Faron Pharmaceuticals Oy (FARN) Earnings Call Transcript & Summary

Good afternoon. Welcome to join our presentation on year '22. I'm here with our CFO, Toni Hänninen.

Good afternoon from my side as well, and welcome.

We are very happy really to describe the year '22, which is so transformative for us, and excited about the prospects what we have for this year, and we plan to go over those with you. And obviously, as you are well aware, we are a public company, and we will be making a lot of forward-looking statements, and this is to disclaim really those. And we move on, and I'll let Toni to start. Toni, please.

Thank you, Markku. So [indiscernible] glance so just to recap who we are. Faron, a biotech company from Turku, we are dual listed in Helsinki and London. Our market cap, roughly EUR 45 million. We are very pleased to see the development of the market cap in the last 6 months since we last spoke. The market cap has gone up roughly 80%. So very pleased to see the results that are driving that. On the key financial and corporate information. So cash balances, we had, at the end of the year, EUR 7 million, which is roughly the same as we had a year before, so stable cash balances throughout the year. The loss for the financial period was EUR 28.7 million. As you see, it's quite a lot larger than we had a year ago. This is mainly driven by the R&D expenses as we have accelerated our pipeline, and we have really accelerated also our U.S. expansion, as we communicated earlier. We currently have half a dozen people in the U.S. And then on the net asset side, we had minus EUR 11.5 million of net assets. And what's very important now to highlight at the end is the fundraising activities that we conducted. So we had 2 fundraises in last year, one in June and one in October, totaling EUR 13.4 million. And here, we welcomed the Leukemia and Lymphoma Society from the U.S. As a shareholder, we are part of their TAP program. On top of that, in February, we obtained up to EUR 30 million debt funding from IPF partners, of which we drew $10 million upon signing in February, and we have potential for further tranches of those EUR 20 million, which are possible under certain conditions. And then post period in the beginning of this year, we raised EUR 12 million from existing and new shareholders. And here, we are very happy that LLS participated with their second investment, which was a lot larger than the first investment earlier in the year. On the team side, we have really added a lot of people in our team. So our newest addition, Dr. Hollmén as the Chief Science Officer. Then Dr. Juho Jalkanen -- sorry, Marie-Louise joined in the beginning of the year as a new CMO based in Boston, and she's been really driving the clinical programs that Markku will explain to you a little bit later. Dr. Juho Jalkanen promoted the COO as well as then Juuso Vakkuri, Vesa Karvonen in HR and in Legal Counsel and Capacity. On the Board side, we welcomed Eric Ostrowski, as a new board member, a great addition to our team. It's been very pleasure working with him. And then on the program-specific advisers, Dr. Mika Kontro, who's really supporting the BEXMAB program. And with that, thank you from my side. I'll hand it over back to Markku.st year, one in June and one in October, totaling EUR 13.4 million. And here, we welcomed the Leukemia and Lymphoma Society from the U.S. As a shareholder, we are part of their TAP program. On top of that, in February, we obtained up to EUR 30 million debt funding from IPF partners, of which we drew $10 million upon signing in February, and we have potential for further tranches of those EUR 20 million, which are possible under certain conditions. And then post period in the beginning of this year, we raised EUR 12 million from existing and new shareholders. And here, we are very happy that LLS participated with their second investment, which was a lot larger than the first investment earlier in the year. On the team side, we have really added a lot of people in our team. So our newest addition, Dr. Hollmén as the Chief Science Officer. Then Dr. Juho Jalkanen -- sorry, Marie-Louise joined in the beginning of the year as a new CMO based in Boston, and she's been really driving the clinical programs that Markku will explain to you a little bit later. Dr. Juho Jalkanen promoted the COO as well as then Juuso Vakkuri, Vesa Karvonen in HR and in Legal Counsel and Capacity. On the Board side, we welcomed Eric Ostrowski, as a new board member, a great addition to our team. It's been very pleasure working with him. And then on the program-specific advisers, Dr. Mika Kontro, who's really supporting the BEXMAB program. And with that, thank you from my side. I'll hand it over back to Markku.

