Good morning, welcome to Circio. My name is Erik Digman Wiklund, and I am the CEO. Today, I will take you through a company update on what's been happening in Circio during this year so far. To begin, please take note of our important disclaimer. We're a listed company. We have a new ticker, CRNA. Follow us on the Oslo Stock Exchange. Starting off, let's look at the highlights for 2023 so far. This has been a big year for the company so far. Earlier in the Q1, we made the strategic decision to shift our focus to fully prioritize our circular RNA platform. This is largely driven by strong internal, external interest in the space. We see several investments, deals being made. We believe we have a unique technology, a differentiated approach, and we want to take advantage of our early mover advantage in this exciting new area. Therefore, we have now retooled the company, and we're fully focusing on accelerating our circular RNA development. To reflect this, we also made the decision to change the name of the company from Targovax to Circio. Circ reflects circular RNA, and IO stands for immunotherapy, and both hints to our legacy as an immunotherapy company, and also reflects that we believe immunotherapy will also be an important component of the company moving forward. There is also a new ticker on the Oslo Stock Exchange. As I mentioned, we are now trading under CRNA. As we have now retooled and become more of a preclinical company than we were before, unfortunately, our Chief Medical Officer, Lone Ottesen, as well as VP and Head of Regulatory Affairs, Ingunn Lindvig, have resigned and decided to join other Nordic biotechs. In addition to that, we have streamlined the organization to be more of a scientific team, and as such, we have an overall headcount reduction of roughly 40%, and our operations are mainly now scientific and based at the Karolinska Institutet in Stockholm. In addition, on the corporate side, we secured an important financing during the first half of the year. We have secured access to NOK 300 million in a convertible bond facility by Atlas Capital Markets, based in London. We have received several questions relating to this financing facility, and we'll come back to that in the Q&A session later. On circular RNA, we've made important progress. We have maybe stayed a little bit silent on exactly what we're doing and the data. This is for two reasons. One is that we want to file important IP. We want to get that out of the way. We don't want to take any risk when it comes to IP. The other is competitive. We want to not reveal too much about exactly what we're doing because we believe we have a unique and differentiated approach. What I can tell you is that we've generated important proof of concept data, and we are starting to build this platform. Far, we've shown that our circular RNA designs in our setup have a 15 x extended half-life as compared to linear mRNA. Half-life is one of the major drawbacks, short durability of mRNA, and this is really where circular RNA can make a difference. We're able to show that this in our system clearly is advantageous. We've to date filed now two important patent applications. One is concerning the general design of our circVec vector approach, and the second, which was filed this year, relates to how this is deployed in certain vector types. We have scanned the opportunity landscape, assessed our technology, and we believe we see three major focus areas. One is in cancer gene therapy, the second is using our platform in rare genetic diseases, and third, as a novel vaccine concept. I will come back to circular RNA and show you a bit of our emerging data. Our KRAS program is also advancing well. We have initiated two investigator-sponsored trials, one in the U.S. at University of Kansas, the second at Oslo University Hospital. The first patient has been dosed in the University of Kansas trial. The first patient is enrolled in the Oslo University trial. We do anticipate that the first patient will be dosed in Oslo very soon. Moving on to an update on the circular RNA program. As we've said before, there is massive interest in RNA therapeutics at the moment, and in particular, circular RNA. In general, the post-pandemic years, 2022, 2023, has been viewed as really unfavorable for biotech financing. There is one exception, RNA deals. As you can see here, actually, RNA deals, even in 2022 and 2023, has been significantly larger total deal value when comparing to pre-pandemic levels. We've seen that roughly $1 billion raised for private financing rounds. Actually, year to date, 2023 is even higher than that. Now, what's interesting is that 40%, or more than 40% of this deal value has gone to circular RNA projects, or projects which have a significant circular RNA component. This just shows that there is strong interest in this. It clearly outperforms mRNA-based approaches when it comes to attracting deal value. Here is a list of, or an overview of companies that have launched and deals that have been made.... Maybe most famously, Orna Therapeutics and Laronde, they launched back in 2021, I think really opened people's eyes to this space, both raising something significant financings. What they are doing is making synthetic circular RNA. They produce circular RNA in a factory, the idea is to use then the circular RNA as a kind of circular mRNA format that they plan to bring into patients. Following on that, Orna was able to do a very significant platform deal with Merck late last year. This year so far, we've seen two significant financings in the US, Orbital Therapeutics launching with a $270 million Series A, subsequently, ReNAgade Therapeutics with a $300 million Series A. Both of these are kind of broader, place, but a significant component of what they communicate that they will do is centered