Hello, and welcome to the Medicenna Therapeutics fiscal Q2 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. Please be advised 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. 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 quarter ended September 30, 2021. If you have not yet 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 and 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 the MDNA11, MDNA55 and BiSKITs programs, the potential of the Superkine platform, partnering activities, cash runway, and the presentation of additional data. All statements other than statements of historical facts included in this conference call, including the future plans and objectives of the company, 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 and 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 in Form 40-F of the company, and in 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 we'll turn the call over to Dr. Fahar Merchant, President and Chief Executive Officer of Medicenna Therapeutics. Fahar. Thanks, Dan, and thanks to those who have joined us today to discuss our fiscal Q2 2022 corporate update. In addition to Dan, I am joined by Dr. Maen Hussein, our Chief Medical Officer, Rosemina Merchant, our Chief Development Officer, and Elizabeth Williams, our Chief Financial Officer. This is an exciting time for Medicenna as our accomplishments over the past months have us advancing towards key positive inflection points with the potential to differentiate our IL-2 program and provide clinical validation of our Superkine platform. Today, we will review some of these recent accomplishments, outline our clinical and corporate strategy, and set the stage for what to expect over the coming months by discussing the clinical, scientific and corporate objectives we are working towards. Let's start with some of our recent accomplishments, beginning with our MDNA11 program. As a reminder, MDNA11 is our beta-only long-acting IL-2 super agonist that we believe is well positioned to be a best-in-class cytokine in the immunotherapy treatment landscape. Last quarter, we initiate our phase I/II ABILITY study of MDNA11, expanding our clinical pipeline. Patient dosing in the trial is currently underway in Australia, and we recently received IND clearance from the FDA to expand the trial to the United States. In addition, we are planning to further expand the study to sites in Canada and the United Kingdom and expect regulatory submissions for these jurisdictions to be complete before the end of the calendar year. While I let Mann speak in more detail about the trial, I will say now that we are very pleased with the progress being made and remain on track to provide a preliminary update on safety, PK/PD, and biomarker data from patients in the early cohorts enrolled in the dose escalation phase of the study by the end of calendar 2021, as well as an initial efficacy data update from the dose escalation portion of the study by mid 2022. The update in calendar 2021 will be an important check to confirm that the best-in-class properties we see in our murine and non-human primate studies are being replicated in humans, which we believe will correlate to a more efficacious drug when compared with other IL-2 variants in clinical development. Staying with our MDNA11 program, we also recently reported data from murine and IND-enabling non-human primate studies at the SITC meeting. These data reinforce our belief that MDNA11 has the potential to be a best-in-class therapy and highlight the advantages of its differentiated beta-only approach to selectively target this key IL-2 receptor subunit. Non-human primate data indicate that MDNA11 may overcome the safety and PK challenges of recombinant human IL-2, which is known as Proleukin, and approved for the treatment of advanced renal cell carcinoma and metastatic melanoma. They also show that by selectively targeting the IL-2 receptor beta subunit and avoiding the IL-2 receptor alpha subunit, MDNA11 preferentially induced durable proliferation and expansion of anticancer immune cells with limited stimulation of pro-tumor Treg cells. We believe this beta-only activation of the IL-2 receptor will translate to enhanced efficacy in comparison to Proleukin and other not-alpha IL-2 versions that are in the clinic. In a murine colon cancer model, data showed that MDNA11 alone or in combination with an anti-PD-1 checkpoint inhibitor led to tumor growth inhibition and dose-dependent durable complete responses in all mice, even though tumor growth rate was not inhibited by anti-PD-1 monotherapy. Additionally, initial treatment with MDNA11 alone or in combination with anti-PD-1 provided long-term protection against subsequent tumor rechallenge by inducing antigen-specific memory CD8 T cells. We believe these collective results, which Mina will be discussing in more detail shortly, provide a strong scientific rationale for our ABILITY Study and highlight the potential of MDNA11 to overcome the shortcomings associated with Proleukin and competing not-alpha IL-2s in the clinic. Shifting gears, I'd like now to