Cellectar BioSciences, Inc. Aktie

Hello, and welcome to The Platform Behind the Pipeline, Cellectar Biosciences' educational webinar. [Operator Instructions] Also as a reminder, this conference is being recorded today.

Anne Marie, you may begin.

Thank you, operator. This is Anne Marie Fields, Managing Director at Precision AQ. Good morning, and welcome to Cellectar Biosciences' educational webinar on The Platform Behind the Pipeline. Joining us today from Cellectar are Jim Caruso, President and CEO, who will provide opening remarks, and Jarrod Longcor, Chief Operating Officer, who will review the scientific and clinical rationale behind the company's phospholipid ether platform underlying its promising clinical development pipeline of radiopharmaceuticals.

I want to remind participants that the information discussed on today's webinar is covered under the safe harbor provisions of the Private Securities Litigation Reform Act. I caution listeners that management will be making forward-looking statements. Actual results could differ materially from those stated or implied by our forward-looking statements due to risks and uncertainties associated with the business. These forward-looking statements are qualified in their entirety by these cautionary statements and in the company's SEC filings. The content of this webinar contains time-sensitive information that is accurate only as of the date of this live broadcast, August 18, 2026. The company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this webinar.

As a reminder, the webinar is being recorded and archived. After management's prepared remarks, we'll open the line for your questions.

I'll now turn the call over to Jim Caruso. Jim?

Thank you, Anne Marie. Good morning, and thank you all for joining us today for what we expect to be an engaging and educational session. On behalf of the entire Cellectar Biosciences team, I appreciate the opportunity to share our vision for what we believe represents a differentiated and potentially transformative approach to targeted cancer therapy.

At Cellectar, our mission is straightforward: deliver better outcomes for patients facing serious cancers while creating meaningful long-term value through innovative science and a scalable technology platform.

Next slide. Over the past decade, oncology has experienced remarkable advances. We've seen the emergence of targeted therapies, immunotherapies, antibody drug conjugates, and most recently, a new generation of radiopharmaceuticals. Yet despite this progress, many cancers remain difficult to treat and patients continue to face relapse, resistance, and limited therapeutic options. We believe one of the fundamental challenges is not simply identifying the right therapeutic payload. It's delivering that payload precisely, selectively, and consistently to cancer cells while minimizing impact on healthy tissue.

This belief has guided the development of our phospholipid ether or PLE delivery platform. What makes this platform compelling is that it was designed around a feature shared by many forms of cancer, rather than a single biomarker, antigen, or mutation. As a result, we believe it has the potential to overcome some of the limitations associated with highly target-specific approaches, and creates opportunities across a broad range of hematologic and solid tumors.

Next slide. Today, our lead clinical program, Iopofosine I 131, is demonstrating the potential of this approach in Waldenstrom's macroglobulinemia, a rare and incurable B-cell malignancy where patients still need treatment options. The encouraging clinical results generated to date, including strong response rates in heavily pretreated patients and recent regulatory momentum, provide important validation of the platform's underlying biology and targeting capabilities.

However, from our perspective, Waldenstrom's is only the beginning. Over time, the true opportunity lies in the versatility of the platform itself. As the targeting properties are inherent to the phospholipid ether scaffold, we believe that technology can serve as a delivery engine for multiple therapeutic modalities. We've already demonstrated this concept with radiopharmaceuticals, and we're advancing a pipeline that includes beta emitters, alpha emitters, Auger emitters, and potentially other payload classes over time.

The vision is not a single product, but a platform capable of generating multiple product opportunities across multiple indications.

Now, importantly, this creates value on multiple levels. For patients, it offers the potential for more selective targeting and a broader application across cancers that have historically been difficult to treat. For patients, and then for physicians, it represents a potential new approach that is independent of traditional antigen targeting. And finally, for investors, it establishes a foundation for a diversified pipeline, supported by common scientific engines, where each new program can build upon the knowledge, validation, and infrastructure established by those programs that came before it.

As the radiopharmaceutical field continues to evolve, we believe the winners will be those companies that pair compelling payloads with novel targeting approaches. Our goal is to be at the forefront of that evolution. Today's webinar is designed to explain why. To achieve this objective, it's important to understand the science that underpins our platform, what phospholipid ethers are, why they selectively accumulate in cancer cells, and how this mechanism may enable the delivery of a wide range of therapies across multiple tumor types.

With that as background, I will now turn the presentation over to Jarrod Longcor, our Chief Operating Officer, who will walk you through the biology, the platform architecture, and the growing body of evidence supporting what we believe is the next-generation approach to targeted cancer therapy. Thank you. Jarrod, over to you.

Thank you, Jim, and welcome, everyone. Thank you for your time today. So as Jim mentioned, and I'll say it -- I'll lay it out this way. Essentially, when we look at this, the problem that exists is not a new problem for targeting cancer. It comes with a host of issues.

Starting at the early part of the 20th century, it was once dreamed that antibodies were going to be the solution. They were cast by Dr. Ehrlich as a potential magic bullet to solve all of disease problems throughout humanity. In hindsight, obviously, that was an aggressive position for him to take and has not quite proven true. The reasons for that are enunciated here on this slide. What we see and what really drives the difficulty in tumor selection starts with the tumor itself, the inherent heterogeneity of any single tumor given the potential for both evolution of the tumor over the course of time, meaning that they can upregulate or downregulate various antigens on their surface for which you are targeting, thereby making your targeting ligand obsolete.

Additionally, the microenvironment becomes a significant barrier to entry. Not only does it create infrastructure that and -- a dense stroma that the antibody or peptide might have to get through, but also in the case of some cancers, particularly things like pancreatic cancer, it can increase the internal pressure and, thereby, keep the targeting ligand from penetrating into the microenvironment and reducing its capabilities. At the end of the day, in all cases, whether you're doing an antibody-drug conjugate, a peptide drug conjugate, the last step of it is once you do bind one of the last great barriers is the drug is then internalized in most cases. And if it goes in via endocytosis and then you have to do endosomal escape, which in and of itself creates an additional problem. The endosome is highly lytic and can break down whatever the payload is, but it can also prevent the payload from escaping and getting to its end target.

All of these reasons create a need -- an unmet need for future new products that solve for this. As we were talking about, we believe that our phospholipid ether or Phospholipid Drug Conjugate platform does solve that.

As you can see here, just as a basic outline, the scaffold is we have a polar phosphocholine headgroup, followed by a long hydrophobic alkyl chain. This alkyl chain is where we then are able to attach various payloads on the one end and allow us to target to the tumor and get retention within the tumor, specifically over the course of time.

Now often, we get asked, are we -- were we the first group to pursue or develop phospholipid ethers? And the answer to that is, no. Actually, we are essentially the third generation of this. Our phospholipid ethers are mimetic of a natural occurring class of phospholipids known as alkyl phospholipids or APLs. The original APLs, which are identified here, of edelfosine and miltefosine, were originally developed and thought to be potential drugs on their own. However, they were limited by GI toxicity, they were being given orally, and resulted in high -- requirement of high -- lot of drug to be delivered, resulting in significant GI toxicity.

In order to overcome that, a second generation of molecules was created, perifosine and erufosine. These, while overcoming the challenges with gastric upset, they developed a new problem, which was plasma stability and then also hemolytic issues associated with the infusion. When we come to an iopofosine or Cellectar's phospholipid ethers, what we have done has basically solved the problem for IV hemolysis and reengineered it to allow it, instead of being the actual treatment, to target it as a payload delivery, much like an antibody, and thereby enhancing the therapeutic index and generating more efficacious drugs.

So how does this tumor targeting occur? How do we get the molecule there? And what happens? The phospholipid ethers actually target micro domains on the cell surface, particularly on the cancer cell surface. These micro domains are known as lipid rafts. Lipid rafts do exist on normal and diseased tissue. In normal tissue, however, these are small, transiently formed micro domains that rapidly dissipate in a few nanoseconds. When you look at what happens in a tumor cell, however, these micro domains get large. They become a few hundred micrometers in size. They become stabilized on the order of days, 7 to 10 days, to be exact, depending on the different tissue types. And they become signaling hubs for the tumor itself to allow them to be -- continue to be pro-oncogenic.

Taking advantage of that, our molecules then bind to it. This all happens again because of a metabolic change in the tumor that requires the overutilization of lipids. Many have heard about and understand the overutilization of the Warburg effect for glycolysis and glucose. However, most tumors are in an anaerobic environment. In an anaerobic environment, glycolysis is very limited. And so therefore, the tumor shift to using beta oxidative pathway and the breakdown of phospholipids and long-chain fatty acids, which our molecules are mimetic of and allows it to get the enhanced target.

To give you a case -- to give you some examples of this. On the left, on the far left, what you're looking at is a co-culture tumor cell, A549, which is a lung cancer cell, and a normal fibroblast cell. The red stain you see is the staining for lipid rafts. And as you can see, the normal fibroblast cell is barely visible in the image while the A549 cell lights up very brightly with significant lipid rafts presence. As you look across, whether it's prostate cancer, pancreatic cancer, lung cancer, kidney cancer, we see this is consistent across all tumor types we've tested. To date, we tested over 180 different tumor types in cell culture and validated that they all possess, at varying levels, but all possess some concentration, significant concentration, I should say, of lipid rafts.

To validate that the target -- that this is what we're targeting and that, when we knock it out, we actually see a reduction. On the other side of the slide, what you can see is now with a phospholipid ether conjugated to a fluorescent molecule, you can see, again, in the A549 cells, we get the uptake in the left image. However, when we use cyclodextrins, which actually pull out the cholesterol and disrupt the lipid rafts, doesn't disrupt them completely, but takes out about 60% to 70% of it, you can see a corresponding reduction in the uptake of the phospholipid ether with the fluorescent tag attached to it, thereby confirming that this is our predominant mechanism of entry into the tumor cell.

So how does this play out? How do we actually get there and go through this process? One of the interesting thing is, obviously, as the phospholipid ether is circulating, it eventually has to get out of the circulation and into the microenvironment. That has actually done, interestingly enough, via the high concentration or high binding -- that we are highly bound to protein, particularly albumin. And albumin has a tendency to accumulate in the tumor microenvironment. Taking advantage of that, our molecules are then transported directly into the microenvironment where they then transition off of the albumin and bind to the membrane via the lipid rafts. These rafts act as portals, and then we are internalized. That internalization goes through multiple mechanisms.

Importantly and interestingly enough, one of the things that we've discovered over the course of time is that not only do we get good uptake initially, that uptake continues over the period of 48 to 96 hours and then we get retention after that time point, which means we are not effluxed back out of the cell, which is a common method of resistance development for many tumors. That enhances our ability to deliver more drug over the course of time.

Again, looking at this now in a slightly different way, as I mentioned before, normal fibroblasts here, again, now looking instead of looking at the lipid rafts, you're looking at a coculture of taking 2 cancer cells taking up our fluorescently tagged molecule, while a normal fibroblast basically takes up none of it. We tend to get very uniform delivery. In the next image, what you're looking at is ovarian cancer. And you're seeing the uptake across all the cells in the image. So we get near 100% uniform uptake despite the heterogeneity within a single tumor type.

And last and probably most importantly, you're looking at an image -- SPECT image of a patient who actually has metastatic brain tumor that we see the uptake of one of our iopofosine molecules, crossing the blood-brain barrier and getting uptake into the tumor inpatient environment, demonstrating that across the board we see this unique target effect, whether it's in vitro or in vivo [ intake ].

So how does this occur at the cellular level? Again, as you think about this, the molecules, shown here with the little balls at the top on the stick, in the extracellular space, they move along the cell surface. They come upon cholesterol-rich lipid raft regions. They insert into those regions. And then exactly how they penetrate or how they enter the cell usually takes 1 of 2 mechanisms. The most common is through a number of these molecules binding, it triggers or it stimulates what's an ATP-dependent flippases, which then rotates the molecule into the inner leaflet and then deposits into the cytoplasm where the molecule is in transit along the Golgi apparatus network and get delivered to the perinuclear space and particularly to the mitochondria and the endoplasmic reticulum.

Importantly, the second part of the mechanism, which is a little different. So in -- whether it's heme or solid tumor, they both utilize this flippase component. However, when you're in the heme space, you also tend to get more [indiscernible] more endocytic sort of pathway working in as well because there's a higher turnover rate -- slightly higher turnover rate of the lipid rafts. And when they are turned over, they end up undergoing endocytosis.

However, in solid tumors, you see less endocytosis and rather more dependent upon fatty acid synthases and fatty acid-binding proteins to bring the phospholipid ethers in via portals. This difference allows us again to think about payloads and what we target and how we target to the different disease states.

Importantly, it's important to note that the microenvironment actually reinforces in our case and amplifies the effect of our phospholipid ether. The increase in hypoxia and acidic environment actually drives greater utilization of lipid rafts by the tumor. It's stimulating more of them being present and allowing us to have greater targets. Driving -- that also drives the tumor to actually become more of a scavenger of free-floating extracellular lipids in order again to overutilize the beta oxidative pathway. And enhancing the immune evasion of the tumor actually is driven from raft involvement.

So interestingly enough, the tumor microenvironment where, in many other cases, it actually causes resistance and difficulty with your targeting, in our case, it actually drives and reinforces the effect of what we're targeting and allows us to continue to get more drug on board.

I'm not going to spend a lot of time on this. This is a great slide for background information, it is very dense and important. But I think the key takeaway is really that the -- that there are properties that are intrinsic to the scaffolds, whether it was the early generations or the later generations, this ability to bind to the lipid rafts has been consistent throughout. What we did was enhance that in our targeting molecule and then engineer the payload attachment component and the ability then to cross the blood-brain barrier.

All of this helps us with an antigen-independent raft-targeting tumor selectivity, which is important because as we now think about the pharmacokinetics and biodistribution, it really -- it's not about how much we can put in the plasma. So it's not about a plasma concentration as much as it is about membrane exposure that drives our activity.

So again, as I mentioned earlier, the high protein binding helps get us into the microenvironment that increases the accumulation in the tumor microenvironment, the binding to the membrane and the microenvironment creating more hypoxic and more acidic environment, drives more membrane opportunity. We see very little metabolism of these molecules once we enter the cell or even in the circulation. Reduced, as I say here, slow elimination, you see biliary and fecal elimination predominantly. This is not a highly renally excreted drug. Less than 15% of the drug goes through the kidneys, which again slows that elimination and allows you to continue to load into the cancer cells over the course of time. And that prolonged retention allows us again to drive, whether it's in the radiopharmaceutical environment, to take advantage of things that have a longer half-life, or in the other molecules, allows us to deliver different molecules that can be utilized over the course of time.

Now shifting a little bit off of the PLE itself and focusing now on the more pipeline-related aspects of what we're doing here at Cellectar. As you know, we've been developing our iopofosine program. Particularly, this comes sort of with 2 scaffolds that we've done historically. On the imaging side, we have a CLR 124 program, that allows us to use PET imaging as a theranostic pair to the iodine 131 or Iopofosine I 131 if we so desire. At this juncture, most of the time, we just use SPECT-CT because iodine 131 can be targeted in that way -- or imaged in that way, I apologize.

As we think about iopofosine, clinically, we have validated this drug across a number of different arenas. I think it's important that as a targeted radiopharmaceutical, it is truly the first-in-class radio conjugate that takes advantage antigen-independent methodology to gain entry into the tumor and yet maintain and hold on to that specificity of -- tumor specificity over normal tissue.

As you can see on the right, we have validated this, whether it's been in our Waldenstrom study, the CLOVER-WaM study or in multiple myeloma and other B-cell malignancies or even in several solid tumor environments. As it relates to the CLOVER-WaM study, just as a reminder, in the clinical environment, we see that this drug is incredibly effective in these patients. And these are highly refractory and highly resistant patients. In general, these patients are in a 60% to 70% refractoriness to the 2 most commonly drugs: rituximab and BTKis. And yet we see essentially an 84% overall response rate and median duration of around 18 months in these patients. So very effective irrespective of that refractoriness, which is unique to iopofosine.

