Good day, ladies and gentlemen, and welcome to Faron Pharmaceuticals Full Year Results 2020. At this time, all participants are in listen-only mode. Later, we will conduct a question and answer session through the phone lines, and instructions will follow at that time. I will now hand over to CEO and Founder Markku Jalkanen to open the presentation. Please go ahead, sir. Good afternoon, good morning for those in the U.S., many thanks for joining us today for Faron's full-year results update for 2020. We are very happy at taking you through the company's performance over the last year, obviously would like to, of course, to have liked to hold this meeting in person. As ever, we appreciate everyone joining us here today and hope to meet all you in person soon again. Joining me here today is our CFO, Toni Hänninen, he will explain the results financial part later. Let's move on to the moving slide number two. Before we begin the proceedings, I would like to bring your attention the standard disclaimer slide, which is included in the presentation for completeness. Could I have slide number three? We have three target assets, Clever-1, CD73, and AOC3. They all deal with our immune system. Obviously we believe that harnessing the power immune system is the best way to tackle some of those medical conditions where the unmet need is really huge. This hopefully becomes really clear also in our presentation. The first one is targeting a cancer growth and spread. We believe that converting Clever-1 a positive macrophages into a negative ones, we can actually shut off their immune suppressive activities, that is a key thing really to reactivate the immune system. Happy to share some of the recent data also with you today. With the CD73, it's a long-term project where we have really seen a lot of evidence that controlling CD73 on the surface of endothelial cells, you can also regulate and control the organ function. Obviously, if you lose this molecule, you have put your lungs or kidneys in a dangerous situation because they may lose their function due to the leakage of the capillaries into those tissues. We talk about that as well. A few words about this Haematokine project, which is now at the preclinical stage, but hope to really get to move it on the clinics as well. Next slide, please. Out of these three assets, this is the pipeline. Starting with the Clevegen, bexmarilimab, it's the name of the humanized antibody we are using to block the Clever-1 function. We started with the solid tumors. These patients had no options anymore when they entered the MATINS trial. Out of those 10 tumor types, we already have signal in six of them for the clinical benefit. I will show some of the data of that as well. Obviously, this MATINS trial can be expanded all the way to the pivotal part, and those would be really interesting times once we have data collected from the Part II patients, which is still ongoing. We would like to expand also this trial or the treatment to one of the standard combination treatment with the PD-L1 inhibitors, and that is lung. That's about to begin this spring as well. Then the third one is the acute myeloid leukemia, which is a very interesting target for us because these myeloid leukemia cells actually have rather significant expression of Clever-1. Obviously if you could knock that out, it would be interesting to see how much we can actually suppress the replication of these cells, and that data we have seen in ex vivo settings already. With the Traumakine interferon beta project, we are involved in the REMAP-CAP, the global study. We don't exactly know when we get the readout from that. More importantly, we are starting the HIBISCUS trial in the U.S. It's now going at the final ethical round, and hopefully get the first patient in very soon. As we have said for years, this treatment of interferon beta protecting the central organs can be applied widely in other organs as well. One interesting one and large volume one is the acute kidney injury. This is a significant patient number today on this planet due to number of reasons. Obviously that is moving on as well. Could I get the next slide? Now we are moving, really look at the key events on 2020. We have made a significant progress with recruiting the patients to the trial. We have seen a survival benefit among those patients who have responded to the treatment, and I saw that data. We have also learned that we need to increase the dosing frequency of these patients, and that's largely due to the discovery a soluble Clever-1 in the circulation. That finding is much more important that maybe people have not realized because Clever-1 is a direct inhibitor of T-cell activation. Obviously if you would have a soluble Clever-1 around, you can actually suppress T-cell activation in all the locations in those patients. Maybe this is the way how cancer actually could influence on the immune system on the remote locations. Obviously that would be a great advantage for those metastasis cells who actually try to comb into those tissues and start to grow distally. If you can prevent that one, that would be a significant benefit to the patients. With the interferon beta, we are involved in the COVID-19 treatments, both the REMAP-CAP and HIBISCUS are really focusing on those ones. As said earlier, we really would like to also expand this, and we have a very interesting collaboration with the US Army unit