Circio Holding ASA (CRNA) Earnings Call Transcript & Summary

Good morning and welcome to Circio. My name is Erik Digman Wiklund, and I am the CEO. And 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 first quarter, 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 head count reduction of roughly 40%. And our operations are mainly now scientific and based at the Karolinska Institute 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 are doing and the data. This is for 2 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. And 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. So far, we've shown that our circular RNA designs in our setup have a 15x extended half-life, as compared to linear mRNA. And half-life is one of the major drawbacks, and short durability, of mRNA; and this is really where circular RNA can make a difference. And we are able to show that this in our system clearly is advantageous. We've, to date, filed now 2 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 3 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 2 investigator-sponsored trials, 1 in the U.S., at Kansas university; the second, at Oslo University Hospital. The first patient has been dosed in the Kansas trial, and 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, but there is one exception: RNA deals. And as you can see here, actually RNA deals even in 2022 and '23 has been significantly larger total deal value when comparing to pre-pandemic levels. We've seen roughly USD 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. And this just shows that there is strong interest in this. It's -- 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 and, I think, really opened people's eyes to this space, both raising some significant financings. What they are doing is making synthetic circular RNA. They produce circular RNA in a factory. And the idea is you use then the circular RNA as a kind of circular mRNA format that they plan to bring into patients. And 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 2 significant financings in the U.S., Orbital Therapeutics launching with a $270 million Series A and then subsequently ReNAgade Therapeutics with a $300 million Series A. Both of these are kind of [ broader placed ], but a significant component of what they communicate that they will do is centered around circular RNA delivery, so this is really a field that is happening right now. Why are people so excited about circular RNA? Well, 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 circular RNA doesn't have any free ends, so this PAC-MAN, the exonuclease, doesn't have anything to latch onto. And this means it can -- it's resistant to this degradation mechanism and therefore has massively improved stability. And this is really what's getting people excited. You can utilize this to drive an enhanced protein expression. You get extended RNA durability. In addition, because it's stable, you can build in other functionalities such as microRNA sponging, which is a well-described function in the literature, as well as other regulatory formats that you can build in, so 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 the 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. And as far as we see, this is a unique angle that no one else has been taking, so far. And 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. So the concept is we make a DNA vector. It's injected into patients, and 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 genetic cassette late last year. And then we filed additional IP relating to how we deploy this in specific vector types, so 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. And here we've done several analyses and figured out exactly what we think is the best way to design the circular RNA to achieve long half-life, enhanced protein expression; and also demonstrating that we can achieve these other functions as well. So 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 15x extended half-life versus mRNA. In this experiment here, our mRNA had 9 hours half-life, which actually may be a little bit longer than you would normally expect. Our circRNA had 135 hours. That's 15x extended. On the right-hand side, you can see in time course how this plays out over time. So 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. It's 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, but 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 hour is actually capable of producing more protein than the mRNA's. This shows that 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 were looking at the protein level compared to the RNA level at 96 hours, but again it's -- proves the point. And 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. So that's important. The in vivo experiments 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. So 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, so 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. And based on this analysis, you see on the scatter plot in the lower part here we picked the top 10. So 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. So we took those top 10 natural loci and we tested them in our expression system. We called them then L1 to L10 in this graph. On the right-hand side, we'll show you the top 4. So L1 to L4, you can see actually it's L1. Our top prediction turns out to be, by far, the best. So this locus #1 is three- to four-fold better than everything else we found, so we picked this as our lead candidate, the locus 1. So we took then the natural sequence and we tried to express protein as well. On the right-hand side then, in this [ gel ], you see also the L1 is better at expressing protein. So then we say, how can we prove this further? So we took the natural L1 structure or DNA sequence and then we've optimized it. So we played around with various features and tried to make it better. And if you look at the top-hand graph here, you can see we've actually been able to improve on this roughly tenfold, so 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. And 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 are 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, yes, and this is what we are moving forward with. Of course, we're trying to optimize that even further, but what we've then done is taken here the best one from the top part, combined it with this D4 design of the circRNA. And this brings us what we call circVec V1. And on the graph on the right-hand side -- or sorry. On the [ gel ] on the right-hand side, you can see how circVec V1 is performing compared to mRNA. So we have a V1, a V2 and 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, so our circRNA beats the mRNA, but you need to design this right. If you don't design it well, you can see, in V2, the protein expression, as a sort of negative control, is much less efficient. So this shows you, you need to understand what you're doing and you need to optimize this well. And this is 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, and now we view this as a general system that we can deploy in various contexts. So 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 in 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. So 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? And we've also established additional regulatory functions that we now know how to do and can build into the system, such as, for instance, microRNA sponging. And then several of these, we are moving now into in vivo experiments to see how they function in an animal model. And we're also working on combining multiple of these features together, so as you can see, we've made significant progress on all these fronts. So where do we aim to deploy this? As I mentioned before, we see 3 major areas: cancer gene therapy. This means delivering proteins, therapeutic proteins, into solid tumors using our platform. So 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 into the clinic 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 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. So 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. And I think this is maybe where we observe in -- 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, so we're currently exploring how we best can deploy our setup there. So 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 an early pioneer of the field and probably the most experienced circular RNA 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. And 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. So that summarizes where we are on our circular RNA program. Moving on to TG01, our KRAS vaccine. This has also made progress in the -- during this year. We have 2 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 within 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, so 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, yes, as now the kind of first hurdle of this first patient is passed. This trial, we're testing both TG01 monotherapy as well as a PD-1 combination with PD-1 supplied by our strategic collaboration partners at Agenus. The second study is that Oslo University