All right, the final session before lunch, so our next presenting company is Cellectar Biosciences from New Jersey, United States, and Cellectar is focused on oncology, oncology combination therapy, and radiopharmaceuticals, and presenting for Cellectar is their Chief Operating Officer, Jarrod Longcor. Jarrod, over to you. Thank you very much. First, let me apologize. Our CEO, Jim Caruso, was supposed to be here today. He was unable to make the trip due to health issues, and so I'm filling in, as our kind moderator said. I'm Jarrod Longcor, Chief Operating Officer for Cellectar Biosciences. I've been with the company for about nine, almost ten years now. So with that, I'll jump in. We are a NASDAQ-listed company, publicly traded NASDAQ-listed company, forward-looking statements. So obviously, you can all basically disregard everything else I'm going to say for the rest of the day. With that said, as our moderator introduced, Cellectar Biosciences is actually a drug-conjugate-focused company. We were founded to take advantage of our unique delivery platform known as a phospholipid ether. These allow us to essentially conjugate almost anything we want to them and get them targeted and delivered directly to the tumor cells. We only focus on cancer. Our targeting does not go elsewhere. With that said, our lead asset, iopofosine I-131, which is a radiotherapeutic using iodine-131 as the payload, so to speak, was recently completed, about the early part of last year, a phase II study in Waldenstrom's macroglobulinemia. That study was designed to be the first step in an accelerated approval pathway with the FDA, and it was successful. We'll take you through some of that data in a few minutes. We are right now in a process with the FDA of finalizing around a confirmatory study and thereby getting the conditional approval for the asset in Waldenstrom's macroglobulinemia. As I said, we are able to attach just about any payload we want. We have done other radioisotopes in addition to that, and we have a platform that goes outside of that into other areas, which I'm going to take you into now. With that, so why phospholipid ethers? Why a long-chain fatty acid? Well, fundamentally, we have taken advantage of a unique difference in tumor cells. It's a metabolic need of the tumor cell. And fundamentally, we're targeting these regions known as lipid rafts. These are micro-domains in the cell membrane that occur, and they occur because they're pro-survival, pro-metastasis, and really help the tumor to invade and evade treatments. Taking advantage of that is exactly what we're trying to do with this. Why is that important? Because unlike most other epitopes or targets, tumor cells have to have lipid rafts. They have to have them in significant concentration. They have to be stabilized, and they're essentially ubiquitously expressed or present across all tumors, and all tumor cells, making it almost the ideal target. So what did we do? We developed and engineered a novel phospholipid ether molecule that allows us to bind directly to specific areas within the lipid rafts and allow for the uptake directly into the cytoplasm and transit along the Golgi apparatus network and get delivered perinuclear. That comes in important when you start thinking about different molecules that you want to get into the tumor cell, whether that be things like oligonucleotides or certain radioisotopes that they have a very short distance of where their energy is delivered, and you want to get it really right up against the DNA. Because of that and the way this molecule has been designed, we're able to create certain advantages, like I said, diversity of payload, ability to get preferential PK sort of experience, and then also get in the unique protected domains like the CNS and getting into very difficult places. To that end, as I mentioned, we have attached and, in this case, validated essentially every single one of these what I'll call therapeutic treatment modalities, whether it be radioconjugates, cytotoxic small molecules, biologics using peptides for intracellular delivery now, not focusing on the extracellular piece, or nucleic acids such as siRNA and mRNA and getting that into the cell. As we show here on the far right, these are all the different molecules and elements that we've actually tested and validated either in vivo or in clinical trials at this point. The upper pieces up in here are all in clinical trials. All of these have been tested in vitro and in vivo in a host of different animal models and demonstrated that we can not just systemically target the tumor, but actually have activity, which is a bit different in some of these cases than other molecules out there, so now for the rest of this conversation, or this presentation, I should say, I'm going to be focusing us in on the radiotherapeutic space specifically, and what's interesting about us, as I sort of mentioned, we started with I-131, which is a beta emitter. Now, nice things about beta emitters is if you're thinking about, you know, you've got to get something to the general area, beta emitters are great because you can get bystander effect. When you want to get away from that