Hello, and welcome to Medicenna Therapeutics' fiscal first quarter earnings call. All participants are in a listen-only mode. There will be a question-and-answer session at the end of the presentation. 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. Please go ahead. Thank you, operator. 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 June 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 fact 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 U.S. securities law. Now, I will turn the call over to Dr. Fahar Merchant, President and Chief Executive Officer of Medicenna Therapeutics. Fahar? Thanks, Dan, and thanks to all listening for joining us on the call today to discuss our fiscal Q1 2022 corporate update. In addition to Dan, I'm joined by Dr. Mann Muhsin, our Chief Medical Officer, and Liz Williams, our Chief Financial Officer. The last several months have been an important period of execution, during which we achieved key clinical, scientific, and corporate milestones. These milestones have left us poised for sustained success with a steady cadence of catalysts expected over the coming months. On today's call, we will briefly review some of these recent accomplishments, discuss our plans and expectations for the upcoming phase I/II ABILITY-1 study of our selective long-acting IL-2 superagonist, MDNA11, and lay out the clinical, scientific, and corporate objectives we will be working towards as we continue through the remainder of fiscal year 2022 and beyond. Let's start with some recent accomplishments, beginning with our MDNA11 program. Last quarter, we completed the submission of our clinical trial application to a human research ethics committee in Australia in order to commence our phase I/II ABILITY-1 study. Mann is going to speak at length about the clinical trial in a few moments, but what I would like to emphasize now is that we remain on track to start enrollment in the study in Australia during calendar Q3, and we will be expanding additional sites in the U.S., Canada, and U.K. thereafter. We expect the remaining regulatory submissions and approvals for these different jurisdictions to be complete before the end of the calendar year. I will now turn your attention briefly to MDNA55, our IL-4 guided toxin targeting recurrent glioblastoma, or rGBM, the most common and uniformly fatal form of brain cancer. We were very pleased to have data from our phase IIb trial published in a prestigious peer-reviewed journal, "Clinical Cancer Research," last quarter, which provided important external validation for our program. These data were discussed at length during our last earnings call in May. In the interest of time, I will now just emphasize the paper's main finding, which was that the early determination of progression-free survival using modified RECIST criteria appears to be a strong surrogate for overall survival in recurrent GBM. Together with previously presented modified mRANO-based response rates and overall survival data from the study, we believe this finding bodes well for the conduct of the planned phase III MDNA55 trial, where mRANO-based PFS could potentially be a reliable early surrogate for overall survival. Looking forward to our MDNA55 program, we remain in active discussions in pursuit of a partnership to facilitate its further development and commercialization. While the details of these conversations need to remain confidential at this point, we look forward to providing a more thorough update on these activities when appropriate. In the interim, we at Medicenna continue to advance the required regulatory activities associated with MDNA55 GMP manufacturing and future commercial supply for potential market launch. Submission of the phase III protocol to the regulators and selection of a contract manufacturing organization for long-term commercial supply of MDNA55 will be finalized jointly with our future development partner, with the expectation that the phase III registration trial can be initiated in 2022. On the discovery and preclinical front, we recently announced a peer-reviewed publication in Frontiers in Immunology featuring data on MDNA109, which is our IL-2 Superkine platform, which is the precursor of MDNA11. The 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. To provide some brief background, oncolytic adenoviruses lead to selective infection and lysis of cancer cells and can effectively deliver therapeutic levels of cytokines into tumor lesions and also promote anti-tumor immune response. Data presented in the paper showed that compared to treatment with IL-2-armed virus, treatment with MDNA109-armed virus led to superior tumor growth inhibition with a clear tendency towards achieving complete tumor regression. Mechanistic analysis showed that this was due to MDNA109's superior ability to reprogram the tumor microenvironment, as