Lipum AB (publ)

Hello and welcome to today's webcast with Lipum, where the CEO Ola Sandborg and Simeo Peter Hursadius will present the -end-communication for 2024. After the presentation, a Q&A will be held. If you have any questions for the company, you can ask them in the form at the top right. With that said, I leave the floor to you.

Great, thank you Ludvig. And yes, really welcome to this webcast where we get the chance to present our -end-communication for 2024. I am Ola Sandborg, CEO of Lipum, and on my left is Peter Hursadius, our medical manager. I think you will understand a bit during the presentation that he will be needed, he will be valuable in this project. But it's fantastic to take this moment together with you and reflect a bit on 2024 and where we are. So, if you take the next picture, Peter. Let's see, I hope it will be good. So, a bit of summary for 2024 and where we are right now, what have I chosen to say? Yes, it is outstanding results and we are ready for phase two. And it can indeed be a phase to strengthen. It is a very, very interesting time we are in. We have good parts with us in the back and we are really looking now towards the next step, which is phase two. So, from that, if you take the picture again, Peter. So, look a bit at how the year 2024 has played out. So, that's it. You know it from before. We do not have any active commercial activities out there, so sales revenues and the like are not there. But we have some moving revenues and that is directly related to the contribution we have received. And that is a contribution from Vinnova and Sweet Life for a project that we are running. The result after financial posts for the quarter minus 25.7 million and for the whole year 2024 minus 55.5 million. And when we leave the year, we have a cash flow of not more than 7 million in crowns. And we are also six employees compared to five a year ago. And the sixth person is Peter Hofstadius who has come in. Then you can also see that the number of shares at the end of the period has increased significantly. And it is directly linked to the contribution that was made last year. So, at present, there are only 21 million shares in the company. So, change the picture, Peter. But a little bit about what is behind this, what I think about the estimated results. Yes, for the first, and perhaps many of you have already seen, it was so that we came out with information that we have results from the phase 1 study yesterday. And it is so that all healthy care workers and patients who are included in the study, they have been able to follow up during the development period of 90 days. And with that we can share top-line data. And that is actually why I have Peter with me today. So that we can present a little more in detail for you so that you get a complete picture. But when the complete clinical study report is completed, we see that it is available at the end of March. We have a little more work to do with the top-line data, the excess data that we share today. In addition to that, the planning of the coming phase 2 study has begun to take shape. And it is actually so that the results from the phase 1 study are very important for the design and the formation of the next study. But as also those who have a good memory know, we started the production and study of drugs last year in April. And to produce biological drugs takes time. And there we do this work together with our partner AtexBiologics and then the production and study of drugs continues. So we are in many different perspectives actually in progress before the phase 2 study with the planning. Another central task in our activity has been to look at the reality mechanism that we can see for sol 116. So how does sol 116 work when it is injected into the body of a person? The research cooperation we have together at the KHA continues to be in the plan. And we are actually approaching the final stages of this reality mechanism. But then I will be able to present it at a later date. And then a very positive task that came in on our board or a news actually happened in December when we got to know that we had received even more support for the company. And it is the financing for Eurostars, where they have given us and the Norwegian company Age Labs a contribution of roughly 11 million kronor in total. And this is then a support for us to be able to develop a companion diagnosis, a diagnostic tool where one can best predict expected effects of a given bandage. And this is linked to sol 116. Eurostars has taken this decision to support us and they do it in collaboration with the Swedish part of NOVA and in Norway. And then I have mentioned that Peter H. Stadius has been the new medical chief since earlier, but he is an important part of the work we do with phase 1 and phase 2 studies. But change the picture, Peter. As you probably know, the company's vision is to support an active and improved quality of life for all who suffer from chronic inflammatory diseases. And with that, our mission is to develop a safer and more effective treatment for chronic inflammatory diseases for those who have significant medical needs. And what does this mean? What are we talking about, if you change, Peter? Yes, the area we have mainly focused on at the moment has been rheumatoid arthritis or lead cancer rheumatism, as you might say in Swedish in any case. But we know that there is a need for patients who suffer from this disease. Despite the fact that there have been many good treatments in the last 10, 15, maybe 20 years. The biological drugs have changed the lives of many patients, and TNF Alpha Hemma has been the one that has driven it. But even the drug cartons have come a little later. But despite the access to these drugs, there is a medical need that remains. And we know that 30 to 40 percent of patients do not get what they expected from a first-line treatment. And even that additional 30 to 40 percent of patients lose effect over time. So it is still up to 75 percent of patients who do not get a sustained effect over the years. So the problem is there, the need is there, and that is mainly what we are focusing on. And in terms of our product, Sol 116, which focuses on a new protein, BSSL, we see the possibilities of helping patients via an alternative route compared to the drugs that are available at the moment. So if you change the picture, Peter, this is our cornerstone for what we are focusing our work on. Yes, of course, in the clinical program, which you will hear about in the next few days, about the results of phase 1 study, but also that we work more in the clinical work to clarify the mechanism of action, the diagnosis, as I mentioned earlier, and also to look at additional areas of use of Sol 116. And the third cornerstone that is important to us, yes, is the ongoing work to find the right partners, which may be part of the development of our product, but also that it can be the implementation and other forms of financing that are also attractive and important to look at. So with that, I thought I would leave the floor to you, Peter, so you can give us some details and pieces of evidence from the results from phase 1 study.