briefly discuss MDNA55, which is our phase III-ready empowered IL-4 Superkine being developed as a treatment for recurrent glioblastoma. As some of you may recall, our phase IIb trial showed that a single treatment with MDNA55 led to a doubling in the overall survival when compared to a matched external control arm. Based on these and other data, we have aligned with the FDA on an innovative hybrid phase III trial design that allows for two-thirds of the control subjects to be from a matched external control arm. This trial design was recently featured in a peer-reviewed manuscript published in The Lancet Oncology and in an oral presentation at the Society for Neuro-Oncology and American Society of Clinical Oncology's first annual conference on CNS clinical trials. We have recently secured the FDA's agreement on deferring any pediatric clinical trials with MDNA55 to occur only after the adult phase III trial is completed, instead of having to conduct a pediatric study in parallel with the adult study. This approach substantially de-risks the conduct of the registration trial in adults by the potential partner. In the interim, we continue to advance the required regulatory activities associated with MDNA55 GMP manufacturing and future commercial supply for potential market launch so that the program can be advanced as efficiently as possible once a partnership is established. On the discovery and preclinical effort, last quarter, we were pleased to announce a peer-reviewed publication in Frontiers in Immunology featuring data on MDNA109, which is our IL-2 Superkine platform and the precursor of MDNA11. This paper, which was independently authored by researchers at the University of Helsinki and other institutions, evaluated oncolytic adenoviruses that were either unarmed, armed to code for MDNA109, or armed with wild-type IL-2 in a hamster pancreatic cancer model. Results showed that compared to wild-type IL-2, MDNA109 was better able to reprogram the tumor microenvironment, which led to superior tumor growth inhibition with an MDNA109 armed virus compared to an IL-2 armed virus in a pancreatic tumor model. These and other results from the paper externally validate the versatility of the MDNA109 platform and its potential to overcome limitations associated with less active versions of IL-2, such as native IL-2, particularly in immunologically cold tumors, such as pancreatic cancer, where a great unmet need exists today. Going forward, we expect the versatility offered by our Superkine platform to continue to power our discovery and preclinical programs as we seek to develop next generation Superkine-based therapies such as those derived from our BiSKITs platform. As a reminder, our BiSKITs platform enables the design of bespoke immunotherapeutic agents that incorporate two functionally non-overlapping mechanisms of action so as to potentially achieve synergistic therapeutic effects. This may allow for the treatment of more aggressive and recalcitrant tumors, where a simultaneous two-pronged approach may be necessary to improve safety and efficacy. BiSKITs comprise a Superkine that is then fused to a second anticancer agent, such as another Superkine, an antibody, or a checkpoint inhibitor. An example of a BiSKIT comprising two Superkines is MDNA19-MDNA413, which is another promising long-acting therapeutic candidate that combines an IL-2 superagonist with an IL-4 IL-13 super-antagonist to potentially overcome tumor resistance mechanisms to immunotherapies and can be a viable treatment option for immunologically cold tumors. Examples of BiSKITs include fusions of our IL-2 Superkines with checkpoint inhibitors such as an anti-PD-1 antibody in the cis mode, or an anti-PD-L1 antibody in the trans orientation. These agents can potentially provide superior anti-tumor effect compared to traditional checkpoint inhibitors in monotherapy settings by enabling T-cell activation while simultaneously stimulating pathways to suppress T-cell exhaustion and inhibiting tolerance of the immune system to tumor cells and antigens. They may also offer important intellectual property advantages and crucial lifecycle management and patent extension as first generation checkpoint inhibitors begin to come off patent in the coming years, and highlight one of the key advantages of our Superkine platform. Unlike others who utilize inefficient chemical synthesis or conjugation techniques such as PEGylation to improve pharmacokinetic profiles of cytokines, our Superkine platform is independent of such manufacturing challenges and instead uses protein scaffolds such as albumin, as is the case with MDNA11. Our highly selective and tunable Superkines and BiSKITs are generated using directed evolution, allowing them to be genetically fused with other biologics such as targeting antibodies, checkpoint inhibitors, other cytokines, or they can be used to arm oncolytic viruses, CAR T-cells, and cell-based therapies to further enhance their efficacy. These versatile options are not available with PEGylated IL-2s. Our manufacturing platform simplifies the scalability of the