Faron Pharmaceuticals Oy (FARN) Earnings Call Transcript & Summary

Hello, everyone. I'm Faron CEO, Markku Jalkanen, and welcome to listen our annual results '21 presentation. I'm here with our CFO, Toni.

Hey, everybody.

And as you know, we are a public company, and I would like to start the show with reminding you about the disclaimer. We will be making also forward-looking statements, and it's important that you understand that. We have been focusing on our immune system and help the conditions where we build up a life-threatening conditions. And we do have 3 different target molecules, we can activate our immune system, and that is the key asset we have at the moment. And that is in the middle of this graph, the target molecule, being CLEVER-1. And we can inhibit for block the activation of that receptor by using humanized antibody called bexmarilimab, we call it bex to be more simple. And that, I spend most of the time on, when I'm talking about the progress we have made in '21. On top, we have second target molecule called CD73. That is a local producer of anti-inflammatory compound called adenosine. And it's a key and gatekeeper to break down the ATP and ADP from our circulations. And those are really dangerous molecules to have, especially if we have inflammation and escalation of that ongoing. And obviously, the Traumakine project is the key there, and we will discuss a little bit about that as well. And then we have a third one. We have learned to multiply the hematopoietic stem cells, and that project is called Haematokine. We believe that we have made significant progress, and we probably will have, hopefully, news this year. And really even think about it to get to the clinic. But we come to that one later on this year and not spend too much time on it. So with that, I let Toni to continue.

Thank you, Markku. So far, at a glance, just to have a recap. So far, we are dual listed here in London, where we are today, and also in Helsinki since 2019. Our market cap hovers around EUR 160 million. We have raised all in all since the inception of the company, EUR 150 million. Being public after 2015, probably EUR 100 million. And most recently, at the end of February, we announced a debt funding agreement with IPF for EUR 30 million -- or up to EUR 30 million, already drew EUR 10 million. And we are located in 3 locations. So our headquarters is in Turku in Finland. We have, last year, started to build our U.S. entity significantly. We are currently 3 people in the U.S., and we are hiring there, mainly clinical people, clinical staff, regulatory staff as well as IR functions as we speak. Our total headcount is 40 people. And we've been in business since 2006. If you look at last year's key financial and corporate information. So our cash balances at the end of the year were EUR 6.9 million, so up from EUR 4.1 million a year ago. So despite -- especially in the second half of last year, we had a very challenging biotech capital markets, as most of you have also seen. We managed to raise more funds than we run in our operations. For the loss of the period was EUR 21 million. So mainly the increase driven compared to prior year is with the acceleration of the pipeline and increased R&D expenses. Our net assets at the end of the year were positive EUR 2.9 million compared to negative a year ago, also the year before. And we did 2 fundraises last year, raising EUR 25.6 million. The first one being in February and second one being in October of last year. And post period, at the end of February, as mentioned, we entered an agreement with IPF Partners for up to EUR 30 million debt funding. Drew EUR 10 million. And there's further EUR 20 million available, subject to certain conditions met. And from our team, so we're very fortunate to have top specialists and top scientists in our team. So to highlight here: Sirpa Jalkanen; Professor Hollmén; and most recently, Marie-Louise Fjällskog, who joined us at the beginning of January as the CMO in Boston. She's located at our Boston office, but today actually here in London. And so she brings along roughly 30 years of experience in clinical oncology and really the experience from the industry. And we are extremely fortunate to have her on board. Further, we are supported by the Scientific Advisory Board that comes with a significant experience [ in the sense ]. And with that, I'll hand back to Markku.

