Good afternoon, everyone. I'm Josh Bowers from the London Healthcare Banking team. It's my pleasure today to introduce Michael and the team from Nykode. Give a brief presentation, you all know the drill, and then some Q&A afterwards. With that, hand over to Mikkel. Thank you very much, Josh, and thanks for the invite to the entire JPMorgan team here. Always a pleasure. Today, we're gonna go through an introduction to Nykode Therapeutics, give an insight into the technology and the lead programs, as well as our growth strategy. We assume you're all familiar with the forward-looking statement. On that note, we'll skip forward to a very brief, high-level introduction to Nykode. Nykode is a clinical-stage immunotherapy company. We are entirely focused on leveraging our unique proprietary immunotherapy platform, which, in one sentence, targets the antigens to the antigen-presenting cells. And we use that to drive a immune... a tailor-made immune response, which we right now focus in the field of oncology and autoimmune diseases, but we also have applicability in the infectious disease settings. From the oncology point of view, our platform is validated and de-risked through very strong clinical responses, showing both a long durability of the immune responses, as well as very convincing survival data. We have also announced a ambitious, aspirational focused strategy to take our lead asset, VB10.16, forward towards the market in advanced cervical cancer, as well as head and neck. We see and have embarked also on reaping the further commercial potential that is in the early stage adjuvant setting for the same cancer types. We've seen, on the back of the interesting data that was shown from some of the mRNA companies also, interesting data in the early setting. So we also want to check what we can do with our technology in the mRNA setting, and that also showed that regardless of whether we use DNA or mRNA, we still see the same benefit of applying our technology to the cancer vaccine. We've embarked on exploring the same modality in the autoimmune disease setting. I'll show you the mechanisms of actions for each of those settings in a couple of slides, which, of course, constitute as significant commercial upside for us as the oncology field. We believe in partnerships and have entered two strategic partnerships, both transformational and sizable, with top-tier biopharma companies from the US: Genentech in 2020, and Regeneron in 2021. Company is well-capitalized, with $159 million in cash at the end of third quarter. We did a private placement, or directed placement, sorry, in October last year, and listed at the Oslo Stock Exchange. So this cash gets us easily the next couple of years into the future to really realize our growth strategy. As the company grows, we've also been focusing on building a leadership team and organization with a solid track record in drug development, drug discovery. I'm happy to have with me here, both the Co-Founder and Chief Business Officer, Agnete, sitting here, and behind her, the Chairman of the Board, Martin Nicklasson. So if there's time, they're also happy to take a few questions in the end. Just a quick look at our partnerships with Genentech and Regeneron. Back in 2020, we entered the partnership with Genentech, centered around our individualized cancer vaccine. I'll tell you more about that program later, VB10.NEO. That deal gave us $200 million in upfront and additional access to potentially $550 million in downstream milestones, plus, of course, royalties on sale. The year after, we entered a multi-program deal with Regeneron, centered around five different programs, three on oncology, two on infectious diseases. That program gave us $50 million upfront, plus additional $875 million in potential downstream milestones, and again, royalties on sales. So of course, these deals, we are immensely proud of, and also serve to both validate and de-risk the entire investment case. Quick look at the pipeline, which is really a testament to the diversity of our assets, as well as our platform's ability to quickly and effectively generate new assets that we can take into development. So you'll see us spanning a nice range of different tumor types, both with our off-the-shelf vaccines, as well as the fully individualized. You'll also see us present in the infectious disease with the two Regeneron programs, as well as moving slowly into the autoimmune disease program. Look at it a little bit differently, when we look at just zooming our oncology programs, we really see, our technology, playing out both in the advanced recurrent metastatic setting, as well in, as into the more early stage settings, where you will see most of the other cancer vaccine companies focusing. So we will be focusing on building a balanced portfolio of assets that spans both the advanced, setting as well as early-stage cancers across a number of tumor types, in the future. Quick look at the mechanism of action. The fellow you have on