Okay. Good morning, everyone, and welcome to our next session. I'm Sarah Nick from H.C. Wainwright's healthcare research team, and it's my pleasure to introduce Cantargia, Nasdaq Stockholm ticker C-A-N-T-A, a clinical stage biotech built around IL1RAP, a target that sits at the intersection of tumor immune suppression and chemotherapy resistance. Its lead antibody, nadunolimab, is being advanced in pancreatic cancer and higher risk MDS with a second-generation IL1RAP franchise behind it. Presenting today on behalf of the company is CEO Hilde Steineger. Please join me in welcoming them. Hilde, the floor is yours. Thank you. Thank you for having me, and welcome. Hilde Steineger, CEO of Cantargia, Swedish-based biotech company. We are in the business of inflammatory signaling. Inflammatory signaling is an important component of- Sorry about that. You want me to start over? No. All right. Inflammatory signaling is an important part of serious disease, and not that well-drugged. It's not due to the challenge of finding the right target. However, it is due to blocking the right way and the right target. We are convinced that our way of blocking the inflammatory signals that I'll walk you through is the right way, because if you block too narrow, the disease will find a way to counteract your effect and find a way through your blockage. While if you block too broad, you will then risk of hampering your patient's own inflammatory defense system. Again, it's important to block the right way. We're listed in Stockholm Stock Exchange, so this is our forward-looking statements. Interleukin receptor accessory protein, IL1RAP, is a co-receptor for three important interleukin signaling molecules, interleukin 1, 33, and 36. By having one target that can block all of these interleukin signaling, it makes the target very versatile. The biology connects both the innate and the adaptive immune system, and we have seen preclinical and clinical effect in multiple disease areas, both in oncology and in inflammation. In oncology with clinical effect in MDS and AML, and I'll walk you through our initiative there, in PDAC, and in non-small lung cancer, all very impressive results. In the inflammatory field, we have already developed a phase I product that was sold to Otsuka a year ago. This versatile target then is an engine to create new antibodies, and we are in the middle of developing a bispecific and an ADC antibody. This is our IL1RAP focused pipeline. As mentioned, we have a PDAC program where we're entering into a phase I-B with daraxonrasib early next year. We'll also have some very interesting data coming out of our MDS AML trial that we are doing together with MD Anderson Cancer Center. In autoimmune, we have our bispecific program and our phase I asset, as mentioned, acquired by Otsuka. Very competent and experienced management team. We've been doing drug development in big pharma, big biotech, and small biotech for many decades. It's a very complementary team, and I'm happy to lead such an accomplished team. We'll start with leukemia and myeloid malignancies, especially MDS and AML. The reason I want to start with that is that this is our near-term milestone coming up close to Christmas this year. Leukemic diseases such as AML and MDS are driven by the leukemic stem cells, and chemotherapy is the standard of care. Chemotherapy will take you only this far and will leave a reservoir of leukemic stem cells in the bone marrow that will seed the disease, and the disease will continue to progress. The cool part of IL1RAP is that normal hematopoietic stem cells express very low levels of IL1RAP, while the leukemic, the malignant cells, have very high levels of IL1RAP, meaning that you can target the malignant cells and leave the healthy one that will support you getting healthy after chemotherapy. It acts by a dual mode of action. It blocks interleukin-1 which is an important part of proliferation for leukemic stem cells. In addition, it marks and labels the malignant cells for killing of the patient's own immune system, illustrated here by a natural killer cells. By flagging the leukemic cells, by blocking their signal, but keeping the healthy cells alive and healthy enough to progress further, we believe that this is the most perfect target to treat leukemic stem cell diseases. Leukemic stem cells are a very diverse group. MDS patients are roughly 400,000 globally in prevalence. It is defined as blast cells in your bone marrow, less than 20%. When the blast cells go over 20%, the patient is then diagnosed with AML. The standard of care of both these diseases is chemotherapy. MDS is split with a new category of defining the group IPSS-R into six groups from very low to very high. The high and very high constitute 30%-40% of the MDS patient population. Of these patients, 30%-40% will progress into AML. AML is a very serious disease. Only 10%-30% will have an overall survival of 10%-30% in five years. Again, chemotherapy is the standard of care, and there are very few targeted therapies. Our trial that we are conducting together with MD Anderson Cancer Center as an investigator-initiated trial, it is a phase I-B/IIa study, and the phase I-B has now concluded. We saw no safety signal of concern, and the combination on top of chemotherapy was very well