Good day, and thank you for standing by. Welcome to the Aktis Oncology conference call. At this time, all participants are in a listen-only mode. After the speakers' presentation, there will be a question and answer session. To ask a question during this session, you will need to press star one one on your telephone. You will hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the conference over to your speaker today, Alex Lobo, investor relations. Please go ahead, sir. Thank you, Michelle. Before we begin, I'd like to remind you that today's remarks will include forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. We ask that you refer to our filings on sec.gov, including our most recent annual report on Form 10-K, filed with the SEC on March 30th, 2026, for a full list of risks and uncertainties. Actual results may differ materially from those indicated by these statements. Unless required by securities law, Aktis does not undertake any obligation to update these statements regarding the future or to confirm these statements in relation to actual events. With that, I'd like to turn your call over to Matt Roden, President and CEO. Thank you, Alex, and thank you everyone for joining today's call, which is in reference to our May 21st press release summarizing the two posters on AKY-2519 to be presented at the ASCO annual meeting on May 30th. Joining me on the call today is our Chief Medical Officer, Akos Czibere, as well as two distinguished guests, Dr. Oliver Sartor of the Transformational Prostate Cancer Research Center, and Dr. Timothy Yap from The University of Texas MD Anderson Cancer Center. In addition, the entire executive committee from Aktis will be available for the question and answer session. In terms of the agenda, I will kick us off with some introductory comments. Akos will summarize the imaging and dosimetry data for AKY-2519, which will be presented in two posters at the upcoming ASCO annual meeting. Akos will then moderate a fireside chat with Dr. Oliver Sartor and Dr. Tim Yap, and lastly, we'll host a Q&A session with the management team and our distinguished guests. To get us started, a reminder that Aktis Oncology aims to expand the reach of targeted radiopharmaceuticals to large patient populations that have no radiopharmaceutical option or where persistent unmet needs remain. Aktis was assembled with all the necessary elements to serve as a leader in the field. From our proprietary miniprotein radioconjugate discovery platform, thus far, we've progressed two programs to the clinic under IND, both of which have multi-tumor and multi-indication potentials. Today, we'll be focused on our second program, AKY-2519, an exemplar of our vision to address several important solid tumor patient populations, including those where unmet needs persist, such as bladder, prostate, lung, breast, colorectal, head and neck cancers, and various other tumor types. In addition to developing novel first-in-class radiopharmaceuticals, our strategy has been to be in control of the infrastructure required to deliver for patients. Our resilient, scalable supply chain, robust portfolio of isotope supply, combined with a strong balance sheet and an accomplished leadership team, positions us well to expand patient access to radiopharmaceuticals. Turning now to the opportunity for AKY-2519. In prostate cancer, PLUVICTO is an important treatment option for patients. Despite its success, there continues to be unmet needs, and in particular, for orthogonal treatment approaches such as ours, which hits a differentiated target in B7-H3 and delivers a differentiated payload with the alpha-emitting isotope actinium-225. Of note, PSMA expression can vary in tumors, leading to suboptimal responses to PSMA-targeting therapies. Secondly, there's acquired resistance to various PSMA-targeted agents, including beta emitters, and given PSMA expression patterns, PSMA radioligands can be retained in the salivary glands, leading to xerostomia that can significantly erode quality of life with PSMA-targeting therapies. This liability is not expected to be observed with B7-H3 targeting, since there's no reported expression of B7-H3 in the salivary glands. In metastatic castration-resistant prostate cancer, it has been shown that B7-H3 is overexpressed in about 90% of patients' tumor samples, while normal tissue protein expression is quite restricted and, again, not reported to be present in the salivary glands. Lastly, while we see a compelling opportunity in prostate cancer, AKY-2519 is not just about prostate. Given the B7-H3 overexpression in multiple other tumor types, and with AKY-2519 being a potentially first-in-class fast clearing radiopharmaceutical, we seek to unlock multiple whitespace opportunities in large patient populations, such as colorectal cancers and various forms of lung cancers. Now turning to slide six, which describes why we employ mini-proteins as targeting moieties for radioconjugates