Good morning and welcome to Cellectar Biosciences' CLOVER-WaM Pivotal Study 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 risk and uncertainties that could differ materially from those forecast 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 because 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 the 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. Please go ahead, sir. Thank you, Operator. As a reminder to the group, there will be a question-and-answer segment available post this call. Good morning to everyone. It is our pleasure to host this Key Thought Leader event to review the impressive results from the CLOVER-WaM Pivotal Study evaluating iopofosine I 131 in Waldenstrom's macroglobulinemia, or WM. To provide a brief overview of the disease landscape, commercial market, and insight into the growing community-based infrastructure to support the increasing use of radiotherapeutics. Please allow me to introduce the medical experts participating in today's call, as well as Cellectar executives. It is my pleasure to introduce Dr. Sikander Ailawadhi, Professor of Medicine at Mayo Clinic, Jacksonville, Florida, and the Global Lead Investigator for the CLOVER-WaM Pivotal Study. We are also excited to have Dr. Michael Morris, a Diagnostic Radiology and Nuclear Medicine Physician, Co-founder of United Theranostics, and the Medical Director of Advanced Molecular Imaging and Therapy and United Theranostics Centers of Excellence. From management, we have our Chief Operating Officer, Jarrod Longcor, Chief Commercial Officer, Shane Lea, and Chad Kolean, Chief Financial Officer. Company's Senior Vice President, Medical, Dr. Andrei Shustov, is taking his scheduled vacation, and I insisted that he enjoy that time with his family. With us today, we have, obviously, Jarrod and Dr. Sikander Ailawadhi, who can address any medical issues. In terms of the agenda for today's event, for those of you that are new to the Cellectar story, I will provide a brief corporate overview, review our platform technology, and discuss the unique features and benefits of iopofosine for WM. We will then hear from Dr. Ailawadhi, who will review the CLOVER-WaM study results. Dr. Morris will follow with insights into the use of iopofosine and radiotherapeutics in the community. I will close with a brief WM market summary. In terms of our company summary, Cellectar is focused on the development of orphan and ultra-orphan adult and pediatric oncology indications, indications that we believe the company can effectively compete and win both in the clinic as well as on the market. The foundation of our development focus is our PDC drug conjugate cancer targeting platform. Our lead phospholipid drug conjugate is iopofosine I-131, a small molecule targeted radiotherapeutic which exceeded the primary endpoint in our pivotal study in WM. Iopofosine possesses a differentiated product profile with activity beyond WM in B-cell malignancies such as relapsed refractory multiple myeloma and DLBCL. Iopofosine has also demonstrated the capacity to cross the blood-brain barrier and is currently in a Phase 1b for pediatric malignant brain tumors. We have developed a highly efficient and effective supply, manufacturing, and distribution logistics chain with scalable production capacity to meet product demand. We plan to file our NDA for WM in Q4 2024, and the financing that we announced this past Monday provides funding through initial commercialization. In terms of our mechanism of action, this slide provides that level of background. As you may know, cancer cells are known for their ability to aggressively scavenge nutrients from their microenvironment, with lipids being a critical nutrient. These cells utilize specialized microdomains on their surface, known as lipid rafts, to capture and transport lipids. As lipids bind to these rafts, the region depolarizes, allowing direct transport of the lipids into the cytoplasm. Tumor lipid rafts differ significantly from those on normal cells. They are larger, more stable, typically persisting for 10 to 14 days, and far more abundant on the cell surface. The lipid rafts on healthy cells are small, dissipate in a few milliseconds, and are very limited in number, thereby limiting or preventing PDC entry and sparing the healthy tissue. Our phospholipid ethers, which are mimetics of a naturally occurring subclass of lipids, are specifically designed to target these tumor-specific lipid rafts. By exploiting the tumor's metabolic dependency on lipid uptake, these phospholipid ethers enhance the delivery and the retention of therapeutic payloads. In the case of iopofosine I-131, this targeted delivery results in a significantly higher concentration of I-131 within the tumor cells compared to many other delivery methods. This increased retention enhances the isotope's ability to induce double-stranded DNA breaks, leading to effective destruction of the tumor cells. In terms of our therapeutic franchises, our PDC platform is comprised of four conjugate franchises, which are listed on the left side of the slide and include nucleic acids, biologics, cytotoxic molecules, and radioisotopes. We have developed drug conjugates for these payloads and have completed extensive preclinical proof-of-concept work in each area. Our radiotherapeutic franchise is furthest along, and we have successfully conjugated nearly all available isotopes with our platform, including most beta and alpha emitters. We are currently advancing one of our actinium-based conjugates through IND-enabling studies in preparation for a Phase I study in a solid tumor. Of course, our preferred beta emitter of choice is iodine I-131, which is the payload for iopofosine I-131, our lead asset with exciting data in a variety of B-cell malignancies, including Waldenstrom's. Let's now turn the call to Dr. Sikander Ailawadhi to review the impressive iopofosine data from our CLOVER-WaM Pivotal Study in WM. Sikander? Thank you, Jim. First, I would like to say thank you to the patients and their families for participating in the CLOVER-WaM study. Based upon my experience with the drug and the patients I've treated, I believe that iopofosine I-131 is addressing a number of important unmet medical needs for patients