around circular RNA delivery. This is really a field that is happening right now. Why are people so excited about circular RNA? The biggest advantage of circular RNA is that circular RNA, by not having a free end, are resistant to degradation mechanisms in the cell. You see these Pac-Mans that we've drawn on the mRNA, they are called exonucleases, and they tend to degrade mRNA from the free end, and then the mRNA is broken down in a few hours normally. The circRNA doesn't have any free ends, so this Pac-Man, the exonuclease, doesn't have anything to latch on to, and this means it's resistant to this degradation mechanism, and therefore has a massively improved stability. This is really what's getting people excited. You can utilize this to drive and enhance protein expression. You get extended RNA durability. In addition, because it's stable, you can build in other functionalities, such as micro-RNA sponging, which is a well-described function in the literature, as well as other regulatory formats that you can build in. We view this as a very interesting toolbox that allows you to not only have a more stable RNA format that can express protein in a better way and more durable way, but also achieve other goals at the same time. What differentiates us from the other players in this space is that we are not making synthetic RNA. Our product is DNA-based. We make DNA vectors that carry the instructions for the cell to manufacture the circular RNA itself. As far as we see, this is a unique angle that no one else has been taking so far. We're working on building out our understanding of this, building out our system, and filing relevant IP to cover up the territory, for Circio. The concept is we make a DNA vector, it's injected into patients, and then in the patient, the circular RNA will be produced and then drive robust and durable protein expression. The core part of our technology is what we call circVec. circVec, in essence, is a genetic cassette. It's a piece of DNA that we can put into any vector, and this piece of DNA carries the instructions for the cell to produce circular RNA. We have filed patent applications covering the design of this of this genetic cassette late last year. Then we filed additional IP relating to how we deploy this in specific vector types. This design is extremely important. We have unique insight into how you do this most efficiently. The second bit is how you design the circular RNA. This is very important, especially for how much protein you get and how durable the circular RNA itself is. Here we've done several analysis and figured out exactly what we think is the best way to design the circular RNA to achieve long half-life, enhance protein expression, and also demonstrating that we can achieve these other functions as well. That's our concept. How does it work? Well, so far, we have been able to show in our in vitro systems in cell culture that we have a 15 x expanded half-life versus mRNA. In this experiment here, our mRNA had nine hours half-life, which actually may be a little bit longer than you would normally expect. Our circRNA had 135 hours. That's 15 x extended. On the right-hand side, you can see a time course, how this plays out over time. If you look at 48 hours, on the left side of the graph, there is RNA, and on the right side, there is protein made from this RNA. On the left-hand side, you can see circRNA at 48 hours is a little bit less than mRNA. The circRNA production is not perfect, so you get fewer copies of circRNA early on, and mRNA, there is more. At 96 hours, exactly what we expect to happen is happening. You see the circRNA is increasing. It's accumulating because it's stable at 96 hours. There is more circRNA than mRNA. The mRNA, in fact, has dropped by 80% after 96 hours. This is precisely the hypothesis, and it's confirming what we're expecting to happen. Interestingly, on the protein expression, now, the circRNA and mRNA here is expressing the exact same protein. The fewer copies of circRNA at 48 hours are actually capable of producing more protein than the mRNA. This shows the circRNA is more efficient at protein expression than a normal mRNA. At 96 hours, this difference increases. There is even more protein from the circRNA, it accumulates, whereas the mRNA is dropping off. Now, protein is much more stable than RNA, so protein hangs around for longer. That's why the difference is smaller when you're looking at the protein level compared to the RNA level at 96 hours. Again, this proves the point. What we're doing now is that we're replicating this type of experiment in in vivo models to show that this holds true when you're in an animal in a biological system, and we anticipate that the difference will be even greater. In the mouse model, we can also run the experiment for longer, so the aim here is to try and see over time, how long does this actually last? That's important in vivo experiments that have started, and we believe this will sort of apply to our circRNA concept in general, and irrespective of what therapeutic area you may want to use it in. How were we able to achieve this? Well, this is a little bit of a complicated slide, but I will try to explain it very simply. What we did first is that we looked in the human genome at all circRNAs that existed. More tens of thousands of circular RNA are naturally expressed in humans. We did deep analysis of sequencing data from human RNA, NGS data sets, and we looked for where do we get the most efficient production of circular RNA naturally. Based on this analysis, you see in the scatter plot in the lower part here, we picked the top 10. We found what we analyzed to be the top 10 natural genetic loci of genes, if you want to call it that, for circRNA production in humans. We took those top 10 natural loci, and we tested them in our