Yeah. No, the cubs. Cubs. Who are you talking about? Good afternoon. Welcome back to session. My name is Matt Gardner. I'll be your moderator for this afternoon. Our first presenting company in the afternoon session is Cellectar Biosciences from Florham Park, New Jersey. As a Westfield guy, I have great pride introducing you here, Jim. Cellectar is focused on oncology, platform technology, and radiopharmaceuticals, and presenting for Cellectar is Jim Caruso, the CEO. Thank you, Matt. And obviously, thank you for all of you participating in the conference today. Cellectar Biosciences is traded on the NASDAQ under the stock symbol CLRB. Here's the obligatory safe harbor statement. Certainly, we'd direct your attention to our K and our Qs on file with the SEC. Cellectar Biosciences is, as by way of background, focused on the delivery of research and development of oncology, pediatric, and adult indications. The foundation of this focus is our phospholipid ether, or what we call PLE, delivery moiety. And we've had the capacity to attach any conjugate, or therapeutic payload to our delivery vehicle and be able to target cancer, cancer cells, stem cells, etc., and spare healthy tissue. The benefit of that is an enhanced therapeutic window, which increases efficacy and reduces adverse events. Today, we'll be talking predominantly about our phospholipid radioconjugates, or PRCs. Our lead PRC is iodine-131, or CLR 131. We had an exceptional data set reported from our phase II-B study, CLOVER WaM, for Waldenstrom's macroglobulinemia. Waldenstrom's is a liquid tumor, a hematologic malignancy. Our study was done in a highly relapsed, refractory patient population. The data was excellent, in alignment with the FDA. Our primary endpoint was response rate, or major response rate. That major response rate that we agreed upon was 20% in this highly relapsed, refractory patient population. As the data unfolded, we achieved a response rate of just under 60% at 58.2% major response rate. In addition, we had an overall response rate of 84%, and a disease control. Almost every patient benefited from the drug with a disease control rate just under 99%. Based on this data, or predominantly based on this data, we achieved breakthrough designation from the FDA and in parallel received the EMA's equivalent to breakthrough designation in the U.S.. It's called PRIME designation. Based on our PRIME designation and ongoing discussions with our friends across the pond at the EMA, we recently received confirmation of eligibility to submit a conditional marketing authorization to the EMA, to the agency. We have a submission readiness meeting in the first quarter of this year, and our application is anticipated in early 3Q 2026. We are in parallel preparing our U.S. FDA accelerated application, and we'll talk to that in greater detail. In terms of, you know, how do we take advantage of these assets and create value both for our stockholders and expansion for the company itself, we'll focus on the execution of our study in triple-negative breast cancer with our Auger emitter, CLR 125. That study has been initiated in the first quarter of this year, and we'll spend a little bit more time discussing that. The market obviously is large, and there's little to no available treatments in this relapsed, refractory patient population. We also have at the ready, phase I ready, CLR 225 for pancreatic cancer. We'll talk a little bit later on in the presentation in terms of how we select the right isotope for the right tumor, taking advantage of the pan-targeting of our delivery moiety. Obviously, in the near term, we believe there's real value creation here with iodine- 131, or CLR 131. We have the potential now, based on our application timeline, which is in alignment with the EMA in terms of timing, to be approved and on market in the EMA, in the first half of 2027. We are continuing to finalize our NDA application, waiting on final CSR data, and we'll talk about timing of additional subset data, from our CLOVER WaM phase II-B study, as well as updates on DOR and PFS over the course of this year. Obviously, as part of our commercialization, both ex-U.S. and in the U.S., we continue to evaluate, based on our discussions with third parties, optimal partnerships, to take full advantage of WM and iopofosine both in the E.U. and in the U.S.. We're obviously also having discussions relative to our platform, which is very, very unique and has a number of different opportunities beyond the Auger emitter, beta emitter, and our alpha program. This stacks up our pipeline. We talked to iopofosine and WM. I think it's important to note that we have expansive data in other B-cell malignancies as well, and we'll have an opportunity to briefly talk to DLBCL WM a little bit later on in this presentation, where the data is also very, very good in much more aggressive hematologic malignancies. In terms of high-grade glioma, our pediatric study to phase I-B was very, very impressive, both from an activity perspective, but interestingly, almost doubling what you would typically see from a progression-free survival perspective with current on-market or non-indicated agents typically used for this patient population. And then, as you can see, the early pipeline, we're being very thoughtful in