and partially funded also by the Department of Defense, as we have announced. That was related more to the trauma treated patients. Obviously there the risk is that they may have a lung injury as well and develop ARDS. We believe that interferon beta treatment is really proper treatment for those patients. That in line, I ask Toni to explain the next slide, which is the final. Thank you, Markku. Warm welcome from my side also for everybody online. We closed the year with EUR 4.1 million in the bank, and the loss for the financial year of 2020 was EUR 16.9 million, which was EUR 3.6 million higher than the year before. This was mainly driven by one third to our additional headcounts. We increased our headcount by 25% last year. The two thirds is by clinical trial expenditure and the CMC buildup. Our net assets at the end of the year were a -EUR 1.8 million, and we did during the period in April of last year, a EUR 14 million fundraise very successfully, virtually for the first time. Additionally to that, we received EUR 7.9 million of grants, loans, and guarantees from Business Finland, the European Innovation Council and Finnvera. Out of these EUR 7.9 million, EUR 2.2 million was dispersed to the company last year. The remaining EUR 5.7 million will come post period as we are speaking now. Additionally post period in February of this year, we did additional fundraise of EUR 15 million by issuing 3.5 million shares. Over back to you. Thank you, Toni. Thank you. Let's move on to the next slide. We focus on macrophage guided immune therapy, our lead asset. Next slide, please. What we have learned in the past is that when we knock out Clever-1 function on these tumor associated macrophages, we can convert them back to the immune system activating a phenotype, then now secreting many of the chemokines and factors which are known to be involved in immune activation. Obviously this is a key thing if you really would like to get the antigen from the tumor to be presented to our immune system, and you get then T cells to respond to that. The surprise was really when we started to look at the treatment cycle and look at the soluble Clever-1. You can notice that on the right hand side, a lower panel, that within a week after dosing, we actually reach back the original baseline. Meaning that the three-week interval is not really high enough to treat these patients properly. I'm glad to say that we are now in the middle of increasing this frequency and also dosing with these patients. In general, the soluble Clever-1 amounts are increased. You can see that on the upper panel compare to normal control. Obviously this could be a key thing for us also maybe to predict which of the patients actually are the best responders in our future activities. That assay development and measurements are ongoing while we speak. Not only we target any more a tumor associated macrophages, we also would like to remove the soluble Clever-1 from the plasma, blood, and tissues in order to get the maximal T cell activation. Maybe this molecule also could be the one that actually can prevent a immune checkpoint inhibitors to work, because at the same time you have an inhibitor that actually prevents the T cell activation whenever you are giving treatments to activate the T cells. Obviously giving significant evidence that the combinations of these checkpoint inhibitors actually could be a really important part of our development work in the future. Next slide, please. This monotherapy, what we are doing at the moment is really with the patients who have a progressive disease. They are difficult to treat. All the other ones have been failed previously. They may have seen three, four, six, seven lines of treatments previously. As I said earlier, this provides us a really a significant combination potential. As the product itself, bexmarilimab seems to be extremely safe, well tolerated, the combinations would be then a really possible to expand to a number of other checkpoint inhibitors. Obviously this would then provide us an opportunity really to challenge the current treatments. Let's look at what's going on. Next slide, please. MATINS Part II is ongoing. I will explain the Part I data in a minute, we already have six cohort groups out of these 10 different cancer types who have shown early clinical benefit. This is a stabilization of the disease or then even seeing a partial response. Obviously these six, ovarian, hepatocellular, cutaneous melanoma, colorectal, cholangiocarcinoma, and gastric cancer, they all are candidates to move on to the pivotal part. We are waiting the data to be completed somewhere later this spring in order to make the right analysis of all of these individual cohorts before we can make the decision which of them actually will be taken further to the pivotal part. First to expand to 30 patients and then later on really to the size that actually would allow us to go to the regulators and ask marketing approval. Let's look at the Part I data for a minute. Next slide, please. Top line safety data on left-hand side, and as you can see, there is really no grade three and four adverse events. The one infected seroma, I don't believe it's really caused by the drug itself, but it was listed in those, and it's here. Also the Grade 1 and 2, very rare. These are something you can see with the patients when you infuse antibody like we do. Again, not necessarily related to