manufacturing process and leads to improved IL-2 receptor beta binding affinity compared to pegylated IL-2, further differentiating our Superkine and BiSKITs platform from competing approaches. Finally, using albumin as a scaffold has the potential for localizing our Superkines to the tumor microenvironment and tumor-draining lymph nodes, which function as sites of T-cell invigoration required for immunotherapy and checkpoint blockade. Looking forward, we remain committed to our BiSKITs program, given its potential to create fusions with antibodies, other Superkines, and checkpoint inhibitors. We are currently advancing multiple candidates through the discovery and optimization process. We plan to conclude the candidate selection and declare a lead candidate by the end of the calendar year. In addition to our recent clinical and scientific accomplishments, we also strengthened the intellectual property portfolio, protecting our Superkine platform with the issuance of a U.S. patent. This patent covers methods of treating a wide range of cancers with IL-2 variants such as MDNA11, and has claims that specifically focus on agents with enhanced affinity for IL-2 receptor beta, which, as I mentioned earlier, is a key point of differentiation for our IL-2 Superkines. This latest patent adds to a long list of issued and filed patents in major jurisdictions around the world, which collectively provide foundational composition type protection for MDNA11 and our broader IL-2 Superkine platform. Lastly, before handing the call off to Mann, I'd like to highlight an important corporate accomplishment from last quarter, which was the appointment of Dr. John Sampson to our board of directors. John is an immuno-oncology expert who brings extensive experience in clinical trial design and execution to our board, as well as deep knowledge of the regulatory process. He is currently the Robert H. and Gloria Wilkins Professor of Neurosurgery at Duke University, President of Duke's Private Diagnostic Clinic, and a member of the prestigious National Academy of Medicine. The insights he's provided have already proven to be valuable, and I look forward to his continued contribution to Medicenna's long-term growth and clinical strategy. With that, I will hand the call off to Maen to provide some more details on our MDNA11 program. Maen, please go ahead. Thank you, Fahar, and good morning, everyone. It's my pleasure to speak today about our beta-only long-acting IL-2 superagonist, MDNA11, and the advancements we have made in the last few months. As Fahar alluded to, this molecule was engineered to overcome the shortcomings of Proleukin and other modified IL-2s in the development landscape that rely solely on the not alpha approach. Proleukin's shortcomings stem from a number of limitations, including its dismal pharmacokinetic profile and preferential affinity for IL-2 receptor alpha compared to IL-2 receptor beta. Stimulation of IL-2 receptor alpha leads to the activation of Tregs, which is generally associated with unfavorable prognosis in cancer, can limit antitumor response, and cause extreme toxicity due to cytokine release syndrome, pulmonary edema, or vascular leak syndrome. These safety issues, together with Proleukin's poor pharmacokinetic profile, necessitates dosing in the ICU every eight hours. In an attempt to overcome these limitations, others have modified Proleukin to be a PEGylated, not-alpha IL-2. While the PEGylation of Proleukin does reduce IL-2 receptor alpha binding by steric hindrance and improve its half-life, it also considerably interferes with and reduces IL-2 receptor beta binding, which is crucial for activation of cancer-killing immune cells that are the target vectors of IL-2 therapies. We believe this is the reason that these PEGylated, not-alpha IL-2 variants have produced suboptimal clinical results to date when compared to Proleukin. Now, rather than utilizing PEGylation to improve half-life and avoid binding to IL-2 receptor alpha, we took a completely new approach when engineering MDNA11. First and foremost, using directed evolution, five mutations in the core of IL-2 improved the binding affinity for the IL-2 receptor beta by up to 200-fold when compared to Proleukin, and is the basis of our MDNA109 molecule. Beginning with MDNA109, we fused this IL-2 superagonist to albumin to improve its half-life, as Fahar mentioned earlier. Using albumin rather than PEG allows for a simpler, more homogeneous manufacturing process with no batch-to-batch variations while maintaining potent IL-2 receptor beta binding affinity. Finally, two additional mutations further enhanced selectivity towards the beta receptor and restricting binding to IL-2 receptor alpha. The net results of the design objective was to construct a differentiated and active beta-specific long-acting IL-2 that has the potential of tumor accumulation without multiple liabilities of PEGylation and achieve the optimal balance of safety and efficacy, as demonstrated in the data generated thus far. The results presented at the SITC meeting that Fahar previewed earlier demonstrate