Cellectar Biosciences INC NEW Investor update
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Hello, and welcome to the Platform Behind the Pipeline, Cellectar Biosciences Educational Webinar. We ask that you please hold all questions until the completion of the formal remarks, at which time you will be given instructions for the question and answer session. Also, as a reminder, this conference is being recorded today. If you have any objections, please disconnect at this time. 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 of 1995. 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 will open the line for your questions. I will 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 have 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 the 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. 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. 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. As Jim mentioned, I will 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 and dense stroma that the antibody or peptide may 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 are 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 it goes in via endocytosis. 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 head group 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. Often we get asked, were we the first group to pursue or develop phospholipid ethers? The answer to that is no. Actually, we are essentially the third generation of this. Our phospholipid ethers are a mimetic of a naturally 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 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 iopofosine or Cellectar phospholipid ethers, what we have done is basically solved the problem for IV hemolysis and re-engineered 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. 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 surface. These microdomains are known as lipid rafts. Lipid rafts do exist on normal and diseased tissue. In normal tissue, however, these are small, transiently 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, 7-10 days to be exact, depending on the different tissue type. They become signaling hubs for the tumor itself to allow them to 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.
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