We're back. The next company on today's RedChip Biotech Investor Conference is GT Biopharma, ticker GTBP on the Nasdaq. Presenting today will be Michael Breen, the Chairman and CEO. Michael, are you there? I'm here, Craig. Can you hear me? I can hear you loud and clear. I see you have your presentation already up. Yep. That is just what we wanted. Thank you very much. Let me get some formalities out of the way. First, I'll read the safe harbor statement. This segment may contain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements pertaining to future financial and/or operating results, along with other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management, constitute forward-looking statements. Any statements that are not historical facts should also be considered forward-looking statements. Of course, forward-looking statements involve risks and uncertainties. To our viewers, you can ask a question at any time by pressing the Q&A button at the bottom middle of your Zoom window. Then there will be a text box. You can type your question in and send it to us. Michael, if you're ready, please go right ahead. I'm ready, Craig. Thank you very much for that introduction. Let me just announce all of my viewers. Our company is GT Biopharma, Inc. We're listed on Nasdaq under the ticker GTBP, as you can see there on the first page of our presentation. We are an oncology research company. We use NK or natural killer cell therapies to treat cancer and autoimmune disease, among other different ailments. If we just move on to our next page of the presentation. You see, there, obviously, that's the disclaimer, which Craig has already kindly covered off for me, so I won't bother with that too much. Let me get just straight into it. As I said, our company is a natural killer or NK cell engager company. That's the main thrust of our research and the science that we have harnessed. The body has its own natural killer cells. When it comes to cancer and autoimmune disease, something has basically gone wrong in the body's natural immune system that it no longer operates as it should and fails to either identify and/or kill either the cancer cells or the autoimmune disease. What our technology does is it essentially engages the body's natural killer cells to give it greater activation, proliferation, and persistence. In so doing, it effectively, what we colloquially call, it turbocharges the body's natural immune system to overcome various different cancers and also, as explained, autoimmune disease. It's a protein therapy, and as I said, it harnesses the body's natural killing part, the NK cells. Please understand it's not an NK cell therapy. That's a very different thing, even though the names sound very similar. Ours is an engager, and it engages the natural killer cells to, as I say, help it activate, proliferate, and give it persistence. Our technology is what we call a platform technology. Our molecule, our drug, has three functional parts to it. It has a CD16 part. It has something called interleukin-15, which is what we call a payload that actually helps to provide various ways of killing the cancer cells. Then we have what's called a binder. As I say, it's got three functional parts. When I say it's a platform technology, that means that essentially the molecule stays fundamentally the same, apart from we swap out the binder element of the molecule depending on which type of cancer or autoimmune disease we're trying to target. For example, in our original proof of concept phase I, first-in-human trial for blood cancer patients for acute myeloid leukemia, the target was CD33. I'll come on to explain what we did in 2021 with our first blood cancer trial. I'll also talk a little bit about our second-generation blood cancer trial that we're currently halfway through. I'll also talk about our solid tumor trial, which we're about to commence. As I say, we had a blood cancer trial in 2021 for AML, and I'll run you through the different results in relation to that. I'll explain how it differs and how the second-generation molecule has significantly improved upon the first-generation molecule. We have a number of different candidates, as I've explained. We've got a blood cancer ongoing trial, we've got a solid tumor trial coming up, and then we also have an autoimmune disease candidate for the treatment of lupus and other autoimmune disorders. You can see there at the bottom, we talk about the management team and our depth of expertise in all stages of oncology drug development, and the fact that we, as of January 2026, had approximately $9 million in cash at bank, which is sufficient to take us through to Q4 of this year. If we move on to the next slide. As I said, I'm going to talk a little bit about our phase I trial for blood cancer for AML and MDS, which we conducted in 2021. This has subsequently been supplanted. Just to give you a little bit more detail, we had six different dose levels or six different cohorts ranging from 5 mcg per kg per day at dose level one, all the way up to 150 mcg per kg per day, which is dose level six or cohort six. You can see here that there were three blocks of 96 hours' worth of infusions, with a three-day rest in between each