Good day, and thank you for standing by. Welcome to the MP0712 update call. At this time, all participants are on a listen-only mode. After the speaker's presentation, there'll be a question-and-answer session. To ask a question during the session, you'll need to press star 11 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 11 again. Please be advised today's conference is being recorded. I would now like to hand the conference over to your speaker today, Patrick Amstutz, CEO. Please go ahead. Thanks for opening the call and the kind introduction. My name is Patrick Amstutz, and a warm welcome from my side to this webcast. We are here today to share the first Radio-DARPin human image and talk about the LEAP program and talk about the study to come. It was roughly two years ago when we signed the collaboration agreement with our partner, Orano Med, who will also be named several times in this webcast, that we come together and pioneer radiotherapy. Today, we are opening the clinical chapter of this story. I'm joined by Danny Steiner, Head of Radio Strategy. I have Philippe Legenne with me, our Chief Medic, and Michael Stumpp, who is the Program Lead. He will be mostly for the Q&A part of the webcast. Just two hours ago, Danny presented this data at the TRP conference in Amsterdam, the story behind the molecule, the mode of action, and he will be recapping that so that all of you hear this firsthand. We will hear Philippe's perspective of the clinical relevance and also the study design, and all of us can ask questions to the experts. Before kicking off, I just want to share a few thoughts on why this is a special moment for myself, but also Molecular Partners and the radiotherapy field. First of all, this is unique to this field that we have the opportunity, before we actually start the phase I, to have meaningful clinical imaging data of humans to de-risk, to understand, and to really speed up the development. That makes it also very cost-effective for us to develop such drugs. MP0712, especially with this mode of action that we will be discussing, capitalizes on the rapid internalization of DLL3, a target I will just come to, to improve a therapeutic index to then help patients. That will be most the core of this talk. This target, DLL3, is on cancers, mostly lung cancer, where we have a high medical need, and we need very potent approaches to create the therapeutic effect like radiotherapy. Let's kick off and move to the first slide, which is actually the disclaimer. We will be making forward-looking statements, but also going to now the slide number three that is sort of the introduction. I shared with you that it was only in January 2024 that we started and signed the deal with Orano Med. What you see here is really the combination of two cutting-edge technologies. On the one side, the DARPin, and on the other side, the isotope, in this case, lead-212. Together, we create a new modality, and that's what we're talking about today. We have engineered the DARPin to be kidney cells, and especially, we have optimized the half-life for matching the disease and the target, and Danny will be talking about that. While Orano Med is the leader and the pioneer in targeted alpha therapy, and we like lead and alpha as it deposits high energy in short time. For us, and this is important, I will come to that, is in short time means high impact. We have a low probability of escape and resistance and a great potential to synergize with IO approaches. If I frame the problem we're trying to solve, and Danny will talk about it, it's really we have a small cell lung cancer patient in front of us with a very fast-growing tumor, high chemo resistance, and a low copy number target. How did we go about to solve that conundrum to come up with a candidate that actually has the potential to help this patient? Danny, over to you. How did we try that, and how did we succeed? Thank you, Patrick. Very happy to present here from Amsterdam. Just been on the stage on sharing this data two hours ago. If we move to slide number four, and I'm now fully focusing on the first program coming out of the Orano Med collaboration, the DLL3 MP0712 lead-based program. What you see on slide number four is preclinical data showing on the left-hand side nice tumor accumulation at the four and 24-hour time points, low kidney values, and as per design, as Patrick mentioned before, elevated blood levels needed for the high tumor accumulation. On the right-hand side, you see the molecule is very efficacious at these two different dose levels, leading to strong tumor regression and complete tumor control. The key question that was raised here now several times at the conference, how did you manage for targeting such low expression numbers, and that's illustrated on slide number five, how did you manage to get such high tumor uptake while only having a couple of hundreds of receptors per cell? To understand this better, one from a scientific curiosity perspective, but also to inform us on next programs that are in our pipeline and new programs to be nominated, we investigated this, which is depicted on the next slide number six. Let me guide you through that data. On the left-hand side, you see a cell