A Randomized, Double-blind, Placebo-controlled, 104-week Proof-of-concept Study to Evaluate the Efficacy of Intravenous Prasinezumab in Participants With Parkinson's Disease Carrying a Severe Mutation in the GBA Gene

This is a proof-of-concept trial to investigate the efficacy of prasinezumab to slow or prevent cognitive decline in people with Parkinson's disease carrying a severe mutation in the GBA (glucocerebrosidase) gene. The duration of the intervention per patient will be 104 weeks with monthly infusions. The investigators plan to enroll 120 participants (60 participants per treatment arm). This study will be conducted across Europe in the following countries: France, Germany, Italy, Luxembourg, Spain, Sweden, UK.

Start Date01 Dec 2025

Sponsor / Collaborator-

NCT07174310

/ RecruitingPhase 3

A Phase III, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study to Evaluate the Efficacy and Safety of Intravenous Prasinezumab in Participants With Early-Stage Parkinson's Disease

The purpose of this study is to evaluate the efficacy, safety, and pharmacokinetics (PK) of prasinezumab compared with placebo in participants with early-stage Parkinson's disease (PD) on stable symptomatic monotherapy with levodopa.

Start Date24 Nov 2025

Sponsor / Collaborator

Roche Holding AG

[+1]

NCT04777331

/ Active, not recruitingPhase 2

A Phase IIB, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study to Evaluate the Efficacy and Safety of Intravenous Prasinezumab in Participants With Early Parkinson's Disease

This is a multicenter, randomized, double-blind, placebo-controlled study that will evaluate the efficacy and safety of intravenous (IV) prasinezumab versus placebo in participants with Early Parkinson's Disease (PD) who are on stable symptomatic PD medication.

Start Date05 May 2021

Sponsor / Collaborator

Hoffmann-La Roche, Inc.

[+1]

100 Clinical Results associated with Prasinezumab

100 Translational Medicine associated with Prasinezumab

100 Patents (Medical) associated with Prasinezumab

Literatures (Medical) associated with Prasinezumab

01 Apr 2026·CURRENT OPINION IN NEUROBIOLOGY

The challenges of experimental pharmacology in identifying novel treatments for Parkinson's disease

Review

Author: Huot, Philippe ; Teil, Margaux

An important part of the field of experimental pharmacology encompasses the study of the effects of molecules in animals. In the case of Parkinson's disease (PD), animal models have played an invaluable role in refining our understanding of the disease, in characterizing the effect of new compounds on the illness, and in bringing new treatments to the clinic. Indeed, it is now hardly conceivable that a drug would be tested in humans if several parameters pertaining to safety, toxicology, efficacy, etc. had not previously been evaluated in animal models. Quite unfortunately, efficacy in experimental models of PD does not necessarily guarantee positive clinical outcomes. In this article, which primarily focusses on the past five years, we review drugs that entered clinical trials for the treatment of levodopa-induced dyskinesia, parkinsonism, disease modification, and had previously been assessed in animal models of PD. The drugs discussed are buspirone, JM-010, befiradol, mesdopetam, foliglurax, dipraglurant, tavapadon, prasinezumab, cinpanemab, nilotinib, minzasolmin, exenatide, NLY01, liraglutide, lixisenatide, and semaglutide. For each molecule, we examine how previous preclinical studies succeeded or failed in predicting efficacy in clinical trials and discuss possible ways to optimize animal-model design and selection to maximize the probability of translational success.

04 Nov 2025·Cureus Journal of Medical Science

Immunotherapy in Early Parkinson's Disease: A Biomarker-Driven Trial Framework for Secondary Prevention

Review

Author: Kniazev, Roman

Parkinson's disease (PD) is characterized by α-synuclein aggregation and progressive dopaminergic neuron loss that begins years before motor symptoms appear. This prolonged premotor phase creates an opportunity for intervention before extensive neurodegeneration. Biomarkers, including α-synuclein seed amplification assays, standardized peripheral tissue biopsies (e.g., skin biopsies for phosphorylated α-syn), neuroimaging, fluid biomarkers, genetics, and digital measures, now detect prodromal PD biology in at-risk individuals and enable secondary-prevention-style trials. Immunotherapy targeting misfolded α-synuclein is a leading disease-modification strategy. Passive approaches (monoclonal antibodies) and active vaccines have shown target engagement in preclinical models and early trials. Phase 1/2 α-synuclein antibody trials have shown mainly mild-to-moderate infusion reactions and no reproducible CNS inflammatory toxicity. Although primary efficacy endpoints have not yet been achieved overall, prasinezumab has indicated exploratory slowing in faster progressors and digital measures. MEDI1341 has demonstrated Phase 1 target engagement with acceptable safety, and Lu AF82422 has shown Phase 1 target engagement, along with promising subgroup trends in MSA, and scheduled Phase 3. Meanwhile, cinpanemab was negative. However, signals of slowed progression in subgroups underscore the importance of treating earlier and selecting patients with biomarker-confirmed pathology. This review synthesizes evidence supporting early, biomarker-anchored intervention and the status of α-synuclein immunotherapies. Treating PD at the prodromal stage aims to preserve vulnerable neurons and alter the disease course; continued advances in biomarkers and trial design are essential to realize this potential. We emphasize biomarkers that verify α-synuclein pathology during the asymptomatic phase and argue for a secondary-prevention model that treats the underlying biology before symptoms to maximize disease-modifying potential. We also propose a practical, biomarker-guided trial blueprint for secondary prevention, with explicit screening funnels and endpoint hierarchies.

01 Apr 2025·MOVEMENT DISORDERS

Prasinezumab: A Bayesian Perspective on Its Efficacy

Article

Author: Mirella Russo MD, MSc ; Stefano L. Sensi MD, PhD ; Dario Calisi MD, MSc ; Tommaso Costa PhD

