Good day, ladies and gentlemen, and welcome to Faron Pharmaceuticals' unaudited Half-Year Financial Results for the six months ended June the 30th, 2021. 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. Participants can also submit questions through the webcast page using the Ask a Question button. I will now hand over to the CEO of Faron, Dr. Markku Jalkanen, to open the presentation. Please go ahead. Thank you very much, operator. Good afternoon or good morning for those in the U.S., and thank you for joining us this conference call, where we go over the presentation for the first six months of this year. Would be really nice to see you all, but obviously, this is the time where we need to do it this way, but hope to really soon get over this one. I am here also with our CFO, Toni Hänninen, who is in Zurich. Hello, Toni. Good morning and good afternoon. With that, could I get the next slide, please? Slide number two, please. Just to remind you that there will be some forward-looking statements during the presentation, and this is just to disclaim those. Next slide, please. As you know, we really have been focusing on the immune therapies, where we maximize the system we have to defend ourselves in this rather hostile world. Our main target is Clever-1, that we believe is the main cause of this immune suppression around the sites where one example is the tumor. We believe that it actually could produce a signal, "hide me," for the cancer cells, and obviously, that is really important to remove if we want to target a removal of cancer. We have a very interesting position here. We have all the efficacy. We have a number of new cancer cohorts, and this is going to move on to the pivotal phase after further experimentation later this year, and we are all excited. The next slide, please. The pipeline illustrated in the next slide is just an example where we are at the moment. The original MATINS trial has become a platform of ours. There we can test various combinations and individual cohorts, and as we have already released, we now have four different cancer cohorts where we have early efficacy demonstrated. The MATINS patients are last-line patients in the cancer treatments, and we are using a monotherapy. When you evaluate the results, keep that in mind. We anticipate really to move on to additional trials on the second half of this year, so very exciting time for us at the moment. We also have made significant progress with Traumakine, the second asset. I will tell that more about as well. Looking the slide number five, the significant progress is really illustrated with the fact that now we have a cutaneous melanoma, gastric cancer, cholangiocarcinoma, and hepatocellular carcinoma showing a disease control rate that is from 30%-40%. As again, this is a standalone treatment post other treatments these patients have gone through previously. Additional trials are really planning to start, and I will go some of them over. At the same time, we have really secured patents in U.S. and Japan to really protect bexmarilimab. More importantly, we have succeeded really to get the companion diagnostics to really measure Clever-1 from the tumor samples, and this is really important aspect as well. Traumakine now has part of this phase II, phase III trial in the U.S. We call it HIBISCUS. There we have a significant support from the Department of Defense. With that one, we believe that we can finally solve the problem in which order the current treatments should take place in those patients. Obviously, we are in favor of starting that with interferon beta, Traumakine, and then continue with additional medication if needed. It's very exciting project as well. Please ask the next slide number six, and ask really Toni to look at the numbers from this first six months of this year. Sure. Thanks, Markku. Highlights of the first six months of the year, 2021. Our cash balances at the end of the period were EUR 7.0 million, and our operating loss was EUR 10.4 million, which was an increase compared to prior year. This is mainly driven by the EUR 3.5 million increase in the R&D expenses due to the acceleration of our pipeline assets, where Markku just gave you the highlights, and will elaborate a little bit later more details. The net assets were EUR 2.8 million at the end of the period. Earlier in the year, in February, we did a EUR 15 million gross equity raise from new and existing shareholders, including the EIC, which first time invested in a publicly traded company. We were very pleased and very excited about that participation. Also early in the year, as Markku mentioned, we had a commitment of $6.1 million from the U.S. DoD to support the HIBISCUS trial, where we announced yesterday the first patient in. With that, I'll hand over back to Markku. Next slide, please. Thank you, Toni. Let's move on and look at the bexmarilimab. This is really a humanized anti-Clever-1 antibody, and this is really the summary. The few things which makes it really unique. The target is unique. We are the only one at the moment who is doing it, and if this target is really in charge of hiding the cancer cells from our immune system, it's important really to unlock it. We also know that it's very safe at the moment, really haven't seen the dose-limiting toxicity and all the