Cantargia AB (publ)

Thank you and welcome. My name is Magnus Persson. I'm the chairman of the board of the company. By background, I'm a medical doctor and a scientist, and I have more than three decades of professional life science investing experience. You're not used to see me at these calls, and I'm here since I would like to shed a little bit of light on the recent transition of management. The board decided after careful consideration that it was time to introduce new energy to the company and to find a manager with more transactional, commercial and international experience. Damien Maron is a board member and thus knows the company very well and is generally well suited for the job. And he has volunteered to step in as our CEO. We I and the board wish to thank Göran Forsberg for his 11 years as CEO of Cantardia and to stress that there was nothing untoward behind our decision to transition management. So with that, I would like to leave the word to Damian and I will... So Damian, the floor is yours.

Thank you very much, Magnus. Thank you. I am very excited to be leading Kantarga at this time. We've got a number of very interesting opportunities in our portfolio. My intention during my tenure here is to drive and to accelerate the value creation for all of our stakeholders on the back of these opportunities. Just to give you a brief introduction to myself, I've actually been 40 years now in the pharma and biotech industry. I'm a scientist by training, a pharmacologist and cell biologist. I did about 10 years in big pharma R&D, most of that in clinical development. I then had a couple of business roles, then was head of business development for 3M Healthcare in Europe for five years. Moved into the biotech industry in 2002, a company called Mycox in the south of France, which was publicly listed. I helped raise there over 250 million euros and did deals with Merck and with Pfizer and with some biotechs. I moved into CEOing in 2008. I subsequently CEOed four companies, two of which were acquired, one by Roche for a rather nice sum of money, another by another biotech. I IPOed one of my companies on the Euronext in Paris. and unfortunately also had to close one down because we couldn't see a way forward for the company. I moved into having a portfolio of board positions about eight years ago, and I also do advisory work with a boutique healthcare transaction advisory firm. So here we are today. Let's have a look at the events of the fourth quarter and since that date. So we reported positive new results on biomarkers and on safety from the ongoing clinical phase one study with Can10, our immune and inflammatory asset. Looking at Naginolimab, we had new results from the clinical studies, SESTA4 and Kappa4, where we tested Naginolimab in combination with chemotherapy in several cancers. We saw positive signals of effect, particularly in non-small cell lung cancer. and in gastrointestinal cancers. Going back to CAN10, we expanded the study to explore higher doses of the antibody based on the positive results we saw and the very good tolerability. Finally, in Q4, we carried out a right issue, which generated proceeds of 120 million sec before the deduction of the issuing expenses. And obviously, as Magnus has just spoken about, Since the reporting period, Joram Furstberg has stepped down as CEO, and I am now leading the company forward. So first of all, I'm going to spend a few minutes on CAN10, our antibody in autoimmune inflammatory disease. This is going to be Generating results in the next few weeks, starting in the next few weeks from the multiple ascending dose part of the study. So that's why I'm focusing on this first. Just first of all, the design of that study, that first in human study. So we have already completed that single ascending dose portion of the study and reported interesting first results. Eventually, we did 10 dose cohorts. As I have just mentioned, we increased the number of cohorts based on the results we saw. We are now in the multiple ascending dose portion of the study where we will give four doses, two weeks apart, either to healthy volunteers or to groups of patients with plaque psoriasis. There'll be two dose cohorts for the volunteers and two dose cohorts for plaque psoriasis are planned. The healthy volunteers allows us to look at higher doses and prepare for our phase two study that I will tell you more about in just a moment. And the plaque psoriasis patients will enable us to look at mechanistic studies and biomarkers in an immune inflammatory skin disease. So if we take a look at some of those results that we saw in the single ascending dose part of the study. So as in the multiple ascending dose, the cohorts were blinded and placebo-controlled. So in each dose cohort, we had six subjects on CAN10 and two subjects on placebo. We have reported nine