Hi, everyone, and welcome. Thank you for joining us. I'm Michael Lubinski, your host. On behalf of Investor TV, welcome to today's interview with GT Biopharma. I am really, really excited about this interview. But before we get started, I just have to go over a couple of disclaimers. This webinar is being disseminated on behalf of GT Biopharma and may contain forward-looking statements. Investor TV is not a registered broker-dealer or investment advisor and is serving solely as the host of this event. We will also be taking questions directly from the audience, so please be sure to leave your questions down below. All right, that's it. Let's get into it. GT Biopharma is a clinical-stage immuno-oncology company that is developing new cancer therapies through its proprietary TriKE platform. I know what you're thinking. This may sound like a mouthful, but to put it in really simple terms, GT Biopharma is working on ways to help the body's own immune system better recognize and attack cancer cells. The company is already advancing programs across the blood cancers and solid tumors and trades on the Nasdaq under the ticker GTBP. Today, I'm joined by Executive Chairman and CEO, Michael Breen, and Dr. Jeffrey Miller, the company's Consulting Senior Medical Director. We're going to talk about the company's platform, where the programs stand today, and the milestones investors should be watching for. Gentlemen, thank you for being here. It really is a pleasure to speak with you both. Thank you, Michael. We're delighted to be here and very excited to present some information on our company. I actually studied biology and neuroscience in graduate school, so I've been especially looking forward to this conversation. It's just one of those full circle moments for me, where I get to speak to you about a field that I first encountered in the classroom, and which at the time, honestly, sounded like science fiction. Dr. Miller, maybe to kick us off, you could bring us up the corporate presentation and just give us a big picture overview of GT Biopharma, what you're building, and what problems you're looking to solve. Great. Give me one second here to click the right buttons. Sure. Take your time. Is that the correct screen? It is right now. Exactly. Perfect. Thank you very much. Okay, great. Okay. Thanks, everybody. I am delighted to be here. Just a little bit of an introduction on myself. As mentioned, I am a consultant for GT Biopharma. I am also a physician, and my job is really to take care of patients with cancer, which has been my motivation to focus my efforts on NK cell therapy for the past 30 years. I am going to take you through some of the journey about how we got there. There are some just very big highlighting things that I wanted to start off with. I think it is very clear that things have been changing in medical oncology. We started off with chemotherapy and radiation therapy, and I think what is going to derive the future of cancer therapy is something called immunotherapy, ways to stimulate the immune system to be very specific for that cancer cell. I think all of us have friends, family, hopefully not yourselves, that have had cancer and have gone through chemotherapy, which not only targets the tumor, but also has many, many side effects of normal tissues. I think what we are trying to do overall on our platform that I am going to cover today is just some very basic steps about how to specifically target the immune system to the cancer cell while not having any of the side effects that one might see with chemotherapy or radiation therapy. There are a number of engagers that have been out here. I am not going to go through all of these. This has been a big market driver in a lot of different fields, and I will go through the specifics as I go through the discussion. Michael, should I continue on, or do you have further questions for me now? No, I think you should continue on with the presentation, and I will jump in at the end with some questions. Sounds great. Okay, thanks. I wanted to start off, one of our first forays into the clinic is a molecule called GTB-3550, and this is a molecule that was designed to target CD33, which is present on AML cells in MDS, which is myelodysplastic syndrome. We treated a number of different patients, and this is really taking you into a background of where we are today. The therapy was given as a continuous infusion in 96-hour blocks for three weeks in a row, and this was followed by a weekend off after each block of therapy. We went through six individual dose cohorts. There were two patients in each of these cohorts, and I wanted to take you through a very exciting summary of what we found in this early study that was completed a couple of years ago. The first thing is, this is the number of activated NK cells circulating in one's blood. When the NK cell infusion was on, remember, this is a 96-hour infusion, so day three, day 10, and day 17 is the Wednesday while the infusion was going. You see all these cells at these peak areas get very highly activated. When you look on the Monday after the next infusion cycle, you see that this is followed by a period of rest. This gives you this seesaw pattern that you see on this graph. The most important thing to me as an NK cell biologist is what did we do with the NK cells circulating in the blood? That's represented by this right panel. You could see, again, when the infusion is on at day three, day 10, and day 17, cells get activated. They get pushed out of the blood into tissue, which is where we want them to be. Then again, on day eight, after the