Medivir AB (publ) (MVIR) Earnings Call Transcript & Summary

Good day, and welcome to the Medivir Fourth Quarter 2022 Earnings Call. [Operator Instructions] Please note this event is being recorded. I would now like to turn the conference over to Jens Lindberg, CEO. Please go ahead.

Thank you, and welcome, everyone, to our quarterly call. And operator, if we move to the next slide, Slide 2, please. So joining me in the room here at Medivir is our CFO, Magnus Christensen, who will go through the financial highlights towards the end of the call. And our CSO, Fredrik Öberg, who will take the science section of the call in the middle. And with that, let's jump into sort of the an agenda for today. So operator, if we move 2 slides ahead or actually 3 slides ahead to Slide 5, please. Highlights during last quarter, I think we've -- 2022 was a year of sort of moving our lead project fostrox forward with as much speed as we possibly could. And Q4 was sort of clearly on the same focus. We are quite happy with the continued strong recruitment we've seen in the fostrox study, and we're now eagerly anticipating sort of moving to the next phase in the near term to set the recommended Phase II dose. And we're very encouraged with the interest we've seen in the study in terms of recruiting patients into both of the combination arms. During Q4, we had an important pre-IND meeting with the FDA, which we completed and positive feedback on the overall development plan. So we're very much looking forward to opening the IND in 2023 in order to be able to include U.S. sites in our sort of future development plan. We have new data presented at SITC conference in Boston continuing to show sort of efficacy of fostrox together in combination in this time with anti-PD1, combining fostrox with either anti-PD1s or TKIs is at the core of our strategy. So good to see that we continue to see that additive efficacy across nonclinical tumor models, and we are eagerly looking forward to hopefully showing that in the clinic as well. And finally, on the people front, we recruited a permanent Chief Medical Officer, Pia Baumann, who is joining us from AstraZeneca, and she is actually making her first day here at Medivir on Monday, so coming soon. On the outside of fostrox, we look at the other portfolio, some movement in Q4, we can see that IGM or we know the IGM Biosciences, who are in the dose escalation phase of the combination of their DR5 agonist, IGM-8444 together with birinapant continues to enroll patients in that fourth cohort. And as of Q4, still no DLTs observed to date. So progressing nicely in that combination. Then INFEX Therapeutics, they announced that -- actually early this year that the MBLI program received FDA QIDP designation, the MET-X Program. That's also encouraging with sort of all the benefits that come with the QIDP designation. We've also seen that they received patented status in Q4, and they are moving swiftly towards entering the clinical one with the MET-X Program. And then finally, Tango Therapeutics who we out-licensed the preclinical USP1 program to a couple of years ago, they have now selected their first drug candidate from this preclinical program, the TNG348. And they have also now they are opening an IND in 2023. So additional compounds from the Medivir research moving towards entering the clinic. If we move to the -- next slide, please, operator, Slide 6. So as I mentioned, I'll start with the people side first. So Pia Baumann, who is a sort of trained oncologist from Karolinska Institute and has spent a good number of years in smaller biotech companies and larger pharmaceutical companies is joining us on Monday. Lot of experience in development of sort of pharmaceutical compounds in the field of oncology, has a lot of experience engaging with regulatory authorities, et cetera. So we feel that her experience will fit in very nicely with where we are with the current set of lead program, fostrox, and the efforts that we're driving as we move towards the next phase of our clinical development. So eagerly looking forward to Pia joining us on Monday. And then before -- as we go into the portfolio, this is our pipeline overview, which we have shown many times before. And we will, of course, spend a bit of time on our in-house program, the lead program of fostroxacitabine bralpamide and then we'll make some additional comments regarding a couple of our partnering programs as well towards the end of the call. And next slide, please. Slide 8. And so as we move into fostroxacitabine or fostrox as we call it for short. As we are about to sort of now sort of soon enter Phase IIa and move into the next phase of the development, but we thought we would sort of take a sort of semi-step back and just to sort of kind of briefly walk through why do we think the compound sort of has promised in HCC and perhaps even more importantly, what sort of -- how did we come about developing this particular compound knowing that sort of historically traditional chemotherapy hasn't fared so well in HCC. But we think -- we feel quite positive about sort of having found a way to make HCC patients sort of benefit from chemotherapy as well. But to sort of take us through that journey and how we came about developing the compound, I'll leave it to Fredrik to walk us through that. So operator, if you move to the next slide, please, Slide 9.