the left side of this slide here is really the core of our technology. We we call it a Vaccibody. It's a fusion protein consisting of three different domains. In the lower dark purple part, you have the antigens, that's the ones we want to create an immune response to, or decrease an immune response to, if we're talking about the autoimmune field... In the middle, we have a dimerization unit, which function is to make sure that the protein comes together as a homodimer. That increases the strength of the signal. And in the top you have what we very often refer to as the secret source. That's the targeting unit. The targeting unit will always be a ligand that binds to a receptor or surface molecule on the antigen-presenting cells. That's the core of our technology. In all our cancer vaccines, we use the CCL3L1 molecule, or the MIP-1 alpha. It binds to the receptor on the antigen-presenting cells, and it has two very interesting features. First, it's a chemoattractant for APCs, so when it's injected into the environment, you'll find an influx of the APCs coming to the site of the injection. Once it binds to the surface of the APCs and internalize, because it is internalized via the CCL3L1 molecule, it activates not only the classical pathway, which leads to CD4 activation, but also the cross-presentation pathway, which leads to a very strong and broad CD8 T cell response, which, of course, is exactly what you want in a cancer vaccine. Now, we don't administer the product as a protein. We could. Our technology and our IP platform is agnostic, but for various different reasons, we are also coming to it later, we administer it as a DNA plasmid, and we inject it into the muscle via a needle-free injector. It enters the muscle cells, and gets expressed and secreted into environment, and then, we have the whole immune response starting from there. We could also do this, as an mRNA. We've shown that in preclinical models. It gives the same added benefit. We could do it via viral vector, or we could do it as a, purified protein. If you take a, a deep dive into our lead asset, VB10.16, is a, therapeutic cancer, a vaccine candidate, directed towards via HPV16, driven cancer types, so, mainly, head and neck and cervical cancer, plus a host of additional cancer types that are driven by, by the virus. We include in the antigen part, the E6 and E7 protein from, from the, HPV16 virus. Same targeting unit as we use in all our cancer programs, CCL3L1. This program is currently in phase II, wholly owned by Nykode. We're not giving away any commercial rights to this program at this time point. Now, HPV16-driven cancer type does represent a huge commercial opportunity with a high medical need. We are focusing on cervical and head and neck to begin with. Cervical is the lead indication for us, and as you see on this slide here, we see more than 130,000 new cases of HPV16-driven cancer types alone in the U.S. and Europe each year. Approximately a third of these are cervical cancer. Very poor prognosis, so less than 5% of the women that present with recurrent or metastatic cancer are alive after five years. We also see, and that's perhaps a little bit surprising, increasing incidences of the HPV16-driven cancer types. We get this question very often, whether the prophylactic vaccines and the rollout of those are not slowly undermining the market for this kind of therapeutic vaccines, and I'm inclined to say, unfortunately not. We do look at still increasing incidences, partly due to the fact that the rollout of the vaccine is not as good as we had hoped for, but also because of changes of lifestyle. So for the next 10 years, we will continue to see an increasing addressable patient population for this vaccine. We did, back in 2023, release the data from our VB-C-02 trial, phase II trial, where we assessed VB10.16 in combination with Roche's checkpoint inhibitor, atezolizumab, in patients that were second-line or more, with advanced cervical cancer. What you see on the left is the key data, objective response rate, PFS, and overall survival for the arm that had vaccine plus atezolizumab, compared to the published data for checkpoint inhibitors in a comparable patient population. On the right, you see the data from TIVDAK, which we contemplate will be the competitor for us when we reach the market. So you see, with an objective response rate of 29% in the PD-L1 positive patient population, which is the one we focus on here, versus for all the checkpoint inhibitors, between 16, 17, and 18%, and a median overall survival, not reached at the time point of the reporting here, so estimated to be more than 25 months, versus what you see with the checkpoint inhibitors in monotherapy, 10-13.9 months. We see a near doubling of the numbers that you expect to see with a checkpoint inhibitor monotherapy. Compared to TIVDAK, as I said, which will be our competitors. Also here, we see a very strong competitive profile, which makes us, of course, very comfortable we have