+ Reactive Fe2+ 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 | Pall, et al. Metallomics, 2024. Efflux iron from cell (ferroportin) Increase iron storage (ferritin) Buffering Fe2+ in labile iron pool PCBP: Poly(rC)-binding proteins 1 2 Fe3+ Fe2+ ZIP8 ZIP14 Transferrin receptor Labile iron Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ Fe2+ ATH434 ATH434 PCBP PCBP 1 Fe2+ PCBP 2 Fe 3+ Tf Fe 3+ PCBP Enzyme PCBP ATH434 ROS Fe2+ Fe2+ Fe2+ 3 11 Chaperone mechanisms: 3 Treatment approach: Address underlying pathology 12 Based on mechanism of action, ATH434 is a potential disease modifying therapy Preserve neurons and oligodendrocyte cell function Reduce α-synuclein aggregation and oxidative injury Chaperone excess labile iron in the CNS Stabilize function or slow decline ATH434: Small molecule drug candidate 13 Broad treatment potential Potential to treat many neurodegenerative diseases (e.g., Parkinson’s, Friedreich 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 ATH434 consistently improved motor performance by reducing α-synuclein aggregation and preserving neurons Target Disease Model Midbrain iron (incl. s. nigra) α-Synuclein Preserve neurons/ function Clinical observations MSA1 PLP-α-syn Improved motor performance MSA2 PLP-α-syn to Improved motor performance Parkinson’s Monkey MPTP to n/a Improved motor performance Parkinson’s Mouse MPTP Improved motor performance Parkinson’s Mouse A53T Improved motor performance Parkinson’s Mouse tau knockout Improved motor performance Multiple models of neurodegenerative disease demonstrate ATH434 efficacy Stable 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 ATH434 clinical development program in MSA Diligent approach to de-risk development program 16 • Observational study in 21 participants with clinically probable 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 *Biomarkers of progression in Multiple System Atrophy (bioMUSE).; Biomarkers: Biomarkers:; MRI, Fluid, Digital BioMUSE natural history study results 17 bioMUSE Advanced MRI methods Structural mapping Sources: Presentations/Posters on file, including Claassen et al, MDS Conference 2021 and 2022. Optimized patient selection in Phase 2 trials Precision biomarker assessment Differentiated MSA from Parkinson’s disease (PD) Identified ”iron signature” of early MSA Revised selection criteria in ATH434‐201 and ATH434-202 protocols to exclude PD patients Novel strategies for measuring brain iron in individual regions Improved precision of volume measurements State of the art methods enabled precise measurements of brain iron and volume with MRI α-synuclein SAA in CSF Iron content in pallidum ATH434-201: Randomized, double-blind, placebo-controlled study 18 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: MSA Rating Scale 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 1 : 1 : 1 Importance of the Unified MSA Rating Scale Part I (UMSARS I) 19 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 endpoint to support approval for the treatment of MSA Proposed primary endpoint in Phase 3 Placebo ATH434-201 50 mg twice daily ATH434-201 75 mg twice daily N=22 N=25 N=24 Age (y) 61.3 (6.6) 63.1 (6.1) 63.9 (6.7) Gender (% male) 63.6% 52.0% 62.5% Duration of motor symptoms (y) 2.5 (0.8) 2.6 (0.8) 2.3 (0.9) Modified UMSARS I 16.9 (3.9) 15.2 (5.4) 14.4 (4.4) Motor score of Parkinson plus scale1 57.6 (14.2) 47.8 (18.4) 48.9 (16.8) Plasma NfL (pg/mL) 34.9 (12.5) 31.1 (9.1) 32.3 (9.0) CSF aggregating α-syn SAA (+) 91% 92% 96% OH symptom assessment 13.5 (9.8) 13.8 (13.2) 15.0 (12.2) Clinical phenotype: MSA-P (%) 59.1% 60.0% 70.8% Severe orthostatic hypotension 4.5% 4.0% 29.2% 20 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 !" !