Nykode Therapeutics As

Greetings, and welcome to the NICODE Therapeutics Q1 2026 Financial Results Presentation. At this time, all participants are in listening mode. A question and answer session will follow the formal presentation. You may ask a question at any time by typing it into the Ask a Question feature on your screen. As a reminder, this conference is being recorded. It's now my pleasure to turn the call over to NICODE CEO, Michael Engsig. Please go ahead, sir.

Thank you very much, Kevin. And also from my side, a very warm welcome to all our listeners to this, our first quarter webcast on this beautiful summer day in Oslo. A quick look at our forward-looking statement, which I think you are all familiar. On that basis, we will move forward. As usual, it is a pleasure to have with me today, Anita Fredriksson, our co-founder, chief scientific officer, and head of business development As well as how our chief financial officer. Taking you through the highlights of of the quarter that the deep dive into some of the data and of course, the financial numbers also. So, for the new listeners, a very quick recap, my code is a chemical stage immunotherapy company. focus on leveraging our antigen-presenting cell targeted immunotherapy platform to discover new immunotherapies within oncology and autoimmune diseases. Our lead asset is Abisuba, which we are developing in first-line head and neck. But we also have very high conviction in EB10neo, our individualized neoantigen therapy platform, as well as our autoimmune disease program. We're well capitalized with funding taking us into 2028, which is on the other side of all important inflection points. It's been a busy quarter with a lot of progress, in particular on Abhisuva, but also interesting movement on our other programs. For Abhisuva, we dosed the first patient in the randomized phase two trial ability, which marks transition from preparation into execution. Of course, a very important milestone, which sets us on track to release the interim data in 2027. We also, at the ICMA conference back in March, reported the interim data from the CO3 part one trial, which also tests Abesuga in combination with Keytruga or Pembrolizumab in first-line head and neck patients. will take you through some of the data at a later point in this call here. We further elaborated some of the data at a presentation at the AECR one month later, which provided further conviction to our immunogenicity data. We've reported some progress on our autoimmune disease platform, showing the ability to also drive immune modulation in human cells, a very important point on our path towards a drug. And then we've showcased our activities in the AI accelerating drug design world at the Nexus conference. We'll just say a little bit about that and we get to that in this presentation here. Brief update on Abizuga. As you know, we are currently focused on generating data from the first randomized trial with Abizuga. We've chosen first-line head and neck for several reasons. One, it is a significant addressable patient population. And two, only one in five patients benefit from the standard of care. And even with a 12-month medial mobile survival, there is plenty of room for further improvement population. In addition to that, we see that most of the drug development for first-line head and neck is focused on the HPV-negative patient population, whereas Abisuva is focused on the HPV-positive patient population. But there is further upside for Abisuva. In addition to head and neck, we see a very large addressable patient population in the other cancer types driven by HPV-16 infections. of which we have already generated very convincing data in the cervical cancer. So we do see further significant upside for our basula in the future. At the ECLO conference, we show interim data showing the overall from the 13 patients that were enrolled into the Part 1 trial. Part one was focused at investigating three different doses of Abizuga on top of standard of care, which is Keytruda, for this patient population. We reported an objective response rate of 39% in these 13 patients, which should be compared to what has been reported for the standard of care, so Keytruda alone, which is around 19%. So close to a doubling, or slightly more than a doubling, if you compare those two numbers, that corresponds very well to what we saw in the CO2 trial where we investigated apesuva on top of atezolizumab in the advanced cervical cancer setting. So with those two trials now, we do see a strong trend towards an additive effect of apesuva on top of checkpoint inhibitors. At the AACR, both at the ICMA conference and subsequently at the AACR conference, we provided further details on the immunogenicity data, which we've always said is extremely important for any immune therapy with the mechanism of action of Apizuga. You do need to see a strong correlation between the immune response to the antigens And the chemical outcome, what we see on this slide here is an ability to drive a very strong antigen-specific immune response towards the two targets, E6 and E7. We just chose to show you one slide. This one is probably the strongest slide showing the ability to drive this response in all patients dosed with six or nine milligram. Again, it aligns well with what we saw in the CO2 trial when we tested this in cervical cancer patients. So, it adds to the very, very strong trend we see with Abizuga. This, of course, all this data strengthens our conviction that Ability, a randomized phase two trial, and first line head and neck, is the right next step for FabriZuga. Shown here on this slide is the design of Ability. And as I mentioned, we have moved from the phase of starting up the trial into execution. We are now approved in seven. different EU countries in addition to the approval we received in UK before year end. We saw the first patient dose in May and we've already seen multiple sites being opened up and starting the search for patients. Our focus going forward is to expand the number of countries and sites for availability so we can make sure we have the sufficient number of sites engaged to recruit the approximately 100 patients in a timely fashion. Of course, everything is aimed at generating the first interim readout in 2027. With those words, I'll hand over to Auneide to take us through an update on DB10 Neo.

