Good morning. Welcome to Circio and beautiful Oslo. My name is Erik Digman Wiklund. I'm the CEO of Circio. Together with me today, I have CTO, Dr. Thomas Hansen, and we will provide you an R&D update as well as a company update, so welcome to you all. During this presentation, first I will provide a general background to our technology to bring everyone up to speed, then Thomas will take over, and he will go through the latest development on our CircVec platform, where we've established now what we call CircVec Generation 3.0, which takes our circular mRNA expression technology to a completely new level compared to previous generations, and we will also summarize the recent status of our in vivo work, where we're now really starting to see strong protein expression and expanded half-life of our circular mRNAs in vivo. At the end, I will discuss how we're planning to use this technology in a therapeutic setting. At the end, there will be brief information about the warrant exercise period and how to proceed to exercise warrants for those who are holders. With that, I will start the presentation. When we talk about circular RNA, it's important to understand the basic molecular biology. What we are doing is actually building a DNA format expression system, and this DNA carries the instructions for the body's own cells to produce the circular RNA. We give our DNA, either in a virus or a DNA format, deliver it to patient cells, and then inside the cell, the cell itself produces the circular RNA, and this circular RNA carries the instructions to make a protein. This you can utilize for a variety of purposes: genetic medicine, vaccines, cell therapy, etc. It's really a platform that can be deployed in multiple settings, which is unique and powerful. And we call this expression system CircVec. Now, how does this compare to other mRNA therapeutics and circular RNA therapeutics? And we try to illustrate that with this overview slide. So I believe now everyone is familiar with BioNTech and Moderna, who are the pioneers in mRNA vaccines. You can see that's on the bottom here. What they are doing is synthetic mRNA or in vitro transcribed mRNA, which is packaged into small particles called LNPs. Now, if you inject LNP format mRNA into patients, you get expression for two or three days. Now, that's really good if you want to make a transient protein expression or for a vaccine. And that's validated. It's been very commercially successful in the COVID vaccines. But it's only transient. It means you can only get a short window of expression. It's really not relevant in something like genetic medicine or a chronic disease where you need permanent expression, permanent delivery of the therapeutic. Circular RNA in the same format, synthetically produced, packaged in LNPs, gives you a robust advantage over the synthetic mRNA. The most famous company in this space is called Orna Therapeutics. What they are achieving is seven to ten days expression in vivo. That's what we have seen. Now, this is three to five times better than mRNA, but it's still only transient. It means this will be good for vaccines. I think it's likely to outcompete the linear mRNA vaccines and other situations where you want the transient expression, but it's still nowhere near what you need in the context of gene therapy or cell therapy or chronic disease. This is where we come in. With our CircVec technology, we are allowing the advantages of circular RNA to be captured in these other areas. We have built an expression system which can give you durability for months or years. We're not really competing against these other circular RNA companies. We are simply enabling the advantages of circular RNA to be leveraged in other therapeutic areas. I think that's a very important differentiation to make. This is also something that is starting to be picked up by industry and the life science media. There has been a lot of coverage of circular RNA. Recently also, people have gotten their eyes up to our approach. We've been featured in a number of international life science publications. This not only serves as a validation of what we're doing, but this coverage has also enabled us to really raise the profile and visibility of the company internationally and helped us access partners and investors, so with that background, I now hand you over to CTO Thomas Hansen to take you through some of the recent developments on our CircVec platform. Over to you, Thomas. I'll just quickly unmute. Thank you, Erik. Welcome all. My name is Thomas Hansen. I'm the CTO at Circio, and I'm happy to now take you through the technical development at Circio, where we have been developing and optimizing CircVec, and now we are at Generation 3.0, so that will be the first part. I'll also take you through some of the in vivo data that we have generated within the last couple of months, so the very updated data, some of this is from last week, so stay tuned for that, and then I'll pass the word back to Erik that will then take you through the last couple of chapters for this presentation, so the first slide, I think, captures nicely what we're trying to do at Circio and why we think the CircVec or circular RNA modality is powerful and interesting. And that's due to the stability of the circular RNA. So we basically measure a 15 times increased stability using circular RNA. So the stability is typically measured in half-life. So here we have the empirically measured half-life in vitro, which is 135 hours for circular RNA versus nine hours for mRNA. These estimates are likely sort of conservative due to some technical aspects, the proliferation of cells, the transient nature of the experiment. Not going to go into too much detail, but I'll revisit this number later