dose groups from 1 to 400 milligrams so far. In terms of safety, which is always clearly a very important parameter in a first-in-human study, we have seen no safety signals of any significance whatsoever, which is clearly very comforting. We have been able to demonstrate, as you see in the bottom right, bottom left, excuse me, in the bottom left of the slide, you can see that we have full receptor occupancy documented at CMAQ starting from about the middle of the dose cohort range from say cohort five and on and upwards. And you can see that we have that occupancy in monocytes and in neutrophils. We have also shown potent pharmacodynamic effects on IL-1 and IL-36, two of the key cytokines, inflammatory cytokines we aim to block with CAN-10, both at C-max on the day of dosing, so the maximum concentration that the drug reaches in the blood, but also eight days later from that single dose on day one. And so you see on the right-hand side, you see, first of all, the day one results, where you can see a complete abrogation of the activity of IL-36. It can no longer induce IL-6 release, which is what we are measuring, and that you see again really significantly from dose five onwards, cohort five onwards. And you see at day eight, perhaps even more impressive results, that you really see the abrogation starting again from around dose cohort five, but very strongly. And that, I remind you, is from a dose given eight days previously. So after this successful SAD, we have moved into the MAD part of the study. We are building towards a study in hydrodinatus separativa, or HS. That's going to be our initial indication for a phase two study with CAN10. So HS is a severe study. chronic inflammatory skin disease. As you can see from the pictures on the right hand side of the slide, you can see varying degrees of severity of the disease in those pictures. Patients get nodules, get scars, and eventually they get what are called draining tunnels in their skin, which are very unpleasant and very painful indeed. You can see underneath a graphic of how the different stages affect the skin layer, causing more and more destruction and inflammation. It is a disease with several inflammatory components involved in the pathology, and this is one of the reasons we believe, obviously, that CANTEN can be very helpful, given that it affects multiple cytokines in the IL-1 family. It has an estimated prevalence of 0.7 to 1.2%, so there are a lot of patients with this disease, even if it's not particularly well known in the way that, say, atopic dermatitis or psoriasis are. There are current treatments, but they are somewhat inadequate. So up until recently, antibiotic steroids. Then we have Humira, the anti-TNF antibody. Recently, we have antibodies against the cytokine IL-17. They are Cosentix and Bimxelix. And with those products, about 50% of patients respond in trials, which of course means 50% don't. And what's more, patients can become refractory to those treatments. So there is a very, very large medical need in this area. And just talking to you about why Can-10 is particularly well-suited to this indication. We affect through our interaction with the IL-1 wrap, the IL-1 receptor accessory protein. We affect the production of or the activity of IL-1 alpha and IL-1 beta, the IL-1 cytokines, but also IL-33. through its ST2 receptor and also the IL-36 receptor complex affecting IL-36 alpha, beta and gamma. Why are these important? Because they are associated with different facets of this disease. The IL-1 drives inflammation, IL-33 drives itch and IL-36 is seen as being quite responsible for the development of the draining tunnels. Interestingly, and very importantly, we have clinical proof of concept for at least the IL-1 and the IL-36 approach. So there are antibodies in development, one targeting IL-1, which has shown some efficacy in HS. That's called lutecizumab. And one targeting IL-36 called spasolimab, which has been shown to have effect on the draining tunnels. We know that we block all three of these cytokines, so we're expecting one treatment to be able to combine the treatment effect of both lutecizumab and spasolimab and add extra efficacy on top of that. So we are going to be moving forward with that program through the year. Now, moving to naginolimab. So for naginolimab, we have published results in PDAC, pancreatic ductal laryngocalcinoma, showing a very strong benefit in patients, particularly those who enter the study with a high level of IL-1 wrap. And in fact, as well as those patients entering with a high level, it's also known, it's been demonstrated that having a high IL-1 wrap is a very poor prognostic factor in pancreatic cancer. Because we saw these very interesting results, we have a diagnostic test in development to be able to have a companion diagnostic to Naginolimab that will identify