Welcome to Medivir Q2 Report 2026. For the first part of the conference call, the participants will be in listen-only mode. During the questions and answers session, participants are able to ask questions by dialing pound key five on their telephone keypad. Now I will hand the conference over to CEO Jens Lindberg. Please go ahead. Thank you, operator, and welcome everyone to Medivir's webcast covering the second quarter of 2026. Looking back, this was the quarter where a lot of things came together for us. The phase I-B/II-A data for fostrox in combination with lenvatinib was published in "Clinical Cancer Research," which is one of oncology's most cited journals. We also took the important sort of exciting next step as the first patient was dosed in the randomized FLEX-HCC study in Korea. We secured funding to take MIV-711 into a second rare bone indication, Perthes disease, through an oversubscribed directed share issue of approximately SEK 140 million. Pia will take you through the clinical progress in both fostrox and MIV-711, and Patrik will cover the financial details. With three funded phase II studies and a strengthened balance sheet, we are in the strongest position that we have been in in many years. Let me start with the three things we would like you to take away from the quarter. First, for fostrox. In June, final safety efficacy data from the phase I-B/II-A study of fostrox plus lenvatinib were published in "Clinical Cancer Research," a peer-reviewed confirmation that our liver-targeted mechanism delivers tumor-selective efficacy without impairing liver function, and a very important validation for when we speak with investigators, regulators, and potential partners. As I mentioned, in May, the first patient was dosed in FLEX-HCC, the randomized phase II study, and we continue to see super strong engagement among the Korean investigators, and recruitment is progressing very well to include all the patients within the 12 months. Second, for MIV-711. Through the directed share issue, we are now taking MIV-711 into Perthes disease, which is the second rare bone indication where we already have orphan designation and rare pediatric disease designation from the FDA. In parallel with that work, the study design for the proof of concept study in Osteogenesis Imperfecta has been finalized and preparations are progressing very well. Building two rare bone indications on the same established safety profile multiplies the value inside the single drug candidate. Third, our financial position. The directed share issue of approximately SEK 140 million was oversubscribed and brought in new institutional investors, and we ended the quarter with SEK 253+ million in cash, and we now have funding in place for all three phase II studies. Let me stop there. Just to highlight our pipeline of first-in-class programs and the one change that you see on this slide from the previous quarter is the Perthes disease, where we are now then in the planning phase of the phase II proof of concept study. We will not speak too much about it today, but Vetbiolix, our partner in developing MIV-701, they continue to recruit patients or dogs into their study, with estimated readout in fourth quarter of their ongoing randomized study. That is an important value driver for us as well in the coming period. Apart from myself, as I mentioned, our Chief Medical Officer, Pia Baumann, will go through the programs. Patrik, our CFO, will cover the financials, and Fredrik Öberg, our CSO, is here for our question-and-answer session as well. With that, let me hand over to Pia, who will take you through the published phase I-B/II-A data for fostrox and the start of the FLEX-HCC study. Thanks so much, Jens. Let me just first start with a reminder of why fostrox is different. This is an oral prodrug that is activated in the liver, which means that we deliver the active substance, which is troxacitabine, where the tumor is and keep systemic exposure low. I know we have said this before, but this is really important. This is confirmed also by the biopsies from our study, where we can see DNA damage in the tumor tissue and no DNA damage in the surrounding healthy liver tissue. That really translates into what we see clinically. In combination with lenvatinib, we see efficacy substantially beyond what has been reported in second-line HCC, including in the recently presented IMbrave 251 study with atezolizumab and bevacizumab refractory patients. We see a combination with our drug that is really well-tolerated. These final data from our study were published, as Jens mentioned, in Clinical Cancer Research in June this year. Our strategic point is really unchanged. There is still no approved treatment in second-line advanced liver cancer. That is a first-to-market opportunity in a market worth more than $2.5 billion annually. I know that we are coming back a little bit in that in the summary from Jens. This is why FLEX-HCC study that is ongoing in Korea is now our highest clinical priority for the moment. Next slide. A few words on the publication itself, because it is an important milestone for this program. The full safety and efficacy data set from the phase I-B/II-A study is now published in the peer-reviewed Journal of Clinical Cancer Research. Professor Hong-Jae Chon, which is also our primary investigator in the FLEX-HCC study, is the first author. The clinical message I would emphasize is the one that you can see in this title, Tumor Control Without Deterioration of Liver Function. In many other tumor types, it is the metastatic disease. I am sure you are aware of this. It is the metastatic disease that drives mortality. In