Good afternoon, and good morning for those in America. Welcome to the H1 2022 results of Faron Pharmaceuticals. My name is Markku Jalkanen. I'm Faron's CEO, and I'm here with our CFO, Toni Hänninen. Good morning. As always, we will making also forward-looking statements, and that's the reason why I want to show this corporate disclaimer. You have seen this before. Really would like to focus now today on our Bexmarilimab, Bex, like we call it shortly, because we believe that that would be a really revolutionary way of improving our current cancer treatments. We think that especially in the combination front, we can improve the immune system to be activated against the cancer cells in order to really remove them from us. We have built an accelerated program really to move on faster, especially in the spring. We still work on Traumakine as well, and we will hopefully be able to tell more later this year about that. For Bex, we have really built now very experienced clinical oncology team, led by our new CMO, Marie-Louise Fjällskog. I'm really impressed by the work they have done. Toni will talk more about the cash position, how we have been able to strengthen that, and what the future will look like in that front as well. Looking at the pipeline, we have now treated more than 200 patients with Bexmarilimab, significant number. We have 10 different cancer groups really involved in that. We have very compelling 12-month survival data obtained, and I will update that one. It is really the responders who normally do not really get any response for the current other immuno-oncology treatments. On top of it, we now can identify the patients who get this response, and obviously that will be a really important part also for our future planning and execution of the trials. Again, I will open that bit more. During this period we started a new, completely new, Bexmarilimab study, BEXMAB, and that is on the first hematological malignancy, acute myeloid leukemia, or where the myeloid cells are involved, so they're in these awful diseases where we have limited possibilities to really treat the patients at the moment. Toni will also show some of the significant worldwide expansion of our patent rights and also talk about the financials. Let's see and look at the pipeline and I will obviously show also later on the plans regarding the pipeline progress we anticipate to take place during the next, eight to 12 months. MATINS is coming to the end. We have pretty much now recruited the part one and part two, and obviously that will continue provide additional information which we anticipate to be really useful when we go to talk to the regulator, especially the FDA. The principal investigator-driven Bexmarilimab lung study in San Antonio is about to start. As I said earlier, we have a combination also for that, and that protocol hopefully will be ready really for the review on the second half of this year. Bexmarilimab now initiated. The Traumakine will be focusing purely to the ischemia-reperfusion injury, where we can avoid any dexamethasone or steroid use at the same time, and that is the main really remark over there. We will come up with the plans so that hopefully early next year, we have a really straightforward way to move on with this. Obviously, the ischemia-reperfusion injury is an area where patients have tremendous need to be helped to avoid their death. Also, in the activation of the bone marrow, whatever the cause has been to set it off, we have a plans really to have anticipated IND submission early next year. All of these are the background and at the moment, Bexmarilimab is really taking almost 85%-90% of the resources we are using to do the clinical development. Now I ask Toni to talk about the financial highlights. Thank you, Markku. From the financial highlights, before we go into our numbers, maybe look a little bit on the market side. Last 18 months, we operate in a very, very challenging market. The biotech market, in fact, on the stock exchange, has gone down roughly 50% in the last 18 months from its all-time high. With that, I'm very pleased to announce and report that we were able to strengthen our cash position from EUR 7 million- EUR 9.9 million in this first six months of this year. Also last year, we were able to improve our cash position every time we reported to the market. Across the last 18 months, consistently, we have improved our cash position every time we have reported to the market. Big thank you to the team. I know it's been very, very hard work, dedication, a lot of resilience, so very proud of the achievement of the team here. On the operating loss side, our operating loss is EUR 13.4 million, up from EUR 10 million, so roughly EUR 3 million difference here, mainly driven by the buildup of the U.S. entity and acceleration of the pipeline and the R&D activities that Markku will talk about later, in more detail. Our net assets were negative EUR 5.2 million, and as announced in February, we strengthened our cash position through the funding agreement with IPF Partners, where we drew EUR 10 million. There's further potential for another EUR 5 million+ EUR 15 million under certain conditions met. In June, we conducted a private placement of EUR 4.5 million. The actual full private placement was EUR 5 million, but out of that, half a million settled on the H2 side early July. In our reported numbers, we show EUR 4.5 million of private placement, issuing 2 million new shares to existing and new shareholders. As a part of this equity raise, we were able to attract LLS, The Leukemia & Lymphoma Society, as new investor. Leukemia & Lymphoma Society is a New York-based nonprofit organization, the biggest and the oldest in the world that is specializing in blood cancers. What they normally do in their investment due diligence, they look at our team, our science, and also assess our capability of bringing our therapy