As I mentioned, when we think about this, the breadth of the opportunity here goes well beyond just Waldenstrom's. Obviously, we've got significant data and evidence in multiple myeloma, similarly in diffuse large B-cell lymphoma. And then smaller quantity of data, but across the rest of the non-Hodgkin's lymphoma, we have demonstrated that this drug is very effective across the B-cell malignancy arena.

Similarly, we've seen activity -- good activity in pediatric high-grade glioma, again, taking advantage of our ability to cross the blood-brain barrier with this compound, and deliver effective doses to the brain, as well as looking at it in combination in head and neck cancer where it was combined in an investigator-initiated trial with external beam radiation to reduce the potential sequelae associated with EBRT.

As we move forward, one of the other unique advantages of this is that we're able to quickly and efficiently modify the molecule to bring on other isotopes. This allows us when necessary or when desired to actually identify the right isotope for the right tumor. Because as we talked about before, at one level, you have to understand that the physical properties of the isotope you're delivering are going to impact both the microenvironment and the targeting ligand's capability. But at the end of the day, really it's going to be about the tumor kinetics and tumor resistance profiles that come up that will drive your activity.

And so in this case, what we're showing you here is our CLR 125 Auger-emitting isotope showing excellent uptake in vivo, in the animal model and getting very nice activity in this triple-negative breast cancer model that we ran.

Moving beyond that or having done that work, we've now advanced that program into a Phase Ib dose-finding study, as you can see here. This study has been launched in 4 centers in the U.S. at the moment, and we are rapidly enrolling and very excited about providing data later this year or early next year as it relates to it.

If we move beyond that, you can see we then can move to our alpha emitter program with actinium. You can see here in a number of different animal models where we've demonstrated good activity across pancreatic cancer and excellent knockdown when we get to the right dose levels in the models.

Importantly, when we think about alpha emitters in particular and the potential toxicities, what we're showing you here is that the infused drug -- percent infused drug per gram in tissue remains incredibly low other than in a tumor where you see somewhere between 10% to 15% or 18% infused drug into the tumor microenvironment. And the only other real reservoir of drug is in the plasma or in the blood compartment. You see nearly nothing collecting at any significant level in any of the other tissues.

Moving further into our programs, we've tested with astatine. Again, in this environment, looking at triple-negative breast cancer again and looking at various doses. And all this goes to us trying to pick the right isotope for the right tumor type over and over and over again, creating models that allow us to get to a more effective and accurate treatment for patients.

Here we looked at lead-212, which is what I'll call a hybrid radioisotope where it's also looked at in triple-negative breast cancer. In lead-212, I call it a hybrid because it has both a beta emission as well as an alpha emission that come off that impact both efficacy and safety profile. In this case, you can see, it was very -- it was efficacious and very safe in the animal model.

Similarly, if we go back to beta emitters with lutetium, you can see again where we can get very good control of the tumor in a breast cancer model and excellent survival with patients -- or in the mice. However, when we start to move beyond the radioisotope and look at other molecules, it's important to know that while we list them here, we have essentially tested every single -- and validated every single one of these modalities in animal models or preclinically in vitro. We've done small molecules, siRNA and mRNA from an oligo perspective as well as various peptides, whether they be degraders or glues or just peptide as a whole. As we look forward to that, we think this offers us a lot of flexibility moving beyond the effects of radiotherapy and allow us to consider, again, not just the radiotherapeutic, what is the right radiotherapy for the tumor type, but now what is the right other treatment modality may be optimized to give patients and doctors different choices and to overcome various resistance.

To that end, as you can see here, in various -- again, in various models of -- in vitro models of breast cancer, whether JIMT-1, SKBR or triple-negative, you can see highly effective, highly active small molecule payload being delivered with nanomolar activity for the most part. And then when we moved it into the animal model at the bottom, you can see whether it's the low dose or the higher dose blue or green line, highly effective with no rebound of the tumor at those doses, resulting in very effective outcome in this case.

When we move to siRNA and mRNA, again, looking at the oligos, we do think this offers a very interesting modality in the future as we move towards this. That modality is because it can provide greater specificity, we can either knock in genes of interest to turn them on to either make -- I'll call it make the tumor hot and recognizable by various immune response systems, or we can knock down various genes with the siRNA or RNAi approach that will allow us to either shut down a particular gene of interest or, again, shutdown pathways that would have been -- the tumor is using to hide the tumor from the immune system.

To that end, on the left, what I'm showing you is in vivo data from an animal model where we took a housekeeping gene. And we were able to take that housekeeping gene and knock it down from anywhere from 20%, depending on the payload, to approximately 70% knockdown in that 72-hour window. Very effective. This was a housekeeping gene. It was known that it would not be cytotoxic. We were doing this just as a proof of concept.

On the right, however, what we've done is design new siRNAs that are cytotoxic. And you can see we can get nanomolar activity with these, whether siRNA-1 or siRNA-2 across different lymphoma cell lines and demonstrate really nice activity and complete knockout of the tumor cells in vitro.

As we think going forward, again, as I mentioned before, PROTACs, molecular glues, we think these are really nice attributes. And one of the great problems that they have is entry into the tumor cell and getting over that. The lipid raft-type mechanism for entry allows us to solve that because again we're getting directly into the cytoplasm and then releasing the payload and it overcomes the issues with getting through the cell membrane that is often a problem with these drugs. It allows us really to get after the undruggable targets to date.

So as we think about this, not only do we think we've demonstrated that we've created a really unique platform for radiopharmaceutical drug delivery, but also a platform that allows us to expand much further beyond that -- the single element of radioisotopes, and move into what are interesting and unique opportunities as we move. We've done this through engineering the linker and release components, remapping our biodistribution, and focusing on what we do best, which is understanding how these drugs -- or these molecules are targeted and how to take advantage of that to drive payloads into the tumor and the tumor microenvironment.

So as we would say, and as Jim mentioned at the beginning, this is not a platform -- it's not just a drug. It is truly a platform. It is a unique platform in that it is truly receptor-independent. It allows us to target almost uniformly across any tumor type and more uniformly in any tumor. It allows us to take advantage of the information that we've gathered to date on how iopofosine behaves and then leverage that across the rest of the platform and allows us to then generate new payloads more effectively and more efficiently and allowing us to bring new technologies forward much faster.

With that, I'd like to turn the call back over to the operator where we can -- are ready now to take questions.

[Operator Instructions] Our first question comes from Kevin DeGeeter at Ladenburg Thalmann & Co. Inc.

I really appreciate, really comprehensive webinar today. A couple of questions. As the company's pipeline expands more into solid tumor space, can you just talk about tissue type and specific tissue types where you think this phospholipid raft-based targeting modality may offer benefits compared to some of the other modalities we've seen in the radiopharmaceutical space that are in reasonably advanced or commercial stage of development?

Yes. So I think because the lipid raft is universally present essentially across the various tissue types, the tumor types that are in the various tissues, I think we have the ability to adjust, as what I would say, and to continue to identify spaces where there is -- continues to be significant unmet medical need and challenges. It's not by accident that we have done a lot of testing in triple-negative breast cancer because we do see that as significant unmet need. And we do think that this offers a unique advantage in that arena, particularly the ability to use an Auger. Because of our perinuclear delivery, you get right next to the DNA what is required for an Auger to be effective. And we think that gives us a significant advantage there.

I think beyond that, obviously, as we've done with the actinium program and focused in places like pancreatic cancer or some of the other unmet needs, while staying away from what I call where traditional radiopharma has gone. So where are we avoiding? We're not as focused and we -- while we've done some limited work, we don't see ourselves pursuing opportunities in the prostate cancer arena. I don't see us going after neuroendocrine tumors. And I say that in a sense, when we talk about pancreatic, we're talking about PDAC specifically, so pancreatic ductal adenocarcinoma, rather than pancreatic neuroendocrine tumors. And we see those as key differentiators for the drug.

We also see opportunities, as you start to think about some of the more unique or even smaller markets than some of those big ones like breast cancer, you can get into some of the gastric tumors that are very unique, like cholangiocarcinoma and places like that where there really hasn't been much development, whether it be radiopharmaceutical or otherwise, where patients have significant need. So hopefully, that answers.

That's great. And then just a follow-up, specifically with regard to tumors and malignancies with high concentration of stromal tissue like PDAC. Can you just talk a little bit about kind of the binding modality or [ MOAD ] with kind of the lipid raft and sort of the more dense stromal tissue, kind of how well have you been able to sort of characterize the relative binding bulk in terms of affinity, but also in terms of duration of kind of binding specific in a more stromal cell intense environment?

Yes. So if -- you can correct me if I get this wrong, but I'm thinking where you're headed is, in that more stromal-based environment, what's happening in the sense of, are we seeing similar uptake as we see in a less dense environment? Or are we losing some of our binding to the actual tumor cell because of what's going on in the microenvironment? Am I sort of capturing...

Yes.

And so what I would say is our -- so the affinity for the actual lipid rafts remains incredibly high. One of the things, and I didn't put it on here, but one of the other areas that we talked about, and it's not so much stromally based, but just to give you a sense of overcoming what I'll call maybe protected compartments or difficult-to-access compartments, we also evaluated -- we've done some early work, is what I'll say, in osteomyelitis and osteosarcoma.

And so in environments where you have a very difficult -- historically a very difficult time of getting other targeting ligands to penetrate what we see as our target ligand, these phospholipid ethers still penetrate really well. I think for us, to your question specifically around like in pancreatic cancer and overcoming the stromal and microenvironment challenges that exist, I think there are 2 aspects.

One, you get the change in the microenvironment that actually enhances or increases the presence of lipid rafts on the tumor cell, which then makes -- gives you a lot more, so to speak, targets, and I sort of skipped over this. But unlike antibodies or peptides, which bind in a 1:1 ratio to their target, one of the benefits of lipid rafts because they become quite large is you're able to bind 20, 30, 40 molecules with the same lipid raft before it gets -- before it undergoes that flipping -- that flippase ATP-driven internalization. And that allows you to actually get more drug in. So that's sort of some of the elements that I think play to our benefit.

As it relates to actual increased affinity, the other part that I think plays to our benefit is that what you still see is that highly protein-bound albumin event still drives this into the microenvironments, such as in those stromal environments, which allows us to get more drug into the space, is what I'll call it. And then as long as it -- what you see is the disassociation from the albumin to the lipid raft regions remains incredibly high. So that affinity to the lipid rafts remains incredibly high despite all of that.

And so we may be losing percentage of infused drug per gram of tissue into the tumor in that kind of environment in theory, but we're actually getting more into the microenvironment. And I think that's why you see that things, like with our alpha emitter program, you see really high -- a stronger activity profile than maybe you might expect if we were using something more of a beta-emitting or an Auger-emitting because you don't necessarily need to be fully internalized with those.

That's great. And then just one clarification and then I'll get back in the queue. You mentioned or you spoke about blood-brain barrier penetration. Were you referring to the phospholipid ether alone or conjugated with the various radiopharmaceutical or other kind of payload? Just kind of, if you could just clarify that for us.

No, that's great question. And what we've seen is -- the short answer is, yes. So we've definitely seen it with the conjugation to the radioisotopes, the images we showed were either with I 131 or with 124, where we saw in both cases, we saw a significant uptake into the various tumors, brain tumors when we did it, and obviously, in the pediatric center when we did the clinical trial in high-grade glioma.

We've also seen it in vivo in animal models where we use a fluorescently tagged payload. And why I stress that is because fluorescently tagged payload, unlike an isotope, which is basically a single atom, a fluorescent tagged molecule starts to behave and look a lot more like a small molecule or a peptide bound to the targeting ligand. And thereby, you're still seeing that crossing of the blood-brain barrier.

Now I will say the challenge for us with the blood-brain barrier is that we do not necessarily see any uptake or coalesce concentration of material in patients without a brain tumor. So we don't know what will cross the blood-brain barrier when there's no tumor present. What we know is we cross the blood-brain barrier when there's tumor present. Is that due to some disruption of the blood-brain barrier? Possibly. Probably. I mean that's been my working hypothesis, is that the blood-brain barrier is slightly disrupted, and therefore, we're able to penetrate and our molecules cross pretty easily because we're small and we slip through. We can't validate that we do it otherwise.

And so I'd just say that in the sense of that would then indicate that potentially with larger invasive tumors, we might see higher uptake, and in smaller micrometastatic tissue, we might see smaller uptake or more limited uptake into those environments. And so those are things that we continue to explore and try to better understand exactly how we're getting across the blood-brain barrier, and how does that play into then the PK profile, both in the brain compartment as well as in the circulation compartment.

Our next question comes from Kemp Dolliver at Brookline Capital Markets.

Thank you for taking my question and sharing all this information today. So first question relates to the other modalities you mentioned. And to put you on the spot a bit, which one of those modalities would you pursue first?

Yes, Kemp, way to put me on the spot. If all things were equal, let me -- money not an issue, all things equal, I would probably -- my preference would probably be to pursue the oligo strategy first. I think it's a real game-changing sort of strategy, unlike many of the other oligo-targeting approaches, they're getting better. But we actually have a platform here that I think is much more effective at getting the oligos cross into the tumor cell, getting them to be expressed. We do -- in this case, we don't require any cleavage. So it allows us to get them in there, get them to where they need to be essentially. And it allows us to drive what I'll call a much more specific outcome for patients, right?

Because if you're knocking down a gene that is overexpressed in the tumor, but it's not really expressed in normal tissue all that much, you're not going to see any off-target effect. And this allows you to get to very effective treatments.

That said, living in the world we live in, we have the most and more complete data on the small molecules because that's where we started. And so that's the easiest, after radiopharmaceutical, probably the easiest and fastest to get into clinical development, would be the small molecule arena.

And the only other thing I would add to that, Kemp, is with all of these assets, we have pretty impressive intellectual property, but with the oligos in general, I think, Jarrod would agree that our intellectual property portfolio is extremely extensive in and around that area of research.

Yes, absolutely.

Right. And a related question on the radiopharmaceuticals. So given that you've evaluated 170 tumors, if money were no object, what would you pursue, that you're not pursuing now?

I was going to say, I pursued WM. So I mean, I -- it's a great question. I think something I would like to -- that's a hard question for me to answer, I'll be honest. I mean I could see going after -- we've looked in pediatric high-grade glioma a little bit. I think adult glioma would be a very interesting opportunity for us to pursue. I think that creates a -- there's a significant unmet need that still remains there, and this could provide a very nice modality to address that.

And then I think, obviously, there are a number of other areas in my head that I think remain significantly challenged. Colorectal cancer continues to grow as a market and continues to be problematic from treatment modalities. So those might be 2 areas.

And Kemp, that's a great question, obviously. But I'll remind the audience that we're so laser-focused right now on getting Waldenstrom's macroglobulinemia across the finish line from a regulatory perspective for 131. And then once approved in WM, I'll state the obvious, we'll have an opportunity to expand via NCCN guidelines and investigator-sponsored studies to build upon the data that we currently have in a wide variety of hematologic malignancy. As Jarrod mentioned earlier, a highly challenging patient population in multiple myeloma, some really nice responses in DLBCL, as well as other non-Hodgkin lymphoma.

So we see that -- we view those areas from a hematologic perspective post approval in WM, assuming approval, as really low-hanging fruit.

There are no further questions on the line. I will now turn the call back over to Jim Caruso for any closing remarks.

Thank you, operator. Certainly, thank you to all the participants. Jarrod, really nice job. You covered a lot of dense information in an abbreviated amount of time, and I thought it was not only succinct, but very clear. And so I thank you for that. As always, your work in the area is simply outstanding.

