Good afternoon, Europe. Good morning, U.S.A. Welcome to the Faron Pharmaceuticals EHA 2026 webcast. My name is Juho Jalkanen, the Chief Executive Officer of Faron Pharmaceuticals. On to the next slide, please. Today, with great pleasure, we are happy to present what was presented over the weekend at European Hematology Association annual meeting in Stockholm, Sweden. Here presenting the actual data and in the Congress is Dr. Mika Kontro from Helsinki University Hospital, the Principal Investigator of the BEXMAB phase I/II trial. After that, as many of you may know and are eagerly waiting for the next phase IIb, our Chief Medical Officer, Dr. Petri Bono, will be presenting on how is the startup of the trial progressing. Before we go more deeper into the data and upcoming next trial, I would like to lay out a higher level big picture coming from. Next slide, please. As many of you may remember, ASH end of 2025 left the high-risk MDS field, I would say devastated after the phase III VERONA failure with Venetoclax. It left a vacuum in late-stage programs. What has actually since then happened is a plethora of upcoming new companies, even new drugs, to the field of high-risk MDS, which we are delighted to see. With the recent developments, though, we are happy to be in a lead position going further, and especially what still differentiates us from the crowd is our novel mode of action, having the possibility to really induce hematopoiesis and make the bone marrow healthier for these high-risk MDS patients. A lot of these different programs we're seeing, unfortunately, they are reruns of BCL-2 inhibitors, CD47 inhibitors, and kinase inhibitors. To mention and highlighting, nice to see also immune modulation, immunotherapy pickup in this field. Want to highlight the anti-galectin-9 from Galecto and the PI3K gamma inhibitor from Stelexis BioSciences. Those are good to be looking for in the future when it comes to immune modulation in high-risk MDS. This is the current state of the field, coming back from, I would say, maybe some depressed moods at ASH. At EHA, I think there is positive enthusiasm generating in the field and looking very much forward to these upcoming data readouts in the field that hopefully there will be something new for the high-risk MDS population. With these words and enthusiasm for the future, let's go see the latest from the BEXMAB trial reported on EHA. Next slide, and over to you, Dr. Kontro. Thank you, Juho. Can I have a first slide? Very briefly about the mode of action of Bexmarilimab. Basically, when monocytes and macrophages express Clever-1, it's kind of immunosuppressive molecule. Bexmarilimab is monoclonal antibody against Clever-1. When Clever-1 is inhibited in monocytes, it leads to enhanced immune activation. What we see in the patient samples, we see enhanced expression of antigen-presenting molecules, activation of T cells, and also activation of cytokines. Basically, these all make the monocytes more aggressive, and that may lead to better disease control. Actually, Clever-1 is also expressed on the myeloid blast cells, and there is emerging data that when we inhibit with Bexmarilimab Clever-1 on the blast cells, it may have an effect on the mitochondrial function of these cells and basically enhance the cell killing. Next slide, please. This is actually data that we showed at ESMO last fall. We actually observed that when we have good Clever-1 target engagement, we have more complete responses. Meaning that this shows good relationship between target engagement with bexmarilimab and response. As mentioned, the more target it engage, the better responses we have. Next slide, please. This is the overview of phase I, phase II BEXMAB trial. The trial recruited both treatment-naïve high-risk MDS patients. We had 20 patients or 21 patients, also the trial recruited HMA-failed high-risk MDS patient population. The trial was recruiting across 10 sites in U.S., U.K., and Finland. It was a combinational study with azacitidine, which is a hypomethylating agent. In the phase one, we evaluated three different dose levels, one, three, and six milligrams per kilogram. For phase II, we included patients with HMA-failed high-risk MDS and explored two dose levels. I want to underline on the right-hand side that actually very many of these patients that were included had a very high-risk disease as defined by IPSS-R, also TP53 mutations, which are commonly associated with very poor outcome, were highly prevalent in this patient population. When looking at treatment-naïve patient population, actually 57% of the patients were very high IPSS-M disease, which is currently more and more used for classification of the MDS. Next slide, please. This is the data from frontline patient population. In summary, we have observed a complete remission rate as per IWG 2006 criteria to be 45%, overall response rate extremely good, 85%. What we have already previously shown, the responses continued to be maintained with the AZA plus Bex combination, we have shown that there is high clearance of blast cells. We have also good response rate in TP53 mutated disease. At this meeting, we also reported the duration of complete remission, it's currently over 16 months, which is very encouraging in this patient population. Next slide, please. When looking at the data on HMA-failed MDS patient population, the overall response rate in this patient population is 64%, we still see good responses and duration of response. Next slide, please. Discussing briefly about the toxicity. In general, we can say that safety profile remains to be very promising. We have to remind ourselves that this patient population is rather fragile and elderly patient population, even though we haven't seen any Grade five Bex-related AEs in this patient population. Next slide, please. Adding a bit more granularity to the data. When looking at the most common treatment-related Adverse Events, it's mainly related in hematopoietic toxicity, which is quite common in this