Warm welcome to Herantis Pharma's webcast where we'll present HER-096 phase I-B clinical trial's top-line data. We will present the data, and this presentation is followed by a Q&A session. During the webcast, please, you can enter your questions in the dashboard. Let's start. My name is Antti Vuolanto. I'm the CEO of Herantis, and together with me in the studio, we have our CSO, Henri Huttunen, and CFO, Tone Kvåle. Before going into the actual presentation, just a reminder of forward-looking statements as a necessity, and then we can actually start the actual webcast content. Just a reminder, Herantis Pharma, we are a clinical stage public company residing here in Helsinki, and we are developing HER-096 as our lead asset. That is a potentially game-changing therapy that can become the first disease-modifying and neurorestorative treatment for Parkinson's disease. Short recap about the background. HER-096 is a mimic of a protein called Cerebral Dopamine Neurotrophic Factor, CDNF. Previously, we have studied CDNF in preclinical and clinical studies with very promising results, and the challenge with CDNF protein was the route of administration. With HER-096, we have exactly the same mechanism of action, same activity, but we can use simple, patient-friendly subcutaneous administration. Now we are in the webcast for presenting the phase I-B top-line data. Very happy to announce that we have met, or the trial has met, the primary and secondary endpoints for safety and tolerability. These data, of course, strongly support advancing HER-096 into phase II proof-of-concept clinical trials. We expect further data by releasing the full dataset, including the biomarker data, before the end of 2025. Also reminding that there is a high unmet clinical need in Parkinson's disease. The current treatments can treat the symptoms, but currently nothing can prevent the progression of the disease. This is exactly what we want to do, to stop the progression of the disease at the early stage of the disease. We want to also be a strong player in the rapidly growing market for pharmaceuticals for Parkinson's disease. That is a high-level introduction of the company. Just want to remind you also about the phase I objectives. Clinical development or drug development is divided in non-clinical development and clinical development. We have received very compelling data with preclinical studies showing the proof of concept of HER-096 described earlier. We have previously conducted a phase I-A clinical study to demonstrate the safety and pharmacokinetics in healthy volunteers. Now we are pleased to announce the great data with phase I-B study where we have established safety in Parkinson's patients, pharmacokinetics in Parkinson's patients, and also establishing dosing for phase II. Let us continue with the actual presentation of the data by our CSO, Henri Huttunen. Please. Thank you, Antti. Let's begin by the study design. The study was divided into two parts. There was a brief part one where we studied elderly, healthy volunteers who received a single subcutaneous dose of 300 mg of HER-096. The purpose of this was to study the safety of the higher dose in elderly individuals and also to extend the cerebrospinal fluid pharmacokinetic data to later time points to complement our phase I-A PK dataset. This was completed already last autumn, and we reported this part one data briefly in November 2024. The main part of the study was part two. In this part of the study, we recruited 24 subjects with Parkinson's disease, who were divided into two cohorts, 12 subjects each. The two cohorts received either 200 mg or 300 mg doses of HER-096 subcutaneously, two injections per week for four weeks. Each of these two cohorts had four placebo subjects and eight subjects receiving active drug. This was a repeated dosing study. The primary endpoint of the study was to assess the safety and tolerability of repeated dosing of HER-096 in Parkinson's patients, and the secondary endpoint related to pharmacokinetics of repeated dosing. We also are doing quite extensive exploratory biomarker work related to the phase I-B study, focusing on assessment of biological response to treatment. It is important to keep in mind throughout the presentation that the primary endpoint was safety and tolerability, and the secondary endpoint was pharmacokinetics. For part one, which was the aged healthy individuals, single dose, we recruited individuals aged between 50 - 75. The main key inclusion exclusion criteria here are fairly simple, fairly standard, phase I criteria, except for the age range. The part two key inclusion and exclusion criteria are a little bit more extensive, and here are listed the most important ones. Importantly, the subjects had to have clinically established diagnosis of Parkinson's, early idiopathic disease, staged with modified Hoehn and Yahr scale up to 2.5, with bradykinesia and one of the other cardinal signs, without any other known or suspected cause of Parkinson's. Also, all subjects had a brain dopamine transporter SPECT or PET imaging result, and the purpose of this was to confirm the dopaminergic deficit to confirm the Parkinson's diagnosis. Patients were