Hello, and welcome to the Medicenna Therapeutics Fiscal Year-End Earnings Call. All participants are now in a listen-only mode. There will be a question and answer session at the end of this call. If anyone should need operator assistance during the conference, please press star zero on your telephone keypad. Please be advised that this call is being recorded at the company's request. I would now like to turn the call over to Dan Ferry of LifeSci Advisors. Dan, please go ahead. Thank you, operator, and thank you all for participating in today's conference call. This morning, Medicenna issued a press release providing financial results and corporate updates for the fiscal year ended March 31, 2022. If you have not seen the press release, it is available on the investors page of Medicenna's website. Before we begin, I would like to remind you that certain statements and information shared during this call constitute forward-looking information within the meaning of applicable securities laws. All statements other than statements of historical facts shared during this call and that relate to the future operations of the company and other statements that are not historical facts, including statements related to the clinical potential and development of MDNA11, MDNA55, and the BiSKITs programs, potential of the Superkine platform, partnering activities, cash runway, the presentation of additional data and other milestones are forward-looking statements that are subject to risks and uncertainties. There can be no assurance that such statements will prove to be accurate, and actual results in future events could differ materially from those anticipated in such statements. Important factors that could cause actual results to differ materially from the company's expectations include the risks detailed in the recently filed annual information form, Management's Discussion and Analysis and Form 20-F of the company and other filings made by the company with the applicable securities regulators from time to time in Canada and the United States. Listeners are cautioned that assumptions used in the preparation of any forward-looking information may prove to be incorrect. Events or circumstances may cause actual results to differ materially from those predicted as a result of numerous known and unknown risks, uncertainties, and other factors, many of which are beyond the control of the company. You are cautioned not to place undue reliance on any forward-looking information. Such information, although considered reasonable by management, may prove to be incorrect and actual results may differ materially from those anticipated. Forward-looking statements contained in this conference call are expressly qualified by this cautionary statement. Except as required by law, we do not intend and do not assume any obligation to update or revise publicly any of the included forward-looking statements, only as expressly required by Canadian and United States securities law. Now, I will turn the call over to Dr. Fahar Merchant, President and Chief Executive Officer of Medicenna Therapeutics. Fahar? Thank you, Dan, and, thanks to all of you joining us on today's call. In addition to Dan, I'm joined by Dr. Martin Bexon, our acting Chief Medical Officer, and Liz Williams, our Chief Financial Officer. With the considerable progress made in the past fiscal year, we believe that we are now at the cusp of what is an exciting and pivotal time for Medicenna. This is being driven by the progress we have made with the initiation and advancement of the phase I/II ABILITY study in patients with advanced solid tumors, which is the first clinical study of our differentiated beta-only long-acting IL-2 superagonist, MDNA11, and the promising signs of clinical activity we are reporting in the early stage of our dose escalation portion of the trial. During the past 12 months, despite being in the midst of a global pandemic, we completed all of the CMC activities associated with GMP-compliant manufacturing of MDNA11 for the phase I/II ABILITY study. The IND-enabling studies required for regulatory submissions to commence first in human clinical trials with MDNA11 and secured clearance of the various applications submitted to regulatory agencies in Australia, U.S., and Canada. As a result, we are well underway in our dose escalation portion of the ABILITY study and continue to enroll patients at multiple clinical sites in diverse geographic regions to establish the recommended phase IIthe dose for the dose expansion phase of the study, both as a single agent and in combination with a checkpoint inhibitor. We have continued to also build our pipeline of new long-acting IL-4 and IL-13 super antagonists, as well as our BiSKITs, such as the NTPDase1 MDNA19 CD39-targeting fusion protein. Furthermore, we have completed a comprehensive commercial opportunity analysis of our MDNA55 program for treatment of recurrent glioblastoma and other brain cancers. With compelling clinical data and an attractive registration pathway, MDNA55 scored highly among KOLs in Europe and the U.S. and was rated very favorably by payers for reimbursement based on projected pricing. We look forward to a positive outcome as we advance our discussions with interested parties. Finally, we close the year-end with a strong cash balance of $20.5 million. We have made modifications to our budget in order to extend the cash runway well into Q2 calendar 2023, taking us well past our anticipated first substantial clinical efficacy readouts from the ABILITY study. In the phase 1/2 ABILITY clinical study of MDNA11 in patients with advanced and metastatic solid tumors, the primary objectives are to investigate safety and tolerability and determine the recommended phase II dose, while the secondary objectives are to evaluate pharmacokinetics, pharmacodynamics, immunogenicity, and preliminary antitumor activity in both the monotherapy and the combination arms of the study. Since dosing the first patient in the ABILITY study this past September, we have observed very encouraging data in the first three dose escalation cohorts, consistent with MDNA11's anticipated differentiation from competing IL-2 programs. MDNA11 is demonstrating an acceptable safety and tolerability profile, as well as promising early signs of clinical activity in the first eight patients while dose escalation continues to enroll in cohort 4. Although it is too early to draw meaningful conclusions on efficacy potential of MDNA11 from the dose escalation portion of the clinical trial, we have seen very encouraging