Absolutely. And then I want to start by saying that this is a little bit of a challenge, a little bit like a late Christmas Eve for a clinical pharmacologist and doctor, when you break the code to a phase 1 study or victim's phase 1. It is very exciting to see the results, of course, and we did that in December. We completed the study just before Christmas Eve, actually, and then we have a little bit of time in January and February to collect all the data and start analyzing it. And what you will hear now, just as Ola said, is top-line data. It is data on primary, secondary, L-point, and it is also parts of the exploratory analysis. So there will be more information, as you will hear here today, is the important top-line data. And the protein language is LPN 116.01, our study, and it is our first study in both healthy trial patients and R-rata patients. Before I get started with going into some details, I just want to fly over quickly and say that we have seen a good safety profile, good tolerability and a predictable pharmacology profile. And we had a handling time of around 20 days, which gives the possibility that a monthly dosage or LRG will return to that. Also very interesting, I think, is that we have had the opportunity to, with our antibody, Sol 116, home BSSL both to healthy trial patients and R-rata patients. Looking a little closer now at what we have done, and many of you who are listening today already know that Sol 116 is a humanized monoclonal antibody. And it is a new protein, and it is not a new protein, but it is a protein that has not been studied in the inflammatory part of the body. While we have found that it has a very important part in our clinical trials. And we will be able to share that with, as Ona said, all our other cases, our mode of action. The study design of this study is a randomized, double-blind, placebo-controlled study that naturally fills all the foundations for a well-informed study. The primary and secondary goals have been safety, tolerability and pharmacogenetics. In that way, the study is extremely interesting, but a little less interesting because it is the study of the pharmacodynamic advantages of the product that we will study in phase 2 later. But I will come back to that. The explorative ones were among other things BSSL, but we have also studied the other inflammatory parameters and cytokines. The study design is quite straightforward. We had three parts, and the first part was the so-called ascending dose. The sing, that is, we give one dose of Sol116 in an increasing dose. And these types of drugs represent each cohort, and each cohort consisted of six people who got Sol116 and two people who got placebo. And as you can see, the first dose was almost homeopathic, 0.075 mg, and we ended up with 6.075 mg per kilo body weight subcutaneous. Then we had two other parts. The lower part consisted of eight people, and the third part consisted of patients. In the same way, six people got Sol116 and two people got placebo. And then we had another single dose, the one where we had an increased dose of these healthy patients with four doses and three milligrams per kilo body weight. So here are the patients, baseline characteristics, as you say in English, the base world, or how we want to translate this. I will start by lasering it so that you can see where I am lasering. So, and what you see here are the single dose groups here, the error group here, and the multiple dose group, or the increased dosage with four errors. And age-wise, the average age was about 55 years, and the other group was about 55 years, and the other group was about 55 years. So, the first group was a little younger. We had a distribution between men and women, and this is good, I think. We had a little over 40 percent of women in the entire study. And since this is a disease that mainly affects women, it is very good that we have as many women as possible. Otherwise, it is a bit difficult to get women in the whole study. It is often men who are generally voluntary. But we thought that was very good. We had a mixed ethnic background, of course, white Europeans. This was a study that went to the Netherlands, I should add. And so there have been a number of other ethnic backgrounds. So, and what I also think is very good for the quality of the analysis is that all patients and healthy volunteers could complete the study with a result, except one who came to the hospital and got a relapse, and that was our placebo group. But all patients were included in the medical analysis. We found specific patients for RA, and I'm sure most of you are also very interested, although we are very few in this study. So, they filled out all the ACR-LEAR 2010 criteria for RA. They had been treated with methotrexate for 12 weeks before they entered the study. They were treated well, and they also received methotrexate as a base treatment in both arms, both in the one they received, Sol F-16 and Caselbo. They all had mild RA, as I mentioned when they entered the study and underwent the study. This is important, and I will come back to that. The diagnosis had patients with some spread sclerosis, one had spores, three had moderate or moderate, and three had mild. And we don't know exactly, because we don't have any registration on that, unfortunately. But it was a mixed result, and they had their diagnosis set between 2010 and 2023. And then we didn't have any protocol deviations, which is good. Most of them were just minor, and that means that they took the test a few hours later, or the analysis was done an hour later than it was supposed to be done, which will not affect the results we present here today. Primary objective, the important thing with a phase 1 study, is to be able to show safety and tolerability. What is the difference between safety and tolerability? Safety is defined as the things we can see objectively in patients or the medical care staff, objective findings on side effects, which are presented and arise after they have received their treatment, be it placebo or active treatment. Tolerability is the subjective experience that the patient has of the placebo treatment. And one way to do that is if they are still in the study during the entire study, that is, if they don't stop. It's a rough way of tolerability, and there are several, but then I have said it again, because I think it is important to point when we look at these data. And this is very encouraging. If we look at the same thing, we have the single group, we have the R-group, and we have the multi-dose group. Hello? The water interrupted me unfortunately, but I'll tell you later. Good. Then we see here, and we classify the PEAE, and it is treatment, emergent, adverse event. What is important to understand here is that it is side effects that occur after you have received treatment, regardless of whether it is Soledad 6 or placebo, or it is a side effect that existed and became worse after you have received restricted treatment. So that is the definition. If we look at the TIAE, you can see that they are the same number, not exactly percent, in each group, placebo or Soledad 6. That is exactly what we want to see, and that is why we have also controlled placebo, to be able to look at this. Everyone who has received their treatment, will get different types of side effects, even if they receive placebo. In this group, you see up to -40% placebo effects, so it is important to have with you when designing an effect study. If we look at the difficult TIAE, you see that there is a zero over the whole line, up to a placebo patient in the multiple dose group. That patient received a ST-reinforced treatment, and then left the study. That was not considered as a treatment, but the treatment was placebo. Down below, you see those who are considered as the