first cycle of therapy, after the second cycle, or after the third cycle, you see this tremendous dose-dependent expansion of NK cells in the peripheral blood. Here we're trying to increase the immune cells that we think will be targeting to the cancers. This has been very exciting to us. Again, this trial is our- I'm going to jump in for one second there. If you can go back for one slide. Absolutely. When you're saying NK cells, I just want to say this more for the audience that may not be familiar- Yeah you're referring to natural killer cells, right? Yes, that's correct. I use the abbreviation NK cells, but these are natural killer cells. Let me take even a step back for that, Michael, for the audience. There are many types of white blood cells in the blood. NK cells are a subset of white blood cells that we think has the potential to attack cancer. Many of you have probably heard about T cells or another type of lymphocyte that are in the blood. They can be targeted as well, and the audience is probably familiar with gene-modified chimeric antigen receptor, or CAR- T cells, that have been FDA-approved, and there's a number of products out there. Like T cells, we know that NK cells have cytolytic granules. They can recognize their targets. They make holes in the tumor targets. They put in cytolytic proteins that make the target cell lyse. This is why we're excited about NK cells. It also reminds me, since T cell products are out there, why do we think that NK cells are better? I think the simplest answer is we think that they're going to have a better safety profile and be easier to export. We're hoping that these will be safer molecules. They're not as activatable as T cells, but we think that they will have the same potential to kill tumor targets. So whenever I say NK cells, I'm talking about those natural occurring endogenous NK cells in the body. Well said. Appreciate the explanation. In that early clinical trial that we completed, we were very excited. Starting at doses of 25 microgram per kilogram per day of the continuously infused products, we saw four patients who had a decrease in the number of blasts that were present in their bone marrow, and this was compared to a pre-bone marrow biopsy. Here is all the detail, which I'm not going to go through, of the blast cell decreases that we saw in this trial. This was exciting for us, and I'm going to go through really our future-looking platform. We now have a 2nd generation camelid TriKE molecule. This started in, is in phase I testing now. The first cohorts have been enrolled and we continue to move forward, and I'm going to give you a little bit of a summary as to the rationale in why we got to this 2nd generation camelid TriKE. We now have a B7-H3 targeted TriKE that is in the clinic now. It started earlier this year. The first patient was dosed in May of 2026, and we continue to dose patients in that trial. Again, this is the trial that I already just reviewed to you, as the proof of concept data as to why we're moving forward into some of these different platforms. What is a TriKE? In very simple terms, you could see that these blue cells are NK cells, and this gold-colored cell is a tumor target. What I like to tell picturally, and this is a very high electron microscope view of an NK cell recognizing a target, and I like to think that this handshake here emanating from the NK cell is what our TriKE protein does. It binds to the NK cell surface. It binds to the tumor, allowing this NK cell to be pulled in to make a hole in these tumor targets and deliver all of its cytotoxic chemicals to ultimately lead to tumor kill. I'll talk about some differences as I go through this between NK cells, T cells, and some of the competitor molecules that have been out there. This is a picture of our protein. We call this Tri because there are three functional domains. The orange domain here is an engager, which is now a VHH or camelid version, and I'll tell you in more simple terms in a subsequent slide what that means. This binds to the NK cell, delivers a very potent activation signal to the NK cell. At the same time, this linear protein, which I'm outlining here, and is also shown here brings an IL-15 molecule. An IL-15 is a cytokine molecule that also stimulates the NK cell. One of the unique aspects of the TriKE molecule is that there are really two activating components in this linear sequence, and again, something measuring what we call a tumor-associated antigen. For AML, this is CD33, and for the solid tumor targets, it's B7-H3. There are a number of different tumor targets. Many of these are classic single chain Fvs. Some of them are nanobodies, especially our B7-H3 is our first all nanobody or dual nanobody TriKE molecule. This is really just giving all of the platforms that are being explored pre-clinically. The clinical programs right now are CD33, the B7-H3 in solid tumors. I will talk a little bit for the CD19 about our plans to get into autoimmune disease. Let's first just at a very basic way look at how these TriKE molecules work. Before I start this visual presentation, what you are looking at here is a very tiny fluid micro well. The green cells here are AML cells that are living, and the blue cell is a single natural killer cell, or NK cell. In the gray here is just the solution of this micro well containing our TriKE molecule. What you see here is that the NK cells have the propensity to crawl around and to search around. When a target gets killed, it turns red. The process that is being demonstrated in this video movie is a process called serial killing. If we put