Greetings, welcome to the Faron Pharmaceuticals BEXMAB study update. At this time, all participants are in a listen-only mode. A question and answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. I would now like to turn the call over to your host, Dan Ferry of LifeSci Advisors. Thank you. You may begin. Thank you, operator. Good morning, everyone, and welcome to the Faron Pharmaceuticals conference call to discuss the positive BEXMAB data from phase I/II trial cohorts in patients with relapsed refractory AML and MDS, and next steps for the program. A press release highlighting these updates is available on the Investors page of the corporate website at faron.com. We will be conducting a question and answer session at the end of the call. Before we begin, I would like to remind everyone that this conference call and webcast will contain forward-looking statements regarding our regulatory, product development, and commercialization plans and research activities. These statements are subject to risks and uncertainties that could cause actual results to materially differ from those forecasted. A description of these risks can be found on the Disclaimer page of our corporate investor presentation, located on the company website. Presenting on the call today are Dr. Markku Jalkanen, Founder and Chief Executive Officer, and Dr. Marie-Louise Fjällskog, Faron's Chief Medical Officer. Additional members of the Faron leadership team will be joining the question and answer session at the end of today's presentation. They also include James O'Brien, Chief Financial Officer. I would now like to turn the call over to Dr. Markku Jalkanen, CEO of Faron. Markku? Thank you, Dan. Good morning and afternoon, depending where you are. We all know that cancer cells are very smart, and they do have very clever way to hide our immune system. They do this by attracting immune suppressive cells around them, so that they will change the microenvironment to hide our immune defense, and by doing that will allow them to grow and metastasis. The main cell type that can actually do that are the myeloid cells born in the bone marrow and then travel in the circulation and called monocytes, and then they go to the tissue, they are called macrophages. This special type of immune suppressive macrophages have a receptor called CLEVER-1, and the antibody called Bexmarilimab, or Bex, like we call it shortly, can block the function of this CLEVER-1 molecule on the surfaces, and that will convert these immune suppressive macrophages into immune activators. This immune activation requires antigen presentation capacity, and we have shown that already in many occasions. With that, we can actually activate the innate immunity, and for that, also the activation of immune cells. The CLEVER-1 anti-protein antibody is a typical IgG4 antibody used in many occasion, and it really blocks the receptor activation on the surface of these cells, and with that one, we can remove the immune suppression. We have very good safety profile in more than 200 patients already shown in the advanced solid tumors, but more interestingly, the hematologic malignancies is very good target because some of them really express the same receptor. Therefore, if I could get the next slide, I would like to present the mode of action, which is really evident with the patients we are now treating. We have a dualistic mode of action. We can activate the immunity by activating these myeloid cells, like shown on the left side of this slide. This activation could really lead a result in the activation or antigen presentation, and again, if those are the cancer antigens, obviously that will really target then the cancer cells. On top of it, these myeloid leukemia cells also express the CLEVER-1, and now we have a direct target. If you now block CLEVER-1 on the surface of these acute myeloid leukemia cells, you reduce their viability by preventing their oxidative phosphorylation and ATP production. This is a very attractive mode of actions really, to prevent the blast proliferation in those leukemia cells. That really is the target of our BEXMAB study, which will be soon introduced by our CMO, Marie-Louise Fjällskog. If you have a next slide, I just wanted to share with you one more thing before letting Marie-Louise to talk. That is that we already have seen in these leukemia patients that we do activate the immune reaction to the point where the antigen presentation on the left-hand side has been increased by increasing the dose. Here I have 1 mg per kg and 3 mg per kg. You can really see the increase in the antigen presentation capacity. At the same time, you have increased number of lymphocytes, especially CD8 cells, accumulating in the bone marrow. This really tells us we are activating this immune system in these leukemia patients. Obviously that is exactly we want to reach. Now it's really time to look at what the outcome of these patient treatments have been over the time. Obviously really looking at the most recent data from 6 per mg dosing cohort. With this, I would like to really transfer the voice to Marie-Louise, please. ... Thank you very much, Markku. The BEXMAB study is a phase I/II study where we are evaluating the additional Bex to standard of care in myeloid malignancies. The study has 2 treatment arms. We call it the doublet. In the doublet, we have added Bex to standard of care azacitidine in the indications of MDS, relapsed refractory AML, and patients with MDS that failed prior HMA-based therapy. The