What does Medicenna do? In fact, what we focus on is interleukins. We call these Superkines. These are engineered interleukins that are derived from naturally occurring IL-2, IL-4, and IL-13. These particular interleukins and the basis of these Superkines essentially have evolved from the very early work done by Chris Garcia at Stanford University. Focusing first on our most active clinical program at the moment is MDNA11. It's an IL-2 super agonist currently being pursued in phase I to clinical trials in advanced metastatic solid tumors. This is where we'll be generating the bulk of the data that we'll share with everyone in the coming this year. First and foremost, we'll have more data on our monotherapy expansion arm. We'll have data on our escalation with combination with KEYTRUDA. We will start our combination combo expansion portion of the phase II trial with KEYTRUDA as well. All of this will be disclosed in the coming weeks. Bulk of it, obviously, coming at the AACR meeting at a conference where we are presenting data on April 28th. Subsequently, in the second half of this year, we will have a complete set of data on the monotherapy, and we will have top-line data on combination with KEYTRUDA. We would have completed enrollment in the ability study in the third quarter of this year. Looking at a second program where we will not have any data except for the fact that we have a phase III ready program. This is driven by our interleukin-4 asset. This is for treatment of recurrent glioblastoma, which is a program that is phase III ready. This is a program that we're looking to partner, hopefully, sometime this year as well. Finally, a really exciting asset that we are continuing to build on. This is based on what we call bifunctional Superkines, being looked at in different immunotherapies, not only immuno-oncology, but, as I'll show you later on, in autoimmune as well as inflammatory diseases as well. We will advance these two programs that are in this BiSKITs platform into readiness for IND-enabling studies before the end of this year. What are Superkines? Really, the Superkines are a version of engineered IL-2, IL-4, or IL-13 that have used this technology known as directed evolution to generate a library of these interleukins that have variations in binding affinities, variations in their ability to signal pathways, ability to alter the fate of your immune cells, et cetera. Therefore, what we have is a series of different Superkines that can be either super agonists or completely opposite in them being super antagonists, and then, of course, anything in between. Each one of these interleukin-2, interleukin-4, and interleuikin-13 Superkines that we are developing, we believe, have potentially pipeline in a product opportunity. As I said, we are a clinical stage company. We have multiple programs in different stages, early, mid, and late stage. It is a nice balanced pipeline with a focus, although initially in immuno-oncology, but the potential to enter into autoimmune disease and inflammatory diseases with our earlier stage assets. Today, we'll spend most of our time looking at the data from our MDNA11 ability study, both monotherapy and combination, and briefly mention the phase III readiness of our GBM program and talk about our earlier stage assets. Let's start with MDNA11. Now, MDNA11, as I mentioned to you, is an IL-2 program. It's a next-generation IL-2. For those who are familiar with the IL-2 space, have probably been hearing and have been accustomed to a series of failures. I think we recently had a fifth failure in the IL-2 space. A couple of those IL-2 programs that also failed were subject to large multi-billion dollar partnerships with other oncology companies to see how IL-2 could be used, either on its own or in combination with checkpoint inhibitors. We know that the IL-2 space, the IL-2 candidate molecule, has a considerable amount of promise in the IO space. What have been the challenges? Hopefully, this is where MDNA11 comes into play. Let's go back to the 1990s, where an IL-2 was approved for treating metastatic melanoma as well as kidney cancer. This IL-2, known as PROLEUKIN, currently marketed by Iovance, is basically very similar to a human IL-2. The problem with this IL-2 is that although it did show benefit in a small percentage of patients, the challenge is that the IL-2 binds, first and foremost, very efficiently with a receptor known as the high-affinity receptor that is on the extreme left, which comprises the alpha, beta, and gamma chains. That affinity pretty much drives the ability of IL-2 to, first and foremost, stimulate your immunosuppressive Treg cells, not the cancer-fighting immune cells, namely the CD8 T cells or your NK cells, which primarily express only the beta-gamma receptor. What has, of course, happened with IL-2 was that, first, it was stimulating at low doses immune suppression. Second, because of the alpha receptor being expressed on endothelial cells, it was causing vascular leak syndrome and therefore incredibly toxic. Patients, therefore, needed