Good day, and welcome to the Molecular Partners First Half 2023 Results Conference Call. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question-and-answer session. If you would like to ask a question during this time, simply press star followed by the number one on your telephone keypad. If you would like to withdraw your question, again, press the star one. Thank you. Seth Lewis, Senior Vice President, Investor Relations, you may begin your conference. Thanks, Rob. Good morning, everybody, and good afternoon to our friends in Europe. My name is Seth Lewis, Senior Vice President, Investor Relations, and I'm joined on the call this morning by Robert Hendriks, Senior Vice President of Finance, and Patrick Amstutz, Chief Executive Officer. Management will be making a few prepared remarks, and then we'll open up for questions. A set of slides is available on our website, molecularpartners.com, under the Investors Presentations tab. We'll refer to the slides as we go through today's presentation. Please note, management will be making certain forward-looking statements throughout today's call, and that things may change materially from the time that this call has taken place, and we refer you to our website and latest SEC filings to ensure the most up-to-date and accurate information available to you. For those of you listening to this on replay, this call was recorded on August 25, 2023. Turning to slide three, with today's call, Patrick will take us through the highlights of the first half, along with a few updates subsequent to the quarters. Robert will provide an overview of our financial results, and then Patrick can provide a bit more in-depth information into the programs and outlook for 2023 and beyond, and then we'll take your questions. Before I hand over to Patrick, I just want to take a minute and highlight my enthusiasm for where the company is at this moment in time. Many of you who have followed us know that last year, 2022, started on such a high note with the success of ensovibep, and then thankfully, the pandemic waned, but so did the potential for near-term revenues and procurement of government stockpiles for ensovibep, and we all saw, you know, how that has affected all of us. Now, that's a trade-off that we are glad to make, but back then, you know, we told you that we were well-financed to move forward in the rest of the programs, and everything was on track and, you know, strong from an internal perspective. Today is really the one of those days where we're gonna start to show you that that is so true. Since then, we're able to show positive data with MP0317 at ASCO. 533 is now in the clinics, and it's making its way through dose escalation and entering a phase where we can see a real opportunity to help patients. I'm just personally very proud of the team and all we've accomplished in this past year, and I wanted to highlight that before we started. With that said, let me pass it over to Patrick for an overview of the first half. Hey, thanks, Seth, and thanks also for the overview that I'm totally backing up. I'm now on slide number four, and I will just kick off with setting the stage just for those who are new to the story, what are DARPins and what is our strategy? DARPin stands for Designed Ankyrin Repeat Proteins. These are somewhat bridging the gap between small molecules, and antibodies or large molecules. They're, they're a tenth the size of an antibody, and we really use that either for the small size in our Radio DARPin therapy approach, or we use the small size then to create multispecific, like 533 or 317, that I will be talking about. We have been doing this a while, and so we have also seven clinical stage compounds, of which six have shown results, and each of them really did exactly what it was meant to do. So we have also a lot of clinical validation on not only the scaffold, but also the modes of action and our ability to predict that. Now to the strategy. So how do we apply the, our approach? The first and foremost is we are focusing on the unique DARPin solution. So we solve problems, and I will talk about the problems, that other engineering approaches with other small molecule antibodies will struggle to do so. So it's all about the DARPin uniqueness, meaning if we want to have a solution, that has to be meaningful, and it also is very difficult to be copied by others. The meaningfulness is the next part. So we're aiming for true patient value, and true means for us a big delta over current standard of care, a high medical need. You will see some of these patients are really that blind and have no other hope than our drugs. Early clinical readout, very important. We, as a small biotech, we don't have the funds to run huge head-to-head trials to find out if we are marginally better than another compound. So we invest in finding drugs that in their phase I, early phase, 20, 30 patients really show themselves. And that is really also very much the hope then for 533, our AML drug. And we don't do that alone. We do partner with world-class partners, and we use the partnership open. It can be an academic, it can be a biotech, or it also can be a large pharmaceutical company. Let's move to slide number five and just quickly look at what have we achieved in the last year. What are the highlights of the first half of 2023? 533 is on top for a reason. It is the key asset where we see most value being built. It's a tetraspecific or a trispecific T-cell engager, but so it has four specificities. We started early in the year with the first patient dosed. We have seven sites open in Europe, and we are now in dose level four. I will talk about that, and that's really where exactly we want it to be, so great execution. Now entering the zone where we expect activity. 