Good morning. Welcome to Y-mAbs Therapeutics' virtual radiopharmaceutical R&D update webcast and Conference Call. As a reminder, today's conference will be recorded. I would now like to turn the call over to Y-mAbs Head of Investor Relations, Courtney Dugan. Please go ahead. Thank you, Operator. Good morning, everyone. Welcome to the Y-mAbs virtual radiopharmaceutical R&D update webcast and Conference Call. We issued a press release this morning before the market open, highlighting key takeaways from today's discussion. The press release and accompanying slides are available on the IR section of our website. Let me quickly remind you that the following discussion contains certain statements that are considered forward-looking statements, as defined in the Private Securities Litigation Reform Act of 1995. Such statements include, but are not limited to, statements about preclinical and clinical data, regulatory matters, clinical trial timing and plans, the achievement of clinical and commercial milestones, the potential benefits of the company's programs and product candidates, and other statements that are not historical facts. Because forward-looking statements involve risks and uncertainties, actual results may differ materially from those expressed or implied by such statements due to a variety of factors, including those risk factors discussed in the company's previously filed report on Form 10-K for the year ended December 31, 2024, as supplemented by the risk factors discussed in the company's quarterly report on Form 10-Q for the quarter ended March 31, 2025. I will now turn the call over to our President and Chief Executive Officer, Mike Rossi. Thank you for joining us today during our virtual radiopharmaceutical R&D update. Joining me today is Natalie Tucker, our Radiopharmaceutical Business Unit Head, and Norman LaFrance, our Chief Medical and Development Officer. We also have our Chief Financial Officer, Pete Frenshu, joining during the Q&A portion of today's update. I will make a few opening remarks and then hand the call over to Natalie. At Y-mAbs, our vision is to pioneer and develop next-generation therapies, leveraging our novel immunotherapy and radiopharmaceutical platforms to transform patient care for a broad range of diseases, starting with cancer. Y-mAbs Therapeutics was founded 10 years ago with the urgent mission to make innovative cancer therapies available to patients worldwide. Since then, we have brought an important and differentiated antibody therapy, Danyelza, to market in the pediatric oncology space, meeting our mission of helping to improve the lives of patients and their families. Danyelza has provided and continues to provide invaluable quality time for patients with relapsed refractory high-risk neuroblastoma in the bone and bone marrow out of the hospital setting, giving the gift of childhood back to patients. This legacy of impact and improving people's lives is something we are working to expand with our radiopharmaceutical platform and programs. With the establishment of two distinct business units announced earlier this year, we have the people and resources in place to further maximize the full potential of Danyelza in and beyond neuroblastoma, while at the same time accelerating the strategic advancement of our novel self-assembling and disassembling pre-targeted radioimmunotherapy, or SOTTA-PRIT technology platform and programs across targeted disease areas. We are excited to provide you with several updates across our radiopharmaceutical business today. Within our radiopharmaceutical business, we have five strategic enablers, which define our vision for growth, which you can see here. Each of these addresses a significant gap in the current radiopharma space. First, we believe pre-targeting will address the challenge of off-target toxicity associated with many radiopharmaceuticals. Second, we are working toward building a fully operational theranostic platform encompassing both novel radioimmunotherapies and accompanying diagnostic tools. Third, we will leverage the multi-isotope modularity of our platform, which will pair the appropriate isotope to the patient-specific disease characteristics. Fourth, we're putting our investment toward strategic R&D and clinical advancement rather than building large manufacturing facilities for complicated radiochemistries. Lastly, we are enhancing physician participation in patient treatment, allowing for a more collaborative and efficient treatment patient journey. Let me touch on these areas a bit more. By executing our vision for our radiopharmaceutical business, we are well positioned to potentially disrupt both the existing treatment paradigm and the commercial pathway for radiopharmaceuticals with much lower cost and increased access for patients and physicians alike. As I mentioned with SOTTA, we have no need to spend hundreds of millions of dollars on new infrastructure and physical manufacturing plants. With our pre-targeted approach, the assembly of the protein and radioisotope happens in the patient as opposed to a radiopharmaceutical production facility. This allows us to focus our investments on strategic R&D and clinical advancement of high-value target programs and helps keep our overall cost of goods down. Physician participation is a challenge right now with current radioimmunotherapies. Oncology and nuclear medicine largely operate independently when delivering radiopharmaceuticals. SOTTA better utilizes the existing physician infrastructure as the first dose or the pre-targeted dose can be administered anywhere by the oncologist. After the appropriate clearance interval, the patient will receive the isotope injection by a radiation oncologist or a nuclear medicine physician. With SOTTA, each physician plays a role in the delivery of the therapy. SOTTA is patient-centric in it can accommodate a variety of different isotopes using modular designs. Physicians would essentially personalize their radioimmunotherapy treatment for a specific patient. Finally, with SOTTA's pre-targeted approach, we can deliver an optimal therapeutic dose directly to the tumor while significantly decreasing potential off-target toxicity. Let's take a quick look at the progress we have made over the past year and a half. Since joining the company in November 2023, Y-mAbs Therapeutics has reinforced its commitment to radiopharmaceuticals and is leading a brand new generation of truly patient-centric theranostics. 2024 was a year of execution for Y-mAbs Therapeutics. In the past 12 months alone, we have brought an incredible level of radiopharma expertise, in particular with Dr. Norman LaFrance and Natalie Tucker, and many others across our clinical, quality, regulatory, and scientific teams. We have learned a lot from our GD2 SOTTA phase I, part A data, and the additional molecule optimization work has been completed. We have set a path for strategic growth and clinical advancement, which we will share with you today. Looking to 2026 and 2027, we have several potential high-value inflection points and clinical milestones ahead. You will hear more about this later today. Today, we will report on the progress of our radiopharmaceutical pipeline and release the results of our completed trial 1001 part A data, including our plans for future studies. Let me pass the call to Natalie, who will discuss the results from phase I, part A of our GD2 SOTTA trial 1001. Thank you, Mike. I want to highlight the important takeaways and learnings gained from recent insights across our SOTTA platform. First and foremost, we are pleased to achieve the primary endpoint of trial 1001 Part A. The GD2 SOTTA is safe and well tolerated. This indicates that we will be able to advance this, our first ever in-human SOTTA program, through further clinical development and continue to execute on new additional programs, which I will speak about later. In addition, in Part A, we confirmed that the pharmacokinetics of our GD2 SOTTA protein and our Luzoda radiohaptin behaved as expected based on our preclinical studies with allometric scaling to human models. Importantly, the GD2 SOTTA PK presented close patient-to-patient repeatability within cohorts, which validates the performance of our protein and is imperative for determining the optimal time of Luzoda administration. Within our operations, we are moving forward with improvements to streamline our study design and overall operations in order to accelerate our clinical trials. Recent insights collected will