Thank you, Toni. So obviously, we have really focused now in our Bexmarilimab program. We have our own trials ongoing and under design. You all know the MATINS, which are pretty much coming to the end, and we are really excited of the possibility to get the feedback from FDA during the first quarter or in April latest. Then we have this very exciting first hematological cancer with extremely interesting results, and I'm going to spend some time with that as well. The combo with the PD-1 or PD-L1 blockade, it's also moving on and that first protocol has been already approved by the Finnish authorities, and it's under review in U.S. at the moment. So a very exciting thing. I've also say that you may have noticed that we are initiating a collaboration with Fred Hutch, Cancer Center in Seattle in U.S. and that is related to a cytokine relay syndrome, which is a very common side effect of any cell therapies given to the cancer patients. And we are about to initiate a clinical trial collaboration with them based on the intravenous interferon-beta use, and we will be announcing further during the year once we progress to the point when the trial is about to start. So wait that also during this year. Now the potential of Bexmarilimab, in my mind, is tremendous. The rationality here is really very simple. Roughly 90% of the cancer-related debts are really related to the resistance of the treatments. So in order to really get that over, we have to learn to control the myeloid cells, which originally come from the bone marrow and build this resistance by setting up a immune suppressive elements to protect the cancer and the growth. And we just believe that the solution is very simple, you reprogram these macrophages, and we do that with humanized antibody called Bexmarilimab, and I'm really focusing a lot of that. We already know the opportunity for us. We could go to the last-line as we have very interesting results that the extension of the oral survival of those patients had no options anymore. The combination makes a lot of sense because the biomarkers indicate that we are helping those patients who are resistant to the PD-1 blockade. Then the third one is really to target cells, cancer cells, which actually carry the same target molecules, and those are the hematological malignancies, which have a myeloid background. So extremely interesting way of moving on. And the mode of action of Bexmarilimab, which we have been studying for a long time, is really based on the fact that they -- these macrophages when they are in the tumor can produce do not show me signal. In other words, they hide the cancer. This is a physiological situation in some of the physiological regulatory pathways, one example of being pregnancy. So this tumor have just adapted the same system as to hide the embryo now they hide themselves so that the host immune system can not recognize the tumor as a foreign material. What we do with the CLEVER-1 blocking using the Bexmarilimab antibody is to reactivate immune activator gene read, and that will produce the activation and then produce a phenotype that can actually present the cancer to the host immune system. So they produced some signal in the presence of the Bexmarilimab. And obviously, this is what we have been aiming for a long time. Based on the work with the MATINS, we have really now set up the table for the progress. We know that Bexmarilimab is extremely well tolerated. We have more than 250 patients already treated. We know what the dosing is, the range. And then we also have biomarkers, which can help us really to enrich the patient selection. We are needed. And we know for sure that Bexmarilimab ignites the immune reaction in cold tumors, and I have fresh data to demonstrate that even further what we have provided previously. Out of these MATINS, we are looking what the last-line structure would be, and that's the feedback from FDA, hopefully, by -- latest by April. But obviously, we also learned from that feedback, what the BEXCOMBO actually would move on even if we have that protocol already in, but there is a statement about the dosing. And then the BEXMAB, it's practically a separate from these because now we are dealing with the hematological malignancies and it's a very unique opportunity for us. This is schematic presentation on the dual activity of Bexmarilimab in these type of the cancers. Obviously, we hope to able to activate the circulating monocytes to become immune activators. We have seen that in humans order previously with the MATINS patients that will take place. So it should take place also with these malignant patients. So activation of the immunity. But then on top of it, we have a second direct effect on these leukemia cells, and that is blocking the CLEVER-1 on them. That will already use the oxidation capacity oxidative oscillation, and that will run out the cell from ATP. And ATP for these cells is the fuel they need in order to maintain their shape and viability. And when that happens, we have evidence that the combination of this BEX treatment with the standard of care will really reduce the viability of these cells. So no wonder we have started to see the control of these cancer cells in those patients. And as you can see in this picture, there may be even a third mode of action, and that is that Bexmarilimab can actually bring monocytes very close to the malignant cells because they are binding to the same receptor. So very interesting opportunity more of action-wise. So outsmarting cancer, a CLEVER approach. So let's look at what we have at the moment. We started everything with the MATINS trial. You are familiar with that one. So those escalation test indications and their expansion and now we have a data that we have a benefit in the overall survival in certain indications, not all of them. And that material was sent to FDA and looking forward, really the interactions with them. And I'm not really going to say what that outcome will be, but it's a very exciting time for us really to have a discussion with the FDA during the H1 and then move on also with this one. So well-tolerated immune activation, taking place in patients who have lost that. Clinical benefit observed up to 30% to 40% in certain cancer indication within the last-line patients and having biomarkers now available, including interferon-gamma, but also the intratumoral CLEVER-1 stabilin. That is becoming most likely connected to our next trial setting in all of those because obviously, would like to establish the way really to identify the patients who have the highest probability for the treatment. This is one example from the MATINS trial. On the right-hand side, you can see the extension of this overall survival. We had roughly threefold longer survival of those patients who had achieved disease control. Remember, these patients had no options. Their average survival was only 4.2 months, which describes how desperate the situation with those patients really was. And we extended that almost to 15 months. Then on the left-hand side, you can see that the ones who have the response, and that's the red curve, they increased their interferon-gamma production. You can see how dramatic difference there are between these 2. So this really tells us that the innate immunity and the immune system is really now activated and maybe that is really the benefit we really provide for the patients and maybe also for the PD-1 blockade. PD-1 blockade works only with the patients who already have T-cells around the tumor and you activate them and then make them to attack the tumor. This combination, what we are thinking changing cold tumor into hot one is a concept that is well accepted already in the literate, so that has to be done in order to really increase the efficacy of the PD-1 treatment with the various tumors. And I promised you some exciting new data and here it comes. This is what they call a volcano plot. This is the MATINS data, looking at the patients who had the response on the left-hand side and the patients who didn't on the right-hand side. Now these different raptions in the left-hand side picture described the situation prior BEX treatment. This is the biopsy from the intratumoral side of the tumor. And the right-hand side in the same picture indicates post-BEX treatment between the