Good afternoon, everybody. Thanks for joining us at the 46th Annual Canaccord Genuity Growth Conference here in Boston. I'm John Newman, one of the biotech analysts here at the firm. Very excited to have TuHURA with us today, and the CEO, Jim Bianco. Jim? Thanks. Good afternoon. Before we get started, as typical with presentations of this variety, we will be making forward-looking statements, and we refer you to our SEC filings for more information on the company. We are a phase III immuno-oncology company. We have three distinct technologies and therapeutics, and we're focused in two strategic areas: primary resistance and acquired resistance to cancer immunotherapies. Just by way of a summary, we have a phase III trial that's ongoing, accelerated approval, frontline Merkel cell carcinoma. I'll walk you through that, both the technology and where we are from the status. We expect to complete enrollment in the second half of next year and top-line data about the end of the year, early 2028. We'll show you the trial design that we worked out with the Oncology Center of Excellence. We do not need a confirmatory trial. This has embedded a key secondary endpoint that would satisfy that requirement. Just to manage the risk of all of the changes at the FDA, we have a Special Protocol Assessment agreement with the agency for that study. Our second asset is a VISTA- inhibiting antibody. We're the only company that is focusing that type of therapeutic in so-called molecularly defined subsets of AML. We're about to put that into a phase I-B/II study. Craig Tendler, who's one of our board members, Craig ran Global IO for J&J for 25 years. He brought bleximenib into clinical practice, clinical development before he left. So Craig is taking on the leadership for moving that program through his phase I/II effort. We'll close it out briefly talking about a really novel class of antibody-drug conjugates. We're going to have proof of concept in the first set of animal models later this year. But we are the only immune targeting antibody-drug conjugate in pre-clinical development. We have a couple of meetings that we're presenting at in the second half of the year. Lastly, our largest shareholder stepped up for us, provided us with a $50 million credit facility. This is interest only. It's a five-year term. I'll go through a little bit more of detail, but clearly for us, a very non-dilutive source of operating capital from somebody that owns 18% of the company. Obviously, his interest is not to be diluted, but playing the equity play in the company in terms of the true value as this portfolio moves towards approval. With regards to some upcoming milestones, as I mentioned, the phase III top-line result is late next year, early 2028. We are going to talk a little bit about at ESMO mini-conference on some of the preliminary results. It is not really a basket trial. This is in the first-line treatment of patients with deep-seated tumors, so we are doing an IR-guided trial for IFx, first-line Merkel cell carcinoma plus pembro. They would not be eligible for the inclusion criteria for the phase III. I mentioned starting the mutated NPM1 mutated AML study. We should start that. We should get FDA clearance next month, and then start the trial shortly after that. Lastly, we will have our first proof of concept data. We should have some pretty interesting data. I am pretty sure ASH will take a number of the abstracts that we submitted this year. All right, let me tell you a little bit about Merkel cell carcinoma. Not a lot of people know about this skin malignancy, if you will. It is unlike basal cell, unlike melanoma. This is not a, quote-unquote, "immunologic or immunogenic tumor." It is a very aggressive polyoma viral-driven tumor, so it is a viral oncogene. About actually 3,900 new cases a year, 25% of those patients will present with local disease that are treated with curative intent and given checkpoint inhibitors. But 75% of these patients will present with advanced metastatic disease, Keytruda and/or avelumab as the frontline standard of care. Importantly, half of these patients will not respond. If they do not respond, there is no alternative therapies. That is the addressable unmet medical need population that we went after, and I will show you some of that data, why we think it could be successful in a clinical study. We are going to try to increase the response rate to Keytruda in the first-line treatment of patients with advanced or metastatic Merkel cell carcinoma. Even though it is only 3,000 patients in an addressable target population, it would become the new standard of care if this trial is successful. We think that even though it is a relatively small number, i.e., an orphan indication, it could still be commercially attractive given the fact that you will replace the current standard of care with a new standard of care. All right. Let me tell you how IFx, this technology works. How do you overcome primary resistance? The basis by which tumors, 80% of tumors do not respond to checkpoint inhibitors is that you do not have an activated immune response against the tumor. If you do not have activated T cells, you do not have activated checkpoints to inhibit. There is no checkpoint to release T cells to become amplified and proliferate and have anti-tumor activity. The whole industry has been searching for how do you make a tumor look foreign to your immune system. You need to have a specific immune response against the tumor. There has been a lot of approaches of activating immune responses that are systemic. They do not really work, right? What IFx does is it takes a plasmid DNA that encodes for a bacterial protein. You inject it in a tumor, and that bacterial protein is transported to the surface of the tumor cell. Now the tumor cell has a bacterial protein which has a very specific pattern, molecular