Greetings, welcome to the Nykode Therapeutics webcast. At this time, all participants are in a listen only mode. You may ask a question at any time by typing it into the ask a question feature on your screen. It's now my pleasure to turn the call over to CEO Michael Engsig. Please go ahead, sir. Thank you very much, Kevin, and a very warm welcome to everybody listening in to this call here, where we will take you through the data for the final analysis of C-02, which we reported yesterday. I'm sure you sensed from our presentation here that we are extremely enthusiastic about these results. Just a quick look at the forward looking statement, which you're all familiar with. Quickly move forward. With me today, I'm very happy to have Agnete Fredriksen, our Co-founder and Chief Business Officer, and Klaus Edvardsen, our Chief Development Officer, who will be taking you through the data in details. Just to frame today's presentation, what we're talking about today is the final analysis of the data from C-02, which was exploring VB10.16 in combination with atezolizumab in patients with advanced cervical cancer. For those of you who have followed us also last year, we reported the positive interim results from this trial back in May and were, in particular, encouraged by the long durability of the responses and the long stabilization of the patients that we saw in those patients that had already stayed in the trial for some time at that time point. The big question for everybody was, will this durability and stabilization turn into real survival benefit for the patients in the final analysis? We are extremely happy to report that indeed, it did turn into a survival benefit. With 16.9 months in the overall population and more than 25 months, meaning not reached for the median overall survival in the PD-L1 positive patients, we can say that we have really demonstrated survival benefit here. The PD-L1 positive patient population is particularly interesting for us because that's the population that we will primarily target in the next development activities. The ORR, so the overall response rate and the disease control rate that we saw in the interim analysis were confirmed. Again, we are intrigued by the PD-L1 positive subpopulation, where we saw an ORR of 29% and a disease control rate of 75%. The favorable safety profile that we saw in the interim analysis were confirmed, and that's important not only for the patients and the women in this trial here, but also for the product candidate, again, with a thought to the target populations where we intend to develop this product. For those who are interested in the translational science, again, we saw a very strong correlation between the antigen-specific immune response and the associated clinical outcome, which is important for any therapeutic cancer vaccine that you want to develop and bring to the market. Again, we think these data are unique and very strongly indicates the vaccine effect. Now, there's a subpopulation that we are also very interested in. That's the one called PD-L1 positive with one prior line of systemic anticancer treatment. That's because the next trial that we intend to be running in advanced cervical cancer will be targeting a population that is very close to this one. Here we saw what I'd like to characterize as a mind-boggling progression-free survival of 16.9 months. Overall survival, median overall survival was not reached, more than 25 months and ORR of 40% and disease control rate of 80%. In together, we find these data strongly indicates a differentiated and long-lasting clinical activity of VB10.16 in combination with atezolizumab compared to what you would expect to see with a checkpoint inhibitor therapy alone. Just a quick introduction to the company for those of you who are new to Nykode. Nykode is a clinical stage immunotherapy company. We are entirely dedicated to leveraging our unique and proprietary vaccine technology platform, which uniquely targets antigens to antigen-presenting cells, which in turn, generates a strong CD8 T cell response, which has been shown to correlate with clinical responses in solid tumors. The technology is modular in its build-up, which gives us a large degree of versatility and flexibility. That means that we can easily incorporate new antigens and adapt the products to new diseases across oncology, infectious diseases and autoimmunity. We are very dedicated to advancing our wholly owned lead asset, VB10.16, which we'll be talking about today. Today, as we mentioned, we'll be reporting the final data from the C-02 trial, and we'll be focusing a lot of the today's presentation on durability parameters. We have also announced that we'll be starting a potential registrational study in advanced cervical cancer, and we'll initiate that trial towards the end of 2023. We are expanding this program into head and neck with the start of C-03 trial in the first half of 2023, a trial that we're running in collaboration with Merck, who is supplying the KEYTRUDA. In Nykode, we believe in partnerships. We've entered a number of partnerships, including two game-changing out-licensing deals with Genentech and Regeneron. The company is well capitalized with a cash position of more than $200 million at the end of fourth quarter, which fully funds all the activities that you'll be hearing about today and takes us well into the next couple of years. With those words, I'm going to hand over