signs of CD8 T and NK cell activation and proliferation in the periphery in most patients treated so far, as well as early signs of tumor control in three out of eight patients. Further, the PD data was from peripheral blood sampling, and we expect that this PD data may have a different profile and durability of activation of cancer-fighting immune cells in the tumor and the tumor-draining lymph nodes. Given that the therapy is well-tolerated as we escalated from 3 µg per kilogram in cohort 1 to 30 µg per kilogram in cohort 3, Medicenna has implemented a step-up dosing regimen in all subsequent dose escalations. Cohort 4 is currently enrolling at the target dose of 60 µg per kilogram following two priming doses at 30 µg per kilogram. As we continue to escalate, we could see different dynamics emerge at higher doses. We therefore look forward to data updates throughout 2022 for more safety, PK, PD, and efficacy data. In the second half of 2022, we expect more fulsome data for MDNA11, as well as early data from the single agent dose expansion cohorts in a restricted number of tumor types, such as metastatic melanoma and advanced renal cell carcinoma. Management expects approximately 10 more patients in the dose escalation portion of the study in addition to 13 patients already enrolled to date in cohorts one to four. With encouraging PK, PD, and safety data and early signs of tumor control in three out of eight patients in cohorts one to three,, we expect more meaningful signals of efficacy at higher doses as we continue with the dose escalation portion of the ABILITY study. As the ABILITY study has advanced over the past fiscal year, we have been consistently monitoring the data it has generated, changes in the regulatory environment, as well as data reported from clinical trials of other IL-2 variants. Although recent clinical results from trials of pegylated IL-2 have not shown clinical efficacy, it is important to note three key points. First, IL-2 is a validated target that, when administered at high doses, it is known to drive meaningful clinical benefit. Second, MDNA11 is clearly differentiated from these competing agents in ways that we expect will translate to superior efficacy. The data we have seen from the ABILITY study supports this view, which is a topic Martin will cover in more detail. Third, we have the benefit of leveraging the learnings from recent trials of competing IL-2 variants to optimize our clinical development plans in a data-driven manner to increase our chances of success. One of these learnings comes from early safety data that shows modest adverse events such as fever or chills, being more prevalent after the initial dose of MDNA11 than after subsequent doses. Based on this observation in the clinic and in non-human primate studies, and to ensure we are able to achieve a maximum MDNA11 dose before reaching dose-limiting toxicities, we are utilizing a step-up dosing strategy from cohort four onwards. This strategy entails first treating patients with two priming doses to habituate them to MDNA11 before stepping up to the higher fixed dose that is being evaluated. This is expected to increase our chances of identifying MDNA11's optimum dose and is in line with FDA's recently released Project Optimus initiative, which encourages companies to do more early on in clinical development to find the optimal dose for oncology drugs. Given the dose-dependent PD effects and early signs of clinical activity MDNA11 has displayed thus far in the ABILITY study, ensuring that we are able to identify its optimum recommended phase two dose will further improve our chances of clinical success. A failure to reach the optimal dose is something that may have hampered other IL-2 programs, such as the pegylated variant I mentioned earlier. While the step-up dosing regimen we are pursuing with MDNA11 will allow us to achieve higher doses and position the ABILITY study for success, it does take longer to dose each patient as two priming doses are required before administering the target dose. This has impacted our follow-up period for each patient to eight weeks instead of four weeks when using the fixed-dose approach. Thus, enrollment in the fourth and subsequent cohorts will take longer and delay our ability to collect patient scans following the target dose. We expect updated PK/PD data from cohort four in July 2022. First follow-up CT scans at the higher dose cohort 4 in Q3 of calendar 2022, with a full set of efficacy data for all dose escalation cohorts in Q4 of calendar 2022. To help ensure the MDNA11 program is advanced as efficiently as possible, we made it a point this past fiscal year to assemble world-class advisory councils, including our Development Advisory Committee and Scientific and Clinical Advisory Boards. These include some of the world's leading experts on drug development and cancer immunotherapy, which allows us to gain invaluable insights and complementary perspectives on our drug discovery and development efforts. These have been crucial to the advancement of not only MDNA11, but also to the advancement of our preclinical-stage Superkines and BiSKITs. We recently highlighted two of these preclinical assets in posters at the AACR meeting this past April. One poster focused on Fc-MDNA413, which is derived from our Superkine platform and consists of an IL-13 super-antagonist fused to the Fc domain for half-life extension, and a second poster featured a preclinical candidate from our BiSKITs program. As a reminder, BiSKITs are bifunctional Superkines designed to combine two distinct and synergistic immunotherapy mechanisms of action into a single molecule. This poster outlined preclinical studies on a BiSKIT consisting of an anti-PD-1 antibody linked to an IL-2 superagonist similar to MDNA11. We believe our ability to incorporate checkpoint inhibitors, which are widely successful commercial drugs, into novel BiSKITs may provide important intellectual property advantages as the first generation of checkpoint inhibitors come off patent. This, in turn, could spark valuable collaborations with the leading developers of these agents. Over the past 12 months, we have seen that some of the world's renowned academic labs have independently published results demonstrating the exceptional potential of our core MDNA109 IL-2 Superkine platform when incorporated in oncolytic viruses, CAR-T-based therapies, conditionally activated Superkines, or when combined with STING agonists. This provides external validation of our Superkine platform, especially the MDNA11 