cycle 3 and 4 when the second biopsy was taken. The different names of these transcripts indicate on the left-hand side that there is a significant immune suppression in the tumor. But post-BEX treatment on the right-hand side, you get the readout of these genes, which mainly are the genes known to be in the active inflammation and immune reaction. There are some very many well-known gene products. So this conversion from immune suppression into an immune activation is localized in intratumoral macrophages because that was ever analyzed and is a significant also statistically. If you then look at the nonresponding patients, it's totally flat and nothing has taken place there. So the association is very strong in here, and this is really the final evidence that we can activate the intratumoral macrophages like we have claimed for quite a while already. Very nice data. And obviously, we are looking forward to publish this data later on the spring time. So very nice results really to move on. We also learned from that same kind of situation that if you have high CLEVER-1 expression within this tumor, the content is also reduced. So there is no wonder that if we prestain these immunohistological sections, there is a statistical significant finding with the intratumoral presence of CLEVER-1 stabilin, not within the trauma or within the whole tumor. It has to be really intratumoral analysis of CLEVER-1 stabilin. And obviously, this is something we are looking for really to combine with our clinical trials and hopefully become a standard companion diagnostic tool for us and for the next set of other trials. Again, very significant milestone achieved last year. So just looking one example of these last-line patients, and this is the cancer. You can see this dramatic difference between responder and nonresponders. And obviously, this would be a typical thing, which could actually further develop in our last-line protocol after the FDA feedback. But let's see how we are going to learn and what we are going to learn from there. But the BEXCOMBO is really supported also from the findings in the literature. If you have high interferon-gamma level, you have a response. That's the block on the top. And if you have a low interferon-gamma, those are resistant to the PD-1 treatment. So obviously, if we can now with Bexmarilimab, really increase the interferon-gamma levels, they obviously have a chance really to react now to the PD-1 treatment. This combination therapy is really the target of the BEXCOMBO. Obviously, we would like to get to the first line and down on the left side, you can see our candidate trials indications. We would like to move on. First, head and neck cancer, where the PD-1 blockade is not very effective. Then urothelial cancer and then also I would like to move on to the lung because there are still space to help those patients as well. So this is almost ready to go. And obviously, we are looking forward really to have resources also to initiate this trial sometime this year. So another very exciting trial to move on. But then the hematological malignancies. We have known for some time that this myeloid-derived cancer types, really express CLEVER-1 and that is illustrated on the right-hand side where the different myeloid malignancies are analyzed, and you can see the red dots, which actually illustrate individual cells, how they have been stained for the CLEVER-1 positivity. There are also information in the literature, higher expression, you have CLEVER-1 on the surface of these cells first at the outcome of the patient survival will be. So there is evidence already in the literature that by blocking the CLEVER-1 you actually could have a chance to help these patients. And again, I -- so again, the same picture. Activated immunity on the left side, blocking the CLEVER-1 function to reduce the viability and maybe even the third one to get the monocyte close to these cells. And obviously, if they are in the circulation, that is very easy to take place. So with this treatment, we set up the BEXMAB study, it's very simple in a way because we have a duplet study, starting with azacitidine, which is the standard of care in many of these different myeloid AML. And then we also have a possibility to move on to the triplet, where we also combine the most recent chemo treatment on these patients, and that is combining azacitidine, Venetoclax, and then BEXCOMBO -- Bexmarilimab. And as we have already reported late in the year, this is a very interesting situation for us. Out of the first dosing cohort, which was on 1 mg/kg every week, we already have started to see a very positive response. We lost out of these 5 patients one to another trial who had this IDH-mutant. There is a separate treatment protocol for that one. So we cannot to do anything for that one. And the third patient had a fatal and nonrelated adverse event infection, which it's rather normal with these patients. So there was nothing. But if we look at 3 other ones, one complete responder at this time point and 2 partial responders. So it's like 3 out of 5 already have a response to these patients. This trial is now moving on, obviously, and we are looking forward later in the spring to look at the second cohort that is 3 mg/kg. Our dose evaluation committee did recently a decision to move on to the 6 mg/kg because there are no dose-limiting toxicity yet, but maybe we stopped there because we already have this high efficacy. And also the triplet, the first triplet cohort has been recruited. We have a very promising situation here. If you look at also, this is from that one because this patients can be also monitored from the blood samples as they can be monitored from the bone marrow but here is an example of a patient where the patient is losing these cancer cells. They are called blasts. And you can see down the stainings and loss of these cells. And then on top of it, the number counts. And here, we can see how the remission has been produced. And as you can see, below 5% representation of these blasts cells in the blood actually indicate that we have interemission. In other words, the cancer have been under control. This is really an example from the Helsinki University Hospital Base, nothing else really to say about that. But the whole point here is that we have MATINS trial extension possible using last-line randomized trial, would that be bile duct or something else? It depends on the feedback from FDA. They may also propose all comers, but let's see what they say. Then the combination initiate that and then accelerate the BEXMAB as much as we can because, obviously, that is where we have the fastest way to the market at the moment as there are no that many treatments to help these patients. And roughly 90% of the patients will die with the diagnosed AML within the first 5 years. So the medical need is to remain over there, and we are really looking forward to help these patients. And all with this setting, we believe that we have a very interesting news flow during the first half of the year, maybe also on the second one, but this we pretty much know at the moment. So there will be additional information provided with the MATINS data and also especially with the BEXMAB data on these hematological malignancies. So we believe that this illustration of the outcome of these different trial and the data and then building that into 3 different programs will be significant for us during the year '23. And we are really working hard in order to get there. And as Toni already indicated, we have really expanded our activities on the U.S. side. For the BEXMAB, we will add additional 4 sites during the springtime in order to really have access to the U.S.-based patients. And all those 4 sites, we are activating are the major U.S.-based sites and are also very well known. So really looking forward also to provide additional data on those patients who are recruited on the U.S. side. So with this, I'm clearly now closing our presentation today, and we want to thank you. And obviously, we are very happy to answer to any of the questions you may have. And please, you have the link to type in your questions provided earlier today and use that one really to send them, and we will then discuss further on whatever is bothering your mind. Thank you again.