terms of level of investment here with a variety of alpha emitters as well as beta emitters. This is an important slide, on a number of different levels. To orient you to the slide, the far left, you'll see the program, and then immediately to the right of the program is the total study cost. And then we have the time and events associated with the study itself and the execution of the study and those milestones and catalysts associated with it as well, as well as the cost of the study over the duration, or the cost of the study over the duration of the entire trial. And you can see we'll start with our phase I-B, triple-negative breast cancer. We're just really aggressively launching that now in Q1 of 2026. We should have, and we'll talk to the design of the study in a moment, imaging data in Q1, and we'll receive initial response data in the first half of the year as well for triple-negative breast cancer. Then, as we dose find, we'll move into the expansion arm. I'm gonna talk to this in greater detail and some of the benefits. Over the course of the year, you can see, you know, from Q1, Q2, Q3, Q4, we're gonna have a number of different catalysts. The imaging data here, the dosimetry data, is very, very important because what it will do, very early on, is demonstrate the capacity of this, our delivery vehicle in combination with the Auger emitter to target the triple-negative breast cancer. We'll be able to clearly demonstrate the amount of drug we're getting to the tumor and have some early activity data, all of this in the first half of the year. We view this as being very, very meaningful, not only because triple-negative breast cancer is a substantial market and it is a solid tumor, it's further validation beyond CLR 124 and 131, clinical data. We view this as being very, very substantial, not only from a street perspective but also based on our discussions with third parties, from a partnership and additional collaboration from an investment standpoint with other assets in our early pipeline. CLR 225, I cited earlier, this program, similar to 125, costs about the same. Here, though, we're standing by on this. We'll be very thoughtful in terms of the timing, to initiate this opportunity in pancreatic cancer, obviously another, important segment for us. And then we've chatted a little bit about iopofosine, but here you can see what's important: zero clinical cost, right, prior to approval ex-U.S.. And why is that significant? In the U.S., they require the initiation of the study prior to approving an accelerated approval for the asset. Here, ex-U.S., you can see we received the CMA eligibility. We were submitting in and around the early part of the third quarter, and we fully expect an approval, and then the subsequent commercialization there in early 2027. In the U.S., again, this is something that we look at and would initiate post a partnership. Those discussions are currently ongoing. And even though the study costs $42 million here, what we would do is initiate the study within a month or two, submit our NDA application, essentially waiting on the final CSR here to do that. Then, at approximately six months, the FDA reviews the application, but they're really just looking at also the initiation of the study: is it substantially ongoing? And then they'll weigh in on an approval. So potentially here, from the initiation of the study, within six to eight months, you can have an approval here in the U.S., although the total study's $42 million, we're estimating approximately $15 million to approval. If you look at the bottom here, the callout, this is substantial, right? So for those agents or drugs that have breakthrough designation, the FDA approval rate is 79%. And for the EMA, with this past pathway we're following with CMA eligibility, those agents with CMA eligibility have an 80% approval rating. So we're sitting, you know, 80% plus, in terms of likelihood of success with the approval process, both in the U.S. as well as the E.U. We're gonna talk very quickly here about the mechanism of action. PLE, it conjugated to any variety of isotope, creates our PRCs. It is universally targeted. Here's the lipid raft. We'll talk to that in a moment. We've demonstrated the capacity to have CNS penetration across the blood-brain barrier and treat a variety of malignant brain tumors. And as I mentioned earlier, you know, with the lipid raft as a target, we have the capacity based on lipid membrane flipping to deliver the drug intracellularly. This approach really overcomes most of the issues with drug-conjugate challenges. You can see up top in terms of the enhanced targeting, limited resistance, especially with the radiotherapeutic, and no need for bystander effect. Very quickly here, in terms of the lipid raft, it plays a significant role in cancer. As you can see, it facilitates processes, cell signaling, proliferation, survival, invasion, metastases, drug resistance. You look over to the far right from a cancer targeting perspective, for our moiety, this is ideal, right? I mean, it's present uniformly across a broad array of tumor cells and tumor types. It's heavily prevalent on tumor cells versus healthy tissue. As cited earlier, you know, this is the recipe for success. It stabilizes on tumors for up to 10 days, allows the