to Agnete, our Co-founder and Chief Business Officer, to take us in through a short recap on the technology platform. Yes. Thank you, Michael. VB10.16 is based on the platform technology that we call the Vaccibody platform technology that uniquely targets the antigens to antigen presenting cells. We've so far chosen to work with the plasmid DNA format. We also have IP for making these unique Vaccibody molecules or in other vector formats like mRNA, viral vectors or recombinant proteins. The products we have in the clinic today is on purpose made on the plasmid DNA backbone. The unique thing with the Vaccibody molecule is that we have the antigen linked through a dimerization unit to a targeting unit that binds specifically to a certain important cell type called antigen presenting cells, which is very important in order to trigger an immune response. This is also the way we can make sure we control the immune response. The immune response can go in different directions, and by choosing the targeting unit of choice, we can direct the immune response into the profile that is desired for specific diseases. Can we go to the next slide, please? For VB10.16 plasmid DNA-based vaccine, simply formulated in PBS, we deliver it with a needle-free jet injector, that makes sure that the DNA plasmid is transfecting cells in the muscle, and these muscle cells start then to produce and secrete the Vaccibody protein. Since the orange part with the targeting unit that is unique for the Nykode technology is a inflammatory chemokine, its first important feature is to attract this specific cell type called antigen presenting cells, where all antigens needs to be delivered to these cells in order to initiate an immune response. We make sure that that happens more effectively by having the antigen presenting cells infiltrating the muscle and ending up as the neighboring cell to the cell that's producing constantly new Vaccibody proteins. When it binds, it will be internalized inside the cell, and that's the other important feature of VB10.16 and other products based on the same platform is every molecule we make with the same targeting unit will be taken up into the cross-presentation pathway. That's the way we control that the immune responses to the antigen is primarily a strong and broad CD8 T cell response and not only focused on CD4 helper T cell responses, for instance. It's these CD8 T cell responses that can go and recognize the antigens in the tumor. All tumor cells that express the antigens we have in the vaccine will then be recognized by these CD8 T cells and be able to kill them. This principle we employ among different products. If you go to the next slide. Our rich and diverse product pipeline is based currently on the same format with the same targeting unit and the same dimerization unit and all on the plasmid DNA backbone so far, which means that the products you see here covering products within the off-the-shelf oncology vaccines as well as individualized personalized cancer vaccines that we work with together with Roche Genentech, they all use the same platform technology. You could also be pretty confident that the data we show you today with VB10.16 has transferability across to other programs that we develop together with Regeneron and Genentech and also future products that we will take into the clinic ourselves. Next slide, please. VB10.16 specifically has this particular targeting unit with the CCL3L1 unique chemokine dimerization unit. And the antigenic unit we have incorporated the full length HPV16 E7 and E6 antigens. HPV16 is the most prevalent oncogenic HPV strain, so an important target, and it's wholly owned by Nykode, so not affected by any of the partnerships that we have so far. Let's see how this performs in cervical cancer patients, and I hand it over to Klaus to get through that. Thank you, Agnete. Let me just remind you all that cancers driven by HPV and specifically here obviously HPV16, because that's the vaccine construct that we have been utilizing, still significant. The major cancers driven by HPV is head and neck and cervical cancer, and then there is a number of minor indications that are, although important, I will come back to that towards the end of the presentation. Just for the unmet need, especially if you look at advanced stage cervical cancer, female diagnosed with that will very unlikely be alive five years after that diagnosis. There is a desperate need for new treatment paradigms and modalities in that setting. One could obviously speculate that based on the prophylactic HPV vaccine, that we would be looking into a diminishing number of cancers with the HPV driven background. That's not the case. There is an expected increase over years to come in those cancers, and that's obviously likely because of a limited uptake or not a full uptake of the prophylactic vaccine and obviously the fact that non-prophylactic vaccine will be 100% efficacious. Next slide, please. Just a few words before I actually go into the actual data. What would be considered good in such a setting? Meaning what would be competitive, what would actually offer an a different treatment possibility for female with advanced cervical cancer? To do that, we have listed the treatment options that potentially all dependent on geography would be available for female with that cancer type. That's chemotherapy. It's one of the checkpoint inhibitor, KEYTRUDA pembrolizumab, nivolumab, ipilimumab, and