HCC, patients most often die from liver decompensation, and it is frequently caused by local tumor progression. The treatment goal is to control the tumor in the liver without compromising the liver function. That is a balance most systemic therapies struggle with. What you see in the figures here are the liver function parameters during the full treatment time. It is transaminase and something called the ALBI score, where you measure liver function. It is across, as I said, the treatment cycles. All of these, they remain stable over time. In other words, we achieve tumor control without deterioration of liver function. That is what keeps patients fit enough, not only to continue the treatment, in this case the study, but also to receive subsequent therapy. Can we go to the next slide? I would also like to comment on the IMbrave 251 study that was presented at ASCO this year because it is highly relevant for how we think about the second line. This study was large. It was over 550 patients asking whether it makes sense to continue immunotherapy after progression on an immunotherapy. Note if you press one more time. Yeah, already do that. Note how favorable the patient population was. The patient had to receive at least four cycles of atezolizumab plus bevacizumab as prior treatment. On that prior treatment, they needed to have documented disease control, meaning stable disease, partial response, or complete response on at least two tumor assessment. In other words, these patients who had done well on the first treatment, that is the patients who were included here. Even in that selected population, adding continued immunotherapy to a TKI, in this case lenvatinib, gave no benefit, neither in the overall survival nor in the progression-free survival. The response rate remained below 8%. For us, the conclusion is clear. Continuing immunotherapy is not the answer after immunotherapy failure. The second line remains open, and what is needed is a new mechanism of action, and that is precisely where fostrox is positioned. Can you go to the next slide? Against that background, let me mention our own efficacy data in this context. It looks a little bit different than we have shown before, but it is also to show in the context of IMbrave 251. Here, more than 75% of the patients treated with fostrox plus lenvatinib experienced tumor shrinkage, and the objective response rate was 24%. They had a time to progression, I know Jens already said that, of 10.9 months, and the median duration of response was more than seven months. We actually see that the longest response is still ongoing beyond 36 months. The part of this figure that might be interesting, again, in the context of IMbrave 251, is the color coding on this figure. The orange bars are the patients who were primary refractory on their prior therapy. In other words, those who never responded to first-line treatment. In this study, they also had tumor reduction. Patients benefited from fostrox largely independent on how they responded in the previous line, which is not what we usually see in this setting. It speaks to a generally different mechanism that is needed in the post-immunotherapy setting. This is the dataset that gives us the confidence to run this randomized comparison, and that is the FLEX-HCC study. Can we go to the next slide? This is the study design for this study, and it is 80 patients with advanced second-line HCC, all with one prior immunotherapy regimen before, and they have a preserved liver function and good performance status. They are randomized one-to-one between fostrox plus lenvatinib or lenvatinib alone. The primary endpoint for this study is objective response rate assessed by a blinded independent central review. They also look at the duration of response, progression-free survival, overall survival, safety, a secondary endpoint. The tumor assessment is done by CT or MRI every six weeks. The study is run with the Korean Cancer Study Group across 12 hospitals, and as I said before, Professor Chon is the principal investigator. The first patient in this study was dosed in May, and the enrollment is really progressing well and very much in line with our plan to include all patients within 12 months. We expect top-line results from this study in the second half of 2027. There are two things that makes this design attractive. We generate robust comparative data through an established research consortium, and the design allows for rapid readouts. Let me just move into MIV-711, our cathepsin K inhibitor. As Jens said, we are now developing this drug or this molecule into two rare bone indications. Both these diseases are driven by excessive bone resorption, and in both, there is no approved drug treatment today. I will start with Perthes disease. Perthes disease, or it is also called Legg-Calvé-Perthes disease. It affects around one in 1,500 children, most often boys, most often between four and eight years of age, so relatively early. What happens is that, for unknown reason, the blood supply to the femoral head is suddenly disrupted. What happens is that the bone dies, and the dead bone is then resorbed faster than new bone can be formed. The effect of that is that the femoral head collapses and deforms while the child continues to walk and put weight on the femoral head. Today, we have no disease-modifying medication to offer to these children. What is used is bracing and surgery, and it addresses only the acute symptoms, but they do not change the underlying process, and the majority are left with permanent damage to the hip. Most develop debilitating osteoarthritis as adults, and around 20% will need total hip replacement