with Waldenstrom's macroglobulinemia and that these results demonstrate a clear potential for iopofosine I-131 to bring meaningful benefit to these patients. As you will see, these patients are the most refractory WM patients reported in a clinical trial to date and would likely experience less than 10% major response rate with the currently available standard of care therapeutic options. I will start my review with the summary of the pivotal study design and patient characteristics enrolled in the CLOVER-WaM study prior to providing you the results. The CLOVER-WaM Pivotal Trial is a global, open-label, single-arm study examining iopofosine I-131 in Waldenstrom's macroglobulinemia patients with symptomatic disease progression. Patients enrolled in the trial had histologically and serologically confirmed WM and ECOG Performance Status of 0-2 and have received at least two prior lines of therapy, including those who received prior BTK inhibitor. Note that this study included WM patients with central nervous system involvement, also known as Bing-Neill syndrome, given the ability of iopofosine I-131 to cross the blood-brain barrier. Patients were dosed in two cycles, the first cycle occurring on days 1 and 15, and the second cycle on days 57 and 71 from the study entry, respectively. The primary endpoint of the trial was a major response rate greater or equal to 20%, which is defined as a partial response or better according to the IWWM-6 modified criteria. The reason for the 20% major response rate was the fact that there are no available treatments that provide meaningful responses in this patient population. In fact, typically, these patients do not have a major or even a minor response, and physicians accept stable disease as a positive therapeutic outcome. Key secondary endpoints included overall response rate, duration of response, and treatment-free survival. The study enrolled 65 patients, of whom 55 patients met the criteria for MITT efficacy population, defined as patients who have received greater than 60 millicurie total administered dose of iopofosine I-131. Response data reported today is on the MITT population with the data cutoff date of May 31, 2024. The median age was 70 years, with the oldest patient being 88 years old. The median number of prior therapies was 4, with a range from 2 to 14. 71% of patients were previously treated with a BTK inhibitor, 91% were treated with rituximab, and 84% received prior multi-agent chemotherapy. Over 90% of patients were refractory to at least one class of drug, with the refractoriness to BTK inhibitors reported as 67%, rituximab 60%, and traditional cytotoxic chemotherapy was 56% of patients exposed to these treatments. 40% of all MITT patients were considered dual-class refractory, which is refractory to a BTK inhibitor and rituximab, and 27% were triple-class refractory, which is refractory to a BTK inhibitor, rituximab, and conventional cytotoxic chemotherapy. Of those patients exposed to two classes, 65% were refractory for and for those exposed to all three classes. 54% were refractory. Overall, this represents the most refractory WM patient population reported in clinical trials to date. Let me also note that more than half, 55% of the MITT patients in the CLOVER-WaM study were considered medium or high risk based on the IPSSWM score, which is a recognized negative prognostic factor for progression-free survival and overall survival in WM patients treated with available therapies. Further, approximately 30% of study patients were found to have the wild-type MYD88 gene, a known genomic factor conferring resistance to BTK inhibitor therapy. Between the refractoriness and these prognostic indicators, one would expect limited responses and duration of response of approximately six months. The study achieved its primary endpoint with a major response rate of 56.4%, with a 95% confidence interval of 42%-67%, which means the lower bound of 42% was more than double the FDA-agreed response rate of 20%. The 80% overall response rate means that 8 out of 10 patients experienced a meaningful reduction in their IgM levels, which is the protein that causes damage to organs and other disease-related side effects. Additionally, the CR or VGPR was 7.3%, which is typically not even seen in late-line patients. Several patients are still under observed potential conversion to a CR or VGPR. Importantly, similar rates of overall responses were demonstrated in patients with prior BTK inhibitor therapy, an overall response rate of 72%, and those with MYD88 wild-type tumors, the high-risk prognostic marker I mentioned, with an overall response rate of 81%, with dual-class refractory patients, so refractory to BTK inhibitor and rituximab, and also triple-class refractory, which is refractory to BTK inhibitor, rituximab, and conventional cytotoxic chemotherapy tumors. Responses were observed in 65% and 54% of patients, respectively. As can be seen on the waterfall plot showing best response by patient, 54 of 55 or 98% of the patients experienced stable disease or better. IgM levels were reduced in 96% of patients. It is quite rare for cancer therapies to produce these kinds of responses across all patient types, as demonstrated by the distribution of the patients to the right side of the graph. Furthermore, it can be hypothesized that, based upon iopofosine I-131's mechanism of action, the reason the patients experience these kinds of reductions in IgM is due to its ability to kill tumor cells and thereby reduce the patient's actual tumor volume and disease burden. Importantly, major responses were shown to be durable, with the median duration of response having not been reached, with a median follow-up of 9.7 months and a maximum duration of 29 months and ongoing. Based upon the Kaplan-Meier analysis performed on the first 26 patients with a major response, the probability of duration of response at 18 months was 78%. Five patients were not included in the Kaplan-Meier analysis as they were too early in their responses to be assessed. As these results continue to mature, we expect further improvement in durability. In the Kaplan-Meier analysis performed on 41 patients with overall responses, the median duration of response was