the antibody, but yes, they are there, but very low number. The preliminary efficacy from this part one, 30 patients. We had two partial responders, seven stable disease or mixed responses in those target lesions. When I talk about this, these are always image analysis of those target lesions. These are not opinions. They are really hardcore data. If you drop out the lowest concentration, 0.1 mg/kg, we have roughly one third of the disease control already at this stage of these patients. Obviously, this is a very exciting outcome. We also learned that when we give bexmarilimab to these patients, we increase the peripheral natural killer cell count. Obviously, that is really important if we believe that we can activate the innate immunity. The reason why innate immunity is so important is that that is the only way you can actually generate additional T cell response, T cell repertoire. If that happens against the cancer antigens, you know that you become kind of vaccinated against those antigens, that would be a significant benefit because then you could assume that you are treated for good, really, against that cancer types. Let's move on and look at some examples. Next slide, please. These are Part I patients. We have MSI negative colorectal cancer. Arrows pointing the shrinking lung metastasis in this patient. The second is a refractory melanoma patient. Again, you can see the rather massive metastasis going away from the lung, and at the same time, all the interstitial tissue was removed, and the patient really felt much better after this one. These are now Part I patients. We started to look at Part II. Next slide. We wanted to show that they are all progressive diseases, and that's on the left side. As you can see, this is 83 patients, and all of them have a progressive disease before they enter the trial. If you look at the overall survival of the patients who had a clinical benefit, that's on the right-hand side. Out of those 100 patient follow-up, which is the four cycles, we only lost one of them. The ones who had no response, roughly 85% of them died. Obviously, this is important information for us for two reasons. First, this is an additional efficacy signal, which we can see. Secondly, now we start to identify the patients and can analyze them further who are the potential responders to this treatment. Obviously, we are happy to tell more about this later this spring once we have completed the analysis with the full cohort sizes. Be patient, stay with us. We will do it. Just a few more months, and hopefully, we have the answer to all of these. Could we have the next slide, please? This is also supported from number of other reasons. This is a genetic analysis looking at the data banks. Here we have a total tumor pools. Red one, high expression for Clever-1. That's a stabilin gene that is analyzed here, and that's encoding for Clever-1. The blue one is the low expression. Significant difference in the mortality. If you then move on and look at the immune therapy response. If you have a high expression of Clever-1, you have a really low survival prediction. Significant difference to the blue line, where we have a low expression of a Clever-1. The same is also shown in this pooled way, where you can see the individual levels of transcript analysis, and high expressions of Clever-1 have really a much, much higher mortality tendency, because already with these patient numbers, which are not that many, you have a p- value very low. Very promising support as well. The next slide, please. This is my favorite slide. This is looking at negative checkpoint molecules post-treatment. We have a pre-dose and then seven days later. The red one shows, again, T-cell activation or immune system activation by increased CD25 expression. That is interleukin- 2 receptor, some chemokines. Good. Very good. Especially the naive cells are responding, which is really nice. Look at the blue ones. That is a decline in expression. Very familiar molecule, CTLA4, PD-L1, even PD-1. One bexmarilimab treatment can regulate the expression of these negative checkpoint molecules to the point where actually the current other treatments are trying to do at the moment. Obviously, this is extremely important finding. We know today that this will last also for one week, so we really need to increase the dosing frequency. As said earlier, that's ongoing at the moment. On the right-hand side, you can also look at the increased number of the effector cells in those patients who responded, which is really good result and explains why we actually have a clinical benefit in those patients. Next slide. If you look at the revolution of the checkpoint inhibitors, what has happened in the past. These inhibitors are expected to sell EUR 50 billion in 2025. If you look at the efficacy between the placebo and in this case a pembrolizumab, that is a KEYTRUDA from Merck, you can see, yes, it is beneficial to the patients, but it's not that dramatic. If we can now combine this treatment with our treatment shown in the next slide, we may have a significant step up, and now we may have a possibility to treat maybe half of these patients. That is our aim directly with the combining the PD-1, PD-L1 treatments with the bexmarilimab. Obviously, if we can really demonstrate this increase in the efficacy and outcome of the patients, this is a very significant commercial opportunity as well, and that is