asset. Looking forward, we expect the continued advancement of our preclinical Superkines and BiSKITs, and to provide important value creation opportunities to supplement our lead MDNA11 program. With that, I will now turn the call over to Martin to discuss the ABILITY study status, recent data, and future outlook. Martin? Thanks, Fahar. Since our last earnings call in February, we reported pharmacodynamic data from the ABILITY study's third dose escalation cohort and are currently enrolling patients in cohort 4, with clinical trial sites open in the United States, Canada, and Australia. We have not observed any dose-limiting toxicities in the study to date and remain on track to report additional PK/PD data at the end of July at the Cytokine Summit to be held in Boston. In the second half of calendar 2022, we expect to identify MDNA11's recommended phase II dose and initiate the study's single-agent expansion phase. Before moving on to discuss the ABILITY study's recent data and what we believe it means for the program. I'd first like to provide some context by briefly mentioning the recently reported results of the randomized phase III trials evaluating a different IL-2 variant in patients with previously untreated advanced melanoma and metastatic renal cell carcinoma. For those of you who may be unfamiliar with this trial, it evaluated a pegylated IL-2 in combination with the checkpoint inhibitor Opdivo versus therapy with a tyrosine kinase inhibitor. An analysis of the data from the trial showed no clinical benefit in the double therapy arm. While the results from this other program are obviously disappointing for patients, I should emphasize that we do not expect them to be applicable to MDNA11. In fact, seeing the results of this trial have provided us with valuable learnings that we believe will increase our chance of success with MDNA11, which is something I will discuss shortly. Before I do this, however, I would like to explain why we believe MDNA11 is positioned to overcome the shortcomings that have affected pegylated IL-2 variants and how the ABILITY study's recent data strongly support this hypothesis. I'll begin by emphasizing a point Fahar made earlier, which is that IL-2 is a validated immunotherapy target since high-dose IL-2 is required to bind and activate effector immune cells via the intermediate receptor comprising the IL-2 beta receptor and has been approved for the treatment of renal cell carcinoma and metastatic melanoma. We therefore know that successful stimulation of the IL-2 receptor complex via the beta receptor can drive meaningful clinical benefits as high dose native IL-2 or Proleukin has shown efficacy. The rationale behind developing IL-2 variants such as MDNA11 or pegylated IL-2s is to improve upon Proleukin's poor safety profile due to its ability to bind to the high affinity receptor, which also comprises the IL-2 alpha receptor. Consequently, Proleukin's pharmacokinetic profile necessitates dosing in the ICU every eight hours for five days, which severely restricts treatment durations and therefore overall drug exposure and uptake. Given that the toxicity associated with Proleukin seems to be linked to its affinity for the IL-2 receptor alpha, the next generation IL-2 programs have focused on reducing affinity for this receptor subunit. While pegylation is able to decrease IL-2 receptor alpha binding affinity and improve half-life, we are of the view that this is a suboptimal approach for a few reasons. A key limitation of using pegylation to decrease IL-2 receptor alpha binding affinity is that it also leads to a reduction in binding to the IL-2 receptor beta, which is critical for the activation of the anticancer immune cells that drive response to IL-2 therapies. This is in stark contrast to MDNA11, which has significantly enhanced affinity for IL-2 receptor beta. Additionally, past data has shown that pegylated IL-2s are not truly non-alpha molecules, since all PEG moieties will gradually dissociate from IL-2 following administration, which leads to unintended IL-2 receptor alpha binding, resulting in toxicity and may also activate pro-tumor Treg cells, which are known to limit the efficacy of immunotherapies. Based on both MDNA's inherent design and all the data we have seen from the ABILITY Study to date, we are confident that its long-acting beta-only IL-2 binding approach is the best approach to improve patient outcomes while overcoming the concerns associated with Proleukin. As a reminder, MDNA11 was engineered using direct evolution to enhance binding to the IL-2 receptor beta, resulting in a 30-fold improved binding compared to that of Proleukin and has two additional mutations that avoid its ability to bind to the IL-2 receptor alpha, therefore avoiding Treg stimulation and improving its safety profile. Finally, to improve its pharmacokinetics, the engineered IL-2 is fused directly to albumin, a protein scaffold that is known to improve tumor accumulation and localization in tumor-draining lymph nodes. As I alluded to earlier, these features are expected to translate to enhanced efficacy and safety compared to other IL-2 programs. The ABILITY Study's preliminary data indicate that MDNA11 is behaving in the clinic very much as it was designed to do. We have observed dose-dependent preferential stimulation of anticancer immune cells with limited stimulation of pro-tumor Tregs and no significant increases in eosinophils which are associated with toxicity. Notably, MDNA11 induced increases in cancer-fighting immune cells are greater than those seen with competing agents administered at equivalent IL-2 doses. This provides strong evidence that MDNA's superior preclinical results are translating in the clinic as expected and may therefore demonstrate superior efficacy as the ABILITY Study continues to advance. Diving a little deeper into the recent ABILITY study PD data, we can see a biological profile emerging that is well in line with what we're aiming to achieve. On our last earnings call, I mentioned we hope to see higher levels of CD8 and natural killer cell stimulation relative to T-reg activation in the ABILITY study subsequent cohorts. This is exactly what we saw with our recent data from cohort 3 as CD8 positive T to T-reg and NK to T-reg ratios increased by 2.6-fold and 4.4-fold over baseline respectively. I also mentioned hoping to see increases in markers of immune cell activation. I'm pleased to say that we are successful on this front as meaningful post-treatment increases in both CD25 positive and ICOS positive CD8 T cells were