Cellectar Biosciences, Inc. (CLRB) Earnings Call Transcript & Summary

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 phospholipids 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 up-regulate or down-regulate 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 in -- 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 phosphorylcholine headgroup, followed by a long [ hydrophilic ] APL chain. This apple 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 phospholipid known as alkylphospholipids or APLs. The original APLs, which are identified here, of edelfosine and lipofuscin, 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, [ pirofosine and irofasine ]. 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 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 microdomains on the cell surface, particularly on the cancer cell service. These microdomains are known as lipid rafts. Lipid rafts do exist on normal and disease tissue. In normal tissue, however, these are small, [ transitally ] formed microdomains that rapidly dissipate in a few nanoseconds. When you look at what happens in a tumor cell, however, these microdomains 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 [indiscernible]. 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 oxidated pathway and the breakdown of phospholipids and long-chain fatty acids, which are molecules [indiscernible] 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 fire blast cell. The red stain you see is the staining for lipid rafts. And as you can see, the normal fiber blast cell is barely visible in the image while the A549 cell lights up very brightly with significant lipid raft [indiscernible]. 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 and 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, 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 macro environment. That has actually done, interestingly enough, via the high concentration or high binding that we are highly bound 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 internalize. 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 e-fluxed 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 RAPs, you're looking at a coculture of taking 2 cancer cells taking up our fluorescently tag 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 -- spec 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 [indiscernible]. So how does this occur at the cellular level? Again, as you think about this, the molecules, shown here with the little bow at the top and the stick, in the extracellular space, they move along the cell surface. They come upon cholesterol-rich lipid RAF 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 [ flip ] basis, which then rotates the molecule into the inner leaflet and then deposit 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 reticular. 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 flip-based component. However, when you're in the heme space, you also tend to get 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 scare of free-floating extracellular lipids in order again to overutilize the beta oxidate pathway. And enhancing the immune evasion of the tumor actually is driven from RAF 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 RAF-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. Reduce, as I say here, slow elimination, you see [indiscernible] 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 [ atheranostic ] pair to the iodine 131 or Iopofosine I 131 if we so desire. At this juncture, most of the time, we just use SPECT because iodine 131 can be 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 BTKi's. 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 Waldenstroms. 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 ligands 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 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 bottles. 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 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 [ LED 212 ], which is what I'll call a hybrid radioisotope where it's also looked at in triple-negative breast cancer. In LED 212, I call it a hybrid because it has both a beta emission as well as an alpha admission 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 validate 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 [ GEN1-SKPR ] 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 sRNA 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-1 ] 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 sRNAs 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, pro tags, 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 RAF 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 -- it's not just a drug. It is truly a platform. It is a unique platform and 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 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 RAF-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 [ RMOID ] 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 strongly 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 of 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 flip-based [ 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 a 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, yes, if you could just clarify that for us.