required to have stable clinical disease state with either no current symptomatic medication or stable treatment, including either levodopa, dopamine agonists, or monoamine oxidase- B inhibitor. If we look at the exclusion criteria, there are a few important ones: history or current clinically significant medical conditions, including cancer, major psychiatric disorder, or other neurological disorders than Parkinson's. Also, if there were indications in the brain MRI of a clinically significant brain pathology, the patient had to be excluded from the study. There were exclusion criteria related to late-stage Parkinson's phenomena, such as wearing off, dyskinesia, or if the subjects weren't allowed to be on apomorphine infusions, for example, or deep brain stimulation. Just to understand the basic characteristic of patients who were allowed to enter this study. This study was conducted at two clinical sites in Finland, one site in Turku and one site located in Helsinki. This was operated by our clinical CRO partner, CRST. Part one was conducted between September and November last year, and part two was started very late this year, and the last patient last visit took place in mid-August. Overall, we can say that the study was conducted in anticipated timelines and within the budget. As a company, we're, of course, very happy with such performance. Here's the summary of demographic data, basically summarizing age, race, sex, and body mass index. As you can see, there's no significant difference between the groups, particularly in part two. Nothing noteworthy here. If we look at part two, the repeated dosing in Parkinson's patients, you can see some characteristics of the disease here. The modified Hoehn and Yahr scale is the typical scale for describing the stage of the disease. As mentioned with the inclusion exclusion criteria, 2.5 was set as the highest allowed stage. There's a little bit of imbalance in distribution, which is typical for a small randomized clinical study. For example, here we can see that both placebo and 200 mg groups have perhaps more subjects who are stage 1 and 1.5 compared to a 300 mg group that has more patients relatively at stage 2 or 2.5. In general, this is not unusual, just to keep in mind when going through the data. The UPDRS is the Unified Parkinson's Disease Rating Scale. It is a scoring system to describe the patient's state and severity of symptoms. The part three is a clinician assessment, particularly focusing on the motor symptoms. As you can see here, the groups were fairly evenly distributed in terms of the UPDRS. The UPDRS total score includes the part two, so the clinician assessment, but also on top of that has some patient-reported parameters. Time from diagnosis, time from first symptoms are also listed here. You can just get an idea of the average duration of the disease in these subjects, again, fairly evenly distributed among the groups. As mentioned, the patients were allowed to use symptomatic Parkinson's medication, and here's a table summarizing the medication use. All patients used one to three symptomatic medications. The dopamine agonists, DOPA, levodopa, and monoamine oxidase- B inhibitors are all related to maintaining and increasing the dopamine level in the brain. They operate slightly differently, but they share the same principle of alleviating motor symptoms by restoring dopamine levels. Beta blockers are not necessarily Parkinson's medications. They can be sometimes used to control peripheral adrenergic activity, which may help in control of tremor amplitude, for example. Now, conclusions on the part one, the single 300 mg dose. The safety data overall was well aligned with our previously phase I-A data. There was nothing unusual. The subjects displayed very similar injection site reactions. There was nothing in systemic adverse events. The pharmacokinetic data was as expected. For the rest of the presentation today, we will focus on the part two, the repeated dosing in patients. This table summarizes the adverse events in the part two. Overall, you can see on top line a summary of any adverse events, then a breakdown for treatment emergent adverse events, related, drug-related, suspected drug-related treatment emergent adverse events, severe treatment emergent adverse events, and any serious adverse events. This is a typical way to categorize different types of adverse events in clinical trials. Overall, we can say that there was only one serious adverse event. This was in the placebo group, and it was noted at the very late stage, basically at the end of the follow-up period. We can conclude that this serious adverse event, which was a bladder neoplasm, had nothing to do with HER-096 because the patient was never exposed to the drug. Overall, adverse events, there's slightly more in the higher dose group. Overall, all patients reported at least some adverse events in all of these groups except in placebo where there was only seven out of eight reporting AEs. This gives an overview of the safety data. In general, it is important to emphasize that the majority of these adverse events were related to the injection site. There were very few systemic adverse events, nothing