Okay. To the questions. There has already been a couple of questions, starting with BEXMAB. How is BEXMAB recruitment progressing and has it been difficult to get patients from Finland? And related, when will the first site sites open in the U.S?

It has been amazing effect after announcing the first response results with the BEXMAB trial. I don't know if the word goes around, but we have a lineup of patients here in Finland at the moment. So as soon as we opened the new cohort 6 mg/kg, we believe that we can recruit that in a few weeks' time. We opened the first site in U.S. That is a City of Hope Hospital close to L.A., really well-known hospital over there. And the second one will be MD Anderson, in Houston, again, very well known. Third one will be Yale. You must recognize that one. And then third one in North Carolina University Hospital. We had a meeting at -- ASH meeting, American Society of Hematology in December. And when the same data I presented here today was shared with them we had a lineup of sites who wanted to join the trial. So we believe that the progress of BEXMAB will be extremely fast. And obviously, the acceleration is good for us, but also I want to remind that it also will increase our cost. And then obviously, every patient will be carefully controlled when they come in and hopefully with the data and with the other ways, we can move on as fast as we can possibly do. And then also with that data, have further discussion with the regulators on the possible pathway all the way to the market. But that remains to be seen and obviously, we will be announcing all those steps later this year.

Okay. Continuing with BEXMAB an analyst question. In BEXMAB, which malignancies will you focus on? Do you expect some to recruit faster moving forward? And how do you intend to monitor these patients? How long do you intend to monitor these patients?