Thank you, Toni. So then really moving on to bex. Very typical humanized antibody blocking the function of CLEVER-1. Antibody have a strong IP around it in most of the territories. Very recently also in Europe, the patent extension will go to 2037 and it may be even beyond that. So proprietary target molecule and no direct competition at the moment. And what is really interesting about this situation, what we have in the cancer biology at the moment and also the treatments, we all are appreciating the fact that we have a new immuno-oncology products really treating people. But the limit here is the responder rates. In general, we have roughly 20% of the people who would have a permanent benefit out of these current immuno-oncology treatments, mainly targeting PD-1 or PD-L1 target molecules. So why is that? And can that be changed? This also has a significant opportunity because if you look at these refractory populations, what they are in indications-wise, it's roughly 160,000 failed treatments alone with the PD-1 inhibitors in U.S. and EU. And the main reason for that is a silent immune system. So these treatments cannot activate the patient immune system other than the existing T cells. They do not generate additional elements which are required to ignite immunity. So that is really important, that we should provide that also for these treatments in order to really increase the response rates. There have been a lot of combination studies ongoing, but that builds up a significant risk of having serious side effects. And that is, for example, seen. If you have 2 immuno-oncology products used at the same time, you really increase all kind of a side effects. We believe that bex is clearly well positioned to really provide now the ignition of the immunity and then provide the treatment success also for this previously refractory patient population. And obviously, that just alone in the existing treatment pool is a significant business opportunity, and that's what we are after really in the future. CLEVER-1 has a control over the phenotype of these myeloid cells that might create to the tumor and hide the tumor from the host immune system. This hide me signal is practically produced only by 2 cell types: Regulatory T cells, but they are hosted and nursed by this myeloid cell. So it's a combination of 2 cell types. And if we don't activate the myeloid cells well, like the way tumor wants to, you cannot build this hide me signal around the tumor cells. What bex does, it blocks the CLEVER-1 and completely reprogram these myeloid cells to become activator of the immune system. We have seen this in many, many ways, including the increased secretion of cytokines leading to immune activation, also representing capacity of these cells to the different antigen material will increase a number of other activations. So we convert immune hiding signal to immune activation. And this is a critical thing in those patients where tumor has already taken over the patient immune system in order to keep it silent. And this is another schematic view on it. We have no an information today at a very detailed level how this plays -- takes place. It's really, really looking at the [ necronation ] pathways of these cells, which are part of this mTOR signaling pathways. And this keeps the hide me signal and degrades all the material, which they are not available for the antigen presentation. And with bex treatment, you inactivate that one and you activate, like I said earlier, completely different gene transcriptions. Very dramatic change. And it just shows the plasticity of these cells, which are meant to be around us to control our immune system in both ways. But here, we need to activate the immune system, and that is the reason why we want to really do it. And in the cancer patients, this benefit could be extended also to remote locations because we know that there is a [ cell perform ] of CLEVER-1 that actually could be T cell inhibitor also in the remote locations. So with this concept, we have really carried out MATINS Phase I/II trial. You have heard about it and we are pretty much at the end of this development today. We already know today that it's very safe. We have first efficacy cohorts identified. Very significant number-wise, because if you reach 30% to 40% of clinical benefit rates in the patient pool, which is the last line and had no options anymore, that is a very significant clinical indication that we may have a successful further progressing with our program. Currently, we are finalizing the dosing. That is really important to understand. And we need to look also a number of biomarker data from this patient pool with roughly 200 patients. And then further conclusions for the optimal dosing and then move on. As you can see, I'm already indicating a melanoma. On the right-hand side, I put it up for the very clear reason. We have some exciting data on melanoma, but not claiming yet that, that would be the only one and we would be focusing on it. But as we have the data, I would like to share that with you. So now thinking the year '21. I think that we have been able to confirm all the earlier key findings we have been telling to the markets. Bex definitely is well tolerated and safe. There are no Grade 4 or 5 adverse events related to the treatment. We have seen autoimmune cases, which is the typical, to be expected, but they have been able to control with the steroids. Clinical benefit, as I mentioned, I will focus on that with a few additional slides. And it's very interesting that you have a pool of patients who actually respond -- or at this stage. And obviously, that has led us to understand what is the immune markers you actually could look at to really pinpoint and identify the best responders. And we have very promising data really to focus on baseline levels of interferon-gamma, TNF-alpha and also interleukin 6 and 8. And then we also have now finally spilled -- it was challenging to get a good [Audio Gap] Also in the physiological settings. And the most exciting one and very clear one is the pregnancy. In order to isolate the embryo from mother's host immune system, we need to prevent the activation against the embryonic material because that's foreign to the mother. It could be totally foreign in the normal family case, since it's like half genes from mother and half of father. But there's no immune reaction. What happens is that the same cells now with tumors have picked up to benefit themselves are also used in this physiological setting and built the immune barrier. And that's the reason why women can have a pregnancy, healthy baby can be born. Very important. And there is no side effects of this reaction. And maybe that partially explains why we have so good safety with mode of action. Very important part. The few immune reactions I mentioned earlier, I said they have been possible to really control with the steroids. Now then looking at the efficacy. On the left hand side, you can see these 10 different cohorts. We had completely negative ones. We