And as we formally conclude today, I'd like to leave you with one final thought. Throughout the presentation, we discussed phospholipid ethers, radioconjugates, payloads as well as the platform technology, certainly appreciative of the questions that were provided. Ultimately, what drives our work is the belief, that innovation matters most when it has the potential to change lives of patients facing serious cancers. We are pursuing a vision that extends well beyond a single product or a single indication. And hopefully, that came across today as part of our discussion.

We believe the opportunity is to establish a new paradigm for targeted delivery, one capable of unlocking the full potential of radiopharmaceuticals, and as discussed over time, a broad range of therapeutic modalities. If successful, the impact could reach certainly well beyond Waldenstrom's macroglobulinemia, creating opportunities across numerous cancers where significant unmet medical need remains.

None of this progress happens by chance. It is the result of years of dedication, scientific rigor, unwavering commitment from an exceptional team. And I remain proud of the researchers, clinicians, operational leaders and employees across Cellectar who continue to push the boundaries of what is possible each and every day. Most importantly, we owe a tremendous debt of gratitude to the patients and families who place their trust in our clinical research, as well as physicians, nurses, investigators and study coordinators who make these advances possible. Their commitment is the foundation upon which every medical breakthrough is built.

While there is still important work ahead, we believe we are at an exciting point in our evolution. We have a clinically validated platform, expanding developmental opportunities and meaningful upcoming milestones, and a clear focus on translating motivation into better outcomes for patients and long-term value for shareholders. Thank you.

Thank you for joining today's call. You may now disconnect.

Good morning, ladies and gentlemen. Thank you for standing by, and welcome. [Operator Instructions] Please be advised that today's call may be recorded.

I will now hand the call over to Anne Marie Fields, Managing Director of Precision AQ. Please go ahead.

Thank you, operator. Good morning and welcome to Cellectar Biosciences' Second Quarter 2026 Financial Results and Business Update Conference Call. Joining us today from Cellectar are Jim Caruso, President and CEO, who will provide an overview of the company's progress before turning the call over to Chad Kolean, CFO, for a financial review of the quarter. Following this, Jarrod Longcor, Chief Operating Officer, will give an update on the company's progress and plans for its promising clinical development pipeline of radiopharmaceuticals.

Cellectar issued a press release earlier this morning detailing the content of today's call. A copy can be found on the Investor page of Cellectar's corporate website. I want to remind callers that the information discussed on the call today is covered under the safe harbor provisions of the Private Securities Litigation Reform Act. I caution listeners that management will be making forward-looking statements. Actual results could differ materially from those stated or implied by our forward-looking statements due to risks and uncertainties associated with the business. These forward-looking statements are qualified in their entirety by the cautionary statements contained in today's press release and in our SEC filings.

The content of this conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, August 13, 2026. The company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call and webcast. As a reminder, this conference call and webcast are being recorded and archived. We will begin the call with prepared remarks and then open the line to your questions.

I'll now turn the call over to Jim Caruso. Jim?

Thank you, Anne Marie, and thank you all for joining us this morning. The second quarter marked an especially productive period for Cellectar as we continued making meaningful progress across every area of our business, including clinical development, regulatory action, pipeline advancement, platform expansion, and strengthening of our financials.

Our near-term priority remains clear: advancing iopofosine I 131 for patients with relapsed or refractory, Waldenstrom's macroglobulinemia, or WM, particularly those patients whose disease has progressed following earlier lines of treatment, including BTK inhibitor therapy. We believe this represents a significant unmet medical need and an attractive opportunity to bring a differentiated treatment option to patients who currently face limited therapeutic alternatives.

During the quarter, we took several important steps to move this strategy forward. First, we reported the full 12-month follow-up results from the CLOVER-WaM study. These data further reinforced both the depth and durability of response achieved with iopofosine and demonstrated that the study successfully met both its primary and secondary endpoints. Taken together, we believe the totality of evidence generated to date continues to support iopofosine's potential to become an important treatment option for WM patients.

Second, we continue to build an increasingly compelling clinical data set for iopofosine. We presented new data at ASCO 2026 from the CLOVER-WaM study highlighting outcomes in patients treated immediately following BTKi therapy, a challenging patient population. These results demonstrated a 79.2% major response rate, an 87.5% overall response rate, and 100% clinical benefit rate, and encouraging durability with a median duration of response of 16 months.

Most importantly, we have now initiated site activation activities for our planned confirmatory Phase III study. This represents a critical milestone in our regulatory strategy. Once necessary site activation and ongoing patient enrollment is achieved, we expect to be in a position to submit our new drug application under the FDA's accelerated approval program in mid-2027. Based upon the breakthrough designation awarded to iopofosine I 131 for relapsed/refractory WM, an approximate 6-month review is anticipated.

To support these efforts, we were pleased to complete an oversubscribed financing in May that has the potential to provide up to $140 million in capital, including $35 million upfront and up to $105 million tied to future milestones. This financing significantly strengthens our balance sheet and provides the resources needed to execute our WM strategy, advance our regulatory initiatives, and continue investing in our broader radiopharmaceutical pipeline. Beyond WM, we continue to advance the broader opportunity represented by our phospholipid drug conjugate, or PDC, platform.

The PDC platform is a highly differentiated targeting technology designed to selectively deliver therapeutic payloads to cancer cells, including primary tumors, metastatic lesions, and cancer stem cells. Importantly, the platform is highly versatile and can be combined with a variety of payloads and isotopes, including beta-emitting, Auger-emitting and alpha-emitting radiotherapeutics.

We believe the success we are seeing with iopofosine is validating the platform and creating a strong foundation for future pipeline expansion. Today, in addition to discussing our progress with iopofosine, we will also review advancements in CLR 125, our Auger-emitting program in solid tumors, and discuss how we plan to leverage the platform to build a next-generation radiopharmaceutical franchise.

With that overview, I'll turn the call over to Chad for the financial review.

Thank you, Jim, and good morning, everyone. First, I will spend a couple of minutes on the financing that Jim mentioned. As he stated, the transaction provided the company with the current and anticipated future funding to support our strategy to obtain approval for iopofosine I 131. The company received $35 million gross upfront, or approximately $31.7 million net, for common shares and prefunded warrants. Additionally, we issued three tranches of approximately 13.2 million warrants each, all of which are currently exercisable at a strike price of $2.65. Furthermore, these warrants are callable for cash by the company if the respective milestone and related criteria are met.

Each tranche of warrants, A, B, and C, has a milestone associated with it. The Tranche A warrants, which expire on July 7, 2027, have a milestone of first patient enrolled in the confirmatory study for iopofosine I 131 in Waldenstrom Macroglobulinemia, or WM, patients. The Tranche B warrants, which expire July 7, 2028, have the milestone of the FDA's acceptance of a new drug application for iopofosine. The Tranche C warrants, which expire July 7, 2031, have a milestone of approval by the FDA of iopofosine for marketing.

In addition to achieving the milestones, two additional criteria must be met for the warrants to be callable. First, the volume-weighted average price, or VWAP, for the company's stock must be at least $3.45 for 20 consecutive trading days. Second, the trading liquidity based upon a VWAP must average a minimum of $500,000 for those same 20 trading days.

The milestone timing is designed to provide the necessary funding through the anticipated study initiation, submission to FDA and approval. We believe this structure, provided it occurs as designed, supports the company's capital needs through initial commercialization of iopofosine.

Now, for our financial results for the period ended June 30, 2026. We ended the second quarter with cash and cash equivalents of approximately $34.0 million compared to $13.2 million as of December 31, 2025, which reflects the cash generated from the initial portion of the May financing.

Turning now to our operating results. Research and development expenses for the 3 months ended June 30, 2026, were approximately $4.6 million compared to approximately $2.4 million for the 3 months ended June 30, 2025. The overall increase in R&D largely reflected increased clinical study activity to support our CLR 125 study in triple-negative breast cancer and initiation of the confirmatory study of iopofosine I 131 in WM.

General and administrative expenses for the 3 months ended June 30, 2026, were $2.6 million compared to $3.6 million for the same period in 2025. The decrease in G&A was driven primarily by reduced professional fees, pre-commercialization efforts, and personnel costs.

Net loss for the 3 months ended June 30, 2026, was $6.9 million, or $0.57 per share, compared with $5.4 million, or $3.39 per share, during the 3 months ended June 30, 2025. The enhanced strength of our balance sheet enables our ability to effectively advance our clinical and regulatory programs.

Now I will turn the call over to Jarrod to discuss the regulatory and clinical advancements we've been making during the first half of 2026.

Thank you, Chad, and good morning, everyone. As Jim noted, we continue to make meaningful progress across our clinical, regulatory and development initiatives and believe Cellectar is entering an important phase of execution with multiple value-driving milestones ahead. Our primary focus remains advancing iopofosine I 131 to potential registration in WM, where we have generated a compelling body of clinical evidence and established a clear regulatory path forward. We have been encouraged by the consistency of the data emerging from the global CLOVER-WaM study, which continues to demonstrate meaningful and durable responses in a patient population with significant unmet medical need.

During the quarter, we expanded that clinical evidence base with two important data updates. First, we presented new analyses at ASCO, highlighting outcomes in patients treated immediately following BTKi inhibitor therapy, a particularly challenging setting where treatment options remain limited. And as Jim mentioned a few minutes ago, we demonstrated an approximately 80% major response rate and 16 months of durability in these patients. We also reported the full 12-month follow-up data set from the CLOVER-WaM study on all patients, which further reinforced the durability, with a median durability of 17.8 months and approximately 62% of patients achieving a major response, and the depth of the response observed with iopofosine increasing over time with a very good partial response and complete response rate increasing to 14.5% in these late-line highly refractory patients.

Importantly, we are now translating these clinical achievements into regulatory and operational execution. We have initiated site activation activities for our planned Phase III confirmatory trial and expect the first sites to open in the coming months, a key milestone in the development strategy. This study is designed to support long-term registration requirements while also enabling us to submit our planned accelerated approval pathway filing in the United States in 2027.

We view the initiation of patient dosing in this trial as a significant upcoming catalyst and believe that could occur late this year or early next year and is an important step toward bringing iopofosine to patients who urgently need new treatment options.

Beyond WM, we continue to broaden the opportunity for both iopofosine and our proprietary phospholipid drug conjugate, or PDC, platform. Our recently published multiple myeloma data in the peer-reviewed journal, Cancers, further support the differentiated mechanism of action of iopofosine and highlight its potential applicability across a range of B-cell malignancies, including WM, multiple myeloma, diffuse large B-cell lymphoma, or DLBCL, and other difficult-to-treat hematologic cancers where new therapeutic options are urgently needed.

At the same time, we are advancing the next generation of our radiopharmaceutical pipeline, which recently enrolled and dosed the first patients in our Phase Ib trial of CLR 125 in triple-negative breast cancer, and remain on track to report initial dosimetry, safety and efficacy data later this year or early next year.

Taken together, we believe these accomplishments underscore the growing validation of our platform, the strength of our development strategy and a significant opportunity ahead. In tandem, we continue to advance what we believe is one of the most innovative, differentiated, and versatile targeting platforms in radiopharmaceutical development today.

Our proprietary PDC platform was designed to selectively target cancer cells through a mechanism that is independent of specific tumor mutation or surface antigens. We believe this enables near-universal tumor targeting across hematologic malignancies as well as solid tumors while providing a flexible delivery vehicle for multiple therapeutic payloads.

The platform has already generated clinical validation through iopofosine and serves as the foundation of our next-generation pipeline, including CLR 125, our Auger-emitting radiotherapeutic program, and CLR 225, our alpha-emitting program. We believe these programs represent significant long-term value creation opportunities and demonstrate the range of the platform across multiple cancer indications.

One of the unique strengths of the PDC platform is its flexibility. By leveraging the similar targeting backbone with different therapeutic payloads, we have the potential to develop multiple product candidates addressing a range of tumor types while capitalizing on the extensive knowledge we've already accumulated regarding tumor uptake, biodistribution and safety.

To provide additional insight into this opportunity, we'll be hosting an educational webinar on August 18. During this event, members of our management team will discuss the scientific foundation of the PDC platform, its differentiated targeting capabilities, the progress we have made across clinical programs, and the significant future opportunities we see for the platform. We encourage you all to join us for what we believe will be an informative and engaging discussion about long-term potential of Cellectar's technology and pipeline. Overall, we are pleased with the progress made across our clinical, regulatory, and pipeline initiatives during the first half of the year. We believe we are well positioned for the next stage of development and remain focused on executing against the milestones ahead.

With that, I'll turn the call back to Jim for closing remarks.

Okay. Thank you, Jarrod. As we look ahead, we believe Cellectar is entering an important and exciting, as well as transformational period. Our immediate focus is executing on the next steps required to advance iopofosine in WM. With compelling clinical data, active site initiation efforts already underway and a clear regulatory path forward, we are working toward the start of our confirmatory Phase III study, which we view as a critical catalyst and an important step toward our planned accelerated approval submission, which remains on target for the first half of the year in the United States.

At the same time, we are well positioned financially, following the oversubscribed financing completed earlier this year, which provides us with the resources necessary to execute our near-term objectives. Importantly, as Jarrod just reviewed, we believe the opportunity extends far beyond a single product.

The progress we are making with iopofosine continues to validate the underlying strength of our PDC platform and further reinforces our confidence in expanding the technology across additional radiopharmaceutical programs, including our Auger-emitting and alpha-emitting product candidates for solid tumors. To this end, I encourage listeners to participate in our educational webinar on August 18.

Our vision is to build a leading radiopharmaceutical company founded on versatile, clinically validated delivery platform capable of generating multiple product opportunities across both hematologic and solid tumor indications. With strong momentum across our regulatory, clinical and corporate initiatives, we look forward to sharing additional milestones throughout the remainder of 2026 and into 2027.

I would like to thank our employees, as always, investigators, most importantly, patients, our stockholders and partners for their continued support and commitment to our mission.

Operator, we're now prepared to take questions.

[Operator Instructions] And your first question comes from Kevin DeGeeter from Ladenburg.

Appreciate the update. Exciting time. A couple of questions from myself. First off, on the Phase III WM program. Can you just walk us through a little bit more granularity, the rate-limiting steps to first patient enrolled? I think you've mentioned your site activation, presumably IRB, but kind of any other factors that may drive kind of your guidance to be, earlier kind of 4Q versus 1Q '27? And then can you just clarify what triggers potential FDA submission. Is it a specific number of patients enrolled, a more qualitative criteria? Just a little bit more granularity there would be helpful.

All right. Terrific. First of all, Kevin, thank you for your participation today in support of the company. It's very much appreciated. That is a significant question. And as you would expect, there's an enormous amount of work that goes into initiating the confirmatory study, especially one of this size. And we're very pleased with the progress that we've made to date, and we're particularly happy with the response from not only those academic catchment centers that treat a significant portion of the relapsed/refractory WM population, but also from community networks, integrated oncology delivery networks that typically treat these patients or diagnose these patients, as well as treat out in the general community, certainly in the first handful of lines of therapy, prior to referring to one of these institutions that are world-renowned for the treatment of highly refractory WM.

So we're looking at all customer segments, even, quite frankly, community-based institutions that also see a significant amount of patients. By way of background, 15 states in the United States essentially control 80% of the population for WM. So it is highly targeted. And in and around those geographic communities, all of these segments, the integrated oncology delivery networks, community-based hospitals, as well as those academic centers, provide treatment for this patient population. So the net -- having said that, we're very pleased with where we currently sit. We're on target from a timing perspective. I'll have Jarrod talk to the details of your questions, but we still view on that kind of March-April time frame as our submission for accelerated approval with our friends at the FDA. Jarrod?

Sure. So, as you mentioned, there's a number of steps that go into the -- obviously, the start-up process, just sort of lay out a few, I mean, generally, the way the process actually starts is that, and I'll just sort of give probably way too much granularity here, but at the time of beginning the process, right, where you start is the contracting with the CRO and getting the documentation in place with the CRO. And that means not just the contract, but it's all the supporting documentation. So all of the necessary investigator letters, all of the necessary documents for the operation of the study and the SOPs and making sure everything lines up.