The refractory or remission relapse patients would be way forward for us. If you really think about there is a significant population, and those patients do not have any options. And we have had those already in our trial. They come in in the second cohort, which I have seen what they are. But then it's a kind of a strategy we have to think about once we have a little bit more data on these patients, which of the form of AML, we actually would like to take further because the treatment protocols are a little bit different on all of those. And also the combination of azacitidine and BEX has been completely safe. So BEX has not added any risk of having additional adverse events. And same seems to be case also with the BCL2 inhibitor venetoclax. But venetoclax and azacitidine combination can produce toxic or adverse events. So we have to be careful how fast we're actually going to develop that one. So we probably like to start on the later stages of the patients, but consider all the time, can we really move on in the front and initiate the separate cohort that obviously requires an amendment to the protocol, but we are ready to do that if the data is supporting that really strongly.

Okay. So and related questions still from analysts, how does Bexmarilimab compared to other AML MDS therapies that are being pursued?

The -- if you think about the biologics, I don't often want to say that some of this are better than ours. But if you think about anti-CD47 treatment, it actually never showed a stand-alone activity like we have already seen with the BEXMAB. And obviously, the mode of action don't eat me signal is targeting a different pathway than Bexmarilimab. And one of the strategies actually could be here that we actually combine them. But again, that has to be based on the data, what we obtain from our own trial, and luckily, that is accumulating really fast. Other than that, what is ongoing, all of us need more data, but something has to be really taking place in order to help these patients within the next 10 years or so.

Okay. Good. Then a bit more general question on Bexmarilimab. How do the companion diagnostics compare across the different patient groups? I mean, in liquid and solid tumors and are the biomarkers similar?

If it start with the solid tumors, we have seen a correlation between intratumoral positivity of the CLEVER-1 and the outcome of the Bexmarilimab efficacy. So that correlation is already there. And obviously, we have provided this information to the authorities. And we are ready to set up the essay to the trials. It's already verified and it's suitable for the standard hospital diagnostic system. I don't want to say the commercial system, what are used at the moment, but it's available to us. So obviously, we will continue to use that. The solid -- that the hematological malignancies are a bit different, but they are easy to analyze just looking in the self-service CLEVER-1 positivity, and that is developing at the same time while we do it. And obviously, I would like to learn if the correlation is as strong as we have seen on the solid tumor part also with the hematological malignancies. So maybe we can one point also to select these patients based on the CLEVER-1 positivity. And that analysis is rather standard also at the university hospitals or hospitals that treat these patients.

Yes. And then from another analyst-related question, in the Phase III trial for Bexmarilimab in the monotherapy do we expect to be selecting patients with the biomarker?

As I said earlier, we're also waiting the response from the regulators on that matter. These patients, last-line patients had very few options. And as we have seen, we have highest responder rates in certain indications and less in the other ones. They may propose us that you take all of them in, and then you just follow and have built up a statistical system for those who are CLEVER-1 positive and for those who have less expression of CLEVER-1 and the outcome could be different. But remember that these last-line patients have no options anymore, and we all want to help them. So I'm open to both of these. And also, would that be 1:1randomization or 2:1 randomization could also be advised by the regulators. So let's see later in the spring what the outcome will be, then I can tell you more about it.

Okay. Still on the monotherapy trial going forward, do you have a confirmed date for the meeting with the FDA? And how long after the meeting do you expect to get their formal feedback?

It's in March and post-meeting, they have 30 days time to provide a written opinion which usually is a letter they send out.

Okay. Still one more question regarding BEX. Are there clinical observations of antibodies against BEX. And if so, can the problem or any problem there be sold by increasing the dose of BEX?

Dosing with a solid advanced tumor patients showed that if you start to go higher up, I'm now meaning like 10 mg/kilo up to 30 mg/kilo, we start to see bell-shaped. So it's not helping us really to increase the Bexmarilimab dosing. The frequency itself has not shown that much of a difference. Is it once a week or every 3 weeks? And if you think about the mode of action, we need to ignite the immunity. We don't need to maintain that once it has been ignited. So you then have a [indiscernible] of dynamic effect later on. And if that ends up or results in activation of naive cells to recognize the tumor antigens that's kind of a vaccination against the tumor antigens and that does not disappear. It will stay with the patient. So the dosing could be something that we may have a range. And once we are using that within the range, it will not help us if we increase the dosing. So obviously, this is also very good on the economical side because you don't need to go high up with the Bexmarilimab. So if it's only 1 mg/kg, it's very decent dose and will reduce also the risk of any side effects. We have seen very few antibodies being born against Bexmarilimab and also that is very good because usually, the regulators want us or want people really to also measure the neutralizing antibodies against your drug, which is now to take place against the antibodies. But we really haven't seen that much in those patients we have been measuring from the MATINS trial.