benefit our entire platform and support the strategic advancement of high-value targets. Now, let's dive into results from Part A, our GD2 SOTTA phase I clinical trial 1001. Earlier this year, we shared an initial look into data from Part A of trial 1001. Today, we will provide a more comprehensive overview of safety, PK, and dosimetry from the six dosing cohorts in Part A. Additionally, we will share how we are using this data in collaboration with feedback from our KOLs to pave the way for the next steps in both our GD2 SOTTA program and benefit our entire platform and operations across an expanded therapeutic and molecular imaging pipeline. We will begin with the trial background and design. Following extensive preclinical and IND enabling studies with GD2 SOTTA and Luzoda, trial 1001 was initiated in 2023 as a first-in-human study of this novel pre-targeting approach. Seven study sites have been activated to date. The key objective of the phase I study was safety. Secondarily, we evaluated the PK, dose symmetry, and immunogenicity of GD2 SOTTA Luzoda. The original phase I design included three parts, A, B, and C. In Part A, which we're reviewing today, the GD2 SOTTA protein was given over increasing doses from 0.3, 1, and 3 milligrams per kilogram, with varying clearance intervals spanning two to five days. A few key items to note. The trial covered multiple indications, including sarcoma, melanoma, small cell lung cancer, and in the final cohort, high-risk neuroblastoma. Patients were eligible with recurrent or refractory metastatic solid tumors with evaluable disease and standard ECOG in liver, renal, and hematological functions. We restricted prior systemic treatment within three weeks of dosing with GD2 SOTTA. For Part A, the design was split into imaging and therapy stages. All participants first underwent the imaging stage where they were evaluated with CT anatomical imaging. A maximum of five lesions were selected to follow by the local study site team. Patients subsequently received a dose of GD2 SOTTA protein followed by a clearance interval and a 30-milligram dose of Luzoda. All participants had blood drawn to monitor GD2 protein and Luzoda pharmacokinetics, as well as GD2 SOTTA immunogenicity, and received nuclear imaging to determine tumor uptake and radiation-absorbed doses to the tumor and organs. Tumor uptake was determined qualitatively as a clear difference in lesion-to-background activity with a contrast-to-noise ratio greater than three. Like target lesion determination, tumor uptake was assessed locally and at the discretion of the site. At least one of the target lesions had to show positive uptake, as determined by the site, to become eligible for the therapy stage, where they subsequently received another dose of GD2 SOTTA protein and a therapeutic dose of Luzoda, either 100 or 200 millicurie. Only the previously selected lesions were eligible for evaluation of tumor uptake. As noted, we had a heavily pretreated multi-indication patient population. Of the 31 patients screened, 23 were enrolled and treated with GD2 SOTTA protein in the imaging phase. Reasons for screen failures varied, including no measurable disease, lab values out of inclusion criteria, and serious intercurrent illness, among others. All 23 patients are included in our safety set. Twenty-two patients subsequently received Luzoda following GD2 SOTTA protein administration. These patients are included in our imaging set. Of the nine patients with tumor uptake, as determined per protocol, seven went on to the therapy stage, with three receiving 200 millicuries of Luzoda and four receiving 100 millicuries. Two of these patients withdrew before completing their final day 43 blood draw. Across all 23 patients enrolled, we had nearly equal representation for male and females across a wide range of ages spanning 16- 76. Patients were heavily pretreated with radiotherapy, surgery, chemotherapy, and immunotherapy. Most were metastatic to the liver, bone, lung, and/or brain, and there was a wide range of tumor lesion sizes. Of patients selected for imaging, an average of 3.1 tumors were selected per patient by the site for further evaluation. As previously noted, the determination of tumor uptake was conducted locally and per the discretion of the site staff. As we showed during our full year 2024 earnings call, nine participants showed tumor uptake per protocol across sarcoma and melanoma. The small cell lung cancer and the two enrolled high-risk neuroblastoma adult patients did not show uptake. Notably, these high-risk neuroblastoma patients were over the age of 16 and heavily treated with prior GD2-directed therapy. Our Chief Medical and Development Officer, Dr. Norman LaFrance, will now present our safety, PK, and dosimetry data. Thank you, Natalie. Part A of trial 1001 was our first in-human study of the SOTTA-based pre-targeting platform with safety as the primary objective. As you will see, an acceptable robust safety profile was met. As previously reported, Part A demonstrated a robust safety signal. Administration of GD2 SOTTA up to 3 mg per kg and Luzoda up to 200 millicuries with clearance intervals ranging from two to five days was shown to be safe and well tolerated across all six dosing cohorts. Importantly, there were no dose-limiting toxicities or treatment-related serious adverse events observed and no adverse event trends across the dosing cohorts. Per protocol, the DLT observation period was six weeks from the first GD2 SOTTA administration. Dose-limiting toxicity evaluable patients, therefore, included patients who completed both imaging and therapy stages, effectively receiving two doses of GD2 SOTTA and two doses of Luzoda, as well as those who were on study for six weeks from the first GD2 SOTTA administration. A significant finding in our safety analysis was the majority of AEs were not related to the treatment. Those that were related were predominantly grade 1, 70%, and grade 2, 27.5%. The single Grade 3 related adverse event was abdominal pain the day of the first GD2 SOTTA administration, which we'll cover later as one of the three adverse events of special interest. To emphasize, we did not observe any DLTs or treatment-related serious adverse events over the six cohorts. In this data-rich slide, the most common AEs were nausea, lymphopenia, and constipation. However, going back to our demographics, the 23 patients enrolled had diverse primary cancers, were metastatic and progressive, had undergone a number of pretreatments ranging from surgery to immunotherapy, and were on significant concomitant meds to address their cancer. Hence, the AE profile is not surprising. For related AEs, the most common observed included nausea and chills of grades 1 and 2, all of which resolved spontaneously or with minor treatment. Notably, we did not see any dose-dependent AE trends that you would expect to see with the usual GD2 binding, such as pain or hypotension, even with increasing amounts of protein over the study cohorts, indicating, as expected, that the GD2 SOTTA construct, at least to the 3 mg per kg currently studied, does not share nor is as severe as the existing anti-GD2 therapies. Similarly, and despite the fact that seven patients received two doses of Luzoda, totaling up to 230 millicurries, we did not see any dose-dependent radiation-related adverse event trends. To that end, we saw only two patients with a total of three adverse events of special interest. One patient reported abdominal pain with the first GD2 SOTTA protein effusion and did not continue with the subsequent Luzoda dose. The pain observed was non-serious, and the patient recovered on the same day. Notably, this patient had a prior history of cancer pain, nausea, and diarrhea, and had been treated with con meds to manage those. A second patient had a history of elevated liver enzymes, which were maintained following the imaging stage and eventually reached Grade 3 while on study. However, they were deemed non-serious and unrelated to study drug. In summary, the safety data from phase I confirms the safety observations that GD2 SOTTA protein and Luzoda pre-targeting platform provide a robust, well-tolerated approach delivering radioactivity to the tumor without any notable dose-dependent adverse effect trends. Secondary objectives of the 1001 trial included analysis of the GD2 SOTTA protein PK, the Luzoda PK, and tumor and organ dosimetry. This section will show that the PK of our GD2 SOTTA product is dose-dependent, predictable