in a molecule here that did not have the IL-15 component and just a bike molecule recognizing NK cells in the tumor target, we would not see serial killing. We might see one killing of the NK cell in its tumor target. This is really bringing a unique aspect of each of the functional domains to mediate serial killing, which we think is ultimately going to be important for anti-tumor activity when we give this to patients. I already showed you early on that the 1st generation molecule gives us NK proliferation and activation in vivo. We know that we already saw a hint of some anti-tumor activity in this earlier trial. There was no loss of the CD16 molecule on the NK cell surface. I did not show it to you today, but we have all the translational data to back up that point. To our expectation, if you will, we saw very few side effects with this 1st generation TriKE. We saw one Grade I cytokine release fever, cytokine release syndrome, which was a transient fever. This also occurred in a second patient at a higher dose, and these patients were given acetaminophen or TYLENOL, and this was totally self-limited and resolved on our own. I already pointed out to you the data slide about how we saw blast cell decreases. We know that this molecule has a very short half-life when you look in the serum, and we have done these pharmacokinetic studies. Remember, these have engaging molecules to bind to cell types in the body. We have some reason to believe, because the effect of the drug is sustained at least for a couple of weeks, that that binding of other components in the body is giving it a longer biologic half-life than its serum half-life, which is listed here in certainly under three hours. Really, how did we make the pivot? Let me go into a little bit more detail. I am trying not to be overly technical here, but human antibodies are shown in this cartoon here. These human antibodies, these are the antibodies that protect us against infection and mononucleosis when we all got this in college. These are comprised of recognition domains in the lighter blues here, containing a variable heavy and light chains. What we know about llamas or sharks or many other species is they have different antibodies called camelid antibodies. These are defined by a recognition sequence called an antibody or a VHH or a single domain sequence. What we did is we developed a proprietary anti-CD16 camelid sequence. Again, this is figured in orange here to bind to the NK cell surface. When we tested this in an animal model of leukemia, better tumor control is a lower dot on this curve. There's a lot of tumor here when you give no treatment. When we gave our single chain Fv TriKE or the 1st generation TriKE, we saw a moderate degree of activity. But when we gave the camelid 2nd generation TriKE, we saw really far superior clinical activity, much better tumor kill. This was really the rationale to only move this 2nd generation platform using the anti-camelid CD16 sequence. We can go through questions if you have them. Where are we in the competitive landscape? There are many companies that are talking about developing NK cell engagers. Innate Pharma engages CD16 in a secondary receptor called NKp46. Dragonfly Therapeutics recognizes CD16 and NKG2D. What sets us aside as very unique from these different platforms is we think IL-15, the co-stimulator brought into this immunologic synapse, is far superior than any of these competing molecules, which at least pre-clinically we've tested in the laboratory. Again, Affimed was out there clinically with something that only recognized CD16A, and this molecule is not really continuing clinically. We know that Innate Pharma has a molecule recognizing instead of CD33, CD123 in AML, and they've had a number of different reports showing at least preliminary clinical activity. I want to really emphasize here that what we have here is an immune engager to work on your own endogenous NK cells. Our therapy is a protein therapy, it's not a cell therapy product. This is really in contrast to Fate Therapeutics, which is giving induced pluripotent stem cell-derived NK cells, or Nkarta, which has their own platform of an NK cell therapy where they're giving living cells. The engagers are protein therapy, including our TriKE platform, which comes in a bottle just like monoclonal antibodies and does not require the giving of live cells, although that may be a combination that we want to test in the future. I think the goal of the research is to get beyond acute myelogenous leukemia or myelodysplastic syndrome, and this is where we became very excited about a protein called B7-H3. B7-H3 is in a family of immune checkpoint inhibitors. Why it's important here is it's widely expressed on a number of different solid tumors, and I'll tell you the eligibility of this trial in a few minutes. We also know that the higher the B7-H3 expressed on your primary tumor, this correlates with poor prognosis, so we thought it would be a perfect target to generate a TriKE molecule. This is really a cartoon rendering of that molecule. Again, we have a camelid component recognizing B7-H3 in the tumor. In the purple here is the camelid anti-CD16 recognizing the NK cell. In this reddish molecule here, this is the IL-15 co-stimulatory molecule to be brought to the immune synapse. If you label this TriKE sequence with a red dye, you could stain cells, and this is picking up this red dye. If we look at a sarcoma tumor target that expresses B7-H3, you can see that there's a high degree of staining in this histogram here. But if we take the exact same cell line, knock out