patient population. Next slide, please. When looking at Grade three or higher Adverse Events, basically a bit more serious Adverse Events, again, these are mainly based on hematopoietic toxicity. Febrile neutropenia was observed in 32.7% of the patients. Perhaps it's good to remind you that actually this was not just the frontline patient population, but also the HMA-failed patient population. In addition, the patients were not required to receive prophylactic antibiotic therapy as a study therapy. Next slide, please. Looking at some of the very interesting data that we actually presented first time at EHA meeting. This data comes from the patients that have been treated in the BEXMAB trial. On the left-hand side, you can see the data of the hematopoietic status of the patient. Basically, what we were capable of showing is that when the patient received AZA plus Bex combination, the number of or the proportion of hematopoietic progenitor cells is increasing, and this might be also relating to less transfusions and hematologic improvement. When looking at the right-hand side, we also observed that while the patients were receiving AZA plus Bex, we actually had a higher number of cytotoxic CD8 T cells, and quite interestingly, also a decrease of exhausted TIM-3 positive T cells. Next slide, please. This data was also presented first time at EHA. This is the patients that were evaluated at baseline and achieved response or not. We observed that there was higher proportion of both CD8 and CD4 central memory T cells, which actually can then be differentiated using Bexmarilimab plus Azacitidine. Interestingly also, we observed less terminal effector cytotoxic T cells in the patients that did not achieve treatment response. Basically, this shows that the patients that achieved CR had a best capacity to activate their T cell responses while receiving AZA plus Bex therapy. Next slide. Thank you, Mika. Very nice biomarker data. Really, I would say capturing and highlighting the effect of the Bex has on the immune system and activating the immune system and activating also hematopoiesis in this Again, very frail patients. Next up, over to our CMO, Dr. Bono, on where are we with starting the upcoming phase IIb. Thank you, Juho. Could I get the next slide, please? All right. Bexmarilimab, the randomized placebo control double-blinded phase IIb trial, schema shown here. First of all, population, newly diagnosed MDS patients with morphologically confirmed higher risk MDS and eligible for standard of care Azacitidine treatment and not eligible at time of screening to stem cell transplant. In the trial, patients will be randomized into three arms. Arm A, BEX 1 mg per kilo plus Azacitidine. Arm B, BEX 3 mg per kilo plus Azacitidine. Finally, arm C, placebo plus Azacitidine. Patients will be treated with BEX with weekly infusions, and patients who receive CR as their best response may proceed after three months to biweekly treatment or every other week infusion. That means why there is Q2-week if some way. Remember that usually Bex is given every week in the BEXMAB trial, but there's a possibility to move over to every two-week dosing. Primary analysis in the trial that will happen three months after last patient's first visit, and all the results will be stratified according to IPSS-M risk category that will be used in the trial and also according to baseline bone marrow blast count percentage and TP53 mutational status. Next slide, please. Where are we going currently with the trial preparations? We have earlier announced that Parexel has been selected as a CRO and actively working together with them. We are well underway with the trial preparations, and we are on track to really have the first patients enrolled to the trial already in early October. Protocol is ready. Protocol is signed. Informed consent forms are ready. Country selection and site feasibilities they have been done. First sites have already been qualified and are on track to be activated already in October. A study global PI, Professor Amer Zeidan from Yale, will be the global PI, then in EU, Mika Kontro will be the coordinating European PI and also Finland will be the reporting member state in EU. From U.K., the coordinating investigator will be Dr. Austin Kulasekararaj from King's London. Next slide, please. Here are the planned sites. If we start with the U.S. sites, the study will first be most likely enrolling first patient from U.S., although U.K. and our list is also very fast in opening. We will have here familiar sites from BEXMAB such as Yale, MD Anderson, City of Hope in California. In addition to that, University of Wisconsin, University of Colorado, Vanderbilt, Mass General for Boston, Dana-Farber/Harvard Cancer Center, as well as Moffitt Cancer Center in Tampa in Florida. In Europe, we will have countries Finland, Spain, Italy, France, and also Poland and Czech Republic. Not to forget, U.K., there will be sites also, four sites probably in U.K. Altogether, the planned number of sites is 35, and as a reminder, the study will have altogether 90 patients, 30 patients per arm, from these 35 sites. There's a nice geographical spread across Europe as well as across U.S. Next slide, please. Maybe then as a takeaway from the newest update of BEXMAB trial here at the end. Lots of interest in Mika's presentation. Data nicely maturing towards better with safety. We have earlier at ASH when we reported, we have in the frontline a bit longer than nine months median follow-up of the patients. Now we had bit more than 14 months median follow-up of the patients. Five months more follow-up, five months more time for safety evaluation. Safety profile remains actually numbers very similar to earlier, which is good news. The safety profile remains very good in this longer follow-up. The efficacy, strong response rates, strong CR rates, and very importantly, CR rate is 45% in the overall treatment line population, and 70% in TP53 mutants. Someone who may remember the ASH waterfall