Thank you, Jens. So I mean, as you all know, traditional chemotherapy is the mainstay of cancer treatment still, and it has a lot of goods in the treatment of cancer. However, in HCC, this has not been the case. And when we initiated this project, we analyzed why this was not the case. And one of the key challenges is, of course, balancing systemic toxicities versus the clinical efficacy in the liver. So our analysis has identified several areas that we thought we would need to address in order to progress such a program. And you see 3 of them highlighted here on this slide. One is, of course, the narrow therapeutic window. So the doses that we need to have an effective drug in the liver would also cause significant systemic toxicity. And this is a challenge. We should also remember that patients with hepatocellular carcinoma actually had 2 diseases at the same time. They have a liver disease, which makes their liver sensitive to liver toxicity and they have the tumor at the same time. So we need to address this as well. And also the liver does have a lot of enzymes inactivating various drugs, some have resistance mechanisms, in particular, for nucleoside drugs that inactivates and deactivate those and therefore lose activity in the liver. So if we move to the next slide, that illustrates how we went about this. So liver-targeted exposure. From the work done in HCC, we did have both nucleoside chemistry and development platforms and also prodrug platforms to develop targeted deliveries to deliver -- to treat survivors. So that could be used that learning to enable higher liver concentrations at lower doses and ensure that we get exposure in the tumor while minimizing systemic toxicity. In order to ensure that we don't hit the normal liver tissue, we need to choose a compound which is cytotoxic to the tumor cells and to do that in many different ways. But of course, one clear differentiation between the liver -- normal liver tissue, and the tumor is proliferation. So not all chemotherapies are the same. Many chemotherapeutics do have toxicities in cells that are not actually growing mitochondrial toxicities, et cetera. So you have liver toxicities of chemotherapies, which are not related directly to the proliferation of the cells. So we needed a compound that linked the cytotoxic effect to the proliferation in order to have this differential tumor selective activity. And to avoid these resistance mechanisms, that's sort of inactivation mechanism in the liver, there are certain unnatural nucleosides that can be used in order to avoid recognition by some cellular enzymes. So with these three aspects, we chose troxacitabine and the pro-drugs that we did. So if we move to Slide 11, then this depicts in a schematic way, the fostrox molecule. And of course, we did examine hundreds of different pro-drug tails in order to find one that enables oral administration and really gives a very high liver selective exposure versus systemic exposure. And the same approach in principle has been used in HCV by approved drugs. The active substance part that does becomes incorporated into DNA and gives the DNA damage and the cytotoxic effect, we chose troxacitabine. It is a chemotherapy that induces DNA damage and cell death. And it had a track record of proven activity, but it did have a too-narrow therapeutic window, which we then addressed with the pro-drug tail. So if we move to Slide 11.

Slide 12.