After that, then you move into the next phase, which is really site identification, where you identify -- which sites you want to target, which countries you want to go to, and so on and so forth from that. That then goes into what's called a feasibility step where you submit to those various sites and investigators a feasibility questionnaire where they again, request -- they get basically a protocol synopsis, they review it, they determine if they're interested in participating, and they provide you with a sense of how many patients they may or may not -- how many patients they might enroll in what time frame.

After that, you move into what's called the qualification phase, which is obviously, with the radiopharmaceutical, it's not like taking an oral antibiotic per se, right? In this case, you've got to have an infusion suite, you got to be able to handle and licensed for handling I 131. And so you have to go through all of that process and you have to collect all that documentation as well. Then you move through and, as you said, you get into the IRB phase. The IRB phase comes, site contracting comes that can sometimes go in parallel, sometimes not. And that depends -- depending, as Jim said, we've got a lot of interest from both community centers as well as academic centers.

When you think about community centers, we can use a central IRB, that allows them to approve more rapidly and move more rapidly. However, some of the more academic centers tend to have a local IRB in addition to that central IRB, so there's an extra IRB review process. In addition to that, many of the academic centers also have an internal committee that have to review the protocol with the final full protocol and statistical analysis plan, where they then vote to participate and go from that step to the next step, which would then be the contracting.

After that, you have to train the centers and begin all that process, and then you do site -- the true site initiation, which allows them to open and begin screening for patients, and then first patient in. That's sort of all of that execution and operational stuff is going on in the background. And as we said in our prepared remarks, we have initiated much of that, and we are on track to have what we believe our first sites open in a handful of months here over the next coming months, with the potential first patient in late this year, early next year.

As it relates to then the FDA submission and what's the gating aspect for that, that is -- the gating aspect by FDA's definition is the site has to be their site. The study has to be initiated and "ongoing." So initiated at the time of submission, ongoing at the time of regulatory action, the definition of which is not defined by the FDA. They will not provide any clear direct guidance on that subject. So you are left to sort of estimate what you think that might be.

We know what they're asking is basically that companies are executing diligently against the confirmatory studies for acceptance of their accelerated approval application, and diligently continue to execute that by the time they are doing regulatory action. Our interpretation of that is that we want to have a number of sites open somewhere -- perhaps 10 to 20 sites open at the time of submission. And we want to be in a position that we've gotten a couple of patients enrolled, preferably at the time of submission, and then having somewhere between 5% or more patients enrolled by the time there's regulatory action, that's 6 to 8 months after the submission goes in. Does that help?

It does. Incredibly granular. And then just separately, on CLR 125, interesting asset. Just kind of talk to us about kind of what the initial learning around, I guess, the dosimetry data and potential time line. I think you kind of called out milestones, but not a specific time line for data update on that exciting program.

Yes. So I'm going to stay very vague on the -- what we know about the dosimetry and so forth. And I think the reason for that is we, to be transparent, we do expect to be able to provide some data later this year. We are looking at the San Antonio Breast Cancer Conference, obviously, has an opportunity, one potential opportunity to present data as it relates to that program, as well as other opportunities as may warrant to provide a data update around the program.

What I can say is we know we've got very good uptake into the tumor. We have distribution that looks as one would predict based on what we know about the targeting ligand and what we've known from iopofosine. And we see that, that it is very much predictable and in line with what we would have expected. And so what we're doing from there is really, as one would expect in a Phase Ib dose-finding study, is optimizing and looking at how we optimize the dose ideally for patients.

And your next question comes from Kemp Dolliver from Brookline Capital Markets.

A couple of questions. So you have started to manufacture -- your supply for your trials. Are you manufacturing any commercial supply for iopofosine I 131 at this point or plan to do so shortly?

Yes. So -- thanks for the question, Kemp. What I would say to you is -- I'm going to say it as a yes, but I'm going to put a qualifier in there. And that qualifier is, obviously we can't manufacture the isotope or the finished product because those are essentially what I'll call near-term just-in-time or nearly just-in-time productions. But the targeting ligand, we do have significant stability data on that, and what we do is we produce that now. We've been producing that essentially at commercial scale for the last several years. And to give you a sense, our -- we've got more than 5 years stability on the ligand. So we generally produce that at large scale and then use that as necessary as we produce it and generate the drugs.

As I said, we have our commercial, and I'll say it for the finished product, we have our commercial infrastructure built out and ready to go. Obviously, when we get a commercial approval -- should we get a commercial approval, let me say it that way, we would then obviously be in a position to relatively quickly turn on that production process and ship drug through our existing logistics chain and production process.

Yes. We have the capacity to scale significantly in terms of patient lives and we could stack very quickly. In fact, what's our max capacity from a patient perspective. It went well beyond any of our potential patient treatment and/or our revenue models. It was very substantial. Close to 1,000...

Yes. We're at about -- I'd say right now, we would easily be able to hit essentially about a 100 patients per week kind of scale with finished products, because as you -- as I'm sure you know, Kemp, the way these things are set up is the production of each unit is essentially done in an individual hot cell. You can obviously, as I'll call them, you daisy chain the hot cells together. In our case, our production runs actually give us considerably more material than we need. And so even just two or three hot cells would provide us more than sufficient supply to hit that sort of 100-ish patient range.

That's great. And that leads into the next question is, how quickly you can launch after receiving the accelerated approval?

So that would be a function of levels of investment and when we determine when to pull particular levers. So it's typically a 12-month period at a minimum to fully lock and load for commercial execution. And really, I think in this particular case, because of the scalable nature of the space, as I cited earlier, 15 states essentially control 80% of the WM lives. But when you look at the actual customers triaging those patients, that number gets even more scalable and smaller. It's one of the attractive reasons this space is, from a commercial perspective, a whiteboard, if you will. There's limited competitive tension in the space. BTKis are the only approved class of medications. They're predominantly used in first line and second line and beyond.

A bunch of inbound inquiries relative to the availability of the drug. So getting back to your original question, we could scale up quickly because it's a targeted environment. But ultimately the time to fully lock and load and mobilize is really a function of when you pull the trigger on certain levels of investment. Now having said that, we also have -- where we are [Technical Difficulty]

digital environment. Because there's limited to no competitive tension there, or [Technical Difficulty]

medical marketing, commercial machinery in the space, it's pretty wide open.

And so for a small company like ours, it could potentially be a consideration to commercialize on our own because a limited amount of oncology spend that would be required to really drive trial use and adoption. However, having said that, we're also discussing with third-party partners that would take that on, as well as world-class, extremely large and efficient commercial organizations that we can also partner with to drive this for us. So all three typical commercial options are on the table for us. We're evaluating all of them. And we believe we could move very quickly in terms of establishing trial use and adoption in the space for limited funds in comparison to other spaces like breast, et cetera, in terms of the cost of doing business.

Great. And my last question is more for the broader industry view, but you do have some toehold in actinium-225, at least not in the clinic yet, but something of interest to you. And so what's your sense of the availability of actinium-225 now versus, say, a year ago?

Great question, Kemp. And I love the fact that it just allows me to just wander off and pontificate for a few hours. I appreciate that opportunity. So what I would say is, yes, a year ago, I would say -- actinium, everybody was considerably concerned about the supply chain for actinium. I don't think that it has fully resolved, but I do think as we have been advancing here and as I think people were expecting, we've gotten new suppliers in place. I think groups like SpectronRx are now up and consistently supplying actinium in addition to the group ITM, Eckert & Ziegler, and then you now have Northstar online. I think you've got a number of other groups, Ionetix and a few others that are coming online in the near future, Nucleus and so forth.

And so I think, where we sit today to where we're going, I think the supply chain is for the sourcing of actinium is opening up a bit. Now I do expect that, as programs advance and the need for larger quantities of actinium for certain programs increases, we may continue to see future constriction and opportunity. And as you know, our strategy here on all of our components for production has been to multisource every piece of the component. So everything from our targeting ligand to each radioisotope we work to work on and then each finished product that gets made, we multisource all of that through various contractors. And in our, what I'll call our collaborative outsourcing model.

And as you probably may or may not be aware, historically, what we've done, and what we've done particularly around actinium, is we put in place our ready supply agreements with a number of parties. I think we're at 4 at this juncture, in order to make sure that we can access and get the supply necessary for our program, both near-term and long-term.

And with no further questions at this time, I will turn it back over to Jim for closing remarks.

Well, terrific. Thank you to everyone who participated in our call today. It's very much appreciated. In particular, our analysts for asking very thoughtful and provoking questions. And operator, with that, we'll conclude our call.

Ladies and gentlemen, this does conclude your call for today. We thank you very much for your participation and you may now disconnect. Have a great day, everyone.

Ladies and gentlemen, thank you for standing by, and welcome. [Operator Instructions] Please be advised that today's conference call may be recorded.

I would now like to hand the conference call over to Anne Marie Fields, Managing Director at Precision AQ. Please go ahead.

Thank you, Vanessa. Good morning, and welcome to Cellectar Biosciences First Quarter 2026 Financial Results and Business Update Conference Call. Joining us today from Cellectar are Jim Caruso, President and CEO; who will provide an overview of the company's progress before turning the call over to Chad Cohen, CFO; for a financial review of the quarter. Following this, Jarrod Longcor, Chief Operating Officer; will give an update on the company's progress and plans for its promising clinical development pipeline of radiopharmaceuticals.

Cellectar issued a press release earlier this morning detailing the content of today's call. A copy can be found on the Investor page of Cellectar's corporate website. I want to remind callers that the information discussed on the call today is covered under the safe harbor provisions of the Private Securities Litigation Reform Act. I caution listeners that management will be making forward-looking statements. Actual results could differ materially from those stated or implied by our forward-looking statements due to risks and uncertainties associated with the business.

These forward-looking statements are qualified in their entirety by the cautionary statements contained in today's press release and in the SEC filings. The content of this conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, May 14, 2026. The company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call and webcast. As a reminder, this conference call and webcast are being recorded and archived. We will begin the call with prepared remarks and then open the line for your questions.

Now let me turn the call over to Jim Caruso. Jim?

Thank you, Anne Marie, and thank you to all for joining us today. The first quarter of 2026 marked a transformational period for Cellectar. Defined by rigorous execution across our clinical, regulatory and financial strategies. We entered the year with momentum. And over the past quarter, that momentum has meaningfully accelerated.

Earlier this month, we reported positive 12-month follow-on data from the Phase IIb CLOVER WaM study evaluating iopofosine I 131 in patients with relapsed or refractory Waldenstrom Macroglobulinemia or WM. These data demonstrated durable and consistent responses across one of the most heavily pretreated and refractory WM populations studied to date, including patients who were both exposed to and refractory to BTKi inhibitors. Importantly, iopofosine met both the primary and secondary endpoints of the study. Reinforcing our confidence in its clinical profile and its potential to address a profound unmet need in WM, particularly for patients who have been previously prescribed to BTKi and are now searching for treatment answers with off-label salvage therapies.

These results take on even greater significance when viewed in the broader disease context. WM is a rare and curable lymphoma affecting a prevalent patient population of approximately 60,000 to 80,000 patients in the U.S. and EU alone with a rapidly growing population of patients progressing after BTKi therapy with no FDA-approved therapies beyond BTKIs. For these patients, therapeutic options are limited, outcomes are suboptimal and the need for new durable treatments is urgent.

With the full 12-month data set now in hand, along with a deep and mature body of clinical evidence, we are advancing our plans to file for accelerated approval with the FDA and to initiate a randomized Phase III confirmatory trial. We believe iopofosine is well positioned to meet regulatory expectations and to become a foundational therapy in the WM treatment landscape. Running in parallel with this clinical momentum, we announced an oversubscribed financing of up to $140 million, led by high-quality long-term health care investors.

This capital materially strengthens our balance sheet and provides the resources necessary to advance iopofosine through our planned Phase III confirmatory study and potential commercialization as well as support the continued advancement of triple-negative breast cancer study as part of our broader radiopharmaceutical pipeline. Taken together, the strength of our iopofosine data and the successful financing represent a clear inflection point for Cellectar. They enable us to move forward decisively from a clinical validation to late-stage execution.

With that overview, I'll now turn the call over to Chad to walk through our financial results.

Thank you, Jim, and good morning, everyone. I'll address our financial results for the period ended March 31, 2026, and the recently completed financing that allows us to accelerate our development of iopofosine I 131. We ended the first quarter with cash and cash equivalents of approximately $8.3 million compared to $13.2 million at the end of 2025. This does not include the results of the financing, which I will address in a moment.

Our research and development expenses for the 3 months ended March 31, 2026, were approximately $3 million compared to approximately $3.4 million for the 3 months ended March 31, 2025. R&D costs declined as the follow-up activities for patients of CLOVER WaM Phase IIb clinical study declined and preclinical product development was reduced. These reductions were partially offset by increased manufacturing spend for both iopofosine and CLR125.

General and administrative expenses for the 3 months ended March 31, 2026, were $2.8 million compared to $3 million for the same period in 2025. The modest decrease in G&A was driven primarily by reduced personnel costs. Net loss for the 3 months ended March 31, 2026, was $5.7 million or $1.33 per share compared with $6.6 million or $4.30 per share during the 3 months ended March 31, 2025.

Importantly, as Jim stated earlier. Earlier this month, we completed an oversubscribed financing for up to $140 million, consisting of an upfront amount of $35 million and up to $105 million in milestone-based capital. As a result, we believe our current cash position enables us to fund planned operations, particularly the initiation of our confirmatory Phase III trial of iopofosine in patients with WM into the second quarter of 2027.

The structure of the milestone-based warrants is designed to provide additional funding at key points in the development of iopofosine. Three tranches of warrants, one tied to each of three milestones were issued for each security the investors purchased upfront.

The first milestone is the initiation of the confirmatory study as demonstrated by the enrollment of the first patient in the study. The second milestone is the acceptance of an NDA submission by the FDA. And the third milestone is the approval of iopofosine by the FDA. Upon the attainment of each milestone, provided our common stock trades above $3.45 with volume exceeding $500,000 per day for 20 consecutive days, the company can call the warrants for cash. The warrants for each milestone represent potential additional funding of $35 million. So the aggregate potential for the 3 milestones is $105 million and when combined with the upfront of $35 million represents the $140 million of total potential funding.

The warrants are all exercisable upon approval of the transaction by the stockholders. Which will be part of our Annual Stockholders' Meeting agenda.

Completion of this offering puts us in a position of financial strength and strategic flexibility, allowing the organization to remain focused on disciplined execution and value creation.

Now I will turn the call over to Jarrod for an operational update, including plans for our promising pipeline of radiopharmaceuticals.

Thank you, Chad, and good morning, everyone. As Jim highlighted, the 12-month CLOVER-WaM results represent a significant milestone for iopofosine for patients living with WM. For some background, patients enrolled in the CLOVER-WaM had a median of four prior lines of therapy with refractory rates from 77% to 75% and 60% in BTKi, rituximab chemotherapy exposed patients, respectively.

Additionally, 58% of patients exposed to both BTKi and rituximab were dual class refractory. Despite this being one of the most heavily pretreated and refractory WM patient populations to date, iopofosine produced robust and durable responses, underscoring the strength of the targeted phospholipid drug conjugate platform. Notably, the primary and secondary endpoints were both achieved in the protocol study population (N=55) with an overall response rate of 83.6% and the primary endpoint of major response rate or MRR, improving to 61.8%. The secondary endpoint of duration of response, or DOR, achieved a median of 17.8 months.

Importantly, greater than 30% of responders maintained their responses beyond 36 months. The median progression-free survival was 13.5 months and the (VGPR/CR) rate was 14.5%. The disease control rate remained stable at 98.2%. In addition, the data demonstrated consistent efficacy in both BTKi exposed and BTKi refractory patients. These results compare favorably with available therapies in the post-BTKi setting, where outcomes remain limited and durability is often modest.