study also has a triplet arm, where we have added Bex to standard of care azacitidine and venetoclax in indications such as newly diagnosed AML that do not tolerate chemotherapy. The study is actively enrolling, and enrollment is going fast. We have 4 very active sites in Finland and 2 in the U.S., City of Hope and MD Anderson. We are very soon opening 2 additional sites in the U.S. Based upon the data that I will share with you with the majority in from the doublet, we have decided to focus on patients that have HMA-failed MDS and relapsed refractory AML. That was a quick background. Let's go to the data. Please go to the next slide. I'm very excited to share the newest data from our ongoing BEXMAB study. This is the third dosing cohort of the doublet in the dose escalation part of the study. What you see here is the cohort in 6 mg per kg, 5 patients. You can see that 3 patients of these 5 have achieved objective responses. You can see a very nice mCR, a narrow CR, so complete remission of the blast in the bone marrow. We also see an mCR in a patient with a frontline MDS. At the bottom of this slide, you see a CR. Complete remission of the blast in the bone marrow, also complete recovery of the blood count. What I also want to share with you is that 4 out of these 5 patients received azacitidine before. They have failed. Reintroducing azacitidine alone to those patients would not lead to very good responses. Based upon this, we can conclude that bexmarilimab is adding to the patient clinical benefit. I would like to walk you through the patients one by one, starting at the top. You see the color coding to the right with the malignancies. The first patient on top is a patient with relapsed refractory AML. This patient received azacitidine and venetoclax prior to going into the study, with the best response of progressive disease. This is an azacitidine-refractory patient. After two cycles on the study, the patient is doing well with a stable disease and is still ongoing. The next patient also received azacitidine and venetoclax before, so relapsed refractory AML, received azacitidine and venetoclax, did well, had a CR, and then relapsed. Now on the study, after three cycles, we see a nice stable disease, and the patient is ongoing. If we go to the third patient, the blue bar, we see a patient with HMA-failed MDS. This patient had azacitidine before going into the study for a long time but relapsed. On our study with azacitidine and Bex, we see a complete remission of the blast in the bone marrow, and we also see that all the blood counts are improving, hemoglobin, neutrophils, and platelets. Not normalized, but improving. The next patient is an MDS patient, frontline, so this patient did not receive any prior therapy. On our study, after 1 cycle of therapy, we see complete remission of the blast in the bone marrow, and we also see normalization of the platelets and a near normal hemoglobin and neutrophils. The last patient on this slide, you see a patient with MDS that failed prior HMA. The patient actually had azacitidine and magrolimab, and the best response was progressive disease. The patient was then put on decitabine and venetoclax, and after failure, came into our study. The patient received two prior lines of HMA-based therapy and failed both of these lines. On this study, we see after one cycle of therapy, a complete remission. This is a complete remission of blast in the bone marrow, but we also see a complete recovery of the blood count. Just to summarize, very excitingly, three out of five patients with objective responses, four of these patients had HMA-based therapy, azacitidine before and are failed. The benefit we see here is highly likely to come from bexmarilimab. Let's go to the next slide. We have already shared the efficacy data from one mg and three mg per kg from this study, but I want to share the totality of the data with you. We have treated 15 patients so far. Five patients at 1 mg per kg, five patients at 3 mg per kg, and five patients at 6 mg per kg. We did see three objective responses in the first dosing cohort, two objective responses in the second, and three in the 6 mg per kg. In total, we see eight objective responses in 15 treated patients. Out of these eight patients, half of them are azacitidine failed and should not respond to azacitidine again. I would love to share a little bit more meat on the bone on these patients. If you start at the top, this is a patient with relapsed refractory AML. This patient had azacitidine before going into the study, but progressed during treatment and therefore was enrolled into our study. After three cycles of therapy, you see a very nice PR, followed by a deepening of the response to a CRi. This is a complete remission of the blast in the bone marrow, but incomplete hematological recovery. I also want to share with you that at cycle six, the patient actually had a complete blood count recovery, so normalization of the hemoglobin, neutrophils, and platelets, and the patient has not received any transfusions since last year. Patient has a very long-standing response and is still on study after 13 months. If we go down to patient number four in the one mg per kg cohort, the blue bar, that is patient with MDS that failed prior HMA. This is a patient with a TP53 mutation, very high-risk MDS patient. Received 2 prior lines of therapy, chemotherapy and azacitidine, and did not respond to any of these therapies. As you know, these patients' only chance for cure is to have a good treatment result and to undergo a stem cell transplantation. In our study, after 2 cycles of therapy, we see a very nice PR, and this PR continued to deepen. After the last PR, as you can see on this slide, the patient had a blast count of 7%, and the investigator decided to take the patient off study to offer a potential cure. The patient underwent a transplantation in February. The last patient in the 1 mg per kg cohort is an MDS patient that is treatment naive. You see, it's a very high-risk patient with mutations that makes it more difficult to treat. As you can see here, it took a while for the patient to respond, but after 4 cycles, a nice PR, that deepened into CR, and the patient was on study almost 1 year. Unfortunately, now transformation to AML and the patient is off study. 