Well, good morning, everyone. Thank you for joining us on this second day of TD Cowen's Oncology Innovation Summit. We're very pleased to be in the Molecular Partners session, and I'm very happy to welcome Patrick Amstutz, who is the CEO of Molecular Partners, and Seth Lewis, who is Senior Vice President of IR and Strategy. Gentlemen, thanks for joining us. Thank you. Hey. Thanks for having us. Thank you. We have a lot of ground to cover, but I was actually hoping to start with some of the basics for those who may be uninitiated on your DARPin platform, and particularly with a focus on your Radio-DARPin platform. Maybe you can describe to me and to the folks listening why DARPins are the right modality for radioligand therapy, and summarize your efforts in that area. No, sure. I can kick off, and Seth can go a bit deeper. In principle, we started as a DARPin platform company, and DARPin stands for Designed Ankyrin Repeat Proteins, but I think in the radio world we're called mini-proteins. Small 15 and smaller kilodalton, high affinity to any given target. Versus antibodies, very short half-life, so fast in, fast out. While for most projects we had to engineer half-life, systemic half-life, obviously this is less the case for radio. The idea is you hook up a DARPin, the vector, to a chelator, you load it with an isotope, and deliver that into the tumor. We have done this now repeatedly, and the lead asset is a DLL3 DARPin called MP0712. Call it the trick is that we have a very broad target universe. Most vectors are peptide or small molecules. They're even faster in and out, but they have to bind to specific groups and I would say the target universe is more limited. For specific situations, and we can talk about those also for our DLL3 asset, the DARPin approach has distinct advantages. It's not that peptides are not good, they just don't cover the whole universe. With our approach, and you can compare it maybe a bit with an Aktis type approach, we open the space for more and different targets, and with that, have a new therapeutic modality established. We also do other modalities with DARPins, but I think for now the focus is radio. I think that's what we should focus on in this call. Seth, anything to add? Definitely, because I want to dive down a little bit more into the question of why DARPin in radio makes sense. MP0712 for DLL3 is going to drive the value of this company for the next 12 months easily, and we can talk about why, and I'm all for that, and I think it's a great asset. We didn't do it for 712. We did it because DARPin can be applied in radio in a multitude of ways, as Patrick was saying, and it's that capability of a DARPin. A DARPin, I'll use visuals here. A DARPin's like a brick. It has one side, which is the randomized surface, which is going to bind to whatever target you want. In the first case, DLL3. The rest of it is very consistent and very conserved, and you can manipulate it a lot. By doing so, we can encode things into the DARPin that are radio-ready, i.e., lower kidney uptake. We have been able to create a class of DARPins that are preferentially passing through the kidney unrecognized, not getting reabsorbed. Whereas if we were to be another treatment modality, we would have to start all over again with a brand-new peptide and have no encoded knowledge in that new peptide as to our new target, what we're solving for kidney, for liver, for bone, whatever the uptake that you're trying to avoid is. We can already build that into the next program, and the next program, and the next program, and we truly have a platform that can derive new targets in a repeatable manner. On top of that, the robustness of the DARPin allows us to switch out isotopes and chelators and keep the constant targeting of the DARPin. What we presented earlier this year, is that you can take, and we did this with two different experiments and two different DARPins, you can look at the biodistribution and swap out lead for actinium, two different alpha isotopes, and have a very similar biodistribution pattern across both of them. You're not doing a completely different program for one isotope and a completely different program for another isotope. We can run experiments swapping out isotopes and chelators and decide what the right isotope is for the right target with the right DARPin. It just gives you a broader applicability on a platform level for ourselves, for patients, and for partners that we could create a multitude of these programs for a lot of different people. Very helpful, an important point of distinction relative to your competition, which we'll talk about in just a minute. Maybe you could first tell us, you mentioned that MP0712 will drive value in the next 12 months. We are anticipating some data over that time span. We've already generated some very interesting data in small cell lung cancer with MP0712. Can you summarize those early data? Then we can talk about next steps. I'm on mute. Patrick, go ahead. What we did is we had a doctor in South Africa who was interested to run a doctor-initiated trial, an IIT, and he dosed patients with the imaging agent of the drug. That's where we used Lead-203. We have a time course and the dosimetry of several patients, and we see specific tumor uptake. From that dosimetry, we can conclude that we have very rapid tumor uptake. Within 24 hours, we don't have all the intermediate time points, we get 80% tumor loading, but it continues to load up to day five. We see that we do clear mostly through kidney, but we have