then the new guy on the block, TIVDAK, that I will come back to at length. What patient population will actually be the relevant comparator is obviously from a checkpoint inhibitor perspective, the PD-L1 positive patient, because every trial would be enriched for PD-L1 positive patients, obviously based on the mode of action. In that setting, I'm not going to read out the underlying median overall survival and median PFS for each of those four treatment modalities, but just to point you to the fact that to be competitive with another treatment in this setting, you would like to see a median PFS above four months and a median overall survival above 14 months. Next slide, please. Just some words about the trial VB-C-02, single arm trial, testing out the concept of adding the HPV16 vaccine VB10.16 on top of the checkpoint inhibitor atezolizumab in patients with advanced cervical cancer. The primary endpoint for the trial was safety and overall response rate assessed by RECIST by an independent blinded review. The key secondary endpoint, duration of response, progression-free survival, overall survival. As Michael already alluded to, it's obviously critically important that when you utilize a vaccine approach that you can actually show that you mount a new response in the patient you do vaccinate. We will show you some preliminary data here because you have to bear in mind that you see the analysis of this data set as a relatively fresh off the press. I can then turn you to the interim analysis for a more comprehensive analysis of immunogenicity at this stage. The trial was conducted in Europe, in six European country. It enrolled 52 patients. The treatment setting here was a nearly 12 months vaccination period where we were starting with a vaccine induction, giving five times every three week, followed by a vaccination maintenance setting where six vaccination was given every six week. That was all concomitantly given with atezolizumab that was given every three week. It was followed by a 12-month follow-up period where in essence, patients would have had an option to continue on atezolizumab. Very few patients did continue on atezolizumab to be specific for patients. That is an important element also to bear in mind when you try to compare this data set in a single arm trial to what you would expect in a monotherapy checkpoint inhibitor setting. Next slide, please. A few words on patient disposition. I'm not going to spend many words on it because in reality, what you see is what you would expect from a patient population with advanced stage cervical cancer. There is, however, one important point to pay attention to, and that is the fraction of PD-L1 positive patients enrolled into this trial. As you can see, it was a little less than half, 48%. That's again, an important parameter to bear in mind when you do the comparison to monotherapy checkpoint inhibitor treatment in a similar setting. Next slide, please. Safety, as already alluded to, it was very well tolerated. You could say in conclusion, and I can start with that you're not seeing much additional adverse event to what you would expect from atezolizumab or any checkpoint inhibitor for that matter in this setting. That can be seen on the left on the slide, where investigator assessed adverse event attributed to the vaccine has been listed. You see those numbers are relatively small, and obviously all mild to moderate. If you look to the right on the slide, you would see that the combined assessment of adverse event was that an adverse event was seen in 67% of the patients. They were primarily mild to moderate, meaning grade one to two, with very, very few patients experiencing anything above that. No serious adverse events were reported related to VB10.16, the vaccine, and there were no deaths related to either VB10.16 nor atezolizumab in the trial. Next slide, please. Let me just draw the key headline results with regard to duration endpoint at this slide, and then I will subsequently get back to all of the clinical endpoint later in the presentation. As you can see, from the table, we were obtaining strong and durable antitumor efficacy across all patients, reaching a median overall survival in the overall patient population of 16.9 months. If you look into the PD-L1 positive subset of patients, which is obviously the relevant comparator to the checkpoint inhibitor monotherapy, the median overall survival was not reached, but at this stage would be at least 25 months. Median PFS in a similar, in a similar setting, PD-L1 positive was 6.3 months. Let me just stop and compare back to the concept contextualization slide, where I was indicating that you at least would have to meet the median PFS of four and an overall survival of above 14 to become relevant. I think it's fair to say that that has been met, and that you, by no doubt can claim that you see a vaccination effect, although you cannot say that in a statistical sense, as it is a single arm trial. No concern claiming vaccination effect. You're not doubling, these two parameters, from what would be expected from a checkpoint inhibitor monotherapy alone. Next slide, please. Just a few words on the observed overall response rate. In the overall patient population, it was 19%, with a disease control rate of 60%. Disease control rate in this setting, meaning that patients derive clinical benefit without actually obtaining a RECIST criteria response, which