expression system. We call them an L1 to L10. In this graph on the right-hand side, we show you the top 4. L1 to L4, you can see actually it's L1. Our top prediction turns out to be by far the best. This locus number 1 is 3- to 4-fold better than everything else we found. We picked this as our lead candidate, the locus 1. We took that, the natural sequence, and we tried to express protein as well. On the right-hand side in this gel, you see also the L1 is better at expressing protein. We say, how can we prove this further? We took the natural L1 structure or DNA sequence, and then we optimized it. We played around with various features and tried to make it better. If you look at the top-hand graph here, you can see we're actually been able to improve on this roughly tenfold. The best natural sequence, we now have something that is tenfold better. This means we now have a setup that is highly efficient for circRNA biogenesis. For each vector we get, we bring in, we get a lot of circRNA produced. The second step is optimizing this for protein expression. That's what we're showing in the lower part of this graph, is various design features to try and optimize protein output. This is here an example from D1 to D12 or 12 different variants, and the difference is actually quite striking. Depending on how you do this, it's a massive difference in the output. D4 is the design that's been best, and this is what we're moving forward with. Of course, we're trying to optimize that even further. What we've then done is taken here the best one from the top part, combine it with this D4 design of the circRNA, and this brings us what we call circVec V1. On the graph on the right-hand side, or sorry, on the, on the gel on the right-hand side, you can see how circVec V1 is performing compared to mRNA. You can do the mRNA, and then when you've done this well, clearly, the circVec expression is much higher than the mRNA. A stronger band means more protein is made. Our circRNA beats the mRNA. You need to design this right. If you don't design it well, you can see in V2, it, the protein expression as a sort of negative control, is much less efficient. This shows you need to optimize this well. This is the key, the key insights that we have made, and we're not aware of anyone else that have developed this sort of technology for vector-based expression. Now we view this as a general system that we can deploy in various contexts. That's how we designed the setup that we have. We have made a lot of progress during the past year. Remember, we only started this actually January of last year. Doing R&D takes time, but here I'll try to give you a flavor of what we've done so far. We've constructed this cassette, the circVec V1, and then we've looked at and optimized the circular RNA biogenesis. We have looked at how it functions in different vector types, both DNA-based vectors and virally-based vectors. We've looked at the protein expression side, how can we express the maximum amount of protein or other types of peptides that you may want to express. We've also established additional regulatory functions that we now know how to do and can build into the system, such as, for instance, micro-RNA sponging. Then several of these we're moving now into in vivo experiments to see how they function in animal model, and we're also working on combining multiple of these features together. As you can see, we've made significant progress on all these fronts. Where do we aim to deploy this? As I mentioned before, we see three major areas. Cancer gene therapy. This means delivering proteins, therapeutic proteins into solid tumors using our platform. This will enable us to achieve a stable and durable supply of therapeutic proteins into solid tumors. Because we have an experience in this area and we have in-house setup with our ONCOS platform, we view this as probably the quickest way to get the circular RNA product in in this area. Second area is in vaccines. Here, our aim is to try and develop a single-dose vaccine format. We believe that this combination of a suitable vector with strong expression from circular RNA really can make a difference in terms of immunogenicity. Initially, our aim is not to bring vaccines into into the clinic ourselves. This is a big undertaking for a small company. Rather, what we want to do here is establish a preclinical proof of concept for our approach and then try to partner with a larger player in the vaccine space. We think this is an opportunity for an early partnering. The third step in our plan is within rare or genetic disease. This, we think long term, has major potential. With a circRNA, you can really start looking at delivering durable protein replacement therapy without the need for genome integration, or, and you may avoid several safety issues that you see with other approaches used in gene therapy. I think this is maybe where we observe among investors and potential partners, that this is really where people think circular RNA long term can make a difference. It still needs to be understood how you get there, but it's obvious that this chemical advantage of circular RNA may be very important in this space in trying to deal with genetic disorders. We're currently exploring how we best can deploy our setup there. To summarize, we think we have a unique edge and advantage, an early mover advantage in this emerging space of circRNA. We have the world-leading experts in-house. Our program is led by Dr. Thomas Hansen, who is the discoverer and early pioneer of the field, and probably the most experienced circRNA scientist in the world. As I hopefully explained and convinced you, we have a differentiated vector delivery platform, which opens new opportunities, and we have several opportunities. This is not just limited to oncology, which has been our