based on preclinical modeling, and demonstrates expected characteristics around CMACs and clearance rates over time. The next few sections will provide more details on these findings. The PK and other preclinical evaluations per standard might be utilized to evaluate our pre-targeting platform. This model was also chosen because GD2 is expressed comparably across tissues, and GD2 SOTTA protein had a comparable binding affinity to GD2 expressing murine and human cell lines. In our murine models, we describe the importance of the concept known as SOTTA trough, which refers to the nadir of circulating SOTTA protein as determined by PK analysis of blood samples over time. The SOTTA trough is a function of the amount of administered GD2 SOTTA protein and the clearance interval prior to the Luzoda administration. Preclinically, we observed that optimal tumor-to-organ ratios were seen when the SOTTA trough was less or equal to 1 microgram per mL prior to giving Luzoda. Using standard scaling coefficients from mouse to human, we modeled the PK profiles of various administered doses of GD2 SOTTA protein, as shown here in the figure on the left. The modeling indicated a longer clearance interval was required to reach the equivalent SOTTA trough threshold seen in the murine experiments for a given scaled protein administered dose. The clinical trial commenced with a study design that sought to investigate the GD2 SOTTA PK over varying protein concentration and clearance interval combinations. As predicted, we observed that higher concentrations of GD2 SOTTA showed slower clearance rates from blood than lower concentrations of GD2 SOTTA, which was highly reproducible when looked at on a per-patient basis by cohort, indicating that even among highly variable patient population, GD2 SOTTA's PK performance is largely a factor of its administered dose. With regard to the SOTTA trough, the highest delivered concentration, 3 mg per kg, did not reach 1 microgram per mL until approximately 120 hours after the administration, which was expected. Lower doses reached the SOTTA trough in less time as evidenced by the 0.3 and 1 mg per kg cohorts. When the GD2 SOTTA PK was normalized by the concentration of the administered protein dose, all dose concentrations had similar CMACs and clearance rates. Interestingly, the 0.3 mg/kg cohort did appear to have a faster clearance rate compared to the other two cohorts. While more data is required to better characterize this difference in our preclinical models, we did see the plasma concentration profiles were dose proportional for doses greater than 20 mg/kg, but lower than dose proportional for doses of 2.5, 4, and 10 mg/kg, which were described to higher levels of monomers at low concentrations having faster clearance than tetramers. Taken together, the first in-human study of the GD2 SOTTA protein and associated PK profiles over varying administered doses shows that GD2 SOTTA protein PK provides a roadmap for determining the SOTTA trough and provides valuable key learnings that can be utilized to further refine murine-to-human modeling for current and future targets. We next evaluated the PK of the radiolabeled half-ton Luzoda to determine by serial blood measurements following its administration. The key takeaway is, unsurprisingly, that Luzoda PK is dependent on both the concentration of the GD2 SOTTA protein at the time of administration and the clearance interval between GD2 SOTTA protein and Luzoda dosing. When Luzoda is plotted against the GD2 SOTTA protein PK, we see a positive correlation between circulating Luzoda and circulating GD2 SOTTA protein. For example, the 3 mg per kg GD2 SOTTA cohort had the highest circulating Luzoda over time. This protein concentration to Luzoda PK is expected and a positive study finding. When looking at Luzoda PK group by cohort, we can further see the impact of the initial GD2 SOTTA protein concentration on elimination rates. The two cohorts at the bottom here are both five-day intervals, one with the 0.3 mg per kg and one with the 1 mg per kg administered GD2 SOTTA. Notably, the top group here is a 3 mg per kg, which is also at a five-day interval. In this case, even though the 3 mg per kg was given after a five-day interval, the higher protein load significantly slowed the elimination of the Luzoda. This reinforces the importance of these data and will allow us to maximize the reduction in circulating GD2 SOTTA protein at the time of Luzoda administration and, most importantly, minimize and mitigate off-target effects. Lastly, we investigated tumor and organ dosimetry. As originally noted, per protocol, up to five target lesions were determined locally by each site via CT prior to GD2 SOTTA protein dosing. Only target lesions identified by the site, which were later deemed to have a contrast-to-noise ratio greater than three on SPECT/CT at the site's discretion, were considered to be uptake positive. Only these tumors were further analyzed by dosimetry. Briefly, serial whole-body planar SPECT imaging supplemented by blood sampling were used for radioactivity measurements following the imaging stage dosing only. Dosimetry was conducted using a hybrid SPECT/CT planar approach using a dose factor-based approach as commonly found in the commercially available OLINDA/ EXM software. Secondarily, in order to understand the performance of our GD2 SOTTA Luzoda complex holistically, we performed an expanded assessment using the TORCH software, which uses voxel-level dose calculations based on the direct Monte Carlo method. In this expanded evaluation, all 22 patients receiving Luzoda were assessed, and all tumors were included for evaluation regardless of their status as a CT-defined target lesion. For the nine patients with protocol-defined uptake, absorbed dose to the target lesions were modest, with organ uptake to the kidney, spleen, and red marrow also evaluated. Unlike what we observed in the preclinical setting and expected in this phase I part A study, no cohort demonstrated an optimal therapeutic index. As a note of clarification, all dosimetry shown is based on the 30 millicuri imaging dose of Luzoda. However, when we expanded the dosimetry assessment to all patients and all tumors, we discovered 16 out of 22 patients had tumor uptake that would have otherwise qualified them for the therapy stage. The column colors here represent the different cohorts, and the table is divided into the original set to the left and the expanded set to the right. All data and calculations were performed with TORCH software. Critically, in the expanded evaluation, we observed a higher tumor uptake in a number of lesions. In some cases, we also observed an improved therapeutic index. Notably, at least two tumors received over one grade, even with the 30 millicurie Luzoda dose. Compared to our original uptake list by indication, we now see that all osteosarcoma patients had uptake in addition to most of the other sarcoma patients. Almost all melanoma patients showed uptake, and the patient with small cell lung cancer also had uptake. Taken together, these indicate GD2 SOTTA is binding despite a variable patient population with heterogeneous GD2-expressing tumors. To further illustrate the power of expanded evaluation, the image on the left shows tumor uptake in a lesion that was not noted as a target lesion. Because the patient had at least one target lesion with uptake, they were eligible per protocol for the therapy stage. The right picture shows a patient who was not eligible because the pre-selected target lesions did not show uptake. However, as evidenced in the image, non-target lesions did show uptake. These data underscore how a broad review of tumors and their uptake is required to better understand the impact of our pre-targeted platform across patients and tumors. Let me now pass the call back to Natalie, who will recap these findings and our key learnings. Thank you, Norman. In summary, the primary objective for part A of our 1001 trial was safety, and we demonstrated a robust safety profile across 23 patients treated with the GD2 SOTTA protein, which includes the 22 patients treated with both the GD2 SOTTA protein and Luzoda. Notably, the safety included seven patients receiving two doses of both protein and radiochelator across the imaging and therapy stages. The GD2 SOTTA protein PK was precise and predictable when evaluated over multiple doses and clearance intervals. Importantly, understanding the GD2 SOTTA protein PK prior to subsequent