Ladies and gentlemen, thank you for being here and welcome to the Prothena Fourth Quarter and Full Year 2020 Financial Results Conference Call. All participants are currently in a listen-only mode. There will be a question-and-answer session following the speakers' presentation. I will now turn the call over to Ellen Rose, Head of Communications. Please, proceed.

Thank you, Michelle. And good morning, everyone, and welcome to Prothena's Investor conference call to review our business progress and our fourth quarter and full-year 2020 financial results and our 2021 financial guidance. Please, review the press release we issued earlier today, which is available on our website at prothena.com and is also attached to a Form 8-K filed today with the SEC. On today's call, Dr. Gene Kinney, our President and Chief Executive Officer will highlight Prothena's recent and 2020 pipeline progress, what distinguishes our scientific platform and our path for sustainable growth. Following Gene's comments, Tran Nguyen, our Chief Operating Officer and Chief Financial Officer will review our financial results and performance for the fourth quarter and full-year of 2020 and 2021 financial guidance. Gene will then provide an overview of our near-term milestones. We will then open the call for Q&A and be joined by Dr. Wagner Zago, our Chief Scientific Officer, and Dr. Radhika Tripuraneni, our Chief Development Officer. Before we begin, I would like to remind you that during the course of today's presentation, we will be making forward-looking statements that are subject to certain risks, uncertainties, and other factors that could cause actual results to differ materially from those referred to in any forward-looking statements. For a discussion of the risks and uncertainties associated with our forward-looking statements, please see our press release issued today, as well as our most recent filings with the SEC. We disclaim any obligation to update our forward-looking statements. And with that, I'd like to turn the call over to Gene.

