Mendus AB (publ) (IMMU) Earnings Call Transcript & Summary

Welcome, everybody, to our first update here with me, the CEO. I have with me today, Alex, who is part of the company nearly forever and Sijme, who you know well, because he presented so much in the past. I'm happy to have those 2 with me. I would like you to give you the first building blocks of the strategy for Immunicum forward. It is work in progress. I clearly stated when I was taking on the job that by the end of September, I will come out and share some first thoughts about the strategy forward with Immunicum with you. So this is the purpose of that meeting today. Of course, this building blocks we are presenting today have to be translated into strategic plans, tactical plans. There will be budgets around that. There will be resource planning around that. That means you will see me frequently in the near future again when I present step-by-step how we want to tackle this new future of Immunicum. I have to put that as a disclaimer up there. I don't expect you to read that in detail, but we are a public company, and you should notice that, please. Immunicum at a glance. I think you are quite familiar with Immunicum. I don't have to spend too much about it. Immunicum is one of the companies that focus on cell therapy and immuno-oncology. And what the vision of that company is really is to add quality to the immuno-oncology space. And spend a lot of time with us so that we show you what makes us unique and why we are a really good addition to the world of immuno-oncology. I have to tell you, being now 1 month with Immunicum that I'm really grateful for the development team there. The reason for that is, if you are talking cell therapy to have a team that has the experience, that has a track record of fulfilling trials to move trials into the finish line is really something that is rare on the planet. On one thing because cell therapy is unique and new; and secondly, that those teams that can perform those clinical trials and do it successfully really hunted by everybody. So I'm happy that we have that team, and I'm happy that this team is dedicated, committed to make those building blocks, which we will present to you happen. I don't want to spend too much time on MERECA. This has been done in the past enough. But when I reviewed the company, the most striking thing about that was, besides something you will show later on, Alex, as part of the preclinical package, this was the tendency we see in MERECA to clearly more complete responses than the standard of care at that point in time and something where I'm really interested and eager to see that evolving, what is happening with the survival of those who had a complete remission. That is not only complete remission, but durability is that an effect. Keep in mind that one of those things we would like to see as a company is that the durability leads to a clear survival benefit for the cancer patients. We have come up with 4 important building blocks of our strategy forward. And it will be Alex, now in the beginning and later Sijme, to explain you this building blocks in more detail. But let me allow you, from my point of view in the beginning already to state where I think it is important to know that as an investor into Immunicum. I think and my team is sharing that that we have to own our own way to the market. So we have to be able to move our cell therapy into the patients. We should not be depending on the grace of any larger pharma company or biotech company to do so. So our own way forward independent. Then, of course, it is important that we have something that is attractive for those who are the big players. Because if we would like to add quality to immuno-oncology, we cannot ignore them or try -- think that the market leaders don't influence us. So we have to be possible to make deals with them, to partner with them and to do that in a way that is highly attractive for them and for us. The other thing is, I believe that a young company like ours, that is going for innovation has to be at the cutting-edge of science and has to deliver breakthrough solutions. Solutions where people later on will say, yes, good, logical, that helps patients and that makes our therapy against cancer, a little bit more effective maybe even more than that. And the other thing is we should put with knowing so much about dendritic cells and having now the first evidence in hand in clinical studies that we should not put all our eggs in one basket. That means we should think about using our know-how, our expertise about dendritic cells to make dendritic cells multiple products to talk about a portfolio that we have multiple options to partner, multiple options to do combinations, multiple options to help patients not dying of cancer. I think it is time now that Alex comes up here and tells you why this what I believe could happen is in his eyes, already happened. There are facts, there are figures, there are data, this universe of oncology is driven by data. And Alex, please show us the universe.