observed in our most recent data release. Taken together, these early pharmacodynamic data suggest that MDNA11 has a biological profile that could translate to superior efficacy, and we look forward to the continued evaluation of this hypothesis in the ABILITY study. Safety data collected in the study to date have been encouraging, as we have not yet recorded any dose-limiting toxicities, which allows for continued dose escalation from 30 µg per kilogram in cohort 3 to 60 µg per kilogram in cohort 4, following two priming doses at 30 µg per kg. Looking ahead, the data we have seen to date gives us confidence in MDNA11's potential to be a best-in-class IL-2 therapy. We see the Superkine inducing a selective and resolute anticancer immune response without the activation of cells associated with toxicity or pro-tumor immune suppression. This indicates that MDNA11 is potentially engaging its intended target. The safety and pharmacokinetic profiles displayed to date are promising and suggest that it can overcome the shortcomings of the only approved IL-2 therapy, Proleukin. We are eagerly anticipating reporting additional clinical data from the trial in the third calendar quarter this year and providing a fulsome clinical update in calendar Q4 across all dose cohorts. With that, I'll turn things over to our CFO, Liz Williams, to discuss the financial results for fiscal year 2022. Liz. Thanks, Martin, and good morning, everyone. Before I begin, I'll note that all references are in Canadian dollars unless otherwise stated. Medicenna remains well capitalized through key anticipated catalysts during the ABILITY study, including single-agent efficacy results. We had cash equivalents, and marketable securities of CAD 20.5 million as of March 31, 2022, which, based on our current projections, is expected to fund our operations late into calendar Q2 of 2023. Net loss for the year ended March 31, 2022 was CAD 22.6 million, or CAD 0.42 per share, compared to a loss of CAD 17.3 million or CAD 0.35 per share for the year ended March 31, 2021. The increase in net loss for the year ended March 31, 2022 compared with the year ended March 31, 2021 was primarily a result of increased expenditures related to the MDNA11 development program, as well as higher general and administrative expenses associated with the company's Nasdaq listing in August 2020. Research and development expenses of CAD 14.7 million were incurred during the year ended March 31, 2022, compared with CAD 10.9 million incurred in the year ended March 31, 2021. The increase in research and development expenses in the current year was primarily attributable to costs associated with the development of MDNA11, including one-time IND enabling studies and manufacturing of GMP materials for the clinical trial, as well as clinical and regulatory costs associated with the initiation of the Phase I/II ABILITY study. General and administrative expenses of CAD 7.8 million were incurred during the year ended March 31, 2022, compared with CAD 6.5 million during the year ended March 31, 2021. The increase in expenditures year-over-year is primarily attributed to a full year of costs associated with Medicenna's Nasdaq listing and corresponding directors' and officers' liability insurance premiums, compared with only eight months of expense in the prior year period. For further details on our financials, please refer to our financial statements and management's discussion and analysis, which will be available on SEDAR and EDGAR, respectively. I'll now hand the call back to Fahar for some concluding remarks prior to the Q&A session. Thanks, Liz. As we look ahead into fiscal 2023, we are pleased to be advancing towards key potential value inflection points, including clinical data from the first three cohorts, as well as PD and PK data from cohort 4 at the Cytokine Summit at the end of July. The pharmacodynamic data we have seen thus far from the three cohorts is encouraging. We have incorporated key early learnings from the trial into its design moving forward and continue to enroll patients in its fourth dose escalation cohort. In parallel, our Superkine and BiSKITs platforms continue to fuel our preclinical efforts, which we expect to provide additional opportunities for pipeline expansion and value creation. I'd like to thank all of those who have contributed to the considerable progress we've made over the past year under challenging circumstances. This includes our employees, partners, investigators, and clinical trial participants and their families. Their efforts have us well positioned for success as we continue our work to generate shareholder value by advancing towards our ultimate goal of developing novel cytokine-based immunotherapies that provide patients with meaningful clinical benefits. With that, we'll now open the lines for questions. Operator. Thank you. We will now be conducting a question-and-answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. One moment please while we poll for your questions. Our first question has come from the line of Matt Biegler with Oppenheimer. Please proceed with your question. Hey, guys. Thanks for the update. Two from us. First, can you comment on the mix of patients you've enrolled in ABILITY so far? It seems like many or most of the patients had tumor types like a sarcoma that you wouldn't really expect to respond to immunotherapy or a checkpoint inhibitor or Proleukin for that matter. Then I had a question maybe on the safety signal that you're seeing so far, just interesting commentary around the priming dose. Seems to us like maybe that's a way to get around some of the CRS-related side effects. With that said, I appreciate the commentary around Bempegaldesleukin, especially 'cause I know that CRS is kind of what they saw, and that's what their dose-limiting toxicities were, I believe. What types of DLTs would you expect now for this drug? You know, maybe something like a neutropenia or changes in blood counts. Because with the non-alphas, we wouldn't really expect to see vascular leak syndrome, right? That's something that obviously Proleukin struggled with. I'm just kind of interested in kind of what you think we should be looking out for in terms of the drug safety profile going forward. Thanks. Great. Thanks, Matt. Thanks for your questions. I'll pass it on to Martin in just a moment. With respect to the tumor types, as you recall, in the clinical trial during the dose escalation portion of the study, we had kept it open to a wide range of tumor types covering a pan-tumor profile of