Good morning, and welcome to Cellectar Biosciences CLOVER-WaM pivotal study top line data call. Today's call is being recorded. Before we begin, I would like to remind everyone that statements made during this call relating to Cellectar's expected future performance, future business prospects, or future events or plans are forward-looking statements as defined under the Private Securities Litigation Reform Act of 1995. Although the company believes that the expectations reflected in such forward-looking statements are based upon reasonable assumptions, actual outcomes and results are subject to risks and uncertainties that could differ materially from those forecasts due to the impact of many factors beyond the control of Cellectar. The company assumes no obligation to update or supplement any forward-looking statements, whether as a result of new information, future events, or otherwise. Participants are directed to the cautionary notes set forth in today's press release, which is available on the investor relations portion of company's website, as well as the risk factors set forth in Cellectar's annual reports filed with the SEC for factors that could cause actual results to differ materially from those anticipated in the forward-looking statements. Note that this conference call has been pre-recorded and as a result, there will not be a question and answer segment. Now, I would like to turn the call over to Jim Caruso, President and Chief Executive Officer of Cellectar. Jim? Thank you, operator, and good morning, everyone. It is my pleasure to announce the full enrollment of the CLOVER-WaM study and to review the exciting top-line results from our pivotal study evaluating iopofosine I 131 in Waldenstrom's macroglobulinemia, or WM. While this call is pre-recorded, we do plan to have an interactive conference call that will be a comprehensive event with participation from WM thought leadership to further review the disease landscape, commercial market, and to discuss the impressive results demonstrated by iopofosine I 131 for the treatment of WM. Before we begin, let me introduce the executives present and provide the order in which they will be speaking. First, we will hear from Dr. Andrei Shustov, Senior Vice President, Medical, who will review the data and results. Then Shane Lea, our Chief Commercial Officer, will provide a market sizing overview and insights from our clinicians, followed by Jarrod Longcor, Chief Operating Officer, who will review our regulatory strategy. Prior to transitioning to Andrei Shustov, allow me to briefly provide an overview of the market, introduce our top-line results, and highlight the transformational impact iopofosine I 131 may have on the treatment of WM. Let's start with the approximate size of the U.S. WM market, validated by third-party commissioned research, which documents an overall market prevalence of 26,000 patients with approximately 10,000+ in the relapsed or refractory setting, and greater than 4,000+ in third line. Not only do we believe the market opportunity for iopofosine I 131 is substantial, but it is also highly concentrated and scalable, which is ideal for a focused and efficient commercial infrastructure. While the relapsed, refractory, and third-line patient populations are difficult to treat overall, our pivotal study patient population is potentially the most challenging composition of WM patients ever evaluated in a clinical study. As we reported this morning, CLOVER-WaM represents, as far as we are aware, the largest study to date in relapsed or refractory WM patients, post-BTKI therapy, and the most refractory WM population ever tested in a clinical study. Patients received a median of 4 prior lines of therapy with a range of 2-14. 50% were refractory to BTKIs, 40% were refractory to rituximab, and 27% were dual-class refractory to BTKI and CD20 antibodies. In addition, approximately 30% represented MYD88 wild type, a genotype with a high resistance profile to BTKIs. Despite these extremely challenging 41 evaluable patients to date, iopofosine I 131 achieved a 75.6% overall response rate and a 61% major response rate, which clearly exceeded the study's statistical significance hurdle and a primary endpoint of a 20% major response rate. In addition, 100% of evaluable patients achieved disease control, experiencing a meaningful reduction in baseline IgM. Based on the nature of WM, iopofosine I 131's mechanism of action and demonstrated CLOVER-WaM efficacy results, we may see a further improvement in the major response rate, as well as the depth of these responses. To elaborate, patients experience improved results over time. In fact, 18 of the first 25 patients enrolled, or 72%, achieved a major response with the benefit of additional follow-up time. The major response rate of 61% achieved by iopofosine I 131 is significantly superior to real-world WM datasets, which demonstrate that for patients previously exposed to a BTKI who then receive salvage therapy, the major response rate ranged from 4%-12%. Further, based upon thought leader input from multiple advisory boards, for those patients that respond to a third-line treatment, the duration of response is approximately six months. In the CLOVER-WaM study, the median duration of response has not yet been reached. A Kaplan-Meier analysis supports a median duration of response no less than 11.4 months in these multi-class refractory patients, which conservatively predicts iopofosine I 131's median duration of response to fall between 1-2 years. In addition to the impressive response rates and durability of response, iopofosine I 131 was well-tolerated, and the safety profile remained consistent with previously reported data. I'm certain that you can appreciate our excitement regarding the efficacy and safety profile demonstrated by iopofosine I 131 in this