Parkinson's disease (PD) is a progressive neurodegenerative disorder featuring aberrant aggregation of α-synuclein (a presynaptic protein implicated in physiological synaptic vesicle trafficking and neurotransmitter release) as a critical modulator of the disease.1, 2 This notion has been further substantiated by the discovery of autosomal dominant variants of PD associated with mutation or triplication of the α-synuclein gene SNCA (PARK1 and PARK4, respectively).3 In PD, α-synuclein undergoes conformational changes (Fig. 1), leading to the formation of insoluble fibrils and intracellular inclusions known as Lewy bodies.4 One of the leading pathogenic theories postulates that these aggregates propagate in a prion-like manner, spreading throughout the brain in a pattern that correlates with disease progression.5-8 Although the link between α-synuclein anomalies and PD has been established, the modalities of this association are still unclear. A revised approach is considering that both a loss of function of a physiological (monomeric) protein9 and a gain of abnormal function could play a role.10, 11 On the one hand, α-synuclein oligomers and fibrils exhibit toxic properties as these aggregates disrupt cellular homeostasis, impair mitochondrial function, and induce oxidative stress, neuroinflammation, and synaptic dysfunction, ultimately leading to neuronal dysfunction and death.10 On the other hand, it has also been hypothesized that the loss of function of α-synuclein (synucleinopenia)9 may consistently affect PD pathophysiology. Due to its main localization at presynaptic terminals, the protein regulates neurotransmitter release and synaptic vesicle dynamics. Thus, its loss of function may impair synaptic transmission. Because α-synuclein is predominantly expressed in dopaminergic neurons, its loss of function may dysregulate dopaminergic signaling pathways.12 Furthermore, α-synuclein is involved in protein degradation pathways, including the ubiquitin-proteasome system and autophagy-lysosomal pathway.13 According to the model, a defective α-synuclein could favor the accumulation of misfolded proteins and protein aggregates, characteristic of PD pathology, thereby generating mixed neuropathology.14 α-Synuclein also interacts with mitochondria, influencing mitochondrial dynamics and function. Thus, a loss of function may disrupt mitochondrial bioenergetics and quality-control mechanisms, leading to mitochondrial impairment and oxidative stress.15 Moreover, α-synuclein has been linked to neuroprotection against excitotoxicity.16 Therefore, its loss of function could compromise neuronal resilience to stressors, making dopaminergic neurons more susceptible to degeneration. Several technical issues challenge the toxic role of α-synuclein. For instance, overexpression of α-synuclein due to SNCA gene multiplication does not necessarily lead to toxicity. High levels of α-synuclein are associated with better outcomes in some studies.9 Preclinical studies in knocked-out α-synuclein mice produced no substantial adverse effects. α-Synuclein knocked-out mice were fertile and showed normal neurodevelopment. However, dopaminergic dysfunction and abnormal motor responses were observed.17 The prion-like propagation of α-synuclein spreads is also questioned. It should also be underlined that the formation of α-synuclein aggregates is a passive, not active, process controlled by thermodynamic principles. Oligomers are indicated as toxic agents, but their real role is elusive because most experimental settings use supersaturated protein levels in which the presence of oligomers is transient, and they usually revert to monomers rather than forming fibers. This challenges the idea that oligomers can persist long enough to exert toxicity.9 This evidence has challenged the gain-of-function hypothesis and suggested that α-synuclein aggregation into Lewy bodies may be a protective mechanism rather than a toxic process. The recent development of disease-modifying therapies (DMTs) for PD has been a turning point. DMTs targeting α-synuclein are also crucial to confirm the "proteinopathy hypothesis," whereas negative results could successfully be the Popperian "falsification element" against it (or at least could demonstrate that the matter is far more complex than a mere protein loss of function; see Fig. 1). One complicating factor is that currently, there are no precise biomarkers for PD, and the assessment of therapy-related changes can be challenging to assess in the short time span of clinical trials. Currently, no DMT has been approved for clinical use. More importantly, PD is still regarded as a disease, even though it better fits the construct of a syndrome.18 That point is worthwhile because it implies the challenging realization of homogeneous cohorts in PD clinical trials. Prasinezumab (PRX002) is a monoclonal immunoglobulin G1 antibody designed to selectively target the soluble and insoluble aggregated forms of α-synuclein, such as oligomers and fibrils, while sparing the physiological, soluble forms of the protein19 (see Supporting Information Data S1 [Preclinical Studies on Prasinezumab section] for the results of preclinical studies). In 2022, the PASADENA phase 2 trial20 assessed the efficacy of prasinezumab in patients with early-stage PD. The results were disappointing.20 Participants were randomly assigned to receive either a placebo or the compound (1500 or 4500 mg) every 4 weeks for 52 weeks. The primary outcome measured changes in the Movement Disorder Society–revised Unified Parkinson's Disease Rating Scale (MDS-UPDRS) scores, with secondary outcomes assessing dopamine transporter levels via single-photon emission computed tomography. Among 316 participants, the MDS-UPDRS scores and dopamine transporter levels did not differ when comparing the treatment and placebo groups.20 Overall, prasinezumab did not significantly affect PD progression compared with placebo, and optimism faded. Nonetheless, a new post hoc analysis was carried out and recently published.21 The post hoc analysis of the PASADENA study showed that the compound might slow motor progression in predefined subpopulations of patients with early-stage PD.21 Although the original study did not meet its primary endpoint (changes in MDS-UPDRS Parts I + II + III scores),20 in the subset of rapidly progressing patients,21 compared with placebo, drug-treated participants showed less worsening in motor signs (MDS-UPDRS Part III). The ongoing PADOVA study (NCT04777331) further investigates the impact of prasinezumab on motor progression in early-stage PD. However, methodological limitations must be accounted for, and longer trials might be required to observe effects in slowly progressing populations. Nonetheless, the recent post hoc analysis of the PASADENA trial raised many questions about the drug's efficacy because it indicated a numerical effect on motor progression in specific subpopulations (ie, fast progressing phenotypes). However, the lack of significant overall effects raises concerns about the robustness of these findings. First, the distinction between "diffuse malignant" and "nondiffuse malignant" phenotypes was made retrospectively and was data driven, which may have introduced a retrospective selection bias.21 The identification of "diffuse malignant" phenotypes at baseline with those with "more rapid" worsening is also problematic, because it conflates baseline features with outcomes. Moreover, the assessment of rapid progression was limited to the time of the observation and could carry a time-window bias and, as acknowledged by the authors of the original study,21 could reflect a different sensitivity to "signal-to-noise ratio" of the clinician's assessment (ie, the greater the change at scales, the greater the amplification of its perception, and vice versa). Furthermore, the prescription monoamine oxidase B inhibitors at baseline is not necessarily associated with a rapid progression of the disease but could depend on different factors, including the prescriber's preferences. Lastly, the mechanism of action of prasinezumab should counter a pathophysiological event that occurs relatively early in the disease course.19 Therefore, the association between drug efficacy and rapidity of clinical worsening, which is not necessarily associated with higher degree of α-synuclein deposition, is somehow confusing. Therefore, we used a Bayesian approach to test the effectiveness of prasinezumab for PD treatment. This provides a new angle on interpreting the trial results and offers critical elements for a constructive debate. This equation helps to calculate the BF for independent groups t test based on the most frequent t statistic. The null hypothesis ( H 0 $$ {H}_0 $$ ) in this test assumes that the population means of two independent groups are equal. Several assumptions underpin this method: the observations in both groups should be random samples, the dependent variable is normally distributed within each population, and the population variances should be equal (ie, the spreads of values in both groups are similar). The BF ( B F 01 $$ B{F}_{01} $$ ) can take values between 0 and infinity. When B F 01 < 1 $$ B{F}_{01}<1 $$ , the evidence favors the alternative hypothesis ( H 1 $$ {H}_1 $$ ); when B F 01 > 1 $$ B{F}_{01}>1 $$ , the evidence supports the null hypothesis ( H 0 $$ {H}_0 $$ ). Importantly, this approach allows for a full comparison of both hypotheses, modeling "what the data should look like when there is an effect." The strength of the evidence depends on how far from 1 the BF is. Jeffreys (1939) proposed conventional thresholds: a BF greater than 3 or less than 1/3 is considered substantial evidence favoring one hypothesis over the other. Anything between 1/3 and 3 is interpreted as weak or anecdotal evidence. For example, if B F 01 = 6 $$ B{F}_{01}=6 $$ , this suggests that the null hypothesis ( H 0 $$ {H}_0 $$ ) is six times more likely than the alternative hypothesis ( H 1 $$ {H}_1 $$ ). In terms of posterior probabilities, this translates to an 86% probability for the null hypothesis ( H 0 $$ {H}_0 $$ ) (calculated as P 01 = B F 01 B F 01 + 1 = 6 7 $$ {P}_{01}=\frac{B{F}_{01}}{B{F}_{01}+1}=\frac{6}{7} $$ ), leaving a 14% probability for the alternative hypothesis ( H 1 $$ {H}_1 $$ ). All Bayesian analyses were performed using the JASP software.22 All results were also tested for robustness using a BF robustness check (see Supporting Information Data S1, Methods: Bayes Factor section). This study employed a Bayesian approach to examine the impact of prasinezumab on the progression of PD symptoms and signs. We used the BF in hypothesis testing. The BF is inherently comparative: it weighs the support for one model against that of another. Moreover, BFs do so by fully conditioning on the observed data. Otherwise, the P value depends on hypothetical outcomes that are more extreme than those observed in the sample. Such practice violates the likelihood principle and results in inconsistent or paradoxical conclusions. The BF can quantify evidence in favor of the null hypothesis. In the Bayesian framework, no special status is attached to either of the hypotheses under test; the BF assesses each model's predictive performance and expresses a preference for the model that made the most accurate forecasts. The fact that the BF can quantify evidence in favor of the null hypothesis can be of substantive importance. For instance, the hypothesis of interest may predict the absence of an effect across a varying set of conditions. Quantifying the null hypothesis is also important to learn whether the observed data provide evidence of absence or absence. Specifically, the possible outcomes of the BF can be assigned to three discrete categories: (1) evidence in favor of H 1 $$ {H}_1 $$ (ie, evidence in favor of the presence of an effect), (2) evidence in favor of H 0 $$ {H}_0 $$ (ie, evidence in favor of the absence of an effect), and (3) evidence that favors neither H 1 $$ {H}_1 $$ nor H 0 $$ {H}_0 $$ . Instead, the P value cannot provide a measure of evidence in favor of the null hypothesis. Finally, the BF is not affected by the sampling plan, that is, the intention with which the data were collected. This irrelevance follows from the likelihood principle, and it means that BFs may be computed and interpreted even when the intention with which the data are collected is ambiguous, unknown, or absent. All these advantages are not available if a classical analysis is performed as was done for the PASADENA trial data. Based on the findings shown in the first table of the source article21 (Table 1), a Bayesian analysis of the results obtained in these subpopulations was carried out. The results of the Bayesian analysis are shown in Table 2. The posterior probability column on the drug's effectiveness indicates no major and clinically relevant difference between the placebo and treated groups. The lack of efficacy applies to the population with and without rapid disease progression. The probability of efficacy is consistently less than 50% and near 50% only for the data-driven subphenotype diffuse malignant subgroup. The results support the notion that the drug's effects cannot be safely assessed. The findings are robust, as depicted in Figure 2, which shows no variation between the two hypotheses as the a priori changes; instead, there is only an increase in the BF for the same hypothesis. Additional analyses are described in Supporting Information Data S1 (Additional Bayesian Analyses section) and support the main results. Thus, there is no substantial evidence of a difference in efficacy between subpopulations with or without rapid progression. Ultimately, these results are consistent with the phase two PASADENA trial, which did not reach the primary end point at 52 weeks. In conclusion, the exploratory analysis to assess whether prasinezumab generates greater benefits on motor progression in prespecified subgroups with faster motor progression using the BF resulted in no supporting evidence. The negative findings related to the anti–α-synuclein approach confirm the many still unknown physiological and pathophysiological mechanisms controlled by the protein. Incorporation of the Bayesian approach in analyzing the efficacy of prasinezumab for the treatment of PD offers a number of important strategies for ongoing and future clinical trials, like adaptive designs to allow real-time decision-making and optimizing the trial parameters.23 The Bayesian framework also provides a probabilistic approach that quantifies uncertainty in treatment effects, thereby better informing decisions by stakeholders about modifications in trials, such as early stopping and expansion or changes in allocation ratios.24 Furthermore, Bayesian hierarchical models enable the assessment of individual variability in treatment responses, providing the groundwork for personalized treatment strategies.25 Beyond statistical and methodological issues, an additional point that should be considered when discussing the unsuccessful attempts to reach DMTs pertains to the disconnect between therapeutic strategies that are envisioned and tested in "clean and sanitized" clinical trials and the more difficult challenges offered by real-world settings. As recently discussed by Brett K. Beaulieu-Jones et al,26 research populations are studied among actively recruited individuals who often receive earlier diagnoses and comply with more consistent follow-ups. In contrast, in real-world populations, patients are diagnosed later in life and often exhibit a more rapid progression because of a combination of selection bias, multiple-hit comorbidity, late access to care, and intrinsic population differences.26 The study also highlighted bias in data collection. The mode of data gathering (actively recruited vs. passively recorded) introduces biases that must be carefully considered in clinical trial design and real-world analyses, ultimately affecting the validity of clinical outcomes. Somehow, the PASADENA trial mirrors findings from the Alzheimer's field in which multiple clinical trials targeting a single protein, amyloid, generated modest or null effects, substantially failing as disease-modifying intervention.27 In that regard, novel insights are promoting a reconceptualization of PD itself as more than a mere "synucleinopathy", but rather a heterogeneous disorder arising from the convergence of multiple pathological processes but ultimately giving a variety of clinical manifestations. Most likely, "there is more than one Parkinson's Disease,"28 and our collective efforts should focus on dissecting the convergent and divergent mechanisms that act inside or outside the central nervous system. Research project: A. Conception, B. Organization, C. Execution; Statistical analysis: A. Design, B. Execution, C. Review and critique; Manuscript: A. Writing of the draft, B. Review and critique. MR: 1A, 1B, 1C, 2C, 3A, 3B. TC: 1A, 1C, 2A, 2B, 2C, 3A, 3B. DC: 1A, 1C, 2C, 3A, 3B. SLS: 1A, 1B, 1C, 2C, 3A, 3B. Open access publishing facilitated by Universita degli Studi Gabriele d'Annunzio Chieti Pescara, as part of the Wiley - CRUI-CARE agreement. S.L.S. is supported by research funding from the Italian Department of Health (RF-2013–02358785 and NET-2011-02346784-1), from the AIRAlzh Onlus (ANCC-COOP), from the Alzheimer's Association—Part the Cloud: Translational Research Funding for Alzheimer's Disease (18PTC-19-602325) and the Alzheimer's Association—GAAIN Exploration to Evaluate Novel Alzheimer's Queries (GEENA-Q-19-596282). The data that support the findings of this study are available from the corresponding author upon reasonable request. Data S1. Supporting Information. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