radiochelator administration is key to informing the optimal trough and clearance interval as related to a given antigen sync and will be incorporated into future study designs. We believe this PK insight and positive safety profile will enable parallel cohort testing, thereby accelerating development. When opening up the tumor uptake analysis beyond the five tumors allowed per protocol and using SPECT/CT as a determining factor, we observed a far greater number of patients with tumor uptake. Critically, this expanded evaluation with concomitant streamlined dosimetry analysis will be built into future designs to allow us to make rapid clinical decisions. Lastly, dosimetry indicated we did not receive tumor uptake or therapeutic index and indicated optimization studies were necessary. We therefore embarked upon a series of preclinical optimization studies with the intent to bring key learnings back to the 1001 trial. In the multivariable preclinical studies on the left conducted earlier this year, we tested each component of the existing GD2 SOTTA Luzoda molecule for optimization. Building permutations of the current molecule and integrating innovative design features, we were able to identify a new molecule with almost double the AUC of tumor uptake compared to our existing molecule used in 1001, with no meaningful change to organ uptake. Our second study, also conducted earlier this year, used our existing GD2 SOTTA protein with the same optimizations as evaluated in study one and a small cell lung cancer model using actinium-225 as the radioisotope. In this study, our optimized molecule was able to achieve greater than fivefold improvement in area under the curve of tumor uptake, again with no meaningful change to organ uptake. As described, we evaluated three components of the existing GD2 SOTTA complex, including the protein itself, the radio halftone, and the formulation. Data indicated no change is required for the GD2 SOTTA protein itself and will allow us to utilize our already existing manufactured protein for ongoing trials. Key changes to the new molecule include a new proprietary half-life and a new formulation. These together are anticipated to increase residence time of the conjugated molecule on the tumor. Our new radiochelator expands our access to a range of isotopes with theranostic applications. Like Luzoda, Proteus binds to SOTTA through an anti-lanthanide dodecadamine with picomolar affinity. Unlike DOTA, Proteus is a universal radiochelator, which, in addition to its better tumor uptake and characteristics, supports a more streamlined development process that can rapidly scale across the therapeutic alphas and betas, as well as optimal diagnostic isotopes for molecular imaging to support patient selection and treatment response monitoring. Proteus will be a key component of our modular platform and will enable isotope modularity as described in our vision for growth. In closing, the combined data from part A of our 1001 trial and the subsequent non-clinical optimization studies are paving the way for the next steps in the 1001 study. We aim to add a bridge study to quickly evaluate Proteus with variable mass doses at six GD2 SOTTA concentration and clearance intervals. We plan for this bridge study to start in the first half of 2026, and we anticipate study results in the second half of 2026. We believe that the molecular improvements will provide a more favorable tumor-to-organ ratio and pave the way for part B, where we will increase the Luzoda administered dose, which we plan to kick off in early 2027 with data results anticipated before the end of 2027. Notably, we are working closely with the FDA on our next IND on a new GD2 PET diagnostic, with filing expected by the end of this year. This GD2 diagnostic will be instrumental in speeding development of this program and will be incorporated into part B to inform patient selection. Now, let's discuss our expanded development pipeline, beginning with a brief overview of our target evaluation. Earlier this year, our team conducted an in-depth target selection work evaluating the next potential high-value targets for our pre-targeting platform. We started with a database of over 1,200 targets and narrowed that down based on incidence, unmet need, and focusing on tumors that are known to have radiation sensitivity. Secondarily, we looked at target-specific attributes such as cellular location, tumor expression, and healthy tissue expression. We landed on 40-50 assets suitable for further evaluation. We then considered market opportunity, competitive intensity, and development risk to prioritize approximately 15 targets for our platform. We force-ranked these 15 targets to develop a mix of archetypes that we believe will diversify our development risk over the coming years. We are focusing short-term activities on targets that are a good fit for our platform and have good scientific validation. As mentioned, the new targets will focus in areas of high unmet need with five-year overall survival rates at or below 50%. These cancers are primarily in three focus areas, namely lung cancers, women's cancers, and gastrointestinal cancers. By focusing on franchise opportunities, we will be able to leverage development and clinical synergies, thereby allowing the appropriate development focus. Aligned with our belief that a theranostic pre-targeting approach will accelerate development, our radiopharmaceutical pipeline now includes molecular imaging. We plan to pair a direct targeted PET diagnostic with each of our therapeutic assets, with the first moving into IND later this year. This molecular imaging asset will be the first of its kind to identify GD2 expression in the clinic. We anticipate the first patient to be dosed early next year. Also notable in our pipeline is our next-generation therapeutic asset focusing on metastatic colorectal cancer. Development of this asset has already begun, with preclinical studies underway. This study leverages our proprietary and universal radiochelator, Proteus, and will be our entry into alpha therapies, with planned testing of actinium-225. Accompanying this target is our diagnostic asset, where testing of both Zirconium-89 and Copper-64 will begin this year. We plan to file an IND on this asset in the first half of 2027 and anticipate the first patient to be dosed in the second half of 2027. Since the beginning of this year, we have completed two optimization studies, and we're currently manufacturing our new universal Proteus. We have redesigned our operations, and we anticipate leveraging learnings from part A to accelerate future and ongoing development. These accomplishments have led to multiple high-value inflection points ahead. First, we plan to submit an IND for our GD2 PET diagnostic later this year using Zirconium-89, and we anticipate to see initial study results in 2026. We believe the benefits of a GD2 diagnostic will not only benefit SOTTA development, but our entire business, helping to expand naxitamab indications as well. We anticipate results from our GD2 bridge study in 2026, and we plan to immediately initiate our dose escalation trial in adult patients and separately initiate a pediatric GD2 SOTTA study upon receipt of meaningful results. To reiterate, we also plan to dose our first metastatic colorectal cancer patient in 2027 using an alpha therapy. I will now pass it back to Mike to close us out for today. Thank you, Natalie. Before we open the call for Q&A, I want to reiterate key takeaways from today's discussion. Data from part A of trial 1001 demonstrates that our GD2 SOTTA protein is safe and well tolerated. In addition, the protein PK can be used to optimize the dosing interval and maximize the therapeutic index. We believe our new universal radiochelator benefits our entire platform, accelerating development, streamlining regulatory efforts, enabling patient-centric treatment through isotope interchangeability. The new target franchise opportunities in oncology we plan to advance are scientifically and commercially fit for purpose and address large unmet medical needs. Together with the proven safety of our SOTTA platform, the precision and predictable PK, and our redesigned operations, we believe we will accelerate the development of our next-generation SOTTA platform. I'm proud of the extensive work and progress our team has made across our radiopharmaceutical business. We believe we are well positioned to potentially disrupt both the existing treatment paradigm and the commercial pathway for radiopharmaceuticals. Thank you. 