Good afternoon, everyone, and thank you for joining us here today. It is my pleasure to introduce Mike Rossi, President and CEO, of Y-mAbs, who will be leading the presentation today, and Bo Kruse, CFO, who will be joining Mike in the Q&A. With that, I'll hand it over to Mike. Thank you, Mike, for joining us here today and sharing your story with us. Well, thank you very much, and welcome to everyone. Thank you very much for attending our presentation of Y-mAbs Technologies, Y-mAbs Therapeutics, excuse me. My name is Mike Rossi. I recently joined in November as the President and CEO, so I'm looking forward to taking you through our novel pre-targeted radiopharmaceutical platform, as well as our antibody-based therapy, DANYELZA. So thank you for attending. As a disclaimer, please note that any of the forward-looking statements may be made today during our presentation, and our disclaimer is available on our investor relations website. So Y-mAbs was founded in 2015, with the specific, clear goal in mind to ensure and provide therapies for both pediatric and adult patients across the globe. Since then, you know, we've been able to really advance our novel platform and move forward on both our monoclonal antibody commercialized product, DANYELZA, which is the first humanized antibody for relapsed refractory high-risk neuroblastoma, as well as continuing to develop our SADA platform, which is a self-assembly and disassembly tetramer that's used to tag radioactivity to specific targeted tumors within the body. The radioimmun platform is exciting. As we know, radiopharmaceuticals are growing in popularity. We see the effect of it, and I think we're well-positioned to have a great discussion today on what that means for the future of the organization. More importantly, we also have DANYELZA, and DANYELZA is our monoclonal antibody that is reaching children today with the high-risk neuroblastoma. We've marketed that product. Now we're a little 2 years past launch, growing that product both in the U.S. and ex-U.S., and continue to grow that across the globe and move it earlier and earlier in the treatment cycle. We've got some great milestones coming this year, which is going to be very exciting. First and foremost, we have the initiation, or we'll have a readout later in the year of our Part A of our Phase 1 GD2-SADA readout. I'll share a little bit of that data today, and the rest of it will be shared in totality as we move forward toward the end of the year at a medical conference. We'll also have our CD38-SADA. That'll be initiated in the first half of this year. We have an approved IND and are working to recruit our first patient, so that'll be two of the SADA targets in first-in-human in the U.S. Additionally, we have some MSK data coming at the end of the year on an osteosarcoma readout for our naxitamab and our DANYELZA product, so we're very, very excited about that. In addition, we are a commercial-stage, self-funding biotech company. As of Q3, we have $87 million in cash and cash equivalents on hand and have financial run rate at our current program levels, as well as our planned program levels well into 2027. So I'm very excited about that. We've reiterated guidance for our 2023. We'll be reporting that formally, and when we bring out our fourth quarter data, as well as providing 2024 guidance at that time. As you see, we have a very significant pipeline, and we're really focused on bringing high-value products to the market and initiating with our partners, both in MSK as well as BCC-initiated trials. We continue to bring these forward in both our naxitamab and our SADA platforms. So our DANYELZA program, we've completed our 201 and our 1230, and additional studies going on that'll be initiated with our BCC partner, so Beat Childhood Cancer, to bring it front line in the high-risk neuroblastoma. In addition, we have our SADA platforms. Our 1001 study is initiated, and I've said we were in phase 1, completing Part A. I'll explain a little bit later about what that means. We'll also be initiating our 1201 later this year in first-in-human in the non-Hodgkin's space for CD38. In the future, we also have two additional SADA molecules that we're further developing that we expect to have first-in-human in 2025, and that includes both our HER2 as well as our B7-H3. We will also further advance and expect this year to initiate an IND for our GD2 SADA in neuroblastoma. Continuing our legacy in the neuroblastoma space in children, and that'll be our pediatric trial with our GD2 SADA. I think now is a good time, as we discuss, to really turn our attention to what the SADA platform is and what that means to the future of the organization. So we're very excited about our novel platform of SADA. When we look at the radiopharmaceutical space, and I've spent the better part of three decades focused on radiopharmaceuticals in both diagnostic and therapies, we know there's challenges in reaching patient care. We know there's challenges in commercialization and infrastructure. Four of the big areas that we look at, one is infrastructure and manufacturing. We see the investment going in to make these pre-targeted molecules. So to make a