# !$ %& %% %" %# ! "#$%&%'( )*+#,%#-. & !' %# '( )% *++, ATH434-201 worsening Modified UMSARS I Change ATH434 − Change Placebo Change Placebo Relative Treatment Effect: Minimal clinically important difference (MCID) on UMSARS I = − 1.5 points 21 Clinically Significant Efficacy on Modified UMSARS Part I Change from Baseline to Week 52 ATH434 50 mg N=25 Placebo N=22 ATH434 75 mg N=24 Difference v. placebo LS mean (SE) Relative treatment effect -3.7 (1.7) 46% -2.7 (1.8) 34% Clinical Analysis Population, incl CSF NfL as covariate Efficacy on Clinical Global Impression of Severity (CGI-S) scale Change from baseline to week 52 22 • CGI-S • 7-point scale • 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 !"! !"# $"! $"# %C'()G+I(+%-./ !"##$B&'()*+#,-.#/ !"#$%&%%' "01+#.-.2 Clinical Analysis Population, incl CSF NfL as covariate ATH434 50 mg ATH434 75 mg Placebo LS mean (SE) Orthostatic Hypotension Symptom Assessment (OHSA) Change from baseline to week 52 10 5 -5 0 Change In OHSA (week S2‒ BL) • Assesses symptoms of low blood pressure when going from sitting to standing (e.g., dizziness / feeling faint / lightheadedness) • Patient reported outcome p=0.08 worsening LS Mean (SE) p=0.14 ATH434 50 mg ATH434 75 mg Placebo 23 Kaufmann, et al. Clin Auton Res 2012.. ATH434-201 Clinical Analysis Population 24 ATH434-201 Step count Total time walking Sit to stand transitions Pendant Wearable movement sensor ATH434-201 50 mg ATH434-201 75 mg Placebo Bouts of walking ATH434 preserved walking in outpatient setting Change from baseline to week 52 Clinical Analysis Population, incl CSF NfL as covariate !"### !$### !%### # C'()*+,-),./+0123(4 ! !"#$#%&' !"#$(#)( *+,-./0/1 !"# !$# !%# !C# # '()*+,-.*-/.*01,234)5 !"#$%&'&( !"#$%#&' !"#$%(#) !"# !$# !%# !C# # '()*+,-.*-/.*01,234)5 !"#$%&'&( !"# !$# # %C'()*+,(+-.'(/,-,0(12'3 !"#$%&'&( 25 1 - Reporting one or more event 2 - None related to Study Drug Placebo ATH434-201 ATH434-201 twice daily 50 mg 75 mg Any Adverse Event (AE) 24 (92.3%) 21 (84.0%) 25 (96.2%) N=25 N=26 N=26 ATH434-201 N (%) of subjects 1 • Similar rates of AEs in ATH434 and placebo participants • No severe or serious AEs related to study drug • No hematologic side effects Severe AEs 2 8 (30.8%) 3 (12.0%) 6 (23.1%) Serious AEs 2 10 (38.5%) 5 (20.0%) 7 (26.9%) 1 (3.8%) 3 (12.0%) 2 (7.7%) 2 (7.7%) 1 (4.0%) 5 (19.2%) 1 (3.8%) 6 (24.0%) 4 (15.4%) 8 (30.8%) 7 (28.0%) 8 (30.8%) 14 (53.8%) 10 (40.0%) 7 (26.9%) Back pain Fatigue Covid-19 Fall UTI Adverse Events Neuroimaging Substantia Nigra Midbrain axial view Putamen / Globus Pallidus Basal ganglia axial view QSM: Quantitative Susceptibility Mapping І QSM overlay: warm colors = higher magnetic susceptibility (iron content) Measuring Iron Content with MRI (QSM) Regional increases in iron in MSA Patient 28 Iron Deposition on MRI in Placebo: Change Baseline → Week 52 ATH434-201 Mean ± 95% CI Iron Deposition on MRI: ATH434 vs. Placebo ATH434-201 MMRM with sex, age, baseline CSF NfL, and baseline iron as covariates 30 ATH434 decouples iron accumulation from clinical worsening Correlation Between Change in Iron and Change in UMSARS I Score at Week 52 Controlling for Sex, Age, Baseline CSF NfL, Baseline QSM Summary: ATH434 Interrupts the Pathologic Process in MSA 31 • Iron accumulates in the basal ganglia of MSA patients, most prominently in the globus pallidus and putamen • QSM allows quantitation of total brain iron but does not distinguish between reactive (toxic in excess) and stable forms of iron • In placebo-treated patients, change in iron strongly