how this meticulously engineered design confirms MDNA11 with best-in-class potential. Pharmacokinetic analysis from the IND-enabling non-human primate studies showed dose proportional increase in exposure as measured by both Cmax and AUC, with corresponding increases in durability of key PD markers. MDNA11 was detected in the serum of non-human primates up to four-five days after dosing, with pharmacodynamic effects lasting more than eight days post-dose. As Fahar mentioned, these pharmacodynamic effects included the induction of anticancer immune cell proliferation and expansion, with limited stimulation of pro-tumoral Tregs. Importantly, MDNA11 also exhibited a favorable safety profile in these non-human primate studies, as its administration did not lead to any of the known safety issues associated with Proleukin that I mentioned earlier. Collectively, these results indicate that MDNA11 can overcome the limitations of Proleukin and other IL-2 variants in the development landscape, thanks to its enhanced beta targeting approach and its potentially superior safety, PK, and PD profiles. We are now working to clinically validate these findings through our ongoing phase I/II ABILITY Study. This study is designed to assess safety, pharmacokinetics, pharmacodynamics, and antitumor activity of various doses of MDNA11 administered intravenously every two weeks in patients with advanced and metastatic solid tumors in frontline as well as relapsed refractory settings. The study will enroll around 80 patients and will include a monotherapy dose escalation phase as well as combination arm to evaluate MDNA11 with a checkpoint inhibitor. During the dose escalation phase, alternative dosing schedules can be examined, and options for intrapatient dose escalation will be included. This should allow us to gain a wealth of information to establish an optimal recommended phase II dose and treatment regimen. Following the trial's dose escalation phase, we plan to conduct a dose expansion phase that will enroll patients with various solid tumors in monotherapy and combination settings. Two tumor types included in this cohort that will be of particular interest are advanced renal cell carcinoma and metastatic melanoma. These tumors are known to respond to Proleukin, but to date have not shown comparable responses to new long-acting IL-2 variants currently in the clinic. We therefore believe evaluating MDNA11 in these tumor types will present an opportunity to demonstrate single agent activity and best-in-class potential. Other tumor types that will be included in the trial are non-small cell lung cancer, both squamous and non-squamous non-small cell lung cancer, some GI tumors, triple-negative breast cancer, and other selected tumors with unmet need to exploit the pan-tumor potential of MDNA11. Looking ahead, the trial remains on track for a preliminary update on safety, PK/PD, and biomarker data from the early dose escalation cohorts of the study by the end of calendar year. All patients enrolled to date in early dose escalation cohorts remain on treatment with no discontinuations, no reported DLTs or SAEs thus far. In addition to the favorable safety and tolerability profile, it's our goal to show by year-end that its PK/PD profile could facilitate dosing every two or three weeks, consistent with extended pharmacodynamic effects following bi-weekly dosing in the non-human primate studies. We hope to demonstrate that MDNA11's profile as the drug of choice when combined with a number of checkpoint inhibitors, irrespective if they have two, three, or six-week treatment cycle. We also plan to analyze peripheral blood biomarkers and immune cell markers. Immune profiling performed by epigenetic analysis will assess markers such as CD3, CD4, CD8b, Foxp3, GNLY for NK, CXCR3, CCR6, CCR7, PD-1, LAG-3, to further confirm drug activity. Immunophenotyping will include markers such as CD45, CD3, CD4, CD8, CD19, CD56, CD25, Ki-67, PD-1, ICOS, CD11c, OX40, CTLA-4, and Foxp3. As part of this study, we intend to collect paired biopsies to assess changes in the tumor microenvironment. Gene expression profiles will be assessed using a panel of 770 cancer-related genes. Furthermore, specific markers such as granzyme B, perforin, interferon gamma expression, and others that are indicative of cell activation will be assessed using NanoString analysis. The NanoString nCounter PanCancer IO 360 Panel on immunofluorescence will be used for CD4, CD8, Foxp3, CD56, CD25, PD-L1, and others. With this comprehensive set of analyses, we hope to observe signs of antitumor immune cell activation, a lack of activation of Treg cells, and a pro-inflammatory and more sensitive tumor microenvironment, which would confirm clinically that MDNA11 is making the tumor microenvironment more responsive, less resistant, with elevated immunogenicity characteristics. This will provide further clinical validation of our promising non-human primate data and would bode well for subsequent clinical data readouts. Speaking of subsequent data readouts, we expect to report an initial update on efficacy data and