Good afternoon, and thank you to everyone joining us at this year's HCW Global Investment Conference. We are pleased to welcome Fahar Merchant, President and CEO of Medicenna. Medicenna is a clinical-stage immunotherapy company focused on oncology and other serious diseases. The company's lead asset, MDNA11, is a long-acting IL-2 Superkine currently being evaluated in the phase I/II ABILITY-1 study. Enrollment is ongoing and remains on track for completion later this quarter. Medicenna is also advancing its phase III-ready IL-4 empowered Superkine for recurrent glioblastoma. In addition, the company has earlier stage preclinical programs targeting autoimmune and inflammatory diseases. Fahar, the floor is yours. Thank you very much. Thank you for the invitation from H.C. Wainwright for presenting today. Also want to thank you all who are listening in today, and apologies for the delay in start of this presentation. As mentioned, we are a clinical-stage company. We have multiple programs that I'll talk about today. We are listed on the Toronto Stock Exchange and also on the OTCQX as well. I will be making forward-looking statements, so I encourage you to review our regulatory filings on SEDAR. Medicenna's focus has really been in programs that are designed to modulate the immune system for treatment of cancers, of autoimmune disease, inflammation, et cetera, using three very important cytokines, namely IL-2, 4, and 13. The backbone of our technology is very much around these engineered cytokines we call Superkines. These Superkines, in turn, are allowing us to generate what we call bifunctional Superkines and also conditionally activated Superkines using our BiSKITs™ and T-MASK™ platforms. Today, I'll talk to you mostly around our clinical data and our regulatory stages that we expect over the next coming weeks and months, and focus really mostly on work we're doing in the clinical space. The three programs that I'll focus today on are bizaxofusp, MDNA11, and MDNA113. Starting with bizaxofusp is an interleukin-4 engineered Superkine that's been fused to a potent payload. Here we have plenty of data in clinical patients who have been treated with recurrent glioblastoma. These are end-stage patients, and I'll share those data with you. What we have shown in our phase IIb clinical trial is a remarkable increase in survival by 100%, or two times the medium expected survival in these end-stage patients, and I'll share those data with you shortly. We will be pursuing certain regulatory aspects in the coming weeks and months, but also the program is well advanced with a phase III design that has been aligned with the FDA, and we plan to partner this asset so that we are able to commence clinical trials next year. The second program is a long-acting IL-2 superagonist. We call it MDNA11. This is a program that we would say is certainly best in class, and I'll explain to you why, and has received substantial amount of coverage from various international labs around the world in testing this approach. We will be providing top-line results from the phase I/II clinical trial as an oral presentation at a major conference coming up. Similarly with bizaxofusp, we will be also presenting newer data at a conference through an oral presentation by a key opinion leader. Finally, we have MDNA113, which is our bifunctional Superkine fused to a NTPD1, and we believe we have potentially best in class, but certainly first in class targeted NTPD1 IL-2. So multiple milestones coming up in the coming weeks and months. First and foremost, as I mentioned, we have two oral presentations, one on bizaxofusp, the second one on MDNA11. We will also have interim data from a separate study with MDNA11, where the drug is being evaluated in a neoadjuvant setting. Also with respect to next year, we plan to partner and commence a phase III registration trial for bizaxofusp, but also potentially phase II registration trials for at least one or more indications for MDNA11 on the back of positive data we have so far. With MDNA113, we have ongoing studies that are IND-enabling studies. We expect to complete those this year, with the plan to commence a phase I/II study next year. This is our pipeline. Of course, it has a great mix of earlier stage programs all the way to programs that are registrational programs. So we have a really good balance of assets here, not only in the oncology space, but as you can see at the bottom, we have MDNA209 and MDNA413, which address the autoimmune space, but also potentially inflammation with MDNA413. Let us focus on the programs that are the most advanced, first and foremost with bizaxofusp. This has Fast Track Orphan Drug designation, and as I said, has alignment with the FDA on a phase III registration trial. If you look at this particular patient population. Patients that are diagnosed with glioblastoma, typically when they are first diagnosed, they will undergo surgery, they will undergo radiation together with chemotherapy, and after the six weeks of radiation chemotherapy, they will receive higher dose chemotherapy until unfortunately, the tumor relapses or recurs, which occurs in all the patients. All the past, this standard of care has been in place for nearly 30 years now, and nothing has changed to help this patient population, particularly when