the B7-H3 protein, apply our TriKE molecule, you get no staining here. This is really important to us biologically because it shows the exquisite sensitivity of binding only to cells that have B7-H3 and not to cells that don't have B7-H3, such as your normal tissues. In the next slide before I start this, because it's really a remarkable summary of all our laboratory testing, I'm showing you in red, and I'll get to that slide in a minute because the movie will start as soon as I click on it. The tumor cells are prostate cancer spheroids that are labeled in red. In all of these conditions, we're giving either NK cells, NK cells plus IL-15, or NK cells plus our TriKE molecule. This is the TriKE-containing sequence. This assay is ongoing for about four or five days. As you can see with the NK cells alone, this is this black halo here, you see very little activity of the tumor target. Same thing with IL-15. But as you can see, the TriKE activates these NK cells to totally dive into this spheroid mass and to obliterate the red, which is the prostate cancer in this model. We have many other examples of head and neck cancer and other tumors that show us exactly the same thing. Really to complete up this portion and to move on, I wanted to tell you the flexibility of the platform. As many of you know, there's been a lot of interest in B-cell malignancies. If you look in the cell therapy market today, most of the cell therapy products are targeting B cells, either in CD19 that's present on lymphoma cells and some leukemia cells, and BCMA, which is present on B cells for multiple myeloma. We have developed a molecule that we, I'm sorry, it just clicked backwards. We have a CD19 targeted TriKE, which we've tested in cancer cells, and we have ongoing studies now, because there's a lot of interest in the field in depleting the B cells that cause autoantibodies in autoimmune diseases such as lupus and myositis. The idea here is that if you target normal B cells making these pathologic antibodies, you can get some control of the autoimmune disease. We initially designed this for B cell malignancies, such as chronic lymphocytic leukemia, but we are doing the testing and exploring manufacturing possibilities to get this CD19 TriKE into the clinic. Remember, the TriKE is a protein therapy to engage NK cells to specific targets. It is not a cell therapy, and we think that this will be easier and more exportable. Michael, do you want to make a comment on the last slide, last two slides here? I actually Yes. Sorry, go ahead, Michael. I just wanted to Yes Keep in mind that I have a bunch of questions about these slides, but for me personally, I am going to wait to the end for all of my questions. Okay. Okay. Thank you. I just want to highlight the people involved in the company. You can see here they're all lined up as it were. Alan Urban is our CFO, Chief Financial Officer. He has a public company background, and he's very, very credentialed. Dr. Miller is, of course, a key opinion leader in the space with more than 20 years of research in this particular space. He is, without a shadow of a doubt, one of the people who is leading the charge with this particular technology in terms of the natural killer cell engager technology. He's ably supported by Dr. Martin Felices, who's associate professor, also out of the University of Minnesota, as Dr. Miller is. We have Chris Henry, who's our CMC and pharmaceutical science consultant. Our independent directors are Hilary Kramer, who's ex Lehman Brothers and Morgan Stanley, David C. Mun-Gavin, who's ex Credit Suisse, and Charles Casamento, who's ex Sanofi, and he was on the business development side. Excellent We really have an excellent team who are very, very experienced, and we're very lucky to have all of these people involved in the company. It's just to highlight, because I'm not a scientist, I come from a commercial background, and I'll explain a little bit about myself later. Just demonstrate that some of the high-value transactions that have completed in the NK cell engager space. You can see there that, dating back as far as 2018, there was a licensed transaction with Sanofi and Affimed, where Sanofi paid Affimed $96 million upfront, with then potential milestones of a further $5 billion. Also, if you look more towards the right, the Dragonfly transaction, it was a single molecule. The most important thing of this is it was a pre-clinical license deal, and it was $300 million upfront on disclosed milestones and 20% royalties. The reason I'm highlighting all of these transactions is just to demonstrate that, if we get this right, and we obviously feel that we're on a very good path to do so, then, commercially, it can be extremely rewarding for our investors. Great, and I think that is it, Michael. Thank you, Jeff. Gentlemen, that was a fantastic presentation, by the way. Very, very thorough. I am going to get you to stop sharing the screen there, Dr. Miller. Thank you. They say sometimes a picture is worth a thousand words. That video is likely worth 10,000 words because I think sometimes it's just really hard to conceptualize these things, but seeing it work in real time just really makes it very, very real. That was really, really cool to see. Dr. Miller, I thought you explained everything extremely well. This might be a challenging question for you because I would like you to try to do it in the most lay terms as possible. For someone that's brand new to GT Biopharma, how is this different from a traditional cancer treatment? Yeah, Michael, that's a great question, and I think I highlighted a little