Great morning, everybody. Thanks for joining us for day three here. Really pleased to have Matt Roden from Aktis with us. I am going to let Matt make some opening remarks, and then we can jump into Q&A. Awesome. Thank you, Matthew. Thank you to you and the entire Morgan Stanley team for hosting us here. We are excited to be here. Also thank you to everybody here in the audience for your interest in tracking our story. Aktis Oncology is a clinical stage oncology company focused on developing a novel set of radiopharmaceuticals or radioligand therapies. We are very excited about this space. We think it is a large new category of anticancer medicines, and we are still in the relatively early era of the development of this category. We like radiopharmaceuticals in part because they are validated. We know how they work, we know why they work. We have seen that they have been successful clinically. We see that they have been successful commercially in terms of patient impact and launch ramp. We also see that the space is, as of today, relatively early in terms of there is only two approved, or I should say, approved products against two targets. The target space for radiopharmaceuticals is wide open. Aktis exists to attempt to bring radiopharmaceuticals to a broad set of patient populations that have no radiopharmaceutical option. The key unlock for that has been our miniprotein radioconjugate platform technology, which enables us to hit a broad array of targets with a clinical or pharmacologic profile that is consistent with what has worked successfully in the radiopharmaceutical space. From that platform, we have advanced two lead programs into the clinic. The first is AKY-1189, which is targeting Nectin-4. Obviously, Nectin-4 is a validated target through PADCEV, which is an approved ADC. It is now projected to have consensus peak sales numbers of about $7 billion, all in bladder cancer. Our clinical development plan is not only in bladder cancer, with now what is a different payload of a radiopharmaceutical versus an ADC, but also to develop outside of bladder cancers into breast and potentially several other tumor types. We think this is an important and large multi-tumor opportunity for us. Our next program is AKY-2519, which is targeting B7-H3, and that, like Nectin-4, we believe has the potential to be first in class among radiopharmaceuticals, and also has a multi-tumor, large patient impact opportunity and obviously commercial launch opportunity. Beyond that, we have several other programs that are, again, leveraging the miniprotein platform. We haven't disclosed anything beyond the fact that there are multiple programs in various stages of earlier development. But we have said that we are tracking towards two additional clinical candidate nominations in the first quarter of 2027. The platform continues to produce, and we're excited about the multiproduct, multi-tumor clinical development plans we have. Further from that, based on the platform technology, we do have a strategic collaboration with Eli Lilly that is worth a total value about in excess of $1.2 billion. This was really to explore or generate new miniprotein radioconjugates against targets that Aktis is not working on. It just expands the impact potential of the platform technology. Of course, Aktis retains 100% commercialization ownership of our entire pipeline, including the lead two programs. Beyond that, we've focused on the other critical component of the story is our supply chain. We are principally prioritizing actinium-225 as the effector isotope. And in order to be in control of our own destiny, we have built a very robust end-to-end supply chain that enables us to, we believe, ramp up to, in the near term, hundreds of patient doses, and then, of course, deliver globally as we advance into later stage development and commercialization. Really it's everything under one roof that you would need to be a leader in the field, all the capabilities and components, and that's what we've been focused on because we're mostly keen to move the needle for patients. At the end of the day, if you can be valuable for patients, then you should be valuable for investors, too. So happy to dig in wherever you'd like. Wonderful. Thanks for that. I thought maybe we could just start at a very high level on some of the components that make radiopharm attractive and how to sort of think about that. At least in my mind, the way I've always thought about radiopharmaceuticals is the most attractive piece is you know that if you deliver an isotope to a tumor, it's going to kill the tumor, right? There's no question about that. There's not a question about resistance, et cetera, that you might see with some other drugs. However, you have to worry about accumulation in tissues or organs that could create enough toxicity that you can't dose high enough, et cetera. Can you talk a little bit about what you see as the benefits and sort of how you've designed your platform to be able to sort of meet that therapeutic window? Yeah, it's a great question. The field of radiopharmaceuticals really started. Well, it started with, of