Slide 12, sorry, that depicts the principle to the left where once daily oral administration provides through the first pass metabolism but it's reaching the liver first and there becoming metabolized into the active metabolite, which is trapped in the liver and thereby minimizing 0systemic exposure and exposing the cancer cells to high enough levels of the cytotoxic drugs. We do know from rats experiments for instance, that we can achieve by dosing orally hundredfold higher levels of the active metabolite in the liver, than if you would give troxacitabine IV as was the case in the clinical studies previously done. So what about selectivity? If we move to Slide 13. You can see it's not a rapidly proliferating tumor. However, we have examined biopsies from patients and there is a clear differentiation. So tumor cells proliferate whereas non-tumor cells, the hepatocytes in the liver do not. That's the left panel. So we were really encouraged when we observed in the Phase I monotherapy that we could actually induce DNA damage in the tumor cells versus not observing any DNA damage to the normal liver cells adjacent around the actual tumor, which was a proof of concept of source demonstrating that we can reach -- with a reasonable dosing of fostrox, we can reach the target and induce a damage in the tumor cells, where it's not affecting the normal liver cells. So in summary, Slide 14, then we have in fostrox, a drug which contains the pro-drug which allows oral administration and liver targeting. And we also have the active substance - the troxacitabine part, which is an unnatural nucleoside and it's a so-called L-nucleoside instead of most other chemotherapies in this class being the natural [ D-enzymatic ]. And this means that it's not really recognized by several enzymes in the cells and such enzymes that are involving resistance mechanisms and toxicity. So therefore, we have a drug that does the job but avoids certain resistance and toxicity mechanisms in normal liver cells. So this is in the area of HCC a unique mechanism. And if we move to Slide 15, as we've spoken about before, there are 2 main mechanisms of action, which dominate the HCC field. One is the checkpoint inhibitors and the other one is tumor -- Tyrosine kinase inhibitors or multikinase inhibitors, TKIs. And there are actually 2 really good scientific rationales for combining with these. And the fact that we have a unique mechanism specs, it's also attractive to combined with other mechanisms. So in terms of stimulating the immune system, we know that inducing DNA damage and cell deaths increases the presentation of tumor antigens and potentially then increases the activity of checkpoint inhibitors, whereas in combination with TKIs, which are anti-angiogenic, the increased lack of oxygen, the hypoxia in the tumor, we know that, that actually increases the levels of the active metabolite of fostrox. So therefore, also creating a situation where you can observe synergy. And we are, as Jens said, eagerly waiting combination data in the clinical trial. But meanwhile, we do have some evidence that this works in preclinical models. So if we move to Slide 16, on the left-hand panel, our immunohistochemistry sections of tumor treated in vivo either with vehicle, the checkpoint inhibitor anti-PD-1 pembrolizumab, fostrox or the combination. And in this case, it's stained for [ CD8 ], which is a T cell marker in brown. The middle panel is a quantification of tumor-infiltrating lymphocytes as they are called this group of immune cells that infiltrate the tumor. And that increase does suggest that fostrox provides a change in the tumor microenvironment, increasing infiltration of tumor-infiltrating lymphocyte, which in turn means that a checkpoint inhibitor combination is a rational way to go. In the right-hand panel, there's a tumor model and HCC model in mice, where it's just a short treatment, 5-day treatment at a suboptimal dose of fostrox, enhances the activity of anti-PD-1. So if you focus on the blue graph -- blue line, which is the activity of the checkpoint inhibitor by itself and the red one, which is the enhancement of adding this relatively short treatment with fostrox early during that tumor growth period. So in summary, we think that we have a situation where we have a drug which is optimized for liver targeting. And it has certain characteristics that allows it to be combined favorably with immune therapies such as anti-PD-1s. So with that, I will leave the word to Jens.