mean that you would need a tumor reduction overall of at least 30%. In the PD-L1 positive patient segment, the overall response rate was 29% with a disease control rate of 75%. If you look at the waterfall plots to the bottom of the slide, overall population to the left, PD-L1 positive to the right, you are obviously seeing the depth of the responders. You are seeing the stipulated line, which is -30% RECIST criteria response. The important take-home message otherwise from the waterfall plot is that you see a significant proportion of patients that do derive clinical benefit, meaning they get a reduction in tumor size. They just do not get a reduction to the -30%, but some of the patient gets very, very close, and we can return to the reason for that in a few slides. Next slide, please. Looking at the spider plot at individual patients, we have broken that down, so that it does not look too much like spaghetti to responders in red and non-responders in blue. If you look to the far left on the deck, you see the non-responders in blue. You obviously see the non-responders as non-responders. There are a number of patients that progress very fast. You also see that there is a significant proportion, close to half, that is actually deriving benefit because you see a stabilization, an almost flat curve from the time you start to see that flattening and then up to the full follow-up of the trial of 12 months. In the red color code, you see the nine responders, and you see the deep responses, and you see that they all accept one patient, keep that response for the duration of the follow-up period. We've also indicated to you, the spider plot for PD-L1 status, and I will only draw your attention to the far right of the slide, where you see the PD-L1 negative patients. There were two responders, one complete response. You see that, and then you see another responder that relapsed relatively fast in the red color coded. Again, here in the blue color coded, you see patients that derive clinical benefit without actually obtaining a RECIST criteria response. We are just indicating here that obviously on two responders, one fast relapse. It is difficult to draw a conclusion as to whether there is an effect of the vaccine in the PD-L1 negative patient segment. If you link it to the stabilization, there is absolutely no doubt that you're also seeing clinical benefit in that patient segment, which is something that we would obviously also return to and try to capture some treatment option for a patient population like that is even higher unmet medical need. Next slide, please. Just a few words on the patients that obtain clinical benefit in the sense of stabilization, again, meaning that they're not responders by RECIST, but they are certainly deriving clinical benefit. If you look at it, we had 28 patients that obtained disease control. 14 of those patients completed the entire treatment, vaccination program for nearly a year, and seven out of those patients are still in follow-up without any evidence of progression. Next slide, please. Now to the Kaplan-Meier curves and the duration endpoint. We start with obviously the durational response that is only assessed in the Kaplan-Meier curve on patients that do obtain a RECIST response, and that landed in the overall patient population at 17.1 months. If you look at it broken down to PD-L1 positivity or negativity, you see that it is still 17.1 months in the PD-L1 positive, indicating that this effect is driven primarily by PD-L1 positivity, but you cannot, as I indicated on the spider plot, say that there is no clinical benefit of treating patients with the vaccine in the PD-L1 negative patient segment. Next slide, please. Looking at the progression-free survival, it reached 4.1 months in the overall patient population. Again, as already indicated, if you look at the PD-L1 positive patient segment, the median PFS landed at 6.3 months. I'm not going to dwell much on the median PFS for the PD-L1 negative segment because of the relatively low number of patients that did derive a response in that patient segment. Now to the final duration endpoint, overall survival, which obviously overall survival is always an important endpoint for obvious reasons. Clearly, if you are looking at patients with advanced cancer, it is likely not possible at that stage to cure any of these patients. Therefore, the critical element for patients obviously become how long can I live without having a burden that is too cumbersome with regard to either adverse event based on the treatment or of the tumor. That overall survival in the overall patient population landed at 16.9 months. As already indicated, if you look at the patients PD-L1 positive, the median overall survival has not been reached at this stage. It is at the current stage, above 25 months, and will obviously increase. Where it lands is not possible to say at this time point. It will unfortunately be only dependent on when patients are not any longer alive. Next slide, please. As indicated, it is important to obviously claim a vaccine effect, or a correlation between the vaccine effect and the clinical effect that you can indicate that you actually mounted an immune response against the antigens that you did vaccinate against. As I said, we are in analysis mode still for this data set, but we just thought that it was important to indicate to you that as we showed at the interim analysis, that if you look