Hello, everybody. I will try to take it rather briefly, the basic. And I start with figure, we are saying that immuno-oncology, next wave of immune primers. And we really believe that combination therapies of immune primers, and when I say immune primer, I mean like adjuvants or even including vaccines and Immunicum Ilixadencel, together with drugs that inhibit tumor immunosuppression could enable the next breakthrough in cancer. We are the first one, when we -- or we -- others, long time ago introduced the chemotherapy, and when we could see that we -- the median Overall Survival was a little bit prolonged, but still the patient died after some years. Then came the immuno-oncology. And by monotherapy, you could see that there was a very special feature with that type of treatment. And that was that you had some type of tail rising, which means that several of the patients actually survived for several years. So instead of being a deadly disease, it became to be a chronic disease in subpopulation. And finally, by combining different types of immunotherapy, you may rise the tail even higher. So hopefully, we will have -- yes, hopefully, the majority of patients treated with different combinations including Ilixadencel, being like 50%, 60%, 70% experience, perhaps not complete response, but the long time response that will lead to long time survival. And just to show you where we are in this field of immune primers, vaccines, adjuvants. If we start with a vaccine approach and with a vaccine that contains a new primer and antigen. And from the start, studies were conducted in the clinical setting where they combine something called tumor-associated antigens. That is antigens that are self-antigens. They are normal antigens, but they are overexpressed in the tumors. And when they produce these antigens, they could be produced as off-the-shelf proteins and then they will combine with some type of immune primer and by that trying to affect a tumor response. However, there is certain challenge with these non -- these self-antigens that are overexpressed. They are not tumor specific. And they are actually the best cytotoxic T cells that recognize these antigens, they have been deleted due to an education of the thymus, leading to deletion of the stronger T cells. So even if you use different immune primers together with those antigens, you certainly see any good effect. And I think there's more than 20 Phase III studies conducted with this approach without any clear success. So just like 5, 6 years ago, the immuno oncology field started to look at these mutation derived tumor antigen. So that is a protein -- parts of proteins that are changed due to the mutation in the tumor. And several big companies have now starting to use these type of neoantigens. They first have to characterize these antigens in the tumor. They have to produce these antigens. And this production is really challenging because it's time consuming, it's expensive, and you just reach to one product per patient. And still, they haven't solved the problem of which primer to use. I mean Neon Therapeutics, they are using poly-IC, and they have done studies that can induce tumor-specific T cells, but they have no good effect on the tumor response still. And then we come to our area, and that's actually to use the tumor itself as a vaccine factory by injecting an immune primer into the tumor, which then contains all type of mutation derived neoantigens. And we are not alone. We have other companies. They are either injecting this Toll Like Receptor ligands. They may inject the STING ligands. They may inject oncolytic viruses. They may even inject the vectors coding for IL-12 unless they're interested on IL-12. But as we see it, based on the data, clinical data that has been published, it appears to be a limited immune priming effect by doing this. And we strongly believe that Ilixadencel is actually the optimal one, the optimal immune primer, and I will try to shortly explain why. And I have to take some steps back and look into the viral space, the virus story, which is that immune primer we know since long time that strong viral infections, they create -- usually creates a strong cytotoxic CD8+T cells response. And I used to call this vaccine a vaccine that -- which has eradicated smallpox as the king of vaccines. He was Dr. Edward Jenner more than 200 years ago, who actually found that or saw that milkmaids milking the cows, they usually got something called cowpox. And they never or very seldom developed smallpox. So then he thought that there was something in this cowpox that affected, when he didn't know about the immune system, but in some way protected people from getting sick with smallpox. So he inoculated material from this cowpox lesions into the skin in healthy humans. In this case, it was young boy 8 years old, I think. And it developed this fantastic vaccine that actually eradicated a very fatal virus infection called small pox. And some years later in 2008, there was a publication about the immune reaction. And they vaccinated healthy volunteers and then they looked for the T cells in the peripheral blood. And what they saw was this huge increase of very specific CD8+T cells producing interferon-gamma, TNF-alpha indicating that these were the cells that actually killed the virus affected