noteworthy, which is also well aligned with our previously phase I-A data. Safety laboratory results on blood and urine, hematology, clinical chemistry assessment, and so on, all samples, all results remained within normal limits throughout the study. There were no trends, no abnormalities that would indicate any safety concerns, and this is again well aligned with the rest of the safety data. Also, the brain MRI results, the brain MRI was done at screening at the end of study visit, and the overall conclusion from the imaging data was that there was nothing suggesting any findings that would relate to this study, no changes during the study. If we take a closer look at the injection site reactions, which you may remember were the majority of the adverse events in total, these are all very typical injection site reactions: pain, bruising, erythema. Anybody ever receiving a vaccination can imagine that it stings a little bit, there's a little bit of bruising and perhaps a little bit of redness, erythema on the skin. This is what we also see with the injections of HER-096. In general, and importantly, the injection site reactions were mostly mild and they were transient. In conclusion, we can say that this is again in line with phase I-A data, with our preclinical toxicology data, and it is very much expected to see these types of injection site reactions with an injectable product. Another important safety assessment for peptides and biological drugs is the assessment of antidrug antibodies. Here we collected samples at pre-dose, so before the first dose, and at the end of the study visit. We had altogether 48 samples, and three of these samples in the antidrug antibody assays were confirmed positive. However, it should be noted that two of these three samples were in a placebo group, and there was one subject that showed both pre-dose and end-of-study samples showed positive signal. This may be just coincidental, and it's quite typical for this type of assays. The only sample that was positive in the groups receiving HER-096 was also pre-dose samples. In conclusion, we can say that there was no evidence in this study of antidrug antibody formation in subjects who received repeated dosing of HER-096 for 28 days. Moving on from general safety to Parkinson's symptoms, we included the Unified Parkinson's Disease Rating Scale, UPDRS, in the study for safety purpose. The conclusion is very clear. There was no change on group level in the UPDRS part three scores. The motor symptoms in these patients receiving HER-096 or placebo remained stable throughout the study. Any further interpretations of motor symptom data are very much limited by the short treatment time and follow-up time also, and the small sample size. I would like to emphasize that this study was not designed or powered to draw any efficacy conclusions. Related to motor symptoms, we also did include a digital health technology tool, Parkinson's KinetiGraph, a wrist-worn smartwatch-like device that continuously collects information and motor features. The purpose of this was to enrich the dataset, but also at the same time to learn how to implement these novel technologies in clinical studies as we anticipate moving to a phase II study, hopefully in the near future. In this study, we have not completed the analysis of the digital biomarker data yet. We have done a preliminary analysis in-house with focusing on the bradykinesia 50 score, which is shown in this graph. Aligned with the UPDRS score, the bradykinesia 50 score does not show any changes in the weekly averages, which are the individual data points in this graph. The full analysis of the digital biomarker data is ongoing with a partner, and we will be reporting this data together with the rest of the biomarker data by the end of the year. Conclusions on safety on the repeated dosing part, this study clearly demonstrated a good safety profile of both single and repeated doses of 200 mg and 300 mgs HER-096. HER-096 was safe and well tolerated in Parkinson's patients. Importantly, all participants finalized the study without disruptions, including unproblematic subcutaneous injections twice weekly for one month. The safety labs, the brain MRIs did not suggest any findings in the safety dataset. Overall, the adverse event profile of HER-096 was good and aligned with our expectations based on previous studies. The one related serious adverse event that was reported in the study was in the placebo group and clearly not related to HER-096 exposure. There was also no evidence of antidrug antibody formation in subjects in this one-month dosing period, which is an important complementary part of the safety dataset. The local reactions in relation to the injection were very common. They were observed both in active and placebo groups, and in general, they were mild and transient. Next, let's move on to the pharmacokinetic data. These graphs show the plasma pharmacokinetic data, the time concentration curves after the first dose and after the last dose, left and right. What we can conclude from these data is that, first of all, these profiles are very much aligned with the PK profile seen after single dose in healthy