treatment, because TIAE and TISAE are not necessarily related to the treatment, they are considered in another scale. You also see that they are a little divided between placebo and active treatment, very good. Then it is indicated that everyone has received the treatment, except for one patient of the 56, which shows a high tolerability. If we look at the secondary goal, it was in immunogenicity, and then the -AptoCov-Cosmetic, after this. In immunogenicity, it is very important to study this type of patient. You all know that the biological drugs we have today make a big and huge difference for the patients, as Ola said. Unfortunately, they are associated with a lot of side effects, and there is always a balance between side effects and side effects, which we have to take into account with other patients, and of course, the benefits of these drugs are greater than the side effects. But there is a big gap here, because if you look at the so-called black box warnings that the FDA has in its pharmacopoeia, you see that more than half of the biological drugs and synthetic drugs that are available for the treatment of RA have a black box warning. It involves infections, difficult infections, cardiovascular side effects, and cancer. There is a risk, even if it is mild, or milder, there is a risk for cancer development. Some of these side effects, of course, are due to the development of Ada, not all, though, it is part of it. We see in our study that we have one patient, an RA patient, who developed a mild type of anti-drug antibodies. That was on day 49, and then you saw that it disappeared on day 90. Should you call it an outlier, or not, we can discuss, or what it could be that is behind this. But in the morning, we basically saw no Ada, which is very obvious. Also, we did not see them in the multiple doses, which could be the one we might have expected to see more, but there were none. So this is very encouraging data. Pharmaceuticals. If you look at this left graph first, you will see all the dosage levels from low to high in single doses. And all have a dosage proportionally predictable curve, that is, the higher the dose, the higher the systemic exposure, we see. And we also get a fairly predictable linearity on the logarithmic scale of elimination. This is very good. This is very good, especially if you look at the red one here, which represents the TadRab patients. It follows the same pharmaceutical genetic profile as the FISCA test subjects. This will be underlined when we design phase two study. If you analyze this data, you will also find that it is half a day, around 20 days. And if you have half a day left, you should have a steady state of around 80 days. That is about four to five times the time. And that was also what we found if we go over to this graph. Then you see the double-edged dosages, that is, four doses, one, two, three and four, and respective days. This curve does not look anything different than the one on the left. It is because we only have three doses of samples here. We do not have a post dose. If we had it on these two and three, the curve would have looked a little better. However, it does not really play a very big role for the final result, I would like to say. Here we found a half-year period of 85 days. The summary shows that we have a very good dose proportionality exposure. It is the same for FISCA volunteers and R.A. patients. We have 20 days of half-year period. This supports, as we understand, a month's dosage, which is to prefer always, the less the better. Many of the biological drugs we have today, such as adenogumab and etanessep, have either one or two injections per week. So if we could have one or more a month, it would have been very good. And -the-state, day 85. BSSL levels are probably very interested in, so are we. Therefore, I have three pictures that will show the various BSSL levels in the various groups. We start with the first, which was single doses, the five on the horts, which only gets one single dose. Here on the Y-axis we have the BSSL in picogram per milliliter. And then we have the dose proportionality, which we followed up with three times. What you directly see visually is exactly what we also point out in the pictures, that after day four, so day three we have a handful of them, we see that there is BSSL in the beginning of the study. But here, after day four, we have no BSSL registration for the day 49, there is 11 persons developing BSSL levels and 63. But here a couple of more, which is why we say that we have day 90 as a breakpoint. So between day four and day 90, there is basically no BSSL registration. If you look at the BSSL levels in the multiple doses, which get four doses, you see the curve is the same. Here you have the night in this way, the same BSSL here, the days here. And at the beginning we have a spread out curve, you could say, of the BSSL world in the beginning of the study. But after day 28, that is, day 29 onwards, we have no BSSL registration for these patients who are on day 116. Except for the one that is there on day 95, we have a total registration of BSSL. We can discuss how it has come here and what it represents. It is always interesting with outliers, you should never lock the mouse on a dataset. It can give interesting insights, so let us see what we can do with it. In the rest, it is just there. What is important to remember in this type of BSSL studies is that we always have one or a couple of patients who do not follow what we see before. They have a different curve. But that said, it is no less interesting to look at. So, then we come to the RA patients. Here you also see at the beginning of the study spread out curves, both among those who have received placebo and those who have received SOAR 116. We had BSSL levels measurable like that in half of the cases on RA patients at the entrance to the study. After day 22, we have a value on the field of those two. After day 22, there are no BSSL levels left for the SOAR 116 patients, except for the patient who is a so-called outlier and who is on the world. What you should remember now is that it is a single dose, not multiple doses. It is only one dose you get. When it was at 2.025, you remember that it looked like this in the first map. So it is one dose down from the highest dose. Another way to do this is to look at how many registrations we could do after day 4. We take a percentage of this, that is, we have taken over 700 BSSL samples in one study. In the single dose group, we had registration of BSSL in 70% of cases after day 4, while only two for SOAR 116. It looked the same for the RA patients and the delta-tickle group. Here you should know that very few patients, of course, are affected by these black spots. If we just take away an outlier here on the 23rd, we end up with more than 8%. It is important to treat this type of statistics with respect and caution. But the trend is very clear. We have a secret of BSSL levels, both among certain test subjects and among RA patients. The conclusion from the whole study is that we have a safe, tolerable treatment with SOAR 116. We see a predictable pharmacogenetics with a dosing line that has 20 days of salivation, which is very good for the monthly dosing or for the fattening. We see a secret of BSSL, among the test subjects and RA patients. We draw the conclusion from this data, that this is very encouraging data. We have managed to establish both primary and secondary objective and explorative objective. BSSL looks very good. We can add our morph protein to our antibody, it is specific. This will lead to the intensification of our efforts to start phase 2. The study will be a proof of concept study, where we statistically get an indication of the effects of this on the disease. I am done with the drawing, Ola, and