Thank you, Ellen. And thank you all for joining us this morning to review our 2020 financial results. It's been an exciting and transformational year for Prothena. As Tran will highlight shortly, we met our 2020 financial guidance and ended the year with a strong cash position. When combined with up to $140 million in potential payments stemming from our collaborations with Roche and Bristol-Myers Squibb, this enables us to fund our pipeline through key upcoming milestones. Over the past year, we've made significant progress advancing new medicines with the potential to change treatment paradigms in multiple indications. In our rare peripheral amyloid disease portfolio, we recently announced plans to initiate the Phase III AFFIRM AL Study of Birtamimab in Mayo Stage IV Patients with AL amyloidosis under a Special Protocol Assessment or SPA Agreement with the FDA, at the unprecedented p-value of 0.10. The significant survival benefit observed in our VITAL study made this agreement possible and we expect to initiate the AFFIRM-AL study by mid-2021. We also announced results from our Phase 1 study of PRX004, including improvements in neuropathy and cardiac function in patients with ATTR amyloidosis. We expect to advance this program into a Phase 2, 3 study in the fourth quarter of this year. In our neurodegenerative disease pipeline, we advanced two programs in our Alzheimer’s Disease portfolio: PRX005, an anti-tau antibody being developed under our Global Neuroscience collaboration with Bristol-Myers Squibb, and PRX012, our proprietary next-generation subcutaneous anti-beta antibody. We continue to expect that the Biogen molecule aducanumab will be approved later this year and we are developing PRX012 to offer a next-generation treatment to enhance patient compliance and access. Last year, we also announced results from part one of the Phase 2 PASADENA study of prasinezumab in patients with early Parkinson's disease. Prasinezumab specifically targets the seed terminus of alpha-synuclein and is the first anti-alpha-synuclein antibody to demonstrate significant slowing of motor progression and improvements on imaging biomarkers consistent with disease modification. Based on these results, we announced that with our partners at Roche, we are advancing prasinezumab into a late-stage Phase 2 study with further details expected in the second quarter. As someone who has devoted the better part of my career to advancing medicines for progressive neurodegenerative diseases, I was particularly encouraged by the consistent signals of efficacy observed in this proof of concept study. This is an exciting time for our company. I'd like to start by highlighting what differentiates Prothena's proven approach that positions us as a leader in developing therapies for diseases caused by protein dysregulation and how we are well-positioned for an extraordinarily productive future. Our unique approach starts with science, specifically our deep understanding of how protein dysregulation contributes to the cause and progression of devastating rare peripheral amyloid and neurodegenerative diseases. This stems from our decades of foundational work in protein biology and understanding the dynamic aspects of protein dysregulation, which subsequently informs our selection of targets. We apply our proven protein dysregulation platform to specifically target the pathogenic forms of the proteins that cause disease. We can simplify this process into the saying, 'epitope matters,' and it certainly starts with selecting the right epitopes to target on a pathogenic protein. Beyond identifying the optimal epitope, we also engineer our molecules to interact with that epitope in a way that is most likely to intercept or halt the underlying disease process. We achieve this by designing molecules with a bias toward pathogenic forms of the protein, specifically or selectively targeting the toxic protein species to alleviate their detrimental effects while leaving the native or healthy form of the protein unaffected in order to maintain normal healthy biological function. This unbiased and empirical methodology is highly customized for each target. In some cases, we may target a cryptic epitope. In others, we may select antibodies with hyperactivity, and yet in other cases, we may select a neoepitope. This customized approach depends on the unique characteristics of each target and underlying disease pathology. After a thorough evaluation of the target with advanced discovery candidates, we have demonstrated consistent and robust biological outcomes in preclinical development. But an optimized molecule is only useful if you can influence biology in a way that results in meaningful clinical benefit for patients. We've now achieved this across multiple programs in our pipeline. Our ability to consistently translate our science into clinical proof of concept is an important distinguishing feature of Prothena today. Key to this consistency is knowing how to design a comprehensive clinical program that tests the biological hypothesis in the right patient populations with the right outcome measures. Our growing pipeline includes therapies with blockbuster potential for diseases with enormous unmet medical need that lack disease-modifying approaches. And importantly, we enjoy a strong capital position that provides the foundation to fund our growing pipeline. Our rare peripheral amyloid portfolio includes birtamimab for AL amyloidosis and PRX004 for ATTR amyloidosis. These molecules have differentiated mechanisms of action from the standard of care therapies that have not demonstrated an improved survival benefit for patients with advanced cardiac disease at high risk for early mortality due to amyloid deposition. The depleter mechanism of Birtamimab and PRX004 directly target and clear the toxic amyloid that deposits in the heart and other vital organs. Earlier this month, we announced our plan to initiate a confirmatory Phase III AFFIRM AL Study of Birtamimab in AL amyloidosis. AFFIRM AL is being conducted under SPA Agreement with the FDA to enable registration at an unprecedented p-value of less than or equal to 0.10 on the primary endpoint of all-cause mortality in Mayo Stage IV patients. We reached agreement with the FDA on this part due to the significant survival benefit observed in our previous VITAL study, where we demonstrated a 59% relative risk reduction in all-cause mortality in Mayo Stage IV patients over nine months. In December, we reported results from our Phase 1 study of PRX004 in ATTR amyloidosis. In this study, after only nine months of treatment with PRX004 in eligible patients, we observed less progression on neuropathy than expected, and in several patients, we observed improvement. We also noted improvement in global longitudinal strain, a key measure of cardiac systolic function in all eligible patients. Turning to the neurodegenerative disease programs in our Alzheimer's disease portfolio, we believe that interventions targeting both tau and Abeta have the potential to reduce clinical decline or prevent the onset of Alzheimer's disease. As such, our pipeline is advancing programs for both antibodies and vaccines. Our two most advanced preclinical programs are the anti-tau antibody PRX005 and the anti-Abeta antibody PRX012. We look forward to sharing preclinical data on PRX005 at an oral presentation at ADPD in March. We've tested a large number of antibodies to epitopes along the tau protein and found that those that target the microtubule binding region effectively block the binding of tau neuron and prevent downstream neurotoxic effects. Understanding this biology increases our confidence in selecting and evaluating PRX005 as a clinical candidate. We look forward to sharing our preclinical data at ADPD. Last year at CTAD, we presented data on PRX012, our next-generation high-potency anti-Abeta antibody. PRX012 has a higher binding strength to amyloid than aducanumab with as much as an 11-fold greater affinity and also recognizes Abeta Pathology to a greater extent demonstrating more extensive plaque area binding at lower antibody concentrations. We are developing PRX012 for subcutaneous administration to improve access to this class of treatment for patients with Alzheimer's disease. I'll conclude by highlighting the results from the Phase 2 Pasadena study of prasinezumab in patients with early Parkinson's disease that we announced last September. In Parkinson's, existing treatments are symptomatic and only address a subset of symptoms. There are currently no treatments available that target the underlying cause of the disease to slow its progression. Prasinezumab is designed to block the cell-to-cell transmission of the aggregated pathogenic forms of alpha-synuclein that are the hallmark of Parkinson's disease, thereby slowing clinical decline. In Pasadena, treatment with prasinezumab resulted in a significantly reduced decline in motor function of 35% versus placebo at one year and delayed time to clinically meaningful worsening of motor progression. This 35% reduction in clinical decline over just 12 months is particularly noteworthy relative to Alzheimer's disease. For aducanumab, we demonstrated reduced cognitive decline of approximately 22% over 18 months. In Pasadena, we also observed improvements on imaging biomarkers and signals of efficacy consistent with disease modification across multiple prespecified secondary endpoints. Our programs address diseases where there are no approved disease-modifying treatments. Each of these programs has the potential to become blockbuster therapies in areas of extraordinarily high unmet need. Our rare peripheral amyloid disease portfolio addresses two orphan disease market opportunities. We are developing Birtamimab and PRX004 in targeted patient populations at high risk for early mortality with a particularly urgent unmet medical need for improved survival. Since the occurrence of many neurological disorders, including both Parkinson's and Alzheimer's disease, increases with advancing age and the worldwide population is aging at a rate never before observed, the magnitude and impact of the pending healthcare crisis in the absence of better therapies is both predictable and alarming. As we've discussed, our proven protein dysregulation platform is our engine for sustainable growth. This year, we expect three programs to initiate late-stage clinical studies: Birtamimab and AL amyloidosis, prasinezumab in Parkinson's disease, and PRX004 in ATTR amyloidosis. Beyond these programs, we expect internal R&D to deliver as many as six INDs for new molecules over the next three years. A combination of potential payments resulting from our collaborations with Roche and Bristol-Myers Squibb, as well as our existing robust cash position, gives us the ability to fund our programs through key milestones. We expect our growing pipeline with programs at every stage of development to facilitate our transition to a fully integrated research, development, and commercial biotechnology company.