a competitive as we move forward. We have, on the back of these positive data, devised a growth strategy for our lead asset, where we will continue on a fast path to market in the advanced cervical cancer setting. So the next trial that we are starting now is VB-C-04. Here we will test checkpoint Sorry VB10.16 on top of atezolizumab in patients that are refractory to the first-line treatment in advanced cervical cancer, so checkpoint inhibition, so plus chemo plus minus bevacizumab. This trial has been discussed with the FDA. We have approval from the IND, and the FDA knows our plans for this program here also, and the first patient will be enrolled imminently. This, of course, represents for us a faster market strategy, so a shorter goal for, for getting the, to the market, and the patients as fast as possible. But we're not stopping here. We've also initiated the first step into head and neck with the VB-C-03 trial. So it's gonna be, vaccine VB10.16 in combination with checkpoint inhibitor in first-line patients, head and neck, testing two different doses. On the back, of course, we'll decide how to, to move forward in, in that program also. And we've announced the start of VB-C-05, or at least the, the, the planning of the VB-C-05 trial, which is our first expansion into, the locally advanced, so the adjuvant setting of, cervical cancer, which of course, represents an even larger commercial opportunity for VB10.16. Out there in the future, we also see opportunities in the locally advanced head and neck setting, in the other hosts of cancer types that are driven by HPV16, plus also the PD-L1 negative patient population, but we have not disclosed any plans for those patients, populations yet. So in together right now, our portfolio of trials includes 4 different trials for VB10.16. VB-C-02 is the one we reported data from in 2023. Next milestone from that one is we will be updating on the overall survival data in the first quarter, so imminently. VB-C-03, first step into head and neck, we have started that trial. So we contemplate to have enrolled, and reached the stage where we can decide which dose to move forward in part two by the end of this year. VB-C-04 will be dosing the first patient imminently. We do expect to have finalized enrollment of that trial in 2024, and be able to report data in the mid of 2025 for that program, from the interim, for the first part. So that's 30 + 30 patients, in a randomized setting. VB-C-05, we are in the planning, of that one. We contemplate that will also, be a combination trial, on top of a checkpoint inhibitor, and we'll be updating the market on both design and choice of checkpoint inhibitor, during this year. Moving from our lead asset, VB10.16, into our individualized cancer vaccine, VB10.NEO, which we run in collaboration with Genentech. So this is the concept, for those of you who follow Moderna, you will be familiar with. This is where we take the biopsy from a patient who presents with a solid tumor. We do a whole genome sequencing, we determine the somatic mutation specific for that patient, and then we use our proprietary algorithm for selecting the best epitopes to target with our vaccines. We then incorporate that into our vaccine technology, which we know drives a long, strong, and broad CD8 T cell response, manufacture it, and of course, then give it back to the patients. We also think that because we use DNA as the modality here, we will have advantages towards the mRNA companies, both in terms of fast production, as well as the cost of goods when we get closer to the market. Here, we have been engaged in two trials, N-01, and we have reported the immune response data from, and the N-02 trial is the one we're running together with Genentech, where we're testing two different doses of VB10.NEO on top of Genentech Roche checkpoint inhibitor, atezolizumab. We did earlier report immune data from the N-01 trial. Here is just a highlight. On the left graph here, you'll see a very consistent, broad response to the epitopes that we include. So we include 20 epitopes into each vaccine, up to 20. You see the percentages of epitopes that are shown to be immunogenic in the patients afterwards, with an average of 53% of the epitopes showing immune responses in the patients. We are far beyond what we've seen reported from the other individualized cancer vaccines. On the right, you see the immune response over time, and two things worth noticing here, a very consistent, slow build-up of a long, sustained immune response while on treatment, but as importantly, also post-treatment, a very strong and durable immune response with a very slight decline over time. Which, of course, tells us we have a technology that is very applicable, not only in the recurrent metastatic setting, but also as we think of moving into the early stage, locally advanced setting across the tumor types. Lately, we reported the expansion of the pipeline by including also the NYK-111, a preclinical program in the colon