pattern or motif. Your innate immune system has cells that have evolved alongside of pathogens, right? It is your first line of defense when you are born until you start having exposure to foreign antigens. In this case, this is a strep protein. TLR4 on your innate immune cells will recognize that as being foreign, and it will engulf, i.e. phagocytize, the entire tumor cell, thinking it is a bacterial protein. What you have done now is you have packaged all of the foreign proteins that are in that tumor, and it is now being presented to newly formed T cells and B cells. You activated an adaptive response with activated tumor-specific T cells and tumor-specific B cells. We know that because in our clinical studies, these patients will make antibodies that recognize the viral oncoproteins and a whole slew, a whole host of other neoepitopes that previously they did not recognize. Then, of course, you will see the data that they will respond to checkpoint inhibitors that they previously failed. This was the basis for the discussion with the FDA. I am just going to go through it briefly. It was a two-stage trial design. It was Merkel cell and squamous cell. We are going to focus on the Merkel cell just because that is where most of the data was generated. IFx is given weekly times one, two, or three weeks. We wanted to see if we had an escalation in the immune response by more repetitive dosing. It is given into skin lesions or nodal lesions or subdermal, not deep lesions, because it is a tuberculin syringe, you cannot have access to it. 23 patients enrolled, 13 had Merkel cell. We will show you how that worked out in terms of responses. Each of the patients with Merkel cell on this slide came in with primary disease, advanced metastatic, were checkpoint inhibitor naive. They received either avelumab or pembrolizumab, right? Either a PD-1 or L-1 inhibitor, and they failed it, meaning they progressed with the first time given a checkpoint inhibitor. That is the PD. They came off the checkpoint inhibitor, and they received IFx in up to three lesions weekly times one, two, or three in each of the cohorts. 28-day observation period. Then they went back on the same class of checkpoint inhibitor without IFx, and you can see the responses that were demonstrated here. The first patient had a CR that lasted 23 months. Second patient, I am going to show you that, had a pathologic CR and a PR that was out 33 months. You can see the duration. Some of these were ongoing at the time of the study cutoff for the data. There were three patients who did not respond. I could tell you antibody-wise, they did not recognize some of the epitopes that the other patients that had antibody generation, i.e., they may not have expressed effectively the protein. It is kind of cool translational work, but what is really cool is the fact these patients are having meaningful, durable clinical responses. This patient in the left panel, this patient got three months of Keytruda, pembrolizumab, developed that large lesion where the blue arrow is in the thigh. That lesion was injected with IFx weekly times two. This was dose level 2. Patient was put back on Keytruda, and you can see that large lesion cavitated. It is about an 80% reduction, was classified radiologically as a PR. It stayed that size for a few months. They excised it, and it was reclassified as a pathologic CR, which was ongoing at the time the data cut off at 23 months. Second patient, we are just showing you when people talk about abscopal-like effects. This patient, again, had two months of Keytruda. By definition, primary resistance is failure to have a response within six months of exposure to a checkpoint inhibitor. So within two months, progressed rapidly, developed these very large, bulky lesions in the abdomen. Those are the blue lines. They had some subdermal lesions that were accessible, so they got injected with IFx times two, was rechallenged with the same class of checkpoint inhibitor, and again, had about an 80% reduction in the so-called reference lesions, PR, and that was ongoing at 19 months. We took this to the FDA, and we are in the same division that cell and gene therapy, Replimune, and the rest are in. But we asked the FDA if we can bring in somebody from the Oncology Center of Excellence. Having worked at a division level and dealing with the office level coming in at the last minute and making changes to essentially what you needed to be approved, so to speak. We started right out at that level. And Dr. Theoret was the deputy director at the time. We showed him that data, and he said, "We have this Project Front Runner initiative, and you are able to show encouraging results that if patients are progressing, they are failing frontline therapy, you can salvage them and get durable responses." So they encouraged us to move it into the frontline, with the theory being, if you can prevent them from progressing, that may actually have more of a benefit to a patient than allowing them essentially to develop resistance and/or failure of the primary treatment. The study design that we agreed to is 118 patient randomized placebo and injection control trial. So it would be IFx as an adjunct to pembro given on its current dose and schedule or pembro plus a placebo injection. We said 21- 25 sites. We are now thinking more in the 40 site range, which we have about 30 of those up enrolling. 