were a bit surprised that with the -- even on melanoma, we have no responders whatsoever. We are not really necessarily giving it up yet, but this is not the focus today. The most promising ones, we have already said them earlier. They are listed here in bold. Melanoma, cholangiocarcinoma, breast cancer, hormone-positive breast cancer, hepato-cell cancer, and breast -- the gastric cancer. And on the right-hand side, you can see these spider plots. [Audio Gap] and you can see that they advance. So in some of these cancers, we have really stabilization of the tumor. In some of the patients, it's already decreasing and this is really a clinical benefit which we can see. In the last line, patients have no options anymore. And the reason why we know that, if you look at this picture on the left-hand side, this is the progression-free survival shown on the left. And you can see red curve and the blue curve. And you can see that they are pretty much aligned, similar ones. But now if you look at the right-hand side, now the red one is the ones who actually got the clinical benefit. And you can see that we increased the overall survival significantly. We have really -- this is now a 6-month data cut post the first image, meaning that it's probably reasonable almost in which some of the patients already 12 months, we haven't really reached the median survival rate. And we know that it's already, with the other population which are not responding, around 15%. So this is remarkable, thinking that this is a monotherapy, alone, last line. And remember also that we do have 21-day washout period before we take them in the treatment. So there shouldn't be any previous effect from any other treatments. Having said that, many of these patients already had gone through the immuno-oncology treatments I referred to at the very beginning. In other words, the patients we are looking at the moment, they have been refractory to the current immuno-oncology treatments. So who are these patients? As said, really started to look the biomarkers and this analysis is still ongoing, but we already know that these patients have really low baseline level of interferon-gamma. That tells us that immune levels, the immunity level, is really low. That's confirmed with the TNF-alpha and also interleukin-6. If you look at these 3 markers alone and make a statistical analysis, we are able to predict the outcome with the 9% certainty. It's extremely high. I don't have that drug analysis slides in here, but that is a very significant. And they may be even further on, because as said earlier, we now have this immuno-histology capacity really to stain all the patient material that come to the trial. And now when it's verified and applied to this commonly used Ventana system, every pathology laboratory on this planet can actually really do the stainings. This was an important milestone for ourselves, and now we have really set it up, and we can really use it in all the patients. And from the MATINS patients, we have roughly 50 to 60 paired samples, pre-dosing and post-dosing levels. And that data accumulate at the moment. And it definitely something that we plan to publish on the second quarter of this year. So people are using often cold tumor and hot tumor definitions. The cold tumor means that you have very low level of our immune cells in that tumor, and that just shows that there has not been the immune activation. And what happens if we have that tumor and if we can now ignite immunity, we saw it earlier in the peripheral blood samples, now we have seen it in the tumors. And we are collecting additional data. But that means that now we have activated the immune system and get the immune cells into the tumor. Interferon-beta, gamma is one example of that activation. But there are a number of other immune markers. And obviously, that is something we follow on also during the next few months. And so having all this data available on the first half of this year, we really made the decision how we are going to move about with the MATINS platform trial. We have 2 options. We make a single-arm study. That's the option one. Or then, we make a randomized study. And the randomization would be against standard of care and doctor can determine whatever they want to do with there. This is very critical to get the approval and opinion from regulators, and our goal is really to go, during the third quarter, to visit FDA after filing the package prior to that and get feeling and understanding, what they see we can do. Both options are as important as they can. And the size, determination will be obviously based on the prediction of the outcome and even rates in those trials. And as said earlier, we are just getting data really to get the understanding on dosing and the best outcome of those trials. Then we are just about to initiate, in collaboration with the principal investigators in San Antonio and Texas, the first line combo. This is the first line setting where the PD-1 inhibition is already as a standard of treatment. And we will initiate this trial in a typical way, increase the bex dosing and then see what the outcome will be. Having said that, we are very interested in additional combinations. And I will spend a few examples why we want to do that. But before getting there, I'd like to also talk about the very exciting myeloid leukemia example. So myeloid means that these leukemia cells have a similar background as these tumor associated macrophages. They come from the same hematopoietic stem cell lineage. And they -- that is the reason why they express CLEVER-1 to their surfaces. So now we have a very dramatic malignancy and we have a CLEVER-1 target on surface of these cells. So you would think that we have a marvelous possibility really to influence on the behavior of those cells. And on the right-hand side, you can see the red color. It's not so visible for me because I'm a green-red colorblind, but hopefully, you can see. Those are the different programs of this myeloid leukemia we can see in humans, and all of them are CLEVER-1 positive. This is very significant. Then in the middle, there is an evidence already that, if you have a high expression of CLEVER-1, that will build resistance. Even the most modern treatment, which is the BCL-2 inhibitor called venetoclax. And this is very encouraging to us because, if we now can really take down the CLEVER-1 expression, that would definitely increase the outcome of the patients' treatments in these populations. In ex vivo settings, we know that if we block CLEVER-1 expression, we practically block the replication of these cells in few days. So it's indicating that, yes, maybe we can really control. So this is pretty much ready to start as well, first in Europe and soon after also on the U.S. side. And MD Anderson in Houston is involved in that study as well. So very exciting. But then back to the solid tumors. Second point, refractory melanoma, as I said, is here. We have first histological stainings. Here, we can see a PD-1 resistant/refractory samples. You can see there are a lot of M2s, they are CLEVER-1 positive, and there are no T cells in that tumor. Typical example of cold tumor, no T cells infiltrated in that. So it's understandable that they cannot fight against this tumor. Then these graphs below those histological pictures, you can see 5 examples of these melanoma patients. 