News (Medical) associated with Prasinezumab

19 Feb 2026

·ir.prothena.com

Prothena Reports Fourth Quarter and Full Year 2025 Financial Results, and Provides Financial Guidance and Business Highlights

Net cash used in operating and investing activities was $23.3 million and $163.7 million for the fourth quarter and full year of 2025, respectively; quarter-end cash and restricted cash position was $308.4 million Prothena expects the full year 2026 net cash used in operating and investing activities to be $50 to $55 million and expects to end the year with approximately $255 million in cash (midpoint). Financial guidance does not include the potential to earn up to $105 million in aggregate clinical milestone payments from strategic partners in 2026 Roche initiated the Phase 3 PARAISO trial evaluating prasinezumab in early-stage Parkinson’s disease in 4Q 2025; primary completion expected in 2029 Novo Nordisk initiated the Phase 3 CLEOPATTRA trial evaluating coramitug in ATTR amyloidosis with cardiomyopathy in 4Q 2025; primary completion expected in 2029 Bristol Myers Squibb fully enrolled the Phase 2 TargetTau-1 trial evaluating BMS-986446 in early Alzheimer’s disease with primary completion expected in 1H 2027, completed a Phase 1 trial evaluating a subcutaneous formulation of BMS-986446 and obtained Fast Track designation from the U.S. FDA for BMS-986446 for the treatment of Alzheimer’s disease Prothena presented preclinical data on its TDP-43 CYTOPE® program at Neuroscience 2025 (SfN) and at the International Symposium on ALS/MND demonstrating the potential of Prothena’s CYTOPE® technology to target intracellular disease pathways At the Extraordinary General Meeting on November 19, 2025 Prothena obtained shareholder approval to reduce share capital to create distributable reserves to support a share redemption program to be conducted in 2026 if deemed appropriate Potential to earn up to $105 million in aggregate clinical milestone payments by end of 2026 related to the advancement of both coramitug for ATTR amyloidosis with cardiomyopathy by Novo Nordisk and PRX019 for neurodegenerative diseases by Bristol Myers Squibb DUBLIN--(BUSINESS WIRE)-- Prothena Corporation plc (NASDAQ:PRTA), a late-stage clinical biotechnology company with a robust pipeline of investigational therapeutics built on protein dysregulation expertise, today reported financial results for the fourth quarter and full year 2025. In addition, the Company provided business highlights and 2026 financial guidance. “In 2025, our partner Roche initiated the Phase 3 PARAISO clinical trial evaluating prasinezumab in early Parkinson’s disease and Novo Nordisk initiated the Phase 3 CLEOPATTRA clinical trial evaluating coramitug in ATTR amyloidosis with cardiomyopathy, both with primary completions expected in 2029. In addition, we expect our partner Bristol Myers Squibb to decide on the potential advancement of PRX019 in 2026 and to complete the ongoing Phase 2 TargetTau-1 clinical trial evaluating BMS-986446 in early Alzheimer’s in 1H 2027. These partnered programs have the potential to earn up to approximately $3 billion in future aggregate milestones in addition to potential future royalties,” said Gene Kinney, Ph.D., President and Chief Executive Officer, Prothena. “We also unveiled our proprietary CYTOPE® technology with presentations at scientific congresses highlighting preclinical data from our TDP-43 CYTOPE® program. In addition, we are evaluating PRX012-TfR, our once-monthly, subcutaneous anti-Aβ antibody combined with transferrin receptor technology for the treatment of Alzheimer’s in preclinical studies. We expect to share more data from our preclinical programs later this year.” 2025 Business Highlights and Upcoming Milestones Updates on Active Clinical Development Portfolio Prasinezumab, a potential first-in-class antibody for the treatment of Parkinson’s disease that is designed to target a key epitope within the C-terminus of alpha-synuclein and is the focus of a worldwide collaboration with Roche. Roche is evaluating prasinezumab in the ongoing Phase 3 PARAISO clinical trial in ~900 participants with early-stage Parkinson's disease; primary completion expected in 2029 ( NCT07174310) Roche has stated that prasinezumab has peak sales potential greater than $3.5 billion (unadjusted) and could be the first disease-modifying treatment for a condition that affects 10 million people worldwide Coramitug (formerly PRX004), a potential first-in-class amyloid depleter antibody for the treatment of ATTR amyloidosis with cardiomyopathy (ATTR-CM) designed to deplete the pathogenic, non-native forms of the transthyretin (TTR) protein, is being developed by Novo Nordisk as part of its up to $1.2 billion acquisition of Prothena’s ATTR amyloidosis business and pipeline. Novo Nordisk is evaluating coramitug in the ongoing Phase 3 CLEOPATTRA clinical trial in ~1280 participants with ATTR-CM; primary completion expected in 2029 ( NCT07207811) Novo Nordisk presented Phase 2 results during a late-breaking session at the American Heart Association Scientific Sessions on November 10, 2025 Potential to earn a clinical milestone in 1H 2026 when prespecified enrollment criteria are met in ongoing Phase 3 clinical trial by Novo Nordisk BMS-986446 (formerly PRX005), a potential best-in-class antibody for the treatment of Alzheimer’s disease that specifically targets a key epitope within the microtubule binding region (MTBR) of tau, a protein implicated in the causal pathophysiology of Alzheimer’s disease. Bristol Myers Squibb is conducting the Phase 2 TargetTau-1 clinical trial in approximately 310 patients with early Alzheimer’s disease; primary completion expected in 1H 2027 ( NCT06268886) Bristol Myers Squibb conducted a Phase 1 open-label single-dose clinical trial to assess a subcutaneous administration ( NCT06955741) BMS-986446 granted Fast Track designation by U.S. FDA as a treatment for Alzheimer’s disease PRX019, a potential treatment of neurodegenerative diseases in development in collaboration with Bristol Myers Squibb. Bristol Myers Squibb obtained the exclusive global license for PRX019 in 2024 Prothena is conducting a Phase 1 first-in-human clinical trial to evaluate the safety, tolerability, immunogenicity, and pharmacokinetics of single ascending and multiple doses in healthy adults with completion expected in 2026 Potential to earn a clinical milestone by end of 2026 should Bristol Myers Squibb decide to further develop PRX019 Updates on Active Preclinical Development Portfolio TDP-43 CYTOPE, a proprietary preclinical program enabling precision intracellular targeting of TDP-43 pathology, a defining pathogenic feature of ALS and other TDP-43 proteinopathies. TDP-43 CYTOPE preclinical data demonstrates the potential of Prothena’s CYTOPE technology to target intracellular disease pathways. Prothena presented a poster at Neuroscience 2025 (Society for Neuroscience) and the International Symposium of ALS/MND demonstrating the potential of TDP-43 CYTOPE in multiple preclinical models PRX012-TfR, a preclinical program combining PRX012, our wholly-owned, single-injection, once-monthly antibody delivered subcutaneously with transferrin receptor technology to potentially improve its product profile. Phase 1 ASCENT clinical program preliminary results demonstrated that patients on the 400 mg dose level of PRX012 for 18 months reached a mean centiloid (CL) level of ~16.0 CL and 9 of 12 achieved amyloid negativity (defined as <24.1 CL). However, the robust plaque clearance was associated with non-competitive rates of ARIA-E. Based on the totality of the results, Prothena is developing PRX012-TfR (transferrin receptor) in preclinical studies while exploring potential partnership opportunities Upcoming Investor Conference Members of the senior management team will present and participate in investor meetings at the following upcoming investor conference: The Citizens Life Sciences Conference on Wednesday, March 11, 2026; fireside chat at 10:10 a.m. ET in Miami, FL Fourth Quarter and Full Year of 2025 Financial Results For the fourth quarter and full year of 2025, Prothena reported net loss of $21.6 million and $244.1 million, respectively, as compared to a net loss of $58.0 million and $122.3 million for the fourth quarter and full year of 2024, respectively. The full year of 2025 net loss includes $30.1 million of restructuring charges associated with the discontinuation of the birtamimab program and the reduction in workforce announced in June 2025, and a $43.2 million net non-cash income tax expense to book a full valuation allowance against its federal deferred tax assets. Net loss per share was $0.40 and $4.53 for the fourth quarter and full year of 2025, respectively, as compared to a net loss per share of $1.08 and $2.27 for the fourth quarter and full year of 2024, respectively. Prothena reported total revenue of $21 thousand and $9.7 million for the fourth quarter and full year of 2025, respectively, as compared to total revenue of $2.1 million and $135.2 million for the fourth quarter and full year of 2024, respectively. Total revenue for the fourth quarter and full year of 2025 was primarily from collaboration revenue from Bristol Myers Squibb related to the partial performance of our PRX019 Phase 1 clinical trial obligation. Total revenue for the full year of 2024, was primarily from collaboration revenue from Bristol Myers Squibb including revenue recognized from the execution of the PRX019 Global License Agreement by Bristol Myers Squibb, which included an $80 million upfront payment in 2024. Research and development (R&D) expenses totaled $14.6 million and $134.9 million for the fourth quarter and full year of 2025, respectively, as compared to $50.2 million and $222.5 million