already predicted and so on by other examples. We are very confident that this will move on really successfully in the future. Next slide, please. Obviously, the pipeline is here to demonstrate first that the MATINS trial cohorts, not all of them. For example, uveal melanoma was disappointing to us because we didn't see any response there. Some of the cohorts will move on all the way to the pivotal part because regulators believe that if you have these patients with no options, already two out of 10 will be looked and analyzed favorably by the regulators. Obviously, that data is coming on later this spring. Moving on to lung cancer model or lung cancer patients with the combination with PD-1, and the acute myeloid leukemia is really exciting one. My own opinion is that we really need to get already on the first-line treatments, and those are the black-blue indications. Ovarian cancer, combination with the standard of treatment, that's a platinum globally used. There you actually could have a rather impressive results as well. Obviously, that is something that we plan to do once we have learned a dosing and having probably demonstrated the efficacy earlier. All right, moving on. Next slide, please. There will be a significant news flow later this first half, and then later on once we move on, and obviously, we are really looking forward to let the market know about the additional information. As time is flying, let's move on to Traumakine, the interferon beta. Next slide, please. Use for the upregulation of CD73. Could I have the next slide, please? Here the aim is what we have been saying for years. We would like to regain CD73 to the surface of the endothelial cells so that they can maintain the endothelial integrity. The reason we are using interferon beta is very simple. They have interferon beta response element. It is our natural defense system, and we do have endogenous interferon beta that is doing it normally. Especially in the viral infections, this is one of the first reactions our immune system actually put up against the viral infections. They want to protect the cells, and that's the reason why they are using this adenosine activation locally to protect the cells. We did earlier, next slide please, a trial in U.K. where we demonstrated that using interferon beta intravenously, I repeat that, intravenously, we can reduce the mortality of these lung injury patients. They are called ARDS because they already have been ventilated. Obviously, you may be considering already earlier treatments in order to reduce the risk of getting to the point where the ventilation is needed. In our next trial, you may remember this, next slide, please. That's the INTEREST trial. We didn't get the similar efficacy. The placebo and the treatment group gave identical mortalities. We were able to explain this. If you look at the ones who have a biomarker response, that's the blue line here on the right-hand side, and those who didn't. You notice that the one who responded showed the biomarker activity is up. They had a strongly reduced mortality, getting close to the original finding. The orange line, where the biomarkers were not upregulated, you can see the mortality is almost 50%. We made a very simple question, what's the difference between these groups? We learn it's the rather significant use of corticosteroids at the same time with the interferon beta. Today we know and have shown and published that corticosteroids can block interferon beta action. I'm a little bit worried about this, that if people use corticosteroids too early on these COVID-19 patients, because it's not shutting off our Traumakine, it's also closing the endogenous pathways to protect those cells in those conditions. Next slide. That is the reason why we are waiting really to start this HIBISCUS study in U.S. We have seven sites now waiting the final ethical approval, ready to go. Here we just make a placebo-controlled randomized study. First interim analysis with the 70 patients, to estimate the final size, moving on to the pivotal part, phase III. This is now control that there is no corticosteroid interference with the interferon beta. It can be used post-Traumakine treatment, but not at the same time. We are really waiting. The next slide shows you why we have been in here. We already have a fast track designation from FDA. We have a Promising Innovative Medicine status from MHRA, we already have orphan drug from European regulators. Obviously this is a ongoing condition now related mostly to the COVID, when COVID is over, I believe that we may have a serious influenza season. Maybe there are some additional COVID variants coming on, which is now indicated in number of articles. This is a condition will stay with us for a long time, that's reason we need to get a new treatments really to rescue those lost lungs. Next slide, please. Looking again, the information coming from these trials starting HIBISCUS. We still do not know when we get the REMAP-CAP read out, but hopefully that is progressing well. Then moving also to other indications. On the right-hand side, you can see the numbers, which these conditions and treatments are targeting, and it is a very significant upside as well. Finally, the news flow for this part. Next slide, please. We have, again, a steady news flow coming in, and obviously very key one is the interim analysis of the HIBISCUS, and we predict that we would get that