you have the next picture. Thank you Peter for a very clear and explanatory presentation of the study results. There are a lot of tasks to be handled, and I think you did that well. I hope that the listeners have the same opinion. I want to conclude by reflecting a little. It has been my first year as CEO of Lipum in 2024, and it has been a fantastic year. There have been a lot of inspiring challenges. The results have really gone in our direction, as you see here, and a lot of delivery. We are keeping a good time plan. I am impressed with the work that has been done. There is no doubt that my predecessor Einar Pontén, who you can see in the picture here, has laid a good foundation for what Peter and I are doing now. I would like to thank the team and the group that really did the daily work. Every day you contribute a lot to the development of our project. In the end, it will be useful for the health of patients in need. I should not forget to thank our partners who are out there for the work. It is not us who are responsible for all parts of the study. We are also responsible for the research that is being carried out. For example, we are QPS, where I mentioned Notex, where it was mentioned earlier about production and study drugs. But I also want to thank those who support our business in the form of shareholders and investors. There is no doubt that we need that. To move on to the next phase two study, there is also a question of being able to get additional support when it comes to financing. But more about that a little further forward. But that kind of work has already begun. As Peter said, it is clear that we now with the results have the security and support needed to enter phase two. And yes, we are on our way. So with these words, I leave it to you Ludvig to be able to share questions and such. But thank you very much.