forward. We are very excited about this partnership, and we have a big thank you for the vote of confidence from LLS and the LLS team. On the next page, we mentioned about the patents that Markku already mentioned. Last year we filed a U.S. patent, and now this year in the first six months, we increased the patent protection in Europe, in Japan, China, South Korea and Mexico, so a lot of large main territories. We continue this work in H2 for the other meaningful, significant territories. Here all of our patents are granted through 2037. This offers a very, very good and solid commercial protection for our Bexmarilimab program. With that, I would like to hand over back to Markku. Thank you, Toni. I'm going to mainly focus really on Bexmarilimab, Bex, like we call it. The data which we have anticipated really to take place again during this period, and that is to provide a survival benefit for the last line patients who had no options anymore for anything than the supportive care. That also means that the current immuno-oncology PD-1 blockade is ineffective. If this really holds up to the whole cancer population, it would be a significant improvement. If you look at this slide, I have shown this before. The patients we are treating coming from this red part, more than 80% of the population, cancer population, who are not responding to the current PD-1 blockade. Obviously, if you look at the market size of this 13% or so, it's already a very significant, some $30 billion at the moment. If you can just double that with any way, that means that the one who can do it actually could have access to the rather significant market. Obviously we hope to be the one that actually can do it. The reason why we think so is that we can really ignite the immunity in those cancer patients who have lost that or not been able to generate. PD-1 blockade works with those who already have activated immune system because they activate the T cells, those T cells that actually can kill the cancer cells. This is a really important aspect to understand why we are so excited about this work we do at the moment. What we plan to do is really complete the MATINS, take the data to FDA, and then build, we believe that it's potentially randomized trial to compare the treated, Bex-treated patients, to standard of care or whatever treatments the doctors may choose at that point. We anticipate that the first combo in San Antonio is about to start, and then we build at the same time a basket trial for Bex combo, which would allow us really to have more selective also in the next steps in that trial. I'm really happy to also report that the BEXMAB, the first hematological malignancy, where the myeloid cells produce the leukemia, is now on the way, and the first cohort hopefully will be soon recruited. Obviously being in an open study, whenever we get the first results, we probably will come up to the market as well. This is a very exciting pipeline at the moment, and it's really focused. Again, I want to thank Marie-Louise Fjällskog really lining up this well. Exciting times for us. Really based on this MATINS trial, we are really finishing the recruitment and then the data analysis. There are two ways of looking at it. First is to look at the occupancy of the Clever-1 in those patients that we get first. Second is really to look at the efficacy and then think about it if the increased frequency of dosing also increase the overall survival of these patients. That will obviously take longer, and then we have to really think about when and how far we take that analysis as well. Currently, from the previous part one and part two in the middle on the left-hand side, we have been able to follow those patients for more than 12- months already. That data you have seen. We have some very interesting patient groups where we have seen a very significant survival effect. This is a 12-month data. On the left-hand side, melanoma and then gallbladder or bile duct cancer on the right-hand side. As you can see, the patients who do get the clinical benefit and also fulfill the criteria of the biomarker analysis, they have a 100% response rate. Look at those who do not, that's only 6%. Those are the blue curves here, and the red one is the effective one. If you look at all 10 cohorts we had in this MATINS trial, we have a 63% response rate in those patients who have a clinical benefit and only 9% in all of the population. Those are also indicated here. Remember, these are the patients who had no any more other options. That red pie part in my slide previously. Then the group, if you compare those who have this benefit to those who do not, you can start to see that they are really the patients who have inactive baseline biomarkers in their circulation. Interferon gamma, TNF-alpha, interleukin-6, typical markers indicating that your baseline is low, you don't have the immune activation. So it's really important to understand. We also know today initial data that if you look at the Clever-1, it's the target, and if especially you look at the intratumoral Clever-1 on the surface of these macrophages, it is a significant correlation to that as well. Obviously we really hope to hopefully be able to report additional data on this front as well. You can also make an analysis, statistical analysis of this, using this, kind of a method, a ROC called, and here you look at the area under the curves between, in the middle you have the line going up and more area you get under these curves, more significant that is. On the left-hand side, you have two of these markers, interferon gamma and TNF-alpha, and you have almost 90% certainty or probability to have a right analysis of this material. If you add all four, interferon gamma, TNF-alpha, interleukin-6 and interleukin-8, it goes more than 90. More than 80 is already excellent predictor, and if you have more than 90, it's outstanding. This is