patients. Not only have we included patients with metastatic melanoma in this study so far in the first eight, patients, we've seen patients, as I've noted, patients with pleomorphic sarcoma, again, metastatic version of that tumor. We've also had patients with pancreatic ductal adenocarcinoma, as well as, you know, patients with squamous cell carcinoma of the tonsil, et cetera. It's a mixed patient population, and as we plan to proceed with the dose expansion phase of the study, we will be focusing very much on metastatic melanoma and renal cell carcinoma with potentially another group of patients that we may if as we see these patients beginning to see benefit during the dose escalation will include that cohort of patients as well. We haven't finalized on the sort of the third group of patients that we may include. Clearly, as you said, you're right. When you look at both the sarcomas that we've seen patients have tumor control, that's encouraging sign considering these patients had rather large tumor masses of over 20 centimeters in total. With that, I will pass it on to Martin, who can sort of give you a bit of background on the safety features of the drug and what we're seeing so far. Okay, Martin? Sure. Thanks, Fahar. I think you've described it well. You know, as with a lot of these first-in-human studies in the lower ranges of a dose range, you know, we do tend to throw the net fairly wide in terms of tumor types in order to expedite that early phase of a study where we're not really expecting to be able to look all that definitively at clinical efficacy, you know, with safety being the dose-limiting consideration. As such, yeah, as Fahar said, we've had a bit of a mixed bag. We certainly had a few metastatic melanomas, but also head and neck cancer, upper GI, a couple sarcomas. You know, not at all atypical in terms of a very early stage dose ranging. Yeah, we will look to narrow that down as we go into the doses where we might expect to see some clinical effects. Maybe just a comment on the safety profile. Sure. I think seems like Martin's line is not coming through, but, Hello? Sorry, Martin, can you Yes, I hear you fine. Okay. I think you are sort of cutting off. Let's see if you can. The question was about what sort of expected- Okay. safety features of DLTs. Yes. We might expect. Yeah. Yeah. What we've seen so far in terms of toxicities, and it is an emerging pattern, I would say is consistent with that that we've seen with a whole range of immuno-oncology agents, by way of what I would term sort of infusion reactions, patients with fevers, with chills and rigors, sometimes some abdominal, sorry, a gastrointestinal upset. I think, you know, this is a pattern certainly in terms of severity. It is consistent with that that I've seen for a whole range of different classes of immune-active drugs, whether those are, you know, bispecifics or monoclonals or, you know, across the families really. What the investigators are telling us are, you know, that these have not been a worrisome event in terms of the clinical experience to date. These are things that are managed easily in the normal ward setting of the clinic with simple measures and so to date, that pattern is reassuring, I think, and as I say, consistent with multiple classes of immune oncology treatment. What do we expect to see by way of DLTs? Well, I think, you know, as you acknowledge, the step-up dosing is designed to minimize the risk of seeing that. I think what we might end up doing is reaching a biologically effective dose without having seen a dose-limiting toxicities. I think if we stay on top of things in the way that we have done to date, that would be my hope that we would go maybe one or two further dose steps. What we're already seeing in terms of the levels of activity pharmacodynamically suggests that we wouldn't need to go a whole lot further than that. Quite possibly, we won't be in a toxicity limited status when we expand for the next phase of the study. Okay. Thank you, Martin. That makes sense. makes sense. Thank you. Thank you. Our next question has come from the line of David Martin with Bloomberg. Please proceed with your questions. Hi. My first question is, could the fever be an early sign that you will see vascular leak syndrome or is it disconnected from VLS? Martin, your thoughts on that? Yeah. I think it's, you know, it's a non-specific finding. As I say, it's the pattern and the severity are more consistent, I would say, with a general IRR pattern seen across multiple classes of IO drug. That isn't to say that it's impossible that some individuals might have features more consistent with VLS. Yeah, it's a bit non-specific is probably the honest answer. There was no sign of eosinophilia at these doses? That's correct. So far, the eosinophil counts have remained outside of the, you know, the high-risk categories that have been described previously with IL-2 therapy. Okay. Next question. Have you taken any of the patients in cohort four to the third step-up dose? Has this strategy been successful as far as reducing the tolerability issues? Sorry. Yeah, Martin, I just wanted to. David, just wanted to, when you say cohort 4 to the next step up, can you clarify a bit more what you mean? Yes, we have p atients that have gone through the priming dose and gone to the 660 µg dose already. That's been the case. Is that what you mean? Yeah. Yeah. How many of those patients has that happened with? You know, are they tolerating the drug at 60? Yeah. We have, as you know, we do have the first eight patients in the study would be monitored for DLTs in this cohort 4, or for that matter, any cohort. Essentially, we've had, if I'm not mistaken, at least two patients that have gone through to the fixed dose of 60 µg, and we haven't seen any DLTs yet. Okay. Which cohort were the three patients with disease control? Were they all in the 30? We had in terms of when looking at target lesions, the first two tumor control patients were at the 10 µg dose. We also had one patient in the 30 µg dose, but in the 30 µg dose, which was the third cohort, we had a total of four patients in that cohort. Out of those four patients, we had three patients where the target lesion was in a sort of call it tumor control, with these patients having signs of additional lesions showing up, but the target lesions had stabilization. Three out of four patients in cohort 3 saw benefit on the target lesions, with one of them not having any additional lesions showing up post-treatment. I'd say too early to break it down, but we've seen, as