at the higher T cell responses, you were seeing a strong statistical correlation between patients that actually did derive a clinical benefit, had a much higher ELISpot count number than patients that did not have any clinical benefit, the ones that did progress early. If you lump all of those responses together and look into the fold increase, same picture, statistical significant in the patients that derive benefit compared to the one that did progress. Next slide, please. Now, just how do we put this into context? I think I have alluded over the entire presentation to the fact that obviously, the comparator here would be what would a patient be expected to do if you had been treated, the PD-L1 positive patient? Obviously, we look into the PD-L1 positive patient segment with regard to the checkpoint inhibitor because of the mode of action, because those trials obviously would be enriched for patients that are PD-L1 positive. Compare that to the patient segment where you have added the vaccine on top of a checkpoint inhibitor, in this case a pembrolizumab, again, in the PD-L1 positive patient segment. If you look at KEYNOTE-158, that's the pembrolizumab trial that tested out in second line, and the cemiplimab in PD-L1 positive in the EMPOWER-Cervical 1 trial, you see a response rate of 17% and 18% respectively, compared to ours, 29%. Then to the median PFS, 6.3 months in ours, 2.1 in pembro, and three months in cemiplimab, more than a doubling of the median PFS. When you look at overall survival, set not reached, but compared to 11 months and 13.9 months respectively in pembrolizumab and cemiplimab, more than a doubling again of that significant endpoint. The last part that I would like to draw your attention to is tisotumab vedotin, TIVDAK, as indicated on the contextualization slide. That is a new treatment option for patients that are failing first-line standard of care in the U.S. First-line standard of care in the U.S. is pembrolizumab plus chemotherapy plus minus bevacizumab. Those patients would have very limited options today because you would likely not re-challenge them with a monotherapy checkpoint inhibitor. You could re-challenge them or not re-challenge them. You could try to treat them with a different chemotherapy setting, or you could try to treat them with tisotumab vedotin. One problem with that compound is that it is with a black box warning. There are significant eye toxicity associated with the compound. There are neuropathy in the optical nerve, meaning that some patients do go blind, and there are some significant ulcerations in the cornea. Anyway, an important comparator to what you potentially could offer patients, if we can get our vaccine registered, which we have every intent to do, obviously not based on this trial, but based on the future program, it will stack up very well to TIVDAK, which obtained a 24% response rate, obviously PD-L1 agnostic because it's a different mode of action, and a median PFS of 4.2 months and a median overall survival of 12.1 months. Next slide, please. Here, Michael alluded to it in the executive summary. We are only giving you this slide and the data here as a prelude to our potential registration effort that I will come to on the next slide, is to look at patients that do fail the first line standard of care in the U.S., as I indicated, would be PD-L1 positive patients because they will be given pembrolizumab chemotherapy plus minus bevacizumab, and they would have failed only one systemic anticancer therapy. If we look at that patient segment in, our C-02 trial, and with the caveat that this patient segment here, they are CPI naive because they were enrolled in Europe. If you look at the numbers, they are pretty compelling. An overall response rate of 40%, a CR rate of 13%, and nearly all female obtaining clinical benefit with a disease control rate of 80%. Median duration of response stays at 17.1 months because it is primarily driven, as said, by PD-L1 positivity. Median PFS increases to 16.9 months, median overall survival was obviously not reached in that segment either. Next slide, please. I'm not going to go over details on this slide. We have in essence at the December update represented to you our future clinical plans. I just wanna draw your attention to the C-04 phase II cervical cancer trial, which is our potential registration program in patients that do fail first-line standard of care in the U.S. That trial is going to be conducted by the Gynecologic Oncology Group. That is the gynecologic collaborative group in the U.S. that everybody would like to conduct their trial with. They have been involved in every approval in gynecologic cancers in the U.S., and they will conduct this trial on our behalf. We expect that trial to open for first patients enrollment before end of this year. I will have to say that there are obviously ongoing negotiations with FDA as to this usability of that design for potential registration, because as already indicated, C-02 enrolled patients that are CPI naive. Here we are talking about patients that will be CPI refractory. We will obviously not take patients that are primary refractory, and you could likely not rescue those. Patients that are secondary refractory, meaning that they have to write a tumor shrinkage. Those data in C-02 would be kind of indicative as long as you can obtain any type of clinical benefit, the vaccine can prolong and keep that benefit for a substantial