Thanks, Gene. Today, we reported results that were in line with our 2020 financial guidance. Net cash used in operating and investing activities was $81 million, compared to our guidance of $75 million to $85 million. Net loss was $111 million, compared to our guidance of $101 million to $118 million. As of December 31, 2020, Prothena had $298 million in cash, cash equivalents, and restricted cash, compared to our guidance of $294 million to $304 million. Also, we continue to have no debt. Please refer to the press release issued today for further details regarding our fourth quarter and year-end 2020 financial results. Turning to our 2021 financial guidance, we expect our full-year 2021 net cash used in operating and investing activities to be $51 million to $74 million, which includes an expected $60 million milestone payment from Roche upon the first patient dosed in the previously announced late-stage Phase II-b study of prasinezumab. We expect to end the year with approximately $235 million in cash, which represents the midpoint of the range. The estimated full-year 2021 net cash used in operating and investing activities is primarily driven by an estimated net loss of $79 million to $111 million, which includes an estimated $20 million of non-cash share-based compensation expense. With that, I will turn the call back over to Gene to summarize our upcoming milestones.

Thanks, Tran. Before we talk about our near-term milestones, I want to first acknowledge and thank our extraordinarily talented employees for their ongoing commitment to advancing our science to help patients. We continue to operate in challenging times and I could not be more proud to work alongside my colleagues at Prothena. I'd also like to thank the patients, their families, clinicians, and study site staff who participate in our studies. Without their support, we could not elucidate the potential value of the new medicines we are developing. Over the past year, our team has delivered multiple clinical milestones, further positioning Prothena as a leader in protein dysregulation. We look forward to communicating multiple R&D milestones over the next 12 to 18 months. Our AFFIRM AL study for Birtamimab, our most advanced program, is expected to initiate in mid-2021. We also expect to report the nine-month study results from the previous VITAL study at a future medical conference. We anticipate that Roche will initiate the late-stage Phase IIb study of prasinezumab in patients with early Parkinson's disease in the second quarter of this year. Prothena will earn a $60 million clinical milestone payment upon the first patient dosed in this study. At the upcoming ADPD conference, new prespecified exploratory subgroup analysis from Part 1 of the Phase 2 Pasadena study of prasinezumab will be highlighted in an oral presentation. We further expect Roche to present results from part 2 of the Pasadena study at a future medical conference. For PRX004, we expect to initiate the Phase II-III study in patients with ATTR cardiomyopathy in the fourth quarter of this year and also plan to present results from our Phase 1 study at a future medical conference. Our portfolio of Alzheimer's disease programs has also advanced. Building on our foundational science and the discovery and development of anti-Abeta antibodies and vaccines, we continue to be highly active in this space with four programs in Alzheimer's disease, including antibody, vaccine, and small molecule approaches. One of these programs, PRX005, is under our Global Neuroscience collaboration with Bristol-Myers Squibb. We expect to file an IND for PRX005 in the third quarter of 2021, triggering a possible U.S. Option Payment of $80 million. Preclinical data for this anti-tau antibody will be presented in an oral presentation at ADPD in March. Finally, we expect to file an IND in the first quarter of 2022 for our anti-Abeta antibody PRX012. So, we are excited about the year ahead. Our team has the capabilities to drive transformational innovation for some of the most devastating diseases affecting society today, and we look forward to providing updates on our programs as they progress. So, at this time, we'll open the call for questions. Michelle?