adverse events related to the drug are really minimal, especially if I compare those, the ones which have been seen with some other checkpoint inhibitors. All of this really mean that we have an opportunity really to transform treatments of cancer by combining with the existing, other treatments. Having this opportunity really to have extensive IP coverage really mean that this opportunity is really significant. Could I have a next slide? As you may recall, the checkpoint inhibitors have improved significantly the outcome of the current cancer treatments, but yet they still help only a portion of these patients, as illustrated here on the left-hand side. In order to improve this outcome, we really need to improve the conditions where these are excised, and we believe that if we can remove these immune suppressive myeloid cells from the tumor site and from the patient, in all occasions, we have much better success in doing that. Next slide, please. Macrophages are around the tumor. You can see that on the right-hand side from these immunohistological stainings. Now we have this diagnostic tool to do it. Macrophages are well preciated to take part in a number of activities which promote the tumor growth and spread. It's accepted well that you need to remove macrophages, but not all of them. Clever-1 is specifying one special group, which seems to have the highest immune suppressive capacity. If you can reprogram those into an antigen-presenting cells, you actually can make them to stimulate the immune system, and that's the whole purpose of the treatment with the bexmarilimab. As shown in the next slide, we really have now worked out a assay that helps us to detect Clever-1 in those tissue samples. They could be tumor biopsies, or they can be samples from the surgical operations, and then we can look at how abundant Clever-1 expression on those macrophages really are. That would help us hopefully also to define the target population in the future, together with some other biomarkers, what we are currently studying in those populations we have been treating. This is a significant milestone and often asked when we get there and now we are there. It's all validated using a commercial analysis kits and an instrumentation which are widely used all over the world. Significant milestone. Next slide, please. That's 11 and 12. Slide number 12. Normally, these tumor-associated macrophages clean everything out, and they are supported by the Clever-1 function. It's a scavenger receptor, but it also maintains the phenotype, which is really effective of removing this material. The whole purpose is really to remove it so that it's not available for the immune activation. In a way, they hide the environment. That's the reason why this is so important for the cancer cells. Cancer cells of these tumor-associated macrophages. As I said earlier in my presentations, the same situation in some of the physiological conditions. If you want to hide embryo from mother's immune system, you are using these same cells. They migrate to placenta. When the pregnancy is over, they disappear. Here, we would like to make the tumor-associated macrophages who are Clever-1 positive to disappear or convert them to antigen-presenting cells. This is a very unique mode of action nobody else has been targeting previously. "Hide me, please," is the begging question the cancer cells is making. Next slide, please. One of the amazing discoveries which we have now confirmed during the first half is really that it's not only present, this Clever-1, on the surface of these macrophages. There's also a soluble form, and we have been able to document that is built in the exosomes which these cells are sending into a circulation. You wonder why is that done? It's very simple. This soluble Clever-1 can directly inhibit T cells. Obviously, if you would like to activate the T cells, for example, using a negative checkpoint inhibitors, maybe it's really important to remove the soluble Clever-1. Soluble Clever-1 has become a target of our development work as well. Obviously, we want to monitor its bearing and also control that the dosing is optimized really to do that. We already know, as shown on the right-hand side of this slide, soluble Clever-1 amounts are increased in cancer patients. Next slide, please. From the animal experimentation, we already know that we can control the tumor growth, start controlling the presence of Clever-1. Several models shown on the left, lung lymphoma and also mammary, but also in the middle, a melanoma, where we also compare that melanoma growth to anti PD-1. If you look carefully, it looks like Clever-1 is more effective in that model than PD-1 negative inhibitor removal. The new thing was that we also figure out that the Clever-1 is heavily expressed by acute myeloid cells, and we have tested those in ex vivo conditions. When we control the Clever-1, we control the replication of these cells. That is one of the reason why we really would like to move on to this first malignant condition where the myeloid cells are involved. Could I have the next slide, please? One interesting thing what we learned from those animal experimentation, that we actually increase the presence of these cytotoxic CD8 cells in those tumors which have been treated with the bexmarilimab or