to be administered the drug in an intensive care unit. Finally, because the molecule is rather small, it clears the kidneys very quickly. What you end up with is really a molecule that needs to be administered and a treatment that needs to be administered every eight hours for five days in an intensive care unit. These were the big challenges. How do you shift and transform a molecule to something that's going to give you the benefits of IL-2 without the negatives? This is where MDNA11 comes in, where we have, by and large, addressed these issues with the objective of getting better patient response, safety, and also less frequent administration of the drug. How have we accomplished this? If you look at this cartoon here, on the left is your engineered IL-2. The first thing that was done was to insert two mutations so that the molecule completely abolishes binding to the alpha domain. Therefore, you are eliminating the potential for stimulating your immunosuppressive Tregs and also have a molecule that is potentially safer. Second was to insert five mutations. Again, this is primarily to boost the binding to the beta receptor. By doing so, we have sort of the ability to substantially boost the population of effector CD8 T cells and NK cells. By virtue of that, changing the pharmacology of IL-2 in such a manner, they are boosting your memory T cells. You are minimizing exhaustion of your natural killer cells, et cetera. This is sort of the end result. Finally, what we needed to do was extend the half-life. This is where linking the molecule to albumin substantially increased the molecular weight so that this drug now can be administered every two weeks, potentially even every three weeks, instead of every eight hours. It is a huge improvement. The key bonus by using albumin is that we know that albumin tends to accumulate in the tumor, in the tumor-draining lymph nodes, et cetera. With that, hopefully, we have got a much better drug. This is our phase I/II trial design. It has four parts to it. On the top left is the monotherapy dose escalation that has been completed. We have established the 90 µg/kg dose as our recommended dose for expansion. At the bottom left, you see the combination arm with KEYTRUDA that is currently ongoing. This is, by the way, a clinical collaboration with Merck, where Merck is supplying the KEYTRUDA to the study. That is nearly in completion. We'll announce results with respect to the combination dose for expansion. This will occur in the coming weeks. The plan will be then to look at a select group of tumor types. Here, both in the mono expansion and combi expansion, what we have is we've selected three different tumor types: cutaneous melanoma, MSI- high/d MMR tumors. These are not tumor-specific or tissue-specific, but biomarker-driven. Then TMB high. This is tumor mutational burden being high in these tumors. This allows us to look at these three different tumor types for which checkpoints have been approved, but only recruiting patients that have failed either primary failure or secondary failure with checkpoint inhibitors. We're looking at end-stage, late-stage patients with MDNA11, either on its own or in combination. Looking at safety, as you know, safety was a big issue, has been a big issue with IL-2 or PROLEUKIN. What we have seen is the majority of adverse events, 92% of them, whether they be in monotherapy or in a combination setting, you're seeing those being mild to moderate grade 1, grade 2, with the majority of them being resolved in 48 hours or less. We've seen some liver function tests increase to showing grade 3 effects, but none of these were symptomatic. We've seen a handful of patients with hypotension. We realized that these patients had adrenal insufficiency, which is something that's not good to have those patients. Therefore, that has resulted in amendment of the protocol. To date, with all the treatments and doses that we've evaluated, both in mono and combination settings, we've not seen DLTs in any patient. We have not seen new safety signals in the combination setting. As far as the pharmacology is concerned, or call it immunodynamics of MDNA11, it's dramatically different than what you will see with other next-generation IL-2 molecules out there. First, what we do see is a dose-related expansion of the immune cells. Primarily, what you see is the expansion of your effector CD4 T cells, the NK cells, and most importantly, the CD8 T cells. You don't see much of expansion of the Tregs. This is important because we do not want to generate immune suppression, but really boost the population of CD8 T cells. All CD8 T cells are not equal. They're different quality of CD8 T cells. Let's look at these data here. As I said, we are seeing this dramatic boost in the population of CD8 T cells. It's important to note that if you look at a number of other second-generation IL-2s, including PROLEUKIN, et cetera, you will see generally that the population of immune cells that get expanded primarily are the NK cells or the natural