317, Seth alluded to, our ASCO abstract, where we could show biological proof of mechanism. We show a favorable safety profile in a mode of action, CD40 agonist, where others, so far were struggling to find that. We are in a class of next-generation CD40s. It's absolutely exciting to see how we can use that biology to support other checkpoint approaches. Radio-DARPins, that is sort of our research focus of the last year. We have made great progress in reducing kidney accumulation. I will talk about why that is important. We have selected DLL3 as our first initial target. We have more in the making, and obviously also in our Novartis collaboration, deserves to note that it's progressing well. On the operational side, I would like to take a moment to also, you will have seen that, to thank Nicola Leupin, our Chief Medical Officer, who is stepping down for the last four years of work. This is a personal decision, so it is not linked to what we are doing. He wanted to take a time out, and I support that also as a personal friend, that he does this. I'm very grateful for what he did, and I'm as grateful that he recruited Philippe Legenne, who is now stepping in seamlessly as acting chief medic. Philippe has set up and run the clinical trials that we will be talking about, and he has an impressive track record going back to J&J, GSK, Novartis, with a focus in oncology, with a focus in the U.S., also important for us, E.U.. He joined us two three years ago from Amgen, where he was the therapeutic area head oncology, hematology in Europe. So thanks to both, and great to have a team that can seamlessly take over in such a moment. Last but not least, and Robert will talk about this on the coming slide, I do want to point out our strong cash position. We have CHF 218 million in cash, and that brings us, and we define the runway well into 2026. With this, it is my pleasure to hand over to Robert, and I will then take the word back just to give you a bit deeper dive into our pipeline. Thank you, Patrick. We're on slide six at the moment. I'd like to briefly run you through the financial highlights and the key figures of the last six months. My name is Robert Hendriks, and I'm the VP of Finance at MP here. The numbers you see are stated in million Swiss francs, and more details can be found in the press release, as well as in the appendix of the presentation. The entire presentation is also available on the website. And then moving on to slide seven. When we are looking at the financial highlights for the past half year, I'd like to focus your attention to three bullets here in particular. As already indicated by Patrick, our cash position, you may recall that last year we ended just under CHF 250 million. We're now at CHF 218 million, so that's a cash growth of CHF 32 million, which is well in line with our expectations. We had no additional cash coming in from collaborations in 2023. Secondly, I'd like to focus on the updated guidance for the full year. We are guiding now that our operating expenses are ending up in the CHF 65 million - CHF 75 million window, and this is down from the previous window of CHF 70 million - CHF 80 million. The reduction is largely based on the actual numbers that we see after the six months and the current expectation of the development of the cost and, of course, also of the workforce. In line with the past, we will not guide on revenue. And to be clear, again, this guidance is subject to the progress and changes in our pipeline. Thirdly, also already mentioned briefly by Patrick, on the runway, we feel that we are now funded well into 2026, and that's a slight change from the into 2026 we had, put out earlier, again, excluding any potential payments from partnerships. And we feel that this runway puts us in a very privileged position in the industry as such. I think that these three bullets combined are important to note as they reflect the, the solid financial state of the company. If I then move on to slide eight, where we see the comparison with last year, the six-month period. Again, focusing on a few numbers. Firstly, if we look at the revenue number, clearly the CHF 0.5 million to this period as compared to the CHF 185 million last year. You may recall that the 2022 number was largely driven by payments that we received from Novartis, from our COVID compounds. And that was, or that is clearly not recurring into 2023. The CHF 3.5 million this year relates entirely to the collaboration with Novartis on Radio-DARPin Therapies. The number has both an element of recharged FTE as well as a recognition of revenue from the upfront of CHF 20 million that we received in late 2021. As per today, we still have around CHF 7 million on the books that will turn into revenue in 2023 and 2024. Secondly, on this page, the operating expenses. You see that they are down for the comparable period. A number of elements are driving this, but just to highlight a few. Early 2022, we did invest largely in the drug substance and the drug product for MP0533 that is currently in the clinic. With this cost not recurring, we did clearly invest also more in our research, our basic research, and the radioligand pipeline. But overall, R&D expense is still seeing a reduction year-on-year. An additional reason for the reduction would also cover the smaller cost we incurred in 2023 for MP0310. That is the compound that we developed together with Amgen, and that is currently no longer progressing. Then on the SG&A side, an element of higher costs we no longer see in 2023 are the professional fees that we did incur in 2022 for