Moreover, iopofosine's fixed dose regimen and manageable safety profile may also provide offer practical advantages for patients and providers. Importantly, these outcomes incorporate key elements that align with the previously described regulatory expectations for iopofosine's eligibility for accelerated approval. We were delighted to have the immediately post-BTKi subgroup analysis from the CLOVER WaM trial selected for presentation at the upcoming ASCO conference, which brings together the world's leading oncologists.

The safety and efficacy of iopofosine observed to date in this subgroup are highly encouraging and underscore its potential to address a significant unmet need for patients who progressed after BTKi therapy. We believe these findings further support the potential for iopofosine to emerge as a differentiated therapeutic option in the post-BTKi setting and as early as the second line of treatment in WM. With the strength and maturity of the total data set, we are advancing with a randomized controlled Phase III confirmatory study, evaluating progression-free survival as the primary endpoint.

We anticipate initiating the study in the late fourth quarter of 2026. Beyond iopofosine, we were delighted to advance our broader pipeline with the recent dosing of the first patients in the Phase Ib trial of CLR125, our OJ emitting radio conjugate in relapsed/refractory triple-negative breast cancer or TNBC. TNBC is an aggressive subtype of breast cancer characterized by the absence of estrogen receptors, progesterone receptors and HER2 protein expression. This lack of common therapeutic targets make TNBC particularly challenging to treat with limited options beyond chemotherapy.

TNBC tends to grow and spread more quickly than other breast cancer types and disproportionately affects younger women and those of African descent. In the U.S., approximately 12% of breast cancer diagnoses are triple-negative breast cancer. CLR125 with its demonstrated selective tumor uptake, promising activity in preclinical models of TNBC gives us confidence in its potential to be an effective treatment for TNBC.

The Phase Ib clinical trial is an open-label dose-finding study in patients with relapsed/refractory TNBC. It will evaluate three dose levels and dosing regimens of CLR125. 32.75 millicuries administered over four cycles or 62.5 millicuries per meter squared over three cycles or 95 millicuries per meter squared over 2 cycles, with approximately 15 patients enrolled per treatment arm with an expansion arm of an additional 15 patients for the recommended Phase II dose.

The study utilizes dosimetry assessments to characterize tumor uptake and distribution, which supports the prediction of safety and therapeutic activity. Clinical endpoints include safety, tolerability as well as preliminary efficacy measures, including tumor response per RECIST criteria and progression-free survival. The study is well underway and our first patients already treated, and we look forward to sharing biodistribution, dosimetry and early clinical efficacy insights as the year progresses.

Overall, 2026 is shaping up to be a year of substantial execution and progress across the organization, and we remain focused on advancing each program with scientific rigor and regulatory discipline.

With that overview of our clinical progress and plans moving forward, I'll turn the call back to Jim for closing remarks.

All right. Thank you, Jarrod. As we look ahead, Cellectar enters the next phase of 2026 with clarity of purpose, strong momentum and the financial resources to execute. The combination of compelling 12-month iopofosine data and a significantly strengthened balance sheet positions us to advance with the initiation of our Phase III confirmatory study and subsequent accelerated approval application.

The WM patient community remains at the heart of our commitment. We continue to hear from and remain motivated by individuals and families affected by WM, particularly those patients with limited treatment options or those that are no longer treatment seekers because of poor or no remaining treatment options. The product profile presented by iopofosine reinforce our belief that this therapy has the potential to be truly meaningful and potentially life-changing for these patients in need.

At the same time, we remain disciplined towards of capital, focused on creating long-term shareholder value by advancing differentiated assets, engaging constructively with regulators and executing against clearly defined milestones.

I want to take this opportunity to thank the entire Cellectar team for their continued dedication and sense of urgency. And I thank our investors for their continued support and conviction. We are committed to delivering on both our mission for patients and our responsibility to shareholders.

With that, operator, we are happy to open the call for questions.

[Operator Instructions] And we have our first question from Kevin DeGeeter with Ladenburg Thalmann.

My first question is on CLOVER WaM and specifically for the BTK experienced patients. did most patients go directly from a BTK inhibitor to study drug in CLOVER WaM or for the patients that did get lines of therapy between a BTK and coming on study drug, what were the most common therapies they received immediately prior to study drug?

Kevin, this is Jim. First of all, thank you for your participation in the call today. And your question is spot on. It's significant on a number of different levels, and I'll ask Jarrod Longcor to address it.

Kevin, briefly, I don't have the number -- the exact number in my head at the moment, but I can say that it was over 50% of patients in the study, who immediately came off BTKi before getting treatment with iopofosine. Most common -- in addition to that as the most common sort of transition, the other would be coming directly off of rituximab either monotherapy or in combination with chemotherapy.

Really helpful. And then with regard to the Phase III program, thanks for the additional color. Can you comment on what the likely comparator arm for the Phase III program will be or at least -- or I think the question I'm ultimately interested is how one might think about potential range of PFS for the control arm population in a potential Phase III population?

Excellent question, Kevin. We've had -- we've engaged our friends at the FDA a number of different times on this. So we've settled in and are aligned on the comparator arm in the study. I could have Jarrod talk to that and provide some additional color.

Yes. So it is a great question. So what we believe the -- or what we've aligned on with the agency on the comparator arm is rituximab, cyclophosphamide, dexamethasone or RCD. It is commonly used in a post-BTKi patient population that tends to have significant adverse events associated with any of the other treatments and provides a comparable sort of outcome to some of the other treatment scenarios. So it makes a good choice.

I will say since you sort of asked the question about how to think about these compounds and how they might behave because obviously, in the literature, what you will find is that RCD, the last time it was significantly sort of challenged or experienced in various studies was pre-BTKi being in the marketplace. And so what you best bet is to look at an article that came out from a group, I'll call it Anna Frustaci out of Italy, where they demonstrated that with any rituximab combination and essentially any salvage therapy, progression-free survival in those patients varied anywhere from about 5.8 to 8.1 months in a post-BTKi exposed patient population and refractory for the earlier numbers. So the 5.8 was a refractory patient population, which in our case, with the pivotal study or the confirmatory study that we're designing, which is essentially an immediate post-BTKi patient population following the frontline therapy. What we expect to see is the vast majority of those patients to be refractory to the BTKis' when they enter into the clinical study.

And the refractory to BTKi population in that salvage therapy, including these RCD combinations were approximately 5.8 months, correct?

Correct.

And out of the Phase II CLOVER WaM, our progression-free survival with iopofosine.

It was over 15 months.

In that same patient population. I think the other element there, Kevin, if you could take a moment and just talk to the powering of the study, the 100 in each arm and based on that differential, your level of confidence relative to how the study was powered.

Yes. So to Jim's point on the powering, what we did was we assumed for the comparator arm, essentially a hazard ratio that corresponds to an 8-month progression-free survival. And for the iopofosine arm, we used a hazard ratio that assumed no greater than a 12-month progression-free survival. So obviously, as Jim just said, our expectation is really that the -- with the vast majority of the patients being BTKi refractory, we're going to see something likely closer to 6 months of progression-free survival of the per arm. And if the patients behave as they did in the CLOVER WaM study, we would expect something closer to 15 months in the iopofosine arm, thereby essentially overpowering the study by a number of patients in order to ensure success.

Makes a lot of sense. And if I could just sneak in one more. I think just one of the questions that might be on investors' minds is just how you're thinking about the potential timing for an NDA submission under accelerated approval for WM.

It's pretty straightforward from our perspective. I mean, we're planning to initiate the study, as Jarrod had cited at the very back end of this year. Once we have the study up and running, enrolling patients, and that may be a couple of 2, 3 months. At that point, we would submit our new drug application.

Please keep in mind that in May of last year, we received our breakthrough designation, which essentially obligates the FDA to -- for a 6-month window prior to regulatory action. So if you initiate at the very back end of this year, wait a couple of 2 or 3 months and then have the FDA action within 6 months of that submission. You're in the second half of 2027 with a potential approval.

[Operator Instructions] There are no further questions at this time.

I will now turn the call over to Jim Caruso for final remarks.

All right. Thank you, operator. I appreciate your assistance today. And certainly, thank you to all conference participants for both your time and continued interest in Cellectar. Have a good day.

And thank you, ladies and gentlemen. This concludes today's conference call. Thank you for your participation. You may now disconnect.

Ladies and gentlemen, thank you for standing by, and welcome. [Operator Instructions] Please be advised that today's conference call may be recorded.

I would now like to hand the conference call over to Anne Marie Fields, Managing Director at Precision AQ. Please go ahead.

Thank you, operator. Good morning, and welcome to Cellectar Biosciences Fourth Quarter and Full Year 2025 Financial Results and Business Update Conference Call. Joining us today from Cellectar are Jim Caruso, President and CEO, who will provide an overview of the company's progress before turning the call over to Chad Kolean, CFO, for a financial review of the quarter and the year. Following this, Jarrod Longcor, Chief Operating Officer, will give an update on the company's progress and plans for its promising clinical development pipeline of radiopharmaceuticals.

Cellectar issued a release earlier this morning detailing the contents of today's call. A copy can be found on the Investor page of Cellectar's corporate website. I want to remind callers that the information discussed on the call today is covered under the safe harbor provision of the Private Securities Litigation Reform Act. I caution listeners that management will be making forward-looking statements. Actual results could differ materially from those stated or implied by our forward-looking statements due to risks and uncertainties associated with the business. These forward-looking statements are qualified in their entirety by the cautionary statements contained in today's press release and in our SEC filings. The content of this conference call contains information that is accurate only as of the date of this live broadcast, March 4, 2026. The company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call and webcast.

As a reminder, this conference call and webcast are being recorded. We will begin the call with prepared remarks and then open the line for your questions.

Let me now turn the call over to Jim Caruso. Jim?

Thank you, Anne Marie, and thank you all for joining us this morning as we review Cellectar's progress throughout the year.

2025 was a productive and strategically meaningful year for Cellectar. Across the organization, we executed with focus and discipline, advancing our lead asset, iopofosine I 131, strengthening our regulatory position in both Europe and the U.S. and progressing our next-generation radiotherapeutic programs supported by our proprietary Phospholipid Drug Conjugate platform.

Let me begin with iopofosine I 131, our late-stage asset in Waldenström's Macroglobulinemia or WM. As discussed in this morning's press release, we ended the year with regulatory alignment in Europe, following guidance from the EMA Scientific Advice Working Party or SAWP. We remain on track to submit a conditional marketing authorization application in the third quarter of 2026, positioning iopofosine for potential approval and European commercialization as early as 2027. This EU regulatory clarity, together with iopofosine's prime designation underscores both the strength of the CLOVER WaM data set and the significant unmet medical need.

As the full 12-month follow-up data become available in early 2026, we are even more convicted on our plans to pursue an NDA under the accelerated approval pathway. These assumptions are supported by iopofosine's FDA breakthrough designation for WM and by our agency dialogue. In addition, we continue engagement and partnering conversations to support the program globally.

Beyond iopofosine, we also made important progress across our broader PDC-based radiotherapeutic pipeline. We initiated the Phase Ib study of CLR 125 and in triple-negative breast cancer or TNBC. CLR 125 is an iodine 125 Auger-emitting agent designed for highly precise tumor targeting and its inhibition represents a key -- initiation represents a key milestone for the second asset. The dose-finding study is ongoing, and we expect early interim data in mid-2026. We also strengthened the infrastructure supporting our alpha-emitting program, CLR 225 through new supply partnerships with ITM Technologies and Ionetix providing commercial scale access to Actinium-225 and Astatine-211 for future clinical development.

Importantly, 2025 also marked significant expansion of our global intellectual property estate with new patents issued across Europe, Asia Pacific, the Middle East as well as the Americas. These patents bolster the protection of iopofosine I 131, CLR-125 and the broader PDC platform.

Finally, we raised approximately $15.2 million over the course of the year, extending our cash runway and enabling ongoing advancement of our pipeline, which positions us to achieve a number of value-creating milestones throughout the year.

With that brief overview, I'll turn the call over to Chad to review our financial results. Chad?

Thank you, Jim, and good morning, everyone. I'll address our financial results for the year ended December 31, 2025.

We ended the year with cash and cash equivalents of $13.2 million as compared to $23.3 million as of December 31, 2024. In the fourth quarter, we raised $5.8 million and now expect that our cash on hand is adequate to fund budgeted operations into third quarter of 2026.

Turning to our results from operations. Research and development expenses for the 3 months ended December 31, 2025, were approximately $11.5 million compared to approximately $26.6 million for the year ended December 31, 2024. The overall decrease in research and development was largely driven by the conclusion of patient enrollment and declining patient follow-up for our CLOVER WaM clinical study modestly offset by increased activity in our preclinical development project costs.

General and administrative expenses for the year ended December 31, 2025, were $11.5 million compared to $25.6 million for the same period in 2024. The decrease in SG&A was primarily driven by deemphasizing pre-commercialization efforts and related personnel cost reductions. Other income was approximately $1.1 million for fiscal 2025, while in 2024, other income was $7.3 million. These amounts are noncash and largely a result of the impact of issuing and marking to market certain warrants. The warrants we issued in 2025 were classified as permanent equity upon issuance, reducing the impact on the statement of operations in comparison to fiscal 2024. Net loss for the full year ended December 31, 2025, was $21.8 million or $8.35 per basic and diluted share compared with $44.6 million or $36.52 per basic share and $41.89 per diluted share during 2024.

Now I will turn the call over to Jarrod for an operational update, including plans for our pipeline of radiopharmaceuticals.

Thank you, Chad, and good morning, everyone. As Jim highlighted, our regulatory and clinical progress in 2025 positions us well for important advances across our pipeline programs and for a milestone-rich 2026. Starting with iopofosine I 131, our interactions with the EMA and FDA have provided us with clear, actionable regulatory paths. In Europe, we are planning to submit this conditional market authorization application later this year. In the U.S., we continue to make strong progress in our regulatory engagement as we work with the FDA on the accelerated approval pathway and the design of our confirmatory Phase III trial to support full registration.

As requested by the FDA in November of 2024, we have now collected 12 months of follow-up on all patients. And based upon further review of the data, agree that a confirmatory study evaluating iopofosine I 131 in a post-BTKi-treated patient population in the second line setting is appropriate. Importantly, this earlier line more than doubles the potential addressable population in the U.S.

As mentioned, we have been analyzing the more mature CLOVER WaM data set, including the full 12-month follow-up for all patients and are very encouraged that the results continue to demonstrate robust and durable clinical benefit over time in this salvage treatment setting, where there are no approved drugs. In addition, new subgroup analysis, particularly within defined high-need patient segments, are emerging as especially promising. We look forward to sharing these findings with regulators as part of our ongoing discussions.

Taken together, we believe the strength and consistency of these data provide a robust foundation for our U.S. and EU registration strategy. Over the remainder of the year, we intend to present our findings, including a minimum of 12-month follow-up on all patients, updates on response data, duration of response, progression-free survival and detailed outcomes in various patient subsets at major medical meetings. We expect these results to be highly compelling to both the clinical community and regulatory decision makers.

Beyond WM, iopofosine continues to show potential across multiple oncology indications, prior data sets in multiple myeloma and diffuse large B-cell lymphoma demonstrated strong activity in these hematologic malignancies and recently, I presented data at the AACR Special Conference on pediatric cancer from a study of iopofosine in relapsed/refractory pediatric high-grade glioma that showed iopofosine to provide meaningful improvements in progression-free survival and overall survival and to be well tolerated with a consistent safety profile.

Iopofosine remains an asset with tremendous global market opportunity and its success supports other assets in our radiopharmaceutical pipeline, including CLR-125 and CLR-225 and further validates our proprietary phospholipid ether delivery mechanism.