in the presentation and discuss further why we think this may be actually an underestimate. But in either case, we see a 15 times enhanced stability. And what that means is when you run an experiment for a longer period of time, that stability kicks in, which makes the RNA accumulate over time. So basically what you see on the right-hand side here is an expression profile where we express a protein called Firefly Luciferase. You can measure that by luminescence, which is handy and easy. And what you can see for, you can see three different CircVec generation: 1.0, 2.0, and 2.1. And for all of them, you can see that the expression profile actually increases over the course of the experiment. And that is due to this enhanced stability of the circular RNA molecule. In contrast, we have the mRNA, which is very unstable here, nine hours. So that quickly sort of reaches peak expression. And then you basically just see a declining expression profile, which is explained by turnover of the system, turnover of the vector. So this is basically, it's peaked already here at 48 hours. For all the CircVecs, you can see that at the very last time point here, they are all superior. So we basically get from the very early design a slight advantage over mRNA, but we have almost 10 times higher expression when we use our CircVec 2.0, sorry, the 2.1 design. So greatly superior expression in vitro when we compare CircVec to mRNA-based expression. So just to take us a quick step back, sort of how did we get to CircVec 2.1? And I'll also introduce the 3.0 in a minute. But just to give you a brief insight into the biogenesis of circular RNA, I'll try to be very brief here because this can become very academic and complex. But basically, I just want to emphasize that circular RNA is a naturally occurring molecule. So this is being expressed all the time within our cells. And the way it's being produced is by a process called backsplicing. So if you have sort of a piece of DNA here, this may encode an mRNA, but at certain positions in our genome, you have this backsplicing occurring that produces your circular RNA. And what we can basically do, and what we did at Circio, we take basically a chunk of our naturally occurring piece of DNA, we put it into an expression vector that then has a promoter that drives RNA expression, and that would actually generate your circular RNA. So of course, we wanted to figure out what was nature's best design. Where do we get the best circular RNA expression naturally? So we did that by characterizing more than 100,000 different circular RNAs that you can identify and quantify using a technology called RNA sequencing. So here you can see each dot represents one circular RNA. So you can see here on the x-axis, that is the expression level of your circular RNA. And this is sort of the corresponding host gene. So that's not so important, but basically from that, you can tease out what circular RNAs are endogenously, are naturally most abundant. And likely that would also translate into that they have a very effective locus for biogenesis. So we screened and selected a bunch of these different dots here, looked how they performed in an expression context, expression cassette context, and then selected the best one for basically our founding father of CircVec. So that is sort of the generation one of CircVecs. So basically, schematically, it's designed like this. So you have a promoter that basically is there to just drive RNA production from a DNA vector. You have these RR sequences, which are naturally derived, so these are the sequences that you find in nature that stimulate and are necessary for the backsplicing to occur, and from that, you then generate a circular RNA, so that circular RNA, you can design as you please. To make the circular RNA protein coding, you put in what we call an IRES element, so this enables protein expression from a circular RNA molecule, and then you have what we call an ORF or an open reading frame, which is basically the recipe for the protein of interest, so that you can express any protein that you like from this technology, and if we try to measure how much protein then did we get from the CircVec 1.1 in this case? So this can be measured by a technology called a Western blot. There's many other ways to do this, but this is a very simple approach that we use in the lab. So here you can basically on a membrane see a band forming corresponding to the protein of interest. So in this case, it's a therapeutic protein. You have a control band that sort of shows you how much protein did you have in total. And this is the level of expression from CircVec 1.1. So this is, of course, not very informative, but it becomes a little bit more informative when we start to look at the development of our CircVec technology. So the CircVec 2.1 generation, the hallmark of that design was a new IRES element that we've identified through a series of IRES screens, which turned out to be much more powerful than what you'll typically find in the literature as the most effective IRES element. And what you can see here for that CircVec 2.1, sorry, the 2.0 design was a dramatic increase or at least a noticeable increase in protein expression. You can see the band here. The intensity is much stronger here compared to here. Then moving on, we focused on the flanking elements. Can we enhance the biogenesis of circular RNA by modulating some of these flanking elements? And yes, we can actually, so it's the same circular RNA that's being produced, but in this case here, it's produced more effectively. So we have more circular RNA molecules being formed, and that translates into higher protein expression as well. So you can see an even further enhancement of protein expression