Thank you so much for the presentation. And just as you mentioned, we go into some questions here. And the first question is, can the only ADA response that is identified be completely excluded, given that the same person later was negative for ADA?

Peter, go ahead. Yes, it is naturally a very relevant question. As I said, I am very interested in outliers myself. You can learn a lot of outliers. And it requires that we look at that patient a little more carefully, because I can give a final assessment. But with that said, I would like to add, as I said, that in all phases 1 studies, especially if we look at this patient category, there is always someone who does not behave properly as it should. If we look at the way we measure BSSL, then we can also discuss exactly how that methodology looks like and where the detection boundaries should be for what detectable boundaries or not. But I want to prepare that patient, as I have done in this presentation, and be open to the fact that there is a value here. In the end, you can do if you at the same time prepare also parallel where that person or where that individual is with their value. So it was a little uncertain answer, possibly, but you should remember that it is only one value we talked about here.

Thank you very much. Is it an EB-rimly conclusion that there are no problems related to immunogenicity?

As I wrote, we had one registration of so-called ADAS. Immunogenicity is a difficult problem, and I mentioned it a little bit with the other biological drugs. It is a concern that can arise both in the beginning of a treatment with biological drugs and even later, depending on how many doses you get, what frequencies you have, if you give up, if you come back, etc. This is a study that has been going on for three months. If we look at ADAS development on other biological drugs, there is a possibility that there may be development later in the future. It should absolutely be said. But if we look at the statistics and see the other biological drugs, then they have ADAS registered, even if they have come during that period, as we have in our application three months. With that said, I think it looks very promising for sol 116, that it only has one and then disappears. I would also like to state that there may also be... The question I am thinking about is why is it on this list? In that case, how can it be that our antibody would not give any antibodies? It is of IgD4 type, our antibody, which has a lower immunogenicity. If we look at the absolute largest of the other biological drugs, it is IgD1. And before going into too much detail, many of you have also felt that it has a higher immunogenicity, if you have IgD1. So there we have one possible explanation.

Thank you very much. Which biomarkers will you study for effect in the continued analysis of your remaining clinical data?

Bionic markers are very exciting. There are several when we look at RNA-passion. The classic biomarkers are naturally CRP and lower ESR, and rosomic acid, talprotectin and so on. There are also some specific ones. And of course we look at cytokines. We will also have cytokines and inflammatory markers for this study. And we will in the final report show how they compare them with the BSF. And just as Ola said, we have several projects where we want to use BSF as a new marker for chronic inflammation, and possibly also a marker for those who may be able to respond to the solar sex treatment. So it will be very interesting to see how these are compatible with each other. The only thing I think, in any case, is that some of you have noticed that the RNA-passion we had in the study only had half the registration of the BSF at the beginning of the study. Then you might think that they should not have had more then, since they were RNA-passion and separately from some private private ones. If it is now that the BSF is an inflammatory marker, then that is a relevant question. But if you look at their intensity of inflammatory disease in their RNA, then it was a very well-treated RNA-passion we had to deal with. The telomere data that I have looked at, as well as the other inflammatory parameters, shows that for example CRP is single-digit on these patients, which gives the conclusion that these patients almost looked like some kind of test subjects in these inflammatory parameters. And thus it is perhaps not so strange that they did not have such high BSF values or no RAUs. I would like to add strongly to our theory that if you push down BSF and add BSF, then you also have a low inflammatory activity. It would have been much more difficult for us to interpret data if they had been higher. So I think this is a positive data to move forward with just looking at BSF as a new chronically inflammatory biomarker.

Thank you very much. If we look a little bit, can you say something about how predictive these biomarkers are in different inflammatory diseases?

