GT Biopharma Inc Aktie

Hi, everyone, and welcome. Thank you for joining us. I'm Michael Lubinsky, your host. On behalf of Investor TV, welcome to today's interview with GT Biopharma. Now 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 adviser 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. Now 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 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 like 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 like 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, click the red button.

Is that the correct screen?

It is right now. Exactly. Perfect. Thank you very much.

Okay. Great. Okay. So thanks, everybody. I'm delighted to be here. Just a little bit of an introduction on myself. As mentioned, I'm a consultant for GT Biopharma. I'm 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. And I'm going to take you through some of the journey about how we got there. So there's some just very big highlighted things that I wanted to start off with.

I think it's very clear that things have been changing in medical oncology. We started off with chemotherapy and radiation therapy. And I think what's going to drive 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.

And I think what we're trying to do overall in our platform that I'm 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'm not going to go through all of these. This has been a big market driver in a lot of different fields, and I'll go through the specifics as I go through the discussion.

So Michael, so 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 -- let's see, this was a molecule that was designed to target CD33, which is present on AML cells and 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 3 weeks in a row, and this was followed by a weekend off after each block of therapy.

We went through 6 individual dose cohorts. There were 2 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. So 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 3, day 10, and day 17 is the Wednesday while the infusion was going, all the cells at this peak areas is very highly activated and when you look on the Monday and after the next infusion cycle, you see that this is followed by a period of rest. And this gives you the see-saw 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, and that's represented by this right panel. So you can see, again, when the infusion is on at day 3, 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.

And then again, on day 8 after the first cycle of therapy after the second cycle here after the third cycle, you see this tremendous dose-dependent expansion of NK cells in the peripheral blood and here, we're trying to increase the immune cells that we think will be targeting to the cancers.

So this has been very exciting to us. Again, this trial...

Jump in for one second there, if you can go back for one slide. When you're saying NK cells, and I just wanted to say this more for the audience that may not be familiar, you're referring to natural killer cells, right?

Yes, that's correct. I use the abbreviation NK cells, but these are natural killer cells. And 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 from 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. And 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 easily -- easier to exploit. 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.

Appreciate the explanation.

So 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 4 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. Again, here is all the detail, which I'm not going to go through of the blast cell decreases that we saw in this trial.

So this was excited for us, and I'm going to go through really our future-looking platform. We now have a second-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 second-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.

And again, this is the trial that I already just reviewed to you as kind of the proof-of-concept data as to why we're moving forward into some of these different platforms. So 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'd like to tell picturely, and this is a very high electron microscope view of an NK cell recognizing a target.

And I'd 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. And 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.

So this is a picture of our protein. We call this Tri because there are 3 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. And 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 and IL-15 is a cytokine molecule that also stimulates the NK cell.

So, one of the unique aspects of the TriKE molecule is that there are really 2 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 Fv. Some of them are nanobodies, especially our B7-H3 is our first all nanobody or dual nanobody TriKE molecule.

And this is really just giving all of the platforms that are being explored preclinically. The clinical programs right now are CD33, the B7-H3 in solid tumors, and I'll talk a little bit for the CD19 about our plans to get into autoimmune disease. So let's first just in a very basic way, look at how these TriKE molecules work.

And before I start this visual presentation, what you're looking at here is a very tiny fluid microwell. The green cells here are AML cells that are living and the blue cell is a single natural killer cell or NK cell. And in the gray here is just the solution of this microwell containing our TriKE molecule. And 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.

And the process that's 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 killing of the NK cell in its tumor target. So 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.

So I already showed you early on that the first-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 didn't show it to you today, but we have all the translational data to back up that point. And really to our expectation, if you will, we saw very few side effects with this first-generation TriKE. We saw 1 grade 1 cytokine release fever -- cytokine release syndrome, which was a transient fever. This also occurred in the 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 side 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've done these pharmacokinetic studies. But remember, these have engaging molecules to bind to cell types in the body. And 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 and certainly under 3 hours.

So really, how did we make the pivot? Let me go into a little bit more detail. I'm trying not to be overly technical here. But human antibodies are shown in this cartoon here. And 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.