tumor response results from the trial mid-2022, which will be followed by additional updates throughout the year. As efficacy data are reported and mature throughout calendar 2022, we are aiming to see objective response rate that meet or exceed those generated with agents in the same drug class, along with deeper responses, improved durability of response, and a more favorable safety profile for comparable patient populations. When coupled with a more convenient dosing regimen compared to Proleukin, results such as these would position MDNA11 as a best-in-class agent that could potentially have a broad therapeutic impact and clinical utility across multiple tumor types, across a wide immunogenicity spectrum, addressing high unmet needs. With the U.S. FDA IND clearance, FIH for MDNA11 trial and other objectives achieved, we believe we are making good progress towards achieving key goals of the MDNA11 program, and we look forward to the ABILITY studies' continued advancements. With that, I'll now hand the call off to our CFO, Elizabeth Williams, to discuss our recent financial results. Liz? Thanks, Mann, and good morning, everyone. Before I begin, I would like to note that all references are in Canadian dollars unless otherwise noted. I'm pleased to report that Medicenna maintained its strong cash position over the last quarter as we had cash equivalents, and marketable securities of CAD 26.7 million as of the quarter close. Based on our current projections, we believe this will be sufficient to fund our operations through to the end of calendar 2022, including through preliminary updates on biomarker PK/PD safety and efficacy data from our phase I/II ABILITY Study of MDNA11. We note an increased cash burn in the current quarter due to cash outflows associated with completing the manufacturing and IND-enabling studies for MDNA11 during the quarter, as well as paying our annual directors' and officers' liability insurance premiums. We've projected a lower quarterly cash burn in the next few quarters as these one-time high-cost activities are now complete. Net loss for the quarter ended September 30, 2021 was CAD 8.2 million or CAD 0.15 per share, compared to a net loss of CAD 3.8 million or CAD 0.08 per share for the quarter ended September 30, 2020. The increase in net loss for the quarter ended September 30, 2021 compared with the quarter ended September 30, 2020, was primarily a result of increased research and development expenditures related to the MDNA11 program, as well as costs associated with the Nasdaq listing, in particular, directors' and officers' insurance premiums in the current period. Research and development expenses of CAD 6.3 million were incurred during the quarter ended September 30, 2021, compared with CAD 2.2 million incurred in the quarter ended September 30, 2020. The increase in R&D expenses in the current year's quarter is primarily attributable to higher CMC costs associated with GLP and GMP manufacturing of MDNA11, which is now predominantly complete, increased preclinical expenses associated with GLP-compliant MDNA11 IND-enabling studies, which are also now predominantly complete, as well as discovery work on the BiSKITs platform and higher salary and benefit costs associated with a larger headcount necessary to support increased activities. General and administrative expenses of CAD 2 million were incurred during the quarter ended September 30, 2021, compared with CAD 1.7 million during the quarter ended September 30, 2020. The increase in expenditures in the current year quarter is primarily attributable to increased directors' and officers' liability insurance premiums due to three months of amortization in the current year versus two months in the prior year, increased stock-based compensation expense due to the timing and value of option grants, and an increase in salary and benefit expenses due to a higher headcount to support ongoing operations. 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. With that, I'll now turn the call back over to Fahar. Thanks, Liz. Before we move on to the Q&A, I'd like to take a moment to again commend Medicenna's employees, partners, and investigators for their accomplishments over the past months. Their ability to execute on our stated milestones and bring MDNA11 to the clinic despite working amid the ever-evolving pandemic is a testament to their talent and dedication. It also gives me confidence in our future outlook and ability to successfully achieve the goals we have set for ourselves on the call today. We believe accomplishing these goals will enable us to grow a robust pipeline of novel Superkines and versatile BiSKITs, which in turn will generate value for shareholders and bring us closer to delivering visionary immunotherapies to patients. We are excited for what lies ahead and will be sure to keep you updated on our progress along the way. With that, we will now open the lines for questions. Operator? Thank you. 