internalization assay where you're basically spiking DARPin, and what you can see, the cell internalizes, the cell expressing DLL3 internalizes this DARPin extremely rapidly. Within 20 minutes, you have more than 50% of the cell bound DARPin internalized. We then, if you move to the middle graph, we tracked what is happening with the DARPin by immunofluorescence assays, and what you can see, the DARPin nicely co-localizes in the endosome, which is stained here in red by this EEA1 marker. You can't see it in the lysosome because the detection of the DARPin is degraded in the lysosome. That will not be able, but you can nicely see it in the endosome. If you move to the right-hand side, and that's probably the most relevant part of that data, you can now do a similar assay against cell binding, but you measure the total fluorescence taken up by the cell, and you expose the cell continuously to DARPin. What you can see is the blue curve where you get a continuous increase in signal of fluorescence inside the cell, which is indicating that the cell can continuously pump in basically this label. The curve would even look more steep by using a radiometal, which is residualizing and staying inside the cell. Here we're looking at fluorescence-labeled data. Integrating this data and moving to the next slide, our hypothesis how this molecule, how the mechanism of achieving high tumor uptake despite the very low expression of DLL3 is twofold. First, from a biology perspective, DLL3 internalizes extremely rapidly and at the same time is extremely rapidly replenished, basically leading to a high apparent receptor density over time. The second aspect, the DARPin that we generated is able to piggyback on that internalization, so allows to follow that rapid internalization, and at the same time, the half-life extension we introduced allows the continuous re-feeding of DARPin, allowing to really continuously reload the tumor with that radioactivity. Finishing all the preclinical package, seeing good efficacy and favorable safety profile, we then decided to move into the clinics. That is depicted on the slide number eight, where we see we took a two-step approach. The first step is using lead-203, which is an imaging isotope with the same characteristics as lead-212. The imaging isotope is used to collect SPECT-CT images, which you basically can use for imaging the patient and for dosimetry calculation, which allows you to inform then the next step, which is the treatment with lead-212 labeled MP0712. Phase I has been submitted. The IND for the phase I in the U.S. has been submitted and is under review and pending of approval by the authorities. We hope to initiate the phase I before the end of this year. In parallel, we received a request from the team around Mike Sathekge, one of the key leading nuclear medical persons at NuMeRI in South Africa, to provide MP0712 for imaging and potentially treating patients with small cell lung cancer or other neuroendocrine tumors. In South Africa, a series of patients have been imaged using lead-203, and Mike Sathekge and his team will be presenting dosimetry and imaging data of the full series of these patients at the Diagnostic World Conference, end of January in Cape Town. Based on support from Mike Sathekge, we got approval to use one of these patient cases out of this series and present to you the data from that patient already today. If you move to slide number nine, quickly going into details of the patient and guiding you through that, if you focus first on the patient characteristic displayed on the left-hand side, it's a 69-year-old smoker, small cell neuroendocrine carcinoma of the lung. At referral, that patient was Stage three with a primary tumor located in the upper part of the lung. Treatment history, radiotherapy, and chemotherapy. Maybe quickly, let me quickly pause here. This profile of that patient with the stage and the pre-treatment history is what we believe gets as close as we can get to patients we would potentially meet in our phase I study in the United States. That patient received 5.1 millicurie of lead-203 labeled MP0712, and based on the assessment of those images, that patient was restaged into Stage four with additional four liver mets detected by that imaging. Let me quickly guide you through the data. I want to start completely on the right-hand side on the colorful image. That is a planar coronal projection. That is how nuclear medics look at these images, where you basically see the orange indicates the more orange or yellow the color, the more radioactivity. What you can nicely see, the radioactivity fully located with the primary lesion, which is indicated with an orange arrow, and the liver metastasis indicated with the blue arrow. If you move then to the left-hand side, the gray images, here, the more radioactivity you have, the darker the area. What you can nicely see, this is like four hours, 24 hours, and 160 hours post-injection. What you can nicely see as per design, we have a high blood pool at the early time point, which decreases over time. Very importantly, we have no uptake or very low uptake in any of the healthy organs such as kidney and liver. Now, focus is zooming in on the