pivotal trial. Please also appreciate iopofosine I 131's differentiated patient-friendly dosing regimen that requires only four approximately 20-minute infusions occurring on days one, 15, 57, and 71, compared to a continuous drug regimen. We believe these data in WM further validate our development strategy for iopofosine I 131 in other areas of high need, including relapse refractory B-cell and plasma cell neoplasms, including CNS malignancies and in pediatric high-grade gliomas. We will now transition to Dr. Andrei Shustov for his review of the CLOVER-WaM data. Andrei? Thank you, Jim. Let me start with a review of the study design and patient enrollment criteria before moving to a review of top-line results. The CLOVER-WaM pivotal trial is a global, open label, single-arm study examining iopofosine I 131 in relapsed and refractory WM patients who require therapy due to symptomatic disease progression. Patients enrolled in the trial had to have histologically and serologically confirmed Waldenström Macroglobulinemia, an ECOG Performance Status of 0-2, and have received at least two lines of prior standard of care therapy, which preferably included treatment with BTK inhibitor. Note that our study also included WM patients with central nervous system involvement, also known as Bing-Neel syndrome, given the ability of iopofosine I 131 to cross the blood-brain barrier. Additionally, we included patients with lymphoplasmacytic lymphoma, establishing CLOVER-WaM as the first study to address these high-need populations. The study protocol target is 50 patients in the MITT population. Data reported today is on 41 available patients, meeting protocol criteria for efficacy assessment at the data cut-off date of January 3, 2024, and having sufficient follow-up after the last administered dose to enable the development of therapeutic effect. Median age was 71 years, with oldest enrolled patient aged 88 years. Patients in the trial received a median of 4 prior lines of therapy, with a range from 2- 14 prior lines. Nearly 90% of available patients were refractory to either rituximab or a BTKI, and 27% were dual-class refractory to both CD20 antibodies and BTKI. 80% of patients were previously treated with a BTKI, of whom 50% were refractory. 91% of patients were exposed to rituximab, of whom 40% were refractory. This represents the most refractory WM patient population reported in clinical trials. Let me also note that nearly half of the patients in CLOVER-WaM study were considered moderate or high risk based on IPSSWM score, which is a recognized negative prognostic factor for progression-free survival and overall survival in WM. Further, nearly 30% of study patients were found to have wild-type MYD88 gene, a known genomic factor conferring resistance to BTKI therapy. Patients in an evaluable group had to receive total administered dose of at least 60 millicurie, with a duration of follow-up of at least 60 days from the last dose of iopofosine I 131, unless they completed all four doses. Patients were dosed in two cycles, the first cycle occurring on days one and 15, and the second cycle on days 57 and 71 from study entry, respectively. The primary endpoint of the trial was major response rate, which is defined as a partial response or better. A partial response was defined as a 50% or more reduction in the disease biological marker IgM. These secondary endpoints included duration of response, progression-free survival, and treatment-free survival. The study achieved its primary endpoint with a major response rate of 61%, with a 99% confidence interval of 0.412-0.777. The overall response rate was 75.6%. Responses were durable, with median DOR not reached at a median follow-up of eight months. The Kaplan-Meier analysis utilized 30 available patients with responses. The confidence interval predicts a median duration of response of no less than 11.4 months in this multi-class refractory patients. Iopofosine I 131 was well-tolerated, with safety profile consistent with previously reported data. Importantly, there were no treatment discontinuations due to drug-related adverse events, no treatment-related deaths, and no clinically significant or life-threatening bleeding events. The most common treatment-related adverse events of Grade 3 or greater, occurring in more than 10% of patients, included thrombocytopenia with 55%, neutropenia with 37%, and anemia with 26%. All patients recovered from treatment-emergent cytopenias. With CLOVER-WaM trial fully enrolled, we are looking forward to the remaining on-study patients completing treatments and procedures, followed by final evaluation. Based on the biology of WM, iopofosine I 131 MOA, and current CLOVER-WaM efficacy results, we expect to see further improvement in the major response rate, as well as the depth of these responses. To elaborate, among the first 25 consecutively enrolled patients in the study, the major response rate at three and six months were 28% and 72%, respectively, a 2.6-fold increase with additional follow-up. The corresponding ORR at three and six months were 64% and 88%, respectively, a 37% relative increase with additional follow-up. With that, it is now my pleasure to turn the call over to Shane Lea for an overview of the WM landscape and patient journey. Shane? Thank you, Andrei. We believe this data regarding iopofosine I 131's top-line results from the CLOVER-WaM pivotal study is truly a triumph for patients. As Jim noted earlier, the patient journey is not an easy one. There's no current standard of care in this relapsed refractory patient group, and there has been no new mechanism of action approved in nearly a decade. Consequently, our market share data show that many patients are treated with the same class of drugs across multiple lines of therapy. There are 26,000 patients living with WM in the United