plot, there were a couple of changes also in the decline in the blast count changes, couple of deeper bars, as well as a bit higher number of 100% decline in the blast numbers. Finally, but very importantly, regulatory agencies take into account that not just the CR rates, but also duration of CR is important when considering approval of novel drugs, for example, in the treatment of higher risk MDS. The duration of CR has increased from earlier 12 months as reported at ASH to 16.1 months now reported by Mika Kontro at the EHA meeting. About a four-month improvement in the duration of CR. Importantly, as a summary, the phase IIb BEXERA trial preparations, they are on track and at the EHA meeting, lots of interest and engagement from principal investigators from both E.U. and U.S. We expect to have a rapid start for the trial. I think this was my last slide, and I give back to Juho. Yes. Thank you, Petri, opening up the Q&A as our investor relations starts getting in those questions. I have a couple to start with now that I have Mika here. We were actually so busy at the conference, didn't have proper time to discuss with Mika that how do you see now Bex in this field compared to others, and how much excitement? To me, it felt that this is the readout that everybody will be looking at in this field. How about you? Yeah. I tend to certainly agree. First of all, I think that what is a really good signal about the upcoming BEXERA trial is that basically all sites that were involved in the earlier BEXMAB trial are very eager to join, and I think that we have also, during the conference, had very good discussions that people are very interested in joining to the trial. With the current results and with the current CR and overall response rate, and also now with longer duration of response data, this is getting more and more interesting and very much looking forward to start also BEXERA here in Helsinki. Thank you. As you said, more and more interesting. Have to do another question for you, Mika. What I hear a lot and what I heard at the Congress is with this response rate in TP53 mutated, where usually response rate is very poor, should we focus solely on that? What's your answer? You perhaps know my answer already beforehand. I think that it actually would be very feasible option also to do and conduct a trial solely on TP53 mutated patient population due to the fact that there is no current available treatment options. All patients are receiving basically Azacitidine plus Venetoclax. Unfortunately, leads to responses. Part responses are quite short-lived. I certainly would be very keen to see the trial, perhaps separate trial to be conducted in that patient population as well. We do know that for FDA, the bar for approval of a compound that improves survival and response rate in TP53 mutated MDS, perhaps also in AML, would be highly valuable. Thank you. Yes, I totally agree. Maybe we will expand into that as our resources expand. My answer to that is we need further data before we just go do TP53 mutated. We will deliver this next Phase IIb. We will learn more, and if needed, we will focus and also, and even possibly solely on TP53 if that is the route. You learn always as you do and collect more data. I have one question to Petri before I let the audience go. You mentioned that there's been good engagement now putting together this trial, collecting the sites. What's it been like getting all these sites? How much work has that been? Of course, lot of work. It's nice that usually at least four times more feasibilities are sent out than actual wind up in the trial, for example, from U.S. 100% of the sites that have been approached, so they have been engaged and want to join our trial. Means that there's a lot of need for new treatments for the patients and the early experience from the existing sites. What the new sites have heard from presentations at various meetings have been positive, so they are eager to jump as a trial site and be part of the development story. Very good response from various PIs. Correct me if I'm wrong because I also get requests, is there already more that we can take along to the trial? We need to limit the trial sites. There would be clearly a lot more interest than how many sites we can open. Need to remember that this is a 90-patient trial, it is not very feasible to open a lot more sites. Okay. Thank you, Petri. Let's open the floor to the audience and questions. Thank you, Juho. The first question goes for Dr. Kontro. The median duration of complete remission is 16.1 months in frontline high-risk MDS. For treating this population today, how meaningful is the 16.1 months compared what's typically seen with azacitidine alone? Yeah, I think that's a great question, what we have thus far been seeing is that the responses have been, as mentioned, quite good. The duration of responses is also related to the fact that how many patients do respond. For example, Azacitidine, the response rate is approximately 25%-30%. Here for frontline patient population, we are looking at complete remission rate of 45%. We have got a better number of patients. For azacitidine, of course, most of the data is a bit outdated, but we are looking perhaps similar numbers with regards of survival instead of complete remission rate. If Petri actually could update on some of the latest data that you have been now going through regarding the duration of responses for AZA. Thank you. Yeah. It is. If you ask me, Mika, how I see the duration of CR, it is clearly shorter than what we have seen here, but of course, depends always compared to early phase trials or randomized control trials. But this 16 months compares very favorably to any studies with the CR duration report. Thank you. The next question. What's the signal that this combination is doing something that the standard of care doesn't? What's the value that Bex add? Maybe I'll go first from a layman perspective. Again, very scientific data presented at EHA and here in this webcast showing