Our first question comes from Jay Olson with Oppenheimer. Your line is open. Please go ahead.

Hey, congrats on all the progress, and thank you for the clear explanation of your strategy and vision for Prothena. The importance of the epitope is really appreciated and since you mentioned the differences between prasinezumab and cinpanemab. Are there other differences between those two molecules besides the epitope and also any feedback on Pasadena part one that you've gotten from the medical community? And then I had a follow-up question, if I could.

Yes, thanks for the questions, Jay. So, very important question. Obviously, we're highlighting in today's discussion is the clear distinction in targeting these proteins at different parts leading to very different biological outcomes. We spend a lot of time in the preclinical space really exploring these proteins to understand the optimal way of targeting, not only where to target them but also considering post-translational modified forms of the protein or phosphorylated forms, for example, versus different misfolded conformations that we want to think about. Ultimately, we adopt an approach that biases our molecule to spare the normal form and function of the protein while specifically going after the more pathological forms. In the case of prasinezumab, that was achieved by using a technique where we carefully examined an antibody that preferred the aggregated forms of the protein over the non-aggregated forms and using very specific genetic and quantitative analysis, we have been able to show that selectivity or preference is over 400-fold. We think that's a key component as well.

It's a little challenging to make a direct comparison between cinpanemab and prasinezumab other than the epitope. But simply because the data around cinpanemab is published later, it is really hard for us to make those comparisons. What we can say is that we spent many years screening the entire synuclein protein and found a consistency for antibodies targeting the C terminal portion of alpha-synuclein, a pathway for prasinezumab. There is consistency in terms of efficacy for those antibodies. The other antibodies that target the N terminal portion did not show that consistency. We consider targeting the N terminal suboptimal regarding efficacy when we did see any. We therefore focused on the C terminal portion.

Thank you. That's super helpful. And then as far and since you have two super high-quality partnerships and now a growing number of wholly-owned assets in the clinic or about to enter the clinic, would you consider partnering Birtamimab or any of the other wholly-owned assets?

Yes, so our plans with Birtamimab are to pursue a commercialization approach with that. Particularly, in the major markets, we are addressing what we believe is the major unmet medical need in that space, which is to improve survival for patients at high risk of early mortality due to amyloid deposition in the heart. So, that would be our current plan, but maybe I'll just ask Tran if you want to speak to that further.

No, I think based on our past experience, we do believe that there is interest fully from strategically partnering Birtamimab given its concentrated hematology call point, and as Gene just said, based on our market research, we are planning to commercialize Birtamimab. Approximately 75% of Mayo Stage IV patients are treated at about 500 amyloidosis centers of excellence and specialty centers across the U.S and Europe, which makes for a very efficient hematology sales force footprint. Given the known diagnosed prevalence in regions such as Japan and China, we may explore some regional partnerships.

Great, thanks for taking the questions.

Hi guys, good morning. Congrats on all the progress. And thanks for this nice pipeline update. I had two quick questions. They both relate to early-stage compounds, one is on the Bristol Celgene collaboration. You talked about how you expect a potential milestone there. Maybe just talk about how that dialogue and ongoing conversations have been with that on that program, the progress, and how confident you are that that milestone will come? Also, just talk a little bit about that target program and conversation. And then the second question is obviously there's a lot more industry interest in Abeta, of course, and we're awaiting a big decision by the FDA. You made some nice comments about your epitope. Can you clarify, is your compound actually more similar to donanemab rather than aducanumab? And maybe just talk about your epitope a little bit more and the comparison between those programs? Thanks.