volunteers in phase I-A study. This is very well aligned with our preclinical pharmacokinetic data, and there's no accumulation after repeated dosing. Perhaps good to remind when looking at these curves that this PK profile is well matched with the planned intermittent dosing regimen as HER-096 has a hit-and-run mechanism of action. Cerebrospinal fluid samples were collected both for the biomarker purposes, but also to further understand the pharmacokinetic properties of HER-096. This graph on the left shows samples that were collected eight hours after the last dose in the part two. You can see that there is, first of all, very clearly there's presence of HER-096 in the cerebrospinal fluid in all subjects. It's very much in the expected concentration range, the average in the 200 mg group being around 80 ng/mL, and in the 300 mg cohort around 140 ng/mL. The slightly wider distribution in the 300 mg group is most likely explained by body size differences. The graph on the right shows a correlation analysis of total plasma exposure, area under the curve on the Y-axis, and then the CSF levels, the single time point CSF levels on the X-axis. We have a high correlation, the R-square being around 0.6. Overall, we are very, very happy with these results. These results, together with our phase I-A data and the part one data from this study, show that 200 mg- 300 mg doses of HER-096 result in cerebrospinal fluid levels that are expected in the expected pharmacologically active level, and very much aligned again with our preclinical data. Now, if we put together a cross-sectional aggregate of the CSF data, so pulling together phase I-A healthy volunteer data and phase I-B healthy volunteer data, we can get a temporal view on the distribution of the data points. This doesn't allow us a full pharmacokinetic parameter determination as these are single time point samples per subject. This is not serial sampling. However, this allows and gives us a very good overview of how quickly HER-096 reaches cerebrospinal fluid compartment and what is the elimination half-life from the CSF. Here we can conclude based on this data that the CSF Tmax lies around 8 to 16 hours, and the CSF half-life is approximately six hours. This is again well aligned with the predicted elimination rate in humans, and it supports dosing in phase II twice weekly. Overall, we can conclude that the primary and secondary objectives of the phase I-B study were met. HER-096 is safe and well tolerated in Parkinson's disease patients. Overall, the phase I-B study was a very clean study that was conducted within anticipated timelines and budget. Pulled together, phase I-A and phase I-B data strongly support advancing HER-096 into a phase II trial to assess efficacy. The top-line data that we're reporting here today doesn't cover all the data from this phase I-B study. As we've indicated before and in yesterday's release as well, there's still data to come towards the end of the year, and this data relates to biomarkers. With this data, we can check three very important boxes: the safety, the pharmacokinetics. We have established also the dosing level, dosing frequency for phase II, but we still have one box to tick, and we are working very hard to get this data together by the end of the year. Biomarkers can mean a lot of things. What do we actually mean by biomarkers? What are we expecting from this dataset? Overall, in general, biomarkers are measurable biological indicators that reflect drug action or alternatively disease state. They have become a critical element of modern drug development, modern clinical trials. They can help to confirm proof of mechanism, target engagement. They can show biological effect before clinical outcomes appear, guide dose selection, identify responders, non-responders, overall reduce time, cost, and risk of failure. Particularly from the partnering point of view, this is very important. This allows us to do better informed go/no-go decisions, helps to de-risk programs by us or our partners. It helps us to design smaller, faster, more informative clinical trials and helps make smarter and faster transition to the next phase. Now, particularly in the phase I-B data, what we are expecting to see or what type of data we are collecting in biomarkers in this study relates, on one hand, to the disease state. Parkinson's disease is a heterogeneous disease. Every subject has a slightly different variation of the disease. The underlying biology is not the same between the patients. That's why it's critically important that we understand this biological background, and we're collecting information related to genetic background, genetic risk. We're collecting a large number of fluid samples, blood, cerebrospinal fluid that would help us to understand the differences between patients. However, this is only one part. The more important part relates to biological response, and this is typically a key question for phase I studies. Can you provide any information, any data that would demonstrate that the human body responds in an expected way to the exposure of the drug? Biological response can mean many things. It can mean safety-related things. It can mean symptom