the implementation of SOX. We started that before our market cap took a dive in first half of last year. What we also see, again, on the SG&A side, is the benefit, already a bit in the first half, but definitely, as an element in the full year guidance, that we have a fairly strongly reduced number of D&O insurance. The market there picked up, and we were able to get a very significant saving. As a general remark, we are and remain diligent and careful when looking at our expenses. We do feel that we are cost-effective, and we run a tight ship, and that remains on course to deliver on the promises. Thirdly, and lastly, a quick view at our FTE number. You see a slight increase year-on-year, to the current 169, and at the end of last year, we were at 175. So again, it's last year... End of last year, a small reduction. Combined, again, we think that these numbers show the strong financial base entering into the second half of 2023. That will allow us to continue to invest in our innovative pipeline and to bring drugs to patients. Thank you for your attention. Any questions, I'm happy to take at the end of the call in the Q&A session. And with that, I hand back to Patrick to tell you more about the R&D programs and the scientific outlook for the year. Patrick, back to you. Hey, thanks, Robert, and thanks also for all the great work you and your team put in to put all of this together. I just echo, we're really cost-effective, as you see, moving forward and keeping the budget well under control. I'm now on slide nine, where I wanna start with the R&D update. Moving to slide number 10, where you see the pipeline chart. You see on the top our clinical two program, 317, 533, that I will talk about. We have immune cell engagers. I will touch on the outlook on those, and then I will also highlight the Radio-DARPin therapy platform. Today, I will not talk about virology, which is earlier in stage, and also not about abicipar. Let's move to 317, the most advanced asset. Just quickly going back to my intro, what is the problem? What is the problem statement there? And the point here is that CD40 is an agonist of cells and, antigen-presenting cells, including B cells, dendritic cells, macrophages. If you now activate, CD40 on a systemic level, and you see that human that is glowing red, that leads to what we would call exaggerated systemic immunity. I was taught by our translational group that's the best way to phrase it, systemic, call it, effect, in this case, turning into side effect. At the same time, these cells, activations of these cells have the potential to turn, call it in very simple terms, a cold tumor into a hot tumor, because this is the beginning of an immune reaction against, tissue, or in this case, hopefully the tumor. So what we try to do is use FAP as a localizer and activator. So it's not only localizing, it's also the clustering, the local cluster of FAP, to bring CD40 together, activate these cells, have no systemic exaggerated immunity, but a lot of local immunity building. We added the next slide, and please, this is by no means exhaustive. It should more highlight how this field of CD40, where many companies see value in this pathway, has evolved over time. Has evolved from full antibodies showing side effects being stopped, moving to two FCs, where the jury is still out, to, I call it, the bispecifics or multispecifics, where we, it's us, Roche and Genmab, that are pioneering that space. And what we can now add to this table from where we sit is the FAP-CD40, and we can talk about presently explored doses of 10 milligrams per kilogram. So far, so good. We also, at this dose so far, see no exaggerated systemic immunity. So from where we sit, we think this is definitely a valid approach to unlock the CD40 activity. On the next slide, I'm now on slide 14. This is a stated update, so I'll quickly focus on the chart. We're now in the last cohort. It's not the highest, but it's the highest per week, so it's the 6B with weekly dosing of MP0317. I'm jumping now to the ASCO results. We presented there the highest dose, but that was every three weeks. On safety, we have a favorable safety profile there. One DLT that was not confirmed, so we could not confirm back that that was a real stopping of the trial at that dose, and we would have to go one down. So far, the highest doses hold, and we are now finishing the trials or the enrollment. We'll look at all the data to then decide at what dose or what dosing regimen would we suggest to move forward. Moving forward would happen in a combination, so we are definitely reaching out to interested parties to run combination trials, as CD40 alone can kick-start the immune system, but it does not. It's not enough just to dose this drug to help the patient. You will need to combine it with other immuno-oncology or other drugs. Just one slide we added here, as sort of seeing is believing, and I like this one here, where you have a biopsy, prior treatment, and post-treatment. On the left-hand side, you see staining for CD40, CD11C, which is for dendritic cells, FAP for the localizer, and then the DARPin. You see, obviously, prior to staining, there's less of at least the dendritic cells and no DARPin. You after dosing, this is cycle two, day eight, you see, the DARPin is now there. It co-localizes with FAP. That's what you would expect, as it binds to FAP. It activates CD40, so you also have more CD40 there, and you now, now see infiltration of the dendritic cells. So this picture really nicely demonstrates what the drug does without any side effects that would hamper it from exaggerated systemic immunity. Let's move to another molecule. This is 533, and you will note one difference from 317. 