Good morning. I'm Jonathan Aschoff, Senior Biotechnology Analyst at Roth Capital. And so and the second company we have this morning is Jim Caruso of Cellectar Biosciences, CEO of Cellectar. Jim, good morning. How you doing? I'm doing very well, Jonathan. As always, we're very appreciative of the invitation to participate in your, your conference and certainly the fireside chat. Thanks. So there's a lot of radiotherapeutic noise going on lately. Good noise, not bad noise. And I would like you to maybe walk us through, you know, your competitive position with your radiotherapeutic among, you know, a lot of the good fortune that's been happening lately. No, absolutely. Great question, and based on the acquisition of Fusion just this morning, a very appropriate question. You know, we believe we're obviously very favorably positioned in the space for a number of reasons. And to your point, with the recent RayzeBio acquisition and then Fusion today, the space is, in fact, white-hot. And there's a lot of interest, certainly from end users interested in future radiotherapeutics. I will start with, when you think about Cellectar Biosciences and our position in the space, we are surprisingly the leader among biotech and pharmaceutical companies in terms of intellectual property. We have the most robust intellectual property portfolio in terms of actual patents and patents granted than any other pharma biotech company, and I think trailing us are companies like Novartis, Lantheus, Bayer, and Biogen. So we're well-positioned, and we've been methodically building out our intellectual property over the course of the last 5, 6, 7 years. So we're very well-positioned there. I think importantly, when you think about the space in general, a lot of interest, and most of, if not all of the research, is built around alpha emitters as we move forward. There's currently 2 approved products in this space, and by the way, they're both beta emitters, right? One for prostate, one for GEP-NETs. There's 8 other products that are in the kind of phase II or pivotal trials associated with radiotherapeutics. 3 of them are for GEP-NETs, and the other 3 are for prostate. There's one that's inpatient treatment for AML, and then, of course, there's iopofosine I-131 with our recently announced top-line data from our pivotal study for Waldenström's macroglobulinemia. Interestingly, with our beta emitter, we do have utility among both solid tumors as well as hematologic malignancies, and our data certainly supports that, making us unique. What does make us very unique is the delivery platform, and that's what differentiates us from a number of companies that are currently in this space, all typically pursuing, as I mentioned, GEP-NETs prostate, with alpha emitters, predominantly actinium. The reason for that is the delivery technology that those companies have. What differentiates us is our delivery platform. Yeah, go into that. Thank you. It's our phospholipid ether. As you know, we can add not only any radioisotope and have proprietary methods of binding, but we also have work done in peptides as well as oligos. But you know, based on your question, we're focused on the radiotherapeutic piece. We've successfully added astatine. We've successfully added actinium-225. We've successfully added lead-212, and have pretty robust preclinical data. In fact, our data is across the board outstanding with the preclinical work. We've chosen actinium-225 in our pancreatic program as our lead alpha emitter program. We have the capacity because of the nature of our delivery platform, being able to have significant uptake and consistent absorption in the tumor. We have the capacity to go with large, bulky tumors, right? So we could target triple-negative breast, we can target ovarian, we can target pancreatic cancers with our delivery vehicle, where almost exclusively, all of these remaining companies in this space need to target these smaller tumors, right? Because of the nature of the delivery vehicle, and, you know, the compound in general, and the epitopes that are present on the cell surface are not spread evenly across the cell surface, so they have a difficult time getting beyond one layer or two and treat a larger tumor. That's why you see this GEP-NETs- Right ... prostate approach with these other companies. For us, we're not restricted to that based on our delivery vehicle and our technology. Yeah, talk about what it is that your drug recognizes and how it gets in, and maybe some quantification of how much of your drug you see in tumor cells versus, you know, wandering around. Typically, it's based on the, you know, tumor biology, right? So it's the payload that we choose and the tumor, and so we do have this capacity to make better decisions in terms of the development of the drug because we have optionality in terms of the payload based on the biology of the tumor. What we typically see is about 20% of our payload actually targets the cancer cell, and you see the uptake and the intracellular penetration with our delivery vehicle, which is very atypical versus other delivery vehicles. Yeah, I mean, talk about the lipid part. Of course ... 