118 patients, one-to-one randomization. But here is the part that was a surprise from the FDA. Marc Theoret came back, and he said, "You have durable responses with pembro." Right? I mean, 75%, if they have a CR, still be a CR at two years, and half have a PR, they are still a PR at two years. If you can take the response rate from 50% to 75%, it is actually 56% to 75%, is how it is powered, you should have a separation in the curves with regards to progression-free survival. And if you put PFS in as a key secondary endpoint, you can get accelerated approval for the response rate endpoint, and then while the data is maturing, when it hits PFS, that would satisfy the requirement for a confirmatory trial. So at the time you are submitting a BLA and receiving approval, you do not have to have ongoing a confirmatory trial, which is the standard model for accelerated approval, i.e., Replimune. Just look at any accelerated approval recently, and typically this endpoint is survival. In this setting, because there are only single-arm studies in the literature, PFS was considered to be of clinical benefit as opposed to a surrogate, and that would satisfy that requirement. Just to make sure that they don't change their mind, he actually encouraged us to do a SPA with the FDA, with the division. We had that study being conducted under an SPA. Again, we're pretty excited about actually having the FDA work with us on a novel design that saves not just time, but a considerable amount of money, and more importantly, really does manage or even mitigate some of the risk associated with a confirmatory trial. I'm going to shift gears. I'm going to talk about TBS-2025. This is a VISTA-inhibiting antibody. In June of 2025, we acquired Kineta to gain rights to their VISTA-inhibiting antibody. This drug was examined in a phase I study as monotherapy in solid tumors, about 44 patients, mono or in combination with pembrolizumab. You may be familiar that Sensei did essentially the same thing with their VISTA-inhibiting antibody. Hummingbird outlicensed theirs, and that company did essentially the same thing. None of them had a response. Why? If you look at the biology of where does VISTA appear naturally in your body, it is a negative checkpoint, meaning it is a regulator of resting cells. It appears to be expressed mostly in the myeloid compartment in the bone marrow, and it's the only checkpoint that's expressed on a resting T cell. Its purpose is to keep T cells from being activated, and its purpose is to keep your neutrophils and other myeloid cells in a state of homeostasis. Why is this relevant to talk about? In 2023, the literature for VISTA really started to grow, recognizing that two of the most frequent mutations, FLT3-ITD and NPM1, I'm sure everyone's familiar with NPM1, with the whole menin inhibitor space, it drives the expression of VISTA on leukemic cells and is believed to be the primary mechanism by which you do not have an immunologic response to AML. That is why you have treatment failure, that is why you have low response rates, and I'll show you. This is patient data in the bottom panel. If you look on the left, that's from The Cancer Genome Atlas for AML. The only checkpoint that is highly expressed is VISTA, and VSIR is the gene. If you look at all the activated checkpoints, none of them are present. In fact, none of those drugs worked in the setting of blood-related cancers like leukemia. The middle panel shows you that if you have FLT3 NPM1 mutations, that's highly upregulated by those mutations. The right-hand panel is from patient samples, the patients whose AML cells expressed or didn't express VISTA. You can see the overall survival on the high expressers obviously was significantly lower. This is a really novel target to go after for a molecularly defined disease. There seems to be a cause and effect, just like NPM1 drives menin to drive leukemogenesis. If you inhibit using a menin inhibitor, you can salvage about 20% of those patients. We went to the FDA, and the FDA essentially gave us the same pathway that they gave to menin inhibitors after menin inhibitors. You take patients, and we're focused on this molecularly defined subset, NPM1 mutated AML that have failed menin inhibitors, will go on to a trial. It's an abbreviated dose escalation because we used the PK/PD to justify a starting dose from the solid tumor data into this liquid tumor application. Again, about 75% of these patients are becoming off menin inhibitors for not responding to them. That's most of the population stream that will come into the phase I study. It represents an unmet medical need, and they were clear that they would consider a response in this group morphologic leukemia-free state. That's essentially an incomplete CR. It's below CR, CRh, and CRi, which we found was interesting. Obviously, it's an unmet medical need because after menin inhibitors, there are no subsequent approved or effective treatments. There's a second stage to the study. In phase II, we'll do dose optimization, and at that point, when we have the RP2D, phase II dose, we can go into a combination study with menin inhibitors. All right. I'm going to close it out here. Bispecific, bifunctional, everyone thinks of kind of a hybrid antibody with two different targets. This is the first class of immune-modulating ADCs. We don't target a tumor. These are not internalized. They're not cytotoxic. They're not cell cycle controlling targeting payloads. Instead, we are the first group to identify, and soon to be announced patent in other presentations, that the delta opioid receptor is highly expressed on myeloid-derived suppressor cells, M2 macrophages, and Tregs, the three normally immunosuppressive cell types that the body makes. If you target the delta receptor with a small molecule inhibitor, you can shut off the expression of multiple immune-suppressing genes and immune-controlling chemokines. You can reprogram the immunosuppressive phenotype of Tregs, macrophages, and MDSCs. If I now link a VISTA-inhibiting antibody to that, you now have the ability to change potentially the immunosuppressive phenotype of the microenvironment, in this case, the bone marrow, and at the same time, allow quiescent T cells to be activated. You can think of the reverse. If I have an activator of a delta opioid receptor, I can make Tregs