killer cells, followed by CD8 T cells. Here, we've completely reversed the situation in that we are actually seeing a massive increase in CD8 T cells, but also an increase in NK cells. By and large, generally, the CD8 T cells dominate. On the right-hand side of this slide, what you see is the quality of CD8 T cells. We're seeing the population of activated CD8 T cells dramatically increase. Also at the bottom, you can see the population of memory, both effector and central memory T cells. Finally, on the extreme right on this slide, what you see is something unique is that we are seeing an increase, a dramatic increase in stem-like CD8 T cells. These stem-like CD8 T cells persist. They stay in your systemic circulation. When the tumor comes back, it is able to invigorate and attack the tumor before it's too late. I think when you look at the totality of these data, what you will generally see is that not only do we see responses, but we see responses that are durable. Now, just a note here that these data are not the latest data. We'll share more recent data at the upcoming conference on the 28th of April at AACR. For now, what you can clearly see here is that patients that have received this drug, and these are advanced-stage patients, they've all failed checkpoint inhibitors, at least one, if not two, different lines of checkpoint inhibitor therapies. We're seeing that 30% response rate. Amongst the high-dose phase II eligible patients, we are seeing a 25% response rate irrespective of tumor type. More interesting is, as you can see at the top, that at the bottom, the time on treatment is extended all the way to 90 weeks. That's two years. Some of these patients have been off study, off treatment. Fortunately, we're not seeing these tumors coming back. When we look at this waterfall plot, what we're seeing is that we are not only achieving PRs that are durable, but also complete responses. Give me an example of the PR patient there. This was a PR in a patient with pancreatic cancer. Okay? Patient had failed gemcitabine, Abraxane. The patient had failed FOLFIRINOX treatment. The patient had failed KEYTRUDA and entered the study about three years ago from today. At that time, received MDNA11 single agent. This patient had metastasis to the liver, as you know, is the most challenging location to treat those particular tumors. What we observed is that the patient's tumor continued to shrink. The patient, unfortunately, went away on an eight-week vacation. Upon coming back, had a new lesion that was then treated with radiation. After radiation, continued to receive MDNA11. That tumor, both the target, the new lesion, the non-target lesions were gone. It's been about 16 months since the patient has stopped receiving treatment. There is no sign of the tumor coming back. This is sort of really exciting. Same thing with the complete responder with melanoma. Patient had multiple failures with immunotherapy. That patient now is approaching two years and has been off treatment for just under a year with no sign of the tumor coming back. Durability is key. I think that is something that's really important to demonstrate the robustness, the potency of this particular approach in treating these patients. When we look at now, this is, mind you, just data from dose escalation. We are enrolling patients with all sorts of tumor types to see what we might see in combination with KEYTRUDA. We're already seeing in tumor types that do not generally respond to checkpoint inhibitors, for instance, anal squamous cell carcinoma, we had a complete response in eight weeks with this patient. With metastatic colorectal cancer, MSS tumors, again, not something that KEYTRUDA would work in these patients. We've seen prolonged PR in these patients. We'll provide updates. You're seeing that you are observing responses in this combination setting despite the fact that these patients have all sorts of different tumor types that generally don't respond to checkpoints as well. All in all, I think we have an asset, a single agent, highly differentiated IL-2 that is showing not only single agent activity, but durability without the penance of safety in this particular approach. Moving on to our second program, this is IL-4 driven therapy for recurrent glioblastoma. I won't spend much time in it, but suffice it to say that GBM has been a challenging, a really difficult tumor type to treat. Here, the focus has been on patients that are recurrent glioblastoma, patients that are not eligible for repeat surgery. These were patients with first or second relapse. At the moment, if you look back at glioblastoma, the drug that was approved some three decades ago is still the standard of care in newly diagnosed GBM. In patients with recurrent GBM, at the moment, there is no good standard of care. In fact, the recommendations are for patients with recurrent GBM to enter a clinical trial. If we look at survival outcomes for recurrent GBM, it's generally six to nine months, but potentially worse in patients where tumors cannot be resected. This