Turning now to CLR-125, our Auger-emitting asset for solid tumors which has the potential to provide extreme precision targeted radiotherapy due to the short distance Auger emission travel, meaning the isotope must be delivered within the cell and near to the nucleus. As Jim noted earlier, we initiated a Phase Ib dose-finding study in TNBC at 2 sites, and we'll be adding additional sites in the second quarter. This study is evaluating 3 dosing regimens with an expansion arm plan once the recommended Phase II dose is determined. We anticipate a steady cadence of results throughout 2026, including early interim dosemetry, safety and preliminary efficacy data.

For CLR-225, our alpha-emitting asset, we completed IND-enabling work and are ready to initiate a Phase I trial pending available funding and continued strategic alignment with corporate objectives. Preclinical studies in pancreatic cancer models have shown compelling tumor inhibition at multiple dose levels, further demonstrating the potential of targeted alpha therapy within our platform.

Across the pipeline, our expanded global patent estate provides long-term protection for iopofosine, CLR-125 and dosing regimens central to our PDC technology. Combined with strengthened isotope supply partnerships, we believe we are well positioned to build sustainable value.

2025 was a year of significant regulatory, clinical and operational advancement, and we look forward to continuing this momentum throughout 2026.

Jim, I'll turn it back to you for closing remarks.

All right. Thanks, Jarrod, for that overview. As you've heard today, 2025 was a year defined by meaningful progress across the entirety of our radiotherapeutic pipeline with strong execution across the organization. We advanced iopofosine toward key regulatory submissions that would accelerate its market approval and get this much needed therapy to patients. We initiated the CLR-125 Phase Ib trial for triple-negative breast cancer, expanded our intellectual property, strengthened supply chain, infrastructure and extended our cash runway. We're entering 2026 with clear vision, strong momentum and a pipeline supported by robust science and regulatory engagement. We expect multiple value-creating milestones in the months and year ahead and remain focused on delivering transformative therapies to patients with difficult-to-treat cancers.

I want to extend my gratitude to our outstanding Cellectar team whose commitment and hard work continue to drive our programs and the company forward. We remain deeply committed to the WM community and are grateful for their strong support and encouragement as we work to bring iopofosine to patients.

Operator, we're ready to open the call for questions.

[Operator Instructions] Your first question comes from Aydin Huseynov with Ladenburg.

Congratulations with the progress in '25 and so far in '26. A couple of questions I have regarding iopofosine. So you're planning to submit in the third quarter for EMA. I'm just curious to understand, can you use the same package that you will submit to EMA? Can you use exactly the same package for the FDA submission as well? And how long after you start the Phase III trial, you can actually initiate that process of submission with the FDA?

Sure. Aydin, first of all, thank you for participating in the call. As always, we appreciate that and your coverage of the company. Let me start and then we'll turn it over to Jarrod to provide some additional details relative to your question.

As you may recall, we've already built out substantial portions of our NDA application and although the format with the EMA is different, there are a lot of similarities in terms of the requested data. So a lot of the work that we've already done in preparation for our NDA submission, we could also apply to the EMA. Jarrod has been providing oversight on this process, and I'll turn it over to him to provide greater detail.

Yes, great question. So the very short answer is, yes, the data itself is essentially the same. And so it's all -- obviously, it's all the CLOVER WaM data. There will be some different, what I'll call, subset analyses that the EMA may have requested that might be a bit different than what the FDA might request. So we're executing on that. And as Jim said, there is just the standard packages are a little different, the ordering and how things come together for the EMA versus the FDA, the actual NDA is a little different from the CMA package development. But otherwise, it is all the same. So as you said, that is pretty much largely taken care of at this point.

And then your second part of your question was, I think, how long to submitting in the U.S. post the initiation of the confirmatory study. Is that correct?

Yes. Yes.

Okay. So the way we're doing that, just to share what -- back when we met with the agency in November 2024, where they basically outlined for us a handful of criteria that were necessary for us to achieve in order to be able to submit for the accelerated approval. Part of what they shared was that for an accelerated approval, a study must be initiated at the time of submission and ongoing, meaning enrolling patients at the time of regulatory action. So what we've taken or the way we're approaching this is about -- we're thinking perhaps a month or two post the initiation of the study, having a handful of sites open, we would then submit the NDA to the FDA. That should allow us to have enrolled 1 or 2 patients essentially at that point. And then over the intervening 6 months because we now have -- remembering that we got breakthrough designation in May of 2025, we are now eligible and have the guaranteed 6-month review under the accelerated approval pathway. And so we would then expect that, that feedback would come in 6 months, and we would want to make sure that we had about 10% of the patients enrolled.

So Jarrod, to summarize that within 7 to 9 months of initiation of the study, we would -- assuming we submitted the NDA in a month or two post initiation, we would have a response from the FDA regarding the accelerated approval. And I think, Aydin, it's also important to point out that at that point in time, they're not reviewing any data out of the confirmatory studies, just a function of the study being initiated is ongoing, and patients are successfully being enrolled.

Understood. Very helpful. And for the Phase III confirmatory study design, I mean, it seems like it is -- the design is okay with both U.S. and EU to get the full approval. But just for modeling purposes, I mean, you're getting into earlier line of therapy, second line post BTK and comparing this to rituximab and standard of care. Trying to understand what it is that we should model in terms of the differences in PFS on iopofosine versus the standard of care. And just to get a better sense in terms of what to expect down the road?

Absolutely. And another great question. Until recently, it was very difficult to give a definitive answer here because nobody has really evaluated any salvage therapy in a post-BTKi-exposed patient population. However, earlier this year or late last year, I guess, early 2025, I got to remember we're in 2026 now. A group out of Italy, where the lead author whose name was Frustaci, they produced data looking at 78 post-BTKi patients irrespective of what salvage therapy they got. So these patients received rituximab, chemo combinations, so like RCD or rituximab bendamustine, they also received -- subsets of them also received pirtobrutinib, so a noncovalent BTKi. They also received proteasome inhibitors, they received venetoclax or BCL-2 inhibitors. So they basically got every alternative salvage therapy. In all cases, these patients, as a median, their PFS was 8 months if they were a second-line patient, irrespective. And what you see is when it was RCD or any of the rituximab combinations, it was sub-8 months as progression-free survival. And so you can clearly model that number because it was -- it's a significant patient population, approximately 78 patients again.

Yes. I think in -- thank you, Jarrod. Very helpful. And I think I can provide some additional color relative to our data. Obviously, I can't report because we haven't publicly disclosed the updated 12-month data, but it will include what we believe to be some very robust durability elements associated with the 12-month data. So we're really excited about the data package. If you -- and everyone was impressed with our clinical data, Aydin, that we have put in play to date. I think the subsequent data based on the 12-month follow-up is going to be viewed as very, very exciting. And the other element here, and you brought this up, it's significant. As you recall, in the CLOVER WaM study, on average, we were the fifth line of therapy, which means 4 lines of therapy prior to the utilization of iopofosine on average. However, under Jarrod's leadership, the team has done substantial analysis, and we've really been able to segment based on the latest data cut that occurred in December of 2025, these patients and the variety of subsets, but also importantly, where they sat in terms of the number of prior treatments. And we will tell you that the -- as you would expect, as you advance further upstream, the data is more and more impressive. And as you cited, second line in the U.S. is the patient population is double that of third line plus. So it really not only does it create opportunities for clinicians to provide their patients with a meaningful treatment option. There's also going to be a lot more of them in the U.S. benefit and globally benefiting from this treatment.

And just historically, so that we don't lose that. Currently right now in the United States and it's increasing in Europe, the BTKis are being predominantly prescribed in the first-line setting, whether that's in combination with rituximab or monotherapy, since the ibrutinib-rituximab study came out showing its potential in the first-line setting, most of the U.S. physicians have transitioned into BTKi in the first-line setting in some form or fashion, which means a second-line setting is a post-BTKi based population today.

Very helpful. And looking at your prior major response rate, they were already high enough 80s and you're going to move to the earlier line of therapy. And typically, the responses increase in early lines of therapy. So just curious to understand your sort of benchmark in the earlier line of therapy. And whether the Phase III trial design will have some sort of top line visual response rates first before we see the TFS maybe at some point, 1 year after we start the trial.

Yes. So the primary endpoint for the confirmatory study is progression-free survival. Obviously, we will be -- a secondary endpoint is going to be major response rates or response rates as a whole and obviously, major response rate is one of them. What I would say is we won't be announcing data from a confirmatory study during enrollment because obviously, that can result in bias being introduced into the study. Even -- and especially in a comparator study, and that would be problematic and would actually negatively impact the review eventually for full approval.

And so Aydin, I'll add to that going in a potentially different direction, were based on the primary endpoint of progression-free survival in that confirmatory study, you can take a look at the Frustaci data and you'll get a sense as to the progression-free survival there. And so this is -- this study is powered in such a way as we introduce our PFS and durability performance for this drug out of the CLOVER WaM study. I think you'll very quickly determine that the way the study is powered for the confirmatory study. It's -- we're setting ourselves up for a high probability of success, assuming the PFS remains consistent with all of the literature and data that we've seen and best case there for PFS is Jarrod discussed was 8.1 months. So we feel very, very comfortable with PFS being the primary endpoint based on the literature.

Very helpful. And the last question I have regarding the current environment in post BTK in U.S. and EU, what do you feel in terms of the enrollment speed and level of interest of PIs and among patients to be participating in this trial once you started?

Yes. So I can say directly that having spoken with every one of the PIs that were in the CLOVER WaM study, the interest from the physician side is extremely high. I can say in a number of cases when I have talked with them recently, they've all felt the delay from a regulatory standpoint and getting to this point is largely unwarranted and that this drug absolutely has a spot in the marketplace and a significant need to fill. So I think that's important from that perspective. I think, again, as patients -- this is a very active patient population. They're very engaged as a community and looking at new therapies. I think as patients and these physicians get a look at the new data that is coming out later this year as we were talking about, so over the remainder of this year. I think everybody is going to be very excited about the ability to participate and have the impact that iopofosine can have for them and their disease in this setting.

Yes. And I would add that in addition to the thought leadership that are very excited about this because they're on the cutting edge. They understand and observe the performance of existing salvage therapies, especially just post first line. And as I think Jarrod stated earlier, BTKIs are used predominantly now either as a monotherapy or a combination with rituximab in first line. So you are already for many of these patients in a salvage therapy mode in the second line. But interesting here, Aydin, in addition to key thought leadership around the globe, really appreciative of the future benefits that this product provides their patients as early as second line. This also tested extremely well with community-based physicians. So we really see this transitioning out of a controlled clinical environment at these world-class institutions or WM catchment centers because of the ease of administration and quite frankly, the lack of artistry required here relative to other oncology drugs, the 4 simple doses. Our community-based physicians are as excited as the thought leaders as well. So I think all constituents, including nuclear medicine, radiation oncology that have a seat at the table in terms of the utilization of this drug, everyone, all constituents are really excited about the opportunity to bring these patients to the many patients that will benefit from this treatment.

Super helpful. And congratulations with the progress so far, and we'll be looking forward to seeing your 12-month data later this year.

The next question comes from Ted Tenthoff with Piper Sandler.

Great. Congrats -- my congratulations to -- on the very hard work and steady progress. You guys deserve a persistence award for sure. Wanted to follow up, 2 questions, if I may. So firstly, and I apologize if I missed this, but what would be the plans to distribute in Europe and can you walk us through a sense of what that second line. Now in Europe, would it be second line too? Or there is actually a little different where you would be getting approved? And what does that patient population look like?

Sure. Thank you, Ted. Great to have you on the call. I appreciate your interest, your continued interest in the company, and you've been very supportive. So we're appreciative of that. I'll have Jarrod launch into this, and then I can fill in any blanks or provide additional color.

Yes. So -- and thank you, Ted. So from a distribution plan, the idea here is that, obviously, Cellectar itself, we will not really commercialize it ourselves in Europe. We are in discussions with various parties that we would partner with to actually do the commercialization in Europe on our behalf in one way or another. So we're looking at partnership as the main thing. Just to give you a sense, we have set up our distribution of a radiotherapeutic in a global sense. So I'll remind you that the CLOVER WaM study was run as a global study, where we had approximately 25 sites in Europe. We had some sites -- a handful of sites also in Asia and Australia. And so we've set up a logistical chain that allows us to ship and cover the globe easily with this product. And I will remind you that for folks that may have forgotten that we have a unique competitive advantage in the marketplace that is often overlooked, which is our time -- shelf life time. Most radiotherapies have a shelf life of about 3 to 7 days max, ours is 21 days. That allows us, and it's not cold chain. That's at room temperature. It allows us to more easily distribute this product globally and make sure that it's conveniently handled by the physicians and by the patients. So that sets up the distribution.

Now the second part of your question was really about in Europe, where would the approval be and what is the size of the market? So in general, just to give you a sense, the size of the European market is generally about 10,000 or so patients in total greater than the U.S. I would say that when we look at the second-line setting, the U.S. market is just a bit south of 12,000 patients in Europe. Its second line setting is generally a bit over 12,000, approaching 13,000 patients is what we've come to learn. And so it's a meaningful patient subset. Now the conditional market authorization would actually be a later line utilization. So it would be a third line or later post-BTKi patient population. That's largely because still in Europe they are transitioning. They're using BTKis more in a first-line setting, but they're more evenly split right now between first-line and second-line utilization of BTKi. So the median would likely be a third line or later sort of position. Upon the confirmatory study, I think it would -- we would be shifting to a second-line setting in Europe.

At this time, Jim will address questions sent electronically. Please go ahead.

So if there's no other questions, we have some that are in the inbox. Jarrod, you up for another question or two? All right. I think I'll decipher this one, what is the benefit of the 12-month data cited in the press release versus your December 2024 data?

Yes. Good question. So what I would say is that reminding folks that the December 2024 data, most of the patients that we had enrolled at that point did not have 12 months of follow-up data on them. They were still essentially shortly post their treatment segment and therefore did not have 12 months. Since that time, we have all patients with at least 12 months of follow-up. And while the data presented at ASH was very good in 2024, I think, as Jim alluded to earlier, this follow-up data is even better. And that is -- what I mean by that is there are improvements in the response rates, there's improvements in durability. There are improvements in progression-free survival. So across the board, we're seeing depth and durability of the responses going out and looking stronger than they did in December 2024.

Jarrod, could you elaborate on the benefit relative to the regulatory pathway with the FDA in the U.S. on the 12-month data?

Yes. So again, in November 2024, the FDA laid out essentially a pathway for accelerated approval that really had 2 key components to it. One was that we needed to have 12 months of follow-up on all patients, which obviously we now have, which allows us to then take that next step. And the next step was really that we needed to have an ongoing confirmatory study in an earlier line of patients, so as to not be competing between our study and commercially available product. At the time, we were a little worried about moving to a second-line setting because we didn't really have data that would say whether we would be better or worse in that line of setting or the same.

Now with the analysis and the 12-month follow-up data, we now know exactly that we perform better in an early line setting as one might expect. But with the confidence now we have the data sets that show and validate that approach. And I think it sets us up very nicely for both the confirmatory study, but then also the execution of the accelerated approval moving forward.

All right. We have 1 more here. It's a layup, which means I'll handle it. Will this data include durability such as PFS and DOR. So PFS, progression-free survival and DOR duration of response?

The answer is yes. Beyond the response data such as major response, complete responses, very good partial responses, the overall response rate metric and clinical benefit rate we will be providing progression-free survival and duration of response not only in the broader population, but an important subset like post-BTKi and refractory BTKi patient populations where this drug appears to be naturally falling post-BTKi based on the regulatory pathways, both in the EU and here in the U.S.

So with that, I'll turn it back over to the operator.

Thank you. We have reached the end of the question-and-answer session. Let me turn the call over to Jim Caruso, President and CEO, for closing remarks. Please go ahead.

All right. Thank you, operator. Thank you to everyone who participated in today's call. We appreciate your time. Have a good day.

Thank you. Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.