Yes, great questions, Mike. Let's start by going backward here. First, regarding Abeta; the PRX012 molecule targets the amino terminus of Abeta. Our own research has indicated that targeting this region provides the optimal ability to interact with both deposited forms that are visible on PET imaging and the aggregated soluble forms, which some believe contribute to the disease. Essentially, you want to eradicate both species, which is accomplished by targeting the immuno terminus of the protein. As with aducanumab, which targets that same region, Birtamimab also specifically looks for a post-translationally modified version of the immuno terminus, critically to target aggregated forms. We think there's consistency here in terms of our observations. It's crucial to also consider elements of clinical design, and choosing the right patients along with the appropriate clinical assessment scales, which is equally important to demonstrating clinical efficacy in our perspective. Next, the dialogue with Bristol-Myers Squibb is strong. We value our collaboration and its added value to the program. Of course, the milestone is contingent on their decision to exercise their option at the right time, which connects with our IND filing.

More importantly, to your point, Bert, the delivery of the IND when we file that will be documented to them as well. There are other documents we send to them in a timely manner. They have a certain timeframe to make their decision on exercising their U.S. rights. We believe we are on track to deliver all necessary documents for them to make their decision. In terms of your question around the players involved, as you know, Bristol had a CNS group back in the day, and they don't anymore. However, when they acquired Celgene, the CNS team came from Celgene. The individuals who did the deal with us are primarily still at Bristol, and key relationships still exist. We have daily to weekly conversations with them, and we continue to plan and collaborate towards the IND and launching our first in-human study.

Good morning, Gene and Tran. Thank you for taking the question, and I appreciate the platform information provided. I have a couple of questions on the platform. But first, about the near-term clinicals, I guess I'm wondering generally about the rate-limiting steps for both AFFIRM and the Phase IIb of Prasinezumab. I'd like to hear more about the operationalization for AFFIRM AL and when you would anticipate that. Additionally, any further information on its size and periodic updates on Prasinezumab beyond just the initial dosing of the first patient.

Let's start with the AFFIRM AL, and maybe Radhika, you can speak to the operational aspects en route to opening that study?

Sure, Gene. It's an exciting time for Prothena as we embark on getting the AFFIRM AL study up and running. Our history in this space and our relationship makes us quite optimistic as we get this study initiated ultimately in mid-2021. The standard activities involved in engaging for the Phase III study regarding site contracts are the main dynamics we are working through. We've got considerable data on Birtamimab that gives us a robust foundational base to communicate to the clinical community, and there's significant excitement to see this study get underway.

You also asked about the size of the study. We anticipate enrolling up to 150 patients total with a two-to-one randomization. As Radhika said, we're excited to see this get rolling. On the Prasinezumab side, we expect Roche to get the Phase IIb study up and running, and we anticipate that at AD, PD, additional analyses of the Pasadena part one study will be discussed based on pre-specified subgroup results.

That’s helpful. Thank you. I have a couple of platform questions, but just one more that I'm thinking about concerning AFFIRM. You mentioned the all-cause mortality in the p-value below 0.10 being unprecedented. How can you provide more insight into your discussions with the agency regarding that p-value?

When we looked at our VITAL study data, we noted what we believed to be a robust survival benefit for Mayo Stage IV patients, translating to a hazard ratio that showcases a 59% relative risk reduction in all-cause mortality, which is meaningful. Each of those events is real and profound, involving individuals, families, and friends. We engaged with external statisticians to review the data thoroughly and sought collaboration with regulators to find a path forward in this population, which resulted in a productive relationship with the FDA. It involved multiple meetings and was centered around understanding the strength of the VITAL data and what would be required for registration. We're pleased that we found common ground with the agency in the form of a special protocol assessment. This underlies what the AFFIRM AL study is—a study that we anticipate will enroll up to 150 patients with an all-cause mortality at a p-value of 0.10, which will enable a registration path combined with our other datasets.

Maybe I'll add, Charles. If we hadn't seen that substantial survival benefit in these patients at high risk, we would not have secured the unprecedented p-value of 0.1. We believe our competitors that lack double-blind placebo-controlled trial data wouldn't have a similar outcome with the FDA, and we're quite eager to initiate AFFIRM AL later this year as has been shared in mid-2021.