not reached, and 18-month duration of response of 72% was projected. Four patients were not included in this analysis due to being too early in their responses. It is important to recall that eight out of 10 patients achieved an overall response, meaning nearly 60% of all patients treated were projected to achieve 18 months of durability. Iopofosine I-131 was well tolerated, with a safety profile consistent with previously reported data and the clinical profile of the patients in the study. Grade 3 or higher treatment emergent adverse events occurring in greater than 10% of patients in safety population, which was 65 patients, were thrombocytopenia in 80%, neutropenia in 69.2%, anemia 44.6%, lymphopenia 13%, and infections 12.3%. Cytopenias were predictable, meaning they initiated and resolved in a similar pattern with the time to nadir consistent across all patients. They were also considered manageable with standard supportive care. Importantly, all patients' cytopenias resolved. It should be noted that patients who were already cytopenic were allowed to enroll as cytopenia is a key driver for treatment and a marker of the disease itself. There was only one AE-related death, which was due to an infection. There were no clinically significant or life-threatening bleeding events. Patients did not experience any treatment-induced peripheral neuropathy, cardiotoxicity, hepatic toxicity, or other off-target effects that can be seen with other treatments. In summary, CLOVER-WaM is the first and largest WM study to date in a median four prior therapies and multi-class refractory patient population, including patients refractory to all available treatment categories. Iopofosine I-131 demonstrated an 80% overall response rate, 56.4% major response rate, 7.3% complete response or very good partial response rate for the entire MITT population. Comparable rates of overall response rate observed across all genomic and clinical cohorts, including dual and triple-class refractory patients. Responses were durable, with median duration of response not reached with an 18-month duration of response of 72% overall and 78% in major responders. Safety profile was consistent with selective targeting of tumor sites and clinically negligible off-target effects outside the hematologic system. Four-dose fixed course of treatment provided quality-of-life advantage for these heavily pretreated patients versus the current therapeutic options. I will now turn the call over to Dr. Morris. Thank you, Dr. Ailawadhi. First, let me echo Dr. Ailawadhi's position that iopofosine I-131 demonstrated promising clinical activity, especially when considering the challenging nature of these patients and their limited treatment options. It is exciting to observe a new potential therapy that may address the unmet needs that currently exist in the WM patient population. As a community-based diagnostic radiologist and nuclear medicine physician, I can say that a novel compound like iopofosine I-131, with its unique features and benefits, including familiar handling in the nuclear medicine department and a rapid, well-tolerated administration process, is highly appreciated both by providers as well as patients. In my practice at United Theranostics, which is a network of community-based radiopharmaceutical imaging and therapy centers, we utilize all of the currently approved diagnostic and therapeutic radiopharmaceuticals, including Lutathera, Pluvicto, Xofigo, radioactive iodine, etc. The center is operated as a central hub for the surrounding community oncologists and other providers who refer their patients to us for both radiopharmaceutical therapy and molecular imaging. We applied the same model with the community hematology oncology groups, which allowed us to seamlessly collaborate in the CLOVER-WaM study. Historically, these patients would have required a referral to a tertiary hospital. However, iopofosine's familiar handling in our freestanding nuclear medicine facility allows for outpatient treatment. This approach permits for close collaboration with our hematology oncology colleagues and provides them convenient access to services and effective products for their patients. It is an approach that is proving to be highly successful and efficient for the healthcare system for patients in our Chesapeake region and throughout the country. Our model is expanding across the U.S. to support the increasing demand for easier patient access to radiopharmaceutical therapy in the outpatient setting. We believe that the advances in radiopharmaceutical therapy and general excitement around the results of these treatment options and the theranostics paradigm of care will continue to drive the need for easier, more convenient access to therapies like iopofosine. Because of this, we have taken the step to create a network of freestanding theranostics centers of excellence, which can provide sustainable, meaningful access to approved radiopharmaceutical therapies and radiopharmaceuticals in clinical trials. Consistent with the FDA and ASCO's advisement on the importance of a diverse population in clinical trials, United Theranostics National Clinical Trial Network is dedicated to investigational radiopharmaceuticals. Currently, we have 3 centers already established, 3 more anticipated in the coming months, and a plan to have a total of 50 network facilities by 2027. You may be wondering how this collaboration and communication between the community hematologist-oncologist and the community nuclear medicine physician works, so I will try to explain. First, the hematologist-oncologist identifies a patient for whom they wish to treat with iopofosine. The patient is then referred to a nuclear medicine theranostics center. As a part of the United Theranostics Clinical Trial Site Network, this theranostics center benefits from strong established relationships with community hematology oncology groups. Patients meet with the on-site radiopharmaceutical therapy authorized user, typically a nuclear medicine physician, to review the treatment plan. An order for iopofosine I-131 is placed with Cellectar, and the dosing dates are scheduled. Throughout treatment, the patient continues to interact with their primary