317 is of the older generation, where we still need the combination trial. 533 is the new generation, the new strategy, and here we do expect stimulation activity. What problem are we solving? AML is not a death, only a deadly disease, it is also complex, and it's complicated because of two or three different things. First, there's different cells with different targets. There is not one clean target like a CD20 on B cells, but you actually have different targets that are expressed on AML cells. And when we speak about AML cells, these are blasts, and in our view, leukemic stem cells. But these targets are also shown on healthy cells to a lesser degree, and especially also likely mono expressing. This is all summarized on slide 17. So there is a way to discriminate, but you need a molecule that can discriminate mono expressing cells from multi or co-expressing cells of these targets. So that's what we set out to do. We created binders to CD33, CD70, CD123, linked them to our T-cell engager. Actually, we're proud that this is the first non-antibody T-cell engager in the clinics now, and has life extended with HSA. In the final combination, we had to screen 8,000, in our case, more than 8,000 combinations, to find those molecules which would do this discrimination. On slide 19, we have depicted on the right-hand side, this Venn diagram, again, showing it. You have the triple expressing cell in the middle. That's in this case, a cell line. We did knock out the individuals, first alone and then the duplets, to quasi-reconstruct from an AML cell line, the situation we expect to see in a patient. We then added MP0533 on the left-hand side, and you see how the line is shifted from the left to the right, so we are less killing the mono expressing, and also the plateau is lower down, so we also don't kill all the cells because the expression level is simply then too low, even at high doses of that respective target. And that's how we want to open a therapeutic window on targets that have been tested, but again, were limited due to killing of healthy cells and side effects. We started this trial early this year, and we're really proud and big thanks to the team for the good progress. It is not an easy disease. You will, you will know that. So also running trials can be difficult, and we, with our very close proximity to these sites, were able to execute flawlessly and now are in dose level four. And you see dose level four is already a bit darker blue, but the next dose levels are really the ones where we expect this molecule to be active, and we expect first signs starting in dose level four. So big thanks to my team for doing it, but also for the, the sites and the KOLs that are really enthusiastic in pushing this trial forward. And this will be the key readout in the second half of this year. Moving now to the Radio-DARPin platform. Slide 24, 22 here shows you sort of the promise and the first problem. What you see on the left-hand side is a prostate cancer patient, PSMA positive, treated with a PSMA-targeting actinium product, and you see within a few cycles, you move to the right side, and this patient is cancer-free. At the same time, you see one first problem, which is the kidney, that larger molecules and protein drugs will bring the radioligand to the, or will bring the radioisotope, I should say, to the kidney and also destroy the kidney. This is not true for small ligands. Moving to slide 23, so the RLTs. At the same time, these RLTs, the ligands, are restricted to targets, or you have a good cavity, and you can make a good high-affinity binder, but that limits your target range. So what we're trying to do is bring the broad target range, high affinity of DARPin that is proven into this class, but also reducing the kidney accumulation. Our team has worked very hard, and we were able to present data at different conferences. Moving to slide 24, and you see, first, we did a stealth DARPin, that's the dark blue checkered line, 80% reduction in this case by re-engineering the surface of this mono DARPin. We added an orthogonal method on top, and that again added 61% reduction. So we're at 14% injected dose per gram in the kidney. As you see on the tumor side, this did not affect the tumor, and that's where we will be focusing next. By slightly engineering half-life and linker, we believe we can bring up the tumor to interesting levels to reach the tumor to kidney of one to one, which is the basis you would need to move a molecule into the IND candidate stage and towards the clinic. So we're very much approaching that, now focusing on increased tumor uptake. I want to mention on slide 25, our great partners, Novartis, leader in this field, and less about the deal than the collaboration. So we're joining forces with them, very much exchanging ideas, results, and learning from them. They are learning from us, and they have two tumor antigens that are exclusive, and we keep all others, including DLL3, which is the one we are moving forward, or it's most advanced in our pipeline. So before turning to the outlook and your questions, let me quickly summarize and actually talk about the outlook. I think this is maybe the most important slide in the whole deck. I'll again start with 533, excited to see initial results, so not only dosing, but also what does the molecule do? And again, we do expect T-cell activity, and with that, we would obviously expand the trial in Europe, but also then to the U.S. We have 317. Here we guide toward 50, when we want to show more data from the higher dose cohorts, and we do believe that the higher doses do help for more activation, and we are engaging with