3 objective responses in 1 mg per kg cohort, and 2 of these patients had received prior azacitidine. If we go to the 3 mg per kg cohort, the 2nd patient there is a patient that received azacitidine for more than 1 year and actually did well and had a complete remission. After relapse, azacitidine was tried again, but the patient progressed very quickly, so no response to single-agent azacitidine. On our study, we see a very nice CRi after 2 cycles of therapy. Complete remission of the blast in the bone marrow, but incomplete hematological recovery. Patient is doing great and is still on study after more than half a year. If we jump down to the last patient in the 3 mgs per kg cohort, we see a patient with frontline MDS, high risk. After 3 cycles, a very nice objective response with an improvement of the platelets. Then we have the 6 mgs per kg data. Just a reminder, we have the mCR in a patient with MDS, HMA failed, and this patient is doing great. Improvement of blood count. The second patient, mCR, frontline MDS. We have recovery of platelets and almost normalization of hemoglobin and neutrophils. The very last patient received 2 prior therapies of azacitidine-based therapy, failed, and got to CR very quickly on our study. Just to summarize again, 8 out of 15 objective responses. Four of these patients had azacitidine and failed and are not expected to respond to azacitidine alone. Therefore, it's highly likely that bexmarilimab has contributed to these nice responses. Let's go to the next slide. On this slide, you see a waterfall plot with the bone marrow blast reductions in our patients. As you can see, most of the patients, a majority of the patients, have very nice reductions of the blast count in the bone marrow. This is important because we want to understand that the drug is really getting into the bone marrow to have the effect there. Very impressive data. Let's go to the next slide. I also want to share a little bit about the safety data. What you see on this slide is adverse events that are potentially related to bexmarilimab, based upon the investigator's knowledge of the patient. I want to share that we did not see any dose-limiting toxicities in the first 3 dosing cohorts. In 15 patients, no dose-limiting toxicities. If you look at the table to the left, we see that most of the treatment-related adverse events are low grade, so grade 1 or grade 2, mild to moderate adverse events. You also see that we have 1 grade 3 and 1 grade 5 event. If you go to the table to the right side, you see that the patient with a grade 3 event had a capillary leak syndrome. This patient responded very promptly, within days, to steroid treatment. The patient is completely recovered and is still ongoing in the study. We also have a patient with hemophagocytic lymphohistiocytosis, also called HLH. This is a condition that is pretty rare, but it occurs in about 1% of all malignancies. It is more common in hematological malignancies. Reports show that up to 10% of patients with AML getting intensive chemotherapy can get HLH. There are also some reports on patients getting HLH on azacitidine and venetoclax. We have evaluated bexmarilimab in more than 200 patients as a single agent in solid tumors, and we did not see any events of HLH. However, since Bex is a macrophage activator, and we know that HLH is characterized by an overactivation of macrophages, we cannot rule out that Bex had something to do with this event. Let's go to the conclusion on the next slide. 3 out of 5 patients in the latest 6 mix per kg cohort responded with CRs and mCRs. 2 of these patients had failed HMA and are not expected to respond to azacitidine alone. 18 of the 15 patients that we have treated so far in the dosing cohort had objective responses. 4 of these are HMA failed and should not respond to azacitidine alone. We have seen some durable responses in the study, and the very first patient on the study, the patient with relapsed refractory AML, has actually stayed on treatment for 13 months now. We are focusing on the HMA failed MDS or relapsed refractory AML patients moving forward with our development, and our intent is to gather sufficient data to apply for a BLA in H1, 2025. Let's go to the last slide, showing a little bit about how we're thinking about the development of Bex. As I mentioned, we are focusing on two different indications, HMA failed, relapsed refractory AML, or HMA failed MDS. We are currently in the left part of the Gantt chart, we are in the phase I dose escalation. We are hoping to decide on the doses to move forward with in phase II by the end of the year. Per the FDA new guidance on dose optimization, we're going to pick two doses from the phase I part of the study