more immunosuppressive. Instead of doing allogeneic Tregs therapies, you can do pharmacologic small molecule ways to modulate autoimmunity. It really does have both a cancer application and obviously the flip side, autoimmune, inflammatory disease, et cetera. We're focused on the cancer side of it. You can read into it that companies may be focused on the other side of it. We really own this space, so to speak. We had a patent issue in less than two years. There is no prior art. There's no other literature. This was recognized by the Scientific Review Committee at ASH. We had an oral presentation last year. I'll venture to guess that we'll have one this year given some of the new information that we have discovered about the coupling of this receptor in immune response. I don't want to focus on MDSCs. I already mentioned that. Some of the things that we're looking at coming up, the orphan drug division of the FDA is very tardy. We should receive orphan drug designation for IFx in Merkel. We should receive it for VISTA and AML. We have two series of patents that are really core technology. They're seminal patents both for VISTA and for the delta opioid receptor antagonist. That should come out in the fourth quarter. As I mentioned, we should be able to start the phase I-B/II study in AML. We have this IR study, as I mentioned, with Keytruda for deep-seated Merkel cell carcinoma, a barometer of what you might expect to see in the phase III study in terms of responses. We're thinking of putting together a mini symposium at ESMO. We certainly will report the preliminary results on the first three or four patients that we have. I think proof of concept with the ADCs, and that's pretty much a full palette for the next four or five months. Five months? Four months. That's it. I think we're good. Great. Thanks very much, Jim. We've got a couple of minutes left here. I've got a number of questions that I could ask, but just wanted to see if there's any questions from the audience first. Okay. One question I have is, with the IFx 2.0 program, you've chosen to advance into the first-line setting. You've chose to do your work there, versus checkpoint-resistant patients. Just curious as to how you came to that decision to go straight to the frontline versus maybe second-line patients. Right. Our initial discussion with the division was just like Replimune, you're in second line, study in second line with progressive disease. We work differently than oncolytic viruses, right? Oncolytic virus relies on a tumor to explode, to release tumor neoantigens, and then your immune system to find them and potentially overcome that resistance. When we brought this to the oncology office, the Oncology Center of Excellence, the Project Front Runner initiative saw the potential that you had high rates of response on rechallenge, right, to a checkpoint inhibitor after your drug, and they were very durable. That if you prevented patients from progressing, and you do that in a randomized fashion, you would take away two aspects. You'd take away the uncertainty of a single-arm trial in patients in the relapse setting, i.e. what RP1 had to deal with, because you have a randomized comparator arm. And two, if you're correct, i.e. you do get a 70%+ response rate in patients before they fail the therapy, then you would establish a new standard of care unequivocally because you have a placebo-controlled trial, that gold standard for phase III design. That is why we moved into the frontline setting. I can tell you most companies like Replimune would feel that this is where you generated the data in second line. The biology would suggest that you should do no worse than what you did in the progressive setting. Teleologically, you should do better if you prevent resistance from developing because you're allowing them on the first shot to have an immunogenic response against the tumor. Okay, great. One question on the TBS-2025 program. Could you remind us again, I know you went through this in the presentation, but what are you looking for internally in the initial data in relapse refractory AML, just to give you a sense as to how the product is performing in that disease setting? Sure. Analogous to menin inhibitors, they looked at the fact that they would achieve a CR, or a CR without full hematologic recovery in patients who had no alternative therapies. The biology suggests that even with menin inhibition, by the way, NPM1 still drives VISTA on the leukemic blast. In patients who are failing a menin inhibitor, can you essentially change the course and tempo of their AML in a phase I study, like Syndax and Kura did? It was their phase I data that they saw their first signal on response with KMT2A and NPM1 mutated blood-related cancers. If we see morphologic leukemia-free state in patients who are getting monotherapy in the phase I, that is adequate to have a discussion with the FDA about what they would need to see in terms of number of patients and overall response in that population. We didn't come up with the MLFS as a response criteria, the FDA did, and they said that they would consider that, and obviously CRh and CRs as well. That's the objective. If you see a signal in the phase I study in the first 17 patients, you'll have that discussion with the FDA. If you show safety and essentially maybe not objective responses at that level, but you still have disease control, going in combination with a menin inhibitor as the next step would make the most sense, given the fact that menin inhibitors have such a low rate overall of response. It's only 20%-25%. Okay, great. Well, it looks like that's all the time that we have today. I'd like to thank you, Jim, for joining us today from TuHURA. I'd like to thank the entire TuHURA team, all the investors in the room here in Boston, and everyone on the webcast. Thank you very much. Thanks, guys.