tissue cells. So now we come to explanation how come that this vaccination had this type of effect. And this is crucial because most immunologies at least before and even now have this view that is that you have virus particles infecting the dendritic cell. By infection this dendritic cell will become activated, will migrate to the lymph node and cross what we call cross-present viral antigens to CD8 cells so that they become activated. But already 20 years ago, the discoverer of these dendritic cells, Ralph Steinman, he was looking for this, what happens when dendritic cells have become infected by this vaccinia virus, and he was very surprised. Because what he saw was that they become enable to migrate. They actually died within days. But before dying, they introduced whole battery of inflammatory factors that you can see as alarm signals. And others have then gone further with this type of theory, really showing that this infected inflammatory disease may produce factors that will instruct the bystander immune system by recruiting certain cells like NK cells and a special subtype of dendritic cells that are cross-presenting DCs. And this will lead to that NK cells will kill the infected cells. The dying cell will be captured by cross-presenting DCs and this cell that will not be infected, it just capture materials from the virus and from the dying cell. They travel to the lymph node and efficiently activate CD8+ T cells. So just once again, we are focusing on this part as the optimal immune primer, the infected dendritic cell approved from a third DC. So what we are doing is actually that we are mimicking -- Ilixadencel is mimicking virally infected DCs. And they are produced by isolating white blood cells, monocytes from healthy blood donors through a process called leukapheresis, we usually get at like 1 billion of monocytes. These monocytes are cultured for 4 days in special media, leading to differentiation into dendritic cells and then we activate these cells, not by a dangerous virus, we activate these cells with certain molecules that mimic a strong viral infection. And that is a combination of Toll Like Receptors 3 ligand, 7/8 ligand together with interferon-gamma. And 18 hours later, they are washed and then cryopreserved. And we have now like 4 years shelf life of these cells. When needed, they are just thawed, washed and we just store and then inject it into the tumor. And for one healthy owner, we get 100 doses of ilixadencel, 10 million cells per dose. And actually 50 patient can be treated by using 100 doses. There is no need for patient matching, no need to genetic modify the cells and no need for tumor material. So it's really an off-the-shelf immune primer still cell based. And just shortly, I think that Sijme used to be the one presenting this cascade. This is a tumor. We are injecting 10 million dendritic cells. And these cells, they believe that they have been affected by very dangerous virus. They are secreting a lot of factors that will induce recruitment of the patient’s immune cells into the tumor. The NK cells they will become activated, they will start to kill tumor cells just locally, leading to the release of the neoantigens. The incoming bystandard bystander DCs will come to the place start, they will start to eat these dying cells and in this environment, full of cytokines produced by Ilixadencel but also like interferon-gamma produced -- that would lead to desymmetrization, migration to the draining lymph node and priming of tumor-specific T cells. So if we go to the tumor models, preclinical tumor models. Then we have chosen the tumor model that is rather hard to beat is, for example, they have to grow for 12 days, they are 100 cubic millimeters big, and they are actually -- this tumor model is PD-1 resistant. So if we treat these tumors with PD-1 you have near to no effect. If we add this standard Toll Like Receptors 3 ligand into the tumor together with PD-1, we have no effect. But when we add Ilixadencel together with PD-1, we will have this growth inhibition. And that means that this is a tumor growth, and you see it is delayed. So the median survival will be prolonged. Then we have combined it with anti-VEGF, which is then mimicking the sunitinib effect. And as you can see, just by giving anti vascular endothelial growth factor, you have some delay, limited effect. But when we add Ilixadencel, we had a clear cut further delayment of tumor progression. And actually, we have like 10% immune -- total complete responses in these tumors. And finally, our late findings when we are combining with CTLA-4. It was really interesting. CTLA-4 treatment monotherapy is affecting the tumor growth. But it does not induce any complete responses. When we add Ilixadencel, we see a 7 out of 10 mice in this experiment. They had a complete tumor response. And when these 7 mice were rechallenged with a tumor at day 60, none of them developed any tumor, indicating that we have induced -- or Ilixadencel induced a immune memory. And finally, we have done additional experiments to look for which cells are needed for this antitumor effect. So we have depleted CD8 cells, CD4 cells or NK cells. And what we saw was that the main contributor to this effect was actually the CD8+T cells. Sven, I think you have some questions. You don't believe me.

