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.

Thank you, Jens. And just before we go into that, just a little bit of a reminder of what is osteogenesis imperfecta. It's also called brittle bone disease. It is a rare hereditary genetic disease, and around one in 15,000 births 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. And the consequences is bone that fracture with minimal or no trauma. In the most more severe forms of OI, non-traumatic fractures can be seen five times or more in a year. But it's 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. and they have significant limitations in their ability to take part in ordinary daily life. There is no approved disease modifying treatment in OI and MEV 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 the next slide. This is the study design and I'm pleased to say that the preparations are well underway. 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 NIV-711 and treated for 12 months. The endpoints are change in bone biomarkers including bone mineral density, pharmacogenetics, 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 the 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 invisible, not invisible, but visible and it's 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's 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 programmes. So with that, let's turn to the financial position and 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 140 million gross or 134 million The issue was oversubscribed, brought in two new institutional investors in Cicero Fonder and Storebrand alongside continued strong support from Carl Bennett AB, Hallberg Management, Link and Nordea Småbolagsfond Norden. The effect on our position is substantial. We ended the quarter with 253.5 million SEK in cash compared with 38.2 million a year earlier, and we assessed that our existing cash is sufficient into 2030. Most importantly, though, we now have funding in place for the three planned phase two studies. And this assessment does not include any proceeds from potential partnering of either Fostrox or MIB711, nor from our existing agreements with VetBiolix and BioCell. So is there one slide to remember from the call today? This is the one. We now have three phase two studies fully funded. Each of them carries a clear value inflection point. FlexHCC is a randomized 80-patient study across 12 hospitals in Korea with the first patient sort of 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 and first five sites have been selected and an external interest is strong in the population of approximately that have a large population of patients across the globe again without approved treatment. Pertus 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. So 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, in sort of behind all the other great pieces of news in the second quarter, this one was a bit hidden, but wanted to sort of stay on this one because this was a big step for us, an important one. We received notice of allowance from the US Patent and Trademark Office for the combination patent covering Fosstrux, Plazolin, Matinib. 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, Canada, etc., we have protection in our key markets until at least And for a program that is now in a randomized phase two, that length of exclusivity in the largest markets is of course significant commercial asset for us. And I think I've mentioned this before, I wanted to kind of 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 company, generic company, to challenge this particular, to try to sort of circumvent this one after the composition of matter has lost its exclusivity. So this is a really, really strong element to strengthening the IP package we have for the compound. So with that, there are some other numbers as well. Patrik?

I will present the financial summary for Q2. And as you can see, all numbers are in million sec. And the net turnover for Q2 was 1.2 million, which was 300,000 lower than Q2 last year. Other external expenses were 17.9 million, which was 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 4.3 million, which was 2.8 million lower than Q2 last year. The total operating costs were 22.4 million, which is 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 minus 21.2 million, which is 2 million better than Q2 last year. And as you can see, the cash flow from operating activities was minus 18.3 million. and we needed to do the direct share issue in two tranches and 130 million was received in June and 10 million was received in July and in total it was 140 million as Jens has said before. Medvir has a strong cash position. The cash balance for end of Q2 was 253.5 million. And the cash is assessed to be sufficient at least into 2030. Yeah, that's financial summary.

Thank you, Patrik. So bear with us. One more slide and then we will move into the Q&A session. So just looking ahead at sort of some of our most important value drivers across our programs. And in our own programs, the priorities are, of course, sort of super clear and continued recruitment in Flex HCC towards full enrollment within 12 months. Clearly, we want to get shorter than that, but we're confident with at least 12 months. Having activated the site activation and startup of the proof of concept study in OI is the next step. And then also, of course, ensuring that we can develop a pediatric formulation as quickly as possible, so we can also start preparations for the proof of concept study in Pertus 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 2 study with MIV701 or VBX1000 as they call it in periodontitis in dogs in the fourth quarter 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 costs 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 FlexHCC in 2027 and continuous strengthening of our IP across territories are also of course key value drivers in the coming period. So 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 Postdoc Mono, have a patent in China that is valid until 2035 or even further. In the FOSDRAC-Mendina combo, which was approved globally in some important markets, you did an excellent job to get the US 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 we do, 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 US patent process? Is it about the same process or is it different?