'cause that sounds pretty unique. Yeah, we have our phospholipid ether is essentially a fatty acid mimetic. And as you know, when you have in the presence of cancer tumors, there's this desire for excess accumulation of fatty acids to support the growth of that cancer cell. You can think of our delivery vehicle as a Trojan horse of sorts. It's a fatty acid mimetic that is now taken into the cancer cell. We're dropped intracellularly, and that's how we are very effective in terms of killing cancer cells. Now, to your point, the major point of difference is that lipid rafts are present on all cancer cells. Now, they're present on all cells, we target cancer cells, and so the lipid raft on a cancer cell, will be available, to, you know, for our delivery vehicle on the scale of 7-13 days, typically. On healthy cells, it's they open and close in milliseconds, and as a result of that, you know, we could target the cancer cell and spare the healthy tissue, which is why, with iopofosine I-131 as an example, we're exclusively our adverse event profile is exclusively cytopenias, which makes sense when you think about the WM patient population, older patient population. They've been treated with 4 or 5 lines of prior therapy, and it's a disease of the bone marrow. So you would expect that this drug is gonna target the bone marrow, and you're gonna have adverse events, you know, associated with that, such as cytopenias. But you don't see neuropathies, you don't see cardiotox, GI tox, hepatic influence, et cetera, et cetera. So it's restricted almost exclusively to cytopenias from an adverse event profile. So enrollment certainly took a bit longer, and therefore data that, you know, versus what I was expecting, but you finally got there, and when you got there, it really looked good. So talk about the lead drug and various aspects of the data that you released in January on Waldenström's- Of course. Macroglobulinemia. Wow, that's pretty impressive that you're, Jonathan. Yeah, we're very pleased with the study, obviously. Our top-line data was off the charts, no doubt about that. And when you think about that patient population, the limited treatment options, and I'll talk through the patient population because it's as important as our top-line data, because it really tells an interesting story. And also tell us, while you're doing that, about what you're doing to identify these patients, 'cause it sounds like you're doing a lot to figure out who they are, where they are, before you're even able to sell it? No, absolutely. We can the commercial piece would be an important element to this, and actually, it's, as I like to say, it's a whiteboard, highly scalable space, great opportunity, and we'll get there. Let's talk. Let's take a step back. Let's talk a little bit about the patient population as I described it. So the most refractory patient population ever studied in WM, highly challenging. Patients on average, 71 years of age. When you look at the IPSSWM scores there, which is a prognostic indicator for performance, we had over 40%, you know, moderate to high risk, which really indicates certainly duration of response historically and has an impact on that, so that piece was highly challenging. Importantly, for me, 4 median lines of therapy, Jonathan, for this patient population- They're sick. Which means very, very sick, and, you know, when you think about the median, right? Half above, half below, but almost exclusively third line and beyond, so third, fourth, fifth line. And there are other studies out there, one or two, that have this kind of third-line median, but it's first, second line and third line, predominantly, right? With very few beyond that. Huge difference in the patient population. And I'll describe some other elements here that further differentiate this study and the challenging patient population, for what you see in some of these other studies. When you look at the BTKi-treated patients, 50% of the patients in this study were refractory to BTKis. 40% of the patients in the study were refractory to rituximab. Those are the two primary agents of choice in this space, and dual refractory was under, just under 30%, which is unheard of in terms of enrollment in clinical trials, right? So we took all comers. We wanted to get a really accurate perspective of this third line or greater patient population, so we wouldn't fool ourselves into thinking we had a tremendous asset. We now know we have a tremendous asset moving forward. And then, as you think beyond that, there's some subtypes or genotypes that are almost extremely challenging to treat, and certainly, the BTKIs are historically refractory against these populations. That's MYD88 wild type. About 27% of the patients in this study were MYD88 wild type that are historically refractory to a BTKI. Said another way, BTKIs are not effective in that patient population, and almost 30% of this population was represented