And what we know about llamas or sharks, or many other species is they have different antibodies called camelid antibodies. And these are defined by a recognition sequence called an antibody or a VHH or a single-domain sequence. So 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. And when we tested this in an animal model of leukemia, better tumor control is a lower dot on this curve.

So, there's a lot of tumor here when you give no treatment. When we gave our single-chain Fv TriKE or the first-generation TriKE, we saw a moderate degree of activity. But when we gave the camelid second-generation TriKE, we saw really far superior clinical activity, much better tumor kill. And this was really the rationale to only move this second-generation platform using the anti-camelid CD16 sequence. And we can go through questions if you have them.

So 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 recognizes CD16 and NKG2D. What sets us aside is 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 preclinically, we've tested in the laboratory.

And 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.

And our therapy is a protein therapy. It's not a cell therapy product. And 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.

So, 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 the 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. And 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. And in this reddish molecule here, this is the IL-15 costimulatory molecule to be brought to the immune synapse. So if you -- if you label this TriKE sequence with a red dye, you could stain cells, and this is picking up this red dye.

And 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. And 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.

So, 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. And in all of these conditions, we're giving either NK cells, NK cells plus IL-15 or NK cells plus our TriKE molecule.

And so this is the TriKE-containing sequence. This assay is ongoing for about 4 or 5 days. As you could 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 could see, the TriKE activates these NK cells to totally dive into the spheroid mass and to obliterate the red, which is the prostate cancer in this model. And we have many other examples of head and neck cancer and other tumors that shows exactly the same thing.

So really to complete up this portion and to move on, I wanted to tell you the flexibility of the platform. So, 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.

So we have developed a molecule that we -- I'm sorry, this click 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 the autoantibodies in autoimmune diseases such as lupus and myositis. And 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 drug into the clinic. And remember, the TriKE is a protein therapy to engage NK cells to specific targets. It's not a cell therapy. And we think that this will be easier and more exportable. So Michael, do you want to make a comment on the last slide -- last 2 slides here?

Sorry, go ahead, Michael. I just wanted just to keep in mind that I have a bunch of questions about these slides. But for me, personally, I'm going to wait to the end for all of my questions. Okay.

Okay. Thank you. So 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. And 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 an Associate Professor also out of the University of Minnesota as Dr. Miller is. And then we have Chris Henry, who is our CMC and Pharmaceutical Science consultant. And then our independent directors are Hilary Kramer, who's ex-Lehman Brothers and Morgan Stanley; David Mun-Gavin, who's ex Credit Suisse; and then Charles Casamento, who's ex-Sanofi, and he was on the business development side.

So, 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. And then 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. But just to demonstrate that some of the high-value transactions that have completed in the NK cell engager space.

You can see there dating back as far as 2018, there was a license transaction with Sanofi and Affimed, where Sanofi paid Affimed $96 million upfront with a 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 preclinical license deal, and it was $300 million upfront undisclosed milestones and 20% royalties. So 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 are on a very good path to do so, then commercially, it can be extremely rewarding for our investors.

Great. And I think that's great. Michael.

Thank you, Jeff.

Gentlemen, that was a fantastic presentation, by the way, very, very thorough. I'm going to get you to stop sharing the screen there, Dr. Miller. So 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. So that was really, really cool to see.

Dr. Miller, I thought you explained everything extremely well. So 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. So for someone that's brand new to GT Biopharma, how is this different from a traditional cancer treatment?

Yes, Michael, so that's a great question. And I think I highlighted a little bit. And 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 2 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 front-end 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 T-CAR 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 got a viral infection, you get fever, your muscle aches. We think that, that may happen with immune activation in these immunotherapies in this TriKE therapy. But we think those symptoms will be very self-limited and controlled and only last while the cells -- while the therapy is in the body.

It sounds like that's not really much of a comparison relative to the side effects of chemotherapy, right? I think most people would take that any day over the other. Sticking towards the science then a little bit. GTB-3650, I hope I said that right, is being 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?