They had similar issues, but I strongly believe that we have made a good argument also in China. But as I said, we don't have a timeline for their response.

Okay, thank you. Thank you very much. Just another question to you. The journal 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?

in Lancet.

I don't think I heard, was it about the Imbrave? What was it about?

No, no, it's an article about the future landscape of HEC treatments and how it's now in a paradigm shift where it's going over from over to different combinations, so to speak. But if you have it, we'll leave the question.

No, I have actually looked into it and 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. But 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. And I think that the learning from our last interaction at ESMO-GI this summer was that not all believe in using systemic treatment, which combination it might be. earlier in the stages, but want to use it later in the lines, which means that FosTrux plus Lanvatenib 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 the lens of where does it strategically put FosTrux plus Lanvatenib, but that is what I took from that paper.

Okay, thank you.

The next question comes from Richard Romanious from Red Eye. Please go ahead.

Good afternoon. I have a few questions. Let's start with IV711 for the leg caliper. 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 that we also need to do sort of 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 sort of a long-term benefit? So we benchmarked, without going into super detail, we benchmarked against other treatments that are similar, non-life-threatening, but would have the similar benefit and similar type of treatment as MIV-711, and also looked at the pricing of rare diseases in general these days. And clearly, we still see a very distinct difference between US and Europe. But with that said, if we look at pricing today, somewhere along the lines of 150,000 to 200,000 US dollars a year in the US, and maybe not 50% in Europe, but let's say 50% to 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 2 million SEK per year from a treatment perspective in the US in terms of how we've estimated it from a market potential.

and treatment during just one more year?

Yeah, treatment, sorry, treatment 12 to 18 months, sort of depending on sort of when the patients sort of start and it progresses. You will probably see some patients likely treated up to 24 months, But 12 to 18 would be most of the patients. So I think it would probably, I mean, again, if we show, 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... taking into consideration that 7-11 has only been tested on adults and there may be additional risks when treating children who are growing.

So 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. And 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 lightened up the requirement to do, for example, start from the beginning to do a dose escalation and so on. So an allometric scaling from the dose that is selected, for example, in adults would be potentially, because, I mean, 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 catapsin K is doing in this population is correct. while we are developing the pediatric formulation, because without that we can't do anything in the pediatric, we can't do a pediatric study in Pertus disease instead. So 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. But of course we will have to monitor the safety very closely with the pediatric, but there is no, and yeah, I can, you can jump in if you want to Fredrik, but the maturity of the enzymes that is responsible for metabolizing MIB711 is mature enough already at two years old. So we don't see that there should be any huge difference when it comes to the drug itself in the pediatric population.

And then I'll pitch in and say the following. We've done, because one of the elements is you also want to make sure that if you treat children and children are growing, that the bone develops as it should in terms of the length of the bones, that that continues. And in the disease modeling work we've done on Pertus disease, that is also an element that we have evaluated, i.e. when they're treated with the kadepsin K, In this case, there 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? And it does. So that's also an element that was important in terms of making anyone, regulators and others, comfortable that, yes, it would be suitable to use Catepsin K in children as well.

And just to add that as well, we didn't say that, but many of the practice 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.

Great answers. That's 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, so I hand the conference back to the speakers for any closing comments.

Thank you. So then 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 MIB 711 became a two-indication program with the funding secured for both Pertus disease and osteogenesis imperfecta, where we've now finalized the study design and moved forward nicely towards starting the study. And we're building two rare disease opportunities on the same established safety profile. With an oversubscribed share issue behind us, 253.5 million in cash funding for all phase two studies, we now have the financial strength to execute on all of these programs. And I would like to thank both new and existing shareholders for the confidence that makes this possible. So with that said, thank you everyone for attending and have a great rest of the day.