3 blue ones with high baseline of interferon-gamma. And then 2 red ones, where we can see that we initiate the baseline from much lower values. Those with the lower values, we can see a significant increase in the interferon-gamma levels. It stays up roughly 20 days and then start to come down. Now out of those 10 cohort patients in this group, the graph on the right-hand side shows the overall survival. There were 3 patients in that group, and I'm happy to say that I checked yesterday, these 3 patients are still alive. This is a previous -- a younger excerpt from the cut-off data, but they are still alive. So here, we have a situation that 30% of the patients in this group already have very extended a survival rate. And obviously, this is very encouraging to us. And we also know that if you look at the data in the literature, it's already known, that the patients who have low interferon-gamma level, they do not do very well in the immuno-oncology treatments, and that's the red curve on the top panel. The ones who have already existing interferon-gamma, they do respond. And obviously, now if you think about the bex treatment, it's the other way around. So we really now have the opportunity to move on the PD-1 blockade resistant population into a responder group. And if that like takes fairly place, this is a significant opportunity clearly for bexmarilimab market-wise. Just to summarize. Early clinical benefit observed in the last line settings as a stand-alone treatment, good safety, biomarker data building up, possibility really to select the patients. And as having good safety of all the combination, we should be really quite relaxed, not really building up a safety problem over there. And now we have clear pathways to move on with the development. And I really would like to thank Marie-Louise joining us and building up the program and really bringing in really good opinions. And we are really on the way, really, to maximize all our effort at the moment, take this forward with the additional resources we got to the company. A few words about Traumakine. You remember, this is the intravenous interferon-beta. We have believed from the very beginning that the only kind of acceptable route of administration is intravenous interferon-beta. This is roughly 150, 200 fold higher bioefficacy per microgram when you do it, if you look at the effect in our key central organs like lung, kidneys or liver. So I know and you know that there have been subcutaneous administration and it's still used for MS, there's an inhaled version of it. And that is okay, maybe to the local activities. But to have a systemic benefit, it has to be intravenous. And we have built the program really to influence on the presence of CD73 on the surface of these capillary endothelia cells. That is the intravenous system we have. And it makes a lot of sense really to have an intravenous administration of the drug so that we have a direct effect, and effect that actually activates the CD73. On the right-hand side, you can see that there also significant number of conditions where this really is needed. They could be natural ones, but they also be made man-made. Man-made examples are all cell-based therapies we actually apply today for the cancer patients. And obviously CAR-T is a very good example of it. But there was an increase in number where we manipulate our immune cells and give them back to the patients. That could drive the cytokine storm. So this cytokine release syndrome is something that actually could prevent the use of these in a higher level of patients and could produce a problem. Especially if we then need to use steroids to slow it down, that actually would immune-activate everything so it's not very useful. So having an agent that actually could upregulate CD73, that is the gatekeeper for the local production of the adenosine, interferon-beta is the one that is doing it. It is our endogenous peptide hormone, remember that you can compare that to insulin which is required for diabetes patients. Here, we need interferon-beta to activate and maintain CD73 on the surface of endothelial cells. If you lose that, you lose the capillary integrity and you lose your [ sense organs ]. We also have looked this in a settings where the trauma is very evident, the causing -- the central. And if you do not upregulate CD73 in these open aortic surgery patients, they all die. However, if you activate CD73, they survive 100%. So it's a clear indication that this is a kind of a defense mechanism against trauma caused by infections or other injuries, and CD73 is really required. And you may recall also that in the INTEREST trial, we noticed that there is a mutation that actually could guide 2 key hormones, what is traumatic conditions. And first one is interferon-beta and the second one are corticosteroids. There is polymorphism within the interferon-beta receptor that actually could divide the combination of interferon-beta and corticosteroids into 2 different signaling pathways. This first existing form that provides a mechanism that corticosteroids activate interferon-gamma expression and the other interferon mechanisms and not activate the mutation-induced a pathway, which is protecting us and including the CD73 expression, there's a significant difference in the mortality outcome. And obviously, this means that we cannot really do trials where corticosteroids are present among these treatment groups, or we need to select them to really identify the patients who have this, what we call TT polymorphic form who are sensitive for corticosteroids, instead of having CT, who are resistant to corticosteroids. And it's very interesting that, population-wise, the anti groups do have a different profile in this. This protective form is very rare in the -- among the Asian populations, meaning that they are very sensitive for this combination use of these 2 drugs. And I think this would be really considered in the future when people are treating anything. So really important kind of a mechanisms really to support our survival in this rather rough environment. I'm not really referring to a man-made conditions. These threats are coming from other biological systems surrounding us. So bex, really, our key focus, we are actually -- in that as much we can. We are refocusing at Traumakine back to the original, where we have been. And then really built up experienced people really to do the further development, and then Toni takes care of the building up for the financing the company. Having said that, we then -- we can move on to the Q&A. And you can see that you can type your question, the box and just click it so that we can see it. And then we will be questioned.