Yes. I think, Michael, the unmet need is the end stage there of their disease. By the way, I'm a bone marrow transplanter by trade. This is how I got interested in leukemia. And remember, if you're 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. So when we started with GTB, having discussions with the FDA, even with our first-generation trial, we were very clear to them, and they were very clear back to us. When you're testing a Phase I agent that doesn't have any clinical data known, you have to start off with the worst patient.

And basically, the patient eligibility in this cohort is the keeping relapsed/refractory, failing standard therapy, and having no other treatment options. And I know it's hard for people to grasp, but that is the way the drug development starts. Once you show activity of molecules, you're allowed to work -- move it further up. And sometimes these newer therapies can become primary therapy. But we always start with the worst patients.

So just on that note then, because it's an early Phase I study, you're basically still trying to determine its safety. So as you're increasing dose levels, what have you basically learned about how patients are tolerating that?

Yes. Just like the first trial with the first-generation TriKE, I think we're 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're 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 second-generation TriKE is a different substance than the first-generation TriKE. We're kind of going back through that stage, and we're 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 -- so what would be the earliest indicators? Like what would you be looking for essentially that would say, okay, this is actually working.

Yes. I think the first thing would be a post-treatment bone marrow biopsy showing a decrease in blasts. I'm a hematologist. That's 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're doing in the second-generation trial compared to what we did previously.

The FDA in the previous study let us do one cycle of therapy. Now we're doing at least 2 cycles of therapy with the opportunity to get up to 4 cycles to hope to get a greater duration of the response if we see it. So that is built into the trial, and that's what we're going to be learning, I hope, over the next 6 months or so.

Fascinating. If we can switch gears for one second and talk a little bit about solid tumors. Again, the TriKE, GTB-5550, that targets B7-H3, right, which is a protein from my -- 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?

Yes. I think -- so, I'm 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's a huge differential in the population infected. There's potentially hundreds of thousands, if not millions of patients affected with solid tumors compared to this very small niche of acute myeloid leukemias.

Actually, it wasn't rare. It was expressed in that many different types of cancers, to be honest with you.

And just to be clear, this 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. So 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.

So this is why we think it's really such a great a pan tumor target because it's not specific to breast or prostate, but the other key piece is that B7-H3 is not present in your heart or your lungs or your skin or your liver. So we think this is going to attack the tumor, but not damage the normal tissues.

Michael, I wanted to kind of bring it over to you for a second. So what became kind of clear to me throughout the presentation was that TriKE is not really -- it's meant to be basically more than a one treatment candidate. So what makes this a real platform in your eyes? And where is GT Biopharma's biggest advantage?

So as Jeff very ably explained, the reason we call it a TriKE is because it's got 3 functional parts to it. And the reason it's a platform technology is that 2 of those functional parts remain constant and all we need to do is swap out what we call the binder part. So as Jeff explained, for AML and MDS, the binder is CD33. And then for the solid tumors, the binder is B7-H3. And then also, as he explained for autoimmune disease, the binder is CD19.

So we're effectively taking our TriKE, which we have more in second-generation form, and we are saying, well, we can use it across all of these other diseases. But it also -- as was shown in I think it was Slide 7, we have other TriKEs in our platform for other targets. So for example, what we call GTB-1050, which is for HIV. So we just -- 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 on to the tumor target.

So that really is platform technology. And 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. And 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 wasn't -- it was not a one-molecule solution. It was platform technology.

So if you have 2 programs now essentially that are enrolling patients. So as the CEO, I was just kind of curious about this. How do you decide where to allocate time, money, funds, resources? How does that work for you?

So it's a very, very simple answer to that question, Michael. We -- as you've rightly identified, we have 2 Phase I first-in-human trials, one for blood cancer, one for solid tumors. The one for solid tumors is -- it's targeting -- it's a basket trial, so it's targeting a number of different solid tumors. So as Dr. Miller explained, it's prostate cancer, breast cancer, bladder cancer, pancreatic cancer, head and neck cancer and lung cancer.

So -- and by the way, the solid tumor space worldwide annually is estimated to be worth $360 billion per annum. So whilst it's great to be focused on solid tumors, we also have -- given it's a platform technology, we're also the next going to be looking at autoimmune disease where the target is CD19. And again, the opportunity in disease market is estimated to be $115 billion per annum worldwide.