area in the past, but we see a much broader potential, and our aim is to try and exploit this platform in various settings. We've also found this quick route to the clinic, potentially in oncology, doing cancer gene therapy, where we can leverage existing know-how and manufacturing capability based on our legacy ONCOS program. That summarizes where we are on our circRNA program. Moving on to TG01, our KRAS vaccine. This has also made progress during this year. We have two very interesting trials running. One is at the University of Kansas. This is in surgically resected pancreatic cancer, where we try to vaccinate patients that have had their tumor removed in surgery and see if we can get rid of residual cancer cells that remain. We received the U.S.IND for this last year. This is the first time TG has received a U.S. IND, that's a big milestone in itself, and the first patient has been dosed. As far as we understand, it's all going well. Hopefully, more patients will be dosed soon, as now the kind of first hurdle of this first patient is passed. This trial, we're testing both TG-01 monotherapy as well as a PD-1 combination, with a PD-1 supplied by our strategic collaboration partners at Aduro. The second study is at Oslo University Hospital. This study has received NoMA approval. It's now actively enrolling. In fact, the first patient has been enrolled. We anticipate very soon this patient will be dosed. In this case, we're vaccinating patients following first-line treatment. We pick patients that didn't get a complete response. See if we can bring the response all the way down after this first-line therapy. In this case, it's a monotherapy-only setting. This will give us important monotherapy data. It's the first time we combine, or we bring TG-01 into multiple myeloma. Between 15% to 20% of myeloma patients are KRAS or NRAS mutants, and we can cover most of these with our vaccine. This will be an important advance in this space, and a significant part of the population in multiple myeloma would fit into potentially receiving this vaccine. This is progressing well. Remember, these are academically sponsored trials, so these are run by the hospitals and medical oncologists at the hospitals. It's also largely externally financed, and we're supporting it. This means that the required bandwidth on our end, and the finance or money we need to put into it, is also limited. It gives us a chance to keep developing TG-01 at low cost to Targovax and allowing us to focus what we do mostly on our circRNA development. This year so far has, in general, been a very important year for cancer vaccines. We have seen the first clinical validation, I would say, that a cancer vaccine actually can work. Data was presented by Moderna at AACR, a large cancer conference back in April, showing that vaccination after surgery in melanoma, using their personalized vaccine, was better than no vaccine in a randomized trial of 150 patients in total. This is the first clinical robust evidence in a randomized setting that a cancer vaccine actually generates clinical benefit. This has been hard in the past for major two reasons, I believe. It's because we have been testing vaccines, maybe in too late-stage patients. They've been too sick, didn't really have a chance to recover or mount the proper immune response. The second reason is that the vaccines have not been combined with anti-PD-1. That's what Moderna did. They went earlier, they went in post-surgery melanoma setting, they combined with anti-PD-1, voila, it looks like it's working. Another maybe less high-profile data set, but nonetheless extremely important for us, was presented at ASCO last week. This vaccine here I show on the picture, on the slide, is called ELI-002. It's from a company called Elicio. They vaccinate against two KRAS mutations. Interestingly, what they showed, this is in exactly the same population that we are treating, post-surgery pancreatic cancer. They showed that this vaccine, dealing with two KRAS mutations, actually was able to clear circulating tumor DNA from blood. They look in blood, can they detect DNA from tumor? In patients where, yes, we can detect the circulating tumor DNA or ctDNA, then they vaccinate, and they look at whether they can clear out this marker. Yes, you see here, actually, in seven out of these patients, there's a complete clearance of the ctDNA. This is really important because this shows that the idea, our concept in the cancer trial actually can work. We believe we have an advantage because our vaccine covers seven mutations versus just two for the other vaccine, as well, that our vaccine is being combined with a PD-1 in this study, versus this other trial, which is a monotherapy trial. This clearance of ctDNA or the biomarker reduction was achieved only with the monotherapy. We think once you bring in the PD-1 inhibitor, it will be even greater. This data makes us even more optimistic about our cancer trial in particular, and that vaccines can work. Importantly, here, we are in earlier setting. It's the same in the myeloma trial. We're testing this out in earlier stage patients. Now maybe this is the way to develop vaccines, hopefully this trial will generate robust data, which will allow us to attract future partnerships and really bring this program, TG program forward. Important updates on KRAS. Finally, let me give you a little summary on HR. Of course, we have now refocused our company to be more of a preclinical organizations, and unfortunately, that means with less clinical activity and less manufacturing activity, we have also had to streamline our organization. Overall, this has led to a 40% reduction in the total headcounts. Obviously, this also comes with the cost advantages, our payroll costs are now lower, as it also means that our cash burn rate is lower. We