But maybe at this stage, I would really ask the first question from the room. We have a Julie Simmonds here from Panmure.

Yes, I have a couple of questions. I suppose firstly just on Traumakine since we've just been talking about that. When do you expect data? And do you have any view on how recruitment is going? I know you're not actively running the trial, but...

It's low. The biggest challenge has been to get the corticosteroid-free patients to the trial. We built what we call door model in order to have a person ordering at the emergency unit really to identify the patients who the GPs where the patient -- who have not really initiated steroid use. It has been slow, and we hope to come up with summary information later this spring.

And the plan is still to do an interim analysis of that one, is it?

Yes, as far as it really goes.

Okay. Excellent. And then you sort of indicated earlier that you're looking at cutaneous melanoma as sort of likely the first indication for bex going forward. Why specifically that one? Why are you so confident about that?

Our understanding is that, currently, the melanoma patients are almost 100% treated with the current immuno-oncology treatment. So they are really refractory ones. But some of the other tumor types have a nascent differences -- natural differences in their treatments. So that would be a very unified trial, by the way, protocol where we can actually spread easily. And we are spreading our sites to new countries while we speak, even including the Australia because the melanoma is quite often what we can see over there and they have really good clinical treatment groups over there. So it makes a lot of sense. But having said that, if you look at the last line, we could actually think about also having [ all those 5 ], the best cohorts and take them as an all-comers and then build a single arm. You can even use the -- what they call synthetic arm to compare. You can actually buy those from certain organizations who have built a historical outcome for those patients and then use that one if it has approval, some of the trials and results, even to the market approval point. But yet, having said that, also the randomization could become. But that definitely will then be higher in size-wise and it move on [ that ].