Hospital, and this study has received NoMA approval. It's now actively enrolling. In fact, the first patient has been enrolled, and we anticipate very soon this patient will be dosed. In this case, we're vaccinating patients following first-line treatment. And we pick patients that didn't get a complete response and then 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, so this will give us important monotherapy data. And it's the first time we combined -- where we bring TG01 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, so 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. So 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, so this means the required bandwidth on our end and the finance or money we need to put into it all is also limited, so it gives us a chance to keep developing TG01 at low cost to Targovax and allowing us to focus what we do mostly on our circular RNA 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 of -- 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 2 reasons, I believe. It's because we have been testing vaccines maybe in too-late-stage patients. They have been too sick, didn't really have a chance to recover [ or mount ] a proper immune response. The second reason is that the vaccines have not been combined with anti-PD-1, and that's what Moderna did. They went earlier. They went in post-surgery melanoma setting. They combined with anti-PD-1, and 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'll show on the picture on the slide is called ELI-002. It's from a company called Elicio. They vaccinate against 2 KRAS mutations. And interestingly, what they showed -- this is in exactly the same population that we are treating, post-surgery pancreatic cancer. And they show that this vaccine, dealing with 2 KRAS mutations, actually was able to clear circulating tumor DNA from blood. So they look in blood. Can they detect DNA from tumor? And 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. And yes, you see here. Actually in 7 out of these patients, it's a complete clearance of the ctDNA. Now this is really important because this shows that idea -- our concept in the Kansas trial actually can work. We believe we have an advantage because our vaccine covers 7 mutations versus just 2 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. So this clearance of ctDNA or the biomarker reduction was achieved only with a monotherapy. We think, once you bring in a PD-1 inhibitor, it will be even greater. This data makes us even more optimistic about our Kansas trial in particular and that vaccines can work. And importantly here, we are in earlier setting. It's the same in the myeloma trials. We're testing this out in earlier-stage patients. So now maybe this is the way to develop vaccines. And hopefully, this trial will generate robust data which will allow us and attract future partnerships; and really bring this program, TG program, forward. So 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 organization's. 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 head count. Obviously this also comes with cost advantages, so our payroll costs are now lower. As -- it also means that our cash burn rate is lower, so we expect going forward less cash burn, less financing needs. So 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 -- 2 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. This -- on this slide, you see now the new management team. It's now more of a scientifically oriented management team. Myself and Lubor Gaal will remain CEO and CFO and 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, 2 years. And she will assume the role of Head of Clinical Development, taking over largely the responsibilities of Lone. And she will manage the TG program as we go forward, but obviously the total capacity needs in that department are now reduced. And 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. So 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. And we are all very enthusiastic about taking Circio forward in this new chapter. So with that, I wrap up the formal part of the presentation and we will take Q&A. We have received several questions beforehand by e-mail. And we were -- 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 e-mail 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've grouped these [ into 2 ] components and translated into English for everyone to understand, but we will try to cover all the aspects that we have received. So with that, I'll move to the Q&A.

And first, there was an article about the circRNA company Laronde published earlier this week by 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 rather dramatic and, of course, very, very unfortunate for Laronde. It seems like there have been problems with the integrity of the data and what they've claimed the technology can do. Now we do things differently, as I explained. We make vectors that make circular RNA inside the cells, so in essence, you could view this as potentially an advantage for our approach or confirming that our approach might be even better. One of the issues here is that apparently the circular RNAs are not as stable in in vivo as has been claimed. What we are doing is bringing in vectors. The vector will have a stability. We'll keep supplying the circular RNA inside the cell over time, so we expect that we will have significantly better durability overcoming this kind of shorter-than-expected turnaround of a synthetic circular RNA. So 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 is trying to figure out exactly how good these are, but potentially overall it lends some validation to our approach being potentially advantageous over bringing in synthetic circular RNA. Secondly, we have summary questions here on Atlas. So of -- as you recall, we have a convertible bond facility set up with an investor in London called Atlas Capital Markets. And this is for up to NOK 300 million over the next 3 years that we can draw in tranches. 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 have -- 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 a miscommunication. I can confirm that Atlas has corrected this breach and repurchased the shares to bring back then the overall volume to 25%. And 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. And we appreciate 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. And we are continuously tracking this in house. I think Atlas themselves are tracking it as well as you, 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 hoped and anticipated it will do. Actually now the share price is trading higher than where both of the previous conversions have been, so 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, so far, we are happy about how this is playing out. We're seeing the facility is 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?" So since the announcement that we were to deprioritize ONCOS-102 in favor of the circular RNA program, we have been in dialogue with potential investors and partners regarding external financing of the program. Unfortunately, we have not been able to generate sufficient interest to be able 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 to -- into development and subsequent registration. If we bring it forward, we want to do it in a proper way in a larger randomized setting. A bit of the issues we've faced 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. And these, 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, in 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, but 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 mid-term. Then 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 we'd maybe work on programs like this for 3, 4 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 1 year, 1.5 years, as I hopefully convinced you in the earlier part of the presentation. However, 2 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 are kind of exploring the potential. At the same time, we are -- 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, so once we have 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, yes. Beyond that, it's hard to promise anything, but my view would be that during 2024 it is possible 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 -- a large Phase II program which was the plan. So comparing to that, we're going to have a burn rate which would have -- is now less than 50% of what it would have been. How large a burn rate will be depends, of course, on how quickly we recruit scientific staff and expand the activities. And this is something we're looking into to find the right kind of balance, but obviously the burn rate will be reduced. We'll report back on this in the Q2 report in August. And of course, with less burn rate, financing needs are also reduced. So that's the advantage of working more on the preclinical side. And 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. So with that, I wrap up this company update. And we'll see you again after summer, for our second quarter presentation at the end of August. So with that, I wish you all a great holiday. And thank you from Circio.