and you want to get more targeted, you move to an alpha emitter like actinium-225 that's become very popular in the last couple of years, and that gives you a much smaller band, but it does have a little bit of bystander effect, a cell or two over kind of thing, rather than broader than that. The last is an Auger emitter, which is essentially an electron emitter. This is very unique, which is you've got to not only get it to the cell, you've got to get it into the cell, and you have to get it perinuclear because it only travels about two nanometers in length, which means in order to be effective, you know where you have to get and what you have to do. We're using our platform because it gives us this unique advantage over other delivery platforms and actually achieves that goal and shows activity and efficacy with Auger emitters. Real fast, our pipeline, how we've set this up, as I mentioned, I-131, our iopofosine I-131 has been tested in quite a number of different indications, particularly in Waldenstrom's macroglobulinemia, which is a mouthful to say, so we'll just call it WM from here on out. It has been tested, as I mentioned, in the phase II study and is right now kicking off the phase III pivotal or phase III study. We've also tested it in multiple myeloma, DLBCL, mantle cell, marginal zone, the PHGG, pediatric high-grade glioma, because we do cross the blood-brain barrier and we do see significant activity there. We are contemplating other what I'll call indolent diseases like mycosis fungoides. We'll spend some of today talking about these two, CLR 121225 and CLR 121125. These are both looking at solid tumors, as I'll talk you through. The first one really focusing on PDAC or pancreatic cancer, and the second one focusing in on triple-negative breast cancer. Then we have the rest of the pipeline with small molecules and some of the other programs that we have. We also think we're pretty unique. This is an example, a sunburst plot of all the different in the inner circle here, you can see the different types of emitters: beta emitter, alpha emitter, Auger emitter, and then the different isotopes being used around here, the indications, and then the companies. A little bit complex, I agree. But from that, the key piece is when you look for the light green, that's us. That's Cellectar Biosciences. We're the only company that's in every single one of those, every single emitter with different isotopes doing different things in different opportunities. Most radiotherapeutics right now are being targeted towards small, I'll call it diffuse, not really diffuse, but smaller tumors. These gastrointestinal, pancreatic, neuroendocrine tumors are generally neuroendocrine tumors rather than things that are large and bulky because it's just harder for the radioisotope to overcome some of the challenges that I was sort of alluding to earlier that our targeting ligand helps us get over. So with that, I'll take you into iopofosine I-131. The important thing here, the left side of the thing, I'm not going to walk you through the whole patient demographics, but the left side is really basically demonstrating for you that these patients were elderly, challenging from the standpoint of they were at risk for many different things. On the right side is really the key component, right? What is it? These patients were highly pretreated. Prior lines of therapy prior to us treating them was four. Importantly, though, was this next bucket down here, this prior treatment and the refractoriness. If you look here, so there are two treatments in Waldenstrom's macroglobulinemia that are predominant. BTKi is predominantly ibrutinib, and after that, rituximab, and I'll show you a graphic on why, you know, how that breaks down in a few minutes, but fundamentally, if you look at those two buckets right there, approximately 75% of patients were refractory to one of the two most common treatments given for this disease, and if you look here, dual refractory was nearly 60% of these patients were refractory to both compounds, which essentially means they had no treatment options available to them. And we enrolled them in this study, and to that end, we saw a really strong outcome. So this endpoint over here is major response rate. That is the regulatory requirement by the FDA. You can see we nearly had a little over 58% of the patients having a major response. But this is the endpoint that matters to clinicians and the patients. Overall response rate, significant reduction in the paraprotein known as IgM in their bloodstream. Nearly 84% of the patients treated with this drug had an overall response rate. At the time, at the last time, a cutoff, which was about 11.4 months and ongoing, PFS and duration response were still ongoing, median not yet met because most of the patients were still over here and did not have an event and so were censored at that point. When we look across the cytogenetics of the patients and the refractory, you know, I don't want to say refractory, but some of the other gene, unique gene populations that are out there, what you can see is irrespective of the cytogenetics, you see a very strong and consistent response in