the tumor relapses and recurs. This is where our focus is and really in the most difficult patient population. These are patients with glioblastoma that have recurred. As you can see from this pie chart here, that three out of four patients at first or second relapse are not good candidates for repeat surgery, for the treatment options for these patients are really limited, and this is where MDNA55 or bizaxofusp has been tested. If you look at patients currently that receive therapy in a recurrent non-resectable population, the median survival is between six and seven months. What we have been able to show with a single dose of MDNA55 or bizaxofusp is that we are able to double survival to nearly 14 months. What is bizaxofusp? Well, it is actually a multi-pronged molecular Trojan horse that addresses some of the biggest challenges that have faced glioblastoma. First and foremost, the way it is delivered allows us to have the drug bypass the blood-brain barrier so that you avoid systemic toxicity completely. Second of all, it is designed so that it is highly selective, and it is targeted where it delivers a potent payload, as you can see on the right-hand side. It delivers this potent payload to tumors, particularly glioblastoma, because they express this particular receptor known as the interleukin-4 receptor. Therefore, it is unique in the sense that healthy brain does not express this particular target. Therefore, we are not constrained or concerned or worried about local toxicity to the brain itself. The big hurdle for glioblastoma has been that this particular tumor is incredibly immunosuppressive. If one was to take a tumor out from these patients, you would find that about half of the tumor is actually made up of these highly immunosuppressive myeloid-derived suppressor cells, or MDSCs. They hide the tumor from the immune system. Therefore, we call these tumors cold tumors. Fortunately, with MDNA55 or bizaxofusp, because it targets the interleukin-4 receptor, what we know is patients that have GBM have myeloid-derived suppressor cells that also express really high levels of the IL-4 receptor. Therefore, we are accomplishing two things. We are targeting the tumor but also purging the immunosuppressive microenvironment at the same time. Finally, the fourth mechanistic aspect of bizaxofusp is that it causes immunogenic cell death of the tumor, meaning that it is releasing tumor antigens into circulation. Post-treatment, we know that after a few weeks or a month or two, we will see that there is a huge amount of infiltration of immune cells in the tumor itself. This allows us to treat the patients just once. In fact, a gram of this drug will treat 4,000 patients. You need only 250 micrograms of this drug to treat a patient. When we look at this data from the phase IIb clinical trial, what you see is the green line is the survival of patients that received the high dose of bizaxofusp in recurrent non-resectable glioblastoma. You can see the median survival of about 13.5 months. We then ran a separate external control arm using the FDA guidance documents on how to run external control arms. So we enrolled patients that had the same inclusion/exclusion criteria as the bizaxofusp study. Then we matched them based on 10 different prognostic factors that we know has an impact on survival of patients with GBM. For instance, we looked at the tumor size, location, we looked at the age of the patients or the Karnofsky Performance Status, et cetera, and we balanced them. Once we balanced those on 10 different prognostic factors, we unblinded the control arm, and what we found was that the median survival in that cohort was just 7.2 months, showing nearly doubling of the survival with a single treatment with bizaxofusp. So, remarkable results here with a single treatment, and the plan going forward in a phase III study would be to allow multiple treatments, therefore, potentially further improving outcomes for this really difficult to treat patient population. We have talked about recurrent GBM, but we also know that patients with newly diagnosed GBM also express the interleukin-4 receptor. We also know that patients with metastasis, that means patients at least we have tested tumors from breast, colon, and renal cancers, and we found that those tumors also express the interleukin-4 receptor. So there is a huge market opportunity, first and foremost, about CAD 800 million for recurrent GBM. But overall, we are looking at a CAD 4 billion market opportunity for CNS tumors in general, including we have seen high expression of this particular target in pediatric tumors as well, whether they be pediatric gliomas or DIPG, et cetera. Moving on to our next program, which is equally exciting, is MDNA11, but it addresses a different population altogether. Where the drug is given systemically, we have two studies currently underway. The first one, ABILITY-1, which is nearing completion of enrollment. We expect to complete enrollment by the end of this month. And another study, which is funded by an external philanthropic organization in Italy that is funding a phase I-B neo-site study in neoadjuvant setting. So we have multiple updates coming up in Q4. But just for those who are not familiar with the IL-2 space, and this is what MDNA11 is. It is a long-acting engineered