hematologist-oncologist for continued monitoring and other required concomitant hematology oncology care and treatment. The dosing schedule for iopofosine I-131 is straightforward, with patients receiving four short administrations over approximately 71 days or so. After the patient's treatment of four doses is concluded, they return to regular follow-up with their hematology oncology physician and may follow up with their nuclear medicine physician on an as-needed basis. The referral process that I outlined is simple and is already well established between the hematologist-oncologist and nuclear medicine physician in our case. Based on my experience, I can say that iopofosine offers advantages, advantageous features for a radiopharmaceutical. These features include the long 17-day shelf life, which allows us to adjust dosing days to accommodate patient schedules, the short administration, and the fact that the product is fully finished upon receipt and is ready to use, which helps to limit radiation exposure to staff in the nuclear medicine facility. It is important for us and patients that their treatment is quick and efficient, especially when handling an I-131-containing radiopharmaceutical, as is the case with iopofosine, which has an administration time that is generally less than 20 minutes, with patients able to be released within approximately 1 hour. This provides for an excellent patient experience and a predictable patient treatment flow. The process consistency allows for convenient scheduling and treatment of the next patient. In summary, we found that iopofosine provides a promising treatment for an underserved WM patient population with limited treatment options, and if approved, will be widely available to patients in the community oncology setting. The drug is familiar to work with in the nuclear medicine facility. It is convenient for the patient, physicians, and staff. The existing United Theranostics Center of Excellence and Clinical Trial Site Network infrastructure, along with iopofosine's authorized user-friendly features, combines to make the collaboration with the community-based hematology oncology physicians nearly effortless. As mentioned previously, we believe that the use of radioisotope-based diagnostics and therapeutics will continue a massive growth trajectory, and community-based theranostics centers such as United Theranostics will expand to support this latest evolution of radiopharmaceutical therapy. Terrific. Thank you, Dr. Morris. Let me briefly talk to the U.S. market. The U.S. WM market is comprised of approximately 26,000 patients living with this incurable disease. It is a concentrated market with high unmet need, limited treatment options, and limited competitive investment. There has not been an FDA-approved new mechanism of action in WM for nearly a decade. These market characteristics provide an opportunity to capture a significant share with a highly targeted and efficient active commercial promotion, utilizing the route to market with an FDA approval. Our third-party claims and epidemiology data show the total U.S. dollarized WM market to be approximately $2.1 billion, with the current relapsed refractory market harboring approximately 11,500 patients with an estimated value of $1 billion. iopofosine I-131 has two very compelling opportunities to capture patient share with imminent marketing approval. The first opportunity to capture patient share exists in the current relapsed refractory market, which is burdened with high unmet need. Nearly 50% of patients in the third line or greater setting are retreated with the same or similar treatment from an earlier line of therapy due to lack of available treatment options. Greater than 60% of these therapies are not FDA-approved and cannot be promoted for the treatment of WM. We also believe the third line or greater market, which is approximately 4,700, expands to 5,700 patients. Approximately 1,000 patients have exhausted all available treatment options. As a result, patients remain either ineligible or intolerant to current market treatments. If approved, iopofosine would provide a new treatment option for these 1,000 patients that unfortunately are out of treatment options. In fact, based on real-world data, major response rates for patients receiving treatment in third line or greater are approximately 10%. iopofosine's novel mechanism of action and strong clinical profile, with the benefit of active promotion, may provide hope for these patients and capture significant share. So with that as a backdrop, let's transition into the promised live Q&A segment. Operator? Thank you. Ladies and gentlemen, we will now begin the question-and-answer session. Should you have any question, please press star followed by the one on your touch-tone phone. You will hear a prompt that your hand has been raised. Should you wish to decline from the polling process, please press the star followed by the two. If you are using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Your first question comes from the line of Ted Tenthoff from Piper. Great. Thank you very much, and thanks for all the detail today. I guess the question about the existing infrastructure to treat, and I appreciate that this builds on current both diagnostic and therapeutic facilities. I wanted to get a sense if you have a concept in terms of what current utilization is. So would this new use in Waldenstrom's fit in with current availability or unused capacity? And how many centers across the country really are able to administer this? Super helpful, and congrats on the data. Thanks. Yeah. Thank you for the question, Ted. We appreciate it. We have observed, and I think most people have this kind of explosion with radiotherapeutics. Historically, they've been used almost exclusively in academic centers. Over the last handful of years, with the advent of new radiotherapeutics, we've seen this now advance into the community where it becomes more and more common. I will also suggest that these large integrated oncology delivery networks that are spread out across the country and really dictate and control large volumes of community-based patient flow have really built out infrastructure to support the anticipated use and growth