like AKY-2519. It starts with the patient. The goal here is to maximize treatment benefit by delivering powerful anticancer activity while minimizing side effects, in particular, protecting the bone marrow, since hematologic toxicities have been dose-limiting for radiopharmaceuticals. However, we also ambitiously wanted to address new targets for radiopharmaceuticals in order to broaden the patient populations benefiting beyond the PSMA, SSTR2, and FAP space. If we're able to do that, we believe radiopharmaceuticals are at an inflection point to becoming a large new category of anticancer medicines. To fit these needs, we employed mini-proteins because we believe that they have all the right characteristics to achieve these goals as radiopharmaceuticals. Namely, their small size enables not only high tumor penetration to deliver the potent anticancer activity of actinium, but also rapid clearance from the plasma to minimize radiation exposure to normal tissues, particularly sparing the bone marrow. However, unlike other small format architectures of radiopharmaceuticals, the massive diversity of our mini-protein screening, as well as their three-dimensional shape, enables us to uniquely select variants with very high affinity and selectivity against a wide variety of molecular targets. This unique combination of properties was employed to enable us to open up the target space and hence new patient populations for radiopharmaceuticals. Turning to the pipeline page, our proprietary platform has given rise to a portfolio of development programs. Our most advanced clinical stage program, AKY-1189, has FDA Fast Track designation and is currently enrolling in a phase I-B clinical trial in the U.S. The trial is on track, and we expect to present preliminary dose escalation data in the first quarter of 2027. The topic of today's call is AKY-2519, for which we have a broad clinical development plan. As you know, we recently initiated the first of two planned phase I-B clinical trials of AKY-2519 in patients with metastatic castration-resistant prostate cancer, enrolling cohorts of both PLUVICTO-naive and PLUVICTO-experienced patients. We expect to report preliminary data from this trial in 2027. The second phase I-B trial is a lung cancer-focused basket trial of B7-H3-expressing tumor types and is on track to open in the second half of this year. Now turning to the ASCO presentations that we'll be discussing today. Clinical investigators will be presenting two AKY-2519 posters side by side on May 30th at ASCO. Poster 3097 reports the imaging, biodistribution, and dosimetry data in 16 patients with metastatic castration-resistant prostate cancer. The findings from this analysis inform the trial design and rationale for ongoing phase I-B trial, AKY-2519. Poster 3098 is reporting PET/CT imaging analyses of patients with various B7-H3-expressing solid tumor types, and the tumor uptake findings of this analysis likewise informed the included tumor types for the upcoming phase I-B lung-focused basket trial. Lastly, a quick word on the key catalysts on page nine. Our plan remains unchanged. We're focused on executing to deliver on a variety of goals, spanning corporate initiatives and program development milestones. Without further ado, I'm happy to turn it over to Akos. Akos? Thank you, Matt. AKY-2519 is our novel, potentially first-in-class miniprotein radioconjugate targeting B7-H3-expressing tumors. Like other miniproteins from our proprietary radioconjugate platform, it combines high affinity with highly selective binding to its target, in this case, B7-H3, with pharmacological properties that allow for deep tumor penetration and retention in cancer cells, along with the rapid clearance from plasma necessary to limit normal tissue exposure. AKY-2519, our now second clinical-stage program, further builds on our vision to bring targeted radiopharmaceuticals to large patient populations with significant unmet need. Let's take a quick look at B7-H3 as a target for anticancer therapies itself. I would consider it biologically de-risked at this point, with several B7-H3-targeting ADCs in large randomized studies in small cell lung cancer and advanced metastatic castration-resistant prostate cancer. Further, we do see B7-H3 as an ideal target for radiopharmaceuticals due to its high expression across multiple tumor types and exceedingly low expression across normal tissues. It is highly expressed, as you know, in prostate cancers, lung cancers, colorectal cancers, and various other solid tumor types where high unmet needs persist. Throughout, there is limited expression in normal tissues. Clinically, expression of B7-H3 has been shown to be also associated with poor prognosis, further highlighting the potential positive impact when targeting B7-H3. Before we dive into the clinical data for AKY-2519 that not only drives our excitement for the program and our platform as a whole, but also forms the basis