No, it's gorgeous. This slide here is the most important slide we present today. And the reason for that is for the first time ever you have shown Alex that you can do complete remission. That means you have a complete response and your mice are not dying anymore. And in addition to that, you have shown if you put the tumor back in the immune control works and can stop any kind of tumor growth. For me, this is the vision, the mission of the company show that it meant, and we really contributed something. Thank you, Alex. For all of those who would like to have the summary of that, a little bit less scientific, what we do there with the immuno-oncology guys, it is -- if you -- I like driving cars. So for me, it looks like remove the hand brake -- you get in your car, remove the hand brake, you release the brake, and you try to push the pedal to the metal, but very little happened. Why? Because you forgot to start the engine. And this is Immunicum, start the engine and all the other things may work. Alex will kill me for that nonscientific thing here. But I hand over to Sijme now, who will put that into building blocks that are more business development driven, corporate development driven and show how we move that forward. Sijme, please?

So yes, with this introduction, we are now ready, of course, to look at what is our situation analysis and what are the development priorities moving forward. So let's start with the pipeline. You've seen this, of course, a few years already, slowly progressing, but getting to the next stage of development. You all have seen the results from Phase II MERECA. And of course, we've now completed that Phase II in combination with kinase inhibitors, the VEGF inhibitors that Alex mentioned in kidney cancer. We have also completed actually some interesting studies in Phase I that is the liver cancer study and also the GIST study or the Gastrointestinal Stromal tumor study. Now these studies have been in combination with kinase inhibitors or TKIs. And we have an ongoing study with another class, which are the checkpoint inhibitors, and you've seen some of the results in the preclinical work that Alex has shown. Now if we look at the completed studies, these have been based on the TKIs, the Kinase inhibitors. We started all the way back in 2012 with a small study in Sweden in kidney cancer because there we had an interesting opportunity to inject into a large kidney tumor and then see if we get a response against the metastasis. So really see the systemic mechanism of ourselves. And that was very positive, but of course, a small study. Based on that, we also expanded it into liver cancer, which is very difficult-to-treat tumor, difficult to treated with other immunotherapies, but we were able to also show a positive immune activation and even a partial response as a monotherapy. Now we've also completed this small study, and we actually published the detailed results in June. And this small study was even in 6 patients done here in Sweden. But it was a very exciting study because these were patients with GIST. So this is a small indication or orphan indication, but patients that were treating -- were treated with the TKI, were already progressing on that TKI, so they would normally move to the next line of therapy and hope for some kind of response there. Instead of doing that, they were given Ilixadencel and see if actually this progression could be reversed. And we saw some very interesting signs there, which again confirm with TKIs we seem to be having a very interesting synergy. Now the biggest proof-of-concept there, of course, came from the Phase II study, the MERECA study. It was a randomized controlled study, so no one can talk about anecdotes anymore. It's a randomized controlled study. We were comparing to groups, even though it was still maybe a small Phase II study. And there we saw the signals of an immunotherapy. Complete responses, which you don't expect from a TKI, more durable responses. And of course, in August, we now reached the median survival in the control group, and we are continuing to follow patients in the experimental group to see what the difference in survival would be. So that's what we call proof-of-concept achieved. Now how to build further on that proof of concept. In kidney cancer, since then, actually a lot has happened, right? It used to be that you were treated with sunitinib after diagnosis. And after progression, you would maybe move to cabozantinib and later also, lenvatinib was added. So these are all similar classes of TKIs marketed by some of the larger pharmaceutical companies. Now then a few years ago, we had the introduction of actually a combination of immunotherapy. So that's the PD-1 CTLA-4 checkpoint inhibitors that Alex has also showed in the preclinical results. So very exciting. Because for the first time, they actually showed that they could induce complete responses in kidney cancer. And this was while we already had the MERECA study ongoing. And then shortly thereafter, we had the introduction and now the approval of this PD-1 checkpoint inhibitor, TKI combinations, and their developments are going quite rapidly. You see Merck, who are marketing KEYTRUDA in first-line, Pfizer with avelumab, but also Pfizer with axitinib, the TKI using those combinations. And recently, we've seen impressive results from BMS with nivolumab and cabozantinib, which is actually from another company. This is really showing that this field is maturing, and there's a lot of large companies going in and trying to take part of the market share of this field. So it's very much an elephant race that we are trying to join. And of course, that is sometimes difficult being a small company. Now the big difference here is that, of course, a few months ago, we announced that we were granted by the FDA RMAT support, so RMAT Designation. Now this was based on their validation of that our Phase II results are exciting. They're very interesting, and they would like to help us how to move this to the market. However, they also indicated to us that RCC is a competitive market, where there are multiple options available to patients. So how to move this best forward in a relatively competitive market? Now if you look on the left, if we were to combine with these PD-1 TKI combinations, you know that you have a requirement for a large study that you would have to compare our triple combination compare to the control group being one of these classes. You would have to choose one or maybe combine different groups in that study. It will be a large study, and we will be very dependent on a partner helping us either with at least the supply of some of these classes, but also preferably the execution of such studies. Because, again, it's an elephant race, you need a large company helping out there. Now in terms of the nivolumab/ipilimumab combination, this is still a differentiated concept with a different type of effect and more complete responses we see in that combination, but it's fighting for market share with these PD-1 