correlates with change in disease severity • In ATH434-treated patients, change in iron weakly correlates with change in disease severity - ATH434 leads to a decoupling of iron accumulation and clinical worsening as assessed by UMSARS I Measuring Brain Volume in MSA Regions of Interest Subject 1 Change in Brain Volume* 0.0000 -0.1000 -0.2000 -0.3000 -0.4000 -0.5000 -0.6000 worsening Z-score ATH434-201 50 mg BID ATH434-201 75 mg BID Placebo 26 weeks 52 weeks ATH434 showed trends in preserving brain volume * MSA Atrophy Index: composite z-score of putamen, GP, cerebellum and brainstem vs. healthy age-matched population Subject 2 ATH434-202: Open label study in advanced MSA 33 1 MSA affected areas by MSA-atrophy index. Trujillo, P. et al Annals of Clin and Trans Neuro, 2025 *ATH434-201 listed for comparative purposes, data are not from a head-to-head study Design Single arm, open-label Objective Assess safety and efficacy in advanced MSA Population Advanced MSA (n=10) Treatment ATH434 75 mg BID x 12 months Brain MRI Biomarkers Volume, Iron Key Clinical Measure UMSARS I ATH434-202 The study indicates the potential of ATH434 to slow disease progression in advanced MSA No serious Adverse Events (AEs) related to study drug AEs consistent with underlying disease Comparable efficacy observed at same dose in double blind study Outcomes: Carefully designed Phase 2 program demonstrates potential for ATH434 in MSA 34 ATH434 demonstrated clinically significant efficacy in slowing disease progression in MSA Both dose levels efficacious on UMSARS I and important secondary endpoints Demonstrated target engagement with reduced iron accumulation in MSA affected brain regions Stabilized orthostatic hypotension, one of the most challenging MSA symptoms to manage Preserved walking in outpatient setting as measured with objective digital biomarker Open-label trial showed comparable safety and efficacy in advanced MSA No safety signals and well-tolerated No serious AEs related to study drug Proposed Phase 3 trial Design 35 N = ~200 Study design: Efficacy Endpoints: Patient criteria: • Clinical diagnosis of MSA • Ambulatory without assistance • No severe impairment • Brain atrophy in MSA affected regions on MRI • Elevated plasma NfL 1 : 1 * Primary endpoint Modified UMSARS I FDA endorsed clinical endpoint 50 mg twice daily ATH434 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; orthostatic SBP – orthostatic systolic blood pressure Secondary endpoints OHSA, Wearable Sensors, Brain Volume by MRI Placebo 12 months treatment Finalize Phase 3 program after end-of-Phase 2 FDA feedback and then initiate trial activities by YE 2026 twice daily * Randomization stratified by screening plasma NfL Efficacy Analysis Includes baseline CSF NfL as covariate Commercial assessment & corporate overview Independent commercial assessment in MSA 37 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 hypotension 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 Target product profile based on positive Phase 2 data ü Reached alignment in Type C meeting related to clinical pharmacology and non-clinical elements ü Reached alignment in Type C meeting related to Chemistry Manufacturing & Controls (CMC) • On track for Type B End-of-Phase 2 meeting mid-year 38 • Initiate start-up activities for the trial by year end • Clinical site identification and qualification • Manufacture and package of clinical drug supply • Expand intellectual property protection • Evaluate additional high-value indications to grow the pipeline • Strengthen the team to enhance organizational capabilities Finalize Regulatory Strategy - Align with U.S. FDA on Phase 3 clinical trial Phase 3 Readiness activities Build for Scalable Growth Well Positioned for 2026 Catalysts ASX: ATH NASDAQ: ATHE APPENDIX 40 41 Inadequately chaperoned cellular iron drives MSA pathology Promotes α-synuclein cross linking1 Directly increases α‐synuclein translation2 ODG toxicity due to limited endogenous glutathione3 Free radicals promote α‐synuclein aggregation4 Impaired lysosomal autophagy5 1Duce JA, et al. Mol Neurodegener. 