the surrogate antibody. You can see that in a increased concentration of cells who are granzyme B positive. Granzyme B is one of those proteinase T cells used to kill the cancer cells. You definitely would like to see that around. When you look at the MATINS patients, you see the same. Those are the red dots in this picture. This is very important finding. This is a post-treatment induction of granzyme B cells in those tumors. At the same time, we also see the increase in the gamma in those patients from the baseline, from the original baseline. Again, indicating that we are activating the immune system. Now the question is, are they targeting the cancer cells? If you really think about that they migrate at the tumor, then they should do it. Next slide, please. The important design of the MATINS really is based on those facts. We collect biology from humans under a bexmarilimab treatment. We learn from that, and then we move on. We can have adaptive designs in the middle, really to modify the cohort in order to get better understanding. As we have indicated, we are now testing the increased frequency in dosing. We started with three-week interval, but we are now getting down to two weeks and to one week. Using that, it then come to the point when we can actually really design the very first pivotal cohorts for next year. Prior to that, really communicate this with the regulators. Along this, then apply the companion diagnostics. Very interestingly, the ESMO abstract that was sent to meeting in September, that was selected as a late-breaking abstract, and that is currently under a preparation for the final form. Hopefully, at the same time when the presentation is taken place at the meeting, we hopefully be able to provide additional information at that time. Next slide, please. When you look at the ones who are responding to the treatment, which you then follow as a RECIST images from those patients, post four cycles or seven cycles, we have a significant disease control in some of the cohorts. Cutaneous melanoma, gastric cancer, cholangiocarcinoma, and hepatocellular carcinoma, in this case. We have some cohorts who have no response whatsoever, like pancreatic carcinoma, uveal melanoma. This is a significant response, 30%-40%. That alone could mean that the regulators really have a feeling that they actually should support us to move on further on to the pivotal phase. The question is, what size of the trials we need to run? That we learn next year. Next slide. If you look at this, you can also look at the individual patients as listed on the left-hand side. More importantly, on the right-hand side, you can see the safety profile. There's hardly no drug related adverse events, as you can see. Look at the grade three or four, which are usually the severe ones, hardly anything, and the same for the grade one and two. This is a significant opportunity, really, for the combination therapies because we are not adding additional toxic risk when combinations are carried out. This may be the reason also why the clinics have been really active in conducting the recruitment. We are close to 160 patients already now recruited. It's really a good sign, because this is done around the corona time. Next slide, please. As said, we need to remove the soluble Clever-1 from the circulation. You can see on the left-hand side, when we are administering bexmarilimab, it goes immediately down on day two. That's on the left-hand side. Already on day eight and later on after two weeks or three weeks, we are back to the baseline. This is the key marker for us really to follow the occupancy of the receptor itself on the surface of the myeloid cells, but also the soluble form. One very interesting pharmacodynamic effect we have observed and already presented previously. This administration takes down some of the negative checkpoint inhibitors. Here we saw one example, and that is the PD-1 level in the peripheral cells, CD4, CD8 in this figure. As you can see, 24 hours post administration of bexmarilimab, we practically lose PD-1 levels. Very important finding and may be the reason why this pharmacodynamic effect then is beneficial in those patients we described earlier. Unique target, unique pharmacodynamic effect, and very safe. It is really an opportunity we would like to continue as fast as we can and move on to the final pivotal phases. Next slide, please. Yeah. If you look at the opportunity number-wise, these all listed cancer cohorts are very significant in size. Look at in the middle, standard of care and the refractory populations. In all of them, it's more than 50% who are still refractory on the first-line or second-line treatments. Obviously these patients need the help, and we are ready to do it as soon as we have data enough really to go out. Next slide, please. The design really to move on to the pivotal part is to continue some of the dosing testings, which are currently ongoing, collect the data, go back to the FDA or EMA, ask advice what size of the pivotal expansion we need to do, plan all the way the marketing approval. This is already ongoing work. The MATINS continue to be a platform. Maybe in the future, we combine there already with PD-1 inhibitors or something else to look at what impact it has even on those who are negative at the moment. That