from CircVec 2.1. And now finally getting to the CircVec 3.0, which very interestingly was actually based on some novel discoveries that we did, where we can put in an auxiliary element, sort of a new element outside of the circular RNA forming cassette that actually turned out to boost expression very dramatically compared to the 2.1. So we thought this was so dramatic that this has to be like a new generation of CircVec vectors. And when we look at the quantification, we can basically see that that element increased the production or the protein production from CircVec four times compared to the 2.1. So you can see we've been through quite some development throughout the years at Circio, and we now have 27 times higher expression using our CircVec cassette than the very early design that we started off with roughly two and a half years ago. So this is extremely powerful. And I'd also like to just point out that current in vivo studies are being based on the 2.0 and 2.1 designs due to the fact that it takes a while to set up these in vivo experiments. So just bear in mind that we would expect four to eight times higher expression now once CircVec 3.0 makes it into a mouse model. So that is the current status in vitro. We are, of course, constantly working on improving CircVec. We are, of course, already now looking at 4.0 as the next milestone, but this is where we are currently, which we believe still is quite remarkable and very interesting. So to take you through the in vivo data, so one approach that we've been used a few times now in vivo is to inject DNA into the hind leg of mice. Here we used a normal Balb/c immunocompetent mouse. We can inject mRNA expressing vectors into one hind leg, in this case, the left hind leg. These mRNA vectors will, of course, express mRNAs that encode, again, the Firefly luciferase, so we can monitor luminescence. In the same mouse, we can inject CircVec, in this case 2.1, into the right hind leg, and then we can monitor expression over time in these mice. We did this at three different dose levels. I'll come back to that, but this is just one mouse here subjected to mRNA or mRNA vectors in the left hind leg and CircVec 2.1 in the right hind leg. And you can see here, if you just look at the left hind leg, mRNA starts off very strong at day two, peaks probably at day 10 or before day 10, and then it seems to decline in expression. And hardly here, which is the last time point of this experiment, we have hardly any detectable mRNA-based expression at day 170, so roughly half a year after the vectors were injected. In contrast, if you look at the CircVec 2.1 here, it starts off a little slower. It takes a little while to build up, but then the stability kicks in. You get a much higher expression. It may peak around four to five weeks into the experiment, and then it may also slowly decline. But still here, half a year into the experiment, very interestingly, we still see noticeable and high expression from the CircVec vectors. So a much better expression and a much more prolonged expression profile compared to mRNA-based vectors. If we quantify this across the different mice, there were four mice in each group and the three different dose levels here, we can see particularly in the low dose setting, we have a dramatic increase in expression from CircVec compared to mVEC or mRNA-based vectors. Still a very noticeable increase in the mid dose, but maybe at high dose, the difference is not as much. We believe that's due to some saturation of the system. But nonetheless, in terms of full chains, we still have almost twice as much expression in the high dose setting. So this is really high doses, so probably not clinically relevant. In the mid dose and low dose, we have from four to actually 15 times higher expression from CircVec at day 170 compared to mRNA-based expression. You can see the development. It builds up, and it may not even have peaked in terms of the full chain. If this experiment would have been, if we did this experiment for a longer period of time, maybe we would have gone to 20 times expression in the end. With such a great data set and all the data we get from these mice, we, of course, want to extract as much information as possible. If you use some bioinformatics and statistical modeling based on the expression profile, you can actually infer what is the expected half-life of the RNA in this situation. Here you can see we did the experiment actually just to show that showing two different settings. We did a similar experiment in immunocompromised mice as we did in immunocompetent. This is data from the mice you just saw. Basically here, if we try to infer the half-life from mRNA, we actually get a nine-hour, which is sort of the best estimate, although there's some level of uncertainty, but that is what you get when you use statistics, and that is completely on par with what we measured in vitro. Here the in vivo estimates and the in vitro estimates are very similar. We get eight hours in this experiment, but also very close to what we estimate in vitro. I think the setup and the approach is valid because we get this very, we actually able to re-identify what we knew in advance. However, if you look at CircVec, in both cases, we see a significantly extended half-life compared to the numbers we got in vitro. I think that boils down to the fact that what we estimated in vitro were probably an underestimate. This may better actually capture the true stability of the circular RNA. It goes from more than 200 hours to more than 600 hours, and in this case, a 75 times longer half-life, 75 times higher stability when we compare circular RNAs to mRNAs. I think that that's much more dramatic than we hitherto thought. Of course, we'll