of a broad clinical development program we are launching here in the U.S. under IND, I do want to take a quick step back. When we started to collaborate with Prof. Mike Sathekge at NuMeRI in South Africa on our first program, AKY-1189, at the beginning of 2024, we were trying to understand two main concepts, given this was the first-ever mini-protein to potentially enter the clinic as an actinium-225 carrying therapeutic. First, does the rapid plasma clearance of our mini-proteins translate to the desired low bone marrow exposure? This is the important one because we do think, and Matt spoke to that earlier, that bone marrow exposure at the end of the day is going to be what will be dose-limiting for radiopharmaceuticals in oncology. Second, with our mini-proteins being readily cleared, what is the potential impact, if any, to the kidneys? With the capabilities and technologies available to us at the time, we were able to investigate those questions, and those data have been presented at the Triple Meeting in the fall of 2024. Fast-forward two years later, we have now advanced our own imaging and dosimetry capabilities, and paired with the new scanners at NuMeRI, we're now together able to ask more questions, like extending the number of normal tissues we can investigate, and also as an access first, get a look at potential tumor doses through dosimetry. Let's dive in with a brief summary of both posters before we take a look at the actual data. First, most important, AKY-2519 and this imaging and dosimetry study was generally well-tolerated with no AEs or infusion-related reactions reported. Second, we observed robust tumor uptake and retention out to at least six days in serial imaging, along with decreasing and limited normal tissue exposure. Tumor uptake by SUV on PET/CT imaging was also observed across multiple tumor types. The robust tumor uptake and retention observed in the SPECT/CT portion of the assessment translated to robust predicted tumor doses with low normal tissue exposure, suggestive of a favorable therapeutic index for AKY-2519 as a therapeutic. Third, but not least, PET/CT imaging analysis also show that AKY-2519 is able to consistently identify lesions that are also identified by PSMA imaging agents when using dedicated PSMA diagnostics, suggesting that B7-H3 may be indeed an excellent target for novel prostate cancer therapies. Overall, these data suggest the potential for AKY-2519 to kill cancer cells across multiple B7-H3-expressing tumor types while minimizing normal tissue radiation exposure in patients. In total, we're going to be presenting across two posters together with our collaborators, data from 34 patients collected across two academic centers in South Africa and Germany. In South Africa, the assessment was focused on mCRPC, where 16 patients underwent PET and serial SPECT/CT imaging utilizing either gallium-68 or lutetium-177 as the respective imaging isotopes. In Germany, patients with different solid tumors expanding beyond prostate cancer received gallium-68 AKY-2519 before undergoing PET/CT imaging to assess tumor uptake. All in all, these data will give us a good, comprehensive view of the biodistribution tumor uptake and retention, as well as the predicted absorbed doses to be delivered to tumors and a range of normal tissues. Pictures tell better stories than I ever could. Let us first take a look at some images from a representative patient with prostate cancer who underwent serial imaging with low-dose lutetium-177 AKY-2519 and PET/CT imaging with gallium-68 AKY-2519. We are starting with a PET/CT image on the top left, and what we see here, a strong uptake in extensive metastatic disease, in particular, nodal disease spread in the pelvis and around the aorta. We also see uptake in a bone lesion that on the PET/CT image is actually hidden behind the liver and at the primary site of the disease as well. From a normal tissue perspective, we observe an initial blushing of the salivary glands as well as the liver here, and the spleen is also visible. We're not seeing much of the kidneys in this two-hour snapshot image. I think, though, more interesting than a two-hour snapshot is the captured activity over time that is pictured in panel B here. These data here, where we utilize low-dose lutetium-177 with serial imaging at three, 24, and 144 hours, are what allows us to translate these visuals or the visuals into predicted absorbed doses. What we're seeing here, again, is a very strong initial uptake at three hours in the metastatic lesions that is preserved and retained at 24 and out to at least 144 hours, the latest imaging time point here. Regarding normal tissues, however, you can see at 24 hours already a clearing of the salivary glands and the liver is retreating well into the background. A nice visual of how the actual dose administered to the patient is distributed between normal tissues and tumor lesions is shown here in the top right panel