TKI combinations. There, we would have the same issue. We would have a need for a partner to do a large study to get it to the market. However, we think that based on our preclinical data, there might be more potential for breakthrough and actually have a more differentiated triple combination in these markets, but still a need for a large study, if you would move into the pivotal right away. And then you have still the good old sunitinib as we call it, where we have proven the synergy with this class, and it is being used in second line. We also see that it is going off patent, and that would create for us a situation where we have more independence of making that combination and doing the development ourselves. However, even in that setting, it's an established drug, and you would have to go head-to-head, showing the difference in this competitive market where multiple treatment options are available. So how to best move that forward? What we have decided and what we are now presenting as our strategy is that what we see as the best move forward in RCC being this competitive market, is actually to take a side step and instead of moving into pivotal and being dependent on a partner helping us out, it's actually better and a more cost-efficient way of using our profile of doing a smaller study to create this concept to pursue this breakthrough effect that we believe is possible based on the preclinical data to capture some of the excitement of partners that based on those data, they could not ignore us and they would have to get us supported through a pivotal program. What we are proposing next to that and what we actually call our first strategic pillar is using our experience with sunitinib as an established synergy, not moving forward in second-line RCC or different line RCC in some kind of large study, but actually sidestepping and use the same concept, but then in an indication that is smaller and where we already have this interesting Phase I data. So sidestepping, using the same combination of sunitinib, having the benefit of independence, but then applying it to a smaller indications where we can more quickly make a difference and get to the market. So that's first pillar, I'm going to tell you a bit more about, we call independence. We combine with a class that is going off patent, and we can do the study ourselves. And it's also more independent because these are niche indications with high unmet needs, limited treatment options available. And therefore, any new innovation is also supported with a fast track to the market. Now GIST and sarcoma are actually under the same umbrella of the sarcomas. The sarcomas are group of cancer types that develop in the connective tissue and GIST is one of them. Now in GIST, we know that with sunitinib, we have already marketed TKI, where we, of course, have the development experience in the second line. And the GIST market, as such, is already around $1.5 billion forecasted for '26, even though there's only 5,000 patients in the U.S. diagnosed every year. If you look at the larger group of sarcomas and soft tissue sarcoma is the other part of the sarcoma umbrella, you actually go up to around 13,000 patients in the U.S. So still a niche indication, an orphan indication. And there also, you see very limited innovation. Immunotherapies are not making the difference or not being pursued that much in the indication. Chemotherapies are given, and we know that with chemotherapies, we can also create an independent combination. So that is actually a combination of indications under the same umbrella that have a similar high unmet need, a similar faster path to the market, where we can apply our already achieved proof-of-concept and get to the market more quickly and more independently. Now we can apply for an orphan designation in those indications, and that will have the benefit that once you get to the market, you would have a more favorable reimbursement and pricing of your therapy and also regulatory path might have lower requirements for your study size and the end points. However, that's, of course, if you get that first to the market. So that's why we are today prioritizing, suggesting to prioritize this indication because if we indeed get it first to market, we believe that we can have a shorter path to the market, but actually a higher return on investment. Now as for the ongoing pillar, that's the second pillar of ILIAD. PD-1 is a checkpoint inhibitor that is now marketed in a number of indications, although with sometimes limited effects. We have ILIAD ongoing in Phase I with pembrolizumab or Keytruda, one of the market leaders. And of course, we already secured a collaboration for the Phase II part of that study. So data is ongoing and will be delivered in the coming years. And of course, we already have the collaboration in place to move that forward into next phase of development. Now for the third pillar, the breakthrough is really where we see, okay, if we can show this exciting preclinical result also in these patients in first-line RCC, this is something that could follow the same path. You generate data, you pursue a collaboration and then, of course, in the end, you're going for some kind of a partnering exit, licensing or an acquisition. And that's really how we try to use these pillars to make our company as attractive as possible for partners, solving their problems that they have in their markets. However, because we're solving their problems, they would actually need us to -- everything all right? Okay sorry -- because we're solving their problems, we would need a partner to step in and take this to the market. You see here, just as an example, the lung cancer market, having such different predictions on the different checkpoint inhibitors that are foreseen to be marketed there. And of course, all of these partners have a different problem that needs solving, and we believe Ilixadencel can add to that. So strategic pillars 2 and 3 are really about creating options for partnering in different indications and different combinations. And then the fourth pillar is an important one. We are currently a platform around Ilixadencel, a very exciting immune primer. But we also know that based on the biology around the Ilixadencel, there's more to pursue. We have all the brainpower in-house to think beyond the current Ilixadencel concept, think about other types of immune cells that can be either complementary as a combination or that can be separately developed. And I just want to give that example. On the left, T cells have paved the way of making this a commercial cell therapy platform, Juno and Kite were the first one, of course, having this pioneering and leading to a certain acquisition by big pharma. We see on the right, some of the companies now generating the next-generation platforms of T cells, and we want to become part of that for the other immune types for the long run. Now I'll leave it at the strategic pillars, and then Sven can talk about how we're going to translate that in the next years.