look more into this going forward, whether this is a better estimate and to see whether this modality is even more powerful than we actually thought so far. Another thing you can do with these numbers, you can then start to calculate then when do we expect peak expression from such a system. You can see with mRNA-based expression, already two to three days into experiment, expression would have peaked, and then it will decline from that point on. CircVec, on the other hand, it takes a while to build up, and the peak expression would be in this case from a bit more than one month into the experiment. So that, of course, also means that we need to run an experiment for a long period of time to fully get the true value of CircVec. So that's, of course, due to the very, very high stability of the circular RNA molecule. Now, we, of course, also need to get our vectors delivered. And one very popular delivery approach in gene therapy is the adeno-associated virus or the AAV virus. The common approach today in gene therapy is that this AAV virus will express an mRNA, and that mRNA encodes a protein. That's a very standard approach, and it's been approved in the clinic. There's a few different therapies using this approach. Now, what we want to do is to, of course, use CircVec in an AAV vector. Instead of expressing an mRNA, we want to express our very stable circular RNA from the AAV and then to get the full benefit of the circular RNA stability and get the enhanced protein expression. When we measure this in vitro and we subject cells to AAV vectors either encoding an mRNA or AAV vectors encoding a circular RNA, we also see an enhancement using CircVec. Not so much after two days, but as you just saw, it takes a while for CircVec to build up. And already after four days, we see twice the expression from CircVec. And I just want to point out that this is actually a 2.0 design due to the fact that AAV viruses take a while to manufacture. So it will always be a little slower to get the most recent technology into an AAV vector-based expression system. Now, when we inject an AAV into mice, we've done a study where we injected it into the tail vein, so systemic delivery, using an AAV that expresses CircVec 2.0 or expresses an mRNA. And this is driven by a muscle and heart-specific promoter. So what happens is basically you will only see signal in heart and muscle in these mice. So this is what you see here, CircVec 2.0, mVEC in a mouse here. And this experiment is ongoing. So this latest readout is from day 30. So this was actually last week. So this is an interim analysis. We plan to run the experiment for longer to, of course, get the full benefit of the circular RNA technology. But basically, you see that the mVEC and circular RNA looks very similar on these images. So this is a high dose on the top and a low dose on the bottom. And maybe easier to just look at the quantification here. You can see they are not separating at this point yet, but of course, we're hoping and believing that the CircVec over time will dominate and we get better expression from 2.0. But still, bear in mind that the 3.0 is expectedly five to 10 times better than 2.0. So when we get that into an AAV, we hope to get maybe one log increased expression compared to mVEC. So this is, of course, what we're working towards. But this is where we are at the moment. And we are actually quite pleased with on par expression, knowing that this is an earlier CircVec generation that we are testing. So this basically leads me to the summary in our ongoing RNA and R&D development. So for the CircVec platform, as I showed you, we have the CircVec 3.0 now with this additional element that boosts expression significantly. What we showcased back in June was a 2.2 CircVec design, which is a codon-optimized approach. This has not yet been included in the 3.0. So already now we have a 3.1 design that's ready to go and expectedly will be even more powerful than what I just showed you. We are working hard on getting the 3.0 into a mouse, either with the intramuscular hind leg injection that I just showed you and with an AAV vector. So this will hopefully be data that we can present early next year. And then critically, we are working on finding a patent to cover the 3.0 design features, which we believe are novel and a very unexpected result. So this is very good for patenting. Moreover, we are doing an in vivo screening program to test CircVec in different tissues and different settings. So actually today, we will initiate an in vivo experiment where we are using LNP-formulated CircVecs that will drive targeting to liver, lung, and spleen to test what is the expression profile from CircVec compared to mRNA-based expression vectors. So this is in part done in collaboration with CerTest and other delivery companies. And we are also testing CircVec in brain to see how that performs in CNS. Furthermore, we have recently entered or will be entering collaboration with different delivery companies that will enable non-viral and redosable delivery of CircVec into different tissues of interest. So we hope to have data on that within the next couple of months or the next half a year. And then, and I think Erik will touch upon that in a minute as well. We, of course, believe that CircVec is extremely powerful, but with the capacity internally, we will likely select one or two internal programs. That we will develop ourselves, and then we hope to establish partnerships in other adjacent areas during next year. But that is all from my part, and I think Erik will take over the next bit and drive you through some of the more therapeutic applications for CircVec. Thanks for your attention. And over to you, Erik. Thank you very much, Thomas, for that