We're looking forward to that initiation and believe this setup may drive enrollments more than anticipated. I have one platform question regarding PRX004, 12, and further ramifications relating to your profile relative to aducanumab and Birtamimab. Beyond what you've mentioned regarding molecule design, what do you think the implications are for CNS penetration?

Given the complexities involved, I'll invite Wagner to elaborate on this further.

So, let's discuss the mechanisms behind ARIA. The contributors to these vascular observations stem from two mechanisms: one being the removal of Abeta from vessels and the second involves the mobilization of Abeta from plaques to perivascular spaces during the antibody clearance process. This mobilization can alter vascular permeability. The incidence of ARIA, especially symptomatic cases, is tied to the Cmax, or maximum concentration of the antibody reached in the brain. By utilizing a subcutaneous delivery method for our program, we anticipate a reduced Cmax while still maintaining a substantial AUC over the course. This could enable not only heightened efficacy but potentially lower instances of ARIA compared to other antibodies. It's essential to note, however, that ARIA would indicate effective clearance of pathogenic Abeta forms from the brain.

When considering blood-brain barrier technologies, our comprehensive understanding—specifically addressing Cmax versus AUC—becomes vital. It's crucial to ensure we do not transiently increase brain concentrations, as this may compromise total exposure. We've structured our approach, particularly with PRX012, to distinguish the aggregated forms of the protein more readily found in the brain, thereby offering our antibodies better access over time to that compartment.

Our next question comes from the line of Bert Hazlett with BTIG. Your line is open. Please go ahead.

Thank you for taking the question. Great discussion this morning. I just have a couple of detailed ones on the tau program regarding Bristol. Could you share expectations for the data for the upcoming program at AD/PD? I would appreciate follow-ups for the Bristol collaboration more generally.

There will be a strong round of preclinical data shared that guided us to target the anti-TBR (tau) portion of tau, demonstrating its impact on blocks and neurotoxic effects downstream from that point. We will continue to release data as we progress, with this first round being a significant milestone.

That’s helpful to frame it. Thank you. Could you remind us of the deliverables to gain the $80 million and $55 million? Also, could you provide color on the lingering presence of individuals who were at Celgene during these discussions at Bristol-Myers?

Upon filing the IND and delivering necessary documents, they will have a timeframe to exercise their option, connecting both the milestone amounts. As for team members, Bristol had a CNS group from Celgene, which still exists in their structure. This includes key relationships from Celgene that we fostered, deepening connections as we collaborate towards the IND.

Hi, thanks for taking the question. A question on Birtamimab development regarding AL amyloidosis in that market moving forward. Given the huge unmet need in Mayo Stage IV patients, what role do you see for Darzalex in treating those patients? Additionally, anything else in development that might benefit them?

Maybe Radhika can speak to this.

It's great to see any therapy that's approved to help these patients. However, I think there's a lack of meaningful survival data from Darzalex that will limit its effectiveness. While it addresses the hematological aspect of care, the ultimate goal is to enhance survival. I believe Birtamimab's role will be pivotal for Mayo Stage IV patients needing effective amyloidosis treatment.

We gained substantial insights from our own data and Darzalex data, learning that advanced Mayo patients require an antibody to deplete toxic tissue forms. The Dara data showcased strong hematological and organ responses, but didn't translate to improved survival outcomes. Our VITAL study showed Birtamimab's 59% relative risk reduction in mortality in Mayo Stage IV patients highlights its necessity in this setting.

Hi guys, good morning. Thanks for taking my question. As companies report, we've been getting guidance on sales and trial enrollment impacted by COVID. Given that AL amyloidosis involves serious patients, how do you view the pandemic's potential influence on this? What impact may vaccination rates have on your internal view of enrollment speed?

Thanks for the question. Radhika, could you provide insight on how we've approached this?

Patients with AL amyloidosis, particularly Mayo Stage IV patients, face extreme risks that make treatment an urgency. Thus, their participation in clinical studies is a priority. Additionally, many clinical institutions have optimized protocols for managing the pandemic after significant experience managing health risks. Overall, we believe these factors align in favor of continued study participation.

Thank you. I would like to turn the conference back over to Gene Kinney for any further remarks.

Great, thank you, Michelle, and thank you all for joining us. We appreciate your interest in Prothena, and over the coming months, we look forward to sharing further updates on our programs. Thank you.

Ladies and gentlemen, thank you for participating in today's conference. This does conclude the program, and you may all disconnect. Everyone, have a great day.