radioactive therapy, you need a specialized facility that can combine your protein or your ligand with your radioactive tracer. You have very limited time to make that delivery, so all of the investment going into that is specialized investment that just doesn't exist today. Physician participation has always been an issue. Most of the physicians that are actually treating and owning the patients can't prescribe radioactive products. They can refer the patient on to somebody who can, but in this case, the oncologist who has been treating the patient needs to refer them to another physician in order to treat. And participation, you know, if you're not doing it yourself, it's not top of mind. So in this case, you know, we have an opportunity to correct that as well. Administration sites. So from an infrastructure across the globe, we need specialized suites, radiotheranostic suites, lead-lined rooms, specialized bathrooms, specialized infusion centers, in order to be able to administer all of the products that we currently have in the market, let alone what's coming. So we have an opportunity here, as we discuss SADA, how we address some of those. And last is continuing drug shortages. As you look at this and you're seeing a ramp-up, it takes a while to build that infrastructure. So you see continuing drug shortages, delays in patient care. As we're trying to get more and more radiopharmaceuticals to individuals, it becomes much more challenging. So our goal is to simplify this process and to solve each one of these problems, and we can talk about what that means. So from an infrastructure point of view, as we start looking at this, we've got some opportunities with SADA. First and foremost, from a toxicity. The way SADA works is we actually inject a cold protein, so that protein is non-radioactive. It gives us the opportunity to get it into the system and to clear it out before the radioactivity comes in. So you'll remove the circulating drug prior to the radioactivity, so what's left is a painted tumor. So by doing that, you increase the dose to the tumor and decrease the toxicity to things like the kidneys, as well as other, you know, salivary glands, lacrimal glands, bone marrow. The shortages, when you look at that infrastructure, by injecting a cold protein first and then the radiotracer later, you no longer need these large facilities to centrally manufacture, release the product, and ship it in such a short period of time in order to infuse it into the patient. In this case, you administer the cold protein in a regular infusion center, allowing the oncologist to participate in the infusion and treatment of their patients. Once that's infused, it's into the body. The PK levels, you allow the drug that's circulating to exit the body and then send them to the nuclear medicine department or imaging centers for the injection of the radiotracer. That then allows you to utilize all of the existing structure in the infusion centers and oncologist offices, freestanding infusion centers, as well as outpatient centers for the cold infusion. And then, again, you're utilizing the nuclear medicine departments and licensed imaging centers for the isotope infusion. Anytime you can utilize the existing infrastructure and get more physician participation with the patient, you're going to have more engagement and much better results as you look forward. The next thing as you look at, overall, which isotopes can be used. I think it's important to understand there's a lot of excitement around things like Lead-212, Lutetium-177, Actinium. We can be isotope-agnostic. As we start moving forward and looking at the SADA molecule, since you're injecting the cold protein and painting the target and preparing it with open receptors to grab the isotope, you're then able to inject the isotope after the fact and choose which isotopes you want to use. So as long as we can create the linkers between the isotope and the SADA target that's already painted on the tumor, you have the ability to switch that out. So something like Lead-212, where the time today is being burned in the manufacturing and release of the pre-targeted conjugate, that's been done before the radioactivity is injected. Now, you take the radioactivity and inject it in the patient, and the tumor seeks based on the SADA molecule that's already attached to the tumor. So as we look at these things from an infrastructure point of view on both manufacturing as well as administration to patients, the ability to choose different isotopes in real time and decreasing toxicity levels to patients while increasing the targeted activity to the, the tumor, we feel is a recipe success- for success with the SADA platform as a targeted radiotherapy platform. One of the big things from an investment point of view, if you look at that, you're no longer putting all of this investment in infrastructure out there in advance in order to plan for the demand that's coming. We can utilize existing contract manufacturing or in-house manufacturing for the cold construct, so the SADA molecules that can sit on the shelf for two or three years as a non-radioactive substance, and then utilize the existing radiopharmaceutical