excellent overview. Now, why does this matter in terms of therapeutic development, and what can we use this technology for? The most obvious place where current technology struggles with durability and expression level is in gene therapy. So gene therapy today is suboptimal in the sense that it's not really potent. You need to give really high doses. They are often toxic and at very high cost. We expect that CircVec should be able to improve the potency of gene therapy by making more protein for a longer period of time, which would enable gene therapy to be developed for new diseases and also to be able to reduce the dosing and reduce the cost of existing gene therapy. So this is where we've chosen to start. We believe it's the lowest hanging fruit for the technology. High durability, high expression level gene therapy. And this can be done either with the AAV format, as Thomas just talked about, or in DNA systems with appropriate delivery technology. But this is a platform. It can be applied more broadly. We're starting to explore how CircVec can enable safer and repeat-dosable cell therapy. And we've established a VLP CircRNA system, which we're planning to develop in this area. We will be telling you more about this in the future. And then longer term, we see chronic disease as an important area, autoimmune disorders, obesity, these kinds of things where you need to have permanent expression of a biologic molecule. So this is where we want to take the platform over time. But for now, then the gene therapy is the lead area we're prioritizing for short-term developments. Of course, what we're talking a lot about now is how we can express protein for longer, and this is really the core functionality of CircVec. We can use CircVec expressing circular mRNA to make protein more effectively and more durably, and this is really important when it comes to gene therapy, as well as any other context like I just described in cell therapy or in chronic disease. However, CircVec enables us to add other functions as well. We can, at the same time, remove an offending mRNA or protein using a knockdown approach, so this is something you can add on in a context where it's relevant. At the same time, we can also use CircVec to neutralize disease-causing non-coding RNA, such as microRNAs inside the cells, so we have this setup where we can make customizable constructs for each specific disease. These can be either mono, bi, or tri-modal, depending on the mode of action that you require in specific disease settings. At the moment, we are doing work to explore exactly what is the best target tissue and the best target diseases for initial CircVec therapeutic development. So we have ongoing AAV experiments, like Thomas pointed to, and we have ongoing DNA, non-viral LNP-formulated DNA experiments. And we're also exploring other delivery chemistries. And we're testing these in vivo in multiple tissues. What we have just shown you is in muscle. That's where we so far have the best data. Heart, cardiomyocytes are similar to muscle cells, so that goes a little bit hand in hand. And we're also interested in lung and brain or central nervous system delivery. So all of these experiments are ongoing or starting soon, and we should have data during December, January, February reading out. And depending on where the results look the best, we will prioritize what diseases to move forward with. And on the list on the right are opportunities we identified in these different areas. And these diseases combined that I show you here represent a patient population of somewhere between 500,000 and 1 million patients, many of whom either do not have any therapies approved at all or are really underserved. So it's a massive unmet medical need in all of these areas. Now, the data we have so far really shows us a big advantage in muscle cells. So we've done analysis to identify what muscle diseases could be specifically interesting for CircVec development going forward. And we've identified these two candidates, limb-girdle muscular dystrophy and myotonic dystrophy. Now, these are quite frequent genetic muscle diseases that cause muscle wasting in different ways. They have 50,000 patients estimated in the USA and EU for limb-girdle, and over 100,000 are diagnosed with myotonic dystrophy. And there are no cures available today. Nothing is approved. And there is very little activity in the gene therapy space. So here we see both an unmet medical need, a business opportunity, and a technological fit for CircVec. For limb-girdle, mainly what you need to do is just make a lot of protein durably. And here we are envisaging a monomodal CircVec to just maximize protein expression. Myotonic dystrophy is a little bit more complicated. And here we think we can really benefit from adding all of these features I just described. So here we're exploring whether we can build tri-modal functionality to really have a multi-pronged approach to bring into the clinic that would be really unique. Maybe a bit more technologically advanced and scientifically more challenging, but a completely differentiated product candidate. So this is what we are working on at the moment to bring into in vivo disease models next year and eventually into clinical development. Now, let me summarize everything you heard today in simple terms. Take-home messages that you should remember: CircVec 3.0. So that's our new generation. This is really powerful. It's 27 times better than CircVec 1.1. And remember, CircVec 1.1 was already 50%-100% better than mRNA expression. So already then, we were outperforming mRNA by one to twofold, depending on the situation. And we've incrementally improved that, and now we're at the 3.0 generation, which is 27 times better. It's four