on the third quarter this year. If everything goes well, it can even be earlier. Finally, a few words about the Haematokine. Next slide. This one and one more. Next slide, please. Here we have a very interesting target. It's AOC3 enzyme. It has several other names as well. What it can do, it can oxidize primary amines. Those are normally arginine or lysine residues of the proteins. When it does, it produces local, converts the amine into a corresponding aldehyde, and that change will release hydrogen peroxide. That hydrogen peroxide is a control element for hematopoietic stem cells. Next slide, please. These reactive oxygen species on the left side, when you lower their concentration around these cells, you make them to proliferate and colonize. Obviously, this is now the aim for us. We could use these in ex vivo settings, making the cells to proliferate either from the donor or from the blood bank, and then give them back. Try to do that in vivo settings. Obviously this is not that huge number of the patients, but they are very much needed when, for example, they have a failure in the graft, for example, but there are some other conditions and obviously really would like to get this project to the clinic as well. All three projects really targeting the immune system, and we believe very strongly that all of these treatments will find their way to the market because they are really targeting the huge unmet medical need. COVID-19 is just giving us an example where that need is rather practical today among us. With this word, would like to then have the final slide to look at the news which we believe are coming in. Additional MATINS cohort data from trial Part II. Selection of the first pivotal cohort to be expanded. Obviously that is possible to do once we have determined the final dosing frequency and level. Then initiation of those other trials, and when we have a first patient in all of those, we obviously will inform the market. With the Traumakine, HIBISCUS start, hopefully get some information from REMAP-CAP, and then also really continue the further development of these indications, what we had in that pipeline chart in order to really be ready to move on. For both of these, bexmarilimab and Traumakine, we are now establishing the brand new state-of-the-art manufacturing facilities and that is in collaboration with AGC, contract manufacturing organization. I can just report that pretty much they are in timeline what we have anticipated. Obviously that is really important once we expand the use of them also in the market situations. That's what we are at the moment. Finally, just thanking you and have the final slide. Next slide. That brings me to the end of our presentation today, and I would now like to hand back to the operator for any possible questions you may have. Thank you very much. Okay. Ladies and gentlemen, your question-and-answer session will now begin. If you wish to ask a question please key star and then one on your telephone. If you decide to withdraw your question simply key star two. All questions will be answered in the order received and you will be advised when to ask your question. All other lines will remain in listen-only. Just to remind you, if you wish to ask a question please key star and then one on your telephone. Okay, our first question comes from Miles Dixon from Peel Hunt. Please go ahead. You're live in the call. Many thanks. Hi there, Markku and Toni. Two questions from me. I think firstly on the bexmarilimab, you've shown some impressive data on the, not only now the messenger RNA expression and the correlation, but also the soluble Clever-1. You alluded to us potentially being able to hear about some data later on in the year. Do you actually expect there to be a difference between the responding patients and the non-responding patients? Has it changed how you're collecting data from current patients? Thank you. That is a very attractive possibility. Obviously, we have to now carefully look at it. We have a lab-based assay to do it. We are also building a sophisticated assay that actually could be validated and brought in whenever, especially if it becomes a part of the companion diagnostic system. It also could be that it is not only the soluble Clever-1. It could be combination with some other parameters. Obviously, that is the reason why we have to really look carefully at the data for the individual cohorts. It could turn out that in some of the cancer types, these signals are better than the other ones. We need to understand that because obviously if you want to move to the pivotal part, you would like to optimize the patient population you want to treat. This is a very exciting time for us and definitely we'll have a lot of activities really to be reported later in the year. Thanks, Markku. Similarly on the, well, really INTEREST trial versus HIBISCUS. It's a fascinating difference that you've got when you extract the corticosteroid impact out of that INTEREST trial group. I know that, for instance, the corticosteroid is a reason for exclusion in HIBISCUS, but is there a dedicated time period between when interferon beta may be administered and then corticosteroid in the HIBISCUS trial? Thank you. Thank you. It's again, very good questions. We have indicated many times that corticosteroids may be at the best service in the final stage of this kind of an injury in the lungs when the fibrotic process