Morning still to everyone. I'm Hilde Steininger, CEO of Cantargia. Next slide, please. This is our Oh, I have a clicker. Yep. Perfect. We're listed on Nasdaq Stockholm, and hence we have a forward-looking statement. We deal with inflammatory signals, and inflammatory signals are an important part of serious disease, and many of these serious diseases are not drugged well. That is not due to the fact that there's not an obvious target. There's a lot of good targets in inflammatory signaling and inflammatory diseases. However, it's about knocking and blocking the right way. If you block too narrow, the disease will find a way around it and counteract your effects. If you block too broad, you risk bringing the patient's immune system down along with you. We believe that our target, Interleukin-1 receptor accessory protein, IL1RAP, is a very good target to do exactly the right kind of blocking. IL1RAP is a co-receptor for three different interleukin receptors, IL1, IL33, and IL36. By being able to target three interleukin receptors more or less at the same time, either full block or blocking over the whole span of the three receptors, this target has shown to be very versatile. We have clinical results from MDS and AML, and I'll come back to that, as well as PDAC and non-small cell lung cancer. We also have very interesting preclinical results in the inflammatory pathways, which is a part of our CANxx engine. Our pipeline looks like this. Those of you who follow Cantargia close know that we have now announced that we will do a combination study with daroxadrecept. I'll come back to that, but daroxadrecept was just recently approved for second line for PDAC. We also have a very interesting collaboration with MD Anderson Cancer Center in MDS and AML, and even though it's an investigator-initiated trial, the results coming out of that can be used in further regulatory filings. Our CANxx and CAN14 is developing nicely. We have a bispecific product in mid preclinical development, and we plan to announce the target closer to Christmas this year. CAN10, as you might remember, was sold to Otsuka, and they are developing the product nicely, and it remains an important part of our portfolio. Let's turn to MDS and AML, myeloid malignancies. The standard of care in myeloid malignancies is chemotherapy. However, chemotherapy leaves a reservoir of malignant cells dormant, who can again be awakened and be a sort of seeding progression of the disease. In addition, the chemotherapy would target also the healthy cells, putting the patient at vulnerable risk for inflammatory and infection diseases. The cool thing about IL1RAP is that it is highly expressed in the leukemic stem cells, so the malignant cells in the bone marrow, and it is not expressed in the normal hematopoietic cells. That means we are able to target the malignant cells but spare the normal ones that the patient will need to recover. MDS and AML are part of the same disease area, and in MDS, there are approximately 400,000 patients globally, and it is characterized as less than 20% blast cells, or the cells that are malignant, in the bone marrow. It is characterized in six groups from very low until very high. Of these MDS patients, 30%-40% of the high risk will progress into AML. AML is also a highly deadly disease, and 10%-30% survival after 5 years. This is an area with high unmet medical need, and again, standard of care is a combination of chemotherapy. There are few targeted therapies, and we think that our targeted therapy will be one of the most effective ones. The study running by MD Anderson Cancer Center is two cohorts, one in MDS and one in AML, both with 20 patients in each arm. Standard chemotherapy backbone, and we have our first cycle as a standalone nadunolimab treatment. The primary endpoint is safety and tolerability. However, we did see some signals in a data cut that was performed January 2026, of which we saw five out of five patients had complete remission. There is a new data cut that was performed June 30th, which MD Anderson Cancer Center and us will present at ASH and be a part of the ASH abstract. That is under embargo for the time being, but it will be public November 4th. The full data set will be reported in December this year. PDAC is still a very important area for us. A reminder on our clinical effect from our phase 2A study, 73 patients received nadunolimab in combination with standard chemotherapy, GnP. We saw a 13.2 months overall survival as compared to 8.5 and 9 months on GnP. 58% were still alive after 12 months, and this, at that time, was a very promising signal. The landscape changed, and the RAS inhibitor was approved. daroxadrecept had 5 weeks of regulatory interactions and got approved after 5 weeks this summer, and has now and will become the standard of care for second line in PDAC. We believe that by combining our two products, we are not just testing safety, but we are adding something to the efficacy to the patients. We have overlapping pathway. Oops. There is non-overlapping pathways, but crosstalk between the two pathways. However, what also IL1RAP with the one component of ADCC, does is to attack the tumor microenvironment, which the KRAS inhibitors do not. So that is a complementary effect that we think will be of great benefit to the patients. Importantly, all the KRAS in development, also the MEK inhibitors, will be part of the same pathway. There is no product, as far as we know, that address this exact pathway. CAN10? Yep. Our pipeline is a very interesting engine for generating new IL1RAP products. We have more than 500 clones now in our library, and already we have produced two clinical candidates, CAN10 and nadunolimab. This library we have used to generate a bispecific CAN14, and we are also utilizing this target and library to pick an ADC that will come as a later part of our development. Very important engine for Cantargia. To summarize, we have important milestone coming up. At year-end, we will have the MDS/AML data, and we will disclose the second target of CAN14. In Q1 2027, we will have our first patient treated in our combination trial. In mid 2027, we will have the full data readout of the MDS/AML trial. Thank you. Oh, half. Thank you. About to go. Thank you so much. Are there any questions in the room? I was wondering if you could talk a little bit more about the MDS space, maybe the competition within that space. Yeah. Good question. The AML is a bit more crowded, but MDS, as far as we see, has seen a lot of failures in the last three to five years. As of now, there's only one company ahead of us, Faron from Finland, Faron Pharmaceuticals. They are initiating 2B now, but still not very far from us, and we are super happy with our results stacking up to their results. We see this as one of the few areas in leukemia that has quite an open space. Right. So it's a question about the financial situation. You did a raise this summer, wasn't it? How would you describe the situation financially for Cantargia right now? It's good. We are doing what we need to do. We are expanding the MDS/AML study with MD Anderson. We're also investing in our 1B with daroxadrecept. That puts us in a very good position to be able to compete and to combine with RAS inhibitors, second line first and most probably first line will be also with a KRAS. So that will position Cantargia in the perfect spot in PDAC, we think. Also have a question here about a launch plan, how far along you are in terms of thinking about markets, pricing, strategy, positioning on those markets, and so on. Everything, basically. Well, as we know in biotech, it takes quite a few years. We are approaching phase 2A, so that means that we will have to go into a pivotal trial in both PDAC and MDS, a phase 2b/3. That will take also some years. Difficult to estimate exactly when. But yeah, we are some years from market from that. Right. Thank you so much.