Medivir AB (publ)

Thank you, Operator, and welcome everyone to Medivir's webcast covering the second quarter of 2026. And looking back, this was the quarter where a lot of things came together for us. The Phase 1 B2A data for FosTrox in combination with Lamatinib was published in Clinical Cancer Research, which is one of oncology's most cited journals. And 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, Pertus disease, through an oversubscribed directed share issue of approximately 140 million SEK. 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 two studies and a strengthened balance sheet, we are in the strongest position that we have been 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 1 B2A study of FosTrox plus lenvatenib 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. And as I mentioned, in May, the first patient was dosed in FLEX-HCC, the randomized phase 2 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 MIB711, through the directed share issue, we are now taking MIB711 into Pertus 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 140 million was oversubscribed and brought in new institutional investors and we ended the quarter with 253 plus million in cash and we now have funding in place for all three phase two 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 previous quarter is the Pertus disease, where we are now then in the planning phase of the phase two proof-of-concept study. We will not speak too much about it today, but VetBiolix, our partner in developing MIB701, They continue to recruit patients or dogs into their study with estimated readout in the fourth quarter of their ongoing randomized study. So that's an important value driver for us as well in the coming period. So, apart from myself, as I mentioned, our chief medical officer, Pia Baumann, will go through the programs. Partik RCFO will cover the financials, and Fredrik Öberg, our CSO, is here for our question and answer session as well. So, with that, let me hand over to Pia, who will take you through the published Phase 1 B2A 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 troxacitamin, where the tumor is, and keep systemic exposure low. I know we have said this before, but this is really important. And 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 ATC. including in the recently presented EMBRAVE 251 study with atezolizumab and bevacizumab refractory patients. And 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. And 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. And I know that we are coming back a little bit in the summary from Jens. And this is why FLEX-HEC study that is ongoing in Korea is now our highest clinical priority for the moment. So, next slide. A few words on the publication itself, because it's an important milestone for this program. The full safety and efficacy data set from the Phase 1b-2a study is now published in the peer-reviewed Journal of Clinical Cancer Research, and Professor Hongjie Xiong, which is also our primary investigator in the FLEX-HC study, is the first author. The clinical method 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'm sure you are aware of this. It's the metastatic disease that drives mortality. In HCC, patients most often die from liver decompensation, and it's frequently caused by local tumor progression. So the treatment goal is to control the tumor in the liver without compromising the liver function. And that is a balance most systemic therapists struggle with. What you see in the figures here are the liver function parameters during the full treatment time. And it is transaminase and something called the ALBI score where you measure liver function. And it is across, as I said, the treatment cycles. And all of these, they remain stable over time. In other words, we achieve tumor control without deterioration of liver function. And that is what keeps patients fit enough, not only to continue the treatment, in this case the study, but also to receive subsequent therapy. Next slide. I would also like to comment on the EMBRAVE 2.5.1 study that was presented at ASCO this year, because it's 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. And note, if you press one more time, and note how favourable the patient population was. The patient had to receive at least four cycles of atezolizumab plus bevacizumab as prior treatment. And on that prior treatment, they needed to have documented disease control, meaning stable disease, partial response or complete response, on at least two tumor assessments. In other words, these patients who had done well on the first treatment, that's the patients who were included here. And 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. And 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 Ostrox is positioned. You can 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 Embraer 251. Here, more than 75% of the patients treated with FosDrox plus lenvatinib experienced tumor shrinkage. And the objective response rates 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. And 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 IMBRAVE251 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 Fosterox largely independent on how they responded in the previous line, which is not what we usually see in this setting. And 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. Go to the next slide. This is the study design for this study, and it's 80 patients with advanced second-line HSE, 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 lenvatinibolone. 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. And 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 Shon 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. and 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 readout. So, let me just move into MIV-711, our Catepsin K inhibitor. As Jan 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'll start with Pertus disease. So, Pertus disease, or it's also called leg calvary Pertus disease, it affects around 1 in 1500 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 because the dead bone... 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 systems, but they do not change down the laryngeal process, and the majority are left with permanent damage to the hip. Most develop debilitating osteoarthritis as adults, and around 20% will need a total hip replacement later on. Or actually earlier on, because it happens earlier than it does in the normal population. So 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 treatments. That is exactly the type of situation where MEV711 can make a difference. So, just to explain what happened and where MIB711 comes in and when to intervene in this disease. Pertus 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. and Catepsin K is the key project driving this bone resorption. So by inhibiting catepsin 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 one to two A 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 And why is that? It is because they have pain and they start limping, which brings them to the medical care quickly. And in the Swedish registered data, it shows that around 80% are diagnosed in stage one or two A. So the population we can treat at diagnosis is around 60 to 80% of all patients. And that is not a small subset. With that, I will hand back to Jess.

Thank you Pia. So a few kind of strategic and commercial perspectives on this particular disease. The reason we're moving into this indication is that much of the groundwork is already in place. We've shown, as Pia alluded to, we've shown in the disease specific animal model that MIV711 counteracts the deformity of the femoral head, which is one of the supporting elements for being granted rare pediatric disease designation. And we are building on the same mechanism and same established safety profile that we have documented in the around 250 subjects from phase one, phase two osteoarthritis. And we also have orphan drug designation and rare pediatric disease designation in place granted by the FDA. So through the directed share issue, the phase two 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. And to make sure that we execute with speed, because now the program is getting bigger, we have also sort of strengthened the organization and recruited a highly experienced clinical operations lead who will take responsibility for the operational leadership across the studies in Pertus disease and osteogenesis imperfecta. So importantly, it's not two separate projects. The pediatric formulation work that we do in Pertus will also, and the dose selection work that we'll 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 Pertus disease, the primary market is around 8,800 children a year in Europe and the US. And as Pia commented, we assessed 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. And then on top of that, there's 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 US, five years after marketing approval in US and Europe, and 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 MIV711 as a whole, this is what makes the candidate special, we believe. It is a third generation highly selective catepsin K inhibitor with a substantial clinical package behind it and proven radiographic benefit in phase one, phase two in osteoarthritis. So 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 US dollars and Pertus disease with approximately 1 million US dollars. Orphan drug in both indications, rare pediatric disease designation in Pertus And we will, of course, target rare pediatric disease designation for OI as well. And as I mentioned, I think that's an important element to comment. There are real synergies between the two programs with the development of pediatric formulation and dose selection across Pertus disease and osteogenesis imperfecta. So with that, I'll hand back to Pia for a bit further update on how the OI program is progressing.