all these patients. Additionally, when you slide over here, again, post-BTKi is a unique patient population because they are usually viewed as the most challenging. But also this, p53 mutations, unique in that normally for radiotherapeutics, overcoming p53 mutation is very challenging. It usually requires significantly higher doses of radiation because of the repair mechanisms, DNA repair mechanisms that are turned on. In this case, we saw a very nice response in that, and we're actually seeing that across all the indications where we have tested this drug. From there, a nice waterfall plot showing the efficacy, again, in a slightly different paradigm here across the patients. And what you can see is almost everybody had a reduction in their IgM, which is actually meaningful. So that's why disease control rate was 98.2%. Only one patient was the only patient who did not respond to treatment. There are various reasons for that. They actually had some benefit, but that was essentially the takeaway on here. So how about safety? Great. You got good efficacy, but are you a safe drug? It's radiotherapy. Do we need to be concerned? Fundamentally, no. So interesting. When you look at the general sort of systemic effects that could be happening, these patients aren't having any real issues. The only issues they're having are cytopenias, which you would expect. For those that don't know, Waldenstrom's macroglobulinemia is a disease of the bone marrow. It occurs. It's like multiple myeloma. It's a diffuse disease of the bone marrow. You are delivering a radioisotope. As I said, it's a beta emitter, so it's going to give you a significant sort of bystander effect. And what do you get? You get cytopenias as predicted and expected. You get thrombocytopenia and neutropenia predominantly, and after that, you basically have no other effects. So a very clean drug profile other than that. So from there, where are we? And I sort of alluded to this before. The upper part's a repeat, but let's talk about the regulatory pathway a little bit. Here's where we sit. We've gone to the FDA. We've discussed this study, and basically what they've told us is what we need is an ongoing or an initiated at the time of submission, an initiated confirmatory study, and an ongoing study at the time of regulatory action or approval. What does that study need to look like? Needs to be a randomized controlled trial in approximately 40-60 patients per arm, so around 100 patients total. Key endpoints are going to be major response rate, which I just showed you on, and the second one's going to be progression-free survival, which I also showed you. In both cases, for the comparator that is likely to be chosen here, we will outperform on both those endpoints significantly in this patient population. So we feel very confident that this drug is well positioned for approval in the next 12-18 months. From that, so why Waldenstrom's? Most people don't know this disease because it is a rare orphan indication. Fundamentally, you know, when you look at the relapsed refractory patient population, there's just around 11,500 of these patients out there. If you look at those that are post-third line, you got 5,700 of them, or nearly 6,000 patients. So it's a significant patient population. Importantly, in that third line setting, 1,000. You see 4,700 and 1,000. The 1,000 are patients who have stopped seeking treatment because they've already exhausted all lines of therapy that are available. This is your BTKi and rituximab refractory patients. They're not getting any benefit. They don't see a reason to seek treatment. They need a new mechanism of action, and this offers it to them, which is why we saw a lot of those patients enroll in our study. Interestingly enough, you know, one of the problems with rare diseases is when patients are spread out all over the place. But when you take a look at the history of these patients, what do you see? 80% of Waldenstrom's patients are found in 15 states across the U.S. So it's a very condensed, very manageable patient population to access and get into. When you look over here on the right side, this is what I was sort of mentioning earlier. You know, light green is BTKi. Dark green is rituximab monotherapy. What is interesting in this is irrespective of the line of therapy, what do you see? The exact, almost the exact same percentage of patients receiving treatment all the way through. Why is that important? What that tells you is that the patients that are getting rituximab are switching to a BTKi. When they get the BTKi, they switch back, and they're just trading back and forth, back and forth, back and forth because there aren't other therapies for them. There's nothing approved after the BTKi in a second line setting. So it's a wide open marketplace, which is again why we think this is a very interesting and great opportunity for a new drug. Beyond Waldenstrom's, how does iopofosine I-131 work? Irrespective of the disease states we've looked at, we see great activity. Here, you know, whether it's CNS lymphoma, again, crossing the blood-brain barrier, diffuse large B cell with refractory diffuse large B cells, I mentioned high-grade