expect going forward, less cash burn, less financing needs, that's maybe the advantage, although it, of course, is unfortunate to have to let go of very talented and dedicated colleagues. On the management team side, the two of our clinical development colleagues, Lone Ottesen, our Chief Medical Officer, as well as Ingunn Lindvig, our Head of Regulatory Affairs, both have decided to resign in light of the new priorities in the company and have moved to other Nordic biotechs, and during the month of June, will transition out of the company. On this slide, you see now the new management team. It's now more of a scientifically oriented management team. Myself and Lubor Gaal, we remain CEO and CFO, and so largely running the company. We have Victor and Thomas running our scientific operations. One is an expert in immunology, the other is an expert in RNA molecular biology, and they are building rapidly now our preclinical team. Margrethe, our head of, has been in the company for soon two years, and she will assume the role of head of clinical development, taking over largely the responsibilities of Lone Ottesen, and she will manage the TD program as we go forward. Obviously, the total capacity needs in that department are now reduced. Finally, we have Ola, based in Sweden, who is responsible for manufacturing, and now is looking into how we deal with manufacturing of our novel circular RNA products. With this, I believe we have a very talented, international, and scientifically oriented team with broad drug development experience, all the way from scientific discovery to clinical development and manufacturing. We are all very enthusiastic about taking Circio forward in this new chapter. With that, I wrap up the formal part of the presentation, and we will take Q&A. We have received several questions beforehand by email, and we've also had an open chat here for posting questions during the call. My colleagues will take a look at any questions that came in. Many questions that we received by email have been relating to some news at Laronde, one of our circular RNA peers, that were published this week, as well as the Atlas financings. We grouped these into two components and translated into English for everyone to understand. We'll try to cover all the aspects that we have received. With that, I'll move to the Q&A. First, there was an article about the circRNA company, Laronde, published earlier this week by The Boston Globe and Stat News, reporting issues with the technology and data integrity. How does this impact Circio and your approach? First of all, I must say we're very surprised by seeing this news, and it's very dramatic and of course, very unfortunate for Laronde. It seems like there has been problems with the integrity of the data and what they've claimed the technology can do. We do things differently, as I explained. We make vectors that make circular RNA inside the cells. In essence, you could view this as potentially an advantage for our approach, for confirming that our approach might be even better. One of the issues here is that apparently the circular RNAs are not as stable in vivo as has been claimed. What we are doing is bringing in vectors. The vector will have a stability. It will keep supplying the circular RNA inside the cell over time. We expect that we will have significantly better durability, overcoming this kind of shorter than expected turnaround of a synthetic circular RNA. We think that this just validates the aspects of how we are trying to do this. In general, we don't view this as any evidence that circular RNA doesn't work. It's clear that this still has advantages, and everyone's trying to figure out exactly how good these are. Potentially overall, it lends some validation to our approach being potentially advantageous over bringing in synthetic circular RNA. Secondly, we have a summary question here on Atlas. So, as you recall, we have a convertible bond facility set up with an investor in London called Atlas Capital Markets. This is for up to NOK 300 million over the next three years that we can draw in branches. The question goes: Atlas seems to have breached the maximum trading limitation of 25% of the total weekly volume, according to the agreement following the previous conversion. Has this been corrected, and will there be any consequences for Atlas? We are in close dialogue with our colleagues at Atlas. The breach of the 25% volume, it's correct that during certain days, the volume went over, and it went over during a period of a week. This was due to miscommunication. I can confirm that Atlas has corrected this breach and repurchased the shares to bring back then the overall volume to 25%. This is important. It shows that we and them, we're following this closely. We're dedicated to following the agreement, and we don't expect these issues to arise. It was purely due to a miscommunication. We appreciate the several shareholders noticing this and letting us know. We also, of course, track this on a continuous basis. Atlas has not made any conversions during the period in which they were in breach, so they have repurchased all of the excess shares, and also any period where there has been a breach of the volume will not be utilized for pricing of convertible bonds in the future. How is the cooperation with Atlas working, and how are the bond conversions and trading tracked? Is another question. And will they be allowed to convert again after they recently have breached its trading volume limits? We have agreed that the trading breach has to be cured before another conversion will be allowed, and that has now been cured. We are continuously tracking this in-house. I think Atlas themselves are tracking it as well as you are our shareholders. In terms of cooperation, I would say this is working very well. We