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. Our first question will come from Bill Maughan with Clear Street. Your line is open. Hi. Good morning and thanks. Just thinking through the addressable patient population, I know after infusing the lutetium, you found patients who would not have otherwise qualified. Do you think that this expands, I guess, the definition of what would be a GD2 positive patient? When you layer in a diagnostic on top of that, do you expect to find the broader patient population versus maybe what you would have found earlier, if that makes sense? Do you expect efficacy to be similar in both that initial positive patient population and the expanded positive? Thank you. Bill, thank you for the question. Just as we look at this, just to make sure I'm understanding you correctly, you're asking about expanding beyond the initial nine patients with the positivity. Yeah. As we look at this, I'll kind of set this up and I'll turn over to Norman. As we looked at this, the clear differentiator between the nine and the additional patients is stepping from what the original protocol was and looking at specific predefined tumors on CT to where the uptake occurs throughout the body. In a short answer, I'd say yes, these patients appear to have GD2 positive because they have uptake. When you're binding to those receptors, you're not constrained by what was seen on CT. With nuclear medicine, you have the ability to see that receptor expression regardless of where it is, even at smaller quantities that may not be visible on CT, picked up on CT, or even tumors that have been so heavily pretreated, they've, I want to say, encapsulated, but you've destroyed kind of the receptors that are on those. It's some of the newer metastases, some of the newer untreated that tend to see the uptake. Norman, I'll—. Yeah. Thanks, Mike. Bill, the question makes total sense. You kind of indirectly answered it yourself. Clearly, with the expanded approach to take benefit of not only the anatomical direction of the CT, which Mike just mentioned was the protocol design, we emphasize utilizing all the available information, particularly the targeted information that, as we presented, showed more patients with the GD2 tumor avidity. This is also presented, emphasized, and showed us that the GD2 protein was fine. That's recognizing the GD2 tumors very well and will help us design future protocols utilizing all the information. You brought in a diagnostic. Having patient selection is always desirable. What we found here is the design with the lutetium imaging dose, which many people do, is one option for patient identification. But as you've heard, we're developing a diagnostic, and we feel this will have even better patient identification capabilities, which will likely further expand the success of this GD2 platform. Hopefully, that answers your question. If you want any more clarification, let us know. Yeah. Bill, just one additional thing. The last thing you asked about was efficacy. I think as we look at this, it's clear you can't predict efficacy. What we can predict is the better the GD2 expression or any targeted expression, the better the opportunity to deliver the isotope to the affected cells and then increase your therapeutic index on that. I think that the better we select these patients, the better you see them upfront, the more opportunity you have to have at least similar, if not better, efficacy than you have with other products. Since we've seen it in GD2, do you expect this kind of expanded ability to identify patients to be applicable to other targets as well? Yeah. I think it's really target-independent. As we look at this, the beautiful thing about nuclear medicine is its functional imaging. You actually see what's happening. You see the organ working. In this case, you see the expression. We see it with the other targeted radiopharmaceuticals that are in the market today. You determine the expression first with diagnostics and then go for the therapeutics. With that, it's very common in the targeting to make sure that we target those that have good expression and we're able to treat when the expression is the highest. Thank you very much. The next question will come from Li Waek with Cantor Fitzgerald. Your line is open. Hi. Good morning, guys. Thanks very much for taking our questions. I guess just first one on tumor uptake. It looks like there's some variability here, maybe lower uptake in some tumor types like Ewing's, medulloblastoma, or neuroblastoma. Just wondering why do you think that's the case if these patients are positive for GD2? For the next generation half-life, I mean, what do you hope to achieve with the therapeutic index just from a dosimetry standpoint? Yeah. We'll take that in kind of two parts. First, we'll talk about the tumor uptake, and then we can really dive into kind of what the half-ton will do. What I'll do is turn it over to Norman first to discuss the tumor uptake and the variability, what we see. I think Natalie will be in a good position to talk about the half-ton and what that'll do. Yeah. Thanks, Li. As we pointed out, the phase I was directed to safety, but we opened it up to all tumors that have had prior descriptions of GD2 avidity, which vary by the diagnosis, as everyone knows. What we showed with the additional evaluation with TORCH, that initially when we thought some of the tumors were not showing avidity, it was because basically they were preselected by only CT "target lesion criteria." When we opened that up to include the SPECT data, the lutetium-DOTA imaging dose, many of these other tumors, and we had a slide that showed that all the osteosarcomas, majority of the sarcomas, a lot of the tumor showed the GD2 avidity that was consistent with the published GD2 expression that people know. This gets back to Mike's comments earlier and what I think we've all said, and I've heard from many of you that patient selection ahead of time for GD2 avidity will likely be an important part of the treatment paradigm for GD2. I might emphasize, although there are some tumors like pediatric, early pediatric neuroblastoma that is known to have very high GD2 avidity, there are other tumors that would benefit from this therapy. Sarcoma, for example, osteosarcoma, melanomas, triple-negative breast, there is lung cancer. These are the ones that will likely really be available for a GD2 therapeutic intervention, particularly with the availability of a GD2 diagnostic. Hopefully, that helps. Lee, just as a follow-up to that, the thing to be cognizant of too, all the dosimetry is based on a 30-millicurie dosimetric dose and not the therapeutic doses. When you look at that uptake, it is at the diagnostic levels. It is also that needs to be optimized, which leads us to the radial half-ton change and what our plans are for the future with that. Natalie? Yeah. Sure. Thank you, Li, for the question. Going back in terms of the impact of the optimization on the therapeutic index, just to recap, we're expecting to make two changes, and we're planning on those changes right now, one to the radial half-ton and one to the formulation. The half-ton itself has two big benefits. Number one, it is universal, so we'll be able to use it across all of our different formats, including our diagnostic. Also, critically important, the tumor uptake. You did see in the pre-clinical studies that we saw tumor uptake area under the curve two to five times. What's so important about that, if it wasn't evident, was the time retention on the tumor. Because it retains so long on the tumor, you're able to extend that dosing interval, allow the protein to clear from the blood while you still have tumor retention, and then dose the lutetium. It really does add an improvement to the therapeutic index for that reason. Again, we're seeing those increase in tumor uptake two to five times. In terms of the formulation, we're also doing a change there where we increase the amount of protease that we deliver, effectively increasing the mass. What that actually does is it acts as a clearing agent in a way to clear the protein from the blood so that you can also increase your therapeutic index. What we've seen, it actually marginally reduces the off-tumor effects so that we really see the upside on two fronts, both from the half-ton on the increased tumor uptake as well as the formulation on the decreased off-tumor uptake. Hopefully that