cancer setting here. Here, we are really using our technology to address again a huge unmet need, as you know, but also play across various disease settings here. So we see this cancer vaccine potentially being used both in the setting of high risk polyp patients, which have a very high likelihood of or risk of developing colon cancer, but also in the actual or advanced colon cancer setting. This program here takes advantage of some of our latest technology developments, what we call the fourth module or second generation vaccine. So it's the first time we would be taking the second generation vaccines into the development. We have earlier shown, and as you see here, you will see the fusion protein, the Vaccibody molecule in the middle with the three different domains in the protein. We can in the DNA plasmid add additional cytokines in that, which will be released created in conjunction with the vaccine. So not together, not attached to, but in the vicinity, where we also release the Vaccibody that then attracts the antigen-presenting cells. And we've shown this to drive a stronger immune response preclinically, and we've also shown this to turn into better protection in the challenge models with tumor. So here we're very excited to be taking this technology, this second-generation technology, into development for the first time, potentially with this NYK-111 program. Skipping to our technology as application in the autoimmune disease fields. So you recognize this figure from the start of presentation, where we're talking about oncology. When we look at the autoimmune disease setting, it's basically the same concept we use here. We are focusing on the core of our technology, the Vaccibody protein, which is again a fusion protein of three different domains. We changed the targeting unit here, so we are not addressing the traditional APCs that we would be addressing with the cancer vaccines, but we instead target the tolerogenic dendritic cells. And we've shown and reported that at the last year, that we can by using this approach have an upregulation of antigen-specific regulatory T cells. Recently, at our Capital Market Day in New York last year in September, we also reported that that upregulation of antigen-specific regulatory T cells translates into benefits in our preclinical model. The first one we show here is the NOD model, which is a model for type 1 diabetes, where we included the pre-proinsulin as the antigen targeting unit that are not yet disclosed, but attaches or addresses the tolerogenic dendritic cells. And then also included in this setting here, up to three different of our fourth module technology, the same that we also use, as I mentioned before, in our NIC-111 program here. And what you see on the yellow curve is the NOD mouse spontaneously developing type one diabetes, similar symptoms. On the triangular graph in the middle is when we include our vaccine without any fourth molecule, you see a significant delay and reduction of the risk of developing the type one diabetes symptoms. On the lower one, which is parallel with the X graph, you see where we've included the three fourth molecule programs in there. You see absolutely no development of type one diabetes symptoms in these mice. We then subsequently, this is the first time we show these data, we stopped the vaccination after 16 weeks, and show even after stopping the vaccination, there is a persistent protection against developing the type 1 diabetes symptoms in these mice, which of course gives us a lot of enthusiasm for this asset going forward as a potential medication for type 1 diabetes in the very early stages. We also tested the technology in a model for multiple sclerosis, the EAE model, where it's induced, it's not spontaneous developing here. And again, we do the same thing. We include the antigen in the part here. We test different targeting units in this case here, see the same effect across the range of targeting units here. And again, you see a strong protection and it's reduced risk of developing the MS symptoms in this model here. So the top one is the untreated mice. The middle graph that light purple are the ones treated with the antigen alone, which in this case here is known to give a certain protection, and the lower graph with almost no development of symptoms is our vaccine. We also did the same experiment with here, and here we looked at the release of cytokines. So again, similar protection not shown here, but shown at an earlier stage. And what I really want you to focus on here is the kinetics or the dose-dependent effect on the release of the inflammatory cytokines. In this case, here, we see an almost complete elimination of the inflammatory cytokines by increasing the dose of our vaccines. It gives us a lot of also enthusiasm for this, for this protein. And remember, if we were using our traditional targeting unit and including the same antigen here, we would actually see a dose-dependent increase of these inflammatory