for the fourth quarter and full year of 2024, respectively. The decrease in R&D expenses for the fourth quarter and full year of 2025 compared to the same periods in the prior year was primarily due to lower clinical trial expenses, lower personnel expenses, lower manufacturing and lower consulting expenses. R&D expenses included non-cash share-based compensation expense of $2.1 million and $14.1 million for the fourth quarter and full year of 2025, respectively, as compared to $4.7 million and $20.9 million for the fourth quarter and full year of 2024, respectively. General and administrative (G&A) expenses totaled $12.6 million and $59.4 million for the fourth quarter and full year of 2025, respectively, as compared to $16.8 million and $67.2 million for the fourth quarter and full year of 2024, respectively. The decrease in G&A expenses for the fourth quarter and full year of 2025 compared to the same periods in the prior year was primarily due to lower personnel expenses and lower consulting expenses. G&A expenses included non-cash share-based compensation expense of $5.0 million and $21.5 million for the fourth quarter and full year of 2025, respectively, as compared to $5.8 million and $25.0 million for the fourth quarter and full year of 2024, respectively. Total non-cash share-based compensation expense was $7.1 million for the fourth quarter of 2025 and $37.6 million for the full year of 2025 which included $2.1 million in non-cash share-based compensation expense related to restructuring charges, as compared to $10.5 million and $46.0 million for the fourth quarter and full year of 2024, respectively. As of December 31, 2025, Prothena had $308.4 million in cash, cash equivalents and restricted cash, and no debt. As of February 12, 2026, Prothena had approximately 53.8 million ordinary shares outstanding. 2026 Financial Guidance The Company expects its full year net cash used in operating and investing activities to be $50 to $55 million and to end the year with approximately $255 million (midpoint) in cash, cash equivalents, and restricted cash. The estimated full year 2026 net cash used from operating and investing activities is primarily driven by an estimated net loss of $67 to $72 million, which includes an estimated $24 million of non-cash share-based compensation expense. This financial guidance does not include the potential to earn up to $105 million of aggregate clinical milestone payments from strategic partners in 2026 related to the advancement of both coramitug for ATTR amyloidosis with cardiomyopathy by Novo Nordisk and PRX019 for neurodegenerative diseases by Bristol Myers Squibb. Share Redemption Program Prothena convened an Extraordinary General Meeting of shareholders on November 19, 2025 at which shareholders voted to approve a reduction in Prothena’s share capital to create distributable reserves, which was subsequently confirmed by the Irish High Court. The creation of distributable reserves provides flexibility for the Board of Directors to potentially return capital to shareholders via a share redemption program through open market purchases or other permissible means in 2026. Any such program would be subject to the discretion of the Board of Directors and Prothena’s then-current financial condition. Conference Call Details Prothena management will discuss these results and its 2026 financial guidance during a live audio conference call today, Thursday, February 19, 2026, at 4:30 PM ET. The conference call will be made available on the Company's website at www.prothena.com under the Investors tab in the Events and Presentations section. Following the live audio webcast, a replay will be available on the Company's website for at least 90 days. To access the call via dial-in, please dial +1 (800) 715-9871 (U.S. and Canada toll free) or +1 (646) 307-1963 (international) five minutes prior to the start time and refer to conference ID number 1706941. A replay of the call will be available until February 26, 2026, via dial-in at +1 (800) 770-2030 (U.S. and Canada toll free) or +1 (609) 800-9909 (international), Conference ID Number 1706941. About Prothena Prothena Corporation plc is a late-stage clinical biotechnology company with expertise in protein dysregulation with the potential to change the course of devastating neurodegenerative and rare peripheral amyloid diseases. Fueled by its deep scientific expertise built over decades of research, Prothena is advancing a pipeline of therapeutic candidates for a number of indications and novel targets for which its ability to integrate scientific insights around neurological dysfunction and the biology of misfolded proteins can be leveraged. Prothena’s pipeline includes both wholly-owned and partnered programs being developed for the potential treatment of diseases including Parkinson’s disease, ATTR amyloidosis with cardiomyopathy, Alzheimer’s disease, Amyotrophic lateral sclerosis (ALS) and a number of other neurodegenerative diseases. Prothena is developing and applying its proprietary CYTOPE® technology to target a broad spectrum of intracellular disease pathways in the brain and periphery. For more information, please visit the Company’s website at www.prothena.com and follow the Company on X (formerly Twitter) @ProthenaCorp. Forward-Looking Statements This press release contains forward-looking statements. These statements relate to, among other things, the sufficiency of our cash position to fund advancement of our pipeline and completion of our ongoing clinical trials; the continued advancement of our preclinical and clinical pipeline, including the potential and advancement of our CYTOPE technology and expected milestones in 2026, 2027, and beyond; the treatment potential, designs, proposed mechanisms of action, and potential administration of prasinezumab, coramitug, BMS-986446, PRX019, TDP-43 CYTOPE, and PRX012-TfR; plans for ongoing and future clinical trials of prasinezumab, coramitug, BMS-986446, and PRX019; the expected timing of reporting data from preclinical studies and clinical trials; projections regarding peak sales and patient population for prasinezumab; timing of and amounts we may receive under our collaborations with Novo Nordisk and Bristol Myers Squibb; our anticipated net cash burn from operating and investing activities for 2026 and expected cash balance at the end of 2026; our estimated net loss and non-cash share-based compensation expense for 2026; and the potential to return capital to shareholders via a share redemption program or other permissible means. These statements are based on estimates, projections and assumptions that may prove not to be accurate, and actual results could differ materially from those anticipated due to known and unknown risks, uncertainties and other factors, including but not limited to uncertainties related to the completion of operational and financial closing procedures, audit adjustments and other developments that may arise that would require adjustments to the preliminary financial results included in this press release, as well as those described in the “Risk Factors” sections of our Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission (SEC) on November 6, 2025, discussions of potential risks, uncertainties, and other important factors in our subsequent filings with the SEC, and our Annual Report on Form 10-K to be filed with the SEC for our fiscal year 2025. We undertake no obligation to update publicly any forward-looking statements contained in this press release as a result of new information, future events, or changes in our expectations. PROTHENA CORPORATION PLC CONDENSED CONSOLIDATED STATEMENTS OF OPERATIONS (unaudited - amounts in thousands except per share data) Three Months Ended December 31, Year Ended December 31, 2025 2024 2025 2024 Collaboration revenue $ 21 $ 2,123 $ 9,634 $ 135,107 Revenue from license and intellectual property — — 50 50 Total revenue 21 2,123 9,684 135,157 Operating expenses: Research and development 14,586 50,172 134,852 222,519 General and administrative 12,646 16,848 59,392 67,199 Restructuring costs (3,008 ) — 30,080 — Total operating expenses 24,224 67,020 224,324 289,718 Loss from operations (24,203 ) (64,897 ) (214,640 ) (154,561 ) Other income, net 2,624 5,396 13,811 25,631 Loss before income taxes (21,579 ) (59,501 ) (200,829 ) (128,930 ) Provision for (benefit from) income taxes 10 (1,545 ) 43,263 (6,620 ) Net loss $ (21,589 ) $ (57,956 ) $ (244,092 ) $ (122,310 ) Basic and diluted net loss per ordinary share $ (0.40 ) $ (1.08 ) $ (4.53 ) $ (2.27 ) Shares used to compute basic and diluted net loss per share 53,831 53,815 53,829 53,772 PROTHENA CORPORATION PLC CONDENSED CONSOLIDATED BALANCE SHEETS (unaudited - amounts in thousands) December 31, 2025 2024 Assets Cash and cash equivalents $ 307,531 $ 471,388 Prepaid expenses and other current assets 7,662 14,024 Total current assets 315,193 485,412 Property and equipment, net 2,144 3,081 Operating lease right-of-use assets 8,125 10,708 Restricted cash, non-current 860 860 Other non-current assets 482 47,047 Total non-current assets 11,611 61,696 Total assets $ 326,804 $ 547,108 Liabilities and Shareholders’ Equity Accrued research and development $ 4,329 $ 13,428 Deferred revenue, current 2,664 8,850 Restructuring liability 13,303 — Lease liability, current 2,886 2,610 Other current liabilities 17,661 23,613 Total current liabilities 40,843 48,501 Deferred revenue, non-current — 3,448 Lease liability, non-current 5,487 8,233 Total non-current liabilities 5,487 11,681 Total liabilities 46,330 60,182 Total shareholders’ equity 280,474 486,926 Total liabilities and shareholders’ equity $ 326,804 $ 547,108 Mark Johnson, CFA, Vice President, Investor Relations 650-837-8550 IR@prothena.com Media@prothena.com