addressed your question. Okay. Thank you, guys. Thank you, Lee. The next question comes from John Neumann with Cantor. Your line is open. Hey, guys. Good morning. Thanks for the update, and thanks for taking my question. You have talked a lot about the PET diagnostic going forward, that this will be refined and sort of designed for each specific indication. I'm just wondering if at any point in time going forward, you'll be able to develop an additional assay for GD2, perhaps something more similar to some of the assays used for other targets such as IHC, although that may not be applicable here, or if we should expect that at least for GD2, you'll be relying on the PET diagnostic? Yeah. John, thank you for the question. It is a great question. The challenge with GD2 is something that the industry has been fighting with for a long time. Many institutions have tried. We have tried several different ways to get a conventional IHC in order to move forward. In order to get a validated test, you really need to be able to preserve it. And it's generally a paraffin-based test, which the paraffin destroys the GD2 receptors. So it doesn't allow you to look at it. There's been some fresh frozen that show GD2 expression, but it's very difficult to validate because it is institution by institution. So as hard as we've tried over the years, it's been very difficult to do. That's why it was so exciting to get GD2 SOTTA into patients and actually start seeing that receptor expression. And maybe I'm a bit tainted as a nuclear medicine person, but when you can actually see something live and you see the amount of expression, you see that affinity, it gives you a much better direction on which patients to select, which indications. I think with GD2, and again, I defer to others as well, but I think our best option going forward is a nuclear medicine imaging agent, a PET agent to patient select for GD2, both for radiotherapy as well as Danyelza. One additional question. You mentioned in your prepared remarks that you're looking to potentially have data in the second half of 2026 for the part 2A study with the optimized Proteus radiolabeled half-life. I'm just curious if perhaps maybe internally, will you be able to take a look at PK ahead of that, or should we expect all of that data to sort of come in the second half of 2026? Yeah. John, good question. We're actually building that timeline as we speak. We're looking at both the bridging study as well as the part B as part of that as rolling it forward. For me, the PK is much easier to have those conversations about on a patient-by-patient basis. We've seen a lot of consistency across all of the patients on the PK. It gives us a level of reassurance on how SADA's performing, what that looks like, what the clearance looks like. Ultimately, when we start looking at the therapy and the imaging, I think it's important that we aggregate and look at at least groupings of patients so that we're not looking at this as results coming in from individuals. You want to see what the overall evidence says across a larger group. I'll turn it over to Natalie on kind of what the plan is. I think overall, it's important for us to look at this and aggregate the data so that we know exactly what we're looking at and not make assumptions based on a single patient. Yeah. Good point. Thanks, Mike. And thank you, John, for the question. In terms of that part A2 study for the bridge, I mean, we're really looking at running two parallel cohorts. We mentioned this earlier today in our opportunity to accelerate. That first cohort, number one, we'll be really evaluating. We'll be swapping out that Luzoda for the Lu Proteus and evaluating the safety, PK, and dosimetry. Exactly what you said, our goal and what we've mentioned today is PK really drives our dosing interval and our therapeutic index. We'll be looking at the PK very early, and we want to run a parallel cohort where we also adjust the mass dose, so our formulation change. We are thinking around six patients based on statistics that we could run in parallel. That's why we hope to have that data by the end of 2026. Okay. Great. Thank you. Thank you, John. The next question comes from Alec Stranahan with Bank of America. Your line is open. Hey, guys. Thanks for taking our questions. A few from us. I guess first, are there any optimizations to the tumor binding motif of the GD2-SADA construct you're contemplating to maybe make it a bit stickier for the tumor, or is the path forward really on this piece with the half-ton and the formulation? Secondarily to this, I guess, is this maybe more of a GD2 target issue or a SADA issue in your view, just reading through your other program? Yeah. Good questions. As we look at this, we're not planning on any changes to the GD2 SADA protein itself. For us, it's optimizing the radial half-ton to increase the affinity. That becomes a platform change. When we look at moving forward with the protease, it'll be used on all. GD2, again, the only validated GD2 target is pediatric neuroblastoma. A lot of this is a bit of a learning experience, and it's an N of one. We'll learn more about the additional targets as we move forward on the best way to optimize those. I think also looking at our development plan forward, as Natalie had discussed, we're looking at manufacturing for phase-specific development, which will give us the opportunity to tweak that protein on the high-value targets to make sure that both the lead sequence and the SADA itself has the highest tumor affinity. Combining that with the proprietary radiochelator will allow us to maximize the therapeutic index on these. Natalie, is there anything else? No, I think just going to Alec's question regarding is the issue GD2 itself. I think that speaks to the fact and the importance of having a diagnostic so that we can preselect those patients for therapy because it is a very heterogeneous population of tumors. It is really hard to predict what should be showing uptake and what should not. That GD2 diagnostic will really benefit us as we go into the later studies later next year. Okay. Got it. And then just on the CD38 program, do you think this is also impacted by the planned inclusion of Proteus, or I guess what's sort of the path forward given the first patient, I think, was initiated in the first half of this year in that study? Thanks. Yeah. Good question again. We're continuing with the CD38 study and evaluating each patient as they come in. It will have an effect as we move forward with the program to then take that bridging study, and that'll be completed for that radial half-ton. We could plug that into any of the SADA trials to increase the overall affinity. Ultimately, again, similar to our 10-01 trial, the 12-01 is a safety study with the protein. No change is needed at this point to get the information we need from a safety and a PK. As we start looking at moving into efficacy is where we'll move into the protease. That makes sense. Thanks for the call. Thanks, Alec. The next question comes from Justin Walsh with Jones Trading. Your line is open. Hi. Thanks for taking the question. Maybe the first one. Can you confirm if the new alpha therapies, are those making that you're planning on using the SADA platform for those? Yes. Got it. Maybe you can give us a little bit of color on where you see the opportunity in metastatic castration-resistant prostate cancer. I think that's listed as the new target for the IND submission for staff of 2027. Obviously, there's a lot in PSMA out there, but others are working on some novel targets in prostate cancer. Curious how you view the landscape. I'm sure you can't give too many specifics right now, but just wondering on the positioning. Oh, Get, I appreciate it. I'll turn that over to Norman, who can definitely help walk through that. That's a great question. I guess the short answer is there's applicability of our platform to the PSMA. I'd summarize it that the two-step PRIT is feasible against PSMA even as an internalizing target. We've looked at various clones, some with excellent potential in the castrate-resistant prostate carcinoma. We've done some comparisons, and they're promising. I really can't go into detail now. That's not by being secretive. It's just we have additional data to do. The feasibility, again, for targets that seem to internalize seem to be promising here. We have gotten some very provocative preliminary data. We are running more experiments. Stay tuned for that development. I think