period of time. That's the hypothesis that we're going to test in VB-C-04. We will not spend all money upfront. We will do it adaptive. We enroll a subset of patients. We have indicated 30 patients, look at whether the signal is strong enough, and then enroll up to 100 patients, which is kind of standard for an accelerated approval in this setting, and exactly the conduct that TIVDAK used when they obtained their accelerated approval. Let me just finalize on future plans. The more critical important elements and the likely most important take-home message from the C-02 data. That is, as I already indicated, if you can get any tumor shrinkage, whether it's RECIST, a response or a disease control, what the data in C-02 indicate is that response or stabilization, if you like, can be kept, and it can be kept for a significant period of time. I think that has been indicated by the duration endpoint. And again, do remember that we only vaccinated for one year, and we only gave atezolizumab for the vast majority of patients for one year. You would normally have extended to two years based on the safety profile that's likely nothing that prevent us from doing so in the future. What... Where are we looking where we believe that there would almost be a winner? That is in the adjuvant setting. The adjuvant setting means that you have already treated patients upfront, and you select patients for benefit, meaning they have a shrinkage of their tumor, and then to keep that shrinkage, you use an adjuvant treatment. It's kind of like what you see and what I just described would be a significant benefit with the vaccine. Why, can you ask, do you not start in locally advanced adjuvant? Because standard of care in that setting has not yet been established. There is an ongoing trial that is indicating whether it is good to add pembrolizumab on top of standard of care in that setting, and we are eagerly awaiting the outcome of that. I think it's important to mention here that we are already in collaboration with Merck on a head and neck cancer program where they're looking for a dose escalation, and it will obviously be very natural to continue that collaboration with Merck as soon as we have established what standard of care. Meaning, will it be beneficial to add pembrolizumab into standard of care, then we will add the vaccine and drive an even more prolonged duration of responses. That's the hypothesis. Next slide, please. Here is the concluding slide on the data set that I have just presented. I think I have read out those numbers many, many times. I'm not going to do it again. I'm just going to say that not unexpectedly, that I think this data set is very strong. It is, in my mind, a very clear indication that you can actually talk about a vaccination effect that is not attributed to the atezolizumab component of the efficacy. The results are so encouraging that we will have to find fast way to get this compound available to people with a significant or female with a significant unmet medical need. I think I have only one slide left, though, and that is, of course, to acknowledge the patients, their families and the investigators that took part in this trial. If they had not been willing to do so, we would obviously not have been in a position to present any of the data to you today. Thank you to all of those. Also thank you to Roche for providing atezolizumab to conduct the trial. Let me just finalize it all by putting a few words on what is the market potential. I already indicated that at the first slide. Now just to put it into the full context when we have described our future plans, we will look into the cervical cancer in the second line, the ones that fail first line treatment as indicated. We very clearly look into the adjuvant setting also in cervical cancer, although locally advanced. I briefly mentioned the options in head and neck cancer. As I indicated, there are other HPV-driven cancers. They are smaller indications, but if you lump them together it becomes a reasonable patient number. Obviously it's not only about patient number, it is about unmet need. Those patients have a significant unmet need too. That's anal, vulvar, vaginal, and penile cancers. Our intent is to capture all of that patient segment, which at this stage is approximately 130,000 new cases driven by HPV16 in the U.S. and EU5. By that, I hand the presentation over to Agnete. Yeah. Thank you, Klaus. So today VB10.16 was the focus. It is part of the platform technology that we are developing in Nykode. As you see on this slide, Nykode is more than VB10.16. We VB10.16 falls under the category of HPV-specific antigen delivery and stimulation products within cancer immunotherapy. We can develop more products that are based on the same platform, which we are already doing, for instance, with the personalized vaccines together with Genentech and off-the-shelf vaccines with Regeneron, as well as internal products. We can use the same platform to stimulate the immune system for infectious disease purposes, either in the direction of these unique T cell responses that we see here, or more in the direction of other immune response profiles like antibody responses, et cetera. We can also utilize the technology with certain twists, with the targeting unit particularly, so that we can make sure that we are inducing an inhibitory response and down-regulating the response antigen specifically, which is what we would want