monitoring, but particularly important for us is the pharmacodynamic component. This means how the human body responds to the drug, and particularly in phase I studies, the targeting demonstration of drug target engagement, target pathway modulation, proof of mechanism can serve as a very important go/no-go decision. It can create tremendous value for the program to be able to demonstrate this. There are also, of course, questions related to disease modification. This could be a little bit more to a question leading towards more phase II, particularly because the study that we run here is fairly short in duration. The pharmacodynamic aspects are particularly important for Herantis and HER-096 program because we are working with a target mechanism that is fairly new to clinical drug development. There are no established biomarkers that we could buy an assay, a commercial validated assay for monitoring unfolded protein response pathway activity does not exist. We need to pioneer. We need to produce the data. That's why the phase I-B will be focusing on the pharmacodynamic biological response to the treatment. All this data is expected by the end of the year, and hopefully also the digital biomarker dataset will be fully analyzed and reported by that time. Thank you, Henri, for taking us through the great top-line data that we released yesterday evening. Herantis was the sponsor of the study, but of course, we have not been alone there being able to achieve this data. We would like to thank, of course, the healthy volunteers and, of course, the patients, the Parkinson's patients and their families. Without you, this could not have been possible. In addition to the patients and healthy volunteers, there has been a vast network of partners and suppliers that we have worked with. I would like to highlight the CRST team as a clinical site to enable this clinical study, but of course, there are other persons as well in analytical labs and CROs and other types of organizations as well. Very important support and achievement also, and thanks goes to you as well. I also want to highlight our own Herantis team. As Henri already mentioned, we conducted this study within the preset timeline, within the budget, and it is a great achievement from the Herantis team, and it really shows that we can deliver with this development program. Of course, investors and financing is a crucial part of taking drug development forward, and I would like to especially provide my thanks to two patient organizations that have supported us financially, enabling this study, the Michael J. Fox Foundation and Parkinson's UK, providing us the great financial support for the phase I-B and biomarker program, but also being there and helping us in other aspects as well. As a summary, we achieved great data with phase I-B. The study met the primary and secondary objectives. We have great safety data. We have expected pharmacokinetic data. We have confirmed the dosing for phase II, so we have all the motivation and all the foundation to proceed the program to phase II efficacy trial. The company is currently preparing for that study. At the same time, we are completing the phase I-B biomarker studies and reporting that by the end of the year. Being able to release the top-line data now helps us to continue the partnering discussions, and we will have a very busy autumn being in contact with the potential pharma partners, one-to-one meetings, and participating in different partnering events. That is the ambition of the company, as we have communicated many times before, that we would like to have a partner on board when we go into phase II. That is the emphasis of the company and the management team to enable that to happen. I think we have now completed the webcast in terms of the data review, and now it's time for the Q&A, and our CFO, Tone Kvåle, will come here and host the Q&A session with us. Thank you. We have really many viewers today and a lot of exciting questions, so be prepared. Why will it take two to three months until the full dataset will be reported? This is a very good question, and there are actually several layers explaining that. One is that we have collected a large number of samples, different matrices, blood, CSF, and so on. These are analyzed with different technologies, with different technology providers, service providers globally. Some of these providers have a certain lead time. They cannot deliver the data the next day you send the samples in, so it takes a little while to run these analyses. Even when that's completed, we are only halfway through. The data analysis can be actually very complex too because we have several omics datasets. We're looking at proteomics data. An example is that one proteomics study could have hundreds of thousands of data points. We have multiple time points, 24 patients, groups, and more than 10,000 analytes in each sample. All that provides a very, very rich body of data that requires quite extensive and advanced bioinformatic analysis, and integrating all that data together, together with the clinical data, is just, it is time-consuming. Looking ahead to phase II, what will the trial design look like, and do you