B. All the normal tissues, including kidney, liver, receive a small portion of the dose, with the vast majority being delivered to tumors. This is the profile you want to see for a radiopharmaceutical and a really nice translation of our miniprotein thesis. Looking at predicted absorbed doses, putting some numbers behind the images, we see that the three organs highlighted here for this particular patient are all well below clinical benchmarks, while the tumor doses are very, very robust. For your calculation conveniences, we provide gray per megabecquerel dose coefficients. These are data converted to potential use of actinium-225, even though lutetium-177 was the utilized imaging isotope. We also present a total predicted gray that would be delivered to normal tissues and tumors over a typical four-course therapeutic application of an exemplary 8 MBq dose of actinium-225. We're seeing that tumor doses with AKY-2519 are not only very robust and consistent across various lesion types, but also substantially higher than the absorbed doses to the normal tissues. When we assess tumor doses, we also employ what is called a partial volume correction here, which can adjust for some of the heterogeneity encountered when contouring tumors. I view this as a sensitivity analysis, giving us a better sense of the range for the dose we may deliver to tumors. Numbers, we just look at the nodal disease here and the specific lesion highlighted. It is expected to receive a very healthy or unhealthy for the tumor 122-239 gray over only a four-cycle treatment course at 8 MBq. While the kidneys at the same time over the same treatment course would only receive 9.2 gray, and the salivary glands would only get delivered 3.6 gray. Keep in mind, this is a really clear grader pharmaceutical. Overall, the dosimetry analysis in this patient predict a fairly favorable therapeutic index for actinium-225. Let's take a look at the predicted absorbed dose to some key normal tissues across all 12 patients with available data to do actinium conversions of the original 16 patient lutetium data set. What you can see is that the data is very consistent with what I have just shown you for the individual patient, with those coefficients coming in at 0.04 gray/MBq for bone marrow, 0.31 gray/MBq to the liver, and 0.5 gray/MBq to the kidneys, and only 0.13 gray/MBq to the salivary glands. If we dial this up to a full therapeutic treatment course, we are landing at 1.3 gray to the bone marrow, 9.9 to the liver, 16 gray to the kidneys, and only 4.2 grays to the salivary glands on average here. With that, the normal tissue dosimetry is clearly supportive of repeat dosing as clinically meaningful doses and advancement of the program. Notably, the low exposure to the salivary glands in particular could be a differentiator from PSMA targeted therapies, especially as we think about alpha therapies in this setting. Similar to what I just described for normal tissues, we do see that same level of consistency when we look at the population data for predicted absorbed doses to the tumors, and this is now broken down by various types of lesions. I'm presenting to you the dose coefficients in gray per megabecquerel of administered activity and how that gray would look like following four therapeutic administrations at that exemplary 8 MBq dose. Partial volume correction I spoke about earlier is not done for the primary disease site since there is a spillover effect from the urine-filled bladder, which would artificially inflate those results. Of course, we're doing it again here for the nodal and bone disease across all patients and lesions analyzed. Here, we're seeing for nodal metastasis a substantive predicted absorbed dose of 141 gray-268 gray following four doses at 8 MBq, and for bone disease, we're seeing 48 gray-121 gray delivered. In all of this, while the kidney would only receive 16 gray and the salivary glands, as mentioned earlier, would only receive four gray based on these data. Overall, these data are quite exciting to us and really highlight the potential for AKY-2519 with very strong tumor to normal tissue ratios, and we're looking forward to start dosing patients under IND with actinium-225 AKY-2519. Let's pivot and take a quick look at the tumor uptake of 2519 beyond prostate cancer. Of course, still including more prostate cancer patients here, and this is work now done by the team in Essen, Germany. We can see robust tumor uptake by SUVmax in a patient with adenocarcinoma, non-small cell lung cancer, a patient with recurrent small cell lung cancer, and a patient with recurrent rectal cancer. These images were taken two hours post-injection with gallium-68 AKY-2519. Once again, similar to 11-89, we can use the same binder for both imaging and therapeutic applications. These images clearly support investigation of AKY-2519 across multiple tumor types and inform the design of the basket study, as Matt mentioned earlier. Briefly