Thank you, Michael. Yes, so in VB-10eo, we have a later focus on following the progress of our peers these days, getting closer and closer to expected readouts from both BioNTech and Moderna on their late-stage Phase II and, importantly, Phase III randomized trials with their individualized neoantigen therapy. So these will be extremely important for the future of our own VB10-Neo. We do believe our VB10-Neo meets the requirements for an ideal INT technology and has several advantages over the mRNA technologies that BioNTech and Moderna is pursuing. And we are focusing on a conscious-based strengthening disposition and a few key activities. In this quarter, we have focused on the antigen selection part with our proprietary NeoSelect and also on continuing to improve the supply chain. give you more details on the progress there in the next coming months, including our participation presentation at the 9th International Reaction Summit in July. So you can follow the progress in more detail when we come to this conference. Then some updates on the tolerance program. Over the last year we've seen numerous highlights on on why we want to pursue a antigen specific immunotherapy program with our apc targeted technology we have been able to show strong durable efficacy across disease models. We are constantly improving the number of disease models and we see that on both in a therapeutic and preventative setting. They also give you a bit more detail on the modular APT targeted platform and how using different APT targeting units allows the immunotherapy to get into different cell types and process and different efficiency presented to regulatory T cells and then also proliferating those regulatory T cells in a different manner depending on our unique proprietary APC technology. We have also seen unprecedented induction of both this proliferation of the action-specific regulatory T cells but also importantly the next step in the cascade suppression of effective CD4 and CD8 T cells and also an effect on reducing also antibodies importantly. One of the key features that is important for taking this into the clinic and the commercial setting is to be able to have a convenient delivery and also favorable safety profile in addition to have a technology that can be manufactured as a standard biologic. And we are having a technology that's a fusion protein that can be manufactured through very standard antibody manufacturing procedures, which is reducing the risk for taking this from preclinic to the clinic, as we're seeing now also with our CMC efforts in this program. And today we'll also see a bit more on the human APC translational data that supports that. We do have a path from preclinic to clinic that can be pretty effective when we take that choice. Obviously, it's important for everyone that this technology is being developed as a second program in iCODES on the back of a technology that's been clinically validated in oncology. So, you've seen this mechanism of action figure before, and how our APC targeting is able to induce regulatory T cells and reduce effector B and T cells. Today we will focus mostly on the human translational potential, so see that we have now created human versions where we have human targeting units binding to human APCs. which is the first step of the mechanism of action here in the red figure. And then subsequently these vaccine molecules are taken up by the antigen presenting cells process and epicals presented on MHC molecules to regulatory T cells, which you also see today. We have a set of the system that nicely shows us how effective this is being going through the antigen presenting cells, which we can use in order to identify the optimal human versions of the APC targeting units for clinical use. And then thirdly, these regulatory T cell proliferation, which I'll show you here. So here on this slide, you can see that we have now made human versions of our molecules that bind to human antigen presenting cells. And when we compare that to non-targeted, non-APC targeted version, we can clearly see that we have molecules now that bind to human antigen presenting cells. This is how you see on the figure that it's shifted to the right on the figure. That means that our therapies are binding the relevant cell. And for the right part of this figure, the sophisticated setup where we have looked at how much of the disease epitopes are actually presented on the MHC molecule after the entire molecule has been taken up, processed, and presented, and how much of this is actually then available to be presented to regulatory TSOF. It's the same method, so you can see that if the shades are shifted to the right, you will have more and more of these effective antigen presentation on antigen presenting cells. Again, as you can see, the targeted APT targeted therapy is strongly presenting the antigens to regulatory T-cells. on the HLA class II antigen complex that we're measuring here. So it means we are getting closer and closer to have clinically ready drugs. And then another important factor of our technology is that depending on which APC targeting unit that we are employing in our molecules, we will have a different effect on the immune system. And in this particular system here, we can measure that if we use here a variety of five different APC targeting units, that all look the same when it comes to the disease-relevant antigens. We can see that these five APC-targeted molecules are inducing a different proliferation of reglycerid T cells. and much better proliferation of these regulatory T cells than the non-targeted version. And then the percentage of those that are truly FOXP3 regulatory T cells differs between the different versions of our technology. So all of these methods gives us much more and more insight into how precisely we can modulate the immune system and choose a version of our platform that will be ideal in order to treat a particular autoimmune disease. All of these are proprietary to NICODE, and you can also appreciate that we have a technology that can extremely precisely modulate which cell types that will be triggered for each patient here. Then I think I'll hand over to you, NICO. give us some insights on the AI.