MDNA109 virus induced efficient T cell receptor signaling. It activated cytotoxic anticancer immune cells and inhibited tumor-protecting myeloid cells in the tumor microenvironment. Additionally, MDNA109 virus demonstrated the ability to induce a potent anti-tumor immune memory response to protect previously treated hamsters against re-challenge with pancreatic cancer cells. Collectively, these results 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 colder tumors such as pancreatic cancer, where a great unmet need exists today. Going forward, we plan to continue leveraging the versatility offered by our Superkine platform in our discovery and preclinical programs as we seek to develop next generation Superkine-based therapies such as our BiSKITs platform. In addition to forming the basis of MDNA11, our IL-2 Superkine platform, MDNA109, is also a core component of our BiSKITs program. As a reminder, BiSKITs are highly versatile and targeted bifunctional molecules that comprise of a Superkine fused to a second anticancer therapeutic agent, such as a checkpoint inhibitor or a second Superkine. The BiSKITs platform enables us to design bespoke immunotherapeutic agents that incorporate two synergistic mechanisms required to treat more aggressive and recalcitrant tumors, where a simultaneous two-pronged approach may be necessary to improve safety and efficacy. During the fiscal first quarter, we presented at the AACR annual meeting data on our MDNA19/MDNA413 BiSKIT. These data, which were discussed in detail during our last earnings call in May, demonstrated MDNA19/MDNA413's potent immune modulating effects and its potential to overcome immunotherapy resistance mechanisms and treat immunologically cold tumors. They also showed how the BiSKITs platform can efficiently combine the enhanced immune signaling properties of multiple Superkines, in this case, an IL-2 superagonist and an IL-4/IL-13 superantagonist into a single bifunctional, long-acting therapeutic. Looking forward, we remain very excited about the potential of the BiSKITs platform and expect to declare a lead BiSKIT candidate by the end of the calendar year. Lastly, before I hand the call off, I'd like to highlight two corporate milestones we achieved last quarter. These were the appointments of Doctors Mann Muhsin and Kevin Moulder as CMO and CSO, respectively. You were introduced to Mann and Kevin on our last earnings call, and since then, each has continued to integrate seamlessly into our management team. I look forward to our continued work together, and I'm thrilled that we were able to attract candidates of their caliber to the company. With that, I'll hand the call off to Mann to provide some more details on our MDNA11 Program. Mann, please go ahead. Thank you, Fahar, and good morning, everyone. I'm happy to have the opportunity to speak with you all today about the phase I/II ABILITY-1 study of MDNA11, which is our novel selective and long-acting IL-2 superagonist. As Fahar mentioned, we remain on track to start enrollment in the study in Australia in calendar Q3, and will then be expanding the trial to sites in the U.S., Canada, and U.K. thereafter, in line with our previously stated guidance. One thing I want to emphasize is that we feel reassured in this guidance, even in light of the Australian government's recent COVID-related restrictions. Conversations with our clinical sites, trial investigators, and Australian domiciled CRO have confirmed that the treatment of oncology patients is considered an essential service, and is therefore exempt from COVID restrictions, including travel between different regions. Further, during our conversation with these parties, we were assured that prior government-mandated lockdowns in Australia had minimal impact on enrollment in phase I oncology trials, which adds to our level of confidence. We will, of course, remain in constant contact with our CRO, trial sites, and investigators as the study progresses and will keep the market updated if any material changes occur to our stated timelines. With regards to the design of the ABILITY-1 study, it will be a phase I/II basket study that will evaluate safety pharmacokinetics, pharmacodynamics, and antitumor activity of various doses of intravenously administered MDNA11 every two weeks in patients with advanced solid tumors. It will begin with an MDNA11 monotherapy dose escalation phase, which will be followed by a dose expansion with both an MDNA11 monotherapy arm as well as a combination arm designed to evaluate MDNA with a checkpoint inhibitor. The dose escalation phase will permit alternative dosing schedules and also includes options for intra-patient dose escalation, which will allow us to gain a wealth of information to inform the expansion phases of the study. Patients that will be enrolled in the ABILITY-1 study may have any one of 