times better than 2.1. And all the in vivo data Thomas showed you is with the 2.1. So we're really excited now to bring the 3.0 into in vivo studies to see whether this in vitro advantage also translates in vivo. Half-life. This is important. Now, we've shown before 15 times longer half-life in vitro of circular mRNA versus linear mRNA. And actually, in vivo, it turns out it's much longer. We see up to 75 times longer half-life of our circular mRNA. And this is really important because it means the mRNA you produce can hang around for longer and make more protein. The peak expression is after 38 days instead of two. If this translates in vivo, we believe everyone is going to switch to circular mRNA-based expression in the future. AAV, this is what is the lowest hanging fruit from a technological perspective in terms of a gene therapy to bring to the clinic. We validated that our AAVs work in our 2.0 generation. We get sufficient protein expression. They are on par with mRNA until day 30. We're now following these to see how they perform over time. We anticipate we're starting to see an advantage as this experiment runs on. And now we're rapidly building 3.0 generation AAV constructs that should have boosted expression over what we have seen to date. And finally, muscular dystrophies, we have identified two of these specific diseases representing a patient population of 150,000 patients in total that we think our data suggests CircVec could be ideally suited for. So hopefully that provides you a broad overview and update of what we're doing and explains why we're excited about the technology we're developing. Now, at the end, I will touch upon the exercise of warrants for those who hold those. Now, as you may recall, we did a rights issue back in July 2024. And in that rights issue, everyone who subscribed was also awarded warrants. And the exercise period for these warrants started this morning, December 4, and it lasts for the next two weeks. The warrants are exercisable at the price of NOK 0.6. There are a total of 13.8 million warrants outstanding that can be subscribed for. So this means that the maximum gross proceeds from the warrants will be NOK 8.3 million. And we will publish the outcome of the warrant exercise period on December 19. Shortly thereafter, the shares will be settled for those who have subscribed. Please note that because of the holiday period and several public holidays, that process may be a little bit delayed, but the subscribed shares will be settled as soon as practically possible following the publication of the outcome. How do you subscribe? There is information published on our website as well as here. You need to complete and sign the warrant exercise form, send it to us by email. This is available on the webpage via our press release, and you can also click on the link in this presentation. You then need to transfer your warrants from the account you hold the warrants in to this account number at Nordea. And then in parallel with that, the subscription amount needs to be transferred as well to Circio's bank account as described here. The amount will be the number of warrants multiplied by NOK 0.6. Importantly, the funds need to be in the Circio bank account latest by the end of the subscription period, which is 4:30 P.M. on 18 December 2024. Please don't hesitate to get in touch with us if you have any questions. We have already gotten several questions around oversubscription or investors who did not have warrants who want to subscribe. In theory, oversubscription here is not possible. However, the warrants are transferable, so it means if someone holds warrants they don't plan to utilize, they can be transferred to someone else. You can either sort that out directly or contact us, and we can help facilitate it. We will also do what we can to try to accommodate any additional interest for investment or oversubscription here. So please get in touch with us if that's the case. So hopefully that explains how it's all going to work. And with that, I think we can move to Q&A. And we have a couple of R&D-related questions as well as others, but maybe we start with the R&D questions for Thomas. What are the upcoming milestones for CircVec development, and when do you expect to enter the clinic? Thomas, do you want to give an answer to that? Yeah, so thanks for that question. So that's, of course, an interesting question. So yes, Erik just brought up a slide that I think highlights our timeline thinking. So of course, now we're at the second half of 2024. So we have this AAV9 data that I just showed you and the 3.0 generation, sort of a technical proof of concept. So this has all been done already, more or less, and we set up this brain experiment. But for next year, we will do a number of in vivo experiments using the 3.0 design. We will start to move in some more disease-relevant models, for now focusing on some of these muscular dystrophies that Erik just mentioned, and we'll do some additional optimization. So we hope that the plan currently is by the mid-2026, we'll have a lead candidate selected, and then that will then enter into these R&D enabling study, which will, depending a little bit on the lead candidate design and format, will probably be 12-18 months. So I think the current estimate is within the next three years that we'll be able to enter the clinic with a CircVec design. So I hope that answers the questions. And I can maybe add that we are really working on two tracks in parallel. One is the in vivo testing and understanding technologically how CircVec works, and then bringing it into disease-relevant models to understand how it may improve disease outcomes, and then in parallel, we're also continuously improving our platform and testing