to evaluate in the first part of the phase II to decide on the RP2D. We're going to pick 2 doses, randomize between those doses, just look at the safety data and the efficacy data, and then decide on the RP2D, the recommended phase two dose. We're going to add an amendment, or we're planning to add an amendment to the protocol to turn this into a parallel trial to be able to file for an accelerated approval in H1 2025. We're planning to add a part to the study, a confirmatory trial part to the study, to be able to potentially apply for full approval. With that, I would like to turn back to the Q&A session. Thank you. Thank you. Thank you very much, Marie-Louise. Thank you. At this time, we'll be conducting a question and answer session. If you'd like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Our first question comes from the line of Ashthika Goonewardene with Truist Securities. Please proceed with your question. Hi, this is Jing. I'm speaking for Asthika. I have a question regarding about your this, we can see there is some response was not responded by the some patients. Do you have any good biomarkers which can help to predict the response to this drug? Also, how about the level of other cytokines such as interferon gamma and TNF-alpha or IL-6, IL-8, or, you know, the also especially the PD-L1 or CLEVER-1, you know, are there all these kind of ratios correlated to the clinical benefit of this drug? That's my first question. My second question is I want to ask, so what do you think this drug could be compared, you know, combo study could be compared with other immunotherapy or some novel agents in the development of RNR, AML, or MDS? That's my question. Thank you for taking my question. Thank you very much. I can take the first one. We know from a solid tumor patients that if the baseline levels of the immune indicators are low, you have a better chances to have a response from those. Obviously, we are looking all of these biomarkers at the moment from these patients. I can just tell that we have seen also interferon gamma increase in some of the patients, and those have been that have already responded to their blast number. The trend is very much the same. We also are measuring the CLE-1 content from these patients that actually could predict also the outcome. All this is really underway at the moment, so it's a bit too early really to pinpoint something that is a specific. As we have been advancing with the solid tumor patients, somewhat similar approach will be applied also here. For the second question, Marie-Louise, would you take opinion on what kind of combinations would be really good for us in the future? Yeah. Yes, thank you. Thank you very much. So what I think is very special for us is that we're going in the last line setting, so there are really no good standard of cares in this setting. I think our mechanism of action is very unique, but I do think it would be very interesting to combine with potential other macrophage-targeting therapies, like, for instance, magrolimab. For now, we're focusing on this study, but a lot to come in the future. Okay, great. Thank you. I just have a quick, follow-up question regarding about the duration. Do you have any comments about the response duration in this study from the latest update? Yeah. Marie, is that for you? As I should. Yes, thank you so much. Yes. If you look at this Waterfall plot, you see that we do have. Remember that the patients that have been longest on the study are the 1 mg per kg patients, and the patients in the 6 mg per kg, they, I mean, they have actually only been on for 3 to 4 months. All of the patients are ongoing in the latest cohort, and if we look at the duration of the responses or duration of treatment in the 1 mg per kg and 3 mg per kg, we see very long durations. In the patient with 13 months on study, that is much longer than expected, and we have several other patients as long. When your HMA failed, both in AML and MDS, the median survival is around 5 months. I think we have very interesting duration of therapy so far, but we look forward to maturation of the data. Okay, great. Thank you for taking my question, and also congratulations on the update. Thank you. Welcome. Thank you. Ladies and gentlemen, as a reminder, if you'd like to ask a question, please press star 1 on your telephone keypad. We'll pause a moment to allow for any other questions. Thank you. Our next question comes from line of Miles Dixon with Peel Hunt. Please proceed with your question. Oh, hi there. Thank you for taking the questions, and my apologies if they've already been asked. I had a bit of difficulty dialing in. Firstly, can you let us know across both solid and liquid tumors now, but both in MATINS and BEXMAB, how many patients total have you dosed, and what does the safety profile look like? Secondly, how is the biomarker developing, particularly now that you're in liquid as well as solid? Thirdly, you talked about the long duration of the responses in AML. I was wondering if you could give me some clue as to what you might expect or is typical of those patients without the Bex combo therapy? Thank you. Thank you, Miles. Marie-Louise, maybe you could take these, all three. All right. I'll start with the safety profile. In the MATINS study, we treated patients that received all standard cares. These were last line patients. We treated more than 200 patients with solid tumors. The safety profile looked very good. Drug was very well tolerated, and the majority of the