tumor. What you can nicely see at 24-hour post-injection, you already nicely see the uptake in the primary lesion as well as in the metastasis, which is still obscured by the high blood pool. Once the blood pool is down at 160-hour post-injection, you see even higher intensity of the primary lesion and the metastatic lesions. Zooming out and summarizing this, we see initial high blood pool followed by specific uptake in the primary and the metastatic lesions over time, and a limited accumulation in healthy organs in line with the mode of action of 712 and as well in line with the preclinical data. With this, I'm happy to hand over to Philippe to guide us through the next stages, which are ahead of us with that program. Thank you very much, Danny. We are going to spend minutes on that image, on those images, and I would like to bring a little clinical facet to them. You already spoke about the blood pool at four hours, 24 hours, and 116, but it is interesting to note that this is exactly, in fact, as we had predicted per our preclinical work. We can see that at 24 hours, when the blood pool starts to go big down, then the tumors emerge, and we see them most visible at 116. In fact, this is a very, from a patient standpoint, it's a pretty interesting image. When we were discussing this with the experts, Mike Sathekge first, this is a patient where the prediction of that blood pool evolution and those image evolution makes them think that it's a patient that could have been benefiting if treated. Okay, that's one. I would also want to emphasize two points. One is about the overall value of the SPECT. You mentioned that, Danny, but I want to reemphasize that basically the patient was presented as Stage three, but the value of that SPECT helped requalify that patient as a Stage four. This is important for the patient treatment. This is important for the clinical team to adjust treatment. Okay, that's the third point I want to emphasize, which is important this time for the development and for us developing that product. Basically, it's really the value of those early images that help us inform and de-risk to a good extent the upcoming phase I, which is now going to start very soon. I'm going to move to the next slide on slide 10 and describe a bit the phase I, which we are planning, which we are close to initiating. This i s a phase I, two-way study for small cell lung cancer and other neuroendocrine cancers. That study is a US multi-center study, and obviously, dose escalation around 712 therapy. On the bottom left scheme, some important points. You can see on the blue part that basically we have four dose escalation steps, so pre-compressed dose escalation starting at 75 megabecquerel, which is at effective dose already or close to effective dose. I really want to thank, in a way, all the inputs from the Orano Med experience already on that, and also the interaction that we are having with the FDA, and also the good quality of the prediction, which we had from our preclinical package. Nice compressed design starting at effective level. Obviously, patients will all get an imaging first, and then will be treated alongside one to four doses in the dose escalation. First, we focus on the small cell lung cancer, and then the green box is that at some point, we will branch and open other neuroendocrine cancers in green when we are close to an effective dose on the blue part. If I move on the right part, there is still higher medical need in small cell lung cancer. That means that if we get the right benefits and risks, the right signal of activity and efficacy, which we hope and anticipate, we should be able to still take advantage of a path for accelerated review and approval through in second line plus small cell lung cancer. There is an avenue here, and if we drive quickly and right, we should be able to take that one. Below on the right, you can see that in complement to that, obviously, as soon as we get a confirmed signal, we want to branch and open evaluation of combination with immune checkpoints, which we believe that the mechanism of action of lead and alpha in a way is the optimal complement to immune checkpoint inhibition. We also want to open registration with other neuroendocrine cancers, where there is a higher medical need too. A compressed and, let's say, accelerated path across those developments. That was, I'm going to move to the next slide, which is slide 11. One could think, why DLL3? DLL3, we have heard that obviously the cell engagers have started to be approved, and there are ADCs. In fact, when we speak to experts, there is high appetite for more modalities and specifically radiopharma. Why? Because all those three modalities first are potent and can act in low expressing tumor, low copy numbers. They have that in common in a way. What we can also say is that in the T-cell engagers, the tarlatamab, yes, it's approved. Yes, it's helping patients. It's great, but it still is a moderate response rate with a promising duration of response. We should not forget that there are side effects with T cell engagers, and not every patient can benefit from them, and not every patient is even a candidate for them. It's going to move into first line likely. Next