course, iodine for thyroid cancers, but targeted radiopharmaceuticals started in the early days with monoclonal antibodies, like for example Bexxar or Zevalin. Antibodies were a logical choice at the time for delivering radioisotopes, because we know we can generate antibodies against a wide array of targets. We know you can localize antibodies wherever that target is, and so that would be an obvious way to deliver a radioisotope. Unfortunately, one liability of antibodies is that they're long-circulating. That's often an attractive capacity to an antibody because you want it to stick around, you want area under the curve, you want target coverage, et cetera. But for radiopharmaceuticals, the problem is that now what you're doing is you're keeping the radiation payload in the bloodstream for a long period of time. What has been observed over time with monoclonals is that you have an elevated level, and perhaps unacceptable level, of bone marrow hematotoxicity. The field has largely moved, not entirely, but largely moved to small formats. This is due to the success of, let's say, LUTATHERA and PLUVICTO, both are very small peptides, effectively, that are fast clearing from the bloodstream. In other words, yes, they can hit a target with affinity, but they also are renally cleared through the kidney. They are cleared out relatively quickly in a matter of hours. The field has largely moved to that small format, and we have as well because we think it's a way to maximize the therapeutic index by protecting the bone marrow. When we were starting the company, we effectively had a whiteboard of every permutation you can imagine of all the component parts you were talking about, and we wanted to optimize for what would be an expected patient outcome. At the same time, we wanted to optimize for, well, how do we hit these other targets, and can we use antibodies or antibody fragments or other sort of antibody-like things? Where we landed was with miniproteins, and we are inspired by the work of David Baker, who subsequently won the Nobel Prize on de novo protein design, specifically around miniproteins. Miniproteins are the smallest polypeptides that can achieve a three-dimensional shape. That three-dimensional shape, and of course the variability or diversity that comes with the polypeptide, was the enabler to hit a broad array of targets like an antibody could, but to have, because of its super small size, these are typically around 40, 50 amino acids, but then folded up into a very compact shape. They have the pharmacology of these very small formats like PLUVICTO or LUTATHERA. We felt like that was the Goldilocks scenario of having a binder that could be bone marrow sparing, hopefully limit the normal tissue exposure, but also be able to achieve very high affinity and selective binding against a broad array of targets like an antibody could. It was kind of the perfect mix of all the formats. On top of it, one of the really important things that makes this work is the diversity. We are encoding in our libraries for over 6 billion variants of the miniproteins, and that's across 100 different scaffolds. That's important, and of course, we are also doing generative design, which is now outside of the 6 billion. It's a new search space. It's billions of trillions of variants now that we are looking at through generative AI design. That's been an accelerator to our innovation engine that when we mention we have multiple programs following the lead two, we have multiple programs following the lead two. That's been exciting. The intent here was to deliver something that could really open up the target space but also meet the needs for a patient in terms of maximizing clinical efficacy and safety. Now, on the part of efficacy, there's a lot of debate about what's the right isotope, and it's our point of view that really any isotope that emits energy should kill tumors. A wide array of isotopes should work with this kind of format, and our technology is isotope agnostic. We have used multiple isotopes in our experimental work, and they all work fine. We did prioritize first, and it's not to say that we won't use other therapeutic payloads, but at least in our first iterations here, our first INDs were with actinium-225. Actinium-225 is a very powerful alpha emitting isotope. It exerts, we think, the maximum amount of energy into the tumor if you can localize it there. The purpose there was to, number one, maximize the efficacy impact on patients, because obviously efficacy is the unmet need in cancer. Number two, its 10-day half-life enables us to do a central manufacturing process that enables us to be, again, in control of our own destiny and supply chain such that we can deliver at scale globally. Both were important components for us. It's not to say we couldn't use others later, but that's what the priority has been. We think this is the right combination to maximize patient impact. It's not the only combination. We're sure there's other ways, other formats that can be successful. But this is a way for us to repeatedly generate as many different product candidates as we can with this