what is very important for these patients is that these again are very anemic, neutropenic patients, and the backbone regime of AZA adds to that. What we're seeing from a safety profile and now in the cells we were presenting here, that we actually do not make neutropenia or anemia worse than AZA would. It may even be that we make it even better, and this happens through the production of these new red and white blood cells. Maybe a more sophisticated answer from Dr. Kontro. Thanks, Juho. I think that one perhaps low-hanging fruit, in a sense, how to evaluate this is that what is the additional value of Bexmarilimab is the phase II or HMA failed patient population, which already have been receiving Azacitidine and have progressed while receiving therapy. For this patient population, as I showed previously, we see treatment responses. We see quite good overall survival in this patient population. Perhaps this is also one patient population that illustrates the additive value of Bexmarilimab on the top of Azacitidine. Petri, your view. Maybe to add on that, Mika is very right that RR MDS patient population is a good one to see the added benefit of Bex, but also like to highlight that the target engagement slide that Mika showed in the beginning, so that we have a very nice relationship that the higher target engagement, the higher response. The CR patients got the highest target engagement, and I think that's probably one of the best pieces of data in addition to that RR MDS patient population, what we can get without a randomized trial. Of course, the upcoming randomized trial will then give the definitive answer to the contribution and to the magnitude of contribution. Yeah, I personally like the target engagement slide really a lot in addition to the translational results that Mika showed, the increase in T cell infiltration and antigen presentation, of course, also. Yes, absolutely. Just like to comment for the benefit of the audience. In other words, the more Clever you block, the better response you get. Very nice to see. Next question. Thank you. Safety in an old and high-risk population is always a concern. How would you describe the tolerability so far? This I'll hand over to a practicing physician. Over to you, Dr. Kontro. Yeah. What we have actually been discussing also previously is that, as you mentioned, the patient population is rather fragile, very prone to the toxicities, and basically the toxicity profile is very similar to azacitidine therapy only. Of course, when interpreting this data, we have to remind ourselves that this is now from all patient population, all 55 patients, including de novo patients that haven't been treated before, and also patients with HMA-failed disease. Also, given the fact that what we have been discussing with other investigators in the investigators meetings, it really seems that, as mentioned, also the gut feeling is that the combination is quite well-tolerated and that this was also illustrated by the fact that we haven't had any bexmarilimab-related deaths in the trial. As mentioned, rather well-tolerated therapy option for these patients. Thank you. How do you plan to demonstrate the benefit of Bex regarding the duration of complete responses and overall survival if patients who undergo bone marrow transplant are censored from the follow-up? Dr. Bono? This is taken into account in the trial design, actually it follows exactly new guidance that FDA has provided for industry in the treatment of MDS. Patients who get a good response for the treatment are transferred to stem cell transplant will not be censored. This is how this is handled, and that's taken into account in the trial design. There's a lot of variation how these patients have been reported earlier in various trials, but now there's a clear FDA guidance that how we should do that, and we are following exactly that guidance. Thank you. You have described that Bexmarilimab is not just reducing cancer cells, but helping the body to produce healthy cells again. How important is this dual mode of action? Maybe I go first. To me, that is actually our, I would say, most important differentiator from other more cytotoxic treatments. For this population, this is an extremely valuable aspect of the drug. How about you, Dr. Kontro? Yeah, I agree. Really also looking very much for the randomized data on the topic, so that actually how much we achieve with combination of Bex to the Azacitidine. Do we have a good number of reduced red blood cells and platelet infusions? I think that will be very crucial for this, again, frail patient population. If we have that possibility that we need to transfuse patients less, it's a huge benefit for the patients and huge benefit also for quality of the life of these patients. Thank you. The final last questions. What are the key milestones between now and end of this year, and what should investors watch for this coming year? Petri, over to you. The key milestones are, of course, the launch of the new BEXERA trial, approval from regulatory agencies, submissions in time, and then first patient in in time, and really fast ramp-up of the patient enrollment. That's related to the BEXERA. Another milestone, at ASH meeting, a new updated efficacy will be for the first time told, for example, time to event endpoints in the frontline patient population. We plan to submit an abstract there and then to do a November data cut before the ASH meeting. Of course, not to forget solid tumor trials. We expect that there will be first patients also enrolled in those trials actually quite soon. Thank you, Petri. Then back to you, Juho. Okay. Thank you, everybody. That is a wrap. I would say super exciting times ahead for Bex, both in high-risk MDS and solid tumors, definitely for the high-risk MDS field. Very happy to see a lot of new attempts entering this field, more immunomodulating therapies into this field. I think they're highly needed, exciting times ahead for everybody. Thank you all, have a wonderful day