distribution network and isotope manufacturers to supply the isotopes directly to the hospitals and centers. The way our current structure is today with our clinical trials, we use a contract manufacturer for the cold protein, and we use isotope partners to deliver the isotope on a specific patient basis directly to the hospital. That's scalable and scalable with the current infrastructure that exists across the globe. As we look forward, what is SADA and why does it work? So SADA is a tetramer, and it's a tetramer that, in this case, you have your anti-tumor component that's going to bind to your tumor, as well as your anti-DOTA component, that it will seek out the DOTA... that's circulating attached to lutetium. So it allows us then to have this tetramer attached to the tumor while it's cold. What doesn't get attached to the tumors breaks up into four monomers and is easily excreted through the kidneys. So what we see, and I'll show you a little bit of what the PK curves look like in the elimination of the circulating tumor, meaning not only is it binding to the tumor, it's also being eliminated renally before the isotope injection. And then there becomes a window in which you can inject the isotope to maximize the effect of the drug. You know, just as a little bit of a why, you know, how is this this technology, and why is it important? If you look at this from an IgG or or even from looking at injecting a pre-tagged conjugate, you're going to have an issue where you've got circulating drug and radioactivity in the system seeking out the tumor that's irradiating other things. In this case, you see the diffuse radioactivity within the animal model here. As a SADA, in injecting it, and you look at the curves, you allow the SADA to tag prior to the radioactive injection. As the blood levels of SADA drop and it becomes attached to the tumor, then you inject the radioactivity, what you'll see is focal uptake in the tumor. So from an animal model, you're looking at this and saying, "This is ideal for patients. Can it be replicated?" Our answer to that is yes, and I'll show you a few slides as we go forward. But ideally, what you want to do is maximize uptake in the tumors because dose matters, and we've seen that with other studies. Less dose, less effectiveness. We want to make sure we're maximizing the effectiveness within the tumor. Where are we today? So we're in humans with SADA. So we validated that the SADA molecule, the SADA platform works, that we can do an in vivo tag within a human and inject it. So in Part A, we've got a study design of 15-18 patients. This is a safety study. It's not an efficacy study. But the nice part about radiopharmaceuticals, you can watch the drug work. We've got a secondary gamma that comes off the Lutetium that we're able to image with a gamma camera. So what we've done in this first segment, this is a dose escalation study of trying to understand what the right level of protein, cold protein is, to inject. So we've already completed the first three cohorts and moving on to the fourth cohort this month. With that, we looked at 0.3 mg/kg, 1 mg/kg. Cohort 4, we're moving to 3 mg/kg, and then we'll be moving to 10 mg/kg. That's part A of the study. We're also looking at that window. How much time does it take to clear out the circulating GD2-SADA molecule prior to injecting the radioisotope? The window that we're focusing on is 2-5 days. So with that, our goal coming out of Part A this year is to have a specific protein load that we'll be looking at for the second part B of the study, as well as narrowing the window for maximal opportunity to treat the patient. Having a wide window is very nice, so what we're looking at is: where's the starting point of injection, and where's the last point in which you can inject? Having a window wide enough allows for logistics and delivery of the isotope without running the risk of missing the optimal time of injection. We'll report this out at a medical meeting later this year in totality on what Part A looks like, but I'll give you a little bit of preview what those first couple patients look like. In Part B, we'll be escalating the dose. I said dose matters. So with this, we're focusing on increasing the dose. From what you see today that's approved in the market is all standard 200 millicuries, right? 200 millicurie per dose. For us, we want to scale this up as high as 750 millicuries, understanding we're seeing less toxicity in the kidneys, less retention. So if you don't have the toxicity, let's deliver the highest dose possible over the longest period of time to get the best results. So part of this will be scaling up to see how much we can give while limiting the toxicity. And then Part C, we'll get into the times when we start doing the repeat dosing and start seeing more of the conventional therapy that you do today to start getting the efficacy signals. So these are designed as safety studies and eventually getting to the point where we could see some efficacy. This is where it gets exciting, right? So I look at this, and this is where I get very excited about SADA. This tells me. This is the first patient that tells me that the SADA