Interesting. And then just wondering on the sort of histology that you're now doing -- now you're able to identify CLEVER-1. Obviously, you've got sort of the cancers, but you haven't seen any benefit in those that you have. Are you being able to see a histological difference between those cancer groups?

Yes. And even within the one single group, you -- what wonders me a lot, for example, is the pancreas cancer. There is a tremendous number of a CLEVER and positive macro basis, yet we didn't see anything. But we all know that, that is a very aggressive cancer. And even that 21-day washout period within the trial, it could actually have an impact on the outcome, because having nothing really to slow down the cancer of pancreas cells, and then you go in, you may actually have lost the patient already at that point. So we need to really think about going earlier in that and see, and then look at also the staining results. But you -- we hope to be able to use the data as much as we can, but really to focus on the first one, where we believe has the most successful and most expedient outcome, obviously, is the target for us at the moment.

Excellent. And just a financial question. Obviously, at the end of last year, you've got a number of grants that were sort of rolling through. I'm guessing that some of those are still there for '22 because you were -- so how much have you got left of that that's still coming?

So out of the grants we have from the EU, there's another EUR 600,000 coming, and that's for the bex [ meeting ]. And then from -- based on business spend, we have several smaller ones. I'd say the sum of them really are [ below EUR 300,000 ].

All right. Thank you, Julie.

Thank you, Julie.

Then questions from...

Yes. So a bunch came in. So I'll start with sort of consolidation of a couple for Toni. Update on current cash position? Or 2022 run rate? And any news on the U.S. stock listing?

So I can touch on the cash run rate. So as we mentioned, we had EUR 6.9 million at the end of the year. And we did this IPF funding debt agreement at the end of February, and that's the EUR 10 million that we drew out of that. I mean, so currently, we have the EUR 6.9 million plus EUR 10 million as of now. Obviously, burning all the time. And with that, we are funded until Q4 of this year. And on the second part, maybe on the sub-listing?

Well, we have said that we are building up activities on the U.S. side, focused into -- Toni has said that the focus has been in the clinical group, and Marie-Louise is in charge of really building it up. We'll have -- but many hires also on the second quarter of this year. So it's clinical, regulatory, but also the Wall Street capabilities. And timing of really moving on as Nasdaq-listed company is not really decided yet. But obviously, that is a very big interest to the company at the moment.

Okay. And there was another one sort of capital allocation. It appears that alongside funding the trials, the biggest challenge in front of you is deciding which exciting trial or indication to back. Where do you see the priorities for bex development now? Neoadjuvant, pivotal trial, monotherapy, combination, or all of the above?

The monotherapy would allow probably the fastest way to the market. We may get the conditional approval and then get the completion advised by the regulators. The combination could be also a really very fast, and especially this myeloid malignancy is something where we have an open structure. And if you start to see really the outcome rather fast, that could be really, really fast, really to the market. And we could learn that as soon as we give the first dose to those patients, and that should take place in the second quarter of this year. It's rather soon.

All right. There's one sort of digging into the MATINS trial a bit. So we've treated approximately 193 patients to date. Does that still sort of the number? And then there were 5 indications that show between 30% and 40% disease control rate. Do we expect those to be the 5? Or are there other tumor types that we're still looking at? And then when would we expect data collection to be finalized or stopped in this phase of MATINS?

