I guess last presentation of today, and it's a pleasure here to present BioInvent at the Jefferies Global Healthcare Conference. Maybe some of you have noticed we had a very eventful week last week. We presented at ASCO our latest ovarian cancer data set, and we will discuss that later in more detail. We believe that we are at the brink of developing the new standard of care for recurring ovarian cancer. As you probably will know, there has been no further development since anti-PD-1, anti-PD-L1, anti-CTLA-4. At BioInvent, we are developing a next-generation IO therapeutics, and we currently have two first-in-class programs that have shown strong effects not only in solid but also in liquid cancers, combined with a very good safety profile, which is very important in advanced cancer therapies because there you need to combine products. The company is based in Lund, southern Sweden, and we're quite integrated. That means we have a very interesting platform that allows us to identify new targets and antibodies that could be interesting for immune oncology. Besides this, we have our own manufacturing and our own formulation, and of course, on top of that, clinical development. On this slide, you see our major shareholders. We're listed in Sweden on the Nasdaq Stockholm. As you can see, we have a quite large international shareholder base, Redmile, van Herk, Forbion, HBM, Omega, and others, which are more than 50% of the current ownership. The opportunity that we try to tackle is obviously, as I already said, immune oncology. It's a fast-growing market but still is hampered by a couple of bottlenecks. We are actually focusing on the number 1 bottleneck, which is the immunosuppressive tumor microenvironment, where we have now those two programs that I will discuss today later in more detail. On this slide, you see our portfolio. On top, you have our TNF receptor two program. The antibody there is called BI-1808. We are currently developing this one in ovarian cancer. We just had the presentation last week at ASCO, combined with a very good KOL event. Besides this, we're also developing this in T-cell lymphoma. There we'll have an update coming at EHA next week in Stockholm, also in combination with a KOL event. The second platform program that we are developing is targeting FcγRIIB, very interesting target. We are currently developing this in non-Hodgkin lymphoma, where we also will have the update on the current data set at EHA, also in combination with a KOL event. Besides non-Hodgkin lymphoma, we develop this also in first-line non-small cell lung cancer and uveal melanoma, and there the update will come during the second half of this year, where we have the first readout on that program. I will discuss the two programs a little bit more in detail, and I will start with 1808. Tumor Necrosis Factor Receptor two is a very interesting target that we identified with our first platform in ovarian cancer material that we received from the local hospital in Lund. We found that target upregulated in the tumor microenvironment on T regulatory cells, but only when those cells are in the tumor microenvironment, not in the periphery. That's why we can develop this in solid cancer. At the same time point, the target is also expressed on tumoral T cells, and that allowed us to develop this in T-cell lymphoma. I will discuss both programs in detail. Before I go into the ovarian cancer program, just very briefly, the mechanism of action that we now have characterized quite intensively. I mentioned already, we deplete the most suppressive regulatory cell population of the tumor microenvironment. Besides this, we also activate the myeloid cell compartment, and that basically those two effects lead to recruitment as well as activation of CD8-positive cells into the tumor microenvironment, and those are the cells that you want to have in order to fight cancer. As I said, pre-clinically as well as clinically, we have seen single-agent activity but also strong synergies with anti-PD-1, and that makes sense when you look here at the mode of action. We basically drive the CD8-positive cells into the tumor microenvironment such that pembrolizumab or any other anti-PD-1 can work on those and double the effect, basically. Now on the clinical development, we have done three things, basically. Part A was BI-1808 single-agent dose escalation, where we analyzed the antibody in a number of all comers, and I come to some of the data in a minute. In part B, we started the development also in combination with pembrolizumab. As I said, we saw strong single-agent activity pre-clinically as well as strong synergies with anti-PD-1. That's why we pushed both. Then part C, that is something that I will explain later, has not been started yet, but will be started hopefully by the second half of this year. Some of the data of the single-agent dose escalation. This is, for instance, an ovarian cancer patient, 63-year-old, end-of-the-line patient with all the previous lines of treatment that she should have. Basically, after nine weeks, we could establish a very strong, robust, complete response as a single agent. In the middle panel, you can see also how the regulatory cells behaved. They actually went nicely down during the treatment. Another example is this patient. That is a GIST patient, a 55-year-old male, who received actually 12 previous lines of therapy. There we could install a very robust partial response, which at the end became a complete response. Again, you can see T regulatory cells population is going down, on the right-hand side, you can see the pre-dose, which means a completely cold tumor microenvironment. On the far right, you see then after five weeks after the treatment how the CD8-positive cells infiltrate the tumor microenvironment and basically kill the lesions. Very, very impressive. Based on that, we went into combination therapy with anti-PD-1. To say it up