there. Another challenging piece, CXCR4, a wild type. 10% of those patients of our study were in this study as well. And then, of course, p53 mutated, which is difficult for any agent in any hematologic malignancy, represented 15% of the population. So you could say over half of this patient population, forget about the median of four lines, were the most challenging of patients and with existing agents typically having little to no effect from an activity perspective there as well. So that's the kind of patient population. What's the results? A 61% major response rate, which is off the charts. I think it's important to note that in our discussions with the FDA, we aligned on a major response rate as the primary endpoint in the study, and that target was 20%, so we tripled the target there. Overall response rate, about 76%. And interestingly, we've seen this across all hematologic malignancies, including aggressive multiple myeloma patients in later lines of therapy or an aggressive disease like multiple myeloma in later lines of therapy. You know, a CBR rate or disease control rate, if you will, of 100%, where every patient benefited from treatment with this drug. And so that's data off the charts. I will also say for this kind of 10%-ish of patients that typically respond in third line and beyond with existing agents, so about 1 in 10, I'll do the math. You'll see a duration of response, approximately 6 months. Based on our initial cut and what we put out in the original top-line data in the January timeframe, based on Kaplan-Meier, we're approximately at 12 already. And that data is obviously maturing over time, and so we expect to see that considerably north of the 12 months that we saw with Kaplan-Meier. So you're giving 4 doses, right? Day 1, day 15, 15- to 20-minute infusions, patient inpatient, right? I mean, or outpatient facility. And you're soup to nuts, two hours from the time you're there to the time you're typically released with a 15- to 20-minute infusion, day 1, day 15. You repeat that on day 57 and day 71, and you could potentially enjoy multiple years of treatment-free remission, you know, based on iopofosine. Which in contrast to one of the market leaders, BTKIs, that's an oral agent that is required to be taking every day in perpetuity until the drug no longer works, so you can no longer tolerate the adverse events, right? So a completely different model and from a quality of life perspective, based on the work we've done with patients, obviously very, very attractive. And also from a clinician's perspective, you know, they view the prescription with the BTKi, this kind of endless treatment for the patient, and you have to manage adverse events associated with that to keep the patient on these drugs. So they view this kind of one and done with our drug as really advantageous for on a number of different levels. And because of the nature of the depth of our responses, you know, so when you take a look at that 61% major response rate and a complete response rate of 7%, and we can come back to that as well, the durability of the responses are better because of the depth of our responses. And, and, and as you and I discussed earlier, you know, we actually kill the disease, right? So we kill the cancer cells, where BTKis are suppressing IgM. They have no impact on the disease itself, right? They're just suppressing IgM. As soon as you discontinue the BTKI, within weeks, your serum levels and all associated symptoms are back. With us, we're getting this, you know, potentially multiyear drug-free vacation and, you know, elimination of the symptoms associated with the disease for patients, and that's, you know, that's significant. Now, importantly, this market is ideal for us, a company our size. It's a whiteboard in terms of commercialization. You know, the BTKIs are the only approved drug class in this space, and there's two of them. Rituximab is used there quite frequently, monotherapy, as well as in combination. We just posted a new corporate presentation that was up on our website yesterday. And what we've put in there, I think, which is really interesting for all parties, is the treatment by line of therapy for these WM patients. And essentially, what you see is BTKI, rituximab, BTKI, rituximab, first line, second line, BTKI, rituximab, third line. Why? Because they're retreating and rechallenging these patients with the same therapies because they have limited to no options, and oftentimes they're refractory. And that's why if physicians can get a stable disease in this kind of second, third line setting by rechallenging with the same drugs, they're happy. And that just talks to, you know, the significant opportunity that exists for a drug with the profile, obviously, the activity as well as the safety profile of iopofosine, and then the unique nature of the kind of four doses and done. There's no multinational pharmaceutical machinery in the space in terms of medical marketing, investment there. Thought leader share of mind is widely available. You know, so