a positive tumor-to-kidney ratio also on the early time points, and that gets even better. We do see that we always think that is something we want to discuss for 712, which is the DLL3 asset. We have prolonged the half-life of this because we need to capitalize on the internalization of DLL3 because it's a very low copy number target. We're talking a target with several hundred copies per cell versus 150,000 for PSMA. We need to go for a bit longer half-life. Now, we don't want a very long half-life. We want exactly that sweet spot, and I think we hit the sweet spot. From all the calculations, we see a positive tumor uptake, and we have dosimetry showing that for a dose, and that's our starting dose of 75 megabecquerel, we'll have 2.1 gray on the kidney, and we'll have 0.8 on the red marrow. The 0.8 is the, let's call it almost a surprising number because you see a lot in the blood, but it doesn't penetrate that deep into the bone. That was for us, positive news, and that's sort of the basis. Just to put that into perspective, the EBRT, so the External Beam Radiation Therapy limits for kidney are 23, and bone is 2.3. In principle, the 75 megabecquerel for kidney, we can dose 12x or 10, 11x, versus the red marrow, you could dose three times. We spoke with the agency, the interesting part about marrow is that it recovers. There it is not a cumulative dose. It's a max dose, then we can max out once the marrow is back or the blood cells are back. Kidney, it is cumulative. For the marrow, not. We can actually dose up to 200 megabecquerel. That means we're maxing out on a single one on blood. That's going to be 2.2, and we have around five and a half in the kidney, allowing us to dose four times. That is sort of, as you were asking, that is setting the boundaries for the clinical trial. First dose, 75, highest dose, 200. That is all possible before you actually embark on a full phase I. You get beautiful clinical data verifying a theoretical, still therapeutic window, but it is there before you even have dosed the first patient with Lead-212. Yep. Maybe I can add to that just a bit to put that into the emergence of data throughout the next 12, 18 months, as it were. Here we sit at the precipice of ASCO 2026, and we'll be presenting, obviously, the trial in progress, and we'll be at SNMMI as well, a large nuclear medicine conference, to discuss the trial and meet with our KOLs, and we'll be doing the same at ASCO. We are now actively screening and recruiting patients across five different centers in the U.S. that will expand out to at least eight centers in the U.S. over the second half of this year, if not more. We've actually started to receive more inbound requests from additional PIs, some of whom were previously conflicted with other studies that are now free to do so with us, which is great. What we're really starting to see is all the hard work that the team put in place over the last six months, the clearance of the IND, getting these centers up and operational. These docs are now, as good as their word, calling us with multiple patients at the moment. We're still early days, and we're still first cohort. We're just getting the emergence of that data, the 75 megabecquerel, which is where we're at today, which is great. Safety is the concern at the moment. Once that heme hypothesis that Patrick was talking about, since we decay in the blood pool, is established, that our dosimetry calculations from the imaging work in South Africa hold up and say, "Okay, the decay in the blood is fine. Heme values dip a little bit and then recover." The patient makes their next dose after four weeks. Perfect schedule, four doses across." This study will move very rapidly, and we'll be generating significant data, not only in the second half of this year as it relates to safety and perhaps early case studies of patients who we're seeing from every six weeks, they get another analysis and a scan to see where their tumors are, if there's any efficacy on the early side. Certainly in the first half of next year, as we approach ASCO 2027, we are exactly positioned to be demonstrating significant later-stage data in that phase I in patients with the higher doses that Patrick was referring to, that 100, or I should say 105, 150, 200 megabecquerel dose. Really a significant data set coming over the next 12 months. Throughout the next 12 months. Got it. Okay. Patients are being accrued, and you've dosed some number of patients in that initial dose cohort. Just to make sure it's clear for everybody, this is the Lead-212, MP0712, in refractory small cell lung cancer. You have some data that presumably you can't share with us today, but you have some early data in hand? I think that it would be too much. We're literally screening now, so we don't have data in hand. Let's be clear. Don't look at our faces and think, "Were they hiding something?" We're not. You know our tricks. We literally are dosing patients these days. It's an exciting moment. As you know, there's a lot to be won or lost. In this case, and I want to make the point Seth pointed out, the safety on the blood pool is sort of the bet. As I said, we need to give it a bit longer half-life to accumulate in the tumor versus other approaches. With lead, you get a lot of activity, and that's why I was pointing out to the red marrow, and even on the first patients, and keep in mind, 75-200 is not huge. We're just talking that's more or less three to four-fold. That's not so high. If the 75 looks very clean on safety on blood, meaning