front, so when we combine anti-PD-1, in this case pembrolizumab, with BI-1808, we see a 24% overall response rate, which has to be compared, as you can see here, with pembro alone, which only achieves eight percent. It's actually a factor of three increase, and at the same time point, I didn't mention it so far, we have a very, very good safety profile. It's completely clean and very nice to combine with other drugs. This is the data that we actually presented at ASCO. As I already mentioned, 24% overall response rate, 56% disease control rate. We have activity in both subtypes, which means the high-grade serous as well as the clear cell, which is very important. Most importantly, and that is very differentiating, a very nice progression-free survival endpoint of 10.3 months. If you compare that to the current standard of care, it's actually quite already much better because the standard of care currently has something below ten, so it's around eight months of progression-free survival, which is the combination of pembrolizumab and paclitaxel. We already see it in the combination with pembro increase to 10.3, and this is a very meaningful endpoint because objective response is nice, but what you want as a patient is duration. This you can see very nicely here in this spider plot. You see really long-lasting responses. Another thing that we also saw, which is typical for immunomodulatory drugs, is that you have pseudoprogression. Normally we see the response not at the first scan but at the second scan, which I think is also a good indicator that you really activate the immune response. Basically, we are inducing very tolerable, long-lasting responses in this very underserved patient population. Basically what we're going after, this is a quite complicated slide, but just focus on the bottom part. There you see pembro and paclitaxel. This has become the new standard of care. That was a KEYNOTE study that has been published just a little bit more than a month ago. What we will do is that we compare that alone and in combination with BI-1808, and we expect that we will have a much stronger objective response, but also extended progression-free survival, which is the main endpoint. Based on the available data points that we have, we did some assessment regarding the commercial potential, and we come down to a very conservative estimate of SEK 1.5 billion peak sales, which I think is rather good, and of course, also indicates that the unmet need is very high in this patient population. Switching gears to the T-cell lymphoma. As I already mentioned, T-cell receptor two is also expressed on tumoral T cells, and that's why we tested this there as well. Just to give you some impressions before I go to the collected data. On the left-hand side, you see a PTCL patient, very, very difficult to treat, and you have to focus on the ganglia around the neck that completely disappear after nine weeks of treatment with BI-1808 in monotherapy. On the right-hand side, you see then those very nasty lesions of a CTCL patient that heals very nicely after week 21. What we have in CTCL is actually a combination of immune activation. We see also here CD8-positive cells are infiltrating the skin lesions, but in addition, of course, we also deplete directly and kill directly the tumoral T cells. The data that we'll discuss next week at EHA is here summarized on this slide. You see on top a very strong objective response rate of BI-1808 as a single agent in a heavily pretreated patient population with advanced cutaneous T-cell lymphoma, and a disease control rate of 92%, which is actually quite impressive. We also have already some indication about durability. We have now one complete response Sézary syndrome patient that is ongoing for more than two years. We are testing this program also in combination with pembrolizumab, and we will discuss that also at EHA itself, but also in the KOL event that we have next week. If we plot currently BI-1808 into the landscape of drugs that are used in this field and also developed, on the x-axis, you have the safety, on the y, the efficacy, and you can see that when you have BioInvent or BI-1808 plotted here based on the data that we have currently, we are almost the most efficacious drug. There's only one, which is a CD30 ADC. This one is also very toxic, has a Boxed Warning, and is also limited because you have to be a certain CD30-positive patient, and we are much more broadly usable. Since we have this very good safety profile also in T-cell lymphoma, we expect that we can use the drug also in earlier lines of disease, not only at the end. I think it's a very interesting positioning, and we firmly believe that we can develop BI-1808 as a single agent in the first line of T-cell lymphoma. Just a little bit of timelines. On the top, you see the ovarian cancer. We have done the phase II, part A. We're currently in the phase II, part B, which is ongoing. Some of the data we already have discussed last week, and there will be an update coming during the second half of this year. We'll go by the end of this year for Fast Track designation and then start the dose optimization in combo with pembrolizumab and paclitaxel, as I already have described. That, based on the data, could lead already to a pivotal study at some time point later. In the lower part, you see then the plans for T-cell lymphoma. We have done phase II, part A. Phase II, part B is ongoing in combination with pembro. We are also doing already dose optimization as a monotherapy. During the second half, we'll apply for Breakthrough Therapy designation, hopefully agree the phase II design such that we'll be ready next year for potential pivotal study. We have Orphan Drug Designation, and we have Fast Track designation for this program already. That is all that I can say to BI-1808, our TNFR2 program. Now we'll quickly come to anti-FcγRIIb, our second platform, and the compound there