to it, ADCs are promising antibody drug candidates. Basically, they promise a fairly high response rate, but for every time that we've seen ADCs in development, the duration of response is up to six months. They likely would move in first line. It really opens for this additional modality of radiopharma, which we are part of. We would like to first enter in second line, and we think that there is optimal mechanistical combination with immune checkpoints that could make us good candidates for maintenance in first line. There is space, and there is value for this as long as we move quickly. Those would be the main points I wanted to deliver on that slide. I think I can move to the next one, which in a way is a bit of a conclusion. We heard Patrick and Danny on the preclinical package and on the specificity of DLL3 internalization. I really want to emphasize this point of images today, which are starting to deliver. Again, let's listen to what Mike Sathekge will present at the end of January. This is really a very effective manner to inform and de-risk our phase I. What we have seen so far is highly encouraging. As also Danny mentioned, we have five R&D. It's currently in review, and we are expecting an opening of the first slides before the end of the year and initial data to be generated in 2026. I hope we will be discussing this with you in 2026 on the effect of those first cohorts. That is more or less what I wanted to say. Let me thank, I guess, first, I would like to thank our colleagues from Orano, and this is because of this partnership that we are there and so quickly. Then the NuMeRI Team, which is really working hard on helping those patients and generating some information and precious data. And the MP. Patrick, maybe you want to complement that thing. No, sure. No, and first of all, thanks to you, Philippe, and thanks, Danny, for presenting today. Also, my thanks goes definitely to our partners, and most and foremost to Mike Sathekge, who had the trust to do this trial with us, to the patients and their families that were in these trials. We have those, I think, roughly eight patients so far. Big thanks to all of them making that effort and being part of this trial. I also want to thank really the, yeah, you all for joining this call, for being with us, for joining the new chapter of radiotherapy with, let me summarize my conclusions, let's say, in three dimensions. I think first, we have MP0712, unique mode of action, and really slated to become the leading alpha therapy in small cell lung cancer. With that, we open the opportunity to build a pipeline on similar targets. We have a very good understanding how to now work with these low copy number internalizing targets and our technology. We have the capabilities on top of that to run this fast up to, as we now see, clinical data in a very fast, cost-effective way. The next stop is really phase I, where we want to bring home that value for the patients in the clinical trial opening in the U.S. With that, thanks, and let's open for questions. Thank you, ladies and gentlemen. If you have a question or a comment at this time, please press star 11 on your telephone. If your question has been answered or you wish to move yourself from the queue, please press star 11 again. We'll pause for a moment while we compile our Q&A roster. Our first question comes from Jonathan Chang with Molecular Partners. Your line is open. Hi guys, thanks for taking my questions. First question, what is your latest thinking on where 0712 fits in the evolving small cell lung cancer treatment landscape? Second question, what are the key learnings from this presentation as you think about what other targets could be addressed by a Radio-DARPin-based approach? Thank you. I can kick off, and then maybe I think it's one for Philippe. Where do we think we will fit? I think at this point in time, as Philippe pointed out, I think in a second and maybe third line setting, sort of last line setting in this case, a fast-to-market strategy as there is still a very high unmet medical need. When we speak to doctors, especially for T-cell engagers, the side effect profile can be inhibiting, while we expect that also our side effect profile should look superior to that. Also allowing more an intervention than a full line. Keep in mind, it's going to be two, three, four, five, six treatment cycles, and you're done. That's just one thing to think about. Long term, ideally, as Philippe pointed out, in a first line combined with IO, this seems to be quasi-ideal. We hope that that's sort of also the most logical setting to run a trial showing the combination of alpha therapy with IO to gain really long-term control over these tumors. That's where I personally hope this will go. Use the high medical needs for a fast-to-market strategy combined with a first line strategy in combination. Maybe Philippe, you talk a bit about branching out into other indications than lung. I have read that DLL3 is the next HER2 where more and more indications are coming up. Yes, thank you, Patrick. Just to reemphasize what you said, there is high unmet medical need and no good standard of care in second/third line. That is, small cell lung cancer has been