again showing that we have a very exciting position also to enrich our population among those patients we have been treating previously, obviously then increasing the clinical benefit among those patients. Just to summarize, Bexmarilimab is extremely well tolerated. It's really not giving that much of a grade four or five adverse events. We have seen some immune reactions, which we actually would expect, but those have been possible to treat with the steroids. I mentioned already this clinical benefit with some of the cohorts could go up to 40% of the patient population, and biomarkers can really predict the clinical benefit. One next really thing is to look at if this increase in dose frequency can actually produce better single agent activity, and that's what we have been analyzing also together with those receptor occupancy in order to have a final data to predict and take to the regulators how we want to advance with the next stage of the development. That is on the way. To support the combination strategy we have been building up is really to show in this slide. As we know, the PD-1 blockade mainly activate the cytotoxic T cells. Those are the cells that can kill the cancer cells. They can kill number of other things, but especially within the cancer patients. There's very little evidence that they activate macrophages, which are the immune suppressive ones, the target for us. They may activate interferon gamma and TNF-alpha upregulation because when you activate the T cells, you do that at the same time. There's no sign that they can activate the innate immunity system in order to really activate our immune defense against the new antigens. Another important aspect with the Bexmarilimab treatment is that you really enhance the antigen presentation in order to initiate the immune reaction against those antigens. If you take these arrows and combine them, you get a very significant combined effect on our immune system. It looks like we are now being able to affect everything. These arrows are not necessarily at the same level because they come from the collection of the papers, but it at least gives direction and the reasons why this combination makes a lot of sense and should help the cancer patients once we get on the first line. The BEXMAB combo first line setting directly going to the combination, and then we have been really thinking about the first target, and here we have been thinking really those where the PD-1 blockade is least effective, head and neck, urothelial cancer, and some form of lymphoma, the lung cancer. This is a typical treatment. Look at the dosing first and then increasing the size of the cohorts in order to get the signal and then moving on to the pivotal part when that material is available. Then Bexmarilimab. On the right-hand side, you can see that almost all these myeloid cells these patients carry on are Clever-1 positive. The reason why this is so exciting now, we are really actually treating leukemia cells which also carry the Clever-1. If that Clever-1 is the reason why the immune suppression is so strong in these patients, it would be extremely important to take these cells out from those patients and inactivate them. That's exactly what we try to do. Here the trial is also rather simple. We have started with azacitidine, which is the first chemo treatment typical to these patients, and those combinations are going on. Once that's done, and we have really sense of the dosing, we can then combine that with the brand-new product called Venetoclax, which is also another chemotherapy for these patients. This condition is really fatal. 90% of the patients die within the first five years after recognition of. Also here, what is really nice for us when we do the open study, these patients are regularly examined at both the bone marrow and the blood samples, and obviously that data is collected at the same time. Once that is done, dosing optimization, we can actually move on to the phase II. We are able to start the study because the Bexmarilimab is so well-tolerated with rather significant dosing already. If you look at the protocol, which you can obtain from the ClinicalTrials.gov, the first cohort is already receiving 1 mg per kilo every week, and that is a significant concentration. I'm really looking forward to start to see some data from this trial as well. Future immune therapy can be improved. We have shown single agent activity, which is not that common with the new cancer drugs, well-tolerated. Patients definitely have demonstrated to us that we activate the immune system. We have a strong scientific rationale really to do the combinations. On top of it, really looking at biomarker data, what we have at the moment to really enrich the patient population wherever that is needed. I'm pretty sure that all these different facts are really well received by the regulators when we go and meet them in the future. With that, I'm happy to now really open the Q&A session. Just type your name and question in the question box and click and just submit it to us, and we are happy to answer any further questions you may have to us. Thank you very much. Markku, there's questions coming in. A couple came in as you were speaking, but they're starting more now. I'll start with a few that came in. The first being, could you please tell us more about funding needs to move Bexmarilimab forward to the market? As part of that, is partnering the strategy you are pursuing? I let Toni to answer the first one, but as I said for the partnering activities, now when we are building up the data, more boxes they can tick the partner candidates, and we are really surrounded by the partner candidates. I have also said that this is now the point where we really generate the shareholder value, and I don't want to really be too fast with any conclusion which partner is the right for us. Those discussions are ongoing. Hopefully