of the blocks. Six dose levels and an escalation based on all the way through up to day 28. If we move on to the next slide. Here, this is a really, really good slide to demonstrate to you. Panel A on the left shows you the NK cell activation. You can see the peaks on day three, day 10, and day 17. The different colors you can see there. Blue represents the 5 mcg per kg, red is 10 mcg, 25 mcg is in yellow, 50 mcg is in green, 100 mcg is in black, and 150 mcg is in gray. You can clearly see that as the infusion is ongoing, sort of halfway through, that you get the significant peaks, which demonstrates that the drug is doing exactly what it's supposed to do, which is to activate the natural killer cells in the body. Panel B on the right, again, the same principle, but it's a different thing. It's measuring the increase in the absolute number of NK cells during treatment. Again, you can see that on day eight, day 15, and day 22, you've got those peaks in terms of proliferation, the increase in the absolute number of NK cells. Clearly demonstrates that our drug, at least in our first-generation molecule, demonstrated that it did exactly what we were hoping it would do, which is that it gave activation and also increased, in terms of the proliferation. If we then move on, and that's obviously an endogenous NK cells. Now, here are the results, which are very, very interesting indeed in terms of the different patients treated. You can see that throughout the various different cohorts, we got a significant reduction in blast count levels in the bone marrow. You can see patient number five, who was treated with 25 mcg per kg per day, achieved a 33% reduction in bone marrow blast count. Patient seven, who was treated with 50 mcg per kg per day, got a reduction of 61.7% in bone marrow blast count. Patient nine, who was treated with 100 mcg per kg per day, had a reduction of 63.6% in bone marrow blast count levels. Patient number 11, who was treated with 150 mcg per kg per day, had a reduction in bone marrow blast count levels of 50%. It clearly demonstrated that for these 12 patients treated, as we got to the higher activation levels for a sufficient amount of drug. From 25 mcg all the way up to 150 mcg, we clearly demonstrated very significant reductions in bone marrow blast count, which is a very positive signal and exactly what we were hoping for. This, as I said, relates to what we now refer to as our first-generation molecule, which was GTB-3550, for the phase I trial in 2021. If we move on to the next slide. As I said before, it's a platform technology, which means that we just swap out the binder depending on what kind of cancer, autoimmune disease or other disease we're trying to target. You can see here that we have a rich and deep pipeline. We're now, as I said, in our second-generation molecule, halfway through phase I trial for blood cancer. We've already treated seven patients, and you can see there that the target is CD33. Then that's GTB-3650. Then, as I mentioned earlier, the solid tumor phase I trial will be commencing very shortly, and the target for that is B7-H3. I would also highlight that. Pretty much 90% of all solid tumors highly express B7-H3. We know that a lot of other oncology research companies have gone after B7-H3 as a target. It's a well-regarded, good target that ought to produce good results for solid tumors. We're very, very excited about that. You can see some of the other things that we have in our pipeline. We've got GTB-6550, where the target is HER2. Again, that's for solid tumors. Finally, I'll just highlight GTB-7550, where the target is CD19, and that's for autoimmune disease. CD19 is a very well-regarded, go-to target for autoimmune disease. As I say, we've got a rich and deep pipeline because we have a platform technology where we simply swap out the binder for a different binder, depending on what kind of cancer or other autoimmune disease we're targeting. We move on to the next slide. This is just again, to try and highlight exactly in a cartoon style that we call our molecule a TriKE. It's a trispecific natural killer engager nanobody platform. As I said earlier, it's designed to activate the endogenous NK cells to target specific cancer cells. It's well regarded that it's got great potential for less toxicity than other cellular therapies, such as CAR T therapy, and also less cytokine release syndrome. If we move on to the next slide. This again is a cartoon style just to try and blow up, if you like, the structure of the three parts of the molecule. That's why it's called a TriKE, trispecific. You can see here you've got an anti-CD16 nanobody. That binds a CD16 receptor onto the natural killer cells or the NK cells. You've got, as I said before, the interleukin-15 or IL-15, which acts as a cross-linker that binds the IL-15 receptor onto the NK cells also. The final part, depending on what type of tumor cell you're attacking, you've got the tumor-associated antigen, which binds onto the actual cancer cell or autoimmune cell itself. As I say, it's a tripartite molecule, and you can see there very clearly the function of each part of the three-part structured molecule. We move on to the next slide, please. This is just