later on, or actually earlier on because it happens earlier than during the normal population. This is a disease where the mechanism is well understood, where the need is severe and where, as I said, there are no disease-modifying treatment. That is exactly the type of situation where MIV-711 can make a difference. Just to explain what happened and where MIV-711 comes in and when to intervene in this disease. Perthes progresses through four stages caused by the blood supply loss to the femoral head. First it is the necrosis, then fragmentation, then re-ossification, and finally the remodeling of the femoral head. Cathepsin K is the key protease driving this bone resorption. By inhibiting cathepsin K, we aim to slow the resorption and preserve the shape of the femoral head before severe fragmentation has occurred. That point us to the Stage 1 to 2a that you can see on this slide, and it is consistent with the effect we have demonstrated in the disease-specific animal model that we have done. A good news is that these children present early. Why is that? It is because they have pain and they start limping, which brings them to the medical care quickly. In the Swedish register data, it shows that around 80% are diagnosed in Stage 1 or 2a. The population we can treat at diagnosis is around 60%-80% of all patients, and that is not a small subset. With that, I will hand back to Jens. Thank you, Pia. A few strategic and commercial perspectives on this particular disease. The reason we are moving into this indication is that much of the groundwork is already in place. As Pia alluded to, we have shown in the disease-specific animal model that MIV-711 counteracts the deformity of the femoral head, which is one of the supporting elements for being granted rare pediatric disease designation. We are building on the same mechanism and same established safety profile that we have documented in the around 250 subjects from phase I, phase II osteoarthritis. We also have orphan drug designation and rare pediatric disease designation in place granted by the FDA. Through the directed share issue, the phase II proof of concept is now funded. The next step is, however, to develop the pediatric formulation and then to move into the randomized proof of concept study. To make sure that we execute with speed, because now the program is getting bigger, we have also strengthened the organization and recruited a highly experienced clinical operations lead who will take responsibility for the operational leadership across the studies in Perthes disease and Osteogenesis Imperfecta. Importantly, it is not two separate projects. The pediatric formulation work that we do in Perthes and the dose selection work that we will do will be highly beneficial also for the Osteogenesis Imperfecta program. So, one plus one is more than two in that respect. If we then look at the commercial side of things for Perthes disease, the primary market is around 8,800 children a year in Europe and the U.S. As Pia commented, we assess that around 80% of them would be suitable or accessible for treatment as an orphan drug in a pediatric population, and also being a treatment where you treat not chronically, you treat for a year to 18 months. We see this setting supporting a premium pricing. On top of that, there is of course the opportunity for rare pediatric disease and a priority review voucher, and those are currently valued at around $200 million if they are being sold. Taken together, we estimate annual peak sales of approximately $ 1 billion, five years after marketing approval in the U.S. and Europe. For a program where the designations are already granted and the study is funded, we think that is a very attractive risk reward. Stepping back and looking at MIV-711 as a whole, this is what makes the candidate special, we believe. It is a third generation, highly selective cathepsin K inhibitor with a substantial clinical package behind it and proven radiographic benefit in phase I, phase II in osteoarthritis. What has changed this quarter is now that we have two first to market opportunities from one single candidate, and neither of which has any approved treatments today. OI, with a market potential of over $2.5 billion and Perthes disease with approximately $ 1 billion. Orphan drug in both indications, rare pediatric disease designation in Perthes. We will of course target rare pediatric disease designation for OI as well. As I mentioned, I think that is an important element to comment. There are real synergies between the two programs, with the development of pediatric formulation and dose selection across Perthes disease and Osteogenesis Imperfecta. With that, I will hand back to Pia for a bit further update on how the OI program is progressing. Thank you, Jens. Just before we go into that, just a little bit of a reminder on what is Osteogenesis Imperfecta. It is also called brittle bone disease. It is a rare hereditary genetic disease, and around 1 in 15,000 birth have this disease. The mutation leads to defective or insufficient collagen production that actually leads to this problem with the bones as well. Children are born with it, of course they are born with it. The consequences is bone that fracture with minimal or no trauma. In the more severe forms of OI, non-traumatic fractures can be seen five times or more in a year. It is not only about the fractures. These patients, they live with bone and joint deformities that is often developed already in childhood. They have more common shorter stature and most of all, they have chronic pain. They have significant limitations in their ability to take part in ordinary daily