anticipate it being an international study, and how many patients do you expect to enroll? First of all, we expect it to be an international study. The current view is that the study would be run in Europe, in several countries. We have started discussions with potential investigators and sites. There are a few that we're already deeper in the discussion, so we have some idea where it could be run. It is a little bit premature to speculate on details of the study design. There are several elements that still need to be decided. We're discussing and planning internally together with our advisors things related to study duration, number of patients, which endpoints will be selected. That also depends a little bit on our full dataset on phase I-B. At this stage, we're not ready to provide further details on the phase II design. How much funding is required, and how will you fund the phase II study? What are your plans to raise additional funding? Of course, the data that we released now gives a strong rationale of running the phase II, and as Henri already mentioned, we have been planning for the phase II. However, for finalizing the phase II plans, we need to have the biomarker data analyzed and interpreted. If you just look at, in general, the industry, a phase II proof-of-concept study might cost somewhere around EUR 15 million- EUR 20 million. We are currently looking at different options, how we could resource that kind of a study. Of course, we are looking at partnering. We are looking at potential equity financing. We are also looking at potential grant financing, and of course, when the time comes, then we will have more information about how to practically set up the phase II. There is a lot of interest in disease-modifying therapies for Parkinson's. How is HER-096 different from other approaches in development? That's a very good question. HER-096, first of all, it's the first of a kind treatment targeting unfolded protein response pathway in Parkinson's or in any neurodegenerative disease. Just based on the mechanism of action, it already differs from many other approaches. We also believe that this is a quite unique combination of neuroprotection, restoration of proteostasis, anti-inflammatory effects, and also the ability to promote functional recovery of stress neurons. This, we believe, is the package that makes HER-096 to stand out among the peers. Good. More related to the funding, what kind of funding structure would you prefer if you need additional funding? Is it partnering? Is it more non-dilutive funding from Michael J. Fox and Parkinson's UK? How do you look into the EIC funding opportunity that you still have with the equity which is not spent? Yeah. Basically, if we start with partnering, of course, as we have communicated, as I already mentioned, that's the ambition to find the right partner. Of course, we need to also then think about what kind of a potential partnering deal we might sign or what could be the terms, which we don't know and we can't comment right now. It really depends on that. We are definitely looking at different kinds of non-dilutive grant type of funding opportunities, but of course, those are something that we can't comment right now. The EIC is very strong support for us, and just to remind that we still have approximately EUR 12 million there in their pre-commitment, which they are able to finance 1/3 of any equity financing round if we choose to go that route. As already mentioned, now is the time to look at the different options to see, and then later on, we will select what would be the optimal choice for the company and supporting the phase II and further growth. Good. More question related to biomarkers. What are your hopes and expectations regarding the results of the biomarker measurements? Will there be anything that will hint towards slowing the disease progression? As already pointed out in the presentation, emphasis is largely on the proof of mechanism, pharmacodynamic target pathway modulation type of responses. We do have a set of targeted biomarkers, which means pre-selected biomarkers based on certain criteria, but also a broad approach using untargeted approaches, including proteomics, for example. There are different ways you can expect to see things here. You could see changes in individual targeted markers or then maybe perhaps more on the pathway level in the omics data. For example, unfolded protein response pathway is strongly connected to regulation of gene expression. We would expect to see something on pathway level related to proteomics data, how certain protein markers are changing broadly, not just a single marker, but broadly. Regarding time, the study is still quite short. It is only 28 days. It is a little bit hard to speculate which disease modification-associated biomarkers would be showing clear change in such a short time. I think we'll just need to keep an open mind and see what the data tells us. Which biomarkers were monitored in the study? It is a very, very large group of biomarkers. I don't want here to name a single marker because we're using a very broad combination of targeted and untargeted approaches. Congratulations with the positive