platform is valid and can work. So what we have here is an osteosarcoma patient. With this patient, they received the lowest protein dose in the study, which was 0.3 milligrams per kilogram. At 48 hours post-protein injection, we injected 30 millicuries of lutetium DOTA, which the patient received, and 24 hours after that dose, we did this SPECT scan on the patient to see where the GD2 SADA went. In this case, we see a very, very focal uptake of the osteosarcoma tumor and very little uptake in the healthy tissue outside of the tumor. So what this tells us is, yes, you can inject a pre-targeted, non-radioactive SADA molecule that will then grab the circulating lutetium and concentrate in the tumor. But this is an N of one, right? So you wanna, you know, get excited, but not so excited that you sell the house. As we move on to the next one, this was the next patient. Four lesions were identified on CT scan, another osteosarcoma patient with GD2-expressing tumors. This patient, again, received the smallest protein load at 0.3 milligrams per kilogram, 48-hour lag time and an injection of 200 millicuries of lutetium DOTA. With that, 24 hours later, we did the SPECT CT image on the patient to validate that it was targeting those tumors. If you look at this, there's a direct relationship where all 4 tumors were painted. All 4 tumors concentrated the GD2-SADA lutetium into the tumors with very minimal uptake elsewhere. So in the first 24 hours, massive clearance outside of the tumors. This again tells us that the SADA platform is working and that the GD2 is targeting the GD2 expression on these tumors. This is where I start getting excited, and the house starts going on the market. So why does it work? Why does it get that pre-targeting? So these are some of the first few patients that we took the PK data on. This is the blue line, is 0.3 milligrams per kilogram, while the purple line is at 1 milligram per kilogram. So we saw that initial blood circulating load of the GD2-SADA, and then we see the rapid clearance from the blood. The reason we're using that 2-5-day window is, as you can see, both the 0.3 milligram as the 1, the majority of it has exited the circulating system by the 48-hour point and start going into more of an equilibrium. So at that point, we're looking at being the front end, where you're getting very minimal toxicity, and then continuing out to 5 days to see where the bookend is of that, where you want to cut off the window for doing the injection. So this upfront has given us a lot of direction on what that potential window can look like. We'll be initiating our 1201. This clinical trial is approved by the FDA to start. We're recruiting sites as we speak. We'll go first in patient. We designed it in a very similar way by design. Because not only do we want to validate CD38, we want to validate the process in which we qualify these products in order to get them into patients and into the market. So part of looking at SADA as an entire platform and a factory for producing targets in the targeted radiotherapy space, by developing these clinical trials in a very similar way, we'll be able to compare the results of each trial and start to get some data that compares each product as a platform and potentially creates an opportunity for us to generate the next products in a much more faster development and a quicker point. But it'll be a part A will be dose escalation, part B will be isotope, and part C will be repeating the six cycles. And just to close out on this, you know, we're extremely pleased with how the SADA platform is progressing. What this means, we've got our GD2 trial, our 101 study, that we'll be reporting out at the end of this year. We'll be initiating our CD38 trial. We've got two additional SADA targets in development, heading for 2025, which is the HER2 and the B7-H3, and again, advancing GD2 and starting that in our pediatric neuroblastoma trial as well. So we've got a very much a significant potential to shift the paradigm, get additional physician participation, and utilize the existing infrastructure to solve much of the challenges that occur today in the radiopharmaceutical space. So we're very excited about that. So we'll talk a little bit about the commercial company. So we're, this was a little bit more forward-looking on where the company's going, but what's fueling it, right? Who are we as a company? We've talked about how excited we are about DANYELZA and what it's doing for patients, but also what it's doing for the organization, allow us to be that self-funding biotech. So a few areas. You know, we've got the humanized antibody for relapse, relapsed and refractory, high-risk neuroblastomas, and we're the only one in the market with that. Also, it has some strategic advantages of some of the other anti-GD2s. So we've got outpatient setting, we've got rapid infusion, and we've got minimal toxicities associated with the product. So right now, as we look at the addressable second line in the neuroblastoma market, these are small markets, but it's a high-value, low-volume market that treats an unmet need. For neuroblastoma, it's, you know, it's in children, in infants, it's the most common