drug to accumulate, undergoes the transmembrane flipping process, and delivers the payload intracellularly. With healthy tissue, you know, it's these windows to attach are open for milliseconds, which is why, you know, we target the tumor and have a very clean adverse event profile, sparing healthy tissue. Obviously, you know, based on our preclinical work, we can identify which isotopes work best for which indication. With the delivery moiety staying constant, this allows us to evaluate a series of isotopes in a series of different tumor types and identify which isotope works best for which tumor. This is just an example of three, a variety of three emitters: alpha, beta, and the Auger, and pancreatic breast and triple-negative breast cancer models. Here's the beta emitter. Here's our CLOVER WaM demographics for 131. This was. I'll direct your attention to the bottom, the most refractory WM patient population ever studied in clinical trials. You can review the patient characteristics, and you get it. I'll just direct your attention to the right side here on the patient characteristics. Between BTKi, Rituximab, and chemotherapies, you see a refractory percentage rate going from 60%-77%. As if that wasn't enough of a hurdle, you can see dual refractory patients, BTKi and Ritux, at approximately a 60% refractory rate, and then triple refractory was around 50% as well at 46, 2.4%, extremely challenging patient population. On average, this was a fifth-line therapy for Waldenstrom's macroglobulinemia patients. Then, of course, if you're familiar with the disease, the genotype plays a major role in terms of the difficulty here, as well. As you can see, with the MYD88 wild type and the CXCR4, as well as the P53, percentage of that represented in this patient population, extremely challenging to treat patient population. Now, having said that, as I cited up front earlier, almost every patient benefited. Average fifth-line of therapy here for 131. Disease control 98%, major response rate just under 60%, overall response 84%. Now, our latest DOR and PFS is 11.4 months. We'll have updated data over the course of the year, not only on our subset analysis on some of those genotypes as well as class refractory, from the previous slide, but importantly, PFS and DOR as well. Extremely clean profile here. WM, like, is a disease of the bone marrow. Because this is a targeted agent, obviously you would expect cytopenias. You can see the cytopenias that are listed here, but importantly, symptoms associated with it insignificant. No significant bleeding, a very limited rate of infection, which is substantially lower than what you would typically see in this patient population, regardless of the treatment being used. All of the AEs were treatable, manageable, predictable, and all patients recovered from cytopenias. Importantly, take a look at this last bullet here. The off-target effects were negligible with all non-hematologic AEs less than Grade 2. Here's our confirmatory study. This would be appropriate for both the EU as well as the US. This would be a second line. We'll talk to that in a moment. The benefit of that is we advance further upstream in the treatment paradigm. This would be immediately post BTKi. We'll talk about the market dynamics in a slide or two. And this is, iopofosine I 131 versus a Ritux cyclo dex or RCD. Primary endpoint is PFS. I will say this, you saw our PFS in a fifth-line population, essentially being 11.4. This will be second line, typically for most of these patients, so you would anticipate a greater response rate. And typically, when you evaluate the literature, you're in this approximately six-month best-case scenario PFS for RCD. So we feel very confident about our capacity to win with this clinical trial. Here's some U.S. market data, and this is important as well as we talk a little bit about the E.U. here. As we advance up into second line, there's 11,500 patients in the U.S. Overall prevalence is 26. I'll direct your attention to the 1,000. There's 1,000 patients approximately that are no longer treatment seekers because they've exhausted all of the available treatment options that are essentially sitting on the sidelines looking for an available drug. That in itself is a substantial opportunity, but we look at this as being very, very meaningful. Importantly, 60% of all treatments here are off-label, just talks to the high unmet medical need here. And from just a commercial perspective, simply put, about 80% of all patients are located in 15 states. What does that mean? It's very highly scalable. There's a handful of academic catchment centers, and the majority of these patients are treated in integrated oncology delivery networks. So, minimal commercial medical marketing investment to drive trial use and adoption. There's only one class of approved agents here. They're the BTKis. They're oral. It's a it's a different play. So we feel very, very confident about the the upside opportunity from a market acquisition perspective. I think it's important to note that the EU is approximately 30% larger than the U.S. in terms of patient population. And this does not take into consideration those companies that have reciprocity with the EMA. An example of that would be Canada via Health Canada. In some other areas that 