States, and approximately 4,300 patients require third-line or greater treatment, with an annual third-line incidence of nearly 1,000 patients. Patients have limited options comprised of unapproved therapies, or they may be recommended to a clinical trial. In many cases, this will potentially mean continuous therapy, additional visits to the clinic, either for treatment, blood draws, or monitoring and management of side effects with other drugs. This creates complexity, financial, and treatment burden for patients. Approximately 50% of third-line patients not receiving treatment are likely to consider new treatment options. To date, there is no study published demonstrating such impressive major response rates in which patients were dual refractory to both BTKI and Anti-CD20 antibodies and had received a median of 4 prior therapies. Our review of real-world clinical data beyond second-line treatment in the community shows a major response rate range of 4%-12%. The 61% major response rate for Iopofosine I 131 demonstrated in the pivotal CLOVER-WaM study represents a 5-fold- 15-fold increase in response over the existing unapproved therapies utilized in this setting. 131's distinguished profile is potentially a first-in-class, novel, fixed course of therapy for WM, can be given to patients in just four doses on days one, 15, 57, and 71, with meaningful responses regardless of patient characteristics. Physicians who participated in the study recognized the improvement of patients' quality of life with iopofosine I 131's vastly different profile, especially in such a heavily pretreated population. We are very optimistic that iopofosine I 131's efficacy, safety profile, and fixed dosing schedule will be able to provide a meaningful benefit for WM patients. We believe iopofosine I 131 has the potential to become a new standard of care beyond second-line therapy or post-BTKI treatment. We continue on our planned commercial strategy for iopofosine I 131 to ensure a successful launch if we obtain FDA approval. Our data supports the concentrated nature of the WM market in the United States. In fact, approximately 80% of WM patients are located in 15 states, which will allow for efficient and strategic resource allocation. As previously announced, our plans include establishing collaborations with large community networks to support smart data capabilities, accelerating iopofosine I 131's awareness, and utilizing effective distribution that will simplify access and reimbursement. We look forward to highlighting more details around these plans and they, as they continue to advance. I will now turn the call over to Jarrod Longcor to highlight our regulatory pathway. Jarrod? Thank you, Shane. Let me echo what has already been said, that we believe iopofosine I 131 has demonstrated a remarkable response rate in what appears to be the most refractory multi-class WM patient population ever evaluated in clinical trials. Our goal now is to continue to work closely with the FDA, or US Food and Drug Administration, to bring iopofosine to the market in the United States as rapidly as possible, so that all patients can have access to its potential multiple benefits. To that end, we plan to complete the work of our NDA filing and submit to the FDA for approval in the second half of this year. We have leveraged our Fast Track and Orphan Drug Designation to have significant and productive discussions with the agency and have received helpful guidance on various components and requirements for the filing. We have been pleased, very pleased with the nature of these discussions and the ongoing collaboration with the agency and are working diligently to ensure our submission for iopofosine I 131 addresses all agency-requested elements. Assuming the priority review associated with the Fast Track designation is accepted, we would expect an approximate six-month review period from the date of submission for our NDA. Also, in preparation for our filing and potential approval, we have developed and refined our manufacturing and supply chain network. Unlike other radiopharmaceutical drug developers, we have designed a strategy that provides a seamless and secure supply of iopofosine I 131 without the burden of building and maintaining manufacturing facilities that cost $10 millions to own and operate. We have built a multi-source supply chain network that allows overlapping redundancy from our selected CDMOs. This, combined with our proprietary formulation, provides an off-the-shelf convenience with an industry-leading 17+ day shelf life. Iopofosine I 131 is shipped as a fully finished, ready-to-use product that arrives at the user site with no on-site compounding required. Our distribution logistics are designed to ensure transport and arrival to all treatment centers in under 72 hours, anywhere in the world. We expect this feature will allow clinical dosing centers to have at least 14 days to schedule patients for treatment, providing flexibility that has been historically lacking with targeted radiotherapies. I will now turn the call over to Jim for closing remarks. Jim? Thank you, Jarrod. On behalf of the company, I would like to share our gratitude to the patients and their families, our appreciation to the participating study sites from around the world, and their dedicated staff. I am also extremely proud of our team for the successful completion of this pivotal study and for their ongoing focused execution as we rapidly advance iopofosine I 131 toward potential approval and commercialization. In conclusion, we are very proud of the results today and continue to execute our iopofosine I 131 product development and commercialization plan. Ladies and gentlemen, this concludes your conference call for today. We thank you for participating and ask that you please disconnect your lines. Have a lovely day.