Phase 1Clinical ResultPhase 3Phase 2Financial Statement

06 Nov 2025

·ir.prothena.com

Prothena Reports Third Quarter 2025 Financial Results and Business Highlights

Net cash used in operating and investing activities was $40.6 million and $140.4 million for the third quarter and first nine months of 2025, respectively; quarter-end cash and restricted cash position was $331.7 million Roche to initiate the Phase 3 PARAISO clinical trial evaluating prasinezumab, a potential first-in-class anti-alpha-synuclein antibody, for early-stage Parkinson's disease by end of 2025 Novo Nordisk initiated the Phase 3 CLEOPATTRA clinical trial evaluating coramitug, a potential first-in-class amyloid depleter, for ATTR amyloidosis with cardiomyopathy Novo Nordisk to present Phase 2 results for coramitug during a late-breaking session at the American Heart Association Scientific Sessions on November 10, 2025 Bristol Myers Squibb obtained Fast Track designation from the U.S. FDA for BMS-986446 (PRX005), an anti-MTBR-tau-targeting antibody, for the treatment of Alzheimer’s disease Prothena will convene an Extraordinary General Meeting on November 19, 2025 to obtain shareholder approval on a proposal reducing share capital to create distributable reserves to support a share redemption program to be conducted in 2026 if deemed appropriate Potential to earn up to $105 million in aggregate clinical milestone payments by end of 2026 related to the advancement of coramitug for ATTR amyloidosis with cardiomyopathy by Novo Nordisk and PRX019 for neurodegenerative diseases by Bristol Myers Squibb DUBLIN--(BUSINESS WIRE)-- Prothena Corporation plc (NASDAQ:PRTA), a late-stage clinical biotechnology company with a robust pipeline of investigational therapeutics built on protein dysregulation expertise, today reported financial results for the third quarter and first nine months of 2025 and provided business highlights. “We are pleased with the advancement of our late-stage partnered clinical programs. Novo Nordisk recently initiated the Phase 3 CLEOPATTRA clinical trial evaluating coramitug in ATTR-CM and Roche plans to initiate the Phase 3 PARAISO clinical trial evaluating prasinezumab in early-stage Parkinson’s disease by the end of 2025. Recently, Bristol Myers Squibb obtained Fast Track designation from the U.S. FDA for BMS-986446, an anti-MTBR-tau antibody, for the treatment of Alzheimer’s disease. BMS-986446 is currently in an ongoing Phase 2 trial with primary completion expected in the first half of 2027,” said Gene Kinney, Ph.D., President and Chief Executive Officer, Prothena. “We look forward to Novo Nordisk presenting Phase 2 coramitug results in a late-breaking presentation at the American Heart Association Scientific Sessions 2025. In addition, our Prothena scientists will be presenting a poster on our TDP-43 CYTOPE®, a therapeutic modality enabling cytosolic delivery of macromolecules, which demonstrated a reduction in intracellular TDP-43 pathology in a preclinical ALS mouse model at Neuroscience 2025 hosted by the Society of Neuroscience. We look forward to sharing more about CYTOPE and its potential applications in the future.” Third Quarter, Recent Business Highlights and Upcoming Milestones Updates on Active Clinical Development Portfolio Prasinezumab, a potential first-in-class antibody for the treatment of Parkinson’s disease that is designed to target a key epitope within the C-terminus of alpha-synuclein and is the focus of a worldwide collaboration with Roche. Partner Roche to initiate the Phase 3 PARAISO clinical trial evaluating prasinezumab for early-stage Parkinson's disease by the end of 2025 ( NCT07174310) Roche has stated that prasinezumab has peak sales potential greater than $3.5 billion (unadjusted) and could be the first disease-modifying treatment for a condition that affects 10 million people worldwide Coramitug (formerly PRX004), a potential first-in-class amyloid depleter antibody for the treatment of ATTR amyloidosis with cardiomyopathy (ATTR-CM) designed to deplete the pathogenic, non-native forms of the transthyretin (TTR) protein, is being developed by Novo Nordisk as part of its up to $1.2 billion acquisition of Prothena’s ATTR amyloidosis business and pipeline. Novo Nordisk initiated the Phase 3 CLEOPATTRA clinical trial evaluating coramitug for ATTR-CM ( NCT07207811) Novo Nordisk will present Phase 2 results during a late-breaking session at the American Heart Association Scientific Sessions on November 10, 2025 Expect to earn a clinical milestone when prespecified enrollment criteria are met in ongoing Phase 3 clinical trial by Novo Nordisk BMS-986446 (formerly PRX005), a potential best-in-class antibody for the treatment of Alzheimer’s disease that specifically targets a key epitope within the microtubule binding region (MTBR) of tau, a protein implicated in the causal pathophysiology of Alzheimer’s disease. Bristol Myers Squibb is conducting the Phase 2 TargetTau-1 clinical trial in approximately 310 patients with early Alzheimer’s disease; primary completion expected in 1H 2027 ( NCT06268886) Bristol Myers Squibb is also conducting a Phase 1 open-label single-dose clinical trial to assess a subcutaneous administration; primary completion expected in 2H 2025 ( NCT06955741) BMS-986446 granted Fast Track designation by U.S. FDA as a treatment for Alzheimer’s disease PRX019, a potential treatment of neurodegenerative diseases in development in collaboration with Bristol Myers Squibb. Bristol Myers Squibb obtained the exclusive global license for PRX019 in 2024 Prothena is conducting a Phase 1 first-in-human clinical trial to evaluate the safety, tolerability, immunogenicity, and pharmacokinetics of single ascending and multiple doses in healthy adults with completion expected in 2026 Potential to earn a clinical milestone by end of 2026 should Bristol Myers Squibb decide to further develop PRX019 Upcoming Scientific and Investor Conferences Novo Nordisk to present Phase 2 results for coramitug in a late-breaking session at the American Heart Association Scientific Sessions on November 10, 2025 in New Orleans, LA Title: Primary results from the phase 2 randomized, placebo controlled, blinded trial of the monoclonal antibody coramitug in transthyretin amyloid cardiomyopathy (ATTR-CM) Prothena poster presentation on a TDP-43 CYTOPE®, a proprietary modality enabling cytosolic delivery of macromolecules for precision targeting of intracellular disease targets, in an ALS mouse model at Neuroscience 2025 annual meeting organized by Society for Neuroscience (SfN) on November 19, 2025 in San Diego, CA Title: Treatment with a cell-internalizing antibody targeting pTDP43 reduces intraneuronal pathology in a mouse model of ALS Members of the senior management team will present and participate in investor meetings at the following upcoming investor conferences: Piper Sandler 37th Annual Healthcare Conference on Wednesday, December 3, 2025; fireside chat at 1:00 p.m. ET in New York, NY 8th Annual Evercore Healthcare Conference on Thursday, December 4, 2025; fireside chat at 10:50 a.m. ET in Miami, FL Third Quarter and First Nine Months of 2025 Financial Results For the third quarter and first nine months of 2025, Prothena reported net loss of $36.5 million and $222.5 million, respectively, as compared to a net loss of $59.0 million and $64.4 million for the third quarter and first nine months of 2024, respectively. The first nine months of 2025 includes $33.1 million of restructuring charges associated with the discontinuation of the birtamimab program and the reduction in workforce announced in June 2025, and a $43.2 million net non-cash income tax expense to book a full valuation allowance against its federal deferred tax assets. Net loss per share was $0.68 and $4.13 for the third quarter and first nine months of 2025, respectively, as compared to a net loss per share of $1.10 and $1.20 for the third quarter and first nine months of 2024, respectively. Prothena reported total revenue of $2.4 million and $9.7 million for the third quarter and first nine months of 2025, respectively, as compared to total revenue of $1.0 million and $133.0 million for the third quarter and first nine months of 2024, respectively. Total revenue for the third quarter and first nine months of 2025 was primarily from collaboration revenue from Bristol Myers Squibb related to the partial performance of our PRX019 Phase 1 clinical trial obligation. Total revenue for the first nine months of 2024, was primarily from collaboration revenue from Bristol Myers Squibb. Research and development (R&D) expenses totaled $28.9 million and $120.3 million for the third quarter and first nine months of 2025, respectively, as compared to $50.7 million and $172.3 million for the third quarter and first nine months of 2024, respectively. The decrease in R&D expenses for the third quarter and first nine months of 2025 compared to the same periods in the prior year was primarily due to lower clinical trial expenses, lower personnel expenses, lower manufacturing and lower consulting expenses. R&D expenses included non-cash share-based compensation expense of $2.5 million and $12.0 million for the third quarter and first nine months of 2025, respectively, as compared to $5.1 million and $16.2 million for the third quarter and first nine months of 2024, respectively. General and administrative (G&A) expenses totaled $13.2 million and $46.7 million for the third quarter and first nine months of 2025, respectively, as compared to $16.8 million and $50.4 million for the third quarter and first nine months of 2024, respectively. The decrease in G&A expenses for the third quarter and first nine months of 2025 compared to the same periods in the prior year was primarily due to lower personnel expenses. G&A expenses included non-cash share-based compensation expense of $4.7 million and $16.5 million for the third quarter and first nine months of 2025, respectively, as compared to $5.9 million and $19.2 million for the third quarter and first nine months of 2024, respectively. Total non-cash share-based compensation expense was $7.2 million for the third quarter of 2025 and $30.6 million for the first nine months of 2025 which included $2.1 million in non-cash share-based compensation expense related to restructuring charges, as compared to $11.0 million and $35.4 million for the third quarter and first nine months of 2024, respectively. As of September 30, 2025, Prothena had $331.7 million in cash, cash equivalents and restricted cash, and no debt. As of October 31, 2025, Prothena had approximately 53.8 million ordinary shares outstanding. 2025 Financial Guidance The Company continues to expect its full year net cash used in operating and investing activities to be $170 to $178 million and to end the year with approximately $298 million (midpoint) in cash, cash equivalents, and restricted cash. The estimated full year 2025 net cash used from operating and investing activities is primarily driven by an estimated net loss of $240 to $248 million, which includes an estimated $36 million of non-cash share-based compensation expense and a $44.9 million non-cash income tax expense to book a full valuation allowance against its federal deferred tax assets. Share Redemption Program Prothena will convene an Extraordinary General Meeting (“EGM”) of shareholders on November 19, 2025 to vote on a proposal to approve a reduction in Prothena’s share capital to create distributable reserves, subject to confirmation by the Irish High Court, to support a potential share redemption program. The Board of Directors is seeking shareholder approval of such a proposal to create flexibility to potentially return capital to shareholders via a share redemption program through open market purchases or other permissible means in 2026. Any such program would be subject to the discretion of the Board of Directors and Prothena’s then-current financial condition. About Prothena Prothena Corporation plc is a late-stage clinical biotechnology company with expertise in protein dysregulation and a pipeline of investigational therapeutics with the potential to change the course of devastating neurodegenerative and rare peripheral amyloid diseases. Fueled by its deep scientific expertise built over decades of research, Prothena is advancing a pipeline of therapeutic candidates for a number of indications and novel targets for which its ability to integrate scientific insights around neurological dysfunction and the biology of misfolded proteins can be leveraged. Prothena’s pipeline includes both wholly-owned and partnered programs being developed for the potential treatment of diseases including ATTR amyloidosis with cardiomyopathy, Alzheimer’s disease, Parkinson’s disease and a number of other neurodegenerative diseases. For more information, please visit the Company’s website at www.prothena.com and follow the Company on X (formerly Twitter) @ProthenaCorp. Forward-Looking Statements This press release contains forward-looking statements. These statements relate to, among other things, the sufficiency of our cash position to fund advancement of a broad pipeline and completion of our ongoing clinical trials; the continued advancement of our discovery, preclinical, and clinical pipeline, and expected milestones in 2025, 2026, 2027, and beyond; the treatment potential, designs, proposed mechanisms of action, and potential administration of prasinezumab, coramitug, BMS-986446, and PRX019; plans for ongoing and future clinical trials of prasinezumab, coramitug, BMS-986446, and PRX019; the expected timing of reporting data from pre-clinical studies and clinical trials, including data from Novo Nordisk’s Phase 2 clinical trial evaluating coramitug on November 10, 2025 and our TDP-43 CYTOPE® program on November 19, 2025; projections regarding peak sales and patient population for prasinezumab; timing of and amounts we may receive under our collaborations with Novo Nordisk and Bristol Myers Squibb; our anticipated net cash burn from operating and investing activities for 2025 and expected cash balance at the end of 2025; our estimated net loss and non-cash share-based compensation expense for 2025; and the potential and ability to return capital to shareholders via a share redemption program or other permissible means if shareholders approve a reduction in share capital to create distributable reserves. These statements are based on estimates, projections and assumptions that may prove not to be accurate, and actual results could differ materially from those anticipated due to known and unknown risks, uncertainties and other factors, including but not limited to uncertainties related to the completion of operational and financial closing procedures, audit adjustments and other developments that may arise that would require adjustments to the preliminary financial results included in this press release, as well as those described in the “Risk Factors” sections of our Quarterly Report on Form 10-Q to be filed with the Securities and Exchange Commission (SEC) on November 6, 2025, and discussions of potential risks, uncertainties, and other important factors in our subsequent filings with the SEC. We undertake no obligation to update publicly any forward-looking statements contained in this press release as a result of new information, future events, or changes in our expectations. PROTHENA CORPORATION PLC CONDENSED CONSOLIDATED STATEMENTS OF OPERATIONS (unaudited - amounts in thousands except per share data) Three Months Ended September 30, Nine Months Ended September 30, 2025 2024 2025 2024 Collaboration revenue $ 2,415 $ 970 $ 9,613 $ 132,984 Revenue from license and intellectual property — — 50 50 Total revenue 2,415 970 9,663 133,034 Operating expenses: Research and development 28,938 50,723 120,266 172,347 General and administrative 13,238 16,760 46,746 50,351 Restructuring costs 479 — 33,088 — Total operating expenses 42,655 67,483 200,100 222,698 Loss from operations (40,240 ) (66,513 ) (190,437 ) (89,664 ) Other income, net 3,328 6,677 11,187 20,235 Loss before income taxes (36,912 ) (59,836 ) (179,250 ) (69,429 ) Provision for (benefit from) income taxes (371 ) (835 ) 43,253 (5,075 ) Net loss $ (36,541 ) $ (59,001 ) $ (222,503 ) $ (64,354 ) Basic and diluted net loss per ordinary share $ (0.68 ) $ (1.10 ) $ (4.13 ) $ (1.20 ) Shares used to compute basic and diluted net loss per share 53,830 53,790 53,828 53,757 PROTHENA CORPORATION PLC CONDENSED CONSOLIDATED BALANCE SHEETS (unaudited - amounts in thousands) September 30, December 31, 2025 2024 Assets Cash and cash equivalents $ 330,843 $ 471,388 Prepaid expenses and other current assets 9,131 14,024 Total current assets 339,974 485,412 Property and equipment, net 2,463 3,081 Operating lease right-of-use assets 8,849 10,708 Restricted cash, non-current 860 860 Other non-current assets 482 47,047 Total non-current assets 12,654 61,696 Total assets $ 352,628 $ 547,108 Liabilities and Shareholders’ Equity Accrued research and development $ 9,544 $ 13,428 Deferred revenue, current 2,685 8,850 Restructuring liability 17,614 — Lease liability, current 2,879 2,610 Other current liabilities 18,714 23,613 Total current liabilities 51,436 48,501 Deferred revenue, non-current — 3,448 Lease liability, non-current 6,203 8,233 Total non-current liabilities 6,203 11,681 Total liabilities 57,639 60,182 Total shareholders’ equity 294,989 486,926 Total liabilities and shareholders’ equity $ 352,628 $ 547,108 Mark Johnson, CFA, Vice President, Investor Relations 650-837-8550 IR@prothena.com Media@prothena.com