Good job, Sijme. I think he explained it quite nicely, that we really want to play with the market leader but we don't want to be dependent on them. We need to have our own way forward. We have identified this way forward. Now we will put that into our planning construct. We'll put budgets around that and then come back and tell you what it takes to it. Breakthrough is for me very important. If you are a cutting-edge company, you have to have breakthrough potential. We clearly have that kind of potential. And as I said, I can only repeat that and emphasize that we have the possibility to build a pipeline. And I have the understanding that we have a clear ambition to build a pipeline because there is more than one product possible with dendritic cells. Long-term mission, RMAT has been asked again and again, how important is RMAT for Immunicum. I think very important because it allows us as a small little company out of Stockholm in Europe to talk with the big FDA in the dialogue to get their advice on our dendritic cells. And I'm quite sure and if you read that correct, they say, good job, guys, validate your data, so they give us advice how to move in certain indications move that forward. And RMAT is -- will be of a big help, if we move in our own way to the path forward. We're not depending on anybody. So we have to move more into commercial thinking as well. We are talking combination and combination always means price and we have to get price sensitive. Everybody tells us that there are very high-priced combinations outside the market. So that can only be justified if there is high efficacy or we are moving into indication where there is no treatment alternative. And this is exactly what we as the fast lean company can do. We can take one of those orphan drugs like GIST and sarcoma, move into it, get quickly to the market. And I don't say that we will achieve all those 6, but we opened up, we allow our drug to work on it. And on that path, we have the possibility of the conditional approval. We have the possibility that any time one of the other bigger players can jump in and say, we like that, we want to join the party. And this possibility, we have to generate and we can generate that now. The first thing we had to do is adjust our development strategy, we did it. We are now striving for the orphan drug designations for the GIST sarcoma and one more, which we may need for deal making. And then we have to think about building the portfolio. Because if you listen to Alex, it is absolutely clear that dendritic cell vaccine is a topic for us. And we have to address that topic, should be part of our portfolio. Here we tried to give you a feeling about the time on that without indicating when we do something specific. So this is not a plan that I'm presenting here. We need to do the planning work on that strategic pillars of strategic building blocks. But next time I come here, I'm quite sure, I have talked with my Board, I have the budget for it, and I have a clear plan forward that names, when do we do what? So next to come, it stays exciting. Yes. Just to remind you, we are a nice little company. We still have money in the bank. And we have some major shareholders for which I have to be thankful really that they have trusted us and provide this company here with the support so that it can move now into that exciting future. And I have to say thank you for our nomination committee because they have put together really nice Board. And I'm very happy to work together with that Board part, not only with Michael, but all the others as well. I have really a Board now here that can do immuno-oncology and can support us strongly. On the scientific advisory Board and the way the friends for our company, we will have more friends. We will not limit that too. But it will not be only science, so not only for Alex, it will be for the whole company, and we will have real key opinion leaders there, people there that can open up the doors for us. Just to remind you, preclinical data from Alex, hoping now to see more from the clinical studies. This is our vision. We really want to make sure that we contribute -- at least a subset of patients is no more dying of cancer. That makes us tick. This is our commitment. This is why we get up in the morning to make that happen. Thank you. Questions?