kind of profile. Just last question before we start talking about some of the programs. You talked about your choice of isotope, and you talked about the supply chain there. Can you talk about, from an investment standpoint, where you think you are in terms of the investments that you need to make to have clinical supply through, say, a pivotal program? Yeah, it's a great question. It's one that we're spending a lot of time on now. What we'd like to say is at the moment, we're focused on two things principally. Number one is executing the plan we have, which we're going to talk about in a minute, and the other is planning ahead for scaling for the future. We're planning for success. Right now we're utilizing multiple, we haven't disclosed the number, but there are several commercial actinium supply agreements that we have. We feel very good about where we are with actinium supply. But we've also been working with various contract manufacturers for the final step manufacturing. That's a fee-for-service sort of thing right now. We're also working on opening our first GMP manufacturing facility at our 17 Dry dock facility in Boston, and that will further verticalize our ownership of that supply chain. As we achieve clinical proof of concept, we have already teed up various investments that we need to make, and we have looked at a combination. Would you build facilities, would you buy facilities, would you do some combination of both? We have kind of mapped out what that looks like. There is investment that is required, but if you look at the precedents, it is achievable, and it is not unduly burdensome in terms of the capital expense required to build out that kind of supply chain. The other part of the equation, though, is how many doses do you really need? Fortunately, because our clinical development plans are focused on multiple large tumor types and with global registration programs, we are going to need a lot of doses. We are going to need a lot of volume. That is a good problem to have, but it is still a problem to have. We have focused a lot right now on climbing that mountain of the capacity that we need to build. There is a lot of work going on, and as we go forward, we are going to stage those investments so that we can manage the cost of capital as we build out this capacity. Perfect. We will first talk about AKY-1189, which is your Nectin-4 program, but maybe quickly before we do that, development of radiopharmaceuticals looks a little bit different than maybe a classical oncology therapy. Can you talk about the value of some of the, let us call it, phase 0 work you can do with imaging, and how you think that sets you up for a more traditional phase I program? Yeah. No, it is a really important question, and it is one of the things that we and I think many investors like about radiopharmaceuticals is that you do get added information if you can do a phase 0-like imaging analysis of your molecule in patients. What we did here was we were able to take the binder, which is Nectin-4, B7-H3-targeted cold conjugate, and you can either put actinium on it for treatment purposes, or in this case, use an imaging isotope like gallium or low-dose lutetium or copper-64. Here you are not creating any harm to the tissues because it is not at a level of activity that would cause harm to tissues. But you can do a PET/CT or a SPECT/CT imaging time course to get initial uptake in various different tissues and tumors. You can do a time course to see how it changes over time. Then you can do a dosimetry analysis of what's the absorbed dose of activity in each normal tissue and tumor that you can look at. This is an advantage for us and others in the field because you can ask the question, is a drug doing what it was designed to do? You can see, is it going to the tumor? In the case of our molecules, we can say yes, we see very high initial tumor uptake, and we also see really nice tumor retention in those analyses, so it sticks around in the tumor for a long time. At the same time, the drug is designed to perfuse everywhere. You want to be able to find the tumor wherever it lives, and so it does perfuse the entire body. You do see some background in the early time points, first couple of hours. You see it in the liver, you see it in the kidneys, you see it in salivary glands and other places. You also see in the time course that it washes out of those tissues relatively quickly, and you can quantify how much is in there, and you can then go on to quantify is that within a safety range that would be acceptable. This is an advantage in development because you can feel good about your safety margins going into a real phase I with a therapeutic isotope like actinium-225. You engage investigators, you engage the agencies, the health authorities, and the health authorities, of course, look very closely at the normal tissue dosimetry and the absorbed dose profile. When you see our dose escalation schemas for both lead programs, those initial starting doses of 4 MBq and 6 MBq were supported and aligned with the agency through the clinical imaging data that we're able to gather. This is