Good morning, ladies and gentlemen, and welcome to the Cellectar Biosciences' Third Quarter 2025 Earnings Call. [Operator Instructions] This call is being recorded on Thursday, November 13, 2025. I would now like to turn the conference over to [Technical Difficulty].

Thank you, operator. Good morning, and welcome to Cellectar Biosciences' Third Quarter 2025 Financial Results and Business Update Conference Call. Joining us today from Cellectar are Jim Caruso, President and CEO, who will provide an overview of the company's progress before turning the call over to Chad Kolean, CFO, for a financial review of the quarter. Following this, Jarrod Longcor, Chief Operating Officer, will give an update on the company's progress and plans for its promising clinical development pipeline of radiopharmaceuticals. Cellectar issued a press release earlier this morning detailing the content of today's call. A copy can be found on the Investor page of Cellectar's corporate website.

I want to remind callers that the information discussed on the call today is covered under the safe harbor provisions of the Private Securities Litigation Reform Act. I caution listeners that management will be making forward-looking statements. Actual results could differ materially from those stated or implied by our forward-looking statements due to risks and uncertainties associated with the business. These forward-looking statements are qualified in their entirety by the cautionary statements contained in today's press release and in our SEC filings. The content of this conference call contains time-sensitive information that is accurate only as of the date of this live broadcast, November 13, 2025.

The company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date of this conference call and webcast. As a reminder, this conference call and webcast are being recorded and archived. We'll begin the call with prepared remarks and then open the call to your questions.

I'll now turn the call over to Jim Caruso. Jim?

Thank you, Anne Marie, and thanks to all participants for joining us this morning as we review Cellectar's progress in the third quarter of 2025. I'm pleased to share that we have made significant strides throughout the quarter, marking a period of strong operational execution on key corporate priorities, including the strengthening of our balance sheet, making significant advancements with our global regulatory strategy for iopofosine I 131 Waldenstrom’s macroglobulinemia or WM, and advancing our clinical and preclinical programs. These achievements underscore our commitment to innovation in oncology and position Cellectar as a company with transformative potential as we head into the final stretch of the year and prepare for an impactful 2026.

Let me begin with our lead asset, iopofosine I 131, which continues to show strong promise as a first-in-class radio conjugate therapy for patients with WM. The third quarter brought exciting developments that further validate its potential and may accelerate its path to market. We've been closely collaborating with the EMA to align on a clear regulatory strategy. Importantly, following a thorough review by the EMA's scientific working party, we received confirmation of our eligibility to file for conditional marketing approval in the EU based upon the CLOVER-WaM study, a major milestone that could bring iopofosine to patients as early as 2027.

This endorsement not only reflects the strength of our data and the urgency of the unmet need, but also carries a high probability of success with 80% of such filings ultimately receiving approval. Confirmation of our eligibility to file for a conditional marketing authorization in the EMA gives us further confidence in our regulatory strategy with the U.S. FDA.

As previously reported, the FDA requested 12-month follow-up data on all patients from the CLOVER-WaM study. With the 12-month follow-up data now available, we plan to submit an NDA under the accelerated approval pathway upon initiation of a confirmatory Phase III trial. As you may be aware, in the second quarter of this year, iopofosine was granted breakthrough designation for WM by the FDA. Data from a recent Jefferies research report showed that 79% of oncology drugs, which have been granted breakthrough designation are successfully awarded accelerated approval by the FDA.

The momentum provided by the success of our global regulatory strategy in Europe and our strengthened regulatory position in the U.S. significantly enhance the value of iopofosine, potentially reducing time to commercialization and making it an increasingly attractive opportunity for strategic collaborations. To support these efforts, we are in active discussions with potential partners, both regional and global, who share our vision for iopofosine. These partnerships are designed to provide iopofosine I 131 to patients as quickly as possible to secure nondilutive capital and commercial expertise while preserving long-term value for our shareholders.

With our bolus of positive clinical data, a favorable safety profile, expedited review designations in the U.S. and Europe as well as a compelling commercial market potential, we believe iopofosine I 131 represents an attractive candidate for potential collaborations or partners seeking impactful innovation and oncology assets with accelerated pathways to the global market.

We remain equally excited about the progress from our next-generation radiopharmaceutical pipeline, including our recently initiated Phase Ib study of CLR 125, our Iiodine-125 Auger-emitting agent, which targets solid tumors, such as triple-negative breast cancer; and CLR 225, our actinium alpha-emitting radio conjugate targeting several other solid tumors with significant unmet need, including pancreatic cancer.

We have also been extremely active in showcasing data from these programs at medical meetings throughout the quarter, including posters and oral presentations at the American Association for Cancer Research and Special Conferences in Cancer Research. We encourage everyone to visit the Posters and Publications section of our investor website to view our presentations.

Operationally, we have raised approximately $12.7 million in recent financings to help strengthen our balance sheet and have also engaged in selective supply and trial support agreements with partners to secure the necessary supply of actinium-225 and to complete our Phase I study for CLR 125 for the treatment of triple-negative breast cancer.

In summary, we are closing out 2025 with strong momentum and entering the new year with a clear regulatory path for iopofosine in Europe and the U.S. and maintain the promise of a unique and robust pipeline addressing challenging solid tumor cancers with significant unmet medical need. As a result, we have several near-term milestones to look forward to that we believe place Cellectar in a position of rapid growth. We are energized by the opportunities ahead and remain deeply committed to delivering innovative life-extending therapies to patients with cancers.

With that overview, I'll now turn the call over to Chad Kolean, our Chief Financial Officer, for a review of our financials. Chad?

Thank you, Jim, and good morning, everyone. Here are my comments on our financial results for the third quarter ended September 30, 2025. We ended the quarter with cash and cash equivalents of $12.6 million, which is compared to $23.3 million as of December 31, 2024. In July 2025, we raised a net of $5.8 million through the issuance of common stock, prefunded warrants and new common warrants. And following the close of the third quarter, we raised an additional $5 million net through investors exercise of certain outstanding warrants and the issuance of new common warrants and now expect that our cash on hand is adequate to fund budgeted operations into the third quarter of 2026.

Turning to our results from operations. Research and development expenses for the 3 months ended September 30, 2025, were approximately $2.5 million compared to approximately $5.5 million for the 3 months ended September 30, 2024. The overall decrease in research and development was a result of lower costs related to CLOVER-WaM study, where the patient follow-up effort continues to decline as patients are moving off study. Additionally, manufacturing costs have declined as in the third quarter of 2024, we were investing more heavily in establishing a second manufacturing source for iopofosine, an effort that is now complete.

General and administrative expenses for the 3 months ended September 30, 2025, were $2.3 million compared to $7.8 million for the same period in 2024. The decrease in G&A was primarily driven by a reduction in pre-commercialization and market assessment efforts and lower personnel costs. Net loss for the 3 months ended September 30, 2025, was $4.4 million or $1.41 per basic and diluted common share as compared with $14.7 million or $11.18 per basic and $12.13 per diluted common share during the 3 months ended September 30, 2024.

With that, let me turn the call over to Jarrod for a regulatory and operational update.

Thank you, Chad, and good morning, everyone. As Jim just reviewed, we believe iopofosine I 131 has a high probability of approval in the EU and pending the initiation of the confirmatory study, its approval in the U.S. We have had extensive communications with both the EMA and the U.S. FDA throughout 2025 and look forward to continuing these interactions through the approval process. As a reminder, this is a program that has received EMA prime designation; FDA breakthrough therapy designation for the treatment of WM; 5 rare pediatric disease designations, including most recently one for relapsed/refractory pediatric high-grade glioma; as well as multiple FDA and EMA orphan drug designations.

These rare pediatric disease designations provide eligibility to receive a priority review voucher, which can be used to expedite the review process for future new drug applications or biological licensing applications for any drug or can be sold or transferred to another party. All of these updates have positioned iopofosine as a major value creator heading into the fourth quarter and early 2026 and underscores its potential in strategic collaborations.

Now let's turn to our 2 exciting earlier-stage radio conjugates, CLR 125, our lead Auger-emitter; and CLR 225, our alpha-emitting actinium-based compound. CLR 125 may provide the greatest precision in targeted radiotherapy as the Auger emissions only travel a few nanometers, meaning the isotope has to be delivered within the cell and near the nucleus or the DNA. Our phospholipid ether delivery mechanism provides this necessary targeting to the tumor entry into the cell and transport to the nucleus as validated through clinical studies.

It has been demonstrated that CLR 125 provides significant tumor uptake and depending on the dose results in tumor volume reduction or growth inhibition with no toxicities being noted, including no hematologic toxicities at any of the doses tested across multiple challenging animal models, including triple-negative breast cancer or TNBC and metastatic breast cancer.

The Phase Ib study of CLR 125 in relapsed triple-negative breast cancer will utilize dosimetry to determine tumor versus normal tissue uptake and will evaluate the activity of 3 distinct doses of CLR 125: a dose of 32.75 millicuries per dose for 4 cycles versus 62.5 millicuries per dose for 3 cycles versus 95 millicuries per dose for 2 cycles with 4 doses per cycle in approximately 15 patients per arm with a planned expansion arm in the proposed Phase II dose. The primary endpoint for the study will be to determine the recommended Phase II dose and dosing regimen, and we will also evaluate safety and tolerability as well as initial response assessments for RECIST as well as progression-free survival in patients. We expect to start dosing patients imminently and could have multiple patients dosed by the end of the year.

For the Phase Ib study, we will be partnering with Evestia Clinical for full CRO services with the Mayo Clinic network serving as a treatment center for the trial and Dr. Pooja Advani acting as our lead investigator. The initiation of this trial will be a significant milestone for Cellectar as it brings us closer to being able to evaluate the safety and optimal dosing of CLR 125. We expect to have a dosimetry data and efficacy data throughout 2026.

Moving to CLR 225, our lead alpha-emitting radio conjugate product candidate, which also has shown excellent biodistribution and uptake into solid tumors preclinically with demonstrated activity across multiple solid tumor animal models, including challenging to treat pancreatic and refractory colorectal cancers, CLR 225 has been observed to be well tolerated in these experiments, which we highlighted in our presentation at the AACR Advances in Pancreatic Cancer Research Conference held in Boston in September.

Pending the necessary financing, our Phase I trial for CLR 225 is designed to comprehensively evaluate the compound's biodistribution, safety and tolerability in patients with pancreatic adenocarcinoma. The study will commence with the dosimetry phase aimed at determining the absorb dose in both normal and tumor tissues. Following dosimetry, the study will progress to a dose escalation phase, systematically evaluating increasing doses of CLR 225 to establish the maximum tolerated dose. We believe this approach gives us an opportunity to demonstrate proof of concept for our innovative combination of phospholipid ether or POE technology with alpha emitters, potentially showcasing its radio conjugates' unique ability to safely treat large bulky solid tumors like pancreatic cancer.

We also recently announced a partnership with ITM, wherein they will provide actinium-225 to help support our alpha labeled phospholipid ether radiopharmaceutical candidates, CLR 225. Actinium-225 is a powerful alpha-emitting isotope used in targeted cancer therapies and both -- and is a rare and in limited supply isotope. This collaboration further underscores our strategic approach to a diversified supply chain to ensure the supply of key resources and thereby guaranteeing patient access to these therapies.

All of these updates and more reinforce our position as a premier radiopharmaceutical company to watch as we look towards the end of the year. This is incredible value to be found in the iopofosine story that will aid in spurring the development of CLR 125 and CLR 225 with alignment from U.S. and European agencies. We feel more confident than ever in the position of our programs.

With that overview, let me turn the call back to Jim for closing remarks. Jim?

All right. Thank you, Jarrod. This has been a very successful quarter for our team. We've maintained consistent dialogue with the appropriate global regulatory authorities and feel that iopofosine now maintains its strongest position to marketing approval and commercialization. With our earlier-stage assets, CLR 125 and CLR 225, we have made significant progress advancing these radio conjugates and have recently initiated the Phase Ib study for CLR 125 in triple-negative breast cancer.

Additionally, we've strengthened our balance sheet with runway out to the third quarter of 2026 and are positioned to execute across multiple near-term priorities, including filing for iopofosine conditional marketing approval in the EU, initiation of our CLR 125 Phase Ib clinical trial with important dosimetry and early efficacy data readouts over the first half of 2026.

We continue to advance our plans to file for accelerated approval of iopofosine in the U.S. pending funding required to initiate the Phase III confirmatory study. We remain committed to achieving these key milestones and confident that these achievements will create value over time. We look forward to finishing the year and believe we are in a strong position to bring iopofosine I 131 and our pipeline of radiopharmaceutical therapies to the patients who continue to battle cancers with high unmet need.

With that, operator, we are ready to open the call to questions.

[Operator Instructions]

Your first question comes from Aydin Huseynov, Ladenburg.

Congratulations with the significant progress with the EMA application. I've got a couple of questions. For the EMA strategy and the decision from Scientific Advice Working Party, could you help us better understand the specific data that we're considering before making a recommendation? Because it sounds like they're allowing you to do it post-BTKi, which could be second line. And in your trial, your prior lines, I think the median prior lines were 4 lines. So could you help us better understand what they were looking for?

Aydin, this is Jim. First of all, thanks for your participation in the call today and certainly appreciate your question. As you are likely aware, we put together a very comprehensive data package for our friends across the pond. And as you appropriately identified, we have recently received additional data from CLOVER-WaM relative to post-BTKi, which gives us a high degree of confidence of our capacity to move iopofosine further upstream. And as you suggest, post-BTKi could be as early as the second line. But with that as an opening comment, I'll turn this over to Jarrod to provide some additional detail relative to the package itself and the consumption of that data from the EMA. Jarrod?

Yes. Thanks, Jim. And thank you, Aydin. Great question. So let me sort of try to unpack that a little bit for you. There are a couple of elements. One, the EU prescribing pattern is a bit different than in the U.S. In the U.S. sentiment, as you just outlined, BTKIs now are generally used in the first-line setting, either in monotherapy or in combination, but predominantly in the first-line setting anymore, which would mean a post-BTKi population or post-BKKi approval in the United States is representative of a second line.

However, in Europe, at this time, the post-BTKi ICE population would still be a third-line setting. Generally in Europe, they start with a rituximab combination and continue to follow that with BTKi at this juncture. They are starting to shift to earlier utilization of BTKi, but that hasn't taken over in the vast majority of the 28 member countries at this juncture. So based on that, what the EMA evaluated, what the SAWP evaluated was the totality of our data, so all patient population, but they did focus in on that in their opinion. In Europe at this juncture, the greatest unmet need that would warrant a conditional market authorization is a post-BTKi patient population.

As Jim just alluded to, when we look at that patient population, we have a vast majority of our patients in our CLOVER-WaM study are post-BTKi. And of those, many of them -- obviously, the majority of them responded well to the treatment, did very well. So we do have statistical significance there. And when we look even deeper into that into varying subsets of that where we look at combination of refractoriness across those patients, what you see is a continued high response rate and even in some sets a much higher response rate than that of the general population.

And based on that, the agency, the EMA, the SAWP felt that the drug warranted or should apply for conditional market approval focusing in on that post-BTKi patient population at this time. I'll stop there.

And Aydin, as I think you brought to our attention a handful of months back, approximately 80% of all drugs that apply for conditional marketing authorization that have received eligibility to apply for a conditional marketing authorization are granted the CNA.

Right. Yes, that's great news. And given that -- I know you don't have to run any trial, you just need to submit. And for the FDA, you only need to initiate a Phase III trial. So how much resources do you think you need just to initiate a trial in the U.S. and whether your current balance sheet would be enough? Just to start off, it's only 200 patients, 24 months. And so can you just start the trial and finish it once you have more resources?

Yes. That's a very good question, Aydin. Based on our assessment, the total overall cost of the study in totality, including multiple years of follow-up is approximately $40 million. Importantly, we're estimating approximately $15 million to full patient enrollment and it's $10 million to initiate the trial. I'll have Jarrod in a moment talk to detail around expectations by the FDA for accelerated approval.