bit. Remember, cancer therapy has been slowly improving over a number of years. But initially, before immunotherapy, which has really had most of its success over the past 10 to 15 years, prior to that, if you came in with cancer, you had really two opportunities. You got chemotherapy, which was typically given into a vein in the arm. The chemotherapy would travel to all your systemic tissues, hopefully attack the cancer, but unfortunately give you side effects to normal tissues. I think many of you know with friends and family or yourselves, the side effects are attacking rapidly dividing cells in the body. Hair follicles, that's why your hair falls out. It's a side effect of the therapy. The GI tract, you get many GI side effects of cancer chemotherapeutics. Some more subtle things, as we know that certain chemotherapies attack heart cells and give you less good heart function over time. The same thing is true for radiation, at least where the radiation beam goes. I think the excitement about immunotherapy, and again, it's true for the NK cell engagers that we've talked about today, as well as some of the CAR T therapies that have already been FDA approved as proof of concept. These are very specific therapies. The intent is to have very little side effects of normal tissue. If this works as monotherapy, as we're intending it to do, this will not give you side effects. It will not give you hair loss or GI symptoms. The one thing we know about immunologic agents, though, is it gives you different side effects. Part of them are these transient flu-like symptoms. We know if you've got a viral infection, you get fever, your muscle aches. We think that that may happen with immune activation in these immunotherapies and this TriKE therapy, but we think those symptoms will be very self-limited and controlled, and only last while the therapy is in the body. Sounds like that is not really much of a comparison relative to the side effects of chemotherapy, right? That is true. Correct. I think that most people would take that any day over the other. Yes. I think, sticking towards the science end a little bit, GTB-3650, I hope I said that right, is being- Correct studied in people with acute myeloid leukemia and high-risk myelodysplastic syndrome, whose disease has essentially returned or who have basically stopped responding to treatment. What would you say is the biggest unmet need for those patients today? Yeah. I think, Michael, the unmet need is the end stage they are of their disease. By the way, I am a bone marrow transplanter by trade. This is how I got interested in leukemia. Remember, if you are young and your leukemia responds right away, you get into remission and you go on to a bone marrow transplant, which still has a real chance of delivering cure. This is true in any drug development. When we started with GTB, having discussions with the FDA, even with our 1st generation trial, we were very clear to them, and they were very clear back to us, when you are testing a phase I agent that does not have any clinical data known, you have to start off with the worst patient. Basically, the patient eligibility in this cohort is the keeping relapse refractory, failing standard therapy, and having no other treatment options. I know it is hard for people to grasp, but that is the way that drug development starts. Once you show activity of molecules, you are allowed to work, move it further up, and sometimes these newer therapies can become primary therapy, but we always start with the worst patients. Just on that note then, because it is an early phase I study, you are basically still trying to determine its safety. As you are increasing dose levels, what have you basically learned about how patients are tolerating that? Yeah. Just like the first trial with the 1st generation TriKE, I think, we are starting to see some very light fevers that are controlled with acetaminophen, just like we saw before. The thing that we have to learn now as we go up with the new molecules are we going to see the clinical activity that we hope to see? We are starting to get into the range that, based on the laboratory data in our earlier study, we hope to see clinical activity. But the FDA is always, because the 2nd generation TriKE is a different substance than the 1st generation TriKE, we are going back through that stage and we are hoping to see something. We do bone marrow biopsies before and after therapy. I was just about to ask, actually, what would be the earliest indicators? What would you be looking for, essentially, that would say, "Okay, this is actually working"? Yeah. I think the first thing would be a post-treatment bone marrow biopsy showing a decrease in blast. I am a hematologist. That is not good enough. We have to show that those blasts stay away for a period of time, and we would have follow-up studies to follow that endpoint before. This is very different from what we are doing in the 2nd generation TriKE compared to what we did previously. The FDA in the previous study let us do one cycle of therapy. Now we are doing at least two cycles of therapy with the opportunity to get up to four cycles to hope to get a greater duration of the response if we see it. So that is built into the trial, and that is what we are going to be learning, I hope, over the next six months or so. Fascinating. If we can switch gears for one second and talk a little bit about solid tumors. Again, I hope I have this right. GTB-5550, that targets B7-H3, right? Which is a protein, if I remember correctly, it is found on many cancer cells. So why is B7-H3 an interesting