Well, predictive... Some of them are very specific. These other inflammatory predictors that are used for RNA are very specific. Some are a little more general than others, CRP and SENCAN are all. While Orozomycoid, .P.P. and Sopreskine have a slightly higher predictive value for different types of biomarkers. Let's look at... So it is very detailed, of course. There is a lot of literature on this. What we are doing now is of course looking at how the BSF cell with these inflammatory values can correlate that BSF cell goes up or down in relation to these well-established inflammatory parameters. That data is not available today. I can see that the predictive value varies in the same way as CRP, for example, and SENCAN. We will come back to this in our final report that will come at the end of this month. However, we need even more data, of course, in these projects that Ola described, which we have received funding for, to look at just that. And as a final comment, I would also like to say that having a diagnostic companion is something very interesting. Precision medicine or individual-based medicine is needed more. One size does not fit all. That's just how it is. We may over-treat some and under-treat others when we think of it that way. Therefore, we would like to start by saying that already in this development stage, we are looking for a companion diagnostic for the SON-116. And really looking for those patients who can benefit from our new antibody.

Thank you very much. What did the two measured TEAEs that were identified look like?

Yes, just as I described, we have a classification of these AES in mild, mild and severe. And as I said, it has no relation to what we consider to be the treatment, regardless of the placebo under SON-116. But it was like one patient who had a cycle of tetrahydroxycloid and the other had a serum.

Thank you very much. If you look a little bit in the report you released, you can suspect that capital creation is a priority during the first half of 2025. Can you give an update on how this work continues and perhaps what type of investor or what type of financing you are thinking of?

As it is when it comes to financing Ludvig, there are a few different ways one can go. If we take it on the soft way, we always seek support from different parties, for example from the European Commission, where we have sent in applications and have been in interviews throughout the year. You saw the example here at Eurostars to get support for the business. But there is no doubt that when it comes to the coming step, phase two study, so to be able to start it, we must have the financing secured. That is from our own perspective, it would not be ethical, vulnerable if we could not have ensured that we could carry out the study against the patients who came. But also the authorities are putting that requirement. So for our part, we need to do the work, it is initiated and there will be more information on it. But of course we need support to be able to carry out the study, which hopefully can start in the beginning of 2026 and then roll during that year and into 2027. So we are talking about financing for the coming two, two and a half years approximately.

So if you listen a little bit, is the rough plan of the funding for the coming two in 2026?

Absolutely, that is what we are doing. We have now received the first phase result, which is extremely important to be able to complete the planning and design of the phase two study. The study medicine will be finished producing and as I mentioned, it will be gone. And then there is a process of application to the medical authorities, which should also be done before we can start the study. And of course, also to the authorities, to the CRO, the companies that will help us with the implementation of the study. So 2024 was a year full of activities, I can promise you that 2025 is at least as much. But the goal is to be able to start the study in 2026 and get this well-needed response. Not only that we have a safe and well-tolerated product, but that it also works on the treatment of patients with disease.

You actually came in a little bit on the next question there, but if you as an investor look at the leap, what milestones should you keep an eye on during 2025?

In 2025, you have actually already received the first one today, that we have come to the result of the phase one study, and as Peter was in on, we have the complete report now at the end of March. In addition to that, we are also expecting that the implementation mechanism, mode of action, will come in a form of final report. It looks like right now it is after the summer, hopefully, for that part. And the third milestone this year is that we are able to enter the application to the medical authorities before 2025 is over. So this year is a lot of the year of final review and take the result, alternatively, that we are ready to take the next step.

I can add that maybe this is also due to all the good work that is done on mode of action by the team at Umeå and also at KU, in that there will be some results in the program, although we do not have an exact date, but it is a job that will be published and presented at several time points during this year.

Thank you very much. A little final question, Peter, you have joined IPUM in 2020-2024, you have soon done a bit over your first half year. How has the first time been and how do you see the potential for Sol 116?

It has been a really fun journey, I must admit. I came in, as you said, for a brief half year ago, and then I met this fantastic team. I was at Umeå quite quickly and met the gang behind this Why that also touches me emotionally is that it is precisely so you are with research, that you get a lot of results from something that you think is one thing, but then you find a connection to something else. And then you have the courage to stay with that research, continue it and see if it really was so that BSSR could have an important role in the future of the organization, which I have had. So a stop-mode, a stop-action, a big forward-looking in this part. And then I thought it would be very fun to work with the equipment team, obviously, full-speed forward and Ola, you and I, work well together, we think forward. So it's been a good teamwork and I think forward, this is very exciting. It's better than this, we're not a forward-looking team, so to speak. You have a new operating mechanism in a We have a big need and we have good data that can take us into phase two. It doesn't get any better than that.

That sounds great and it was a perfect conclusion. That was all the questions we had. Thank you so much for presenting us with questions. And thank you to everyone who has watched. Have a great day.