have a continuous open dialogue and try to plan this in the best possible way. Overall, I would like to say that lately, we believe this financing has been working exactly as we had hoped and anticipated it will do. Actually, now the share price is trading higher than where both of the previous conversions have been. This shows that we can utilize this over time, and we can have an increase in share price. I think it also demonstrates that everyone here is incentivized for an increase rather than a decrease in the share price. So far, we are happy about how this is playing out. We're seeing the facilities working, and we see that the share price can hold up despite concerns that have been, because we have built in important safeguards in how the structure is executed. Then we have a question on ONCOS-102. What is happening with ONCOS-102, and have you been able to find a partner? Since the announcement that we were to deprioritize ONCOS-102 in favor of the circular RNA program, we have been in dialogue with the potential investors and partners regarding external financing of the program. Unfortunately, we have not been able to generate sufficient interest to bring it forward at this stage. The program still remains in a shape where it can be reactivated in the future, but we have to be honest that so far, there are no active dialogues that are looking like they may lead to sufficient interest to be able to run the phase II program as planned. We believe that larger program is what is needed. Doing another small trial, we think, would not give the required data to actually bring it sufficiently forward into development and subsequent registration. If we bring it forward, we want to do it in the proper way, in a larger randomized setting. A bit of the issues we face is that oncolytic viruses have had certain headwinds in the industry, illustrated, for instance, just a couple of weeks ago, one of our peers, a company called Oncorus, unfortunately went into bankruptcy due to clinical data that didn't play out as expected. Several of these negative stories and problems in the OV space have made both partners and investors a little bit reluctant to continue investing into oncolytic virus programs. We firmly believe that ONCOS-102 works. We see clear activity. We think this warrants to be brought forward, but I think this market perception just needs to be overcome, and what's probably required is a larger positive data set to really fully confirm for everyone that intratumorally delivered oncolytic viruses are effective and have a future. Until then, we decide to focus on circular RNA, which we believe is the most innovative technology that we have. It's what everyone is looking at at the moment, and also where we have the best opportunity to generate value for shareholders in the short to midterm. There is a question on circRNA: If your circRNA technology is so great and unique, why haven't you been able to get a deal like Orna and others? The answer here is very simple. Doing R&D and development takes time. Remember, we started this from scratch in January of last year. Normally, you would maybe work on programs like this for three, four years before you even announce that you have them and then bring it out. I would say that we've come very, very far in only one year and a year and a half, as I hopefully convinced you in the earlier part of the presentation. However, two aspects are playing in. This space is new. It's new to investors, it's new to partners. People are trying to figure out what is the best way of doing it? What technologies are there? Where can we apply it? So it's a maturing therapeutic area where not everyone has made up their mind how they want to utilize this and kind of exploring the potential. At the same time, we are, I have to admit, even though we make progress, we're relatively early, and we're working hard to get to proof of concept data package that's sufficient enough to be able to get to a partnership. What I can say is that we receive a lot of interest. Many companies and investors want to meet with us, listen to what we have to say. We also get feedback on what they think would be the best approach. Once we have a robust enough data package, I think there is a lot of interest, and we have already dialogues ongoing that are likely to enable us to transact. Beyond that, it's hard to promise anything, but my view would be that during 2024, it is plausible that with good data, we can find a partner in a specific therapeutic area or concept to drive forward. Finally, what is the expected burn rate and financing need following the switch to circRNA and the reduced organization? As I said, percentage-wise, our burn rate will be reduced. Of course, it will be significantly reduced when you compare it to having run a phase II, large phase II program, which was the plan. Comparing to that, we're gonna have a burn rate, which would have is now less than 50% of what it would have been. How large the burn rate will be depends, of course, on how quickly we recruit scientific staff and expand the activities. This is something we're looking into to find the right kind of balance. Obviously, the burn rate will be reduced. We'll report back on this in the Q2 report in August. Of course, with less burn rate, financing needs are also reduced. That's the advantage of working more on the preclinical side. Of course, these are programs that are less capital intensive than running clinical trials and clinical grade manufacturing. I don't think we have received further questions beyond that. I hope we covered what you were interested in learning more about. With that, I wrap up this company update, and we see you again after summer for our Q2 presentation at the end of August. With that, I wish you all a great holiday, and thank you from Circio.