we know that after a few weeks on these patients, you don't have to be a specialist to see. We will have a very good feeling where this drug is. I think that's why for us, even in the first half of this year, we will know if we have a therapeutic index for the safety part. It's, is it 100? Is it under 50? Is it 200? That we'll have to find out. If 75 look good, we feel very confident on the drug. Super exciting next few literally weeks. Give it a month, but then we'll be able to answer a bit more. Okay, great. Should we expect some data to be divulged by the company over the next six months, and what kind of rough contours of that data, what should we expect? Let's be precise. We don't want to dribble out data. That's not going to help. What we will do is we will update on trial progress. Once we go to the next dose cohort, one will know that the safety of the first was good. I think that will tell a lot. I think progress will indirectly show safety, and then we will definitely be able to talk. Don't expect that we will talk about every single patient. That's not the idea. Then I think it becomes more a case study on activity. Then assess that in a year from now, we should have a meaningful data set that we then can release as the data set. Seth? Understood. No, I certainly have intent and have discussions with the team about presenting on the safety and what we're seeing from a profile of the drug in the second half of this year. We will endeavor to do so. If there's case study to point to at that moment, certainly possible. I want to put it in the context that we are in a competitive situation on DLL3. Five years ago, DLL3 was a wasteland. Nobody wanted to be there, and now it's crowded, and they don't know why we'd even go there because it's so busy. Between ourselves, Radio, it's between ourselves and Novartis at this point with Mariana. Those are the active participants in phase I at the moment. With ADC and T-cell engagers, there is room for everyone to play. We believe that we have a significant place in that. What's important for us is that by first half of next year, we are showing our data at a time when others, Amgen, will have a very significant data set coming up in the first half of next year. Obviously the ADCs will continue to do so as well, that we're relevant with a relevant data set at that moment for everybody to appreciate who we are and what we're doing. I'm not saying we're going to hold back, but we're going to be preserving the integrity of that data. Sounds silly. My scientist would say, "He just said what?" We will be preserving the integrity of that data, to be relevant at that point, because we see it as a significant half, first half of 2027, we see as a really significant place to be. Got it. Okay. That's helpful. Well, you mentioned the competitive landscape. You identified a couple of the key players. How do you think MP0712 stacks up and might be differentiated? One of the things you already alluded to was the optionality with the radioisotope. Maybe you could elaborate a little bit more on where it stands in the competitive landscape. Yeah. On a technical point of view, I can just give sort of the update. I think there are, or there was three. We're not that sure where Dara is these days. There is the Rover platform, which has a longer half-life, like ours. That is a longer-lived approach, but that is antibody-based. We have the DARPin with an intermediate half-life, mini-protein, we have the peptide from Mariana. We think from the peptide on Mariana, the fast in, fast out, we can also do that with the DARPin only. We get limitations on tumor loading because we cannot capitalize enough on internalization. That's why we added the half-life piece. We do think it might be that Mariana Oncology has to repeatedly dose several times very often just to get enough mass on the tumor, given that there is not so many receptors at any given point in time, but if you give a longer half-life, it can be internalized. On the OPDIVO approach, that's an antibody type approach, where, in this case, and that was data that was presented last year, we saw more liver uptake than we would have expected, and than we see. We see no uptake in the liver unless we have metastasis there. We are clear through kidney. It seems that our half-life engineering, that is HSA DARPin based versus an Fc based, seems to be favorable for liver uptake. Where that puts us on a competitive landscape, I think these are all approaches that are valuable. As you say, we're the only one who can also switch in lead or actinium. We went lead first. That is a differentiator by itself, but we can also do actinium. Maybe I'll add there that especially because lead is still not limited for clinical trials, but limited for doctors' use. We are getting requests from doctors that would like to use, in their compassionate care setting, actinium, because that's what they have. Definitely something to consider, that if we want to support the doctors to use the drug early on before we are in phase III and are supporting globally. U.S. is no problem. U.S., we have lead. In Europe, lead supply is not so easy. Africa, it's not there. An actinium strategy around more global acceptance for the isotope is also something we're looking into. Okay, great. I failed to mention at the top, if there are any questions from the audience, please feel free to email me at michael.nedelcovych@tdsecurities, and I can pose that question on your behalf. We only have a few minutes left, though, and I want to make