The last question related to the drugs and then we go to the regulatory and corporate questions. Would it be possible to give BEX as an intramuscular or subcutaneous injection in the future?

Thinking that you would like to get the antibody to penetrate to tissues, you may be better off if you give it in an IV formulation because then the concentration peak would help it to penetrate into tissues. Technically, it would be possible to really develop IM or AC form, and that has been also developed some other antibodies. But in our case, we may not think about it that way because we really would like to get the antibody to penetrate into tumor as well. And their higher plasma concentration will help really to take that place.

Okay. Then a question about regulatory. Could further positive BEXMAB data lead to an European application?

Yes. I talk about a lot of FDA. Obviously, we focus on both of them. But we -- as we said, we are increasing our activities in U.S. and FDA is more close regulator there. And then maybe also, I don't know if it's more dynamic, but anyway, you get an opinion that holds up to the end of the development. So if they advise us to do a certain pivotal pathway all the way to the PLA biological application in order to get the marketing authorization. If you have that advice, you can trust that it holds up to the very end, unless something really dramatic will happen. But yes, both Europe and U.S. are in our mind. But as I said, U.S. is very interesting market as well for us at the moment.

There are a couple of questions or multiple questions relating to funding and licensing strategies. So the questions actually, can you -- if you combine them, can you elaborate a bit about the usage of the remaining debt facility, the likelihood, the potential licensing deal discussions, and also eventually whether there is a plan for NASDAQ listing.

Toni, would you like to answer?

Yes, sure. Thank you. That's a great question. So as mentioned earlier, so we have a debt facility with IPF, which consists of 3 tranches. So we drew the first tranche EUR 10 million last year. There is a second tranche, which is EUR 5 million, defined by certain conditions. And then the third one, which is 15%. So we are in active discussions, of course, about the second and the third tranche. So that is definitely an option. Regarding licensing, maybe if you want to -- Markku, say a few words about the licensing, and I can talk about the question on the NASDAQ.

Yes. Thank you. So with the data that we have obtained recently, and as I said, we got the clinician excited, but we have also got excited different licensing candidates which have been discussing with order in the past. We can already see the increasing intensity over there. We will be present in many of the conferences this spring, where we meet all of -- not all of them, but many of these partners who have been interested in this new mode of action to treat the cancer patients. And if you think about the situation in the market at the moment, there are, I guess, 8 approved PD-1 inhibitors at the moment. They all start to run out of their patent period. And obviously, they all want to protect their product or even increase their sales. The one who comes with the new combination that can increase the efficacy of the PD-1 blockade would be the winner. And obviously, we are looking at winner as well. Having said that, we would also have a situation that we can use BEX with all of these PD-1 because -- inhibitors because that would put our position in a much better commercial position. And then I definitely can say that the upside will be humongous. That upside is tremendous. If you think about how much PD-1 blockers are selling at the moment. So we have to be careful with the future decisions, but the interest definitely is there.

Maybe to come back to the NASDAQ listing question. So what we have always done, we looked at the U.S. market very closely. We have a track record here in Europe of fundraising successfully since the beginning of the company in 2006, and we always look at the option of the U.S. listing. Clearly, we are building the activities over there. We are building the capabilities if we choose to pursue such listing. So we continue to follow that and keep that as one option for future funding.

And finally, one corporate matters related question. Can you expand on the reasons for the proposed appointment of Tuomo Patsi as a member of the Board?

Oh, that's extremely easy. Tuomo is one of the few people who have really made a significant carryout from Finland. Even he's visiting nowadays, he has really go over a number of oncology commolizations in his career in smaller biotechs, but especially in the big pharma. He brings in the commercial experience to the Board, which we value high at the moment when we are entering these licensing discussions, and plans, how we are going to commercialize our Bexmarilimab opportunity. So that was really the main reasons. And Tuomo is also a very pleasant person. So I'm really looking forward to with him.

Yes. No further questions from the audience.

Thank you very much for following us and hope to see you soon with the good additional data from Bexmarilimab trials. Thank you very much again. Bye now.

Thank you. Bye-bye.