life. There is no approved disease-modifying treatment in OI. MIV-711, we are addressing the quality of the bone as well, not just the density, by reducing resorption while allowing bone formation to continue. That is the rationale we have tested with our external expert, and it is also the rationale behind the proof of concept study in adult OI that I will talk about next. We can go to next slide. This is the study design, and I am pleased to say that the preparations are well on the way. We will include approximately 20 adult patients with Osteogenesis Imperfecta who have had fractures within the previous five years. They are randomized one to one to two dose levels of MIV-711 and treated for 12 months. The endpoints are change in bone biomarkers, including bone mineral density, pharmacokinetics, safety tolerability, and we will also look at number of fractures occurring during the treatment period. On the operational side, the interest from investigators has been really substantial, and five sites are already approved. Importantly also is that the eligible patients are largely known to these centers already, and they have them in their medical records, which is why we expect enrollment to be really fast. Preparation of clinical activities is progressing as planned, and manufacturing of study drug is on schedule. I would also highlight the commitment that we see from patient organizations both locally and regionally in Europe. They make us be visible, and it is a really good engagement that really matters for us, both for recruitment and for how we design the next development step. With that, I hand back to Jens. Thank you, Pia. There has been such a lot of change over the last couple of quarters, so we want to take a bit of time to go through a bit more detail on all three programs. With that, let us turn to the financial position, and I have a couple of comments on the intellectual property work and the IP positions that we are building. Clearly one of the biggest events in the second quarter was the directed share issue in June, and we raised approximately SEK 140 million gross or SEK 134 million net. The issue was oversubscribed, brought in two new institutional investors in Cicero Fonder and Storebrand, alongside continued strong support from Carl Bennet AB, Hallberg Management AB, Linc AB and Nordea Småbolagsfond Norden. The effect on our position is substantial. We ended the quarter with SEK 253.5 million in cash, compared with SEK 38.2 million a year earlier, and we assess that our existing cash is sufficient into 2030. Most importantly, though, we now have funding in place for the three planned phase II studies. This assessment does not include any proceeds from potential partnering of either fostrox or MIV-711, nor from our existing agreements with Vetbiolix and Biossil. Is there one slide to remember from the call today? This is the one. We now have three phase II studies, fully funded. Each of them carries a clear value inflection point. FLEX-HCC is the randomized 80-patient study across 12 hospitals in Korea, with the first patient dosed in May. Initial recruitment progressing really nicely and expected to be fully recruited in the 12-month period that we have planned for. In OI, the study design is finalized. First five sites have been selected and external interest is strong in a population of approximately that have a large population of patients across the globe. Again, without approved treatment. Perthes disease, the funding is in place. Pediatric formulation work has been initiated ahead of the proof of concept study, and both ODD and rare pediatric disease designations are already granted. Three studies, three indications without approved treatments, and the combined value potential well beyond what our current valuation reflects. One more piece to the value story, and an important one. This, I guess, behind all the other great pieces of news in the second quarter, this one was a bit hidden but wanted to stay on this one because this was a big step for us, an important one. We received notice of allowance from the U.S. Patent and Trademark Office for the combination patent covering fostrox plus lenvatinib in hepatocellular carcinoma and cancer metastasis to the liver. Once that patent is granted, together then with the other approvals we already have in EU, Japan, Australia, and Canada, etc, we have protection in our key markets until at least 2041. For a program that is now in a randomized phase II, that length of exclusivity in the largest markets is, of course, significant commercial asset for us. I think I've mentioned this before, and wanted to stop here and highlight that for a compound as fostrox, which is a liver-targeted compound, i.e., we will be focusing on liver cancer, having a combination patent like this, and where we also develop it in collaboration with lenvatinib. This is in addition to our normal composition of matter patent. This is a very strong patent because these are the areas we will focus on. It will be very difficult for any generic company to challenge this particular to try to circumvent this one after the composition of matter has lost its exclusivity. This is a really strong element to strengthening the IP package we have for the compound. With that, there are some other numbers as well. Patrik? I will present the financial summary for Q2. As you can see, all numbers are in SEK million. The net turnover for Q2 was SEK 1.2 million, which was SEK 300,000 lower than Q2 last year. Other external expenses were SEK 17.9 million, which was SEK 13.4 million higher than Q1 this year, which is mainly due to the successful early recruitment in the