of radiotherapeutics. They either have an existing infrastructure that's already designed to support their clinics. For example, Florida Cancer, which has approximately 99 clinics in the state of Florida, has 16 hubs that allow them to refer patients. They're regionally distributed and positioned so they can service all of their 99 clinics. Florida Cancer is one of many large integrated delivery networks that continue to enhance and expand their capacity for radiotherapeutics. It's providing additional services for patients, and they also believe it gives them an opportunity to enhance their overall product in and around the regions and for the patients and communities that they serve. So with that, I'll turn it over to Jarrod for additional comments. Yeah. And then I'll also open it up to Sikander and to Michael to add in their additional thoughts. But I think it's safe to really address sort of the back end of your question, I think, which is the available capacity right now. Just to give you a sense, based on our investigations, there are approximately 200 centers across the United States right now that are I-131 licensed. And that means they're able to dose liquid I-131 of this nature as of today. There are quite a few centers that are, as Michael sort of alluded to and as Jim just sort of alluded to, that have the capacity for radiopharmaceuticals as a whole but would require the additional licensing, which will take a few months to allow them to come online with I-131. But there is a significant amount of capacity out there. With that, I'll pass it over to Sikander and then let Michael collaborate on. Sure. Thanks a lot, Jarrod. So Ted, excellent question because these logistics are obviously important so the drug reaches every patient who is the appropriate candidate for it. I should say that historically, the 50-60 NCI-designated comprehensive cancer centers that are also including the NCCN comprehensive cancer centers, those were the only designated centers where such medications could be administered. But I'll just say that we don't really get patients from community all the time saying, "Hey, I need my Lutathera," at the academic center, etc., because community has over time developed this capability. So no longer is it the 50-60 NCI-designated comprehensive cancer centers. But as Jarrod mentioned, a lot of this capability is being developed in the community and is going to be expanded further. It's not just a static number. It'll keep increasing, bringing these treatments, the radiotherapeutics, to patients in need everywhere. That's all really helpful. Michael would be. Oh, sorry. Go ahead. Sure. Yes. This is Dr. Michael Morris. I would just add that in a dedicated theranostics center like ours, we're specifically focused in these centers that are really catering to a high volume of radiopharmaceutical patients. We certainly have the capacity to handle the addition of WM patients and also other emerging radiopharmaceuticals in our centers. Our typical centers have anywhere from 4-8 dedicated treatment rooms, and then some markets could have more. We're easily capable of incorporating these into our current clinic workflow and have all of the appropriate licensing to handle I-131 as well as many other radiopharmaceuticals. We're also actively investing and growing our centers' capacities throughout the country and opening new centers constantly. I think that we'll be able to grow our network to meet the need for these and other patients in the radiopharmaceutical space over the coming months and years as well. Great. Thank you for all that color. I appreciate it. Thank you, Ted. Your next question comes from the line of Jeff Jones from Oppenheimer. Please go ahead. Good morning, guys, and congratulations on the data. A great update. One clarification question, a simple one. This looks like about 10 additional patients from what you reported in January, and just wanted to understand if there were additional patients outstanding that would then be included in the regulatory filing. And then a couple of follow-ups. So you are sort of correct, Jeff. I think it's about 14 patients additional from the January date in the efficacy portion and about 20 total patients. I think in the January timeframe, we reported 45 in the safety data set. Now it's 65. So the additional patients in the regulatory filing, no, the 55, if you recall, the target was 50. So we overrolled by 5 in the MITT to ensure that we had sufficient patients to get there. And then in addition to that, obviously, as you will recall, and it should be highlighted, we do have a period of time post-treatment in the what I'll call early follow-up period where patients are able to continue to convert from minor responses to major responses or from PRs to VGPRs, CRs. So we do continue to monitor these patients over the course of time to evaluate those transitions during that window. Great. Thanks, Jarrod. In terms of getting ready for that NDA filing, I know, Jarrod, specifically, there's been a huge focus on the CMC. So are there any outstanding gating factors ahead of that NDA filing that we should be watching? And CMC is always an issue on the radiopharm side. Yeah. Funny that you say it that way. My philosophy on that, if it can go wrong, it does go wrong, and it's always in CMC, it seems like. However, I got to say that we have really, over the years, really focused on our CMC elements. This is why we've created the system and the network we have, this multi-source process from beginning to end, everything from radioisotope all the way to finished product, so that we can always maintain supply. I think from the NDA submission, we have built all of that in. We actually started with the CMC sections well before the study was halfway enrolled so that we could engage with the agency and really understand and stay on top of the CMC. Because as you said, historically, that has been an area where companies much larger than Cellectar have had issues in their launch timing and with their filings. And so we've tried to learn from those experiences and really button down all of those elements so that we could sufficiently address any concerns of the agency ahead of time, in both markets, I will say, both in