phase I-B results. Although not designed for efficacy, were there any exploratory trends that might hint in early efficacy signals? The UPDRS and the PKG bradykinesia 50 data what's available today on group level doesn't indicate anything, and this is exactly what we expected from such a small study that's not powered for assessing efficacy. It is, of course, possible. You never say never. When you dive deeper in the data, you look into complex biomarker data, you never know what you can discover there. I would again remind that the short duration of the study and the small number of patients is limiting any further speculations on symptom improvement at this stage. Were there any differences in the type of adverse events, tolerability, or drug exposure between the 200 mg and the 300 mg cohorts other than injection site reactions? Not really. The number of AEs was slightly higher with the 300 mg group. This may simply relate also to the slightly higher dosing volume. The drug concentration in the drug product was the same. When we increased the dose, we had to increase the injection volume, which per se can increase injection site reactions. Broadly speaking, there's nothing noteworthy between the two groups. Back to phase II study again, what are the main regulatory, logistical, and financial steps required before you can start a phase II? Maybe I will start with that. Of course, when setting up a clinical study, we need to have enough resources for the preparation of the study and applying for the clinical trial authorization. We need to have enough financial resources to actually run the study. As already mentioned, we are looking at different options for resourcing the study. Related to the actual study setup, currently, it seems like it should be pretty straightforward with those plans that we have already created, and we already have preliminarily assessed the regulatory paths and everything related to the investigational drug and such things. We believe that it should be a rather straightforward program to set up the study and practically conduct it if we have the right resources in place. Okay. Based on animal models and testing, is it possible to estimate after how long treatment the clinical symptoms could show change? Mouse are not very good humans. Also, preclinical models, their translatability to the human disease setting is always complicated. It is a very difficult question to give a straightforward answer to, and I believe we don't have many hours to sit here listening to me speculate on that. We can look at some other studies. For example, studies done with an alpha-synuclein antibody, prasinezumab, the PADOVA study, PASADENA study that were conducted by Roche. They, based on their symptomatic data and also digital biomarker data, can make some estimates, and they said in their recent presentations that one year is a realistic timeframe to expect with that mechanism of action. It might be slightly different if you have a sort of like a passive supportive mechanism removing alpha-synuclein compared to an active neuronal functional recovery promoting compound like HER-096. The timeframe could be different. I think the time will tell, and when we're ready, we will come out with the phase II design, and I can guarantee that we have spent a lot of time discussing this time question with our advisors and our team, so we will be confident about the decision. I can continue that also the biomarker data that we are looking at might give us more insight into this time perspective for the phase II. Related to the biomarker plan, is genetic diagnosis included to the prerequisite for the HER-096 therapy? There's no basis for that right now. We included genetic characterization of the patients to understand the underlying differences between the patients and the underlying disease biology. There's nothing in the data that currently suggests that HER-096 would only work in a sub genetically defined subgroup of patients. Also, unfolded protein response pathway is a very general target, if you will, in neurodegeneration, so that also supports that view. In light of these results, what is your best case scenario for getting the product to the market time-wise? That's a very good and important question, which we actually haven't commented yet before, and I won't comment that either right now here. The next step that we foresee is to run a phase II proof-of-concept study, hopefully targeted to start during the next year. It really depends on the signal, the efficacy signal that we might see in that study that will then decide on the next step after the phase II. I would not start speculating about the different options there. Okay. I think that concludes the Q&A session. A lot of really good questions, so there's a lot of enthusiasm among the audience. That's good. Thank you, Tone. I think this concludes our webcast for phase I-B top-line data. I want to emphasize still that the data was really good. We were really happy about what we were achieving, and this gives us a great opportunity to go into phase II efficacy trials. Thank you for listening to us today, and I hope that you will follow our story going forward. Thanks a lot.