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. Our first question today is from Matt Biegler of Oppenheimer. Please proceed with your question. Hey, good morning, guys. Congrats on all the progress. Really looking forward to that first human data later this year. Fahar, I wanted to ask you for your thoughts on the importance of NK cells relative to T cells. Obviously, we've seen really robust expansion in both NK cells and T cells pre-clinically, as you would expect, I think, from MDNA11's mechanism of action. There's some that speculate, or at least that I'm hearing that might not be ideal for optimal safety and efficacy for an IL-2 agonist. Can you just comment on that? Thanks. Thanks, Matt. Thanks for being on the call and this question. You're correct. The issue about NK cells has been controversial, particularly recently. Nevertheless, we feel that NK cells are really important components of immune surveillance mechanism, and that has evolved to protect against tumor progression. We believe the importance of NK cell expansion to modulate the tumor microenvironment and to achieve therapeutic effects in tumor models without eliciting toxicity has already been established, and provides the basis for many different treatment paradigms that are currently using NK cells in different modalities. We believe that the stimulation of NK cells is not detrimental. We believe it is essential for a holistic approach to having the most potential benefit for treating a patient with cancer. I think you need multiple attempts and multiple mechanisms to have a best outcome for the patient. To date, we don't see a potential for toxicity, et cetera, that seems to be claimed by others. We will see how this pans out. Clearly, when we did our non-human primate study, we showed that administration of MDNA11 not only substantially increased the population of NK cells but also naive CD8 T cells. We know that increases in naive CD8 T cells are not associated with any toxicity, et cetera. We feel that the proliferation of NK cells, naive CD8 T cells that are antigen-inexperienced, are not cytotoxic, and therefore, we believe those are also essential to boost therapeutic efficacy. Finally, we've also shown in our mouse studies that MDNA11 not only enhances the proliferation of naive CD8 T cells but also activated effector CD8 T cells as well. We're seeing multiple activities of MDNA11 in the tumor microenvironment, where we see an expansion of effector CD8 T cells, naive CD8 T cells, and NK cells. I think we believe that's probably the best approach. Maen, do you want to add anything to this? Thank you, Fahar. I think you covered it well. Generally speaking, as we know, NK cells nowadays representing a new strategy for cancer immunotherapy and, most of the new research emphasizing on the NK cell roles, the NK cell based therapy become promising and advanced scientific topic and scientific approach to be applied in clinic. NK cells, innate lymphocytes holding the spectrum of functional effect on anti-neoplastic and anti-cancer and, the foremost effector cells against tumor and the innate immunity and, greatly heterogeneous tumor microenvironment would require NK activity. As we know, there are NK cell therapy in the form of chimeric antigen receptor. With reference to safety, we haven't seen those claims actually in clinic having a detrimental safety effect on those patients. Rather, the activity of NK cells and the surveillance and completion of the immunity cycle does indeed require NK activity to prevent recurrence and to have a durable immune response. Yeah, that makes sense to me. Just one quick follow-up. How are you planning on unveiling the year-end update? Should we expect a press release and a conference call or just a press release? Any thoughts around that? Then I'll hop back in the queue. Thanks. Yeah. There isn't any major conference coming up before the end of the year, so most likely it will be in the form of press release. Maen, any thoughts? I believe that will probably the best way for us to communicate those data. Yes. I think we'll need to gather as much information, as much data, and we'll look into number of ways of communicating it, either via company updates or preliminary papers to be submitted in subsequent conference. Fahar, do you have anything else to add? No, I think that's good enough. We might even, you know, based on that, following the press release, we might just have a call similar to the one we've got right now so that, you know, there are questions that could be asked at that point. Okay. Okay. Thank you, Matt. The next question is from David Martin of Bloom Burton. Please proceed with your question. Thank you for taking my questions. Back to the safety question, in NK cells and other things. What doses have you started to date? You mentioned how many patients are in the trial? You mentioned that there'd be no DLTs or SAEs. Do you have commentary on how well the patients are tolerating the drug? We will provide all that information at the end of the year. We'll sort of compile the full set of results from the patients that have enrolled in the early cohorts so that we can provide context within not only the patient data, but also provide additional data that