sure we talk about MP0726, which I believe is the next- Yeah. Candidate in your Radio-DARPin portfolio. Maybe you could tell us a little bit about that, DARPin, the target, and your plans for development there. No, absolutely. Mesothelin, as we know, is a target that has been gone after several times. The problem of mesothelin is that it is cleaved from the surface of cancer cells. There is a high pool of cleaved mesothelin, we call it shed mesothelin, and that is acts as a sponge. If you now would take a DARPin that binds that and put an isotope on it, we would just be in the bloodstream, and we would not even reach the target. We would have a very unfavorable tumor to healthy organ ratio. What our scientists did is they selected a DARPin that does not bind the cleaved form that is freed. It binds the full form and the cleaved form, the stump that is still on the cancer cell. We now have a cancer selective mesothelin, which is needed. I was talking about peptides before. To find a binder like that with a peptide is quasi impossible because there is no groove that would discriminate from that cleavage site there after it's cleaved. That's a mini protein domain. That's why we chose it. It's also internalized, so we also added a bit longer half-life because we don't know how much we can bring on the tumor in what time. The models are less robust, I would say, than DLL3. We said we would go towards compassionate care to really get those numbers in humans that will be much more meaningful. In the clinical setting, the shedding so far was always a negative prognostic marker for other treatments that were targeting meso. We believe we actually have a very strong hypothesis that we can test for radio, and we're also not aware that anybody else is going there. While we said DLL3 is getting crowded, meso for radio is still wide open. Great. What radioisotope are you contemplating as a first foray for this target? Or perhaps both? That's a very good question. Let's go back. The rapid uptake and prolonged staying or residence time on the tumor allows us to be agnostic for DLL3. DLL3 can work for both. From the data we have, also meso can work for both. It has a bit slower uptake, so it leans a bit more towards actinium, but that has not been decided which isotope is it. I personally would like to try both. At least get the dosimetry and then look what the clinical data actually tells us. It's really how fast do you get uptake, and how long is your residence time? I don't want to take the bet if I don't have to. Let's first do dosimetry, take the data, and then decide the isotope. That's the thesis that Seth in the beginning put out. We're likely the only company who can really do that because we have access to lead, we have access to actinium. We are not an isotope company or a vector company. Because we can do that in a compassionate care setting, we don't even have to manufacture under a full GMP. We can just do high quality test, then decide. No matter what isotope we choose first, we can easily switch later. If we would say we go with lead first, doesn't mean lead is then the end product. We will wait until we have data to lock in the clinical phase I isotope. Great. Okay, in our final couple minutes, what is the development path for MP0726 from here in terms of what we on this side of the street might see over the next six to 12 months? Sure. Seth? Yeah. The first up, as Patrick was saying, is the compassionate care setting. In doing so, it's important to be able to calculate and figure out which isotope is the ideal that we would prefer. Shy of that, the IND-enabling work can effectively work in parallel with that. You make sure that there's nothing from a safety perspective that's a giant red flag. Mesothelin is in healthy organ systems in the body as well, especially within the lung lining, the pleura. Each indication has organs of concern. There are very few targets on Earth that are as clean as DLL3, where it is primarily on tumor targets and nothing else, or on tumor cells and nothing else. You want to be mindful of that, but shy of that, getting that study up and running in the second half of this year for the imaging work, being able to present that, then getting toward the IND-enabling studies, and getting the IND filed in 2027 would be the path. Now, that we've seen it once with DLL3 and worked through not only imaging centers, but true PIs that are using radio in their daily practice and are appreciative of what we have to offer, we think that it's going to be a much more expedient path to develop a phase I than obviously our first one here with DLL3 has been. It's been an exceptionally good process with DLL3, but it's just one of those things that'll get easier with time. I shouldn't forget to say that we have a couple other programs going on that have not been announced that are going through animal work right now. We believe at least one of those will be disclosed in the second half of this year, which could also be in a path toward IND within 2027 as well. That's earlier, but could be a much more clear path into the clinics, perhaps even more than mesothelin at this point. Not that mesothelin is complicated, it's just might be that easier because we know better now. Great. Okay. Well, that's a wonderful place to stop at the top of the hour. A lot of data to come, hopefully a new target in the next six months or so. Patrick, Seth, thanks so much for your time, and we look forward to tracking your progress. Hey, thanks, Mike. Appreciate it. Take care. Bye.