target, and what could success in solid tumors mean for GT Biopharma? Yeah. I am a hematologist. We know that the number of new cases of AML in the U.S. is anywhere from 10,000 to 15,000. But when you think about solid tumors such as prostate cancer, breast cancer, lung cancer, ovarian cancer, all the other ones that express B7-H3, there is a huge differential in the population infected. There is potentially hundreds of thousands, if not millions of patients affected with solid tumors compared to this very small niche of acute myeloid leukemias. I actually was not aware it was expressed in that many different types of cancers, to be honest with you. Huge number. Just to be clear, this is for men and women, for breast cancer, the hormonally responsive tumors, and for men, prostate cancer. Each of those diseases in male and females in the lifetime of an individual will affect about 8% of all males and females. When you think of the world's population, this is a huge reach. Both of those tumors express B7-H3 in more than 80% of the solid tumors that develop in patients. This is why we think it is really such a great pan-tumor target, because it is not specific to breast or prostate. The other key piece is that B7-H3 is not present in your heart or your lungs or your skin or your liver. We think this is going to attack the tumor but not damage the normal tissues. Michael, I wanted to bring it over to you for a second. What became clear to me throughout the presentation was that TriKE is meant to be basically more than a one-treatment candidate. What makes this a real platform in your eyes, and where is GT Biopharma's biggest advantage? As Jeff very ably explained, the reason we call it a TriKE is because it's got three functional parts to it. The reason it's a platform technology is that two of those functional parts remain constant, and all we need to do is swap out what we call the binder part. As Jeff explained, for AML and MDS, the binder is CD33, and then for the solid tumors, the binder is B7-H3. Then also as he explained, for autoimmune disease, the binder is CD19. We're effectively taking our TriKE, which we have a now in 2nd generation form, and we are saying, well, we can use it across all of these other diseases. It also, as was shown in, I think it was slide seven, we have other TriKEs in our platform for other targets. For example, what we call GTB-1050, which is for HIV. The main advantage, of course, in all of this is that having already developed the TriKE, all we're really looking at now is changing the binders that's going to have the most and best efficacy for binding onto the tumor target. That really is platform technology. Then of course, commercially, I would be remiss if I didn't mention that when Big Pharma, if it ever comes knocking on our door, they very much like companies with platform technology. If you look at what Gilead, for example, paid for Kite Pharma, I think it was a huge amount of money, but that was predicated on the fact that it was not a one molecule solution, it was platform technology. You have two programs now essentially that are enrolling patients. As the CEO, I was just curious about this, how do you decide where to allocate time, money, funds, resources? How does that work for you? It's a very simple answer to that question, Michael. As you've rightly identified, we have two phase I first in human trials, one for blood cancer, one for solid tumors. The one for solid tumors is a basket trial, so it's targeting a number of different solid tumors. As Dr. Miller explained, it's prostate cancer, breast cancer, bladder cancer, pancreatic cancer, head and neck cancer, and lung cancer. By the way, the solid tumor space worldwide annually is estimated to be worth $360 billion per annum. Whilst it's great to be focused on solid tumors, given it's a platform technology, we're also next going to be looking at and targeting autoimmune disease, where the target is CD19. Again, the opportunity in the autoimmune disease market is estimated to be $115 billion per annum worldwide. To revert back to your question, we've got two trials ongoing, which we're very focused on, and particularly with regard to making sure that we have correct financial resources. I should also maybe just mention that the cost of a trial for our NK cell technology, our Engager technology, is much more cost-effective and is somewhere between $100,000 and $120,000 per patient. Whereas if you compare that with CAR- T technology, where you have to take it out and reprogram it, then it's estimated that it costs $750,000 per patient. And that's a very important thing to focus on. We're very focused on our trials and very focused on the next trial that we're moving towards. I always like to ask this question just because I'm curious about it always. What made you want to take on the role of Executive Chairman and CEO of GT Biopharma at this stage of your career? And I always ask also this, do you personally own any stock in the company? Okay. So they are two excellent questions, and I think those are questions that should always be asked of the CEO and Chairman of any public company. My background is that I was a merger and acquisitions corporate partner in a global law practice. We had 50 offices around the world and 4,000 employees, and I was on the management board of that firm. You get to a point where you've been at the top for a very long time, and then you have to sort of let the new cohort come up, and you move down what we call the escalator. I did that for 25 years. I got an opportunity to join one of my clients, which happened to