is already taking place. There are some information in the literature that, yes, that really helps. To be too early with the corticosteroids to shut off the interferon pathways, that could be a very significant problem. We have solved that by letting the doctors use them post-Traumakine treatment. Now the patients come to the hospital, and they're hospitalized, and for six days they get the Traumakine treatment. If that is not helping them, then the doctors are allowed to use corticosteroids post that six-day treatment. That is the structure what we have within the HIBISCUS. Would three days be enough or some other period? I don't know, but they should not use them at the same time, and that is now controlled in that trial structure. Thank you very much. Okay. Our next question comes from Julie Simmonds from Panmure Gordon. Please go ahead, Julie. You are live in the call. Thank you. Hi, Markku. Hi, Julie. A couple of questions. Firstly, just following on from one from Miles there. With REMAP-CAP, is there likely to be a problem with steroid use in that? I know it wasn't how it was designed originally, but then COVID was sort of thrown in as an extra bit into that trial. Do you have any ideas how are they separating the use of steroids and Traumakine in that? They are separated. They are individual arms, so they should not overlap. Do the doctors really follow that? Yes, they should, and they commit themselves to use a Traumakine as a single agent for the treatment. I know a few of the sites, one, for example, being here in Finland, they follow that advice. That would be a single treatment of interferon beta only. Excellent. We might actually get some useful data out of what is ultimately quite a large trial, the way they're recruiting into that at the moment. Yes. Do you have any idea how much Traumakine has been used, or you don't have access to that? The only information I have is that they have not reached the first interim readout. There is an independent data monitoring committee who is looking at the data all the time. We are really dependent on that readout. Okay, fine. Then on bexmarilimab. With the dosing, clearly when you did part one of MATINS, you looked at different doses, and you didn't actually choose the top one when you moved on to part two. I was just wondering, now you're looking at moving up the dosing. Is it the fact that in part one I suppose it's really a question of is it dosing frequency or concentration that needs to be increased? How is the trial set up to identify which is the factor there? Because clearly, if you're giving a higher amount on a less frequent basis, you might not be seeing the same profile you're seeing currently. That is, again, a very good point. In the part one, we had five patients in each of those dosing cohorts. Obviously, if you had some patients, cancer types, which were not the best candidates and could kind of have a peculiar behavior, they may have fooled us. We started to see some suppression of some markers that actually started to indicate a suppression of the treatment at the highest concentrations, and we got worried if that is the case. That may be more related to those patients more than dosing. Obviously, that is really important now to look at what happens to those patients when you increase the frequency. My own opinion is that if you have a circulating T cell inhibitor around, you don't want to have that. Even for the benefit of the other checkpoint inhibitors, because remember, these are immunological synapse activators or inhibitors, so they need to deal with the T cells, and that's the reason why they are used. Obviously, we would benefit the use of those as well as we benefit the activation of the immune system in other locations as well, not only around the tumor, which is probably critical. Absolutely. The data you've got reading out next on this is going to be what? A more frequent dosing within colorectal cancer patients, is that right? A higher dose will come out at a later point. Have I got that the right way around? That's pretty much the development at the moment. Also we get Part II cohorts analyzed in full size. That was not in this release we did earlier this week. It was really related to that number and the data that was presented to the data monitoring committee, and they were extremely happy and almost thrilled. Maybe that explains why the recruitments have been rather successful along these months and year. I believe that data sometime in quarter two should become available. Obviously, that is very exciting to report to the markets as well. Absolutely. Thanks very much for that. Thank you. Okay. Our next question comes from Jon Berggren from Kepler Cheuvreux. Please go ahead. You're live in the call. Yes. Hi, Markku and Toni. I have four questions, but I guess we can take them one by one if that's okay with you. Okay. The first one regarding the press release you sent out on Monday. You said that the analysis was based on 67 patients, that you have 10 responders that are either partial responders or that have stable disease. You said that you couldn't provide data on overall response rate because you haven't followed all these patients long enough. For those 10 responders that you have, how long have you followed them, and how many of them showed partial response at the time of assessment? That data came after four cycles of the treatment, and one cycle is a three