2017;12(1):45. 2Febbraro F, et al. NeuroReport. 2012;23(9):576-580. 3Thorburne SK, Juurlink BH. Neurochem. 1996;67(3):1014-1022. 4Souza JM, J Biol Chem. 2000;275(24):18344-18349. 5Tanji, K, et al. Neurobiol Dis. 2013;49:190-198. doi 10.3233/JAD-170601 (2018); doi.org/10.3390/ijms25084269 (2024) Christine Kaindlstorfer, Kurt A Jellinger, Sabine Eschlbök, Nadia Stefanova, Günter Weiss, Gregor K Wenning Seojin Lee, Ivan Martinez-Valbuena , Anthony E. Lang, Gabor G. Kovacs 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. Importantly, extensive evidence suggests a molecular relationship between iron accumulation and α-syn pathology. Cellular iron deposition patterns predict clinical subtypes of multiple system atrophy Neurobiology of Disease. 2024. https://doi.org/10.1016/j.nbd.2024.106535 Journal of Alzheimer’s Disease (2018) DOI 10.3233/JAD-170601 42 Reactive iron Generates free radicals Promotes α-synuclein aggregation α-synuclein aggregation Neuronal toxicity Impaired myelin production Oxidative stress Disrupts multiple cellular functions Promotes α-synuclein aggregation Iron is a key driver of the MSA Pathology ATH434 chaperones excess iron to reduce neuronal injury Overwhelms natural iron buffering systems, leading to iron accumulation in MSA brain regions MSA Pathology Cycle Disrupted Control of CNS Iron 4 Key disease drivers 43 Correlation Between Change in Iron and Change in UMSARS I Score at Week 52 ATH434 decouples iron accumulation from clinical worsening Controlling for Sex, Age, Baseline CSF NfL, Baseline QSM ATH434-201: Populations and key endpoints 44 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 Endpoint Change from BL to week 52 Population Biomarker (Primary) Imaging Clinical (Key secondary) Clinical Iron content in s. nigra by MRI Change in Modified UMSARS Part I Randomized 77 ATH434-201 ATH434-202: Open label study in advanced MSA 45 Key objective was to assess efficacy and safety of ATH434 75 mg dose for comparison to 75 mg dose in 201 double-blind study Parameter ATH434-202 75 mg BID N=10 ATH434-201 75mg BID N=24 Age (yr) 64.5 (7.5) 63.9 (6.7) Duration of motor symptoms (yr) 3.9 (1.8) 2.3 (0.9) Modified UMSARS I1 19.2 (5.3) 14.4 (4.4) Motor score of Parkinson Plus Scale2 57.5 (20.4) 48.9 (16.8) Plasma NfL (pg/mL) 42.1 (14.1) 32.3 (9.0) OH Symptom Assessment 16.7 (14.8) 15.0 (12.2) Severe Orthostatic Hypotension 40.0% 29.2% Mean (SD) 1 MSA affected areas by MSA-atrophy index. Trujillo, P. et al Annals of Clin and Trans Neuro, 2025 ATH434-202 Change over 12 Months ATH434-202 75 mg BID N=10 ATH434-201 75mg BID N=24 Modified UMSARS I 3.5 (4.7) 5.6 (5.6) Clinical global impression of change (% stable) 30% 21% Patient global impression of change (% stable) 30% 26.4% Brain volume1 -0.44 (0.14) -0.42 (0.29) Mean (SD) ATH434-202: Key data at 75 mg dose Comparison to double blind study at 12 mo 46 • No serious AEs related to study drug • AEs consistent with underlying disease 1 In MSA affected areas by MSA-atrophy index. Trujillo, P. et al. Annals of Clin and Trans Neuro, 2025 ATH434-202 The 75 mg dose demonstrated comparable efficacy to that observed in the double-blind study