So it's encouraging to see that we -- sort of fostrox seems to sort of stimulate tumor microenvironment in a positive way and sort of create that additive efficacy within the anti-PD-1. This complements sort of previously presented data where we've shown a similar sort of complementary or additive efficacy with TKIs and we will -- we look forward to sharing additional data later in the year where we have, among other things, starting to look at sort of not just sort of single combinations, but triple combinations as well. But that would be for later presentations when we have presented at external [ context ]. And just sort of -- this is the program as it's ongoing and where we are -- oh, sorry, move to the next slide, please. This is the program as it stands now. And as you know, we are sort of exploring 2 different combinations, there's one combination with lenvatinib and with pembrolizumab. As we said, we are -- we've been rapidly accruing patients in the dose escalation, and we are now eagerly looking forward to sort of setting the recommended Phase II dose and moving into the expansion phase sort of in the very near term. And the feedback from sites are also -- they're on as to it because they want to be able to include more patients. So we are having patients in line. So we very much look forward to that Phase IIa start near term. When we decided at the time of study start or design of the study, there was a question whether we should choose one arm or more go with both arms in dose escalation and decision was made to -- no, let's go with both because we never know where the treatment algorithm how it will evolve throughout the year and it turns out that the decision to have both arms was a very good one. But if we move to the next slide, please, this is a relatively busy slide. But if we look at what has happened in this field over the past, let's say, 12-plus months, particularly in the first-line stage of HCC. We know that to on the left-hand side that the IMBrave150 trial that sort of evaluated the combination of atezo/bev versus sorefenib showed positive results and was the first one to be approved as a combination. The interesting part here is that, that has been sort of followed by a number of other combinations that are looking at a little bit the same, combination of a PD-1 and the TKI, various combinations, the AstraZeneca Himalaya trial, the Leap-002 from Eisai and Merck and later camrelizumab plus rivoceranib. And I think that the one thing to point to here is that from the study results perspective, it looks very similar. ORR percentages, relatively the same. Overall survival, relatively the same. So it seems like the combination does work and it does a lot of good for patients, but sort of -- it doesn't really matter which combo you may use, you will get to this point, but you will not get further. So what it has done is it has cemented the combination of atezo/bev as the standard of care in first line. And as most patients then get a PD-L1 in first line, it means that there is an -- physicians are quite eager to move to a different mechanism of action, i.e., TKI monotherapy is becoming sort of the way to go as a standard in second line for those patients where lenvatinib is used sort of -- is preferred in many places, which then highlights the relevance of the fostrox plus lenvatinib arm. And then finally, if you do the same, results will probably be the same. If you continue to use the same type of combinations, results will likely be the same. So what it does highlight for us is that they will likely need to be different modes of action or additional modes of action to take things further, i.e., to improve the clinical benefit in this sort of first-line space. So as we read this and as we look forward, we are very happy with having both arms because it means that perhaps the lenvatinib/fostrox arm is the most relevant arm for the second-line space, which -- and be the arm that would be most relevant to explore in second line to see what improvements can we make beyond TKI monotherapy. But equally, that other arm, the pembrolizumab arm and the dose recommendation for that, could clearly have potential in second line, but it could also be a dose and data that could inform potential opportunities moving into earlier spaces. So that's also data that we need to watch for to see whether there's opportunity to sort of explore additional alternatives beyond the second-line program. So with that, we can move to the next slide, please. So the short version on fostrox, a significant unmet need. I mean benefits for patients as of late with new studies in combinations, but there continues to be a significant unmet need and commercial potential. We do have a unique mechanism of action that then selectively, Fredrik sort of spoke about, targets cancer in the liver and bypasses resistance mechanisms. And that mechanism and being the only sort of chemotherapy in development has a unique and strong potential for attractive combinations. And before we conclude, a couple of words on our other -- a couple of our other programs. So if you move to the next slide, please, and slide -- and we could move one more so to Slide 21. As I mentioned before, our partner, Tango Therapeutics in-licensed the USP program, they announced in Q4 that they are now moving towards clinic. So they have selected a CD from that program, and they will be referred to as TNG348 going forward and they are planning an IND filing in 2023. And in terms of data they've shown -- showing a significant sort of potential opportunity in -- specifically in BRCA1 and BRCA2 mutated cancers. They've shown synergy with PARP inhibitors in both PARP sensitive, but also PARP resistance models. So eagerly looking forward to seeing as they move into the clinical and seeing clinical data. And then finally, sort of in terms of Q4 development, next slide, please, Slide 22. The MET-X program which has moved forward quite nicely in 2022 with regards to both sort of nonclinical data presented, but more importantly, they have received as of late, the QIDP designation in January, which will sort of give them sort of a faster and better sort of path towards the clinic and towards the market as they start to engage with regulatory authorities in the U.S., and they have also communicated the next step is to enter the clinic in 2023. So with that, I will hand it over to Magnus for financial highlights, so you can move forward to Slide 24, operator.

Thank you, Jens. With Slide 24, we can see the financial summary for quarter 4 and for the whole financial year 2022, which I will briefly comment on. From a financial viewpoint, Q4 was a pretty straightforward quarter, the turnover for quarter 4 was SEK 2.3 million, which relates to the royalty income from Xerclear. Year-to-date, the figure is SEK 4.4 million which is lower compared to last year. But then we have in last year included upfront payment from out-licensing deal with IGM related to Birinapant as well a milestone payment when the first patient was dosed in their combination study in Q4 2021. Other external expenses are lower compared to last year in Q4 and relates almost to lower clinical costs. Last year, we had costs for starting up the combination study. Year-to-date, it's around SEK 4 million lower. The operating loss for Q4 is SEK 18.6 million and it's also lower compared to last year, and it's almost due to the lower clinical costs. The cash flow from the operating activity for the quarter amounts to almost minus SEK 25 million, which is in line with our current plan that we have in the company. And the cash position at the end of Q4 is around SEK 117 million. And according to the current plan and with the current expansions that we have, this cash run rate is into Q1 2024. And with this, I will hand over back to Jens.

Yes. So we can move one more Slide operator, and then we'll sum it up. So 2022, sort of continued progress across the portfolio, and in Q4, as mentioned, continued recruitment -- strong recruitment in the fostrox study. And as we look ahead to now sort of 2022 a year of moving that project forward as much as we could 2023 as we sort of move into Phase IIa, generate more data, we are sort of eagerly looking forward to sort of seeing the clinical data and hopefully showing that sort of the nonclinical evidence that we have indicating how the combination provides additive efficacy that's also coming through in the clinic. Then on the other side of the -- other side of the portfolio, and the partnering assets, again, nice progression throughout the year for birinapant, for the MET-X program, for Infex, et cetera. And we are looking forward to 2023, seeing a couple of those sort of preclinical compounds moving into the clinic and opening an IND and we're following closely as well. Of course, the birinapant/IGM8444 combination, as they are also moving towards close of the dose escalation and selection of tumors and moving towards expansion phase for that sort of in a kind of a similar time frame as we are seeing for the fostrox. So with that, thank you for staying with us. Hopefully, we are not too long-winded. We are maybe sometimes a bit too excited about talking about why we believe fostrox is unique and why it's different and why we think it has strong potential. And now we're eagerly looking forward to hopefully showing that clinically as well in 2023. So operator, I think we can stop there and if there are any questions.