be an international private bank, and I joined that as the Managing Director with a brief to grow the business and then prepare it for sale and ultimately sell it, which I managed to do within three years, having doubled the business in size. I also sat on the boards of a couple of hedge funds, which had also been clients. And I came across GT Biopharma with regard to one of those hedge funds, with regard to potential investment, and ultimately, the hedge fund invested. And having done my due diligence, I very much liked the science, I liked Dr. Miller, and I invested personally in the company. However, that was back in 2017. I didn't get involved directly with the company until 2021 when the company was uplisting from the OTC to Nasdaq, and they approached me and said, "Look, we'd really like you," or rather, "The bankers would really like you to join the board as an independent director," because bankers like people with resumes and backgrounds like mine. Having already invested in it personally, that was a pretty easy thing to agree to. It made perfect sense to me. I joined in January 2021 as an independent director, and I remained in that role up until November 2021. We took the company through the uplist on the Nasdaq. Obviously with my corporate law background, a lot of the questions were being deferred to me with regard to how you run a public company. I was then approached by my fellow board members, and they asked me to become the chairman of the company because, and at that point in time, I was already doing that job, to be honest with you. I said, "Yep, sure, no problem." Then they said to me, four months later, "Would you also become the CEO as well as the chairman?" After some thought I said, "Well, okay, but I'm only going to do it on an interim basis. I don't want to do this full time. It's not for me." I was heading towards retirement. Anyway, we interviewed and looked at some potential candidates for the full-time CEO role, but every time we did, my fellow board members said, "But we really like the job you're doing, Michael. We'd like you to stay in it. Michael, I will say this to you. From my experience, the best CEOs are always the ones that are the most reluctant to do it. For some reason, or they don't want to do it, they somehow turn out to be the absolute best CEOs. Look, it's really interesting. I actually haven't heard of too many that have invested in the company beforehand, and that led you to this role. I always say with biotech companies, the asset itself is important, but so is the team. Having a really, really strong team behind you is equally as important as having a good asset or a good drug in this case. Look, there's no question GT Biopharma, but now having met Dr. Miller myself, there's no question GT Biopharma has a really exceptional team. I just want to wrap up with one final question to you, Michael. To our investors, if you had to point to two or three things that people have to watch for this year, what would you say they are? Dr. Miller, you can feel free to jump in if you have something to say about it as well. Without stealing Dr. Miller's thunder, I would say, and I'm looking at this from the perspective as an investor, either a current investor or prospective investor, I would always say the data. You've always got to see what the results are, and we're a long way down the road with regard to our blood cancer trial, phase I, and also with regard to our solid tumor trials. I would say the data which will be coming through shortly, certainly by the end of the year and the early part of next year in both of those trials are the two key milestones that we've got coming. Then if you were looking further into 2027, I would probably say further down that road, we'd be looking at the autoimmune disease space and when we start looking at that more seriously. Yeah. Michael, the only thing I'd have to add to that, and this is really a reminder to the group listening. Phase I dose escalation is very slow. This is the part of the work that I do that I don't like because I'm incredibly impatient. Like Michael said, we all want to know what the answer is, but we can't know what the answer is till we get there. Once we do this dose escalation and pick a dose that we will continue through the phase II studies, we will start to enroll larger number of patients without delays. We have pre-programmed FDA mandated delays to make this process slow to ensure that we have the correct safety metrics to protect patients. That's really important. The other thing that I forgot to mention about GTB-5550, the B7-H3 solid tumor TriKE. There are different expectations of solid tumor patients compared to leukemia patients. Leukemia patients are treated in the hospital where continuous infusion is appropriate. With the 5550 program, this is the first TriKE molecule that is given under the skin as a subcutaneous shot once a day. What we're hoping to do in the phase I study is another readout in figuring out the best dose to bring into phase II studies is what is the frequency. It's currently designed as Monday through Friday, weekend off, two weeks in a row, and then two weeks off, and then repeating those cycles. We're also trying to look at maybe Monday, Wednesday, Friday is more patient-friendly. All of this is being done in the outpatient clinic. If you have a solid tumor, all of that has moved to outpatient therapy, and this is the other very pivotal thing in the solid tumor program that we're starting to test now that I'm very excited about. Patients don't want to be in the hospital for their therapy. They want