different than a T-cell engager or ADC, where you're kind of walking into phase I blind, and you're just doing, let's call it empirical dose finding based on clinical safety and efficacy. Once we're past that stage gate, the dosimetry data is really useful because it's hypothesis-generating. It's also, in my mind, kind of a stage gate. If you see untoward activity in normal tissues, you can do a fast fail approach and then reiterate and maybe come with a different molecule. It's really nice to be able to know that you can fail something quickly without running into a year-long or two-year-long dose escalation. We are starting with just categorically more information about the molecules than you do with other modalities. That's really helpful to us and to our investors. That's exciting. Now that we're in phase I-B, we're in a more traditional oncology dose escalation schema. Now it's all about 28-day DLT observation periods and more traditional safety analyses, safety assessments in standard dose escalation. We're using a BOIN with backfill design. The backfill enables you to accelerate, if you will, the dose finding through the dose escalation. So that's been an exciting thing for us. Now we are into the phase where, at the end of the day, the advancement of these molecules from here, now that we're post the dosimetry phase, the advancement of the molecules from here are now gated on the clinical safety observations and, of course, response. For Nectin-4, maybe just talk a little about what is the timing of that phase I data. Maybe talk about how you selected that range of doses from the imaging data. Then I think importantly, when we see that data, especially given that you have PADCEV, what is the right comparator? What is a good outcome from that study? Yeah. Let me just first start with a few words on the design of the dose escalation. The design of the dose escalation, there are five dose levels, starting at 4 MBq, going up to 12 MBq administration. Then you would give those every 28 days for six cycles. Eligible for the study are, of course, Nectin-4 positive patients as determined by initial imaging with a copper imaging agent. So you have to be uptake positive in the tumor to get into the study. That will include post PADCEV pembro urothelial carcinoma patients. So think of it as second line metastatic plus metastatic. But also other patients with metastatic disease that are Nectin-4 positive are eligible for the study. So this includes things like triple negative breast cancer, ER/PR positive breast cancers, colorectal cancers, head and neck, and some others, lung cancers, non-small cell. Nectin-4 positive patients writ large are allowed into the study. We do have a protected number of slots for the bladder cancer patients, but we will be moving through dose levels here. We did disclose at the time of our IPO early this year that we had cleared the first dose level and were enrolling in the second at the time. So, in terms of what do we need to see, I mean, the purpose of this part one dose escalation is to establish safety at a dose, right? That is the purpose. But of course, we are tracking response as well, RECIST response. But the efficacy question is really more properly assessed under an expansion cohort, which is part two of the study as designed. That said, we are cognizant of, as you said, benchmarks. What are we looking for? Since there is a protected slot of bladder cancer patients and bladder is de-risked for Nectin-4, let us talk about that for a minute. So what we know about post-pembro PADCEV, there is a handful of reports that have described the outcomes and how patients after the pembro PADCEV combo are managed. But probably the most comprehensive is the post EV302 follow-up that was reported by Tom Powles at ASCO. So what that shows is that the most common treatment course post PADCEV in bladder is platinum-based chemotherapy. The outcomes there are not robust, so he has reported around about a 20% response rate and relatively short PFS, three to four months, and less than a year of OS, overall survival. So, this is a difficult. I should say this is a patient population with not a lot of good treatment options. It's really a huge unmet medical need in our view. That's the patient population that is obviously one of the areas of focus for the development of the program, and potentially one of the faster paths to registration. This is an area of focus for us and we're cognizant of that. I just want to double-click on that notion that in dose escalation, it's going to be a mix of tumor types, it's going to be a mix of doses, it's going to be varying degrees of duration of follow-up. The first quarter preliminary data that we're going to describe is going to be a little bit like a work in progress, because backfill will not be complete and we'll be continuing to enroll patients in backfill. It's going to be where we are at the time and what we know about dose at that stage. Nevertheless, we're excited about what we think the potential for the program is, and given the validation from PADCEV and what we know about Nectin-4 expression in other tumor