adverse events in this study were grade 1 and grade 2, mild to moderate. We did see a few immune-related events like pneumonitis, thyroiditis, and so on, but it was less than what is seen with PD-1 inhibitors. The patients with more high degree immune-related adverse event received drug withdrawal and steroids and ended great. In this study, most, in the study with a combination with standard of care, if we look at the bexmarilimab-related adverse events, we also see mostly grade 1 to 2 Bex-related adverse events. As I shared on slide number 10, we did have 1 grade 3 event, where the patient, immune-related event, where the patient was treated with steroids and recovered within days and is still ongoing in the study. We have this patient with a grade 5 HLH, which died from the event. This HLH is known from malignant diseases to occur in about 1% of the patients. It has been shown that up to 10% of AML patients receiving high dose chemotherapy can get HLH, and it's also been described with azacitidine venetoclax alone. Overall, the safety profile looks really good, both as a single agent and in combination. Regarding biomarkers, from the solid tumor study, we know that as Markku mentioned, that patients that have less immune activation in their tumors, they seem to have the most benefit from Bex, and we see an immune activation. We are actively looking for biomarkers in this study, so we're collecting a lot of bone marrow and blood to look at different potential biomarkers, because as you pointed out, it's very important to try to tease out which are the patients that will respond best to therapy. Regarding how would these patients do if they did not go into our study? These patients, all of our patients have received azacitidine before, except for the frontline patients, and they are HMA failed. In this, going through the literature, it looks like those patients have median overall survival of around 5 months. To add something to that, we want to achieve something around 7-8 months at least in the relapsed refractory AML patients. Like the first patients I mentioned, is far beyond 8 months. So 8 months would be that we are adding 3 months to what would be achieved without our study. The first patient that I told you about has been on study for 13 months, and then we have other patients that also have surpassed the 8 months. I hope I remembered your questions, otherwise, please ask again. Yes, very comprehensive. Thank you very much. Thank you. Our next question comes from the line of Julie Simmonds with Panmure Gordon. Please proceed with your question. Thank you. Thank you very much for the presentation on the data. Very interesting. I was wondering, in terms of the trial at the moment, how many dose levels are you planning to be testing? Yeah, how many more do you think you need to go significantly higher than you are at the moment, or we nearly reached the top of the dose ranging? For moving the next phase of the trial into pivotal, do you have any feeling as to how many patients you would need to make the trial pivotal at this stage? Marie-Louise, I think it's your territory again. yes. I'm sorry, what was the first question? I was focusing. Are we going to increase the dosing from 6 mix per kid? Yes. Yes. That is a very good question. We have now tested 3 different doses. We do believe that we are pretty close to the dose where we need to be. We know from the MATINS study that there is like a bell-shaped curve, that first we see an increase in the immune activation, but then it goes down with increase in doses. We're still waiting for the PD data and the biomarker data from the 6 mix per kid cohort, to be able to say if we're done or if we need to add another dose level. I would anticipate that we don't need a lot of more dosing levels, and I am hoping to be able to choose a dose for the phase II by the end of this year. Regarding the second question, we have made some calculations, and we think that the pivotal part of the study, we need around 60 patients. We're aiming at an objective response rate of, like, 20%-25%, and we want to have for... That is for the accelerated approval, because that will be based on objective response rate. If we go into, like, a full approval, we want to prolong the overall survival with at least 2-3 months. We need additional patients to do that. Lovely. Thank you. Thank you. Ladies and gentlemen, that concludes our question and answer session. I'll turn the floor back to Dr. Jalkanen for any final comments. Thank you very much, thank you everybody, listening us and really good questions. You may feel how excited we really are to take this further and obviously, while we are progressing, we'll be report to the markets of that progress. I will also really would like to thank all the investigators who have been involved in the study. I have never seen in my life so much excitement on the clinical side, and I can tell you that as soon as we open these slots, they are taken away right away to the study. It looks really promising. I also want to thank all the KOLs and advisors, finally, also our own employees who have come to the work every day and take all this really move on. Thank you. With this and additional information, you can reach out, either Julia Balanova from us or investor relations, Sharon or Dan Ferry from LifeSci. Thank you again, and with this, we will close the call. Thank you. This concludes today's conference call. You may disconnect your lines at this time. Thank you for your participation.