different delivery systems, so these two tracks move along in parallel, and then eventually what will happen is that we merge them together, take the best delivery, the best vector formats, target disease, and put it all together in order to create a lead therapeutic candidate, and once you have that candidate, you then need to start manufacturing and regulatory enabling, or what we call IND enabling studies that allow you to put it into patients. That typically takes 12 to 18 months before you can start dosing patients from you have the lead candidate, depending on, again, what is the vector format, the disease, etc., that creates certain changes in time and budgets. Hopefully that was the answer to that question. Next question for you, Thomas. Can you explain in layman's terms what the expected advantage will be for CircVec versus current mRNA gene therapy? And how happy are you with the 3.0 performance? Yeah, so let's see how I will do with layman's terms, but basically, we talk a lot about half-life, but basically what that translates into is more and better expression per vector copy. So let's say we have a 10 times better half-life or 10 times better expression from CircVec compared to mRNA. That will either translate into a 10 times better clinical benefit. It may even be that you can now address diseases that were otherwise unaddressable with an mRNA-based approach due to inferior expression profiles. So that would be one aspect that now that this may open new avenues for gene therapy. Or the other aspect, which is maybe more low-hanging, is that in a number of gene therapies, dosing is actually an issue with you have dose-related toxicities. So if you have a 10 times higher expression based on CircVec, perhaps it's possible to now reduce dosing tenfold and then reduce those dose-related toxicities and make a safer and better product. So I think these are the two avenues that we believe would be where CircVec can really shine, and that is better clinical benefit and/or better safety, and with the 3.0, I believe that's the second half of the... So I'm, of course, very excited by the 3.0, particularly because, you know, as a scientist, we try to understand nature. And I think this having something completely novel and in part unforeseen, having that effect on circular RNA biogenesis, I think that not only is very interesting from a technical perspective, but it's also very interesting from a natural sort of biology perspective. So I may be inclined to look into whether this is some overseen, overlooked feature also for the endogenous circular RNAs that may actually be expressed, whether this... So how this all boils together. So I'm very excited about this 3.0 for many different reasons, not only the enhanced expression, but also with the biology and all the questions that actually emerge from such a discovery. So I'm a happy guy. So am I. Thanks, Thomas. I think that nicely leads into the... We had several questions on business development. Are you on track for a business development deal in 2025, as communicated? This is always a very difficult question to answer. It takes two to tango. What I can say is we are getting substantial interest for our platform. We've met with over 100 companies. Several have requested follow-ups. We're under a CDA with multiple. And in many cases, we get specific requests for certain data or applications that the company may be interested in. And then we address these questions, generate the data, and go back to them. So this is ongoing work. We had BioEurope, which was in the early November, where Lubor and I had a very hectic agenda meeting. Many different companies were now building on this new data, as well as BioEurope, to travel to J.P. Morgan in San Francisco in January to follow up. Precisely when our data package is sufficient or there is a good fit is somewhat unpredictable. But I think what I really sense is that the current data we have is making people believe more in what they're seeing. We have now multiple settings, multiple doses. It adds to the body of evidence and the credibility. And the key now is probably to show an advantage with a specific vector format such as AAV or in this disease setting to really get someone to move on with this. But this is ongoing work, and Lubor and I are very positive that this definitely is partnerable. And importantly, it's a platform. We can deploy it in multiple areas. So there is plenty of room for us to move our own programs forward and then partner in adjacent areas. I think at the end, we maybe address some questions around financing and Atlas. We frequently receive these questions. How is the Atlas financing working going forward, and what is the number of outstanding bonds? So the agreement with Atlas, the convertible bond financer who's supporting the company, is that they are covering the company's cash runway until June 2025 at the level of NOK 4 million per month. This helps us have a predictable cash runway, and we access the capital on a month-by-month basis. Going back to the warrant exercise period, if we get more funds during the warrant exercise, then that means we can rely less on Atlas. So we use it only carefully on a need-to basis. To answer the second part of that question, there is currently NOK 24.5 million worth of outstanding convertible bonds that can be converted into shares in the future that are held by Atlas. That includes the December tranche, which we announced earlier this morning. We draw the December funds of NOK 4 million. So with that, I think we covered everything. Thank you all for tuning in to the presentation. Hopefully, this was informative. As always, get in touch with us directly if you have any questions. Thank you from Circio. Thanks. Thank you.