partners for combination trials. And at the same time, we are very much looking forward to our competitors, Roche, mainly hopefully to present some data on their FAP CD40. On the Radio-DARPin side, I was pointing out before that it is all about now tumor accumulation to bring the tumor higher up to reach the one-on-one. We are evaluating more targets that we then can put into that pipeline, and once we want to move forward, we will also need partnerships with the radionuclide, and there we are discussing, and you should also watch out for, collaboration agreement with isotope providers in this space. We will also start to talk about the next generation of DARPins, that, from the platform, and here, keep the switch ideas in mind. Before kind of thanking and opening for questions, let me reiterate what Robert said. So we're running a tight ship. We have CHF 280 million in cash. We're funded well into 2026, so all of the above is well into our cash runway Let me, before opening for questions, thank, first of all, my team. That was super hard work to get all of those trials, all the research that I could only touch on a bit, forward. Great progress, great teamwork, so big thanks for that. Then obviously also the investigator and sites in the clinical trials, and most importantly, all the patients in our trials. With that, I would thank you for your attention and for dialing in and your support of what we're doing, and open for questions. Thank you. At this time, I would like to remind everyone, in order to ask a question, press star, then one on your telephone keypad. Our first question today comes from the line of Diana Graybosch from Leerink Partners. Your line is open. Hi, two questions for me, both on... one on the tetraspecific and then one on CD40. So on the tetraspecific, you say that you think that dose level four is when you start to hit efficacious doses. Can you talk through why specifically the rationale for that dose level four, and if you are seeing PK and PD biomarkers in the clinic that are supportive of your preclinical modeling? And then the second question is about CD40. We recently saw a deal here with Pyxis acquiring Apexigen, and I wonder if you had any thoughts on the valuation of that deal and how your molecule compares to Apexigen CD40. Thank you. Good. I will definitely, I can take the first. So, why dose level four? I mean, and it's a great question, and we have quite some understanding on the modeling, which we do in preclinical stage. So we have a group that is expert in that. They advise on which dose levels we have to take, and maybe I'll start there. As we did not have cross-reactivity to cyno or actually all the other species, we really had to go for a MABEL dosing. So the first doses are so low that you don't expect anything. It's even difficult to measure a PK trace at those levels. You're quasi at your lower level of detection. So this is, and we didn't change any of the coloring, so these are really the predicted activities. Now, obviously there's the clinical signs you follow, and you will want some CRS, but not too much. And we are also measuring all the cells. We are measuring the cell counts, and in this case, unfortunately, it's also survival, as these patients are very ill and will also progress very fast on this, in this disease. So with that together, I think we can easily get a good understanding, is the drug doing something or not? And obviously, blast count and then also regrowth or leukemic stem cells, the MRD negativity, are things we'll be following. Obviously, not for me to comment today, but we will definitely guide and then show an update in the time we get around ASH. On the CD40 Apexigen deal, I find that difficult to judge, so I mean, that's in the eyes of others. Apexigen definitely had nice early data that then maybe was a bit less impressive going forward, but it's always to find the right application for that drug. If Seth or others want to comment on that or more on the deal, please go for it. I would not feel in a position to compare valuations of these drugs. I think our table helps to put aside why we think we are different and why we think we have maybe a more open dose range. But then again, it has no data published except for ours so far, showing that that really opens the therapeutic window and gets the full biological effect possible in the tumor. But Seth, if you want to comment, you are always close to the deals and competitors. Maybe you have an angle on it. Yeah, you know, I obviously, as you said before in the slides, Patch, there are what we consider that second generation with the FC tuned, and clearly from a localization activation perspective, we just have designed the molecule differently. And, you know, I think they're at a time and place, at least in immuno-oncology, that we all are, where, you know, single agent activity is preferred. And while they have shown in their data, I think certainly some limited activity in that regard, you know, we know that folks are looking for a little bit more when it comes to the data and people... This isn't 2019, 2018, whatever it happens to be, and people aren't handing out checks for, you know, a second molecule for their IO-IO franchise. So, from our perspective, having the funding in place and having the ability to further differentiate our data sets among the class, as Patrick referred to, of sort of this next generation with Roche and even the Genentech or Genmab, BioNTech molecule, I think we have a bit of patience and flexibility- Mm-hmm. that maybe they didn't. And I guess that's, I would just comment on that in regards to the valuation question. One quick clarification of the answer