something will come up in the future. Again, really hard to predict because these negotiations usually take place and also all the DD processes, but it looks really exciting. For the financing part, I let Toni to answer. Thanks, Markku. I think on the cash need, as we publicly communicated in our corporate deck, we're looking to bring both BEXMAB and BEXMAB combo into phase II data, we need roughly EUR 50 million. In order to bring into the BLA to the market, another hundred million. As Markku elaborated, we are looking at the different options here, you know, how far will we take it on our own money, so to say, and when do you partner? That's kind of the discussion that we have internally and of course with the board to get the maximum shareholder value. Toni, that's a good transition. There were a couple questions about shareholder value, and I guess, you know, summing them up, what are the upcoming milestones that could have a meaningful impact on shareholder value? I will let that Markku maybe. Thank you. Really good point. It's an additional data. There's nothing wrong with the current data. Believe me, it's so exciting to really deal with the population that has no effective treatment, and we are already showing single agent activity over there. Obviously, the final readout to the point where we can actually take the material to the FDA and get their opinion what they want us to do next. We are mainly focusing on the data from MATINS trial, but obviously these other trials, when they develop, we can additionally then discuss with them. That all is really giving us the patient population where all kind of valuation models can be applied. As we all know, one significant good year life can be priced nowadays in U.K., that is GBP 50,000. You just can make the calculation if the population is 100,000 or more, what kind of a upside we have with this BEX project. Obviously we need data, and that's why we are really working hard, and we really try to accelerate everything as much as we can. Okay. Another one on, you know, sort of what's the regulatory path for BEX, and is the single randomized trial going to be enough? I'm assuming they mean in the MATINS setting. Or do you expect to need additional or two trials? I guess an interim step before you get to a regulatory, a registrational trial. In the last line, if you can have randomized trial with the significant overall survival benefit, normally the regulators take a positive view on it, and that's what we are hoping for, and that is the reason why the meetings are so important that you get pre-advised really for those activities. If you then look at the indications, would that be bile duct cancer, cholangiocarcinoma or melanoma, which already have shown in this cohort what we have currently treated, which have not been enriched or preselected, is already 30%-40%. If you then apply the biomarker, and we can have 50%-60% outcome in the clinical benefit rate, and that overall survival is extended by 12 months, I believe that then the data monitoring committee can actually advise us how far we need to go with that one. We do not necessarily talk about 500 or even 300, it actually could be even smaller. That is the pathway with the randomized trial. These other ones where we have these combinations, there, if we start to see immediately the effect, then that can be easily expanded into a large trial. Obviously that data is still yet to become, and I'm not really predicting how that is going to progress. All right. Then there's one on dose and frequency and where that stands in terms of figuring out what the optimal dose and frequency would be for patients in MATINS. We have pretty much recruited the patients, and the sample analysis for the receptor occupancy is already indicating that we really are not that far away from the optimal dosings what we have. If we want to use the increase in the efficacy and clinical benefit, then we have to utilize the traditional cancer method, and that is the RECIST analysis. Those we take roughly every other three months. Now the question is how long we actually would wait that one. My personal view is that maybe already the receptor occupancy would be enough really to go to the regulators and tell that, you know, we are now done with the dosing and then measured all the PPK and PD analysis, and here is the results. As said earlier, we already have in BEXMAB 1 mg/kg every week and no alarming sign of any toxicity. Maybe we are rather close already with the dosing. One, I guess, for Toni, which is how much should we expect the OpEx to increase for full year relative to 2021? Then any sense of a split between R&D costs and G&A increase as part of that? Okay. Thanks. That's a great question. For this year currently, we spent EUR 13.4 million in the first half of the year. We expect the second half of the year to be actually a little bit lower. It has three reasons. In the MATINS trial, as Markku elaborated, you know, we don't have that many patients coming in the second half as we are doing the preparations for the FDA meeting. Second, on the Traumakine front, the HIBISCUS study was closed. We announced that in April. Third, we had some one-off costs as we are ramping up the U.S. activities in the first half of the year. We expect this to be relatively in line with last year. We don't actually expect an increase. In turn, compared to the first half of the year, well, we are currently estimating we actually have less spend in the second half of the year compared to the first half of the year. The split between the G&A and on the R&D side, we don't expect any material change there. Markku, based on the comments with the FDA meeting or potential advice, I guess the question is really, do you expect them to suggest a trial where there would be a comparator arm in the MATINS setting that would be no comparator? Would there be another treatment