drug is MDNA55. It's an IL-4 engineered. It is high selectivity towards the IL-4 receptor and carries a lethal payload. This drug is administered single once directly in the tumor. Thereafter, what we do see is tumor shrinkage. Subsequently, we have also seen, having conducted some nanostring analysis and gene expression analysis, that we are also targeting the tumor microenvironment at the same time. If we look at the results from the phase II-B clinical trial, when we compare MDNA55 or bizaxofusp versus a very well-balanced external control arm, we are nearly doubling the median survival in these patients from, what, seven months to 13.5 months. Dramatic improvement. This is a program that we look forward to partner this asset with a potential partner. The opportunity is substantial. It's not only recurrent GBM, but potentially newly diagnosed and metastatic tumors that express the target, which is the interleukin-4 receptor. With respect to the preclinical assets, another program very much based on our IL-2 Superkine is MDNA113. This is a BiSKIT. It's a targeted bifunctional Superkine, and it is masked. What it does have is really two different components. It has the benefit of an anti-PD1 and an interleukin-2, which is essentially the same IL-2 that is being used in our MDNA11 program. The approach here is to ensure that the same T cell gets stimulated with our IL-2 and an anti-PD1 at the same time. We've seen some very impressive results, at least preclinically. There is evidence that this approach would be really beneficial for tumors that are difficult to treat. In our approach, and there are many companies pursuing an anti-PD1 with an IL-2 program, is that our IL-2 has already demonstrated single agent activity. The anti-PD1 is a commercial anti-PD1 that is, as you know, going off patent in 2028. An opportunity to really build on this. More importantly, what we have done is we have created this molecule so that it is targeted. We are using interleukin-13, as you can see at the bottom of this on the left-hand side, to do two things. The IL-13 is engineered so it will bind to a tumor-associated antigen, IL-13 receptor alpha 2. A number of tumors, particularly aggressive tumors, express this particular target. By localizing it at the tumor site, what we are able to then do is the drug, while in systemic circulation, we avoid the toxicity with respect to the IL-2 component. More importantly, we localize it at the tumor site on the surface of the tumor cells. That is where it gets activated by tumor-associated proteases, releasing the bifunctional molecule to stimulate the CD8 T cells. We have seen a number of transactions that have taken place. Roche, for instance, acquired Good Therapeutics, a preclinical asset for about $250 million. Another molecule that we are also really excited about is MDNA209. This is an asset. This is identical in structure to our oncology drug, MDNA11. The only difference is it has four additional mutations. It transforms the IL-2 from being a super agonist to a super antagonist. Essentially, it is here driving the ability for us to tame the immune system in autoimmune disease or graft- versus- host disease, et cetera. This is a molecule that blocks both IL-2 and IL-15 receptor binding and the potential to use this in autoimmune disease and graft versus host disease. Finally, with the IL-13 platform, we have an IL-13 Superkine that is selective where it binds only to the type 2 IL-4 receptor. Unlike Sanofi's DUPIXENT, which binds to both the type II and type I IL-4 receptor, this is binding only to the type II receptor. By doing so, it blocks signaling. In essence, we are able to potentially use this approach to treat patients with various inflammatory diseases, be that atopic dermatitis, asthma, et cetera. With that, I will just sort of close by giving a little bit of background where we are as a company. As I said very early on, we are a TSX, OTC QX listed company. Symbol is MDNA. We are headquartered in Toronto. The market cap of the company is about $70 million. Cash on hand being $30 million. With our ongoing cash burn rate of about $5 million a quarter, we have sufficient cash to take us right through the middle of 2026. We have a healthy cash balance. We have, from an insider ownership perspective, 22% ownership with RA Capital and AIGH being two institutional investors, including RA that recently invested in Medicenna last year about this time in a pipe. Analyst coverage by Jones, Katherine Novak, RK from HC Wainwright, David Martin from Bloomberg, and Andrew Dean at McKee Research. Finally, the key highlights here being MDNA11, a data reach time that we'll have lots of data that we'll share in the coming weeks and coming quarters. With bizaxofusp, we continue to look at a potential partnership. Of course, with the BiSKITs, we look forward to sharing more data with respect to its ability to then proceed into IND enabling studies. Hopefully, the plan is to have the molecules ready before the end of this year. With that, I'll end. Thank you very much.