cytokines. So a very strong indication of the proof of concept. As we said, we're also encouraged by the results that are emerging by other cancer vaccines with the mRNA modality. So we set out to explore what kind of benefit we add to that modality. As I said, the IP for our vaccine or our technology is agnostic, so it also covers mRNA and viral vectors. And here, just go forward to this one here. Here, we tested 20 different epitopes in a vaccine giving as mRNA alone, so naked antigens, very similar to what you see with the mRNA cancer vaccine companies on the right, and our vaccine, so mRNA encoding our targeted vaccine, so with the targeting unit in the middle column, and you see here, both on the prime and the boost results, a stronger results, but as interestingly and probably more important for cancer vaccine, a broader response. So you see more different epitopes when we use our targeting vaccine, generating a strong immune response compared to what you see with the antigen-alone mRNA molecule. So it gives us actually some enthusiasm that this our technology will also add benefit for the mRNA technologies. Quick look at the financials. So as I said, we're strongly capitalized with $159 million at the end of third quarter. This gives us sufficient years into the future to realize our growth strategy, which we've been through here. But we've also publicly indicated that we are heading towards the U.S. by announcing we have initiated a process to explore a potential listing on the U.S. Nasdaq. We've not given any indications on the timing for such an event. Finally, a quick look at the catalysts. So we had a busy year last year, and fortunately continue to be busy in 2024. So within the lead asset program, we will be starting up the VB-C-04 imminently, as I said. The IND is in place, and we're just waiting for the first site to start enrolling and dosing, probably over the next couple of weeks. For VB10.16 also, we look forward to report the updated survival data from the VB-C-02 trial in the first quarter. And, of course, we also are pursuing the next indication, and hope to be able to have patient enrolled to allow to pick the dose at the end of the year. For VB-C-03, we are planning to have patient enrolled for the part one of that trial, so that's 60 patients, at the end of the year. Then we'll be on track to report the data by mid 2025. And then, of course, we will continue to keep you updated on our autoimmune program development, as well as our partner programs with Regeneron on Genentech, although it is inherently more difficult to provide guidance on those. With those words, I think we're open for questions, Josh. So a number of companies. Here's a mic for you. I have a few questions. So a number of companies have noted that their algorithm selects truncal mutations, and that's how they argue that even though they're sampling the primary tumor, that's enabling them to also target metastases. Because in the neoadjuvant setting, obviously the surgeon's removing the primary, and your objective is to hit the adjuvant. Can you comment on sort of the ability to actually do that? Yes. So the element of clonality, right? Well, the issue of where is the mutation? Yes. Is it truncal or is it a branch mutation? So, I think we all, and when we talk to our colleagues out there, I think we are all more or less on the same path in terms of the algorithm. First of all, I think we realized pretty early that the algorithm needs to be tailored to the technology modality underneath. So, we would be using different algorithms compared to what you'll be doing if you had a peptide-based or if you had an mRNA. So, that's the first one. We're all focused on finding epitopes that are present not only in the primary tumor, but actually as a clonal one all over the body, also in the metastases. I think we've been focusing on that from the start by mainly two things. We are looking at... We're sampling from as many places as we can when we take the biopsies, and that gives us a good indication of whether a mutation is clonal or not. And second one is we also take the ctDNA expression level into consideration. That was one of the first cancer vaccines that started taking ctDNA into the decision algorithm. That also gives us a feeling for whether the mutations are actually expressed clonally across metastasis also. You don't mind? The follow-on question, though, to that would be, the algorithm essentially is a tool, and so as you look at your clinical pathway, if you make any adjustments to the algorithm, don't you have to start from the beginning as far as your clinical pathway? That's a very good question that I think is inherent for the whole concept of individualized cancer vaccine. So I think even the authorities, the FDA, are still, you know, the juries are still out on how that would work. What is very clear is we need to have a very well-controlled and confined environment, where we have actually stringent control of what we are doing in