10 different solid tumor types, including advanced renal cell carcinoma and metastatic melanoma. These two tumor types are of particular interest as they are known to respond to recombinant human IL-2, also known as Proleukin, but to date, have not shown comparable responses to the new long-acting variants of Proleukin currently in the clinic. We therefore believe that by evaluating MDNA11 in these tumor types will present an opportunity to demonstrate MDNA11's best-in-class potential. Now, what clearly differentiates MDNA11 from Proleukin and other agents in the IL-2 landscape is that it has been engineered so that binding to IL-2 receptor alpha is abolished, whereas binding to IL-2 receptor beta is substantially enhanced. This is crucial, as stimulation of IL-2 receptor alpha leads to preferential activation of tumor-protecting Treg cells that can suppress systemic antitumor immune response and causes extreme toxicity, whereas stimulation of IL-2 receptor beta is key for activation of cancer-killing immune cells that are the target effectors of IL-2 therapies. MDNA11's beta-only IL-2 receptor selectivity gives the molecule the potential to outperform other agents in the IL-2 landscape, which rely entirely on the not alpha approach. What I mean by this is that rather than having reduced IL-2 receptor alpha binding and enhanced IL-2 receptor beta binding compared to Proleukin, as in the case of MDNA11, these competing IL-2 variants were designed to simply reduce IL-2 receptor alpha binding. This was done via pegylation. Now, while pegylation does reduce IL-2 receptor alpha binding and improve half-life, it also considerably interferes with and reduces IL-2 receptor beta binding when compared to Proleukin. We believe this is the reason as to why not alpha-regulated variants have produced suboptimal clinical data to date compared to Proleukin, as these molecules are likely not sufficiently activating cancer-killing immune cells due to their suboptimal IL-2 receptor beta binding affinities. Now, in addition to believing that MDNA11 will outperform competing not alpha IL-2 variants, we also believe that it has the potential to overcome the shortcomings of Proleukin. As I mentioned a few moments ago, Proleukin stimulates IL-2 receptor alpha. This leads to activation of Tregs, which inhibits the antitumor immune response and is associated with unfavorable prognosis in cancer. It also causes extreme toxicity, which necessitates dosing of Proleukin in the ICU. Finally, Proleukin must be dosed every eight hours for nine days due to its poor pharmacokinetic properties. We believe that MDNA11's beta-only selectivity will allow it to overcome the toxicity concerns associated with Proleukin, and its high affinity to beta receptor will also leading to improved efficacy. Additionally, using human albumin as part of the MDNA11 confers improved pharmacokinetic properties on the molecule. This should enable much more convenient dosing schedules, potentially dosing every two or three weeks. We also expect that it will lead to improved tumor accumulation, which in turn would further enhance the molecule's efficacy. Our belief that MDNA11 has the potential to be a best-in-class therapy is supported by a robust preclinical data set. Looking forward, we are eager to bolster this support with the clinical data updates we expect to report from the ABILITY-1 study in the coming months. The first update from the trial, which is expected later this calendar year, will include preliminary safety, PK/PD, and biomarker data from the dose escalation cohorts of the study. From the prospective pharmacokinetics, we aim to see preferential MDNA accumulation in the tumor and albumin-mediated half-life extension that would facilitate dosing every two or three weeks, consistent with an extended PD effect following two weeks dosing in the non-human primate studies. With regard to PD and biomarker data, we will be taking paired biopsies from patients before and during treatment and assessing the changes in the tumor microenvironment. We'll also be looking at the peripheral blood biomarkers and immune cells markers to see signs of anticancer immune cell activation, a lack of activation of Tregs, and pro-inflammatory and sensitive tumor microenvironment, which would confirm that MDNA11 is making the tumor microenvironment more immunogenic, which in turn would bode well for subsequent data readouts. Now, speaking of subsequent data readouts, preliminary efficacy updates from the ABILITY-1 study are expected throughout calendar year 2022, as monotherapy and combination efficacy data from the study are reported and mature throughout 2022. We hope to see objective response rates that meet or exceed those generated with agents in the same drug class, along with improved durability of response and a more favorable safety profile. When coupled