the U.S. as well as in Europe with the EMA, focused on trying to pre-solve those potential issues. Great. Thank you. And then just one last clinical practice question, probably for Dr. Morris. He outlined sort of the referral practice from the hem/onc into these outpatient centers. And as you noted, there's a fairly high degree of cytopenia in these patients. Are the AEs and issues like cytopenia managed in those outpatient centers, or do those patients go back to their referring physician for that management? Yeah. That's a great question. This is Dr. Morris. We work really collaboratively with our hematology-oncology physician colleagues in the care of these patients. So the patients are not being treated in our clinics in isolation from their oncology provider. We are in constant communication. And so typically, if a patient experiences a cytopenia, we would work really closely with the hematology-oncologist to manage those side effects. Of course, we'd be available to the patient and to the oncologist as well through that process. But typically, the treatment for the cytopenias or the following of the cytopenias would be primarily managed by their hematology-oncology provider, and we would be available to provide supportive care. And we would have close communication in deciding when or if the patient can continue on to their next course of treatment or subsequent follow-up care. Great. Really appreciate that. Yep. This is Sikander Ailawadhi from Mayo. I just wanted to add kind of a little bit more explanation to Dr. Morris's excellent answer because so I'm at Mayo Clinic. We have a large number of patients who get referred in. We have a huge catchment area: regional, local, national, etc. So I'll just say that from our experience, also from my experience using iopofosine I-131, when patients are local, they get treated obviously with us. But we have had a lot of patients who come to us from a distance, from South Carolina, from North Carolina, etc. That is where the collaboration between the local hematologist and, let's say, even the academic center comes in extremely handy. And I should say that a lot of these bridges are already made within the cancer space. So patients are referred for CAR-T. Patients are referred for transplant. Patients are referred for certain clinical trials to academic centers. So the local physician is the one who tends to provide all of that in-between care. Typically, we would tell them how frequently to monitor labs, how to handle any cytopenias, etc. The good part was that despite the cytopenias, it was easy for me, for example, a PI, to reach out to the local doctors and say, "Well, this is very predictable. This is the time point when you expect the counts to go down, and this is the time point you expect the counts to come up. So we know the relatively finite time of the supportive care needed. And what would that supportive care look like?" So actually, from a patient standpoint, also, they like the idea that their community hematologist is kept in the loop, and we take care of the patient as a team. So it brings it as a very patient-centric approach of care. So I think this drug is being able to utilize the bonds and the network and the connections that already exist in the cancer world and in cancer treatment landscape. Great. Really appreciate that and that visibility to how you're thinking about this. Guys, congrats again on the data, and talk to you soon. All right. Thank you very much, Jeff. As always, we appreciate your continued support. Thank you. Ladies and gentlemen, should you have any question, please press star followed by one on your touch-tone phone, and you will hear a prompt that your hand has been raised. Your next question, follow-up question, comes from the line of Ted Tenthoff from Piper. Please go ahead. Great. Thank you very much. I appreciate you taking my follow-up questions. So I wanted to go back through kind of the market opportunity here. I'm really getting a sense from the physicians, sort of, how they will envision using iopofosine I-131. So again, this is for later-line patients. I think the numbers that you gave earlier, there's prevalence numbers, I believe, in terms of patients who are currently living with Waldenstrom's. And I guess maybe you could walk us through sort of how a patient, how you would select patients who might be prioritized for iopofosine I-131 in your practice, but I'm assuming that would apply more broadly to treatment across the country. Thanks. Ted, thanks a lot for that question. I think it's extremely insightful for you to think about the patient journey or where this would fit or who would be the most appropriate patient population for the treatment. So of course, if the drug were to be approved, a lot of that would depend on what the label says or what the specific indication the drug is available to a treating physician. But that said, in the current landscape of treatment, the general treatment opportunity options available to me as a clinician are 3 broad categories: monoclonal antibody by itself, which frankly is not of much benefit, and in the view of most of us academicians, it should not be a go-to treatment option. So that's available but almost not helpful. Then there are the BTK inhibitors, which are approved for two of them are approved individually for treatment of Waldenstrom's, but without any line of therapy connotation, so patients could get them anytime. But they come with their baggage of long-term treatment, chronic side effects, and a huge financial toxicity to patients. And then the traditional chemoimmunotherapy, which is cytotoxic chemo plus monoclonal antibody, which is a traditional non-Hodgkin lymphoma-type treatment. In the current landscape, we do not utilize them in any specific order. A patient could go from A to B to C, A to C, A to B, B to A, whatever. So I would say in my mind, there are two legitimate treatment options that we currently use: the BTK inhibitor and chemoimmunotherapy, which we can anticipate getting some benefit for patients, but there are pros and cons. So when we look at the prevalence pool of these patients, we know that the natural history of Waldenstrom's is such that the patient's overall survival is most