to the first one. So how many of the doses are sort of MABEL doses, where you really can measure almost anything? And which is the first dose where you start to see meaningful, and measurable PK/PD? I'll refer to the slide deck where you see, and I mean, this is sort of the way we depicted. We are not in a position to give those levels, but obviously the first two are very low. That's why we're also just dosing one to three patients, so don't expect anything from there. Then those level three is maybe the first where you want to have a bit more patience. I think as of those level three, you expect to actually see drug. And now with those level four, we're entering the zone where we would also start to expect activity. Great. Your next question comes from the line of Richard Vosser from JP Morgan. Your line is open. Hi, thanks for taking my question. Just to follow up on MP0533, probably on that dose level three then or, or maybe the lower doses, can you say anything about the side effect profile at this point in terms of what you've seen, how clean it is? You mentioned you want to see not too much CRS, but some, you know, any color you can give there would be useful. And then just on, you know, MP0317, in terms of partnership discussions, you know, would you look to co-fund those? It sounds like, you know, you need more data first from this weekly cohort, but after that, would you do another trial where you provide drug and co-fund, or how should we think about the partnership? Yeah. Thanks, Richard, for both are great questions that we obviously look into closely. The first, I simply can't comment. So, so we are following the trial, we are looking into that, but at this point in time, we're not commenting. What I can say is that those escalation was seamless. You see where we are. This is really great execution. We had many also investors asking us, are you not a bit aggressive starting an early year and then wanting to show results? Because end of, end of the year with the, the stage you are in, and, and there our confidence and also the, the strong support of the science, really, that's the thing we can add at this point in time. 317, also great question. I think there, it's where we are today. We're in the third generation, the only ones that have really shown data. And I do think also we would rather profit than, than kind of being set back by good data by our competitors in that third generation. We will not fund massively into additional trials for 317, as at one point in time, as I said before, this will be a combination play with another IO drug that is not in our pipeline. It's not there, and we're not acquiring one. So this will be more strategic for a partner. I think it's really about sort of how do we facilitate to get the data of those combinations. As you say, it could be a combination trial, we could co-fund, we could maybe run some safety work to support that. So those are the thoughts. It will not become a major investment, but maybe we'll invest in one or the other safety trial because the combination work would need to be done. But then again, ideally with a partner who has a strong vested interest to move it forward. I hope that helps. These are a bit open questions that at this point in time, we'll have to also answer in an open way. No, sure. That's fine. Thank you. Maybe, Patrick, from my perspective, I can just add. Yeah, just one thought. I think it's a great question, Richard. I think it's important to pull out the fact here that, you know, this, if you ask anybody, you know, within our company, 317, this is, this is a drug. This, this is working as designed. This is doing what we expected it to. It's performing mechanistically as we've asked of it. And, you know, there are other programs historically within MP, throughout our history, where maybe it wasn't the right patient population, or maybe it wasn't the right molecule that was needed because there were other things that were out there at the time that would otherwise be utilized. And, I think with this one, we're being exceptionally thoughtful about how to make sure this program finds its way forward appropriately, because the activity we've seen here is exactly what we would have hoped for it, and the, the enthusiasm and the positivity around this program is high. So I think while we're a bit reserved in what our, you know, public thinking is at the moment, I can only reiterate that the enthusiasm and the expectations for this program are, are high. Thanks, Seth. Your next question comes from the line of Michael Nedelcovych from TD Cowen. Your line is open. Hi, thanks for the question. Patrick, first one on MP0533. When we see the data at the end of the year, can you help us set expectations? What would get you excited when the data are released about future development of the compound? And would it be efficacy, safety? What should we focus on when we see the data? And then the second question is, when we think about MP0533, your Radio-DARPin platform and your Switch-DARPin platform, looking ahead, let's say, two years, what do you anticipate will be the, the major focus of the company and the avenue into which you put your, most of your R&D resources? Yeah, thanks. Obviously, also a very good question. Thanks, Michael. Let's just guide first a bit for MP0533, and it's good that we're here for end of August and ASH in a clinical trial. Timing is just around the corner. So we will not be able to give a lot of data points there, but we definitely will be able to talk about safety at relevant doses, as you pointed out. Are we seeing some CRS, but not too much? Then also on the efficacy, well, do we have responses or not? And