expanding on the PET/CT imaging data, focusing on a cohort of seven prostate cancer patients with SUVs captured, again two hours post-injection, we can now look at SUVmax and SUVmean, as well as the SUV peak across different lesion types. We're consistently seeing very strong uptake, highlighting that 2519 could potentially not only be utilized as a diagnostic in prostate cancer, but is potentially to be highly effective across various types of metastatic lesions, which is of course supported by the robust tumor dosimetry data I discussed earlier. Further to that, here's a little bit of a teaser for you since the work in South Africa included matched pair sampling of PSMA and B7-H3 expression through imaging with PSMA-11 and AKY-2519. I'm showing you two patients here with their MIPs, so maximum intensity projections, and some axials here with SUVmax. When we look at the broader uptake profile for AKY-2519 and PSMA-11, which is a dedicated diagnostic agent used to select patients for PLUVICTO therapy, you can see that AKY-2519 consistently and reliably identifies lesions that are also identified by PSMA-11, suggesting co-expression of B7-H3 and PSMA. The way this was done here is by utilizing a thresholding approach where all lesions above a certain SUV cutoff are colored in red. As a starting point, thresholds established for PSMA were applied to both image sets, and we're going to be doing additional analysis with these data across the full cohort of patients, including optimization specific to B7-H3, and that will be presented at a future conference. These data, however, which are the first comprehensive imaging data of B7-H3 and prostate cancer, clearly demonstrated to be a very promising target for novel therapies here. Let us summarize again before we spend a few minutes on the development program itself. AKY-2519 was well tolerated with no ADEs or infusion-related reactions observed. There was robust tumor uptake and retention that translated to strong tumor doses while keeping normal tissue exposure low. Tumor uptake by SUV was also observed across multiple B7-H3 tumor types. These data support the broad clinical development program of AKY-2519 across multiple tumor types. This is the design of the ongoing prostate cancer study that we spoke about at our last call in earlier May, utilizing copper-64 as the imaging isotope and, of course, the highly potent alpha-emitter actinium-225 as the therapeutic isotope. The study is now enrolling in two cohorts, cohort A for patients who have not received PLUVICTO, and cohort B for patients who have received PLUVICTO. Both cohorts run independent dose escalations across three dose levels, 6, 9, and 12 MBq, of which two can be expanded to up to 30 patients for each of the two cohorts. Now, for the first time, I'm also sharing with you the high-level design of the 2519 basket trial. It follows the same dose escalation schema that you've seen before with backfill, as well as now dedicated expansions for non-small cell lung cancer and a large one for other B7-H3-expressing solid tumors. Protocol is now active on our IND and on track to start dosing patients in the second half of this year. This concludes the presentation piece of the data, and now comes the fun part, as I'm welcoming Dr. Sartor and Dr. Yap to our virtual fireside chat. Thank you both for joining us today. I really want to take this opportunity to sit down with both of you to talk about the data just presented. In addition, I'd like to explore with you what you're seeing in the current treatment landscape for both prostate cancers and more broadly in the B7-H3 space, whether you see continuing unmet need for patients, specifically around other radiopharmaceuticals in development when we think about prostate cancer, and how you see the treatment landscape continuing to evolve for radiopharmaceuticals. Before we dive in, I'd like to ask both of you to introduce yourselves and talk a little bit about your background and experience. Let's start in order of the studies you're going to be also supporting. We'll start with Dr. Sartor. Hi. Dr. Oliver Sartor. I'm a long-time prostate cancer investigational doc. I've been involved with radiopharmaceuticals, believe it or not, since samarium-153 back in the '90s, and then going on to radium-223 and PLUVICTO. It's a pleasure to be here and delighted to be able to sit in the call today. Dr. Yap? Good morning, everyone. Tim Yap here. Thanks so much for having me. I'm a medical oncologist at MD Anderson. I'm the VP and head of clinical development here in our Therapeutics Discovery division, and a professor in our Department of Investigational Cancer Therapeutics, which is our phase I program, where we're developing novel agents, including RLTs but also interesting ADCs and also T-cell engagers as well. Have been involved in phase I clinical trials and early phase studies for about 20 years. Wonderful. Thank you. Dr. Sartor, maybe start