week, so 21 days. If you look at the slide in my presentation, it's roughly 100 days. Obviously we are as excited as you are really to look at the data post seven cycles when the protocol-based imaging is done again. They may do imagings more often than just on those requested, but that is really the data points what we are mainly looking. The whole cohort, not only those 67, but the others which were not included yet in that one, they all moving every day. That is the reason that I believe that we have additional information to provide to the markets. Okay. It was to the dosing schedule. That makes sense then. Okay. Thank you. Yeah. Second one, in terms of the survivor benefit that you also communicated in the same press release, how did you do that analysis? Did you compare responders to non-responders for each indication, or did you just compare responders to non-responders across all indications? All indications, because again, the cohorts are not full in all of the cases. The only one that was full, which was a bit surprising, was uveal melanoma, unfortunately, there were no responders in that group. That may also explain why the overall benefit was less than in the Part I, where we have one third maybe responding. Here we have maybe around 15%. Keep in mind that some of the cohorts had no responders, and that's diluting out, obviously, the previous finding or the numbers. Yes. Got it. Okay. How many patients do you have in total today in the MATINS trial, and how many of these are in the six indications where you have seen early signs of efficacy? The plan is, in part two, have 10 patients for all of those cohorts. In February 21st, if I recall correctly, we had 83 out of 100 already on the trial. I know that it's progressing well, so I believe that we are almost full now with those 100 patients. It means that we have 30 patients from Part 1 and then 100 patients from Part II, and then we should have a full 10-patient cohorts for all of those cancer types. That is why it becomes so important, really, to make the thorough analysis of all of those cohorts and then look at and make the decision, which will then continue with the further expansion and all the way to the pivotal part. I cannot say yet the exact numbers for each of the cohorts. Got it. Thanks. The last question, this may be more for Toni, but can you give some flavor on what the run rate will look like for this year? I think it mostly related to the R&D cost for the new trials that you started and intend to start. Also you said that you increased headcount 25% for last year. Do you expect this trend to continue in this year as well? Thanks. That's a great question. In terms of the headcount, yes, we did increase the headcount by 25% last year. The average was 30, and at the moment we are still in a hiring mode. We are going to have soon roughly 35, 36 people on board, and we have added four people already this year. The trend is absolutely continuing. In terms of the run rate, as Markku showed on the trials, we have the DoD grant, which is then with the HIBISCUS trial, and then on the MATINS is really depending on the recruiting of the patients. What we do see, the cost is relatively upfront, so that's why we had a very steep increase last year, as these cohorts have opening costs and different milestones with our CRO. They're a little bit front-loaded. That gives us then a pretty good control for this year. Okay, thank you. That was my last question. I also wanted to add here that we do have a plan to set up a U.S. unit, because now there's an increase in number activities on the U.S. side, and obviously the communication with FDA is really important. That is part of that expansion of the personal headcount. Okay. Just to remind everybody, if you wish to ask a question, please key star and then one on your telephone. Thank you. Okay, we have a question from Miles Dixon from Peel Hunt. Please go ahead, Miles. You are live in the call. Thank you. Just following up on a question that Julie had earlier on. You were asked about how often you use the Traumakine in REMAP-CAP. I was just wondering, do you expect any data to come out of the Solidarity Trial in terms of how much it was used? Thank you. Thank you. We have really tried to push WHO to get that data to us, as we said in the release, they have not yet provided. It's kind of a pity because based on the agreement we have with them, they actually should do it. FDA already has asked that data to be provided to them as a package when they are going through the approval process. We are reminding them all the time, and I hope that one day we will have it. I just believe that in the Solidarity Trial, they didn't really use intravenous interferon beta. It was all subcutaneous. Maybe that is the reason why they may have difficulties providing the data, if they don't have any patients treated with the intravenous one. Got it. Thanks, Markku. Thank you. Okay, just to remind everybody, if you wish to ask a question, please key star and then one on your telephone. Okay, there are no further questions on the conference line. I will now hand over the presentation to the management team. All right. If there are no further questions, I'd like to thank everybody for your time today. If you do have any further questions, please do get in touch with us directly, and we look forward to really updating you on our progress, hopefully very soon. Thank you.