I would add also, besides your question on prostate, we are looking also at colorectal cancer. There is some very promising data on that target that I will defer to Mike on how much we disclose. Yeah. Justin, as we look at these, for us, we are going to focus in three franchises for what we want to commercialize. Things like prostate, although the platform is very good for that, we will make that decision as we move forward on if it is something that we help somebody else get into the two-step, whether it is something that we consider doing down the road or if it is something that is good enough where it is, At the end of the day, it's all part of the evaluation and both from an internally commercialized product as well as potential BD partnerships. Got it. One more, if I can. I'm curious, as we're kind of moving forward and we have this optimized radial half-ton we're working with, and then also you're moving into trying things with alpha therapies, is there a certain tumor-to-kidney ratio that you define as sort of a SADA success? From broad sense, obviously, I'm sure it's kind of dependent on the particular cancer and some of those other details, but curious what your thoughts are moving forward. Yeah. No. As we look at these, I wouldn't say there's one single number on a tumor kidney, especially difference between alphas and betas. Looking at the overall half-life of the isotope, where we have a lot of flexibility with SADA is using shorter-lived isotopes. If you have a situation where you've got great tumor affinity for a short period of time, using the shortest-lived alpha isotopes gives you the best therapeutic index on that and the best ratio between the tumor and kidney. A lot of the kidney data is all based on external beam. There is so much happening right now in collecting the data on systemic radiotherapy and understanding what the appropriate levels are. Again, the larger the difference between the tumor and the off-target, the better it's going to be. As we look at this, we want to make sure that we're focused on tumor absorption. We're looking at kidney function, liver function, because it's ultimately, is it causing damage both short and long-term? Is it reversible or not? Is that the right way to move forward? Again, with the betas, you want a much bigger tumor-to-kidney ratio. The alphas, maybe not so much, and it gives you a lot more flexibility. With our platform as well, what we know is the lower the nadir in the blood upon injection, the less toxicity you see off-target. To me, the one key for us is making sure that we're injecting at the right period of time, whether it's an alpha or beta, and you will create that differentiation you're looking for. Great. Thanks for taking the questions. Sure. The next question will come from Nicole Germino with Truist. Your line is open. Hi. Good morning. Thanks for taking my question. I noticed that there was no tumor uptake with the two neuroblastoma patients. Can you explain why or was it not enough dose? Should we think of GD2 SOTTA as part of the life cycle management for Danyelza, given that you already have so much expertise in the GD2 space with Danyelza already? Would that be more or is this more of a proof of concept and this will be used as a format to kind of help build the foundation for the pipeline, or will this also be a key target for further clinical and commercial development for GD2? Yeah. We'll break that into the two halves. We'll start with the tumor uptake and what we see on that and what the expectations are. That'll turn over to Norman to talk about that. As far as moving forward with GD2, I'll address that upfront. I think all of these, as we look at them, Danyelza is a fantastic product, and it has its own life cycle plan for continued expansion. That is part of the reason for getting into the GD2 diagnostic for us to be able to really patient select for things like for breast, for lung, for sarcomas. We plan on continuing to invest in Danyelza and move that forward. Now, as far as the GD2 product itself as a SADA GD2, that too may have its opportunities to go after some similar indications, and it may be in conjunction with, it may be sequenced. Time will tell as we develop the evidence on that. It is not a plan to replace Danyelza in any stretch of the imagination. As we look at this, the diagnostic can enhance the opportunity to continue to grow Danyelza. Then the GD2 as a separate commercial product, if we see that it is a benefit to continue that. I'll turn it over to Norman to talk a little bit about the tumor uptake. Yeah. Thanks, Mike. Nicole, it's a good question on neuroblastoma. You'd expect more avidity, which I think is what you're getting at. I want to emphasize both of these were older patients for neuroblastoma, I think one in the 20s, one in the 30s, so in the early 30s. The way I'd approach it, even though neuroblastoma de novo, particularly in the early presentation, kids are two to four years old, for example, oftentimes, it's well known their GD avidity is north of 90 expression, excuse me, is north of 90%. The biology for these older kids typically present in late teenage years and then extend on as we have with these two patients. The biology is different. The GD2 expression likely differs. Importantly, in these patients, there was a lot of pretreatment, multiple pretreatments, all of which I think probably influenced it. Different biology, heavily pretreated. We saw with the data presented over many tumor types, it really was not the antibody issue because we saw avidity across many tumors. When we had the additional evaluation with the TORCH methodology and looked at all the data, we had a broad representation of recognizing tumors if they had GD2 avidity available. I think it was, in this case, these two older patients with the different biology of a later neuroblastoma development were negative. That is what happens. It gets back to Mike's point on having a diagnostic product to be able to patient select. I'll add as a caveat, I just came from the ANR meetings, the Association for Neuroblastoma Research, and a lot of excitement there, a lot of pure antibody approach for their treatments, of course, and much of it GD2. I got as many questions about our diagnostic and the need for that even with the high expression of neuroblastoma. It's not just us waving the flag for a needed diagnostic, I think, as people recognize it's the KOLs. Thank you, Norman. Thank you, Nicole. Our next question will come from Mike Alts with Morgan Stanley. Your line is open. Good morning. Thanks for taking the question. Maybe just to follow up on some of the tumor uptake questions and just curious what other factors might influence the uptake. Sounds like tumor expression or target expression on a tumor is key, but just curious if you're learning other factors that may influence this, for example, tumor size or maybe tumor location. Thanks. Yeah. Mike, I appreciate it. And again, as we look at the variability on tumor uptake, there are several variables. I'll let Norman address that. One thing to keep in mind too on these are these were all heavily pretreated patients, many of which had received anti-GD2 therapy, which we know if you're failing on that therapy, generally, it's a receptor-driven issue. I'll turn it over to Norman to kind of talk about what some of the variables are in there. Yeah. I think we've tried to approach the tumor avidity part and with the extra evaluation. The antibody per se is fine. We showed with the additional evaluation that it was positive in a broad array of tumors that we presented. Importantly, people want to see the osteosarcoma. When you look at all the data, we saw a much better percentage of avidity. I think it points out to really protocol design that you do not limit yourself to, say, an anatomical selection of the biggest tumors. You rattle off some of the criteria that can influence things. The strength of some of the diagnostic process, you could have a small tumor that resolution could be an issue. If you have the avidity or the expression density, you will pick up that tumor. The other advantage is, for example, a GD2 assay was raised. Everyone has tried that for decades. Imaging will give you not only the presence or absence of that target, but the location of the target. At the end of the day, I think having a diagnostic product and making sure you utilize all the data available will be most important. That is, I think, one of the big learnings we had here, that when