So to revert back to your question, we've got 2 trials ongoing, which we're very, very focused on and particularly with regard to making sure that we have correct financial resources. Though 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 it 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. So 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 2 excellent questions. And I think those are questions that should always be asked of the CEO and Chairman of any public company. So 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 like 4,000 employees, and I was on the Management Board of that firm. So you get to a point where you kind of -- 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.

And I got an opportunity then to -- so 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 3 years, having doubled the business in size. I also sat on a couple of hedge -- the Boards have a couple of hedge funds, which had also been clients.

And the -- I came across GT Biopharma with regard to one of those hedge funds with regard to potential investment. And we ultimately, the hedge fund invested. And having done my due diligence, I very much like the science. I like Dr. Miller, and I invested personally in the company. However, I -- 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 because as an independent director because bankers like people with resumes and backgrounds like mine, which -- so having already invested in it personally, that was a pretty easy thing to agree to. It made perfect sense to me. So I joined in January '21 as an independent director, and I remained in that role up until November 2021.

So we took the company through the uplift on the NASDAQ. And 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. So then -- 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. So I said, yes, sure, no problem. And then they said to me, 4 months later, would you also become the Chairman -- sorry, become the CEO as well as the Chairman.

And 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 kind of heading towards retirement. And anyway, we interviewed and looked at some potential candidates for the full-time CEO role. But every time we did my fellow Board members kind of said, but we really like the job you're doing, Michael. So we'd like you to stay in.

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 CEO. So look, it's really interesting. I actually haven't heard of too many that have invested in the company beforehand, and that kind of led you to this role. So I always say with biotech companies like the asset itself is important, but so is the team. And having a really, really strong team behind you is equally as important as having a good asset or a good drug in this case.

So look, there's no question, GT, 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. So to our investors, if you had to point to 2 or 3 things that people have to watch for this year. What would you say they are? And Dr. Miller, you can feel free to jump in if you have something to say about it as well.

So, 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 a prospective investor, I would always say the data. You've always got to see what the results are. And we have obviously -- 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.

So, 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 2 key milestones that we've got coming. And then if you were looking further into 2027, I would probably say further down that road would be looking at the autoimmune disease space and when we start looking at that more seriously.

Yes. And 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 until 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 a larger number of patients without delays.

We have preprogram FDA-mandated delays to make this process slow to ensure that we have the correct safety metrics to protect patients. So 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.

And 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, 2 weeks in a row and then 2 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 a 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 have a pretty clear runway, which is really nice to see, by the way. So we -- look, we do have a couple of questions from the audience, and I do want to be fair and give them some time. So let's just try to take a few minutes and answer as many of these as we can. So I'm 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?

Yes. And Michael, let me give you this is a very simple answer for us. Actually, this is a basket trial. All of the 7 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 he -- 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. And so 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 on therapy.

Okay. It's from James Rev Shark. When will GTB 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.

Yes. Michael, do you want to answer the time point question because we are waiting for the metrics you mentioned, but maybe you can address that question.

So as Dr. Miller explained, we have very prescribed timelines with regard to the dosing for the 3650 blood cancer trial. And in relation to timelines, given that blood cancer is a rare disease, then 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. But obviously, I cannot say on this program, what exactly the timeline is because we've got to be a little bit careful because we're a NASDAQ-listed company. But it will be relatively soon provided that we don't have patients who get too sick once we've enrolled and screened them. So we move as quickly as we can within the prescribed time frame set down by the FDA.

Dr. Miller, this question is for you again. It's 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?

Yes. So I'm not going anywhere until my CEO at home, meaning my wife directs me further, but we have a plan at least for the next 6 or 7 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've been working in the NK cell field since the late 1990s when I had my first faculty position at the university. So I've been doing this for a long time and 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 preclinically 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. So 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. And I really certainly hope we have a round 2 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. So 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. So Orion too would be very welcome, and we would look forward to that very much. So 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. And 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. And 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 Investor TV's YouTube channel. You'll find the links in the chat below. On behalf of Investor TV, thank you again for being here, and have a great rest of your day.