I said, activity as early as the 10 µg dose. All the patients in the third cohort have had scans at this point. Were there any shrinkage, like, disease control can, you know, include a wide range of response of the tumors. Was there any with shrinkage? Yes, there were. Okay. Are the patients still on the drug? You know, what has been the duration of disease control? Yeah. We will provide more of that data, we expect at a conference late in July. We'll hold off on all those other additional data for later on. Okay. Last question. In the third cohort, were there any melanoma or renal cell carcinoma patients who progressed? Again, we'll sort of break it down in more detail at the conference so that we have the ability to compile more information for that conference, and share those data, not only additional PK/PD data, but also the data on individual patient profiles, including type of tumors, tumor burden, and some of the sort of prognostic factors of each of the patients and what the prior treatments were, et cetera. Can you at least say what the third patient who had disease control, what type of tumor they had, like two sarcomas, and what was the third one? Yeah, one was melanoma. Okay. Okay, that's it for me. Thanks. Okay. Thank you. Our next question comes from the line of Catherine Novack with JonesTrading. Please proceed with your questions. Hi. Thanks so much for taking my questions. The first thing I wanna ask, can you remind us of what degree of lymphocyte expansion is associated with clinical responses in IL-2? Given the low baseline count of the patients currently in this study, how translatable are these early dose escalation results? My second question is on the BiSKITs™ program. You know, given the cash runway extending measures you're taking, can you give us an updated timeline on getting the BiSKITs™ into the clinic? Thank you. That's great. With respect to answering your second question first regarding the BiSKITs program, as you know, we have just reported some data at the AACR meeting with the first BiSKITs that we're working on, which is an NTPDase1 IL-2 Superkine fusion. That's a program that we see quite a bit of interest and excitement around. The plans would essentially for us at this moment in time continue to optimize this particular molecule with respect to the NTPDase1 domain. The work that we've done so far is obviously using a mouse version of the NTPDase1. We will be looking to identify the right kind of or potential partnering with a company that has its own human NTPDase1. Until that happens and we've completed additional optimization preclinical studies with the molecule version that would eventually go into the clinic, I would say we are very early in the process to be ready for initiating a clinical trial any time, you know, the next 12 months or so, perhaps more towards the towards the end of 2023. In that scenario, we are not looking at a situation where the impact of our work on the BiSKITs is going to materially impact the spend as it's still very much a research project at the moment. Now, the other question that you raised was around the expansion of the the lymphocytes, et cetera. You're right. At the moment, we actually don't. If you go back to data from other prior studies with Proleukin or others, there's no confirmed correlation with respect to increases in population of specific immune cell types. At least that's demonstrated a correlation between changes in those population versus tumor responses, for instance. However, we have seen that with Proleukin, for instance, increases in lymphocyte counts of about two to three-fold are associated with better outcomes with respect to tumor response and so on. We're already seeing that with MDNA11, although I must say that the baseline counts of these patients have been low. We have as of our sort of going forward with future cohorts, we're sort of screening for patients that have a better lymphocyte count at baseline. As you know, most of the work that has been done with Proleukin and other competing agents out there, you'll see typically that the baseline lymphocyte counts tend to be well above 1,000. That's what we would hope to enroll patients in doing dose escalation going forward at these high doses, including doing the dose expansion so that we can get the patients to benefit the most from the drug. We expect the effect of MDNA11 to be a lot more pronounced going forward as we enroll patients with baseline counts that are more typically used in immunotherapy patients, etc. I don't know if Martin, if you want to add any more to that. No, I don't really have an awful lot. I mean, I think we're continuing to analyze this data and to, you know, look at subpopulations. I think going forward, we have a couple of additional biomarker presentations in the calendar that we'll aim to provide a bit more insight as we go. David- Right. I think what we are really very encouraged about is seeing the level of tumor control in these patients, despite that the baseline lymphocyte counts have been much lower than what would normally be the threshold baseline count. That's for us really compelling with respect to the kind of increases we've seen, and also to see tumor control at these levels, despite the fact these patients have very poor pretreatment or baseline lymphocyte counts or CD8 T-cell counts, NK cell counts, etc. Despite that, what we're seeing in these patients who are heavily pretreated, have large tumor burdens, to see tumor control is, for us, I think at the moment, looks really exciting, particularly as we plan ahead with the higher doses that we are expecting to see, and enroll patients that have a much more reasonable baseline lymphocyte counts in the clinical trial. Look forward to. I would expect much greater increases in actual populations of the CD8 T-cells, NK cells going forward, instead of the first three cohorts where the lymphocyte counts were generally much lower at baseline. Got it. Is that something that we can expect to see starting in cohort four, or can you give me a little bit more granularity on that? I would say that we've set up the protocol. The amendment has now been approved with all three regulatory agencies. We would expect that in cohort five onwards. Okay. Of course, when the dose expansion phase as well. Yes. Yeah. Got it. Appreciate it. Very helpful. Thank you. Our next question has come from the line of RK with H.C. Wainwright. Please proceed with your questions. Thank you. Most of my questions have been answered, but just I have two general questions and probably