we collect from peripheral blood analysis, et cetera, so that we can provide a comprehensive set of results at the end of this year. We are in that phase of dose escalation. You mentioned how many patients we plan to enroll. It's gonna be approximately 80 patients. We estimate about 20 patients in the monotherapy dose escalation phase. How many patients have enrolled to date? We provide that update at the end of this year. Okay. Switching over to MDNA55, you talked about things that were underway so that once a partnership's secured, it can move quickly. That sounds like you are still negotiating for MDNA55. I'm wondering if you can provide some color on that. Are there multiple parties, one party? What's the profile of the interested parties and what are you expecting as far as a partnership, in as much as you can answer any of that? Right. Yes, good question. I have to basically say that we are in active discussions with companies that are covering various geographic areas. With that said, if we complete a partnering deal, we will make an announcement and be in a position to comment further with respect to the type and company that we are working with. Generally, we can say that the partnering process for MDNA55 is progressing well. We are confident that a transaction will be completed. However, we cannot at the moment provide specific timelines, but we'll update the shareholders as soon as we're able to do so. Okay. Just a quick housekeeping. When Liz says you have enough cash to the end of 2022, that's calendar 2022. Does that require some partnership dollars, or can you get there with what you have on the balance sheet? Uh, that's- Yeah, that's. Oh, sorry, Fahar. Go ahead. No, go ahead, Liz. I was going to ask you to answer that. Okay. Yeah, that's calendar 2022, and it does not factor in any cash proceeds other than what we currently have on the balance sheet. Okay, thanks. That's it for me. Thank you. The next question is from Kumar Raja of Brookline Capital Markets. Please proceed with your question. Thanks for taking my questions, and congratulations on all the progress. With regard to the clinical trial sites in Australia, how many sites do you have on board, and when do you expect additional sites to come on board? With regard to the U.S., when do you think you'll be able to start recruiting patients here? Right. With Australia, as you know, that's the geographic location where we first started enrolling patients. We have set a target of having at least four-six sites in place. Most of them are in place or nearing being in place and ready to enroll. We certainly have the enrollment currently underway in Australia. As far as U.S. is concerned, as you know, we just received the approval from the FDA for the IND submission. As we go through the IRB process or the ethics review at different centers, we are proceeding with those activities as well. We expect to have about eight-10 sites in the U.S. also enrolling patients. We think the first patient we are expecting will be soon after New Year in the U.S. The expectation is that the patients in U.S., they can potentially directly go to the monotherapy expansion phase? Depending on how far we are, but it will be mostly we will expect that it'll be dose escalation continuing at that time in January. We expect U.S. patients to also or U.S. sites to be also enrolling in the escalation phase as well. Okay. Finally, in terms of your efforts in autoimmune diseases, are you doing anything in that front? Sorry, can you repeat that question? I'm talking about focus on autoimmune diseases. You used to have some preclinical programs in autoimmune diseases earlier. Right. Yes. Yeah. Right. Yes, there is ongoing activity currently where we are using or exploiting the different IL-2, IL-4, and IL-13 assets or Superkines that we currently have in discovery phases, looking at different autoimmune diseases as well as neuroinflammation. As the activities that are currently being evaluated from a discovery perspective, yes, those activities are actively underway. Thanks so much. You're welcome. The next question is from David Bautz of Zacks Small Cap Research. Please proceed with your question. Hey, good morning, everybody. So you've previously indicated that for the dose expansion phase of ABILITY-1, you're gonna focus on renal cell carcinoma and melanoma patients. I'm just wondering if there is a limitation for these early patients as far as tumor type goes. Yes. Well, I'll pass it on to Mann. Maybe you can elaborate a bit more on that, the dose expansion phase. Sure. Yeah. Thanks for the question. For the dose expansion and as the study design, which is also on ClinicalTrials.gov, what we will have is a 1:1:1 ratio of melanoma to RCC to other selected tumors. Now, the other selected tumors, I'm gonna go over them quickly, include sarcoma, triple-negative breast cancer, pancreatic, as indicated earlier, non-small cell lung cancer, both squamous and non-squamous variants, colorectal, gastric, biliary tract, basal cell carcinoma, bladder, Merkel cell carcinoma, squamous cell carcinoma of head and