FLEX-HCC study. The personal costs were SEK 4.3 million, which was SEK 2.8 million lower than Q2 last year. The total operating costs were SEK 22.4 million, which is SEK 2.6 million lower than Q2 last year, which is mainly related to less employees and therefore the personal costs are lower. The operating loss was SEK -21.2 million, which is SEK 2 million better than Q2 last year. As you can see, the cash flow from operating activities was SEK -18.3 million. We needed to do the direct share issue in two tranches. SEK 130 million was received in June, and SEK 10 million was received in July. In total, it was SEK 140 million, as Jens has said before. Medivir has a strong cash position. The cash balance for end of Q2 was SEK 253.5 million. The cash is assessed to be sufficient at least into 2030. That is the financial summary. Thank you, Patrik. Bear with us one more slide, and then we will move into the Q&A session. Just looking ahead at some of our most important value drivers across our programs. In our own programs, the priorities are of course super clear. Continued recruitment in FLEX-HCC towards full enrollment within 12 months. Clearly, we want to get shorter than that, but we are confident with at least 12 months. Having activated the sites, the startup of the proof of concept study. Site activation, the startup of the proof of concept study in OI is the next step. Then also, of course, ensuring that we can develop a pediatric formulation as quickly as possible so we can also start the preparations for the proof of concept study in Perthes disease. In terms of concrete milestones, the nearest one comes from the work by our partner, Vetbiolix, as they expect top-line results from the phase II study with MIV-701, or VBX-1000 as they call it, in periodontitis in dogs in the fourth quarter of this year, as they continue to progress the recruitment of their study in a very nice fashion. A positive outcome there could generate substantial revenues for us without any material development cost of our own. Beyond that, rare pediatric disease designation in OI, completion of the feasibility work, and regulatory approval of the study design in OI. Top-line results from FLEX-HCC in 2027, and continued strengthening of our IP across territories are also, of course, key value drivers in the coming period. With that said, we stop. We thank everyone for listening to the presentation, and we can open up for Q&A. If you wish to ask a question, please dial pound key five on your telephone keypad to enter the queue. If you wish to withdraw your question, please dial pound key six on your telephone keypad. The next question comes from Hans Engblom from EVM AB. Please go ahead. Hello, guys. Thank you for an excellent presentation. Regarding the IP situation, I consider that you, in relation to fostrox mono, have a patent in China that is valid until 2035 or even further. In the fostrox lenvatinib combo, which was approved globally in some important markets, you did an excellent job to get the U.S. approval. But you haven't got any approval yet in China. You have a pending application. What is the status and the expectations regarding that application? Hi, Hans. As you know, we never get any timelines from the patent offices. But the ball is in the Chinese patent office court, and we do expect a result from them. But we can't really say when they will respond. Can you say whether you have about the same issues that you had in the U.S. patent approach? It's about the same process, or is it different? They had similar issues. I strongly believe that we have made a good argument also in China. I said, we don't have a timeline for their response. Okay. Thank you very much. Just another question to you, the journal The Lancet had recently a very interesting article regarding the future of HCC treatment. Have you any reflections on that article since you didn't mention your presentation? Can you repeat what article it was? The Lancet. I do not think I heard. Was it about the IMbrave 251, or what was it about? No, it is an article about the future landscape of HCC treatments and how it is now in a paradigm shift where it is going over to different combinations, so to speak. Yeah. But if you have it, we will leave the question. Okay. No, I have actually looked into it. I think one of the things, what you are saying, that it is combinations, and obviously there is cell therapy in this combination, but also how to use immunotherapy. What I think is even more important is to understand sort of where the different stages when you start your systemic treatment, and that has not been any conclusion about. I think that the learning from our last interaction at ESMO GI this summer was that not all believe in using systemic treatment, whether it's which combination it might be earlier in the stages, but want to use it later in the line, which means that fostrox plus lenvatinib would still sort of be the right second-line therapy after an immune therapy combination in first line. Obviously, I'm looking at all these publications with a lens of where does it strategically put fostrox plus lenvatinib, but that is what I took from that paper. Okay. Thank you. The next question comes from Richard Ramanius from Redeye. Please go ahead. Good afternoon, I have two questions. Let's start with MIV-711 for the Legg-Calvé-Perthes disease. Could you discuss a bit more how you see the potential pricing for this disease, considering on the one hand, it's extremely rare, which would motivate a high price. On the other hand, it's not a life-threatening disease. No. I think first it's fair to say that we're relatively early in the stage, so