if we develop products to treat autoimmune diseases and, for instance, also allergy. That's an interesting future potential with our technology that builds on what you've seen today, with certain modifications. We will not restrict ourselves to that. Part of the name Nykode, new code, means that we can also use our in-house competence to build in additional modules, novel combinations, and structures. We can also go beyond vaccines and build novel therapeutics with these new codes that we can do, specifically Nykode. Next slide, please. Just an example with building in additional molecules. We have already demonstrated as of last year that we can further improve and control the immune response by building an additional fourth module in the plasmid DNA backbone that secretes a separate cytokine. This is something we can do also with the fifth module and potentially even sixth module in the future. By doing this, we can even further control the immune response. In this figure, as you see, we already see an enhancement in T cell responses and antitumor efficacy for applications within cancer vaccines. If we move to the next slide, that is also a potential we can use for infectious disease purposes to further enhance antibody responses and/or control it in different directions. For immune tolerance, we find here that our technology is very well suited to provide a unique and very specific approach to control the immune response, both through the targeting units that we can specifically design to both induce, but also make sure that the antigens are targeted to certain subtypes of antigen-presenting cells in order to induce regulatory T cells that can down-regulate this response antigen specifically. Here we can also play with the fourth module technology. If you go to the next. To sum this up, we've focused today on immune stimulation for cancer and here the platform really can show its potential by just changing the antigen. We will expect the same unique immune response profile that we believe we've also shown here today in inducing an immune response that correlates with clinical efficacy. We're very excited to also move that into further products. Then, we have a link in infectious diseases as well as what I explained for immune tolerizing vaccines. Then again, with the name of new code, we think also that in the future we can further employ our ability to create novel structures and use that as therapeutic proteins also beyond vaccines. I hand it back to you, Michael, for looking a bit into the future and the finances. Thanks, Agnete. Thanks, Klaus. Just two more slides. First the outlook. As you all noticed today, we announced the positive data from the C-02 trial, which has been an important milestone for us. We will immediately start focusing also on getting the C-03 trial, our expansion into head and neck, started. We are planning to enroll the first patient in the first half 2023. As well as the C-04 trial, the potential registrational trial, which is our next step into the advanced cervical cancer. Here we plan to start the trial and enroll the first patient in the fourth quarter 2023. We will also, as alluded to by Klaus, be updating the survival data. Very importantly today was the final data of C-02, but we still have patients in the trial or following patients from the trial. We will be able to provide updates on survival when we get to the first quarter of 2024. Then we'll be updating the market on the autoimmune program in the third quarter of 2023. A few words on the financial. As I said in the beginning, we are well capitalized with more than $200 million at the end of fourth quarter last year, which will fund all the activities that we described to you and run us a couple of years into the future. We also reiterated our statement that Nykode is continuing to explore a potential listing at the Nasdaq Global Market in the United States. With those words, I think we can open up for questions. Operator? Thank you. If you'd like to ask a question, please type it into the ask a question feature on your screen. One moment, please, while we pull for questions. Our first question is, you mentioned results from subpopulation of PD-L1 positive patients with one prior line of systemic treatment, 40% ORR and 80% DCR. How large is the subpopulation in your study? No, it's a fair question, and it is 16 patients. I also alluded to, it's not part of the formal analysis. It is a prelude for you to get an understanding of why we do believe that there is a likelihood to see a positive outcome in the C-04 trial. Again, with the caveat that I also very clearly stated that there is a difference between a CPI naive and a secondary CPI refractory patient population. That's the context that the presentation should be seen in. Thank you. As a reminder, if you'd like to ask a question, please type it into the ask a question feature on your computer screen. One moment, please, while we pull for further questions. If there are no further questions, I'll turn the floor back over to management for any further closing comments. Very good. Thank you very much. Once again, I'd like to say thanks to everybody for dialing to this call here, and looking forward to keep you updated on the progress in the future. I wish everybody a good day. Thank you. That does conclude today's webcast. You may disconnect your line at this time, and have a wonderful day. We thank you for your participation today.