But the net here is essentially, it's trial initiation, which would allow us to submit the NDA and then have a study which is ongoing, enrolling patients at the time of the FDA assessment of our accelerated approval. And as you know, with Breakthrough Designation and Fast Track, that's approximately 6 months further downstream. Based on the high level of interest in iopofosine by both patients suffering from WM as well as thought leadership in the area, we would expect the study to enroll very, very quickly.

But Jarrod, I think it's fair to say, based on our assessment, approximately $15 million or so to full patient enrollment?

Let me correct that. It's about $28 million to full patient enrollment. It's about $15 million to the point at which we would have sufficient enrollment for the agency to act on an accelerated approval application. So Aydin, if I back you up a little bit, as Jim said, to initiate the study itself because of CRO cost and the start-up costs, that's approximately about $10 million of the $40 million that Jim outlined as the total cost.

Then what happens is, obviously, you get the study started. The requirement, as you alluded to, is initiation of a confirmatory study. Assuming that would happen, then the agency also has the obligation or the statement in the regulations now that the study must be considered ongoing, which they have been updated as some level of enrollment. They have not specified what level of enrollment. We are estimating that somewhere between 10% and 25% of patient enrollment will probably be satisfactory. In our calculation, that is somewhere between 20 and 50 patients. In order to achieve that, we think it would take about $15 million, including the $10 million start-up to achieve that number.

And then obviously, as Jim said, $28 million to get the full enrollment and then $40-ish million to see out the rest of the study, including all of the long-term follow-up. We do believe that if we were to have enough funding to really launch the study and get to that first metric, I think, of having the agency respond to the submission, we would be -- we would absolutely want to initiate and go.

No, I appreciate the question, Aydin. And Jarrod, thank you for the clarification on that. And as a recent -- and I cited in my opening comments, a recent assessment by Jefferies research report identified those oncology drugs with -- that have been awarded breakthrough designation, there's a 79% approval rating for accelerated approvals. And net, both with the EU at approximately 80% likelihood of success. And based on this Jefferies report with the BTD for iopofosine in the U.S., approximately 79%. So we view those as certainly reasonable statistics that stack up in the favor of iopofosine.

Right, right. And given that -- it appears that you will be first launching in Europe, then in the U.S. and given all these MFN discussions. So could you help us understand the pricing potential for iopofosine in Europe and U.S. And also whether you would consider different brands maybe given potentially different labels for EMA and FDA? Just curious to hear your thoughts on this.

Yes, I'll open. We anticipate submitting our application for the CMA in the middle of 2026, if you estimate an approximately 12-month review by our friends across the pond, that's an approximately middle of 2027 marketing or commercial launch ex U.S. And to your point, it's not only Europe, it's 30 major countries, except for China, Japan and the U.S. that would be -- have the capacity to market iopofosine. So it's a significant market size comparable certainly to that of the U.S. when you look at incidence and prevalence numbers for WM.

Now taking a step back before we address the pricing question, and we're not going to give you specific numbers, but we'll give you -- it's clearly a premium-priced opportunity. But as you cited earlier, with the approximate $10 million to initiate our Phase III confirmatory study in the U.S., and with that, as Jarrod cited, approximately 6 months or so to get to the necessary patient enrollment that we would believe would satisfy the FDA's requirement for an accelerated -- for the granting of an accelerated approval, you could actually have a horse race depending on when that study was initiated.

So if, in fact, the study is initiated in the first quarter or second quarter of next year, within 6 months, you're obviously submitting your application to our friends at the FDA. And because of Breakthrough and Fast Track, et cetera, it would be an approximate 6-month review. So in reality, you could have access to the U.S. market and approval in the U.S. market prior to that of the EMA. And so from a pricing perspective, that would certainly make pricing both in the U.S. and ex U.S. a little bit easier.

Jarrod, without providing price points, if you could provide any additional detail for Aydin and our call participants, I think that would be helpful.

Absolutely. And I'm going to go in 2 directions -- or take this in 2 steps again. As you mentioned, Aydin, the Most Favored Nation discussion has resulted in some interesting outcomes. I think as I'm sure you are aware that for pharmaceutical pricing nature that some companies -- some of the larger companies have taken a position of rather than decreasing prices in the U.S., they've taken a strategy of a more flat universal price globally and thereby negotiating harder in Europe and other places for higher prices. And I think that, that is a trend that is going to likely continue. There will likely be some downtick in the U.S. price in order to sort of get them more mirrored, but that there's significant increases in Europe.

Now as it relates to iopofosine directly, obviously, one of the processes that we have to go through is now to work through the HTA process, which was recently -- earlier this year announced, particularly for oncology drugs that this has to be done sort of in parallel with our CMA. That process, I can't -- as Jim sort of alluded to, we're not in a position at this time yet to give specificity on pricing. We have given what we believe and based off our pricing estimates for what we would expect in the U.S. Traditionally, in Europe, those prices can be anywhere from similar to 50-ish percent of that as a whole, but that really comes down to that discussion.

The HTA requirement is for -- even if you do not have a comparator in your clinical study or in your initial -- in our case, in the initial study for CMA, what it would require is that we would do research to evaluate the potential clinical benefit of iopofosine I 131 over comparative drugs. I think the key takeaway on that is that, obviously, based off of the regulatory, the SAWP and in general, the EMA process, the Prime and everything else, there is a significant unmet medical need that this drug is needing. And in their own words, that is essentially driven by the fact that these patients do not have treatment options available to them.

So there is a justification for negotiating higher percentages under that, the more -- the greater the value to the patient and the patient outcomes, the greater the price point can be. And so our expectation is based on the research we have historically done, recognizing that there is no direct comparator that one could utilize that we are in a position of strength to negotiate -- or with a partner, negotiate a stronger price point in Europe.

Yes. Super helpful. Super helpful. And for modeling purposes, it sounds like 2027 is the launch year for both U.S. and EU, which makes it sort of a global launch perspective. Congratulations for the significant progress this quarter.

Yes. Thank you, Aydin. Appreciate your participation. Appreciate the questions.

Our next question comes from Jeff Jones, Oppenheimer.

Congrats on the progress and the regulatory wins so far. So great progress. The -- can you comment at all on how the partnering discussions have evolved since the EU regulatory update and how you're thinking about partnering, be it U.S., Europe or globally?

Jeff, thank you for the question. Much appreciated. Hope you're doing well on your end. Obviously, when we anticipated a positive outcome with our friends across the pond and did the necessary work on the costs associated with our clinical trial, our confirmatory study for the U.S., it became apparent to us to slow play corporate development discussions until we had the blessing certainly from the EMA on our capacity to file.

Obviously, that becomes now iopofosine is a near-term oncology asset in a very robust ex-U.S. market at a minimum. And then when we also -- based on our further communications with the FDA, we're able to really drill down in terms of line of sight and this $10 million to $15 million for upfront-ish to the necessary patients enrolled, as Jarrod cited earlier, in order for us to receive an answer from our friends at the FDA.

We felt as if we would be in a much better position with both of those. And so we kind of, over the early part of the year here or middle part of the year, really slow played our discussions. It also allowed a handful of other companies to kind of get up to speed on their diligence. So we have a number of companies all in -- in and around the same spot in terms of their understanding of where we currently sit, certainly from a regulatory perspective.

And also, quite frankly, the latest data that we've mined from our clinical trial is also very, very supportive of our regulatory approach. So Jarrod has been overseeing and has done a great job in terms of communication on the corporate development side and making certain that we were in a position of strength to optimize the potential value for our stockholders with iopofosine on a number of different fronts. And I'll turn this over to him to provide some additional detail. Jarrod?

Sure. And I'll confess -- Jeff, it's great to talk to you. But I'll confess that I'm not sure that I can add much more detail. Jim did a great job there, explaining exactly where we sit. I would say that we -- obviously, as you get closer and closer to a regulatory approval, the interest and activity heats up, especially when you start to be able to position this sort of as we just talked about with Aydin with the conditional market approval in Europe, the potential to negotiate from a position of strength on pricing through the HTA process, the potential to -- the potential and our approach to manufacture and cost of goods, all of those things puts us in a very positive light in most -- various partners and opportunities. And so we've seen, as Jim said, an increase in that.

I think the second part of your question, which Mike I can dig into a little bit more, which is the strategy. I think we've talked about this before, and we continue to be in this situation. We have ongoing discussions with parties who, I would say, are either globally focused or are focused on the 2 predominant regions right now for radiopharm, which is the U.S. and Europe. We do have various regional conversations ongoing that are advancing rapidly. So those are -- those might be part of those territories or all of those territories. Said another way, it could be solely Europe, could be solely U.S., could be other territories outside of that.

But as Jim alluded to, we have quite a number of parties right now who have either completed or nearly completed their diligence, who have supplied and move forward into the next phases of partnering, and we continue to try to drive that to maximize both the return for the organization and to ensure, as Jim said in his opening remarks, ensure that the drug is developed in such a way that it does get the patient actual benefit.

Great. Really appreciate it, Jarrod. And apologies if I missed this on the call. With respect to 225 and the pancreatic program, I know you're moving -- you're actively moving 125 ahead and that trial is taking off. Any gating items on 225 to begin that trial? Or is that something you would move ahead with absent additional financing? Or is that one pending?

Yes. I believe the team, Jeff, has put us on the precipice of a Phase I ready study there with the pancreatic cancer and 225. It is a function essentially of financing as the gating issue there. Jarrod, any additional color you'd like to provide?

No, I would agree with you. I think that financing is the gating element. And as Jim said, we are -- we currently sit in a position to essentially initiate the study as soon as the capital is in hand, so to speak. We have the CRO, we have the submissions, we have sites. We have everything ready to run for that study. And as you can see, part of the reason we have announced the various supply agreements is because -- particularly around actinium is because what we've done is make sure that we have a consistent supply of actinium so that we are not delayed in any way, shape or form as it relates to actinium sourcing and that supply gets us from where we sit today based off our forecasting all the way through into commercialization on the actinium program. And that's exactly why we've done that. So there are no hiccups or delays on that front as we've seen with other parties.

And so we expect, again, pending the capital, we expect to initiate that Phase I, and I'll call it Phase Ia study. It really -- it is a dose escalation safety study with the dosimetry component. So at the end of the day, what we'd be looking at is clear safety and understanding of the uptake and distribution of the molecule, which we don't expect to be very different than what we've seen historically.

No, Jeff, I was just going to make a comment -- no worries. I was just going to make a comment on how significant we view the -- as an example, the triple-negative breast cancer study. It's a solid tumor. As Jarrod cited, we believe our drug, our conjugate will behave in a very similar manner to what we've observed with other isotopes as well, 124, 125 as well as 131.

And so this is really, I think, for the company and for validation of our platform, very significant. And Jarrod, perhaps you could just expand a little bit for our audience the imaging and dosimetry data that we expect to collect very early on in this study that we believe will be further validating our platform and in particular, our capacity to be very effective in challenging solid tumors.

Sure. And so we're -- I'm going to blend this because it's the same, whether I'm talking about the actinium program in pancreatic cancer with CLR 225 or the triple-negative breast cancer program with CLR 125. In both cases, we're utilizing dosimetry. And for folks that may not be as familiar with the radiopharmaceutical, radiotherapeutic -- targeted radiotherapeutic strategies here, the benefit of dosimetry is unlike other therapies where we take blood samples and we've used that to sort of calculate and guesstimate the amount of uptake into the tumor and their -- and also into other healthy tissues.

In this case, what we're able to do is actually image in the transit of the drug with inside the human body, and we're able to identify exactly where it is at different time points. Utilizing that data, we're then able to calculate both the absorbed dose in the healthy tissue and be able to know when we might achieve a level that would be sort of toxic. And on the other side, we're able to calculate the absorbed dose into the tumor and thereby calculate the expected dose and dosing regimen necessary to be an active therapy in that tumor type.

And utilizing that data, you could get what's called a therapeutic window and you get the opportunity, that is the difference between your therapy dose and when you start to see toxicity. And we expect, as we have seen with iopofosine, that this therapeutic window will be significantly wide enough. Interestingly enough, in the CLR 225 program, back to pancreatic piece for a moment, one of the great challenges in pancreatic cancer is not just the nature of the tumor and the late stage in which patients are diagnosed, but it's also there is, what they call interstitial pressure in the tumor, which prevents most drugs from actually being able to penetrate the tumor because there's fluid pressure pushing back against anything entering.

Interestingly enough, as what we saw when we did this in the [indiscernible] studies. Our phospholipid ethers, again, give us a unique ability to actually penetrate through that and actually get inside the tumor and get deep inside the tumor, which is one of the reasons why we think, particularly in pancreatic cancer, we have a competitive advantage over other programs in that tumor specific. Obviously, in triple-negative breast cancer with the CLR 125, we've seen similar sort of results, but that comes at it from a different perspective, particularly because you have limited targets now in breast cancer and being able to overcome that with our targeting mechanism that is based off [indiscernible].

[Operator Instructions]

Our next question comes from Jonathan Aschoff by ROTH.

Congrats on the regulatory progress. I was curious, just because the full approval is based on PFS, can you remind us where you are in CLOVER-WaM follow-up and where that PFS last came out or at least what it at least is and how that compares to standard of care for WM?

Of course, Jonathan. Thanks for your participation. We have not updated our data since January of last year relative to PFS. And at that point in time, it was very robust and well beyond what you normally would see with salvage therapies in the lines of therapy that we were treating. So Jarrod, if you want to provide some detail there, I think it would be helpful for Jonathan and our audience.

Yes, Jarrod, please to do that. I had 11.4 months after 8 months, but you last said you had follow-up beyond 12 months. I just didn't get any further PFS with that additional follow-up. So I'm kind of just trying to reconcile where it is.

Yes, absolutely. Thank you for confirming what I was about to say. What I was about to say is it was 11.4 months with 8 months of follow-up. We now have 12 months of follow-up on all patients. That is correct. That is -- that was one of the criteria that the FDA for submission for accelerated approval had requested. We now have that.

As you might -- as I'm sure you are aware, basically, where we are in the process, we have not announced additional data. We do not wish -- we're not in a position -- I don't want to say we do not wish, we're not in a position to announce additional data at this juncture, largely in part because we are now in a process of trying to submit this for FDA regulation, and we don't want to be caught in a situation where the FDA may view us as being promotional as it relates to this data prior to a submission.

So at this juncture, the most recent data is that data from January of last year, and that won't be updated in the near term -- or I'll say in the near term, based off of the requirements and discussions with them.

Okay. And by the way, the order for pancreatic is file the IND, get funding, start the trial, correct?

Sort of. So -- sorry, Jim, if I jumped in there too fast. The pancreatic cancer study is one that we're not running in the U.S. So it will be filing and we have filed ex U.S. with the appropriate authority to execute the study and have that acceptance already. So we're in a position now where it is await the capital and then initiate the trial.

No worries. And the only additional information that I'll provide in regards to the PFS question, Jonathan, is that when we did multiple advisory boards with global thought leadership for Waldenstrom’s macroglobulinemia, and what came across very, very clearly was in the patient population. And just for all participants, this was -- iopofosine being used essentially as fifth-line therapy for this patient population.

One, the response rate that we achieved was that 60% range was considered outstanding. And more importantly, they gave us insight that 4 to 6 months of PFS for that patient population would be an excellent outcome. And as you cited yourself with our initial cut of data, we're at approximately 1 year of PFS. So almost doubling or greater the expectation of thought leadership in WM in terms of what would be considered an excellent result for patients.

Okay. There are no further questions at this time. I will now turn the call over to Jim Caruso. Please continue.

Terrific. Thank you, operator. This concludes our call for today. Certainly appreciate the great questions from our analysts and for your participation as well as all participants. Of course, this will be up on our website, and a transcript will be following this call. Thank you all very much.

Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.