[Operator Instructions] The first question comes from Joe Pantginis with H.C. Wainwright.

This is Sarah on for Joe. I have 2 questions. First, have you been in any regulatory -- in any talks with regulatory agencies yet in Korea? And are you able at this time to provide any color on those talks?

The short answer is no, sort of, at this stage, but the regulatory interactions that we've had primarily one as of late has been the pre-IND discussions to open in the U.S. The only regulatory interactions we've had so far in Korea has been sort of opening the current study as we have the Asian sites in terms of sort of regulatory approvals, but nothing further at this point and that will come as we start to see a bit more clinical data.

Okay. And then also kind of following up then on that general region for your development plan. Can you detail any potential recruitment effort to enroll outside of Korea and in general larger area geography?

I mean we're -- from a clinical study perspective, we have 14 sites that are open at the moment, and they are in U.K., Spain and Korea. And I think if we go back to the first half of the year, before we had the Korean sites open, we did have a bit of a challenge in terms of recruiting to the study, and that picked up nicely when the Korean sites came on board. But we also added -- we also made a few initiatives in terms of working closer with the sites. We made some adjustments to the protocol. And that has sort of -- that has also helped pick up the speed. So when we see sort of speed or recruitment pickup in the second half of the year, that is across the different countries. So clearly, getting the Korean sites on board sort of took a first step towards picking up speed. But then we've also seen the Spanish and the U.K. sites also pick up speed. So at the moment, we are seeing sort of a very nice recruitment pace and then sort of across the different countries, we actually have patients kind of waiting in line for those cohorts to be opened.

The next question comes from Jason McCarthy with Maxim.

So wondering what you mainly attribute the accelerated enrollment in Q1 be to? Was it primarily the protocol amendment that sort of relaxed enrollment criteria to include those third-line patients?

No, I wouldn't say primarily. So I think it's -- I mean sort of -- I think we've spoken about before, we've done kind of taken steps in 3 -- a couple of different areas where we've added some additional sites. For example, in Korea, I think in the beginning, we had -- our first plan was to have 4 sites. We added that, so we had 2 additional sites. So that has clearly helped. We have worked quite closely with the sites locally as well to sort of identify patients, and we've been quite active out on site to generate, I mean sort of, interest, excitement and kind of, how should I put this, kind of willingness to participate. So many times, it's just sort of -- if you are -- if we are quiet and if we don't show ourselves on the sites, then there are competing studies that might take precedence. So the more active we can be on sites, which we have been across the different countries, that helps, of course. And then the protocol has also added some to it. But the protocol hasn't been all of it because what we can see is that sort of the majority of the patients are clearly second line patients, and they were eligible as part of the previous protocol. So it has contributed to some extent, but not all of it. So it had a mix of all things, including our sort of stepped up local presence on site.

Got it. And as far as site that are still in total 13, is that correct?

Say that again?

As far as total sites at right now, is that still 13?

No, it is 14 sites. 14 sites. So 6 sites in Korea and 3 sites in U.K. and the remainder in Spain.

Got it. And for the Phase IIa expansion phase, I guess, sort of roughly when we expect that to initiate to just sometime this year?

Yes. I would say sort of. We wrote -- I think we wrote in the press release this morning, and I might have it on the slide here as well, near term. And yes, I mean, sort of we -- as we've said before, we are -- we've been sort of eagerly looking forward to open. We did have an ambitious plan to maybe even be able to sort of open it at the end -- before end of 2022, and that was maybe a bit overly ambitious, but that provides a bit of insight as to sort of the opening -- we're not anticipating the opening of that IIa to be too far away to presently.

[Operator Instructions] The next question comes from Richard Ramanius with Red Eye.

I wanted to continue on the last question that was asked. If you could define or -- as analyst and also investors, what the is one of the main triggers for fostrox that will occur this year that is more or less when do you think the Phase Ib will be finished and when do you think the Phase IIa part might report and then next would be initiation of Phase IIb, when could that be?