abysmal up to very recently. There is a good glimmer of hope with the DLL3 coming in, and tarlatamab is helping the proportion of patients. However, it's only a proportion of patients. It's both, in fact, either tarlatamab or the potential ADCs in development will be moving in the first line. We also know that there is likely preservation of the expression across lines for DLL3. In a way, it's inviting, and really, there is that need will still be there in relapse. We can start there. This is where we should start, and there is where there is a quick path to approval. I think, as Patrick was also mentioning, it's a lot about first line and maintenance. We need to cure those patients or to keep them in the very long status in the maintenance part. Immune checkpoints are well established here. In fact, likely, all the biology points that radiation block immune checkpoints is a great duet. This is likely where I would like to develop that drug just as we get enough of good signal in relapse refractory moving early in. That's for the small cell lung cancer part. If we look at the other neck, and the more this area is now being researched, the more we find that DLL3 is relevant. There is not good standard of care post first line in other neck. Those are the avenues where we can further develop those. This is where we have a plan in our phase in our expansion to start evaluating that signal. Thanks, Philippe. Maybe I actually do love your second question, which is sort of posing towards pipeline build. Where does this leave us? I think it actually, the DLL3 understanding has really led to a renaissance of us looking at ADC targets. When the radiotherapy field started, everybody was saying, "Yeah, yeah, it's going to be like ADC." It turns out that the short-lived peptides are very different than full antibodies because of the internalization that we actually presented to you today. We are in a position to take the best of both worlds, to take targets that are rather low copy number and internalizing fast, as we did show, and build a set of programs around those where we think simple peptides that are fast in, fast out are likely going to be missing part of the therapeutic window. Next to that, we have targets that are just very difficult to reach with peptides, like the mesothelin approach we are doing. If you want, in the third wave, we are also looking into bispecifics. I am not in the room with Danny, but he is our Head of Radio Strategy. I do want to give him the opportunity to talk about this because he is spending a lot of time on that. We literally have three, four targets already in development lined up to be next. That is really because we have built the capability to, after we have a candidate, be able to test it with compassionate care setting, as we have shown you now, in a very fast way. Danny, maybe you add a few words how you see the next wave. I think you would call them waves of targets in our pipeline. Thanks, Patrick. You summarized it really well. I think for me, in the context of 712 and DLL3, the learnings we made, how to piggyback on this rapid internalization, rapid replenishment of low-density target antigens has been extremely valuable in that sense. For me, it almost becomes a strategic imperative to consider this for the future pipeline. That is why we have been starting and have already initiated activities looking at other ADC-validated targets where we say the biology risk in that sense is low, but we can exactly try to duplicate what we have been seeing on DLL3. That will be for us, I say this is wave number one where I feel like we can execute very fast. Thanks. One moment for our next question. Our next question comes from Charles Zhu with LifeSci Capital. Your line is open. Hi, this is Sue Elm for Charles. Thanks for taking that question. How many grades of alpha particle radiation would you expect to have a therapeutically meaningful effect on tumors? Similarly, to what degree are you able to exceed the EBRD radiation dose limits on healthy tissues, given the field's experience on renal dosimetry and updated radiopharmaceutical dosing guidance earlier this year? No, that's a great question. I will just quickly give the short answer, and then I possibly ask Michael or Danny to answer. Just to sort of, I can now reference the advanced cell, very beautiful advanced cell data on PSMA. I think they started to see activity when they were dosing around, I think it was 100, 100 plus, or even less, megabecquerel. That was in their second lowest dose or even lowest dose. The lowest dose had the stable disease on the post-trench and second dose, it was already leading to very good responses. Now, we don't know how much tumor uptake there is at their dose and what their therapeutic index is because that is just not known. We just know how much they gave. If we look at our dose, I think their lowest dose was 60, and we're starting at 75. From that part on, we think we're really on par. Now, how much they reached the tumor versus us, we don't know. The second part is we also are comparing prostate cancer with a lung cancer. We also don't know. I'll be happy. The healthy organs, I mean, that is part of the equation. We will see. I mean, our