again, to further emphasize the modular platform and just to highlight the different types of targets or binders that you would utilize depending on autoimmune disease, breast, or different solid tumors and blood cancers. Just again, to re-emphasize, B7-H3 is for solid tumors, HER2 is for breast and gastric solid tumors. PD-L1 is a pan-tumor target, and we've even got an HIV target also. I said earlier, there's a CD33 for blood cancer, and also CD19 for autoimmune. Next slide. This here you've got, this is actually a microwell, and the green is the blood cancer, and the sort of blue is the TRIKE itself. That's the killer. You'll see that it will target each of the green blood cancers. They will turn red once they've been killed by our molecule in blue. Here's the first one killed, then you see the second one, and it's a serial killer. It keeps targeting, seeking out the blood cancer until they've all been killed. You'll see that in a moment, it will attack the final green blood cancer. As I said, our molecule is blue in there. You can see that it's killed the third bit of blood cancer. As I said earlier, the whole idea is that our molecule drives activation of the body's natural killer cells. It's the immune system that we're trying to turbocharge, and it helps with activation, proliferation, and natural killer cell persistence. Each of those is obviously very, very important to ensure that you produce enough of the natural killer cells, having activated them to overwhelm the cancer and kill it, and give it sufficient persistence to keep killing the cancer until it is all eradicated, as you just saw in that video. I think the video, as always, is much better at clearly explaining so that folks understand very easily how our drug works. It's always much easier when you actually see it in action to see that it actually does work and kills all of the cancer. Next slide, please. This is just talking about our first-generation molecule, which has now been supplanted by our second generation. I'll come on to explain in a moment how it differs. Again, it's just repeating some of the results that we achieved in our trial for blood cancer in 2021. Next slide. We're going to talk a little bit about our second-generation molecules now, which are for blood cancer and solid tumors. We move on to the next slide. Camelid and nanobody technology. You can see here that the IL-15 or interleukin-15 has got some of the characteristics from camelid characteristics of mammals which come from the llamas, camels, and alpaca families. I know it might sound at first to be a little bit strange, but if you think about it, llamas, camels, and alpacas exist in very, very harsh environments, so either in mountainous regions or deserts. The result of that is that they have extremely robust immune systems. That's why we've taken some of the characteristics from those to further boost and give our molecule better efficacy moving forward for second generation. We move on to the next slide. This is just to talk a little bit about our approach versus some of our competitors. As I said, our main differentiator is the IL-15 or interleukin-15. We have found a way to fold it over into our molecule. Interleukin-15 is what we would traditionally refer to as the main part of our secret sauce in our molecule. We've found a way to deliver that IL-15 to have a very effective payload in terms of its interaction with the body's natural killer cells to give proliferation and persistence. Next slide, please. Here is a very, very good video showing on the extreme right. You've got an actual prostate cancer, which is in red, and on the extreme right you can see it's been hit with our B7-H3 TriKE molecule, and it turns black when it's all been killed. I don't know if we can show that one just one more time, just to further emphasize what happens with NK cells alone on the left, NK cells and just IL-15 in the middle, and then our molecule is on the extreme right, and that shows you that the other two don't really do anything to the prostate cancer until our TriKE molecule gets it and, as I say, shows it being all killed in black. That, again, just is to further emphasize that our molecule does work because this is actually prostate cancer being killed in a microwell environment. Next slide, please. I want to talk a little bit about autoimmune disease. The solid tumor market is estimated to be around about the $362 billion per annum worldwide, whereas the autoimmune disease market is somewhere in the region of $115 billion worldwide per annum. Both the markets, by any stretch, are vast markets, with enormous commercial opportunity. As I've said earlier, we hope to be announcing the opening of our solid tumor basket trial very shortly. That will cover all of the main cancers, solid tumor cancers, so that will be prostate cancer, breast cancer, ovarian cancer, head and neck cancer, lung cancer, bladder cancer, and pancreatic cancer. Seven of the major cancers. I would also just highlight that prostate cancer affects one in seven men worldwide at some point in their life, and breast cancer affects one in 12 women. Very, very prolific and therefore very, very important that we do find some sort of a resolution for a more