types, we think it's a really important opportunity for patients. Great. Just given the time, why don't we turn to B7-H3 and- Sure. -maybe just talk a little bit about how you think about that market opportunity relative to Nectin-4. Obviously, both are big. Yeah. The Nectin-4 opportunity is significant. As we mentioned, PADCEV peak sales, consensus peak sales expectation is now around $7 billion peak. That is just in bladder cancer, right? We plan to develop in bladder as well as in other large tumor types like breast cancers and others. We do see this as a multi-indication, multi-tumor, potentially a successful multi-billion dollar program. That said, if you look at the B7-H3 program that we have, obviously B7-H3 is expressed in north of 90% of prostate cancer patients, but also in high proportions of small cell and non-small cell lung cancers. In various other important tumor types where there is still unmet needs. If you were to just, and I am going to make a comment not about the molecule specifically, but rather the end markets or end patient segments we are talking about. The patient segments that could be addressable by B7-H3 is just categorically larger. Right? These are very large end markets. This is something that we think is a really important opportunity that we are going after. One thing that is in common between these two programs is they are both first in class for radiopharmaceuticals. Sometimes someone might say, "Well, why do I need a Nectin-4 RLT when I can use a Nectin-4 ADC or vice versa for B7-H3?" It is just important to keep in mind that these are totally different killing mechanisms, right? These are non-overlapping resistance profiles. These should be additive and potentially even combinable with ADCs down the line. We think it is irrespective of other tumor killing mechanisms, this is a unique killing mechanism that we think is going to be additive to the patient journey. A similar question, obviously you are also in dose escalation with B7-H3. Maybe just talk about the information you had when you picked the dose levels, maybe how that compares to the Nectin-4 dose levels, if there is any information just across that you are going to be able to glean across the programs. Then, prostate cancer, obviously the first key tumor type there and why you picked that versus some of the other choices you could have with B7-H3. Sure. When we first generated imaging data with the B7-H3 molecule called AKY-2519, we were excited to see the profile that we were seeing high tumor uptake in various different tumor types, including prostate, non-small cell, colorectal cancer, and some other patients. That was all reported at ASCO this year. That was exciting. What was also exciting to us and to investigators was that the normal tissue exposure was relatively modest. I have to share that when you have and we have gotten this question a lot from the posters. In the very early time points, you do see a lot of liver, and that is really profusion, not, we believe, target mediated because it does wash out very quickly and the total absorbed dose in the liver is actually quite low. That is an example of how the molecule is kind of doing what it is supposed to do. Right? It's perfusing through the whole body, but it's clearing out of the normal tissues and sticking around in the tumors. In terms of the dose finding piece, what we did was, of course, you look at the absorbed dose profile in the key normal tissues. You look at bone marrow, which is almost categorically dose limiting for radiopharmaceuticals as a category. Bone marrow, kidney, liver, et cetera, and various other normal tissues. Then you ask the question, if I were to give a full course at a certain dose, meaning multiple administrations over time at a certain dose level, would you be below all of the benchmark values of EBRT that people think about? That's like a regulatory thing, right? That's what is required for a starting dose. We did start at a slightly higher dose with B7-H3, not necessarily because the dosimetry data was fundamentally different than Nectin-4. It's just, we asked for a higher dose and got it. At 6 MBq, that's a good starting dose, but it's also steeper with the prostate program. It's also a steeper dose escalation curve, so we're going 6 MBq, 9 MBq, 12 MBq. That we think is also, I think, useful to us in terms of learning more about the molecule faster. The imaging data were exciting to us. We got great feedback from the investigator community, the expert community on the data, because it also showed very long tumor retention in excess of 6 days with very high absorbed dose in the tumors relative to all of the normal tissues. We think that that sets us up for an exciting run at prostate. When we thought about the clinical development program, once we had those data, we took it, of course, to ad boards. The prostate ad board was very enthusiastic about this profile for a couple of reasons. Number one, different target. Just categorically, it's important to have a different target. Number two, the very low exposure to salivary glands. We all know that PSMA is expressed at some level in