My name is Niklas Elmhammer, and I'm an analyst at Redeye Life Science team. I'll start off with a question for Alex, please. Compared to this time last year, you have achieved a lot in -- lot Ilixadencel and the MERECA trial. So what does -- is the feedback you're getting from KOLs, clinicians and so on?

Yes, I can just say that if you look for the -- I'm in contact with continuously like the Swedish ones, they are really pushing forward. We have to do something more. And of course, they're especially asking for this combination with CTLA-4 and PD-1 in first-line mRCC. When I was in Florida in February at this ASCO-SITC meeting, I met a lot of people that thought that this is actually very interesting, especially this clear trend of long time survivors in our MERECA group and also these complete responses. So yes, I've got all like congratulations for a very good study, from not only Swedish, but also international opinion leaders -- key opinion leaders.

And now you're stepping back from the CEO role. So what will be your main priorities?

Yes. I think we will continue to have this. I'm a scientific guy. So I'm really glad to -- I can dig deeper into this area instead of being like something that I have not used to be a CEO. I want to be a Chief Scientific Officer.

And for Sven, I want to ask you, you have alluded this a bit in the presentation, but what makes you excited for joining Immunicum?

I think you could get it already as a feeling when Alex presented, there is a possibility of remissions. That means that we really can alter the response. We have seen already complete responses in clinical setting. You mentioned that, KOL mentioned that again and again. But to have a durable, this is a thing that everybody is exciting. We are waiting for more data out of MERECA, but we need to move that in other indications as well. And we have to move it to patients. We have to make it available for patients as fast as possible. And I think this is the key thing why we had to adjust our development strategy, why to start a Phase III trial, now is not the smartest thing for the company to do. We can create even for our investors, much more bang for the buck when we do prove this remission thing in them.

And you will have a long industry background, and you have been in business development on both sides of the table. So what does it take to attract a partner in biotech?

Data, data, data. And secondly, that we really provide a solution for anybody interested in us, and for patients. So if we just do what we think would be nice, this doesn't help us. If we can solve some of the biggest problems, Bristol-Myers, Pfizer or Merck has, then we are attractive. And if we provide them with data like they expected, then we are their partner. And this requires a dialogue with the pharma. And this is where my network, my experience in addition to what Sijme brings to the table counts because I know these guys now for 10, 20 years. I know what I see. And this is what we try to get into here. And some of the pillars have not been fully through. Because we will go into the dialogue with them first and ask them what -- please, what do we have to show you with Ilixadencel that you get excited, not only us.

And looking on the other side, what is -- what would be ideal partner for you?

I think there comes a little bit of strength from this company. We are one of the few who could develop that. So our partner most likely will look at us and say, wow, this could become a cell therapy powerhouse. So help them and watch what they could do, what they can deliver. And we have seen it with Kite. We have seeded it with Juno and so on. They wait until they are sure this is a powerhouse, and then they acquire it. But Kite was acquired for $2 billion to $3 billion and so on. So -- but it's nothing that happens overnight. You cannot have that happening tomorrow, but you have to be prepared as a company. You have to generate those data they expect, so that they can come and acquire you.

And we have a question regarding the interesting data, preclinical data presented at ESMO. Why do you think you see these strong synergies with anti-CTLA4?

Yes, I think it's -- I mean, it was enough to just combine with CTLA-4. And CTLA-4 has been shown not only to inhibit this negative interaction between T cells and immunosuppressant cells, it's also affecting the T regulatory cells that you find in the tumor. So if you inject Ilixadencel into the tumor, we are inducing tumor-specific T cells. But when they come to the tumor, they will meet these T regs and this will tell ourselves to take it easy now. But by adding CTLA-4, we see a clear-cut difference -- a huge difference. And that's actually the same for the combination with these TKIs, so vascular endothelial grow factor antibodies. Because it has still shown that before everybody thought that VEGF, vascular endothelial grow factor, is something that the tumor produced in order to enhance or enhance angiogenesis because the tumor need more blood in order to grow. But what has been shown is that the vascular endothelial grow factor is actually a very immunosuppressant molecule of protein. So by inhibiting its effect, you are also inhibiting and blocking the immunosuppression, both on T regs, but also immunosuppressant cells, mainly those 2 cells. So I think they are in the same area, but it's totally different drugs.

And could you tell us a little bit about this model that you -- you're investigating? You see a strong effect with CTLA-4 than PD-1?