IL-2. And IL-2, just for your information, was in fact the very first cancer immunotherapy approved. And it was used initially for melanoma and then into renal cell carcinoma. Unfortunately, this particular drug, which is still available today but is rarely used, is that it has a very short half-life, meaning patients have to be treated every eight hours for five days. And it is incredibly toxic. The toxicity is life-threatening, and therefore, the patients have to be administered this drug in an intensive care unit. Certainly, scientifically, it makes sense to work with IL-2, but this is not the version that would be acceptable. So over the past 10 years, there has been a substantial effort to develop what we call second generation interleukin-2, and these have been developed by big pharma, small biotechs, et cetera. Billions of value of transactions have occurred in this particular space, but unfortunately to no avail. Most of these studies have been abandoned or discontinued or companies have wound down their programs simply because they have not shown single agent activity of their IL-2. What is unique about Medicenna's IL-2 or MDNA11 is that it is designed completely differently from all others. And what have we done here with our IL-2 that makes it so different? First and foremost, what we have done is we have inserted two mutations so that the binding to the alpha domain is abolished, and therefore, we are not stimulating your immunosuppressive Tregs. And without alpha binding, we have created a molecule that is substantially safer than the original molecule. The second thing we have done is we have dramatically increased the binding to another receptor that is found on your immune cells called the beta receptor. And this is something that nobody else has done in a commercial or a drug development setting. This boosts the population of the immune cells, it boosts the population of memory cells, stem-like CD8 T cells, prevents exhaustion of natural killer cells, et cetera. We're seeing a very different novel pharmacology with this approach. Then finally, to extend the half-life of this drug, we fused the molecule to human albumin. That not only increases the half-life, but we know the albumin accumulates in the tumor, and it accumulates and localizes in tumor-draining lymph nodes. This is where the immune cells get trained. This is ideal for delivery of MDNA11 so that it accumulates in tumor-draining lymph nodes. Overall, what we see, I share with you, superior efficacy of this drug in a single-agent setting and also combination. The key thing here is the message I want to portray here is this, that our approach of beta-enhanced binding is not something that only we have demonstrated in the clinic, but we have a number of other studies conducted by independent labs worldwide who have published in these top journals from top research labs to show that beta-enhanced IL-2 is the way to go. Whether it's used to arm CAR T-cells, arm oncolytic viruses, combined with TKI inhibitors, combined with STING agonists. Overall, something that is really important that just came out 10 days ago was a publication in Science Advances by the founders of BioNTech. As you know, BioNTech and others are developing mRNA cancer vaccines. What they observed was this particular beta-enhanced IL-2s identical to Medicenna's IL-2 with albumin, was able to dramatically improve in preclinical studies the efficacy of these cancer vaccines. We see the trend here is that MDNA11 has an opportunity widely, not only in on itself or in combination with checkpoints, et cetera, but with other treatment modalities as well. If you look at today, the checkpoint inhibitor space, obviously the hottest space. We've seen dramatic improvements in patient outcomes. About $60 billion of annual sales of checkpoint inhibitors today, but only 30%, one in three of these patients will benefit. The remaining two out of three patients do not benefit. What we have found with MDNA11, either on its own or in combination with KEYTRUDA, where we have a collaboration with Merck, is that in patients who failed checkpoint inhibitors are responding to MDNA11 either on its own or in combination with response rates in the 30%-40% range, which is quite remarkable. We will be presenting newer data at a major conference. As I said, it's an oral presentation coming up in the next few weeks. We will be presenting data on ABILITY-1. We'll be sharing top-line data from 150 patients who have enrolled to date, addressing multiple tumor types, but the focus is going to be on four different expansion cohorts, melanoma, GI tract tumors, endometrial cancer, and a biomarker-driven tumor, MSI-high tumors. These data will be presented at, as I said, a conference. We also have the data from the neoadjuvant study. We'll have interim data. This is an 80-patient study. It's a randomized study comparing head-to-head with a combination of OPDIVO and YERVOY. Lots of news coming around MDNA11 that will drive our regulatory strategy, but also, we have leveraged our IL-2 to dock a bispecific NTPD1. This space has become really exciting. NTPD1s, as you know, over the past 24 months, these bispecific NTPD1s have resulted in transactions worth about $38 billion. Most of these are NTPD1 with another antibody called anti-VEGF. More