we did the initial analysis, a broad array of tumors were positive. We found that the radial half-ton, we had avidity. Sometimes, if you do not have the proper radial half-ton, particularly with the chelate linker for the antibody, you might miss it. It was not an antibody issue. It was the radial half-ton that we discovered and have optimized. Hopefully, that makes sense to you. Thanks for the question. Yeah. Thanks. Thanks, Mike. Yeah. Thank you. The next question will come from Jeff Jones with Oppenheimer. Your line is open. Good morning, guys. Thanks for taking the question. I guess a lot of questions have been answered really on the PKPD. I guess at this point, where's your head in terms of thinking about the optimal isotope delivery timing versus SADA dosing? That seemed to be pretty consistent and just SADA-driven. As part of that, was there any impact of the tumor burden on that SADA trough? Jeff, thank you for the question. As we look at this, I'll turn this over to Natalie, who could talk a little bit about what the optimal window is as well as what we expect on tumor burden. Yeah. Thank you, Mike. Thanks, Jeff, for the question. When we talk about the optimal isotope delivery timing, it really is driven by the PK. I think you mentioned that really it's getting below that trough level and timing the dose of the radiochelator when we reach the nadir. We saw that in our preclinical, and we did see it play out in the human trial, which was really exciting. We are going to use that PK in all of our trials going forward to identify the optimal timing to deliver the radiochelator and the isotope. Your second question, the impact on tumor burden, the tumor burden impacts the trough. We didn't see that, right? Because if you look across cohorts, they were very variable, right? We had six different cohorts of different proteins, protein loads. Yet, at the same point in time, we saw a precise and predictable PK across those cohorts. Those patients presented with anywhere from one to five tumors, but yet we did see that repeatability. Kind of directly answering your question, no, there was no direct impact of the tumor burden on the trough because that PK was quite precise and predictable. Great. Thanks. As we think about the CD38 program and switching to the new half-ton, should we be thinking about a similar timeline for the SADA program for part B, so sort of a 2027 start there? Jeff, I'd say on this, the CD38 is still under review. We've dosed one patient in a very difficult-to-acquire patient population. We're looking at patient by patient, and we'll make those determinations. If it moves forward beyond the safety study, we would absolutely be moving forward with the Proteus radial half-ton. However, that's still very early in that program. All right, guys. Thanks. Appreciate it. Thank you. The next question will come from Chiara Montironi with Van Kempen. Your line is now open. Hello, team. Thanks for taking my question. A quick follow-up regarding the PET diagnostic. I was wondering, would you please help us understand the market opportunity for diagnostic with your SADA approach for GD2 and also beyond GD2? Yeah, Chiara, great question. As we look at the PET diagnostic, I'll let Natalie address kind of what the business case looks like. Going back to any diagnostic, as we look at this radiopharmaceutical space, and I'll use prostate for an example. Right now, the prostate PET diagnostic market is north of $1.5 billion just in the diagnostic, right? In the therapeutic, you're looking at $2 billion-$4 billion at this point. The diagnostics themselves, depending on the size of the patient population, incidence rates, prevalence pools, how it is being used, there are significant opportunities. Even in the rare disease space, like neuroendocrine tumors, we see the diagnostic north of $200 million in sales. Even in the rare disease space, the potential on the diagnostic is very high. In this case, there is a lot of excitement around the GD2, especially because there is no other alternative to determine GD2 expression. There are a lot of patients that really need to be treated, need to be selected. For us, it is an opportunity for us on both the diagnostic and the therapeutic, but more importantly, it is selecting patients that are going to best benefit from the therapies going forward. Natalie, if there is anything you want to add on the diagnostic. Yeah. Thanks, Mike. And thank you for the question. I think Mike spoke pretty well about the opportunity beyond GD2. With this first product on our PET diagnostic that we're going to bring to market, that is specifically for GD2. When we look at the population for our trials, we're going to be looking at pediatric neuroblastoma as well as osteosarcoma and a second cohort, including our adult patients, including neuroblastoma, malignant melanoma, small cell lung cancer, and TMBC, which is identical to our 1001, as you will notice. Really, when you look across all of those different study populations, the opportunity is quite large. If you look at any other diagnostic on the market, I'll take the prostate that Mike gave as an example. You really need to think about it in three different approaches on how a clinical site will use that diagnostic. Obviously, you think about it from the inclusion criteria, but you'll see that the majority of use cases are in the response to treatment as well as the ongoing monitoring. Those can be two to three times the population and the use cases as the inclusion. It is kind of three phases. When you look at your modeling, we need to look at all three of those: the inclusion, the response to treatment, as well as the monitoring when we think about diagnostics. Thank you very much. Thanks, Girl. The next question will come from Kemp Dolliver with Brookline Capital Markets. Your line's open. Great. Thank you. Earlier on, you said that this experience is giving you some potential, I guess, opportunities to speed up execution. Since you're going through this process a few more times, at least in the next couple of years, how much of a benefit should we see with regard to the speed of execution in these early-stage trials? Yeah. Kemp, a very, very good question. I'll turn that over to Natalie. Before I do, just as we walked into this, the GD2 SOTTA and both GD2 and CD38, the goal was to get into patients very quickly and to really start looking at the feasibility of the two-step approach. For us, it was speed into patients, get that information, and understand what we have. Now that we've learned from that, I could let Natalie discuss a little bit of how we plan to get this data much more quickly and how we plan to move forward and benefit from that across multiple products. Thanks, Mike. Thank you, Kemp, for the question. Just kind of talking about speed of execution, I do want to reiterate what we've done since the beginning of the year. We did move into these two business units early in the year. Since then, we've been able to run two preclinical trials in order to optimize our molecule. We've already had that molecule in manufacturing. When you look at speed of execution, we've already started to deliver on our promises there as we've been able to execute a lot since the beginning of the year. When we look at our upcoming trials and our ongoing trials and what we're going to expect to see, you're going to see a lot of benefits when we look at parallel cohorts, number one. That's going to accelerate tremendously. You're also going to see a lot of acceleration when we look at dosimetry. We've been able to identify opportunities to improve with centralized imaging, with real-time dosimetry, and with ways to really gather our data much quicker. With that, we expect to see if you take, for example, our 1001 part A, that's been 14-15 months, but yet on our bridge study, we think we can get it done in about six months. We're looking at accelerating mostly because we've been able to prove the safety of GD2-SADA. Once we've proven the safety, that'll allow us to quickly accelerate going forward. Kemp, Thank you very much. Appreciate everyone for joining. We're up on time. I just want to thank you again for joining today's call and hearing about the progress made across our radiopharmaceutical business. We look forward to providing updates on key milestones and inflection points across our pipeline. Appreciate you joining, and have a great day. Thank you for participating. This does conclude the call for today. You may now disconnect.