we need to see some responses. How that could look, I mean, we'll definitely follow the blast. We will follow how the patients are doing, and we will only be able to see the first part of those responses, obviously, just given the time. So no durability, no how long the response would hold, things like that we will not have, and we will maybe be able in those range five with data and then six, seven to come. So it will be an early data. So managing a big expectation. At the same time, we can see responses, and that's nothing we had with MP0317. So obviously, it's really right in between. I do think it's important that we can show responses then. That's where we are today. This will then create sort of the basis for further planning to exactly what you were asking, how will then the investment space look like? Because you're investing in a molecule that you think can win. Today, we're very positive about five three three. We are we also like, or like, we don't like the outcomes in AML, but we have some follow-up ideas in that space. So if five three three looks good, I'll branch to your second question. We can also work on additional generations of AML drugs, and that's then based on switch concepts and the like. So if five three three looks good, you go fast forward a few years, it could be that we have two, three, four molecules from also a switch platform in AML. That's a scenario that is possible and can materialize. Obviously, RLT is then a bit different. That's, and this would be a therapy, the area focus. RLT is a technology platform focus. We hope to be able to find the Holy Grail of the one-to-one, or even better, make that broadly available to targets. So given we will solve that, the question will be what targets and in what settings? That will be one of our focus areas. Can we also work on target identification, validation for this space? So that's something I would hope to have in a few years, much more clarity, plus the collaboration to secure the isotopes. So if you want to do that. And so you will be, if both work out just on these two settings, there you will have an AML franchise and an RLT franchise that are different, but both are groundbreaking, solving key problems that you today have in the clinics. Thank you. I hope that answered a bit how the thinking, how the outlook can evolve from here. And again, if you would like to ask a question, please press star, then the number one on your telephone keypad. Your next question comes from the line of Laura Faiser from Octavian. Your line is open. Yes, hello, good afternoon. I just may be following up on the questions on 533. I'm wondering here, at what time point we can expect a go, no-go decision from your side, and also what is needed for a go? And then, maybe related to that, I'm also wondering how much R&D budget you need to bring MP0533 to the next value inflection points, and how, in general, we should think about your R&D progression over the next one to two years. Thanks. Yeah, no, thanks for the question. So let's put it like that. I think in the next six months, we can go, let's call it no-go continue. So we will not have the data to double down and, and start to think about a say, a pivotal phase II/III. But what we will see is, do we have effects? Do we have to understand patient characteristics? Are there subgroups? Are there difficult-to-treat subgroups where we are effective? And really form our thinking about what the next steps of development is. And here, the team is already full force on. So they're looking at all of this. We're preparing all scenarios and the corresponding next trials that you would want. Obviously, this is nothing I can put out today, but you can guess we are well prepared. To run the trial from where we sit today to the goal, I think that's where we were guiding with including the expansion cohort there. I think that's those 20-45, and hopefully it will be more to 45 patients. But with 45 patients, we should be in a good position to also then reach the go answer. That's the next year. And this is really where we then could define how the next steps look. But that we would have a drop, that this is valuable to go forward. That's early next year, it's earliest, I would guess. The costs you were asking, so this is not massively expensive. This is well within the budget that Robert was talking about. We're always running these trials. It's in the budget. This is all in what we're doing. Where we would add, obviously, costs is if we start a phase II/III trial, but that's based on good data. Okay, thank you. This ends our question and answer session. Mr. Patrick Amstutz, I turn the call back over to you for some final closing remarks. Yeah, thanks. First of all, thanks again to my team, everyone involved. Also, thanks for all the great questions. I love that we are now focusing on the positive possible outcomes and outlooks. I mean, this is great. To sort of close the circle to test, the last year was all about execution, was to get into the position to now collect the data, to have those forward-looking discussions. I think I'm personally glad we have progressed so well. At this point in time, you can say that was a year of steady, constant progress, but in our field, if you reach that, it means you have no setbacks, and that is everything but normal in our field. So big thanks to my team, but also very happy to be where we are. Looking forward to the next six months and beyond. With that, I would like to close the call and thank you all for your attention and fasten your seatbelt for the months to come. Thanks. This concludes today's conference call. Thank you for your participation. You may now disconnect.