hypothesis is strongly based on that the blood pool will be not toxic. We'll see a drop in blood cell count, but it will come back hopefully fast that we can read those fast. That's what you see on the image. While the healthy organs look very, call it healthy. I mean, that's kind of the image we did show today. Maybe Michael or Danny, you're better on post to give the absolute numbers. I do not see if Danny wants to go first or. I'll go first. Michael goes first. Yeah. No, absolutely. Thanks, Patrick. I hope you can hear me. It is very, very difficult to say and to be sure, but obviously, we designed the protocol together with all the experts believing that we reach this range as of, say, also second, third dose. It is very important to have a safe dose delivered and hopefully within the grace we are expecting to get. The field has a huge range of numbers from, say, double digit, triple digit. It is very, very difficult to say where we will end up. I am very confident with the protocol we designed, we see what we need to see. Danny? Not much to add from my side. I think one of the key questions will be for small cell lung cancer patients is, at which dose levels do they start to respond? I think for healthy organs, we have a pretty good understanding in terms of EBRT limits. We know how much people or other companies are going above these limits for their clinical trials. Tumor uptake and understanding at which level tumor uptake will be sufficient in terms of triggering the desired response, I think that's really something we will need to now explore in the phase I trial, and we will be guided by the data. Thanks. One moment for our next question. Our next question comes from Mike Sathekge. Hi, thanks for the questions. I have three, if you'll allow me. My first question is on the competitive lanes. Can you offer up key points of differentiation between your program and other DLL3 targeted radioligands in clinical development, such as the one from Abdera or that from Novartis? I know the clinical data for 0712 are limited at this point and mainly illustrative, but are there any early hints from the empirical data that suggest your program is indeed differentiated? That's my first question. My second question is on your isotope of choice, lead-212. It seems like the most compelling image in terms of tumor to normal organ ratios is probably from 116 hours post-injection. I think that's several lead-212 half-lives later. I'm just curious whether lead-212 is the right isotope to capture the DLL3 replenishment phenomenon that you describe. I'll stop there. If there's time, I can ask my third question. No, thanks. All great questions. Let me quickly start with the differentiation. Let me start with the Mariana peptides. Mariana gets very nice tumor to kidney ratios. I would say the best published data is 15% injected dose. My guess is that is the max they will get versus our 60%. If you just do the math, a peptide that is not half-life engineered will just be able to load the cell once. We think for these low copy number peptides, the half-life is not ideal. The idea of fast in, fast out is not the best way to go. You might then dose several times that you could do, or you have to half-life engineer the peptide. That is the peptide side. You have the Abderra data. I think there the differentiation is that Abderra, as us, takes a longer half-life. We go with the HSA binder, which we really hope and we see has a very clean blood distribution. The Abderra has an FD-type molecule, so it will bind to immune cells. From the data that is published, you see a much more uptake in the liver. Keep in mind, we did show liver uptake. This is because we have lesions in the liver. The livers of our non-lesion patients look very clean, that I can say. From that point of view, I think we have a differentiation over the Mariana with half-life. We have a differentiation of an FD-type approach by our HSA technology, which for us positions us as the, let's say, winning strategy in this approach. I'm not saying you cannot half-life engineer peptides. You can. As of now, those are the three molecules in the clinic. Your other question is also super interesting. I mean, we also looked at the images and said, "Yeah, sure, why not test other isotopes?" In principle, there is nothing to hinder us from doing that. At the same time, do not underestimate the lead approach. As Danny nicely pointed out, the uptake is also there. You just do not see it because the contrast is so strong. In these images, you always go for the contrast. If you would just take out the liver and cut off the blood pool, you do see uptake much earlier than what you think you see here. Also, Danny presented the fast uptake. We are talking 30 minutes. Within a few cycles, so within 10 hours, we see good uptake. It is just hidden behind the blood pool. At the same time, you are also right. Nothing speaks against a long-lived isotope like actinium that you could also use. What you would not likely want to use is lutetium because our blood pool would be too high. With the long pathway and the broad killing, you would have too much side effect. You see a clean alpha strategy. You see a very good potential for lead and