with a question for you, since we're obviously at Aktis very excited about the data we just presented. Maybe you can share some of your thoughts about these data and how you see them fit into the larger prostate cancer treatment landscape, specifically in the context of the now ongoing phase I-B study in prostate cancer. Yeah. Thank you. I think the data are very impressive. Let's go back to PLUVICTO for a second, because I think that's where the current money is, obviously a multi-billion dollar drug. PLUVICTO is an absolutely fantastic drug for about one-third of the patients. About one-third of the patients, it's really not very impressive at all. Another one of the third, it's kind of in the middle. PLUVICTO's obviously a very good agent, but only for a minority of those who are actually treated. I think there's plenty of opportunity to be able to look at another agent. I'll tell you what I saw when I reviewed the data, was a surprising amount of uptake, even in those that are PSMA PET positive, but also extending, and I know this from other data, to those that are not PSMA PET positive. There's a broad spectrum of PSMA PET positivity, and B7-H3 imaging, as shown here, I thought was absolutely outstanding. If you're looking at the SUVs, you're looking at multiple lesions, multiple patients above 10, which is a really nice cutoff that's been used by Louise Emmett and the Australians, certainly greater than liver. Liver comes in with an SUV of typically around five-ish or so. What we're seeing is lots of uptake, and that portends in a radiopharmaceutical trial the opportunity for nice activity. The other thing that I think was nice was the retention that you see in the tumor, and you see this in Mike Sathekge's lutetium-177 dosimetry data, where you see the retention in the tumor and the washout in the normal tissue. There were two items that I was watching very closely. Number one was the kidney exposure, because that's been an issue that has come up with the SSTR2 ligands with actinium and others. We really have to be careful of the kidney. The way this mini-protein works, it's not really typically cleared by the kidney, thus the renal dosimetry is extremely favorable. The other problem that has been encountered is with the antibodies, and we've seen the long half-life of antibodies translate into substantial bone marrow toxicity. Here we're seeing the rapid clearance and what looks like a very tolerable bone marrow profile. I'm going to call it the trifecta. Really nice retention in the tumor, really minimal exposure to the kidney, and rapid enough clearance to not expose the bone marrow. I think this is very preliminary, very promising data that certainly supports the use of further development. Thank you for that, Dr. Sartor, and I wholeheartedly agree, of course. Maybe just to dive in a little bit deeper into prostate cancer and alpha-emitting radioisotopes and your experience there so far, what normal tissue do you typically see outside of bone marrow as the most dose-limiting when thinking about alpha therapies for prostate cancer? Yeah. Let's look at the landscape just for a brief moment. We have the PSMA-617 actinium, and there we're going to be really worrying about the salivary gland because xerostomia is a substantial issue and can be rate limiting. Next, we go onto the PSMA I&T from AZ, and they're also having significant salivary issues. When you go to the convergent antibody, which is J591, you're starting to look at marrow toxicity being rate limiting. If you look at basically, and I'm going to call it the five that are fairly developed, by the way, the Bayer Trillium, also is under phase III development in the not-too-distant future. There, I think it's going to be a little bit on the kidney and marrow. There's some interesting properties to the Trillium molecule, but nevertheless, so far what we're seeing is salivary and bone marrow, depending on whether or not a small molecule like PSMA-617 or I&T are the marrow, which is going to be true for the antibodies. Thank you. Maybe the last question for you, Dr. Sartor, how do you view the novel fleet of ADCs coming into prostate cancer and how they will compete with radiopharmaceuticals, not just this one specifically, but as a category at large? Whether you view physicians or yourself will prioritize ADC versus RLT, or why not both? Yeah. The ADCs have so far been a bit disappointing. Almost some of the B7-H3 is under further development. AbbVie will end up with an interesting ADC that'll be presenting data here at ASCO. So far, the ADCs have been a little bit disappointing to date. The T-cell engagers have been more interesting, and those we're going to be looking at with xaluritamig and pasritamig coming out of the Amgen and the J&J camps. In terms of the ADCs, I think you probably got a better mousetrap here than the ADCs I've been watching so far. Great. Thank you. Thank you for that, Dr. Sartor. Maybe now we spend