likely not going to be affected for the majority of the patients. They'll be living with the disease. So you can imagine that prevalence pool actually keeps increasing over time. The need for treatment in these patients keeps coming back based on clinical features and parameters. The way I looked at this data when this was released was that the benefit from this drug was across the board, whether the patient was MYD88 wild type or not, whether the patient had high-risk features or not, previously treated with BTK inhibitor or not, refractory to anything or not. And we expected an outcome to be very uniform. So to me, this is a great opportunity. When I talk to patients, I don't say, "Hey, your next treatment is going to be X." We talk to patients in terms, "We have these next treatment options. These are the pros and cons. One has four limited treatments but comes with some expected cytopenias, and you have to be treated at my center or one of the larger centers or something that has theranostic-type capability versus you could be on a drug if you have not had it before, a long-term treatment with a pill but comes with the financial toxicity and the chronic side effects versus you could go to chemoimmunotherapy, fixed duration, but traditional chemotherapy is kind of scary to patients, especially in Waldenstrom's where natural history is very long." So we talk about these options, but I can say that in the relapse refractory setting, which is even second onward, so third line and beyond, we really don't have anything legitimate. There's no point recycling the previous treatment. So I would think across the board, based on the profile we've seen in that relapse setting, this would be a treatment option for patients where the logistics work out and the network works out and the patient can come and get the treatment. I would not say that this fits one patient profile versus the other. At least in my experience using the drug, every patient profile fits this drug and vice versa. Yeah. That's really, really helpful color, especially based on the profound activity that you're seeing from the mechanism. And I really appreciate your point about that being consistent across patients. Thank you very much for taking the time to answer my question. Thank you. Thank you. Your next question comes from the line of Ahu Demir from Ladenburg Thalmann. Please go ahead. Hello. This is Chung for Ahu Demir. I have a couple of questions. The first question is regarding, can you please help us to understand more about the venetoclax in the real world? We know venetoclax were added to the NCCN for the treatment of previously treated WM patients. And in the real world, in your practice, what percentage of patients are using venetoclax? And also follow up with the prior questions. Where do you see the biggest opportunity for the I-131 given all the current options and how it compares with the venetoclax? And I will have a couple of follow-up questions. Thanks. Sure. First of all, thank you for participating in the call. We appreciate the question. I'll provide some epidemiology and actually claims data specific to venetoclax, and then I'll open it up to the group to provide their feedback as well. I mean, obviously, to your point, venetoclax is not approved for the treatment of WM. And interestingly, when you look at real claims data, it gets used about 1% of the time in first line, 1% of all prescriptions in second line. And then in about fourth line or so, it increases to 4% because of the total lack of available treatments. But typically, in lines one through three, you'll see of every 100 prescriptions for WM, one of them being for venetoclax. And then in that kind of, as I mentioned, the later line of therapy, fourth line and beyond, it's approximately 4%. And so that's the actual claims data. So that's the quantifiable number for the number of venetoclax prescriptions currently being used for WM. Thanks for providing that background from the claims data. And thanks a lot for your question. I think it's important to bring up the discussion of BCL-2 inhibitor or venetoclax in the current treatment landscape. That's a very insightful thought thinking about what are we accessing or what's the current landscape truly looking like. In a practitioner's standpoint, I have—we at Mayo Clinic have a large Waldenstrom's population of patients who require treatment. BCL-2 inhibitors or venetoclax, their data stems from a small, very small phase 1/2 trial, single institution experience based on which the patients did not have very deep responses. So the CR VGPR rate was very small. Patients did have disease stabilization to some improvement, not like the major responses being seen with iopofosine I-131. And when patients were stopped from the treatment, because that's the venetoclax paradigm in other diagnoses like CLL, when venetoclax were stopped, the disease grew right away. So all the promises or thoughts that we had around venetoclax and Waldenstrom's, that it would give deeper responses, durable responses, and fixed duration of therapy, at least in the relapse refractory setting, that has not been the case. So the frontline setting, there is no data with venetoclax so far. And so I think venetoclax has not behaved in Waldenstrom's the way it was expected to behave or the way it behaves with other areas like CLL. In our practice, again, a large Waldenstrom's population with a large patient following and on treatment, we use venetoclax relatively infrequently. And I would say the numbers that Jim mentioned of, say, one out of every 100 prescriptions in the relapse refractory setting, I would say maybe we have, say, 2% rather than 1% just being a large academic center. But patients, to me, if I have an available clinical trial, I'm more likely to recommend that clinical trial to a patient rather than venetoclax, which is not necessarily changing the disease biology and natural history much. I hope that answers your question about the current utilization of venetoclax. I know you asked as a follow-up also how the data on iopofosine compares to venetoclax. So I think, again, to me, it's a very far-away comparison because the patient populations are different, the trial characteristics are very