the upside, if you want, for other isotopes. Thanks. Again, ladies and gentlemen, if you have a question or a comment at this time, please press star 11 on your telephone. One moment for our next question. Our next question comes from Chiara Monteroni with Van Lanschot Kempen. Your line is open. Hello team. Congratulations with the update. Thank you very much for taking my question. I was wondering if you could provide more color on what to expect on the first phase I data next year, whether we are going to see some efficacy data points. Also, you have submitted the IND, and we'll start phase I year-end, pending regulatory clearance. I was wondering whether you foresee any risk there. Can you repeat the risk question, which is acoustically couldn't hear the second part of your question? What type of risk do we foresee? Yes. So you just submitted the IND, and we start the phase I year-end pending the clearance from the regulatory FDA. Do you foresee any risk over here? Yes. I think Michael can speak to it. What do we expect in, let's say, the first data set, but also how is, I guess, the question is, and it reaches a bit to regulatory shutdown in the U.S. and our interaction with the authorities. I think, Michael, you are in almost a daily exchange. I think you're best positioned to answer here. Yeah, thanks, Chiara. I indeed was in the U.S. last week in a conference. Obviously, logistics is a key challenge right now because not everyone is working. Many things have been piled up. We are monitoring this very closely. Luckily, our supply is within the U.S., so we do not have to cross the border. Luckily, FDA is really doing a good job in turning around questions. Nothing to look out from there. Should anything change, of course, this will have an effect. Also, starting upsides, of course, everyone needs to be there, the usual routine. We are very confident. We have very good collaboration and team inside to say this should be possible by year-end. Again, we are very grateful to everyone involved who makes this such a smooth process. What I can add in terms of study dynamics, again, we learned a lot from our colleagues from Orano Med, and there is a lot of interest in developing in small cell lung cancer. There is appetite. What we have selected is a team of investigators. It's a combination of, I would say, early starting sites, more on the private side, if I may say, and also academic side. We have a good mix. That is why we think that we should be able to have a good throughput. That is that. I think you were also asking on what type of data, when. Again, every patient gets imaged. We hope that when we start in January, ideally, we would be able to start seeing images fairly quickly. Then patients get quickly, in small cell lung cancer, patients get quickly dosed. I think that should develop fairly quickly in the first part of the year to get some early data. Thanks. Thanks, Chiara. Thank you. One moment for our next question. Our next question is a follow-up question from Mike Nedelcovych with TD Cowen. Your line is open. Hi. Thanks so much for taking my third question. This question is on the regulatory path and supply chain. I'm curious, if the trial enrollment and data cooperate and you can indeed pursue accelerated approval in the U.S., is it at least conceivable that you could have a registrational package in the next, call it, 18 months? If so, do you think that the Orano Med supply chain will be sufficient at that time for a reasonable launch? Thank you. I can start, thanks, Michael. I have high confidence in Orano Med's supply chain ability. I do not think 18 months is a problem. I am not sure everything will go so smoothly because, of course, once we have data, we go again to the agency, some review, some learning. None of my programs has gone as fast as the COVID time. If we had COVID times, I would say yes, absolutely. Generally, I think it is more in the time scale of two years. Quick question will change everything. Thanks, Mike. Thank you. One moment for our next question. Our next question is a follow-up from Chiara Monteroni with Ben Leshment Kempen. Your line is open. You can ask your question. Hi. Sorry. I already submitted my question. If you want, I can find another one. Thanks. Okay. I'm not showing any further questions at this time. I'd like to turn it back to Patrick for any further remarks. No, thanks again for this very good call, for all the questions. We are excited to now be moving towards phase I in the U.S. Obviously, shutdown is hopefully over, and we can progress fast. All questions are going in the right direction. Next stop will definitely be the phase I. Again, with the ambition to be the leading alpha therapy in small cell lung cancer and to branch out and build a pipeline building on this unique differentiation, now with clinical imaging data showing the value of our platform. A big day for us. Very pleased with the outcome and looking forward to generate value in lung cancer with 712 and building a pipeline beyond lung cancer. Thanks. Stay tuned, and we'll be in touch. Ladies and gentlemen, this does conclude today's presentation. You may now disconnect and have a wonderful day. Thanks. You're welcome. Thanks, Kevin.