we also need to do additional pricing work to learn further. What we've done is we've benchmarked, because that's an important element. Is it life-threatening? Is it severe? Is it a chronic? Is it something that you treat for a short period, but you still get a long-term benefit? So we've benchmarked, without going into super detail, we've benchmarked against other treatments that are similar of non-life-threatening, but would have the similar benefit and similar type of treatment as MIV-711, and also looked at pricing of rare diseases in general these days. Clearly, we still see a very distinct difference between U.S. and Europe. But with that said, if we look at pricing today, somewhere along the lines of $150,000-$200,000 a year in the U.S., and maybe not 50% in Europe, but let's say 50%-75% of that. That would be an estimate today in terms of the pricing work that we've done. If you then look ahead a few years in terms of inflation or pricing going up, so somewhere along the lines of SEK 2 million per year from a treatment perspective in the U.S., in terms of how we've estimated it from a market potential. Treatment during just [audio distortion] Yeah, sorry. Treatment in 12-18 months, depending on when the patient start and it progresses there. You will probably see some patients likely treated up to 24 months, but 12-18 months would be most of the patients. I think it would probably, again, if the drug shows clinical benefit and is approved, I would be comfortable assuming an 18 months on average treatment duration. Right, sounds reasonable. Have you taken into consideration that MIV-711 has only been tested on adults, and there may be additional risks when treating children who are growing? We have been looking into that, and we have actually had quite a few discussions around that. We have already investigated safety in adults, as you mentioned, in osteoarthritis. There have been recent change in the FDA regulation as well to make it a little bit more attractive and possible to develop the first indication in the pediatric disease, which means that they have lighten up the requirement to do, for example, start from the beginning to do a dose escalation and so on. An allometric scaling from the dose that is selected, for example, in adults would be potentially, because we still need to have the interactions with the regulatory authorities, but would potentially work. This is why we also are trying to benefit from first doing an investigation when we talk to OI in adults to make sure that we have the proof of concept, our hypothesis of what cathepsin K is doing in this population is correct while we are developing the pediatric formulation. Because without that, we cannot do a pediatric study in Perthes disease instead. That is what Jens talked before about, that we are having this kind of synergies, or we are using another disease as well to come to the place where we actually can do the pediatric study in OI. Of course, we will have to monitor the safety very closely with the pediatric. T here is no, and yeah, y ou can jump in if you want to, Fredrik. The maturity of the enzymes that is responsible for metabolizing MIV-711 is mature enough already at two years old. We do not see that there should be any huge difference when it comes to the drug itself in the pediatric population. I will pitch in and say the following. Because one of the elements is you also want to make sure that if you treat children are growing, that the bone develops as it should in terms of the length of the bones, that continues. In the disease modeling work we have done on Perthes disease, that is also an element that we have evaluated, i.e., when they are treated with the cathepsin K. In this case, it was a pig model. Are the pigs growing as they should? Not just minimizing deformity of the femoral head, but are the bones growing as they should? It does. So that is also an element that was important in terms of making anyone, regulators and others, comfortable that, yes, it would be suitable to use a cathepsin K in children as well. Yeah, just to add that as well. We did not say that, but many of the Perthes children have a shorter leg when they grow up because the disease is impacting the femoral head, which makes it a bit shorter. So that is also important. If you can prevent the destruction of the femoral head, maybe they will not have this leg shortening after the disease. Okay, great answers. That is all for me. Thanks. As a reminder, if you wish to ask a question, please dial pound key five on your telephone keypad. There are no more questions at this time. I hand the conference back to the speakers for any closing comments. Thank you. Before we close the call, let's come back to where we started. This was the quarter where fostrox was validated in a peer-reviewed journal, and where the randomized FLEX-HCC study got well underway with high engagement among the investigators and a strong start to the recruitment. It was also the quarter where MIV-711 became a two-indication program with the funding secured for both Perthes disease and Osteogenesis Imperfecta, where we have now finalized the study design and moved forward nicely towards starting the study. We are building two rare disease opportunities on the same established safety profile. With an oversubscribed share issue behind us, SEK 253.5 million in cash funding for all phase II studies, we now have the financial strength to execute on all of these programs. I would like to thank both new and existing shareholders for the confidence that makes this possible. With that said, thank you everyone for attending, and have a great rest of the day.