with a more convenient dosing regimen, it would clearly position MDNA11 as the best-in-class agent and bode well for its continued clinical development and collaboration opportunities for a variety of indications and combinations. With that, I'd now like to hand the call off to our CFO, Liz 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 35.9 million as of the quarter close. During and subsequent to the quarter end, Medicenna received a total of $1.4 million for the reimbursement of past expenses through our non-dilutive grant from the Cancer Prevention and Research Institute of Texas, further strengthening our cash position. We believe this cash 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-1 study of MDNA11. Net loss for the quarter ended June 30th, 2021, was CAD 6.4 million or CAD 0.12 per share, compared to a loss of CAD 2.4 million or CAD 0.05 per share for the quarter ended June 30th, 2020. The increase in net loss for the quarter ended June 30th, 2021, compared with the quarter ended June 30th, 2020, was primarily a result of increased R&D 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. R&D expenses of CAD 4.3 million were incurred during the quarter ended June 30th, 2021, compared with CAD 1.8 million incurred in the quarter ended June 30th, 2020. The increase in R&D expenses in the current year quarter is primarily attributable to higher CMC costs associated with the GLP and GMP manufacturing of MDNA11 for the ABILITY studies, increased preclinical expenses associated with GLP-compliant MDNA11 IND enabling studies, as well as discovery work on our BiSKITs platform, increased clinical costs due to activities in preparation of the initiation of the ABILITY study. Higher salary and benefit costs associated with increased headcount necessary to support increased activities. These increases in expense in the quarter were partially offset by the reimbursement of expenses from the separate grant. General and administrative expenses of CAD 1.9 million were incurred during the quarter ended June 30, 2021, compared with CAD 0.7 million during the quarter ended June 30, 2020. The increase in expenditures year-over-year is primarily attributable to increased directors and officers liability insurance premiums due to our NASDAQ listing. For further details on our financials, please refer to our financial statements and management's discussion and analysis, which will be available on both SEDAR and EDGAR, respectively. With that, I'll now hand the call back over to Fahar. Thanks, Liz. Before we can move on to the Q&A, I'd like to take a moment to recognize the talent and dedication displayed by the Medicenna team, as well as our partners and investigators over the past months. Thanks to their efforts, our MDNA11 ABILITY-1 study and other programs have continued to advance as planned, despite the ever-evolving circumstances around the pandemic. This has left us poised to achieve a steady cadence of value-creating milestones in line with our previously stated guidance. Looking forward, we expect the continued advancement of these programs to drive our sustained growth and, most importantly, address the unmet needs of the patients. With that, we will now open the lines for questions. Operator? Thank you. If you will like to ask question press star one on your telephone keypad a confirmation tone to indicate your line on the question queue You may press star two if you would like to remove your question from the queue and participant using speaker equipment may be necessary to pick up the handset before pressing any key. Our first question is from Matt Biegler with Oppenheimer. Please proceed. Hey, guys. Thanks for taking our questions. Congrats on the recent progress. Fahar, looking ahead to year-end, just wondering if you could elaborate on what types of translational data you think are most relevant as we look for early signs of efficacy. I'm assuming it's things like Ki-67 induction and potential for regulatory T cells. Just wondering if there are others we should be interested in. Also, I may have missed this, but can you just remind us if you're hoping to get any biopsy data from this trial? Yes. Thanks, Matt. Good to have you join the call today. Certainly, what I will do is both of the questions, I'll pass them along to Mann, who will be better able to provide you with the details on both of those questions. Mann? Thank you, Fahar, and thanks for the question. The study will be looking into an array of immunophenotypes and biomarkers in the peripheral blood. There are certain biomarkers that are known to be associated with T-cell activation, exhaustion, recruitment, and tumor infiltration. The study will examine, for example, CD8 to Treg ratio, as well as change from baseline and level of increase, as well as the increase in the expression, upregulation of biomarkers in favor