effective cancer therapy that they can do as an outpatient, and ideally, once we prove safety, that can be self-administered at home. Much like insulin given to diabetics or any of the new drugs that are out there today that people are starting to administer at home. We're very far away from that, and we have to get these metrics that Michael mentioned, but there are a lot of different delivery nuances that we're really excited about. We also have a pretty clear runway, which is really nice to see, by the way. Look, we do have a couple of questions from the audience, and I do want to be fair and give them some time. Let's just try to take a few minutes and answer as many of these as we can. I am going to pull them up right now. Okay. This is coming from an anonymous user. It says, "For GTB-5550, why did you decide to focus on prostate cancer patients first? And could this treatment eventually work for many different" Well, you did answer the second part, but why did you decide to focus on prostate cancer first? Yeah, Michael, let me give you, this is a very simple answer for us. Actually, this is a basket trial. All of the seven solid tumor diagnoses are eligible for enrollment into the phase I. We focus a little bit on prostate cancer because the PI of the study is a prostate cancer study, and there is a ton of unmet need in his clinic. But all the patients are eligible. We put on breast cancer patients, and we put on other patients as well. These kind of come in the order that we see them, but each of these individual cancers, once we go into phase II, will be analyzed separately. We are trying to get more shots on goal and figure out the opportunity of where this is going to be the most effective to go into therapy. Okay. From James Reese now. "When will GT Biopharma release efficacy data from the current GTB-3650 phase I cohorts, and what are they seeing at the higher dose levels?" It's probably for you, Dr. Miller. Yeah. Michael, do you want to answer the time point question? We are waiting for the metrics you mentioned, but maybe you can address that question. Yeah about release. As Dr. Miller explained, we have very prescribed timelines with regard to the dosing for the GTB-3650 blood cancer trial. In relation to timelines, given that blood cancer is a rare disease, there are not as many patients for that as there are for, say, breast cancer or prostate cancer. But we envisage that it will be relatively soon. Obviously, I cannot say on this program what exactly the timeline is because we have got to be a little bit careful because we are a Nasdaq-listed company. But it will be relatively soon, provided that we do not have patients who get too sick once we have enrolled and screened them. We move as quickly as we can within the prescribed timeframe set down by the FDA. Dr. Miller, this question is for you again. It is actually a general question, and it just says, "How long have you been working with GT Biopharma, and do you plan to stay for a long time? Yeah. I am not going anywhere until my CEO at home, meaning my wife, directs me further. But we have a plan at least for the next six or seven years. But I met GT Biopharma in 2015. They were looking for interesting, really pivoting molecules that could work in cancer, very different than chemotherapy and radiation. I have been working in the NK cell field since the late 1990s when I had my first faculty position at the university. So I have been doing this for a long time. I plan to continue doing it. As Michael knows, some of my aspirational ideas go beyond the limits of what we, the company, can do currently. But this is part of the goal, to come up with good ideas, to prove that they work pre-clinically, to bring things into the clinic as soon as possible. The part of my physician job that I like is seeing patients is a motivating factor to try to do as little as possible in preclinical models and just test it in patients, which is ultimately the most important. This has been my lifelong career. I hope to see it move forward before my family tells me it's time to take a rest. Amazing. Gentlemen, honestly, I can't tell you how much I enjoyed this really. I certainly hope we have a round two sometime in the near future as results come forward. I sincerely wish you both the absolute best of luck. It's truly fascinating, and in many ways, this really did make me miss my science days. Thank you for being here. Delighted, and thank you so much for having us, and thank you for all of the viewers for tuning in and being interested in our company and being able to share with them a little bit about what we've been doing and working towards. The one thing I would also just say is the thing that motivates everybody, and of course, Dr. Miller the most, is trying to find a cure for cancer, and that's vitally important. A round two would be very welcome, and we would look forward to that very much. Thank you. Absolute pleasure. Thank you, Dr. Miller. It really was a pleasure to meet you as well. Thank you. You as well. Thank you. With that, guys, that's all the time we have, and we'll wrap up today's conversation. Again, a sincere thank you to Michael Breen and Dr. Jeffrey Miller for joining us and sharing their perspective. Thank you to everyone who joined us live and sent in their questions. We really appreciate your time and your engagement. A replay of today's discussion will be available shortly on GT Biopharma's website and on InvestorTV's YouTube channel. You'll find the links in the chat below. On behalf of InvestorTV, thank you again for being here, and have a great rest of your day.