is the plan. This is very similar to what was done some 10 years ago for the PD-1, PD-L1 inhibitors. We want to learn when the dosing is optimal. Next slide. Next slide, please. The plan is really to focus on those four cancer cohorts described here. Initiate the neoadjuvant treatment, and then also the combination with the lung cancer, where the PD-1 inhibitor is already as a standard of care, and then initiate this leukemia study. You can see the collaborators we have on the right-hand side. We have a significant pool of clinical experts, oncologists really around us, helping us to design all the protocols for these studies. I wanted to highlight one example, and that is the next slide. That is the neoadjuvant study. Many of the colorectal cancers are really cold tumors. They have a not activated immune system. We do not necessarily know what that is, but some people think that as there are very little mutations, so the genetic burden is so low, they do not activate the system. With this setting, we are going to apply to renal cancer and colorectal cancer. We give the single dose of bexmarilimab two weeks prior to surgical operation. We have a biopsy prior, and then at the time when the clinical operation and surgical operation is conducted, then we get additional samples. If we can really show that with single treatment we can convert these cold tumors hot again, they could become target of checkpoint inhibitors. Very interesting data collected from those tumors. This we get rather soon because we don't necessarily yet look at the efficacy within the short period of the time. It's really to look in the conversion of this. Very important study for us, and it's about to start. Next slide, please. Back to this one. This is really important for us, and I would say, and Toni will go over it later on, 75% of the resources we have, if not more, really go into this development. A few words about the Traumakine. Please, next slide. As we announced yesterday, we now are in the HIBISCUS trial. It's on the left-hand side. Just to remind is that with this Traumakine treatment, we hope to be able to produce locally one of the most anti-inflammatory compounds we have in us, and that's adenosine. It's produced by CD73 and interferon beta is upregulated in CD73 if it's lost from the cell surfaces. The HIBISCUS trial, next slide, is a very simple setting, but very interesting. We run it against dexamethasone. As you may know, dexamethasone has been largely now recommended to be used on the COVID-19 patients, and we have opposed that. We know from the ex vivo and in vivo experimentations that steroids can block the interferon beta signaling pathway. If that happens, you wouldn't have antiviral help from the interferon beta. With this trial now we run them head-to-head, and now we have initiated that in the U.S. We plan to have 10 - 15 sites. We soon have five sites open. Looking the situation after interim analysis after 70 patients, we can then make the further evaluation of this. I also want to share that the IDMC, the Independent Data Monitoring Committee, carefully follow this because obviously they want to see how the two arms are separating from each other so that they can actually follow that and then advise the trial study accordingly. Very important and very pivotal trial for us, and happy to have also the Department of Defense really helping us to conduct this one. Thank you. Next slide. I would now like to let Toni to continue with the corporate highlights. Toni, please. Sure. Thanks, Markku. Next slide, please. A push towards approval. As Markku elaborated, what we've achieved here so far is we see a single agent activity in multiple tumors, which are refractory to standard care. In other words, all existing treatments have failed for these patients where we see activity. In the setting that we've done in MATINS is an all-comer setting, which is showing the clinical benefit here as Markku elaborated. Out of that, these four cohorts or cancer types that Markku mentioned that we are really expanding and accelerating. Hepatocellular carcinoma has a standard of care with 75% refractory to combo treatment. On the second line, melanoma, the market is forecasted to be a billion-dollar market by 2026. On the gastric, we see a significant growth in the Western markets. Asia is already a very high incidence, we see the Western markets significant growth over the next five years. In cholangiocarcinoma, it has a limited market size as currently there is no innovative drug approval on the market. To recap, our pathway here is the checkpoint inhibitors. They have been approved with exactly similar trial sizes, approximately 100, 1-200 patients, and with a very low overall response rate of 10%-20%. Next slide, please. On the back side, what are the near-term catalysts? As you can see here on the slide, we had a very busy first six months or eight months by now, as of today, with multiple milestones that we've achieved. Out of that, we also have a lot of plans and a lot of milestones coming up in the second half of the year. Additional data release in solid tumors. We got the late ESMO, late breaking abstract in ESMO, confirmation of the final dosage and frequency, and the meeting for the pivotal expansion and guidance. The cohorts should be starting