different. And again, cross-trial comparisons are always fraught with lots of issues. But the way I can put it is that with venetoclax, we have not seen fixed duration therapy benefit. We have not seen deep responses or durable responses. Of course, the mechanism of action is active in B-cell lymphoid malignancies. But as a contrast, I'm not going to go into numbers because that would be cross-trial. I would just focus on the characteristics of the drug where iopofosine I 131 is giving us fixed duration therapy, deep responses, and durable responses. And all of those are extremely important when you translate to patient-centered benefits. So quality of life, time away from work, time away from family, days taken off, financial toxicity. When you put all of that together, I think it's better to compare a package versus a package rather than a drug versus a drug. I hope that answers your question. That's very helpful. And my next question is, we saw there are other ongoing trials and generate good responses as well, such as the CAR-T cells or reversible BTKI. Can you highlight some of the key differentiating features of the I-131 compared to these other agents? Again, an extremely important question, and thanks for bringing up the current landscape discussion. So I'll talk about CAR T. So we're a large CAR T center. We do tons of CAR T treatments every year for lymphomas, for multiple myeloma, for leukemia. So CAR T is certainly a promising therapeutic approach for a lot of different cancers. Unfortunately, outside of the acute lymphoblastic leukemia, where it has given responses kind of akin to a cure, we're always a little jittery using that term as a clinician. But it seems that in the B-lymphoid malignancies, which are more mature lymphoid malignancies like non-Hodgkin lymphoma, multiple myeloma, we haven't gotten to that kind of "cure" or that durable long-term responses, which has been the promise or the go-to for CAR T. The Waldenstrom's CAR T trials are relatively early on. You can imagine if we were talking about the logistics and the infrastructure need and access of patients to CLR or iopofosine I-131, Waldenstrom patients are typically older, typically more comorbidities, and access or utilization of CAR T in Waldenstrom, where we know that the utilization of CAR T in other lymphomas like diffuse large B-cell is significantly lower than the prevalence pool. I am a little cautious in how CAR T will change the playing field for our patients with Waldenstrom because in diffuse large B-cell, we have not seen anywhere near the utilization, anywhere near what it was supposed to be or what the prevalence pool is. So I'm a little leery about how we're going to utilize CAR T in Waldenstrom if and when it becomes available, considering patients' age, comorbidities, access to CAR T centers, risk of side effects, time away from family, need for hospitalization, etc. And your follow-up question of how I would think about compare and contrast iopofosine with CAR T or such like treatments, I would, again, when I take a step back, think in terms of how am I explaining treatments to patients. I can talk about a lot of clinical terms and percentages, which could confuse the patient. Or when I talk about simple nuts and bolts logistics, patients tend to take treatment decisions based on what is fixed duration, what is more time at home, chronic side effects, is it approved by insurance or not, how does it affect their pocketbook. Those are very, very important factors that go into treatment decisions. There are many studies showing from multiple myeloma, lymphoma, etc., that in patients' mind, these factors are paramount, unlike what we talk about PFS and OS and ORR, etc., etc. When I compare and contrast in clinical terms, these results are extremely impressive. In terms in which I will be talking to my patients when the drug becomes available, those are also factors that are way more in favor of this drug for patients to likely choose this as a treatment option when they are given all the options. It will help me in a shared decision-making and informed decisions with the patients. That's very helpful. My last question is, I might have a follow-up to answer as well. Just wanted to say that, and emphasize the point that CAR-T specifically may be even more challenging to get access to, of course, compared to radiopharmaceuticals because of the special needs and special places where the patient needs to receive the care compared to an outpatient community-based therapeutic network like what we have at United Theranostics. So I do think that the ease and access for iopofosine I 131 will likely be superior. That's very helpful. Thank you. And my last question is, when do we expect to see the PFS and OS data? And are you still planning to present the full data set at ASH? Thanks. Yeah. So we do expect to—it is still our plan to present at ASH at this juncture. And that is the time frame I would expect that you would start to see the data on PFS and OS. As Sikander, Dr. Ailawadhi just mentioned, OS does not tend to differ all that much between the patients because these patients tend to live with it. But the progression-free survival, we do expect to see some differences. Great. Thank you so much for the question. Congratulations for all this data. Thank you. Thank you. There are no further questions at this time. I would now like to turn the call back to management for final closing comments. Of course. Thank you, Operator. On behalf of the company, I would like to thank Dr. Ailawadhi and Dr. Morris for their participation, thoughtful insights, and candid comments. I would also like to share our gratitude to the patients and their families, our appreciation to participating study sites from around the world, and the respective dedicated staffs. I am honoring our team here at Cellectar for the successful completion of this pivotal trial and for the ongoing focused execution as we urgently advance iopofosine I-131 toward potential approval and commercialization. And of course, we thank all of our participants on today's call. Thank you. Ladies and gentlemen, this concludes your conference call for today. We thank you for participating and ask that you please disconnect your lines.