terms of the algorithm. And I think there will be, as you say, a need to document the effect of any major changes we include there. It's not necessarily the intention to keep on mutating the algorithm. The algorithm is intended to be fairly solid over time. So the algorithm we use now was finalized and validated before we started the clinical trial. We're not changing the algorithm between the patients as we enroll right now. So I, so I agree with you. There will be a need to document control changes for the algorithms as we go forward. So you think you can do documented control changes between phases of trial? So if you were to see something in a phase I, you think the FDA is actually gonna allow you to adjust it for phase II, phase III? No, I, Yeah. Back to start. I don't think... I don't know that we would actually want to change it. Right. But I do agree with you that if we want to change it, we would need to have a solid strategy for documenting the impact of that change. Whether that would be between phase I or II, or whether that would be five years down the road when on the market, when we realize something actually gives a better response, it still needs to be documented that it drives a better response without impacting the safety and so on. But I think it's an interesting question. I think I don't think the FDA really have their minds fully around this one yet. Keep in mind that the epitopes that we're selecting between the patients are completely different medicines. So we are giving each patient very different medicines, and I think it's... We were all a little bit nervous how the authorities would actually respond to that concept five years ago, when we started this. I think they've been very honorable and open for the whole concept of this technology moving into development, even though it's very far from what you've seen before in development, right? If you don't mind, a follow-up? Sure. There has been some noise from some regulators that they might actually look at the algorithm, and so you're producing a different product for every person. Yes. There is some noise about trying to deconvolute what the algorithm's actually doing... even if you don't change it. You know, you saw that with IDEC, where they had a cocktail of antibodies, and then at one point, the government- Yeah -came back and said, "You have to deconvolute the whole thing, Yeah. They had to be sold to Biogen. Yeah. Do you see an inherent risk about having to deconvolute your algorithm towards, when you get towards approval? It's not just you- Yeah but Moderna and everybody else as well. Yeah. No, I don't... First of all, I think it technically would be impossible- Right To try and do that. That would kill the whole concept. And I don't think we've seen any signals from the authorities, neither the FDA or the one you'd be talking to in Europe is the German authorities, not seen any signals in that direction. But it is a new concept that has not been tested before. I think that's why everybody is a little bit nervous, on the edge, on how the authorities will eventually look at this. No, but thank you. That was a great answer. Okay. The last question is that people are talking at the conference, they're a little surprised that Moderna is looking at higher tumor mutational burden patients- Yep where KEYTRUDA works. And yet BioNTech is talking about going after lower TMB patients in pancreatic and CRC. Do you have any idea of what the thinking is behind that? And how do you think about the, probably success versus high TMB versus low TMB? Yeah. I think we've seen across all our trials that we can create a new route. I mean, to their strategy, I... That would be very hard to speculate on, right? Absolutely. I think that's really a matter between are you going for the big markets with slightly higher risk, are you going for something that's slightly more controllable and increase the likelihood of success in that setting? I suspect they will also be expanding on the back of the first trials anyway. From our perspective, we've shown earlier that we can create immune responses independent of whether we have low or high tumor burden. I think we remain very optimistic with our, on the back of our VB-C-02 data that I showed you, in the first part of this presentation here, that we will have a, a place, not only in the locally advanced setting where you see Moderna and BioNTech playing right now, but also the advanced setting, across tumor types, also with our individualized, cancer setting. So I think we, we are a little bit on, on a different path than they are. We right now remain focused on the recurrent metastatic setting, and then, although it's not my place to speculate where Genentech eventually will take it, we, we certainly hope that, they agree with us. There is also a path into the, locally advanced setting across tumor types. Thank you very much. Looks like there's no other questions. Thank you, Mikkel. Very good. Thank you very much for listening.