tolerated. Notably, in this patient group, the phase I-B with a data cutoff in January 2026, five out of five of the patients evaluated had complete remission. Six at that time were still not evaluable. We did a new data cut in June 2026, and that data was submitted as an ASH abstract. The embargo of that abstract will be released on the 4th of November, and the presentation will be held at ASH sometime in between 14th and 16th of December. For us, this is an important milestone, and we are very excited to be able to share with the world our concept of IL1RAP targeting in both MDS and AML. Turning to PDAC. As you know, the landscape has drastically changed with the approval of Rasonque after RASolute 302 showed impressive results in second-line treatment of PDAC patients. First line, however, is still not changed. The standard of care there is still chemotherapy. However, we're all waiting eagerly, of course, with the RASolute-303 to be able to understand how Rasonque might change even first-line treatment. In this changing landscape, Cantargia decided to combine our product with daraxonrasib in a phase I-B study to be able to pivot either to first line or second line, depending on the results that will emerge. Our belief in the combination of daraxonrasib and nadunolimab is based on the fact that we saw impressive results from our first-line treatment in CANFOUR. On top of gemcitabine, we saw a 13.2 months overall survival compared at that time with 9.2 and 8.5 chemotherapy overall survival. At the time it was 12 months, 58% of all patients were still alive. IL1RAP is an important driver of interleukin signaling in pancreatic cancer, and it has been shown by us and also others that IL1RAP is a good prognostic marker for overall survival. If you have high levels of IL1RAP, your survival rate is lower than if you have low levels of IL1RAP. Very interesting, when we treated with nadunolimab in our CANFOUR trial we saw the opposite. We flipped the curve, so the patient that was treated with nadunolimab in the high group had a longer survival than in the group treated with the low IL1RAP. In the high group, we saw 14.2 overall survival rate, and with the low IL1RAP group, we saw 10.2. Striking results. The effect of nadunolimab on its own was impressive, but in this changing landscape, we do need to adapt and we are then combining with daraxonrasib, and it's important to know that we are not hitting the same pathway as all the RAS inhibitors and MEK inhibitors. We have a parallel pathway that we impact. There are crosstalk between the two pathways, but they're non-overlapping. In addition, nadunolimab has another component, the ADCC component, that attracts the tumor microenvironment in a very effective way. None of the RAS inhibitors seem to attract and attack the tumor microenvironment in the same way as nadunolimab. Also important is that the high levels of IL1RAP again strongly correlates to the poor survival, even in KRAS-mutated patients. In this patient population, with the KRAS, especially G12D, there is a high level of IL1RAP. We're initiating a combination study just after Christmas this year, and we are recruiting roughly 15 patients in combination with daraxonrasib, and the primary objective is, of course, to determine safety and tolerability in this patient population. We'll also have some preliminary signs of clinical effect. However, this is a limited number of patients. Turning to our engine, IL1RAP engine, as mentioned, from this monoclonal library, we have now two clinical candidates, CAN10 and CAN04, which is nadunolimab. We are using this platform to develop bispecific antibodies and ADC, antibody drug conjugates. We have more than 500 monoclonal antibodies in the library, which makes this a very interesting agent that are targeting this versatile target. A few words about the Otsuka deal. Total bio dollar deal was $613 million. It's milestone-based and regulatory milestone-based, and the upfront was $33 million. Otsuka will do all the development of the assets, and they also have an exclusive first right on the next generation of some of our antibodies. To us, this was a formative deal. First of all, it was a third-party confirmation of the target, the product, but also a confirmation that there is a commercial proof outside our oncology franchise. I mentioned the next generation. We are working with our first bispecific with IL1RAP. We will target, of course, IL1RAP, but we will disclose the target closer to Christmas this year, and it will be within the autoimmune inflammatory space. In addition, we are working with a targeted ADC, and again, we are looking at either hematology and/or solid tumors, depending on where our preclinical mode of action studies takes us. The upcoming milestones and important events for Cantargia. The year-end will be extremely important for us. We will have the MDS/AML data coming out at ASH, and based on that, we will then be looking how we can progress into a phase II-B, maybe a II-B/III, based on the data coming out of the interim analysis. The full data set will be available summer next year. In addition, we will start in Q1 our combination trial with daraxonrasib, which will of course be subject to regulatory approval. Okay. With that, I think I will conclude. Thank you for listening.