recruiting in the first half of next year. Additionally to that, we have the neoadjuvant study that Markku just elaborated, and also the hematological malignancies, starting in Q4 of this year. At the end, we also do an investigator-driven trial on a PD-1 combination, so not just a single agent. Next slide, please. To recap also on the Traumakine and Hematokine. Traumakine, CMC, the commercial scale preparation is ongoing with AGC, progressing very well. For the HIBISCUS, yesterday, we announced the first patient in, that's the study for COVID supported by the DoD. Out of that, we hope to get the interim analysis as soon as possible, followed by, of course, the presentation in the Military Health System Research Symposium, three map gap readout, and then organ protection data release with the DoD. Last but least, Hematokine is in pre-clinical studies, and we are advancing those pre-clinical studies all the time. With that, I'll hand it over back to Markku, and thank you. Thank you, Toni. This is really the summary of the current situation, and we are extremely excited about the second half of this year because a lot of additional information will be analyzed. As said earlier, especially the biomarker data will be a key thing for being able to hopefully enrich the populations even further and understand how this response is taking place. We have some ideas there, but they have to be confirmed. With all of this, really thank everybody joining us and as said at the beginning, you have now possibility to send questions to us, and I transfer this back to the operator. Thank you very much. Okay, ladies and gentlemen, we will now begin the question- and- answer session for the event. If you wish to ask a question, please key star and then one on your telephone. All questions will be answered in the order received, and you will be advised when to ask your question. All other lines will remain on listen-only. So 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 Jon Berggren from Kepler Cheuvreux. Jon, please go ahead. You're live in the call. Yes. Hi, Markku. Hi, Toni. Hi, Jon. I have a question regarding your main asset, of course. About a year ago when I first talked to you guys, you were pretty focused on investigating what kind of tumors that were high expressers of Clever-1, and that these patients would obviously potentially benefit more from treatment with bexmarilimab. In January, you made this discovery about soluble Clever-1 and that a lot of patients in your trial had abundance of soluble Clever-1, basically. Now, when you had this key opinion leader update in June, you talked a lot about focusing patients with no underlying inflammatory responses and essentially making cold tumors hot, basically. I mean, to filter out high Clever-1 expression tumors in patients who also have soluble Clever-1 with no underlying inflammatory response, that seems kind of complex to me. I know that you accept all comers in trial now, but do you aim to filter out patients with these kind of conditions in the pivotal arms of your trial? Thank you. Thank you. It's a very good point. That is the reason why we have collected a really massive amount of biomarker data, also related to the information. Especially we know that if we have interferon gamma activation ongoing, and if we can help those who have been previously activated, that is really key thing to understand. Is that activation dependent on the presence of Clever-1 positive M2-type macrophages? Now we have a tool to do it. We go back and stain every sample we have from those patients to get a really high-quality data. I can assure that becomes part of this development work in the future. What are the best information really to classify to enrich the patients? We hope to learn this for all of that information. Okay, great. Thank you. That was my only question. Okay, our next question comes from Miles Dixon from Peel Hunt. Miles, please go ahead. You're live in the call. Hi. Thank you. Hi there, Markku, Toni. Hi, Miles. Firstly, hi there. Just to ask firstly on the bexmarilimab, the advanced tumor, the numbers. I seem to remember that you were initially talking about 30% the control, and you're now talking 30%-40% subject, which indications you look in. Is that a consequence of more data coming in, or is it better understanding of the data that you had originally? It's really the accumulation of the data, not all the patients were at the stages we could evaluate them. Now when the full cohorts are available, that is the final number of the data. It's three out of 10 in those three ones, and at the hepatocellular, which is the latest one, it's four out of 10. Great. Thank you. Secondly, this, I think, follows on a little bit from the earlier question. The companion diagnostic and the staining of the antibody, are you now at a stage where you're reasonably confident that there's a quantum or a level of expression in the histology samples where you're able to distinguish responding patients or discriminate on patient outcomes, for instance? It definitely varies. There is an individual levels. How that is connected to the outcome and can that be helped in combination with other biomarkers, that is a crucial thing really to enrich the population and even go further than this 30%-40% response rate in those