cancer in infants. It's heartbreaking, you know, and for us, there was a personal mission in why it's named DANYELZA, who it treated, and how it came to market, and it's definitely something worth taking the time to look at if you have some time later. But at the end of the day, we have the ability to treat these patients in ways that they haven't been treated before in order to extend their lives and put them in a much better place. We continue to launch the product, continue to grow it forward. Q3 reported sales of $20 million, so that's two years post-launch, and we also are continuing to move this earlier and earlier. We launched initially with the majority of the patients being late line or third line. We've moved up to second-line with plans to do some additional studies in partnership with Beat Childhood Cancer to move it into first-line induction in neuroblastomas. We've got—we added 7 sites on just this quarter, so we've moved to 52 treating—from 52 treating sites to 59, which in this space is fantastic. We continue to grow that, as well as the number of practitioners actually prescribing. We have a large ex-U.S., so we've launched in China. We're continuing to grow that. We've gotten 2 approvals in Latin America, and we'll be launching early this year in 2 additional countries. We've got European coverage on a named patient basis that we provide through the WEP program. So we're very excited about this, and this continues to be a driver of who we are and what we are, and we've treated 167 patients to date, which is just, in this space, is absolutely fantastic. So we're increasing the share. We're up to 17% of the anti-GD2 market and continuing to grow that overall.... This slide is extremely important. This, when you look at it, is around Curie scoring. Curie scoring has to do with the bone and bone marrow involvement in neuroendocrine tumors. So by lowering the Curie score, you have better outcomes. In this case, looking at what DANYELZA has done, we've seen a reduction or stabilization in bone disease in 46 of the 48 patients that were treated. So, you know, I won't speak a lot to this, but at the end of the day, this really shows you how DANYELZA is taking bone disease, stabilizing it, and reducing the Curie scoring for better outcomes. So it's, you know, very exciting for us as we go forward. As we look forward, we've got some additional trials that we're working on. We expect to see the initiation of the Beat Childhood Cancer in first line. We'll be supporting that trial, as well as providing DANYELZA for the trial. In addition, we've got additional expansion with Memorial Sloan Kettering, who will have a readout in the second half of this year, probably fourth quarter. That trial is closed, and that was in around osteosarcoma and what GD2, our anti-GD2 can do for that. And then our Ohio State University Comprehensive Cancer Center, and that was target enrollment of 42 patients. So we're continuing to advance DANYELZA and look for additional opportunities to grow the product and reach more patients. Overall, this is a look at both the drug studies in play, as well as the additional indications being looked at in areas of interest. So really a focus, we're in high-risk neuroblastoma, looking at bringing it forward earlier in the care. We're looking at osteosarcoma, soft tissue sarcomas, breast cancer, as well as melanoma. You know, DANYELZA reaches a significant unmet need. So for us, we're gonna continue to invest in that. We've got our studies that are moving forward. We've got our grants. We're continuing the commercialization in high-risk neuroblastoma, and as well as looking at potential advantages over our competitors and what's out there today. So being able to infuse this in the outpatient setting, rapid infusion, minimal toxicity makes DANYELZA, and it should be the drug of choice in this space. So a few takeaways as we come to the end. You know, we've talked about our novel platforms, both in the monoclonal antibodies as well as our SADA platform. We're very excited about that and excited about what the future means. We've got our commercial leverage of a growing DANYELZA product that allows us to go ahead and continue to fund our R&D on a net positive basis. We've got our milestones coming this year that are gonna be important as we move forward as a company and start to advance both of these. And then again, we've talked about our financial independence and our runway well into 2027. But as we bring these products to market, we have the opportunity to then accelerate some of the R&D as we validate these platforms and validate the targets and work with our partners to bring products to market. So let me close by saying I'm very excited about where Y-mAbs is today, what we're doing for patients, but more importantly, what we can do for more patients in the future. Thank you very much. Thank you, Mike, for the very informative presentation, and congratulations on all that your team has achieved in the past year. Thank you. We will now open up for Q&A. If there is no Q&A, we can close out the session. Thank you so much for attending this presentation, and thank you all for joining us here. Thank you all.