131 has done particularly well, this is in a much more aggressive hematologic malignancy, multiple myeloma. You know, the waterfall chart says it all here. Some very challenging patients. You can see 15% of the overall population were quad-class refractory patients. You can see in multiple myeloma in these highly refractory patient populations a 30%–32% overall response rate. And again, almost every patient benefiting with a disease control rate of 96%. Here we have activity, and we're demonstrating CNS lymphoma. That was a complete response, and that's, you know, crossing the blood-brain barrier, CNS penetration directly below that in a very difficult DLBCL patient population a 30% response rate with a 10% CR rate. And you can look at the PFS being extensive in particular with that CR. So that was not a limited response. And then the top right here with the pediatric high-grade glioma. And we saw this in our phase I-B study with the extended PFS, essentially on average doubling than what you would typically see in this patient population. And this was a very impressive study in head and neck, you know, a relapsed or refractory population. You can see a response rate of 73%, with 64% complete response rate. All right. Now we're going to talk about our Auger emitter. We're very excited about this. We just launched into triple-negative breast cancer study, as stated earlier. Interestingly, because of this, our we maintain the same delivery moiety, and we're adding, you know, individual isotopes. 124 and 131, along with 125, are very similar from a molecular structure perspective. The difference is in, you know, how they behave with the variety of neutrons, protons, electrons, et cetera. But the molecular structures are the same. So what holds true for 131 and 124, we would expect for a large part to hold true for 125. And that is the case. As you can see here, what these charts show are the amount of drug that the tumor absorbs, and that's the far right line, directly to the cancerous tumor, tumor cells, and then these other lines are those to normal tissue. What you can see is it's substantial, and there's an area under the curve or a therapeutic window, that's pretty substantial for all three, but 125 was particularly effective here, so we are very excited about 125 in this triple-negative breast cancer indication. As you can see, it demonstrated even with two outstanding performances with 124 and 131, by the way, that have substantial in human clinical data. You can see 125 had the greatest tumor and lowest normal tissue absorbed dose. This supports the lack of off-target effect. This is a heat map, demonstrates biodistribution of CLR 125 in non-tumor-bearing animals. As you can see, it's essentially non-existing, limited to no off-target effects here with the drug. So we are confident in, certainly cautiously optimistic in the potential AE profile the Auger emitter can have. Here, obviously, we're confident also in the potential from an activity perspective. We've evaluated the Auger emitter in a variety of tumor types, successful in most. Here, as you can see, this is a triple-negative breast cancer model. In images A and B, you can see the significant tumor uptake. Then obviously the resulting in growth in inhibition, both at both dose levels here. We even see statistically significant activity at the higher dose. As you would expect from an activity perspective, very strong and the AE, with no signs of end-organ toxicity. This is what this study looks like. As mentioned, it's launched up and running. imaging and therapy study, those scintigraphy data we view as being very, very significant for us. It is in triple-negative breast cancer. You can see the inclusion-exclusion criteria. We are estimating these three study schematics, and we expect to get, based on those scintigraphy, the optimal dose very, very quickly. We're fortunate to have the Mayo Clinic Network performing this triple-negative breast cancer study. From a financial perspective, as of September 30, $12.6 million, we added $5.2 million. In October, it's just under $18 million. We have 4 million+ shares of common stock outstanding, fully diluted at 7.5. So in closing, great opportunity with triple-negative breast cancer. We'll have data in the first quarter from a dosimetry perspective, activity within the first half. So look for those catalysts in the near term. We'll stand by on CLR 225. We continue to be thoughtful in terms of our early preclinical levels of investment, and we have great upside opportunity, both with an approval ex-US in approximately 30-plus countries, plus those countries, from a reciprocity perspective. That market, as I mentioned earlier, 30% larger than the U.S., and we can expect an approval there in 2027, and this phase III confirmatory study that I outlined earlier supports our U.S. FDA opportunity as well. We will continue to evaluate all third-party partnerships. It would be important for us to complete partnership, certainly prior to initiating the phase III confirmatory in the U.S.. With that, I'll ask the team to close down the presentation and open it up for any questions that you may have. Matt. Thank you, sir. All right. The Cellectar team, Jim and Jarrod, will be available in public breakout room number one. Thank you very.