some time with Dr. Yap as we think about 2519 outside of prostate cancer. Dr. Yap, as we're ready to initiate the phase I-B trial, how do you view B7-H3 as a target outside of prostate cancer? What has been your experience? What gets you excited about this outside of prostate? Yeah, thanks, Sartor. To me, B7-H3, and I think certainly to the field in general, we view B7-H3 as really an exceptionally promising target, but importantly, a near universal target for solid tumors. Not just prostate cancer, but certainly plenty of other opportunities as well in addition to prostate cancer. It's primarily based on the data that you've already shown that it is heavily overexpressed across a wide range of different cancers, but minimally expressed in healthy tissues, and therefore really can serve as a very highly specific target to go after developing target therapies against. I think the data speak for themselves in terms of approaches that have been successful, and I do certainly think that B7-H3 is already, if you like, clinically de-risked as a anti-tumor target to go after in the clinic. Yeah. Could you maybe just share with us your one or two favorite solid tumor types that are not prostate cancer for B7-H3, where you see the highest unmet need? Yeah, absolutely. Certainly, small cell lung cancer, I think it's really probably one of the most successful indications for B7-H3 targeting. Of course, I'm really referring to the ADCs, the B7-H3 ADCs, like ifinatamab, deruxtecan, which have shown strong ORR response rates in advanced heavily pre-treated small cell lung cancer. Also beyond small cell lung cancer, I really do think that it is broadly actionable in non-small cell lung cancer as a potential indication, metastatic colorectal cancer, and also head and neck squamous cell carcinomas. Then going even beyond that, B7-H3 is actually highly expressed in tumors like osteosarcoma, and neuroblastoma, so thinking about pediatric solid tumors. Going beyond that as well, it is heavily expressed as well in CNS tumors like glioblastoma. That's the reason why there has been so much interest in targeting B7-H3 out there in terms of ADCs, in terms of T-cell engagers, CAR-Ts, bispecific antibodies. Great, thank you. I think this concludes our fireside chat, and I'll hand it back over to Matt. Great. Thanks, Akos. Thanks, Dr. Sartor and Dr. Yap. Appreciate all the insights shared here. Now we're going to turn it over to the operator to, excuse me, conduct the question and answer session. Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. We ask that you please limit yourself to one question or one follow-up. If you have additional questions, please reenter the Q&A queue and we will take as many as time permits. One moment for our first question. Our first question is going to come from the line of Tyler Van Buren with TD. Your line is open. Please go ahead. Excuse me, this is Ikenna on for Tyler. Congrats on the data, guys. My question is, given that AKY-2519 uses an actinium-225 payload, do these dosimetry results suggest the potential for improved efficacy as the relevant relative tumor uptake compared to PLUVICTO is at least similar, if not improved? Great. Thanks for the question. I'm sorry, please go ahead. No. Yeah, thank you. The answer is yes. You're ending up with the alpha as opposed to the beta. I think everyone would choose an alpha over beta when it comes to any tumor activity. The doses here are clearly what I think will be superior to PLUVICTO with lutetium. I think basically this is very promising, more so than PLUVICTO when it comes to the absorbed doses. All right. Thanks, guys. Thank you. One moment for our next question. Our next question will come from the line of Jonathan Chang with Leerink Partners. Your line is open. Please go ahead. Hi, this is Yiwen Ong for Jonathan. Thanks for taking our question and congrats on the data. How does the patient population in this phase II study compare to the intended population of the phase I study in terms of tumor burden, disease stage in prior treatment, and others? Thank you. Yeah, I can answer this one. The patient population in the South African study was primarily a PLUVICTO-naive patient population, with only a couple patients being PLUVICTO exposed or PSMA-617 exposed for that matter. In the ESMO data set, those seven patients, it's a mix. Understood. Thank you. A mix of- A mix of PLUVICTO-exposed and naive patients. Yep. Thank you. Thank you. One moment for our next question. Our next question will come from the line of Alec Stranahan with Bank of America. Your line is open. Please go ahead. Hey, guys. Thanks for taking our questions. Great to see all the updates. I guess for the company or the KOLs on the call, maybe just to put a finer point and maybe some numbers on a couple important questions that were mentioned. I guess first, based on the literature for B7-H3 and other RLTs, I guess what delta would you want to see in uptake