neck, cutaneous, and OB/GYN tumors, namely uterine, ovarian, and cervical cancers. Those are included in the expansion in the 1:1:1 ratio between melanoma, RCC, and these select tumors. In the escalation, all those patients with all those tumors are actually entering the dose escalation portion of the study as we speak. We don't only have melanoma or RCC, we have also additional tumor types from the cluster tumors I've just mentioned. With the expansion combination, the same ratio is maintained 1-to-1-to-1 ratio of melanoma to RCC to other selected tumors as well. Hopefully that addressed your question, and thank you very much for the question. Yes, that's very helpful. Thank you. As far as the BiSKITs program goes, I'm wondering if you could go over maybe what are the most important considerations or what are the things that you're looking at that are most important for selecting a lead candidate from that program? Well, thanks for that. What we are working on is a number of different potential fusion partners as part of the BiSKITs platform. These two different bifunctional molecules are really, we have, I think, previously indicated different strategies where we have looked at two different superkines of being part of the BiSKITs. We've had an opportunity to share with you data on an antibody, which is a targeting antibody, together with the superkine, as well as data on a checkpoint inhibitor fused to our superkine. These are different various potential fusion partners. We are screening these and of course, the focus as far as oncology is concerned, to identify two distinct functional activities, that would allow us to then subsequently create a molecule or test a molecule that has, providing synergistic effect, very much being, based on clearly different tumor types. We are looking at that, very, very closely. At the moment it's difficult to specifically mention, what is our preference. We'll definitely be able to share a lot more data, and more information towards the end of the year. Okay, thanks for that, and thanks for taking the questions. You're welcome. The next question is from David Martin of Bloom Burton. Please proceed with your question. Yeah. Thanks for letting me have the follow-up. Mann, in his earlier comments, contrasted your approach to the not-alpha approach. I'm wondering if you have some comments on the not-gamma approach. Right. The not-alpha approach, I think, as you know, has been a focus of others at the expense of losing out also on the beta approach. We've seen that with the PEGylation approaches that have been pursued by others, where an attempt to create a not-alpha IL-2 unfortunately has also resulted in a molecule that has a weaker beta. That therefore, not surprisingly, has not shown promising single agent activity so far. Our approach, as you know, is very distinct in the sense that although we are proceeding with a not-alpha approach, we have dramatically improved the binding affinity towards beta. That beta-only strategy is crucial. We feel that the beta-only approach would subsequently require an active gamma based signaling so that we are able to fully take advantage of the selectivity for binding to beta and signaling through gamma. This way, you are able to create a molecule, or our molecule is such that it's not only stimulating your effector CD8 T cells, but to engage your naive CD8 T cells, your NK cells, you also require a signaling through gamma. Because by blocking signaling through gamma, you're not going to be able to engage your naive CD8 T cells and therefore not build a population of inexperienced CD8 T cells that is essential. You're not going to be able to benefit from any potential activity that is required for NK cell activation. We believe that engagement of both beta and gamma is essential. We certainly believe in gamma, blockade, in an autoimmune setting, which is something, that has been demonstrated, by work that has been done by Chris Garcia's lab and for which we already have a program of our own, where high binding to beta subsequently with reduced binding to gamma clearly shows, potential in autoimmune disease. I feel that, the approach that we've got here with, beta binding and gamma signaling is absolutely essential to get a full spectrum of activity from an antitumor perspective, so that we are engaging naive CD8 T cells, effector CD8 T cells, as well as NK cells. That's what we believe is the best approach. Okay, thank you. There are no additional questions at this time. I would like to turn the call back to Fahar Merchant for closing remarks. Thank you all for being on the call today. Really appreciate the calls and questions and answers that we received. We will certainly keep you all updated as we progress to the end of this year with respect to any updates, any new results, et cetera, over the coming weeks and months. Thank you again for joining the call and look forward to giving you more updates in the coming weeks. Thank you. Operator? Ladies and gentlemen, this concludes today's presentation. Thank you once again for your participation. You may now disconnect.