you have given answers to these already, but I'm just trying to make sure. For this Cohort 4 in the ABILITY where you're going to be priming with two doses, I'm assuming these are increasing doses like dose level two and three so that you can increase the exposure before you go to your dose four. Is that yes or no? Is it dose two and dose three? Also what's the timing in timing interval, you know, between the two priming doses and before you get to the final to the fixed dose? Yeah. Just to give you a bit of background here, the first two priming doses are at the 30 µg per kilogram dose, and it is at a dose that is, as we've seen so far, clinically beneficial for the patients. We are not dosing patients at much lower doses. We've actually seen tumor control at the 10 µg dose. Therefore, the 30 µg dose, although we call them priming doses, I would say that those 30 µg doses are substantially effective in stimulating the immune system very profoundly. That's really one of the first things that we are doing here. Then moving on to the 60 µg dose. The interval between treatments has not changed. That's every two weeks, irrespective of whether it's a priming dose or once we reach the fixed dose. The dosing regimen has stayed at once every two weeks. Does that answer your question? The other question I have is, you know, from the data that you have seen so far, in various tumors and also the data from your competitors, you know, what type of tumors do you think are a good target for MDNA11 outside of the two that, you know, you're planning on right now? I would say that, you know, what was very surprising for us to see a stable disease in sort of patients with sarcomas. Both of these are aggressive forms of sarcomas, rare kind of sarcomas, and therefore, considering that these patients had baseline large tumor burdens, to see tumor control was very encouraging in that patient population. As you know, sarcomas are not generally used with IL-2, neither have are they sort of generally used with different immunotherapies or checkpoint inhibitors. That was a novel new finding that we found very encouraging. Going forward, of course, we'll continue to enroll as our protocol mandates that we'll be enrolling patients with different tumor types. However, the focus will have to be on tumor types that generally respond or have a prior history of responding to checkpoint inhibitors, for instance. That's going to be the sort of, our expectation that patients with, prior exposure to checkpoint inhibitors or patients that would normally qualify for immunotherapies would likely do even better. As we continue to enroll patients going forward, we will be, more selective in making sure that the patients that are enrolled in the study, are those patients that normally do respond to immunotherapies rather than those patients that have no, prior, exposure to or, immunotherapies have not been approved for those patients. We are sort of, focusing on, those tumor types that we expect the immune system to play a major role. Although, as I said, in addition to sarcomas, we've had two patients with pancreatic cancer as well. We know that those patients typically again would not respond to checkpoint inhibitors or other immunotherapies. We are fine-tuning the patient population as we escalate the dose with the intent, of course, to get into the dose expansion phase with the right patient population that is likely to benefit most with immunotherapies such as our drug MDNA11. Perfect. Thank you very much for that, Fahar. Appreciate it, and good luck. You're welcome. Thank you. Thank you. Our next question comes from the line of André Uddin with Research Capital. Please proceed with your questions. Hi, Fahar and Liz. Just wondering if you could give us a business development update on the licensing of MDNA55 and how that's progressing. Thanks. Right. Yes. As we put out in our press release, what we've done and of course in the call today also mentioned that we have, as you know, earlier this year, completed a very comprehensive analysis that would be supportive of the commercial potential for MDNA55 with respect to conducting a thorough primary market research and adoption of MDNA55 at different hospitals across both Europe and U.S. following interviews with about 40 different KOLs, 20 in Europe and 20 in the U.S. Of course, also from a market opportunity, whether it's us, ourselves, but nonetheless for partner purposes, for collaboration, we needed to make sure what the pricing might be for MDNA55, which was something that we were able to complete, as well as getting feedback from payers and insurance and reimbursement agencies to find out what kind of expectation there might be. In all these cases, we've seen a very positive feedback from these KOLs, from payers, from insurance companies, reimbursement agencies, et cetera, with respect to what the pricing might be. That was really important for us to have in place, which we now have in place. I would say that our interactions with potential partners address those in that bit of information that was not available. It does give us additional 2 checkboxes that we are progressing with. I think the other key feature of our discussions going forward with potential partners is the fact that localized administration of a drug is something that's sort of discouraged potential partners in the past. Administration of a drug intracranially is something that's not out there. There's nothing approved until very recently, where Daiichi Sankyo announced that they had a virus-based therapy which is being administered directly in the brain tumor as well, which was approved by Japanese authorities. That third bit of information and has substantially improved the profile of MDNA55 from that perspective. Also there is, as you can see, consistent or increased awareness of using an external control arm in different oncology clinical trials. Over a period of this past several months, we've seen quite a bit of renewed interest on MDNA55, and we are progressing and advancing those discussions, and that process continues. We'll provide updates as we get closer to a time when we can make more meaningful announcements regarding a partner. We are definitely fully engaged with the process at the moment. Great. Thank you. Thank you. Our next question has come from the line of Kumaraguru Raja with Brookline Capital Markets. Please proceed with your questions. Hi. Hi, I'm Shubhendu Roy for Kumar Raja. Thank you for taking our questions. With regards to the BiSKITs program, how are you thinking about