we've been very active in this space. We don't need a $50-$70 million OpEx that you typically see with oncology products, especially in years of, you know, early years and in the year of the launch. It will be more along the lines of a $25 million OpEx in 2025 as we think about the launch for this product and moving forward. And the reason for that, it's a highly scalable space. So approximately 80% of the business is in 15 states. Number one, so think about the age of this patient population, obviously elderly. So Sun Belt states are where they typically reside. I mean, Florida and California are outliers in terms of even, you know, representing a greater percentage of the business. And then there's about a handful of 15-20 academic centers that do the majority of kind of the treatment of WM. They're these catchment centers or centers of excellence for WM. And then there are the integrated delivery systems that are highly organized, and you can think about, like, Texas Oncology, AON, Florida Cancer, QCCA, as we think about various regions of the country that are very, very well organized, and all are highly interested in radiotherapeutics, right? So as you mentioned earlier, it's a renaissance with radiotherapeutics. There's a high degree of interest in terms of the technology. It's always been historically very, very effective. And now you have these delivery networks building out the necessary infrastructure to support this next wave of radiotherapeutics. Many of them are already very well-positioned, like a Florida Cancer and Texas Oncology already have that infrastructure in place, and they view radiotherapeutics as a real growth opportunity for them and to differentiate their systems from other, competitors in and around that region. So the net is, highly scalable, minimal investment. When you dollarize that market, it's approximately $2 billion, right? So if you brand it and normalize the, patient population, overall, it's about $2.1 billion. The third line or greater setting represents $500 million, and the relapse refractory population, which we believe we have a very reasonable opportunity to secure in our discussions with the FDA, is about $1 billion, just north of a $1 billion opportunity. So with little to no competition in the space, no counter detailing or share of voice, a highly targeted group, you know, commercial medical marketing investment in and around that $25 million range, will accumulate, you know, real trial use and adoption and upside revenue here, as we think about WM and how to attack that space. I also believe, based on the unique nature of our product profile, the high unmet medical need, and the advisory board work that we've done, both with patients as well as prescribers, this is gonna take on a life of its own in WM. Yeah, I mean, the data look good already. What's going to come, you know, with, what, about 9 more patients in a couple of months? Is that what we have, we have to look forward to? It's a great, great point. Some longer-term data for, you know, the earlier ones. Yeah, so that's a great point. So as you, as you're appropriately stating, back in January, we delivered, 41 efficacy patients to secure the 61%, etc. In the May timeframe, we're on target for... This May update will provide, the full, enrollment for, both safety as well as activity. And we look forward to sharing those results. To your point, you know, we fully expect the response rates to be in and around the same area that we presented with the original 41. And clearly, your duration of response would, you know, naturally, over, over the course of time, increases. And so we'll see a, significant increase, we believe, in the duration that we could- Right ... announce at that point in time as well. I think that'll further validate, you know, the quality of the study and the high performance of this drug in this very challenging patient population. For all these patients, it's four doses, and there's no fifth or sixth. There's nothing more than four, or they can receive further? So that's a great question, right? So for the sake of this discussion, it was the four doses over 71 days. Now, as we noodle on how you take further control of this WM marketplace, one element would be, you know, a retreat with, you know, an additional cycle further downstream. So you get your first two cycles, you're, you know, you're on your way, you're treatment-free for a few years. Maybe your IgM starts coming back up a little bit. There's certainly an opportunity to retreat with another cycle of iopofosine. So that's one consideration. And we could talk about, you know, depending on time and where you want to go next, where we could talk about our clinical development program overall for WM as well. Well, I think, you know, regarding that, we have enough time to go with multiple myeloma. I've always... I have written a lot of notes, right? I've talked a lot about that. Do you intend to do what's necessary to gain, you know, compendia listing or full approval? What's your strategy for multiple? That's