patients. That also may could guide us further to think about what are the best combinations if those are needed. Yes, we get the information from the human material, not anymore from the animals. We all know that it's really important to understand how the human reactions will really take place. Also, I need to remind here that we are really looking last line patients. Many of them have gone through several line of treatments, including chemos, and many of them I know and have seen the data are in really bad conditions when they come to the trial. I just wonder how these things will look when we get further up on the first line or second line. It is really important to understand. Thanks, Markku. Then the last one on the science. This is back on slide 15. You were showing the matching patients in bexmarilimab's effect on CD8. Are you able to quantify that difference between the CD8 expression in the patients pre and post, or is it the law of small numbers and it's just a significant change at this stage? We would like to not only look at that individual cell type, also some other biomarkers among those populations. It's really important to understand what is the CD8 populations we are affecting mostly. As I said earlier, all that data is under the analysis at the moment. Okay, thank you. I'll wait for it. Lastly, perhaps, Toni, just on the financials. I remember in your FY 2020 results, you included a number of grants, loans and loan guarantees that were totaling EUR 7.9 million, but you disclosed EUR 2.1 million in the actual financial results. Does that mean that we can potentially expect the rest to come in in H2 2021 or some of it drift out to the following financial year? Thank you. Thanks, Miles. Exactly. Out of the EUR 7.9 million, that's the four instruments that we announced, and the DoD from the U.S. is on top, $6.1 million. Last year we received out of those funds, EUR 2.2 million on the bank account, and now in H1, there's roughly EUR 300,000 from the Business Finland loan. Those are staged with the milestones, and then we report back to them and then they pay. They always come with a lag. We do continue receiving them now, for a period in H2 and some of them also next year. They're split between the both financial years. Great. Thank you for taking all my questions. Okay. There are currently no further questions on the conference line. We will now move on to the questions received through the webcast page. Our first question, are there plans to expand the HIBISCUS trial beyond the current patient population, potentially to study effectiveness against long COVID? That really is now dependent on the data. We don't need to make the decision in the near future. We need to look at the interim and the finalizing the HIBISCUS data so that the regulators are happy with the outcome and would allow us really to come to the market. That is the aim. At the same time, having said that, we do have a number of experimentations ongoing, and especially all the ischemic conditions where the reperfusion injury will take place potentially are the target groups. The answer is that yes, we are expanding it, and also the ARDS, that is the condition we started with at the INTEREST trial. That condition still requires additional help. We are dreaming to have a mortality rate below 10. Nothing like 30%, 40%, what is today, even with the current treatment with those patients. Okay. Our next question is, will the next MATINS data release include findings from the increased dosing schedules in order to study the effects on soluble Clever-1? There will be data coming out gradually, not necessarily everything at one time. I can't predict in which order it can come. We also need to be careful when we analyze everything and verify if that is correct. I have a feeling that in the quarter three, there will be some new data, also quarter four, additional data. These are really massive amount of data we have collected from those patients, that is probably one of the reasons why the cost of the trial analysis is also significant for us. We need that data. We need to analyze that carefully. The answer is yes, they come out when everything is in proper order. Okay, ladies and gentlemen, that concludes today's question- and- answer session. I will now hand back to Dr. Markku Jalkanen for his concluding remarks. Thank you very much. Thank you for joining this meeting. I hope that you are convinced like us that the bexmarilimab will be a very valuable addition to current treatments. We need to help those who are refractory at the moment. That is really important. If that is done with the bexmarilimab to open and unlock this Clever-1, then we are there. With the HIBISCUS trial, we need COVID-19 patients additional help. There are unvaccinated people. There are new viruses most likely coming around. We now have a Delta. Maybe influenza is waking up and comes in a year or so. These are life-saving drug development we are doing at the moment, and we would like to thank for your support and patience really. I have said to some of the shareholders that longer our cancer trial will last, better off we are, because then we are knowing that the patients are surviving. That is really important. With that, thank you, and we are looking forward to see you again rather soon. Take care.