these high L1 RAP patients who benefit particularly well from the treatment with Naginolimab. This will enable our continued development in that high L1 RAP subgroup. And during this year, we're planning for regulatory interactions about the diagnostic test and the further development of Naginolimab in pancreatic cancer. We also reported results from SESTA4 and KAPPA4 with positive signals of efficacy in both SCLC, lung cancer, and gastrointestinal cancers. Importantly, we are estimating that we will be able to release the initial results from our first randomized control phase two study of Nadjinalimab, the study called TRIFOR, which is in triple negative breast cancer, or TBNC, TMBC, and we expect to release those around mid-2025. know we have spoken about previously we have an acute myeloid leukemia study in the final steps of preparation a study sponsored by the unit u.s department of defense and which will be conducted at the university of texas md anderson cancer center so just to summarize there over overall now we have over 300 patients treated with naginolamab And clearly, there are multiple opportunities here to take adrenolamab forward and make a significant difference to the treatment of patients with these cancers. Just as a reminder, you have seen this data before, but just as a reminder of the efficacy of adrenolamab in PDAC and the differential effect according to IL-1 RAP. So you can see here on these two graphics, the one on the left is the overall survival by IL-1 RAP subgroup. And you can see here that we saw a considerably higher survival rate in the IL-1 RAP high subgroup. And in fact, the OS and IL-1 high RAP group was 14.2 months versus 10.6 months for the IL-1 RAP low patients. And that was statistically significant difference. And you can see on the right what has driven this. You can see the IL-1 RAP high group on the left. You can see where the lines go down. That's where there's a response to treatment. And you can see we had many more and larger responses to adrenolamab in the IL-1 RAP patients versus the IL-1 RAP low. These responses were deeper and more durable with over 11 patients having a 50% or more tumor size reduction. So this really is what drives the interest to move Naginolimab forward into the next stage of development in PDAC. Just finally here, going to say a few words about the milestones we have coming up during 2024, 2025 even, excuse me. So for Naginolimab with PDAC, we are developing, as we said, the CDX and we expect to have user regulatory update around Q2. For TMBC, we expect shortly that the recruitment for the Triforce study will be completed. And as I mentioned, we will have those initial results in mid-year. And we expect reasonably soon to be able to announce the start of the AML study that I spoke about a moment ago. With CAN10, as I mentioned, we will start to bring out the initial MAD results in Q1 and the complete results in Q2. And we're planning towards the start, hopefully, of a phase two study in HS towards the end of the year. We also have our CanXX platform and we may have new results from that and also the preclinical and translational results from Naginolimab and Can10. So I hope you'll agree that's an extensive news flow that we have during 2025. With that, I will hand over to Patrick to talk about the financial results.

Thank you very much, Damian, and I am happy to present to you the... Why is this not working? There we go. So the financial highlights are here on the screen in front of you as reported this morning. And I'd like to say that we see in general on the cost side a reduction both on R&D expenses and on general and administration. both in the quarter and obviously in the full year numbers. So that we ended the year with operating expenses of, or the quarter, sorry, of 40.7%. That was a total reduction of 43%. And if we look at the full year, our operating expenses were at 168.6, total reduction of 42%. And then our net reported loss a little bit lower due to positive impact from our net financial items. But so overall, the message that we have been sharing across the year has sort of continued in the quarter, and the reduction of our clinical activity mainly in adenolamab and less production costs than in the previous comparison period is what's driving this reduction. Now, over to our cash position, we had a net outflow in the quarter of about 26 million. We reported available funds of 33 million, but I would like to, for the purpose of this call and for answering some questions, I would say that we have virtually 140 million on our available funds. 107 million at a issuing institute by the end of the year that we received in early January from the completed rights issue. But obviously for accounting reasons, we are reporting 33, but virtually 140. With that, I hand back over to questions and answers.