option at that stage, or would it be? I mean, I guess what we've said in the past is it would be investigator choice or physician choice. Really, what does that mean? Well, that means depends strongly on the status of the patient. In some of the cases that could be just a supportive therapy because everything may be already used. Some of the doctors still may want to use some chemo treatment that can be allowed. It's really to have a comparator arm where doctors can actually determine what they want to do. Obviously the Bexmarilimab treatment will be the same, but they have a Bexmarilimab. That's practically what it is. Okay. There's a question about any news regarding soluble Clever-1 research and the recent patent application? That is very interesting. We have been rather quiet about it because we want to have a complete understanding how strong inhibitor that is in us. If it's really strong inhibitor of T-cell activation, then part of these Bexmarilimab treatments actually could ease that part as well. We want to really study this to the point that we fully understand. We also want to understand the interaction of the soluble Clever-1 with T cells and maybe some other cells in order to fully understand what are the pathways it's using, and is it totally different from T cell surface Clever-1 on the surface of these immune-suppressing macrophages. If we come up with something once it's kind of well understood. I don't want to put out data that is partially true or it's not completed. That's the strategy we have on that front. Okay. One back to BEXMAB. What's the timeline, or are you planning to expand BEXMAB into sites in the U.S. or other countries? Yes, yes, absolutely. That's ongoing work. Yep. As you know, we have a good relationship with MD Anderson in U.S. already and that will be activated. There are some excellent other sites, and interest has been tremendous because, as I already mentioned, this is such an awful disease that we really need to get some better treatments than we have today. Any thoughts on recent developments of CD47 clinical trials and how, if any, impact this would have on Bexmarilimab? That's a very good question. We all know that CD47 is expressed almost on every mammalian cell type. If you look at the transcript analysis, there are only very few cells where it's not expressed. Instead, if you look at the Stabilin-1, Clever-1 expression, there are only very few cells where it's expressed. So due to this large expression or frequent expression of CD47 on so many cells, it's probably causing the problem what the current developers actually have seen. Just to give an example, it's on the surface of the erythrocytes, and if you have a massive load of anti-CD47 in those patients, you may have a lysis, and that's the reason why the anemia is very evident in those patients. There could be some other problems. Gilead needed to stop their trial, they analyze it, and can they continue that? It is really important that your target molecule is not expressed in that many locations. It just be expressed there where it's needed, and then you can block the function. There were a couple about the U.S. entity and, well, U.S. in general. There's one, are you seeking a U.S. listing? Secondly, can you describe your U.S. organization in the U.S. sorta currently and what you would expect it would look like at the end of the year? We are expanding our clinical group over there. As said earlier, I thank again Marie-Louise Fjällskog, who is really doing excellent work on that front. That's one part. Obviously, we are interested in setting up further regulatory activities over there in order to communicate with FDA effectively. We haven't really said that we are going to be listed in Nasdaq, but obviously, that market is attractive, and I have a feeling that it will recover faster again than in Europe. There are already early signs that biotech is coming up again, and obviously, we should be prepared. Toni Hänninen, if you want to comment on this as well. Sure. Maybe on top of that, on the U.S. side, we also added a resource in IR and communication on the G&A side, so not only on the R&D side. Yes, absolutely. I mean, with high interest, we've always looked to, you know, a potential Nasdaq listing as a means of funding the company and getting better shareholder value there. However, we've seen the last 18 months market has been very challenging. U.S. market has gone down more than the European. Typically, we've seen it recovers faster than the European market, so we continue to monitor the situation. What we've seen in the last couple of months in the capital markets is that there are signs of recovery, stabilization, and we of course hope that this trend continues. We have now internally built a lot of organizational capability to explore this option. Mark, there's one about Traumakine, which is, can we expect any new trial programs for Traumakine? Yes, you can expect. We have this collaboration with the Department of Defense, and obviously that is important that we understand the next steps. This ischemia-reperfusion injury is related to the fact that, if you are on the battlefield, you may lose your arm or leg. These limb injuries, when they have to close the circulation, you get ischemia-reperfusion injury when you reopen it, and that is the dangerous situation, and that is exactly where Traumakine is needed. There are some interesting results we hope to be able to publish later this year, which then actually tell us what kind of a trial design we will have next. It's a bit too early to talk about it, so you need to wait a little bit more. I don't see any other questions that we haven't addressed here in the tool, so I think that's it. All right. I just want to thank everybody making nice questions and we will come back when we have exciting data, and hopefully we will see soon. Thank you very much again. Thank you.