the salivary glands and that all of the PSMA assets have some level of PSMA exposure in the salivary glands. But our level of absorbed dose in the salivary glands was markedly less than what has been reported for the PSMA agent. That's an important potential point of differentiation versus the PSMAs, but these things are all going to live together. You're going to need PSMA agents, and we're going to be the first B7-H3 agent out there. Prostate was an obvious one to go after. I would also point out that we know that targeted radiation in prostate cancers is effective, and so that's one additional layer of risk that's eliminated by this approach. One other thing that we explored and reported on at ASCO was the concordance of uptake with our molecule versus the FDA-approved diagnostic PSMA-11. What you could see is we didn't see any evidence that you're giving something up by using B7-H3 versus PSMA. In other words, we had the same uptake writ large than what you saw with PSMA. We are doing further analysis on that for a future presentation, but we did give a glimpse of that at the ASCO poster. We think it's a super exciting approach, not only for prostate, but in addition to prostate, we have lung. In fact, we have guided to opening our second dose phase I-B, dose escalation protocol with AKY-2519 in a lung-focused basket study, and that is supported by the uptake that we saw in lung and colorectal cancer patients in the imaging analysis. That is, as I mentioned, we guided to opening it second half of this year, and that's totally on track. This is a big, broad multi-tumor opportunity, and we just can't wait to get into data. Just remind us on the prostate data, when will we see the dose escalation data there? What we've said about the, when we opened the prostate study, we were confident we could deliver the first preliminary dose escalation data in 2027, and we certainly stick to that. As we get further into enrollment, we'll probably narrow that. I would just point out that because there's only three dose levels, and because there's a high degree of investigator interest in this program and priority given to this program, it has the potential to, let's say, narrow the gap in timeline between Nectin-4 B7-H3 readouts. Okay. Great. Maybe just one sort of additional question. I think obviously as you get through phase I-B and you get expansion cohort data, the question will be how quickly then can you move to a pivotal program and is that possible versus a traditional phase II to phase III? How should we think about that? Also great question. We are looking at a variety of scenarios, and we're working up plans across both programs, the Nectin-4 and B7-H3 program, for what would it take for registration and what indications would you prioritize, and how would you go about this? That's all part of the planning process we're under right now, and obviously, we're engaging ad boards of top investigators across multiple different disease areas. At the right time, we'll engage the regulatory authorities for their feedback. We have seen in terms of precedent, anywhere from the more traditional way for Nectin-4 would be to go into expansion cohorts because, as I mentioned, the patient population, the dose escalation is a mixed patient population. The proper way to assess efficacy and response is actually to go into an expansion cohort, and that is part of the plan, the part two of the existing NECTINIUM-2 protocol. But we are exploring the question of whether or not there's a different path forward to registration. That's one example. With prostate, again, we haven't said anything yet about registration plans and what the development plan would be, but let's just say we're exploring all paths. We look forward to sharing more when we can. Perfect. Maybe just last question, talk about funding, capital needs, and sort of how you think about progressing the plan from a funding standpoint. Yeah. No, it's also critical for us because what I'm describing here are at least two, and maybe next year there'll be more than two, multi-tumor development programs. Multi-tumor development programs are big, broad, heavy, expensive, but also very rewarding for patient impact and value. We reported $517 million on the balance sheet as of the last reported quarter, with runway into 2029 under the current plan. But you can imagine we had a very high energy IPO earlier this year. In the end, the demand was 18 times over the initial base deal, so many times oversubscribed with very high quality, and we continue to engage with investors on the right time and place to raise additional capital to fund what is really a big and broad opportunity. We're excited about that. We are, of course, contemplating multiple forms of capital, right? There's more than one way to approach this, and so we're contemplating all angles here. I would also add business development is an important piece, right? We have a $1.2 billion deal with Eli Lilly, but that really is very relatively narrow in scope, and so there's a lot of other angles here as well. Wonderful. Matt, thanks for being here. We appreciate it. Thank you, Matthew.