recently, a deal between Takeda and Innovent Biologics was related to an NTPD1 with IL-2. That was an $11 billion transaction with $1 billion up front. We believe this is the next frontier in bifunctional superkines of checkpoint inhibitors where we think, and we have already shown combination approaches there to benefit patients. What is MDNA113? It looks really complex, but it is simple to manufacture. It is unique in the way it has been designed. First and foremost, it is a targeting approach. We are targeting an antigen known as IL-13 receptor alpha-2, which is overexpressed in lots of solid tumors. Second is that we are using an IL-2 that we have demonstrated that works, which is our MDNA11 version of IL-2. Third is that we are leveraging the patent expirations of OPDIVO and KEYTRUDA to use a commercially proven NTPD1. Combining the three together ends up creating a molecule that is targeted, that is switched on only at the tumor site and provides a remarkable number of benefits. A big thing here, which is unique and which is first in class, is the fact that our MDNA113 is targeting the IL-13 receptor alpha-2. As you can see, it is found in many solid tumors. In fact, about 2 million cancer patients diagnosed every year express this particular target. The importance here is that the IL-13 receptor alpha is associated with more aggressive cancers. As you can see an example here for colon cancer on the right-hand side. Patients with IL-13 receptor alpha-2-positive tumors do very poorly compared to patients that do not have that target. We feel that we are addressing a huge unmet need that is currently not being addressed, targeting a unique receptor that is found on cancer cells only. If we compare MDNA11 or rather MDNA113 with other bispecifics that are entering the clinic or just entered or in the clinic, you can see that MDNA11 or MDNA113 really provides so many advantages compared to others. First and foremost, that this is an NTPD1 that we are using is commercially proven. Our IL-2 itself has demonstrated single-agent activity. None others have demonstrated single-agent activity. We are targeting the beta gamma receptor, which we have found from not only our work, but a host of other publications, that that is the best way forward for a better IL-2 design. Unlike anybody else, we are actually targeting the bispecific molecule right at the tumor site and going after the most aggressive tumors out there. Finally, we have a conditional activation, which is unique is that we have it, the drug or the IL-2 component gets activated by two ways. Either that it gets in close proximity to the T cell, that is one, or second of all, the masking is removed by very specific proteases produced by the tumor itself. This in of itself shows that we have a huge opportunity to fill the gap in patients who have to get a better KEYTRUDA or a better OPDIVO out there. Certainly, we have demonstrated that in our combination studies with MDNA11. We also have earlier-stage programs. I will not talk to you about them, but suffice to know that we also have IL-2, which is a super antagonist, which is unlike MDNA11, which is a super agonist. MDNA209 is a super antagonist, therefore very relevant for autoimmune disease. We have seen this particular space, large transactions, a CAD 2 billion deal recently announced where argenx acquired Forte Biosciences. Then on the IL-4/13 blockade is a, we believe, a better version of DUPIXENT, which is a multi-billion dollar, $25 billion a year product for Sanofi. This was also something that was demonstrated in a transaction recently where AbbVie acquired ImmunoGen for about just under $11 billion. As a company, market cap is just CAD 40 million, a great opportunity for participating at this low valuation. Our current cash, with additional cash expected through a sharing agreement, is that takes our runway into second quarter of next year. 92 million outstanding shares, 20% of those are held by insiders, and we are currently covered by four analysts, two in Canada, two in U.S. As you can see, multiple upcoming milestones with our three different programs here. bizaxofusp, data being presented at a conference, at an oral presentation. We have updated data as well and ongoing activities from partnering perspective with bizaxofusp. With MDNA11, we will be completing enrollment in the study this month. We will be reporting top-line data at a presentation. This is an oral presentation at a major conference in Q4. We will have interim data on the neoadjuvant study, and the plan is with those data, the plan is to have an end of phase I meeting with the FDA to see if there is a way forward for at least one, if not more, different tumor indications for a phase II registration trial to get accelerated approval for MDNA11 for one of four different expansion cohorts. Then finally, with MDNA113, we are in completion of IND-related activities are currently ongoing. Plan is to submit the IND and start a phase I study next year. Of course, we have ongoing partnering discussions on MDNA209 and MDNA413. The key takeaway here today is that over the next three to six months, we have multiple clinical and regulatory milestones coming up, each one of them major key value inflection points. With that, I will stop and happy to take any questions. Thank you.