humane way to treat cancer in solid tumor and blood cancer form. As I say, solid autoimmune disease. We move on to the next slide. Our candidate is 7550. I should also just highlight that our second-generation molecule is estimated to be, from all of our preclinical work, somewhere between 10x and 40 x more potent than our first generation. We're very excited also to have a resolution for autoimmune disease. We're hoping to start work with regard to manufacture of our autoimmune disease drug later in this year, early next year. Certainly everything we've seen preclinically is very exciting and very, very positive in terms of the potential. I think the fact that it's, again, camelid and nanobody technology, it's very exciting that we'll get something that will be very helpful with regard to things like lupus and other types of autoimmune diseases. If we move on to the next slide. This is really just to set out who the main players are in our company. That's myself on the extreme left. Alan Urban is our CFO. Dr. Miller, I should highlight, and Dr. Martin Felices are the two main inventors of our science out of the University of Minnesota. It would be no exaggeration to say that Dr. Miller is, without question, one of the key opinion leaders worldwide in the NK cell engager space. He's been at this for 25 years. He speaks all over the world on the subject. He has 170 peer-reviewed articles, and he's a director of the Masonic Cancer Center out of the University of Minnesota. Dr. Martin Felices is assistant professor there at the university, and again, he is very highly regarded in the space of NK engagers generally. Then we have to the right, we've Hilary Kramer, David Mun-Gavin, and Charles Casamento, who are independent directors. I think I'll leave it at that and then hand over to any questions that we may have. I'll maybe stop sharing the screen. Thank you very much for that excellent presentation. We are now live again with your questions, and we've got a lot coming in here. What is the simplest way to think about why the TriKE platform could matter in oncology? I think the simplest way really, Craig, is it's a very humane solution because you're taking the body's natural immune system, you're giving where it's failed for whatever reason to work as it was originally designed, and you're effectively turbocharging it to overcome whatever the disease is that we're specifically trying to target. As I've explained, it's a platform technology with different targets, and it gives the body's natural immune system the ability to kill cancer and also things like lupus. I think it's very important just to say that, in that way, you don't have to subject yourself necessarily to things like chemotherapy, where you poison your blood, or radiation, where you effectively burn the flesh, or even surgery. This is a more humane resolution for cancer. Now, the GTB-5550 IND clearance seemed like an important step. From your perspective, what does that milestone validate for the company? We've already, as I said in the presentation, we've already validated for AML, blood cancer. We know that the molecule works because you've seen in those videos for both blood cancer and also prostate cancer, where you've seen them being killed by our TriKE molecule. In terms of validation, getting clearance from the FDA for the solid tumors is extremely important. We believe that we are going to, through this phase I trial, which is about to commence, demonstrate very clearly the same sorts of results that we have achieved with our first-generation trial in 2021 for blood cancer. Another question about GTB-5550. It's moving into solid tumors, and how are you thinking about the size of the opportunity if early clinical data are supportive? This truly is why it's really very exciting. The first thing I'm going to say, again from a human basis, Craig, solid tumor cancers are very, very prolific. As I said in the presentation, particularly things like breast cancer, which affects 1 in 12 women, and prostate cancer, which unfortunately affects 1 in 7 men. The market is vast. The estimate, as I said, is somewhere in the region of $362 billion worldwide annually. I think that if we achieve a signal in just one of these solid tumor cancers in the trial, that will be completely transformative for our company. Given what we've achieved for blood cancers, we're very optimistic what we might achieve in the data for solid tumors. Michael, we've got 30 seconds for this last one. How should investors think about the progress of GTB-3650 and GTB-3550 in terms of validating your broader platform? 30 seconds. I think we've already achieved that, to be honest, in terms of validation, because you saw the bone marrow blast count reductions for 3550. The second-generation molecule is much, much more potent. It's got camelid technology and nanobody technology, which gives it better binding efficacy. We're very, very optimistic with regard to what will be achieved in the second half of our blood cancer trial later this year. Perfect. Thank you very much, Michael. Great presentation. For more information about GT Biopharma, reach us at 1-800-REDSHIP or write us at GTBP@redchip.com. Michael Breen, thank you very much.