Yes. I mean, the MATINS dose testing and escalation, it's pretty much the recruitment completed. There are not that many patients [ any to run ]. But before we get the data and analyze everything, that will take us maybe to mid-summer, maybe the end of June. And obviously, to then build a package to send to FDA and then have a meeting with them, that probably is the third quarter. So yes, we are getting there. These just take time. You don't get all the pens at once. It's just you need to enrollment. But I want to really thank the sites of doing it. They have been really excited. And one motivation for them is the safe profile because they are not worried about causing any additional problems to the patients, and they're very motivated to take them further. What would then be the final kind of a selection of the cohort? I indicated that it could be melanoma, but it could be pool of these most promising cancer types. And honestly, I also believe that, in the future, maybe the classification of the tumors are not anymore based on the TC origin. So today, we talk pancreas, liver and so on. But maybe we start to profile them totally differently, and that would actually determine the way we treat them. And we have already seen this because we see low gamma interferon patients in all of these indications, not only in melanoma, meaning that they do have immune activation really declined and there is no really kind of immune cells actively migrating around us -- or around the patient's blood, meaning that there is no survivance. And that has to be generated again in order to have the immune activation really take place. So very important decisions to be made on the second quarter, but we are ready to do those.

That's a great lead into this next question, which is really around biomarkers and what -- number one, when can we expect to see more biomarker data? And then how confident are you that the strong correlations observed in the 2 biomarkers is logically explained by the underlying cancer biology? And then the last piece is, do you expect the next round of trials to include a biomarker for patient inclusion? And if so, would it be interferon-gamma?

First, on the timing. Second quarter is the key for us. I have not been aware of additional cancer treatments who actually would predict the outcome this well as bex biomarkers are now doing. Even with the PD-1, you have certain guidance where you have 50%-plus presence of PD-L1 intra-tumor T cells, then your treatment from 1 to 50 is doctor's opinion, and below 1 is -- but we have an extremely high probability to predict. It would be foolish if we do not use that, I would say, that way. We absolutely will be using some sort of a ways really to incorporate that data in our statistical plans or even to the selections. Both ways is acceptable by the regulators.

So one that is -- are we planning to generate additional bex data this year? Which, yes, I know that's certainly additional data from MATINS. But then, are there any updates on licensing negotiations? And how that new data might impact the licensing strategy.

Yes. Well, we are building up the data and everybody is always waiting the data. The final dosing, regulator opinion, for example, if they already approve the plan all the way to the pivotal stage, those are the things which are very attractive for the partnering. The value of the bex is important for us, and that is the reason why we would like to kind of a progress additional data to understand how we can apply this treatment to the patients. If you think about, that all cancer patients would have some sort of immune inactivation taking place, and that allows the tumor to grow either locally or then forming the metastasis, you would even think that bex would be very beneficial to all the patients. Having said that, I know that we need to start with certain populations. But I don't want to do a partnering deal at the point where -- and we cannot really convincingly spell out the full potential of this treatment. It's not the benefit for the shareholders. So please wait a few more quarters, and we will have the data. And having been informed on the numerous discussions, it's ongoing already, I expect something to happen over there. But this is not the focus at the moment. The focus really to generate additional data and build the package to the regulators to move on. And then we have outcome really for the discussions with potential partners. We also have no desire to limit the combinations in 1 or 2 compounds. We actually would rather have a situation where everybody else would like to combinate -- run the combination with bex because that would maximize also the outcome. And maybe at one point, some of the big pharma companies actually could become a little bit nervous if they actually lose this possibility to treat the patients who have no response anymore because that would cut out quite a number of revenue stream for them.

So there was just one more, and I guess specific to the AGM press release that went out this morning. So if you could just give a quick comment on how you see, if Mr. Ostrowski joined the Board. And what role he would play and sort of what skills he brings to the company?

He is a very experienced CFO from the biotech side. He has been also a CFO, a company that was a European originally and then was dual-listed. That was Summit Therapeutics. And we, at the Board level, wanted to have support to our CFO, Toni, to have a discussion partner who could follow all the steps and move more closer to Wall Street. So this was carefully thought out, and it's really to really have an additional kind of a understanding what is critical for the European company to more of the U.S. side. Toni, you can feel -- say what you feel about it, too.

No, I'm excited to have Erik as a support for the program, but not just for myself. Having been -- he has done an listed company, taken that to dual-listing in the U.S. And also been a CFO [ of our U.S. is compare ] at the moment. So very excited to have that support for us as a whole team to work to expand our list development.

That's it in terms of questions that were submitted, Markku.

All right. If there is no additional comments, I just want to thank you, everybody. And keep following us, I think it's really exciting year for us. Thank you.

Thank you.