Financial StatementPhase 2Phase 1Fast TrackAHA

04 Aug 2025

·ir.prothena.com

Prothena Reports Second Quarter 2025 Financial Results and Business Highlights

Net cash used in operating and investing activities was $46.4 million in the second quarter and net cash used in operating and investing activities was $99.8 million for the first six months of 2025; quarter-end cash and restricted cash position was $372.3 million Prothena expects to convene an Extraordinary General Meeting by year-end 2025 to propose that shareholders approve a reduction of share capital to create distributable reserves in order to support a potential share redemption program if deemed appropriate Roche to advance prasinezumab, a potential first-in-class anti-alpha-synuclein antibody targeting a known biological driver of Parkinson’s disease progression, into Phase 3 development for early-stage Parkinson's disease by end of 2025 Initial data from Phase 1 ASCENT clinical trials evaluating PRX012, a potential single-injection once-monthly subcutaneous treatment for millions of patients with presymptomatic or early symptomatic Alzheimer’s disease, expected in August 2025 Potential to earn up to $105 million in aggregate clinical milestone payments in 2026 related to the advancement of coramitug for ATTR amyloidosis with cardiomyopathy by Novo Nordisk and PRX019 for neurodegenerative diseases by Bristol Myers Squibb DUBLIN--(BUSINESS WIRE)-- Prothena Corporation plc (NASDAQ:PRTA), a late-stage clinical biotechnology company with a robust pipeline of investigational therapeutics built on protein dysregulation expertise, today reported financial results for the second quarter and first six months of 2025 and provided business highlights. “We are excited that our partner Roche is advancing prasinezumab into Phase 3 development in early-stage Parkinson’s disease with initiation expected by the end of 2025. Prasinezumab could be the first disease-modifying treatment for a condition that affects 10 million people worldwide. Later this month we plan to share initial data from the Phase 1 ASCENT clinical trials of our wholly-owned PRX012 program in Alzheimer’s disease,” said Gene Kinney, Ph.D., President and Chief Executive Officer, Prothena. “We are also looking forward to data from Novo Nordisk’s Phase 2 clinical trial evaluating coramitug for ATTR amyloidosis with cardiomyopathy expected in the second half of 2025. Bristol Myers Squibb is conducting a Phase 2 TargetTau-1 clinical trial evaluating BMS-986446 in Alzheimer’s disease with completion expected in 2027 and a Phase 1 clinical trial evaluating BMS-986446 in a potential subcutaneous formulation with completion expected in the second half of 2025. In addition, we are conducting a Phase 1 clinical trial for PRX019 in collaboration with Bristol Myers Squibb with expected completion in 2026. Finally, there is a potential for us to earn up to $105 million in aggregate clinical milestone payments if Novo Nordisk advances coramitug and Bristol Myers Squibb decides to advance PRX019.” Second Quarter, Recent Business Highlights and Upcoming Milestones Neurodegenerative Diseases Portfolio Parkinson’s Disease Prasinezumab, a potential first-in-class antibody for the treatment of Parkinson’s disease that is designed to target a key epitope within the C-terminus of alpha-synuclein and is the focus of a worldwide collaboration with Roche. Partner Roche to advance prasinezumab into Phase 3 development for early-stage Parkinson's disease with initiation expected by the end of 2025 Prasinezumab is being investigated in ongoing open label extensions (OLEs) of the Phase 2 PASADENA and Phase 2b PADOVA clinical trials; both clinical trials are being conducted by our partner Roche Roche has stated that prasinezumab has peak sales potential greater than $3 billion (unadjusted) and could be the first disease-modifying treatment for a condition that affects 10 million people worldwide Alzheimer’s Disease PRX012, a wholly-owned potential best-in-class, single-injection once-monthly antibody delivered subcutaneously for the treatment of presymptomatic or early symptomatic Alzheimer’s disease that targets a key epitope at the N-terminus of amyloid beta (Aβ) with high binding potency. The U.S. Food and Drug Administration (FDA) has granted Fast Track designation for PRX012 for the treatment of Alzheimer’s disease. Prothena expects initial data in August from the Phase 1 ASCENT clinical trials Following the data from the Phase 1 ASCENT clinical trials, Prothena expects to advance PRX012 through non-dilutive and capital efficient structures BMS-986446 (formerly PRX005), a potential best-in-class antibody for the treatment of Alzheimer’s disease that specifically targets a key epitope within the microtubule binding region (MTBR) of tau, a protein implicated in the causal pathophysiology of Alzheimer’s disease. Bristol Myers Squibb is conducting the Phase 2 TargetTau-1 clinical trial in approximately 310 patients with early Alzheimer’s disease; primary completion expected in 2027 ( NCT06268886) Bristol Myers Squibb is also conducting a Phase 1 open-label single-dose clinical trial to assess a subcutaneous administration; primary completion expected in 2H 2025 ( NCT06955741) Bristol Myers Squibb is responsible for all communication, development, manufacturing, and commercialization PRX123, a wholly-owned potential first-in-class dual Aβ/tau vaccine designed for the treatment and prevention of Alzheimer’s disease, is a dual-target vaccine targeting key epitopes within the N-terminus of Aβ and MTBR-tau designed to promote amyloid clearance and block the transmission of pathogenic tau. The FDA cleared the investigational new drug (IND) application and granted Fast Track designation for PRX123 for the treatment of Alzheimer’s disease. Prothena expects to advance PRX123 through non-dilutive and capital efficient structures Neurodegenerative Diseases PRX019, a potential treatment of neurodegenerative diseases in development in collaboration with Bristol Myers Squibb. Bristol Myers Squibb obtained the exclusive global license for PRX019 in 2024 Prothena is conducting a Phase 1 first-in-human clinical trial to evaluate the safety, tolerability, immunogenicity, and pharmacokinetics of single ascending and multiple doses in healthy adults with completion expected in 2026 Potential to earn a clinical milestone in 2026 should Bristol Myers Squibb decide to further develop PRX019 Rare Peripheral Amyloid Disease ATTR Amyloidosis Coramitug (formerly PRX004), a potential first-in-class amyloid depleter antibody for the treatment of ATTR amyloidosis with cardiomyopathy (ATTR-CM) designed to deplete the pathogenic, non-native forms of the transthyretin (TTR) protein, is being developed by Novo Nordisk as part of its up to $1.2 billion acquisition of Prothena’s ATTR amyloidosis business and pipeline. Phase 2 clinical trial in 105 patients has completed with results expected in 2H 2025 ( NCT05442047) Coramitug is being evaluated in an ongoing open label extension trial ( NCT06260709) for participants who completed the Phase 2 trial Potential to earn a clinical milestone in 2026 when prespecified enrollment criteria are met in a Phase 2b or Phase 3 clinical trial by Novo Nordisk Second Quarter and First Six Months of 2025 Financial Results For the second quarter and first six months of 2025, Prothena reported net loss of $125.8 million and $186.0 million, respectively, which includes restructuring charges of $32.6 million associated with the discontinuation of the birtamimab program and the reduction in workforce announced in June 2025, and a $44.9 million non-cash income tax expense to book a full valuation allowance against its federal deferred tax asset as compared to a net income of $66.9 million for the second quarter of 2024 and a net loss of $5.4 million for the first six months of 2024, respectively. Net loss per share was $2.34 and $3.45 for the second quarter and first six months of 2025 respectively, as compared to a net income per share on a diluted basis of $1.22 for the second quarter of 2024 and net loss per share of $0.10 the first six months of 2024. Prothena reported total revenue of $4.4 million and $7.2 million for the second quarter and first six months of 2025, respectively, as compared to total revenue of $132.0 million and $132.1 million for the second quarter and first six months of 2024. Total revenue for the second quarter and first six months of 2025 was primarily from collaboration revenue from Bristol Myers Squibb related to the partial performance of our PRX019 Phase 1 clinical trial obligation. Total revenue for the second quarter and first six months of 2024, was primarily from collaboration revenue from Bristol Myers Squibb. Research and development (R&D) expenses totaled $40.5 million and $91.3 million for the second quarter and first six months of 2025, respectively, as compared to $57.5 million and $121.6 million for the second quarter and first six months of 2024, respectively. The decrease in R&D expenses for the second quarter and first six months of 2025 compared to the same periods in the prior year was primarily due to lower clinical trial expenses, lower manufacturing and lower personnel expenses. R&D expenses included non-cash share-based compensation expense of $4.7 million and $9.5 million for the second quarter and first six months of 