is BI-1206. FcγRIIb is also a very interesting target. It's on one side expressed on tumoral B cells. That's why we can develop in non-Hodgkin lymphoma, and that actually blocks a very important resistance mechanism to anti-CD20-based therapy. Since it's also expressed on dendritic cells in a tumor microenvironment, we also developed this in first-line non-small cell lung cancer and uveal melanoma. I will start with the non-Hodgkin lymphoma first. Obviously, everybody will know non-Hodgkin lymphoma is a very competitive space. You have bispecifics, you have CAR-Ts and other programs. When you talk to KOLs and also treating oncologists, anti-CD20-based therapy will remain core and center because it works very well and is very safe. The only problem with that is every patient, and literally every patient will become refractory at some time point of his or her disease. That's where we come in, because with BI-1206, we can block a very important part of the resistance mechanism. At the same time, BI-1206 is a subcutaneous formulated antibody, so it's a very convenient two-ml injection and also with a very tolerable toxicity profile. No nasty side effects, which means we can use it very nicely in combination. The positioning and differentiation actually to the competition that you can see here. You have lenalidomide-based regimens, bispecifics, you have CAR-Ts. You can see when you look at the very far right of the slides, they are actually quite heavily associated with adverse events, mainly cytopenias and also neutropenias. That is actually very bad because the patient population that we are targeting here is elderly and frail, and they don't tolerate any toxicity. Those side effects, actually, they lead to increased infection rates, especially with severe infection. That means you cure the patient of cancer, but he or she might die at the end of severe infections. That's where we come in because we have the same efficacy as I will show you on the next slide, but no associated severe toxicities, which I think is excellent and tailor-made for this patient population. The data that we'll discuss next week at EHA and also in conjunction with the KOL event is summarized here on this slide. You see that we have a very strong 80% ORR and a disease control rate of 100%. You see that we have activity across different subtypes in non-Hodgkin lymphoma, so follicular lymphoma, marginal zone lymphoma, and mantle cell lymphoma. The treatment has been very well tolerated and no safety and tolerability concerns. This is the spider plot where you can see long-lasting responses. We now have complete responses that are more than three years in complete response after the end of the study, which is also, I think, great for the patients and exactly also what regulators would like to see. When we look at the timelines and plans, we have recruited all the patients into the phase II-A signal-seeking. Now across this year, there will be some follow-up, but also during this year already want to agree the pivotal phase II design, apply for Breakthrough Therapy designation such that we will be ready also there next year for a pivotal study. Last but not least, BI-1206 in first-line non-small cell lung cancer and uveal melanoma. Just to recap again. FcγRIIB is expressed on dendritic cells in a tumor microenvironment, and it's the only inhibitor receptor of the innate immune system. That's why it makes sense to test it also in the context of solid cancer. What we did in the first setting, we were focusing on patients that have received two or three lines of either anti-PD-1 or anti-PD-L1-containing regimens and do not respond anymore. There we saw actually very nice responses in combination with pembrolizumab. This is a uveal melanoma patient who received several lines of ICIs and also chemo did not respond anymore, and we could induce a very strong and long-lasting partial response. Very impressive. Same for cutaneous melanoma, and it's just a few examples that I have here today. Also, a patient who received, I think, three lines of ICIs, and I think at the end, partial response was the best response after ipilimumab and nivolumab, and then progressed again. Then we came in and basically induced a very strong complete response. With that data, we went to MSD, discussed it with them, and we agreed that we went into first-line non-small cell lung cancer as well as uveal melanoma. We have done de-escalation already, and we are currently in the middle part, which is called signal seeking. At the end, we would like to treat 30 non-small cell lung cancer patients and 12 patients with uveal melanoma, and we expect to have the first readout of that study during the second half of this year. I would like to end with the expected key milestones for this year. We had already last week a very important milestone for the ovarian cancer program of BI-1808, where we really had this very nice, long-lasting progression-free survival, which I think is currently very competitive compared to the standard of care, but also to the ADCs, which are very short-lived. Next week we will have the T-cell lymphoma data at EHA in combination with KOL event, and it will be monotherapy as well as combination data. We also have at EHA the non-Hodgkin lymphoma data set, also in combination with a KOL event. During the second half of this year, 1206 first readout for first-line non-small cell lung cancer and uveal melanoma. Next year, we will be as busy as this year, so we have then two pivotal studies that will be ready to start, and the main value driver at the moment, that is why I also started with that at the beginning, is the ovarian cancer data set. That, of course, will further mature. By second half of this year, we'll start the comparison with the standard of care, plus the standard of care in combination with 1808, where we'll have the first readout by second half of next year. Thank you very much.