a great point. So as you know, we have a very rich database with multiple myeloma. And, you know, with WM, let's assume, you know, we're on target with our submission in the back half of this year. Let's assume we get NDA approval, and they review this in a six-month timeframe. You know, you're on the market clearly in the, you know, the early part of the first half of next year. And having said that, what does your multiple myeloma non-labeled uptake look like, right? Because it's a very crowded market. There's a ton of different, options there. It's one of the reasons why we elected not to pursue multiple myeloma through a regulatory pathway. Obviously, there's cost involved above and beyond what we were required for WM, but it's a very crowded market, a lot of spend, a lot of investment in that space, and it's very fluid in terms of treatment availability. We believe our current data set is certainly rich enough that allows us to secure NCCN guideline support. So I walked through that WM process and the first half on market, because once you're on market, that allows, you know, the utilization of this drug for, for multiple myeloma. We fully believe our data set is rich enough. To your point, regardless of that patient subtype in multiple myeloma, you're at a 40%-60% response rate, right? High risk, quad/penta refractory, triple-class refractory patients- Yeah. 6-line patients. These are last laggards. Last laggers, and the data was off the charts. So for an aggressive disease like multiple myeloma, getting those types of responses made sense for us. Obviously, in WM, we fully anticipated to get, you know, not only robust responses, but durable responses as well, based on the nature of our drug and mechanism and the disease itself. So you can look at the multiple myeloma there as something that I believe we would secure NCCN guideline listing. From a clinical development perspective, beyond multiple myeloma, you know, you can think about us advancing at the first line, right? With this drug. When you, when you have a 7% complete response rate in this patient population, you can only imagine, you know, what you would look like in first line, right? Yeah. In a naive patient. The difference between first line and second line, and third line, these patients fall off a cliff in terms of response rates, right? Right. You see that in multiple myeloma as well. In first line, in a healthier patient, naive patient, I mean, how high is high with a complete response rate for us? So clearly, we envision ourselves, regardless of where we sit with this first to market indication, further exploiting, you know, the quality of this drug and advancing further upstream, which is a classical development approach, obviously. Right. With any indication, for us, with WM. Well, I think it'd also be highly desirable to have, you know, four interactions for a treatment first line, and be able to let it rip and see how long that benefits- Yeah ... you know, rather than coming in and taking a much more cumbersome treatment path with what they're given first line. Sure. Now- I mean, think about rituximab or Rituxan, as an example, and, you know, those are arduous treatments, right? Combination chemo immunotherapies are not, are not easy. And so something like this that is, you know, very safe, very quick, and to your point, in first line, are you getting a couple, two, three, four years? You know, who knows? It's gonna be safer. And it has, to your point, a very safe adverse event profile for this patient population. And so, you know, we look forward to further advancing and controlling the WM space. And then there's also some logical, inexpensive, highly efficient plays. You talked about NCCN guidelines for multiple myeloma. We see, you know, mycosis fungoides, you know, a sister indication to WM, something we can do, you know, an investigator-sponsored study at a world-class academic center, and do a small n there and put together, we believe, data that would not be dissimilar to what we're seeing in WM and providing a, you know, an NCCN opportunity there. Something that we're very interested in is marginal zone. We believe this drug will work very, very well there, very meaningful market. That may cost a little bit more if we elect ultimately to go down that pathway, but I think you could, you could see mycosis fungoides and marginal zone as being, you know, two diseases that this drug should work very, very well in, and quite frankly, high unmet medical needs still exist there, right? And so those are the types of spaces with limited to no competition, high unmet medical need, where a company like ours could transition into very efficiently, both from a cost perspective and once there, compete, if we elected to do so on our own from a commercial perspective, you know, with, with targeted investments. So, you know, that's kind of the, you know, WM as in the near term, as you think about our approach there. We're gonna have to end it there, Jim. Thank you very much. Oh, I appreciate it. Okay. Thanks much.