2025, respectively, as compared to $5.6 million and $11.1 million for the second quarter and first six months of 2024, respectively. General and administrative (G&A) expenses totaled $15.9 million and $33.5 million for the second quarter and first six months of 2025, respectively, as compared to $16.1 million and $33.6 million for the second quarter and first six months of 2024, respectively. G&A expenses included non-cash share-based compensation expense of $5.7 million and $11.8 million for the second quarter and first six months of 2025, respectively, as compared to $6.4 million and $13.3 million for the second quarter and first six months of 2024, respectively. Restructuring costs totaled $32.6 million for the second quarter and first six months of 2025, as compared to nil for the second quarter and first six months of 2024. Restructuring charges incurred for the second quarter and first six months of 2025 primarily consist of employee termination benefits in connection with the reduction in workforce announced in June 2025 and contract termination costs primarily associated with exit fees relating to third-party manufacturers that were contracted for commercial supplies of birtamimab. Employee termination benefits include severance costs, employee-related benefits, and non-cash share-based compensation expense related to the acceleration of stock options. Restructuring costs included non-cash share-based compensation expense of $2.1 million for the second quarter and first six months of 2025, as compared to nil for the second quarter and first six months of 2024. Total non-cash share-based compensation expense was $12.4 million and $23.4 million for the second quarter and first six months of 2025 respectively, as compared to $12.0 million and $24.4 million for the second quarter and first six months of 2024, respectively. As of June 30, 2025, Prothena had $372.3 million in cash, cash equivalents and restricted cash, and no debt. As of July 25, 2025, Prothena had approximately 53.8 million ordinary shares outstanding. 2025 Financial Guidance The Company continues to expect its full year net cash used in operating and investing activities to be $170 to $178 million and to end the year with approximately $298 million (midpoint) in cash, cash equivalents, and restricted cash. The estimated full year 2025 net cash used from operating and investing activities is primarily driven by an estimated net loss of $240 to $248 million, which includes an estimated $36 million of non-cash share-based compensation expense and a $44.9 million non-cash income tax expense to book a full valuation allowance against its federal deferred tax assets. Share Redemption Program Prothena expects to convene an Extraordinary General Meeting (“EGM”) of shareholders by year-end 2025 to vote on a proposal to approve a reduction in Prothena’s share capital to create distributable reserves, subject to confirmation by the Irish High Court, to support a potential share redemption program. The Board of Directors intends to seek shareholder approval of such a proposal to create flexibility to potentially return capital to shareholders via a share redemption program through open market purchases or other permissible means. Any such program would be subject to the discretion of the Board of Directors and Prothena’s then-current financial condition. About Prothena Prothena Corporation plc is a late-stage clinical biotechnology company with expertise in protein dysregulation and a pipeline of investigational therapeutics with the potential to change the course of devastating neurodegenerative and rare peripheral amyloid diseases. Fueled by its deep scientific expertise built over decades of research, Prothena is advancing a pipeline of therapeutic candidates for a number of indications and novel targets for which its ability to integrate scientific insights around neurological dysfunction and the biology of misfolded proteins can be leveraged. Prothena’s pipeline includes both wholly-owned and partnered programs being developed for the potential treatment of diseases including ATTR amyloidosis with cardiomyopathy, Alzheimer’s disease, Parkinson’s disease and a number of other neurodegenerative diseases. For more information, please visit the Company’s website at www.prothena.com and follow the Company on X (formerly Twitter) @ProthenaCorp. Forward-Looking Statements This press release contains forward-looking statements. These statements relate to, among other things, the sufficiency of our cash position to fund advancement of a broad pipeline and completion of our ongoing clinical trials; the continued advancement of our discovery, preclinical, and clinical pipeline, and expected milestones in 2025, 2026, 2027, and beyond; the treatment potential, designs, proposed mechanisms of action, and potential administration of PRX012, BMS-986446/PRX005, PRX123, prasinezumab, PRX019, and coramitug/PRX004; plans for ongoing and future clinical trials of PRX012, BMS-986446/PRX005, PRX123, prasinezumab, PRX019, and coramitug/PRX004, including Roche’s expected advancement of prasinezumab into Phase 3 development for early-stage Parkinson's disease with initiation expected by the end of 2025; the expected timing of reporting data from clinical trials, including initial data from our ongoing Phase 1 clinical trials evaluating PRX012 in August 2025; potential to advance our PRX012 and PRX123 programs through non-dilutive and capital efficient structures; timing of and amounts we may receive under our collaborations with Novo Nordisk and Bristol Myers Squibb; our anticipated net cash burn from operating and investing activities for 2025 and expected cash balance at the end of 2025; our expectation to convene an EGM by year-end 2025; the potential and ability to return capital to shareholders via a share redemption program or other permissible means if shareholders approve a reduction in share capital to create distributable reserves; and our estimated net loss and non-cash share-based compensation expense for 2025. These statements are based on estimates, projections and assumptions that may prove not to be accurate, and actual results could differ materially from those anticipated due to known and unknown risks, uncertainties and other factors, including but not limited to uncertainties related to the completion of operational and financial closing procedures, audit adjustments and other developments that may arise that would require adjustments to the preliminary financial results included in this press release, as well as those described in the “Risk Factors” sections of our Quarterly Report on Form 10-Q to be filed with the Securities and Exchange Commission (SEC) on August 4, 2025, and discussions of potential risks, uncertainties, and other important factors in our subsequent filings with the SEC. We undertake no obligation to update publicly any forward-looking statements contained in this press release as a result of new information, future events, or changes in our expectations. PROTHENA CORPORATION PLC CONDENSED CONSOLIDATED STATEMENTS OF OPERATIONS (unaudited - amounts in thousands except per share data) Three Months Ended June 30, Six Months Ended June 30, 2025 2024 2025 2024 Collaboration revenue 4,420 132,014 $ 7,198 $ 132,014 Revenue from license and intellectual property — — 50 50 Total revenue 4,420 132,014 7,248 132,064 Operating expenses: Research and development 40,517 57,510 91,328 121,624 General and administrative 15,910 16,127 33,508 33,591 Restructuring costs 32,609 — 32,609 — Total operating expenses 89,036 73,637 157,445 155,215 Income (loss) from operations (84,616 ) 58,377 (150,197 ) (23,151 ) Other income, net 3,651 6,470 7,859 13,558 Income (loss) before income taxes (80,965 ) 64,847 (142,338 ) (9,593 ) Provision for (benefit from) income taxes 44,802 (2,039 ) 43,624 (4,240 ) Net Income (loss) $ (125,767 ) $ 66,886 $ (185,962 ) $ (5,353 ) Basic net income (loss) per ordinary share $ (2.34 ) $ 1.24 $ (3.45 ) $ (0.10 ) Diluted net income (loss) per ordinary share $ (2.34 ) $ 1.22 $ (3.45 ) $ (0.10 ) Shares used to compute basic net income (loss) per share 53,827 53,767 53,827 53,740 Shares used to compute diluted net income (loss) per share 53,827 55,043 53,827 53,740 PROTHENA CORPORATION PLC CONDENSED CONSOLIDATED BALANCE SHEETS (unaudited - amounts in thousands) June 30, December 31, 2025 2024 Assets Cash and cash equivalents $ 371,435 $ 471,388 Prepaid expenses and other current assets 14,040 14,024 Total current assets 385,475 485,412 Property and equipment, net 2,690 3,081 Operating lease right-of-use assets 9,563 10,708 Restricted cash, non-current 860 860 Other non-current assets 478 47,047 Total non-current assets 13,591 61,696 Total assets $ 399,066 $ 547,108 Liabilities and Shareholders’ Equity Accrued research and development 10,929 13,428 Deferred revenue, current 5,100 8,850 Restructuring liability 30,330 — Lease liability, current 2,853 2,610 Other current liabilities 18,595 23,613 Total current liabilities 67,807 48,501 Deferred revenue, non-current — 3,448 Lease liability, non-current 6,928 8,233 Total non-current liabilities 6,928 11,681 Total liabilities 74,735 60,182 Total shareholders’ equity 324,331 486,926 Total liabilities and shareholders’ equity $ 399,066 $ 547,108 Mark Johnson, CFA, Vice President, Investor Relations 650-417-1974, mark.johnson@prothena.com