between tumor and normal tissues? Then what uptake in tumor correlates with response? Is this really that SUVmax that was mentioned or maybe a different metric? Thank you. Alec, thanks for the question. I'm going to start with Akos, and we'll go to Dr. Sartor and Yap. I would point you to panel E in that case study slide that we presented in this deck. If you're thinking about what ratio do I want to see, that's exactly what you want to see, right? You have all the normal tissues squished, squeezed to the left, and all the tumors are to the right. The way this plot works is it's basically the distribution of the actual dose administered, right? What proportion of the dose goes to what tissue versus tumor. Yep. I don't know if Dr. Sartor or Dr. Yap has a view on translation of SUVmax mean peak/dosimetry data to potential efficacy. Yep. Couple of comments from Oliver here. Number one is there's a huge difference in the absorbed dose that can be taken in a normal tissue and the toxicity that results. The bone marrow is quite sensitive. The kidney is moderately sensitive, whereas the liver is not sensitive. The salivary is sort of stuck in there in the middle. When you think about the dosimetry, you have to think not about normal tissues, but which normal tissue are you referring to? That's why when I had my little opportunity in the fireside chat to talk about renal and salivary, this is where I think you have really exceptional data here. Secondly, the minimum and the maximum on the SUVs that you see in a PET scan can be a little bit misleading because really it's the retention of the isotope that matters. I think that's what you nicely see in the lutetium-177 dosimetry from South Africa. You see the retention. The whole game here is the area under the curve, particularly during the half-life of the administered isotope, in this case, actinium. You can see that the absorbed dose is going to be quite large because of the retention, not the individual SUVmax, but the retention is what counts. Yeah, I totally agree with what Oliver just said. In particular here, we have a massive opportunity in developing a B7-H3 targeting RLT, which is differentiated to the other B7-H3 targeting classes of agents out there. As you think about antibody-drug conjugates, we do see a lot of toxicities. I think that's something that has very much been overlooked and minimized. I think these drugs, we shouldn't forget, are chemotherapy agents at the end of the day, and they do have a narrow therapeutic index. So we do see high rates of myelosuppression, 40%- 50% grade three or greater toxicities, which can be very dose-limiting or are dose-limiting for many patients out there. So I really do think that we have a really differentiated opportunity here with this BC083 targeting RLT. Very helpful. Thank you. Thank you. One moment for our next question. Our next question is coming from the line of Alex Ramsey with William Blair. Your line is open. Please go ahead. Hi, thank you for taking our question. Our question is related to the extrapolation of lutetium-177 to actinium-225, and specifically, we're wondering how the translation accounts for the recoil effect of actinium-225 and potential release of isotope from the chelator upon emission of the first alpha particle, and also how that effect could impact the calculation of total absorbed dose. Thanks again for the question. Yeah, I'll take that one. The mathematical model that we use to convert lutetium-177 to actinium-225 accounts for all daughter emissions and the increased biological potency of the alpha emitter. It's the full delivery of all the emissions at the site or the lesion site or organ. I might briefly comment if I might. Yeah, go ahead. The first alpha emission is going to be purely targeted because you're still in the chelate. With recoil, the second alpha emission has an extremely short half-life, and that extremely short half-life, seconds, microseconds, I forget the exact number, but it's not going to wander at all. The third emission is from bismuth, and that's where some wandering can occur because it's a little over 40 minutes, but most of the data would indicate that the tumor still is retaining the majority of the alpha. Then the last alpha, which is, of course, unchelated, is going to be relatively short-lived after that. I think it's reasonable to take the four alphas when you're doing the dosimetry calculations, even though only the first is actually part of the chelate. Thank you. I'm showing no further questions at this time, and I would like to hand the conference back over to Matt Roden for closing remarks. Well, thanks everybody for joining today, and a special thanks to Dr. Sartor and Dr. Yap for your additional comments here. This will conclude our call today, and let us know if you have any follow-up questions. Thanks, and have a great day. This concludes today's conference call. Thank you for participating, and you may now disconnect.