it? For the IL-13 MDNA413 and the MDNA109 programs, do you plan to test it further in non-human primates before taking it to the clinic? If you can provide some color on the sort of indications you want to test it in. Thank you. Right. As I mentioned earlier, the NTPDase1 IL-2 BiSKIT, that particular molecule, as I said, so far we've been working with the mouse version of NTPDase1 to be able to demonstrate whether this concept or this approach is feasible, which we have done. Of course, the next steps typically will be to identify the right human version of NTPDase1 that we could fuse our IL-2 with. Whether that comes with us bringing it into Medicenna, which is something we are not planning to do. Our preference is, of course, to work with companies that have checkpoint inhibitors. Going forward, we'll be looking at analyzing and approaching different potential collaborators that we can use or work together with their checkpoint inhibitors that are in the clinic or already in the marketplace so that this sort of provides some additional comfort that we are not starting from scratch with a different checkpoint inhibitor. Medicenna clearly does not have a checkpoint inhibitor program. That process will proceed. As we've done in the past, including with our IL-2 Superkine program, particularly with MDNA11, we'll generally take programs. We like to identify a ideal candidate to take into the clinic, but sometimes you end up in situations where you have two molecules that are just as good as each other and we might do some pilot non-human primate studies. These are not being planned in the next 9-12 months. These are obviously further away from that point. Nevertheless, we expect that we would be in a position to pursue with IND-enabling studies towards the sort of the second half of next year with these bifunctional superkines. With the 413 molecule, we've seen that it works not only on itself, particularly in cold tumors, but also when combined with our MDNA11, and therefore there'll be some additional optimization that we plan to work on. Our 413 molecule is currently fused to the Fc domain. We expect to do further optimization with the right protein scaffold. It might be trying it with albumin, for instance, et cetera. Again, that molecule, although we have demonstrated proof of concept in mouse models, that molecule is again not quite ready for non-human primates or IND-enabling studies at this stage. There's further work to be done, and we will continue to report more data at conferences, with respect to these new optimized versions of both the BiSKITs as well as the MDNA413 molecule as well. Okay. Great. Yeah. Yeah, that's very useful. Thank you. Just with regards to the ABILITY study, you are planning to do some combination studies with checkpoint inhibitors. When do you think you could initiate those combination studies? Also, when you recruit the patients, would they have failed CPI treatment or would they be naive? Any timelines that you can share with that? Yeah. The combination study is part of our phase I/II ABILITY study at the moment. Once we've established the recommended phase II dose, the next step, of course, is to conduct the dose expansion phase of the study with the single-agent monotherapy. That will help us identify which of the three different patient populations are benefiting in a single-agent setting. We certainly want to see single-agent activity. We want to see tumor responses. We expect that is a reasonable threshold for us to get there. The plan is to combine MDNA11 with an NTPDase1 molecule that's already in the market. We will announce that in the future. The plan is, obviously, toward the first half of next year would be the right time for us to proceed with initially optimizing the dose in the combination setting before we expand into the combination setting. Typically what happens is, although we will have the recommended phase II dose in a single-agent setting, it is very likely that we will, when we combine the two therapies and administer them at the same time, it's not unusual to start at the RP2 dose minus one level in the combination setting before finalizing the dose in the dose expansion phase of the combination arm as well. That's more likely, as I said, in the first half of next year. Thank you so much. You're welcome. Thank you. Our next question comes from the line of David Bautz with Zacks Research. Please proceed with your questions. Hey, good morning, everyone. Just one question on MDNA11 for me. For your pharmacodynamic results that you've seen so far with T cell and natural killer cell responses, have those been consistent across the different tumor types in the study, or have you seen any other patient characteristics that kinda correlate with those responses? Obviously the number of patients, it's just eight patients and therefore difficult to make a judgment as to what correlations, if any, exist. As I mentioned, we've seen changes or expansion of the CD8 T cells, NK cells, et cetera, across all different tumor types. That is really encouraging. It's irrespective of what tumor type, but of course, each patient has a different baseline levels, so that might have some kind of impact. We haven't got enough data at this moment. With data on just eight patients, it's difficult for us to correlate those numbers with different tumor types, et cetera. We would expect to get more data as we continue to enroll more patients and see if there are any trends coming through. I would expect that we'll probably see more of that during the dose expansion phase of the study. We'll be able to see more clearly if these PD changes are occurring based on other tumor characteristics or patient profile or not. Okay, great. Thanks for taking the question. You're welcome. Thank you. We have reached the end of our question and answer session. I'd now like to hand the call back over to Fahar Merchant for any closing remarks. Well, I would say thank you, operator, and thanks again to all of you who have joined us today. Clearly we're excited with the data that we've seen so far, although these are the early first three cohorts that are the lowest dose cohorts in the study so far. As we escalate, we hope to see further benefit of MDNA11 in this difficult to treat patient population. We will be providing periodic updates over the coming months on our progress. Finally, let me wish everyone a very good day. Thank you. Ladies and gentlemen, this does conclude today's presentation. Thank you once again for your participation. You may now disconnect your lines.