Phase 1Phase 2VaccineFinancial StatementLicense out/in

100 Deals associated with Prasinezumab

External Link

KEGG	Wiki	ATC	Drug Bank
D11420	-	-	DB14788

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Young onset Parkinson disease	Phase 3	United States	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	China	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	Australia	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	Austria	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	Brazil	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	Canada	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	Denmark	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	France	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	Germany	F. Hoffmann-La Roche Ltd.	15 Jan 2026
Young onset Parkinson disease	Phase 3	Italy	F. Hoffmann-La Roche Ltd.	15 Jan 2026

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04777331 (PADOVA, CTgov)	Phase 2	Parkinson Disease	586	placebo+prasinezumab (DBT Period: Placebo)	rpsnaaflgf(aqgaavaakg) = cxumwizofp tfrrijmkbi (cialuncyso, klpdapgdup - wppnltcerv) View more	-	02 Dec 2025
				Prasinezumab (DBT Period: Prasinezumab)	rpsnaaflgf(aqgaavaakg) = upullaiuks tfrrijmkbi (cialuncyso, sexigzhves - uldeueotlw) View more
NCT04777331 (PADOVA, MDS2025)	Phase 2	Parkinson Disease	589	Prasinezumab	wujqinogih(xbibnmqrvh): Difference in adjusted means = -2.18 (95.0% CI, -3.87 to -0.49), P-Value = 0.0117 View more	Positive	05 Oct 2025
				Placebo
NCT04777331 (PADOVA, Company_Website) Manual	Phase 2	Parkinson Disease	586	Prasinezumab	nfspubhrnt(pdpbtppzbf): HR = 0.84 (95% CI, 0.69 - 1.01), P-Value = 0.0657 Not Met	Negative	18 Dec 2024
				Placebo
NCT03100149 (PASADENA, AAN2023)	Phase 2	Parkinson Disease alpha-synuclein	316	Prasinezumab 1500 mg	txrdjxjenh(nvhbmteczr) = qxlzzdbays wlcnotqrno (ksiheagwfd ) View more	-	25 Apr 2023
				Placebo+Prasinezumab 1500 mg	txrdjxjenh(nvhbmteczr) = ivjqbzwrjo wlcnotqrno (ksiheagwfd ) View more
NCT03100149 (PASADENA, MDS2022)	Phase 2	Parkinson Disease α-synuclein	-	Prasinezumab 1500 mg	oliqqaztim(tmpvaraljq) = bqmjlyratr vqakemwexr (evprixonlz ) View more	-	15 Sep 2022
				Prasinezumab 4500 mg	oliqqaztim(tmpvaraljq) = duuyubvpcx vqakemwexr (evprixonlz ) View more
NCT03100149 (PASADENA, Pubmed \| N Engl J Med)	Phase 2	Parkinson Disease α-synuclein	316	Prasinezumab 1500 mg	orpuxagexp(mnnfqvkqha) = infusion reactions occurred in 19.0% and 34.0%, respectively stfrqyjlye (qazqfxxbhh ) View more	Negative	04 Aug 2022
				Prasinezumab 4500 mg
NCT03100149 (PASADENA, CTgov)	Phase 2	Parkinson Disease	316	Placebo (Part 1: Placebo)	kwcfmkurjb(xkmkxhybmw) = rlgadskawk rvynoegysm (cvfvpgddvp, 1.221) View more	-	08 Feb 2021
				RO7046015 (Part 1: RO7046015 Low Dose)	kwcfmkurjb(xkmkxhybmw) = osfexmoaie rvynoegysm (cvfvpgddvp, 1.225) View more
NCT03100149 (PASADENA, Pubmed \| Front Neurol)	Phase 2	Parkinson Disease	316	Prasinezumab 1,500 mg	pvzxgbagth(ukghpwmvlv) = mnoawokgpk kwprtagczz (roogkwbopx )	-	01 Jan 2021
				Prasinezumab 4,500 mg	pvzxgbagth(ukghpwmvlv) = admgutkrqb kwprtagczz (roogkwbopx )
NCT02157714 (Pubmed \| JAMA Neurol) Manual	Phase 1	Parkinson Disease	80	PRX002	kkbxiikmcu(djbnswqpvy) = viiggxhqej awqzvnzuem (ekacnjhvsv ) View more	Positive	01 Oct 2018
				Placebo	kkbxiikmcu(djbnswqpvy) = cvzvjrpslm awqzvnzuem (ekacnjhvsv )
EAN2017	Phase 1	Parkinson Disease alpha-synuclein	80	PRX002 0.3 mg/kg	rlvbibmsgg(wqhwslumdm) = TEAEs experienced by â¥5% of patients and >placebo were constipation ishqpyrdno (ifovlydaze ) View more	Positive	13 Jul 2017
				PRX002 1 mg/kg

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