glioma in pediatric, head and neck cancer, or even multiple myeloma. You can see in all of these refractory recurrent diseases, we get very high overall response rates, high CR rates. So it's a very effective drug when it gets, and it can get to the tumor. So from that, I'm going to now shift for the last about 10 minutes of this presentation into our earlier stage programs. Alpha emitters. So as I mentioned earlier, alpha emitters, they have a shorter distance. They're very active. It's sort of the difference. So with a beta emitter, you're shooting like a rifle shot. With an alpha emitter, you're shooting like a cannonball at the DNA. So you're getting a very different sort of effect. In this case, this is looking at pancreatic cancer, as it says at the top. A single infusion after allowing the tumor to grow, what do we see? Very nice dose response across the animals, very effective that the two of the higher doses both knock down the tumor with almost near total regression off a single infusion in a highly refractory pancreatic cancer. You see nice uptake into the tumor, and this is very predictive and repeats exactly what we essentially saw with the iopofosine I-131 program. From there, everybody else using actinium is right now looking at prostate, metastatic prostate cancer in the bone marrow. So from a comparator's perspective, how do we stack up when we look at prostate cancer? And here you go. Two different models of prostate cancer. Again, very straightforward dosing. You can see total knockdown, near total knockdown in this model, and you get absolute knockdown in the second model. So very effective compound and irrespective again of where we're treating it and very nice survival benefit being received by the mice. We're good at curing mice. So where are we going next with this? We're going into a phase I dose escalation study. What you have here is sort of a demographic of it. What we're thinking is single ascending dose escalation in one arm, and then the next arm looking at a multi-dose sort of component. We do believe with pancreatic cancer, because of the density of the tumor and the complexity of the tumor microenvironment, it's going to take likely more than a single dose to be effective. And we sort of lay that out. We do have up here the idea that it would be a three by three design. We may switch to a Bayesian sort of approach to make that a bit more faster to enroll. So from there, the other place where the next phase I study we're about to initiate is a phase I with the, as I mentioned, the Auger emitter. Because of the unique nature of our delivery vehicle being able to get into the tumor cell, get to the perinuclear space, and actually break up the DNA. And so what you have here is a mouse model where we image the uptake of the Auger, in this case I-125, and you can see down here. This is again a single low dose. You know, there were two doses, but this is a relatively low dose with only two microcuries being delivered, and you get significant knockdown of the tumor. This is in a triple-negative breast cancer model, MDA, which is a very refractory model. And so this was an incredibly nice outcome. You can see sort of the generalized as you move through the uptake mean and max of where the drug goes in the body in the animals. Very nice profile. From that, quickly into the financials. As of September last year, we had 34.5 or $34.3 million on hand. We have really focused in, you know, we don't have any debt. We have a handful of warrants. These warrants are pretty straightforward, vanilla warrants, nothing major. We do look to and are planning to raise additional capital later this year, particularly in support of that confirmatory study for the iopofosine program. We're looking at almost any means of supporting that program at this juncture. Overall, again, our focus is to really rapidly advance our programs. We have the iopofosine program right now. In the near term, we're really going to focus on getting the accelerated approval and clarity on that confirmatory study with the FDA. We're also linking that because we have PRIME designation in Europe. We're linking that with the EMA program so that we can get essentially a near global launch of the drug at one time. As I said, we have validated our PDC platform across many of these treatment paradigms, as well as a number of indications to give you a sense. We've tested the drugs in over 100 different animal models at this point, and I think it's about 20 different clinical settings. Very, very broad sort of data package that we have around the programs and understanding. As I mentioned, the 1225 and the 125 program are both expected to go into phase I studies here in the next, in the first half of the year, likely yet in the first quarter, at least for one of them. And we continue to look to various partnership scenarios around our platform and across our platform to enhance stockholder revenue. So with that, I want to thank you for your attention and wish you have a great day. All right. Thank you, Jarrod. So the Q&A will follow in breakout room one, but we still have like five minutes left. If anyone wants to ask questions, please shoot.