I think what we -- if we take them in first -- and if we start with Phase Ib. So the Phase Ib will conclude at different times for the 2 different arms. I think we've been reasonably open in the past that the fostrox, we're recruiting nicely. So we're very happy with the recruitment base. But we can also see that the lenvatinib arm has been recruiting with sort of at a slightly higher speed, but the interest in the pembro arm is very good as well. But the lenvatinib arm, I think has recruited a bit faster. So it will sort of very likely conclude first and conclude earlier, and that's the one that we anticipate that 1b to conclude sort of in that -- sort of, as I said, in the near term. And then as soon as that concludes, we will initiate the IIa sort of soon after that. Meaning then that Phase Ib beginning of the year for the lenvatinib arm and then -- initiating Phase IIa, meaning that sort of Phase IIa date back more in the second half of the year. And then if you then do the kind of the math and the planning, that would mean Phase IIb starts in 2024 as we have communicated previously. So sort of Phase Ib beginning in 2022, phase IIa second half -- sorry, '23, Phase IIa second half of 2023 and then Phase IIb starts in 2024.

Okay. So I guess there might be a delay of a 2 months between the two different arms than when the Phase IIb -- sorry IIa part initiates or something like that?

Yes, that will be -- it's difficult to say sort of the timing between the two. We are quite sort of comfortable in sort of saying that sort of 1 of the 2 arms would open in the near term. The other arm, it sort of -- it depends a little bit on the number of cohorts and how far you go, et cetera. So I wouldn't say -- I think it could very well be 2 months, but it's difficult to say and promise that. But the one we are eagerly awaiting at least the first arm to open -- Phase II arm to open in the near term.

Okay. You mentioned -- you almost answered my second question because you mentioned it's more interesting to carry [ TKI ] arm. So would you say the waiting list is longer on that one because you said people are waiting to be enrolled in the expansion part, does that relates more to the TKI part? And would that also be particularly in the Korean sites?

No, I think we sort of -- the interesting bit is that we are -- waiting list we have on both arms. We have been accruing the lenvatinib sort of combination arm a bit faster. So maybe there's been a few more additional patients from a kind of waiting list perspective. But we're seeing -- the waiting list is there on both arms, and we have patients across the 3 different countries on that waiting list. So I wouldn't say that sort of -- I mean there's a bit more Korean patients for the fact that we have than the other countries because we have in 6 sites. That's quite a few in Korea. And HCC is more common in Asia than it is in Europe. So by mass, you would have more patients. So maybe there's a bit more Korean patients on the waiting list, but we're seeing similar interest and engagements and patients waiting across the 3 countries.

Okay. Okay. Makes sense. Lastly, I wanted to ask you about the Tango project. You mentioned they will submit an IND this year. Do you think they could initiate the Phase I trial this year because I assume that will be associated with the milestone payment?

The answer on the last one is, yes, i.e., on the milestone payment. And clearly, you don't open an IND unless you -- I mean they're opening an IND because of intention to move into the clinic and move into Phase I. There will always be a bit of time lag between IND and Phase I. So it depends a little bit on how quick they are on opening the IND, but sort of -- yes, we are anticipating sort of as they communicated now that they're opening an IND, that means that they are intent on moving into Phase I and Phase I will provide a milestone payment. I don't know if Magnus wants to comment anything further on that?

No, that's correct. But we have not disclosed yet the amount on milestone.

This concludes our question-and-answer session. I would like to turn the conference back over to Jens Lindberg for any closing remarks.

Thank you. And operator, we can move to Slide 27 just to sort of say that sort of upcoming activities at sort of a number of different conferences. We are also, from a data perspective, our next time for data sharing will be at the AACR Conference, where we will sort of this kind of be sharing additional nonclinical data, building on what we've shown today. And as I alluded to earlier, we're looking at both combinations, but we're also starting to look towards sort of triple combinations and seeing how fostrox -- adding fostrox on top of 2 other drugs, what that looks like from a clinical perspective. But with that, thank you all for calling in. Thank you all for engaging. We are happy with the progress we have seen under 2022, but we are even more so looking forward to sort of starting to see the first clinical data on both the combination arms and hopefully rapidly taking the fostrox program forward in primary liver cancer. So thank you all.

The conference has now concluded. Thank you for attending today's presentation. You may now disconnect.