of clinical benefit driven by immune cell activation, such as Ki-67, which you indicated in the question, ICOS, CD25, PD-1, OX40, CTLA4, and many others. Furthermore, we will anticipate some favorable trends in increases in the surrogate efficacy markers. We will expect also albumin-mediated half-life extension, preferential biodistribution in the tumor, and Th1 bias in the tumor microenvironment, as measured by increased T-cell priming, trafficking, and infiltration TILs. In paired biopsies, as well as markers such as CD3, CD4, CD8, B, FOXP3, GNLY, and natural killer cells marker, and will assess major cell lineages, T-cell subtypes, CXCR3, CXCR6, and CCR7. Exhaustion markers, classically PD-1 and LAG-3. Finally, we will study gene expression patterns using the NanoString IO360 panel, which is commonly used in IO agents. Based on the preclinical data, the half-life of MDNA11 seemed to be longer than comparable novel agents in the drug class, allowing for dosing every two or three weeks, and that is what the ABILITY study will evaluate, and those markers should map well with this half-life extension. Furthermore, the pharmacodynamic markers associated with the MDNA11 treatment seem to substantially outlast the pharmacokinetic trends. The half-life flexibility is significant because it will enable our agent, MDNA11, to be combined with all checkpoint inhibitors, whether the backbone treatment has a cycle of two weeks or three weeks, or even for four weeks, we will be considering that given the pharmacokinetic marker that substantially outlasts the pharmacokinetic markers. I hope I answered your question to the level of detail that you would like, and feel free to follow up if you have any follow-up questions. Thank you. Yes. Thank you for the detailed response, Mann. That seems consistent with the preclinical data, which is cool. Fahar, I wanted to ask a follow-up just relating to the IL-2 field more broadly. As you know, it's getting pretty crowded with several entrants also testing new approaches like conditional activation, targeted IL-2. Maybe if you could just speak to why you believed an optimized version of Proleukin, which is effectively what MDNA11 is, why that's the best approach to take. Thanks for taking my question. Yeah. Thanks, Matt. Clearly, yes, you're right. There's lots of different approaches being pursued with respect to the IL-2 space, and we are aware of those. Generally, I would say, first and foremost, I would like to make it very clear that although we sort of classify our program very much like an optimized version of Proleukin, in fact, our molecule is far from it, so that although you might look at the other candidates that are in the clinic very much as optimized versions of Proleukin, MDNA11 actually is dramatically different from Proleukin in the sense that not only does it have the extension of half-life, which is common with all other interleukins that are in the clinic at the moment. I think the important differentiation here is clearly that not only do we reduce binding to CD25 and therefore have reduced alpha dependency, our molecule has been engineered so that it has substantially better affinity for beta or CD122. This is where the big difference is between the work that's being currently in the clinic versus the work we are doing, and therefore, I believe we have that unique differentiation and the desire for selective binding to CD122 and therefore preferentially stimulating naive CD8 T cells, NK cells, as well as the effector T cells, is crucial with the approach that we are pursuing. Now, yes, there are other approaches for localization, for instance, using ways of tumor-based activation using conditionally activated IL-2. Again, remember that those IL-2s tend to be similar to Proleukin, and there is a whole bunch of dependency of those particular tumor types because remember, activation of those tumors or at the tumor site itself will be dependent on what kind of tumor it is, whether it is producing the required protease to activate the IL-2, et cetera. There will be quite a lot of variability from tumor type to tumor type, patient to patient, and we can never expect that the dosing regimen, et cetera, that is established will work in multiple tumor types or not, because there's so much other dependencies as well. Yes, there are potential ways of localization. What we have achieved with MDNA11 is that by virtue of us fusing our molecule to albumin, there is considerable amount of data to also support the fact that molecules like MDNA11 that have an albumin domain tend to passively accumulate in the tumor itself, as well as we know from data that they accumulate in tumor-draining lymph nodes. Both of those accumulations of our IL-2 are crucial because they provide, we believe, a much better safety profile, but also localized stimulation of the immune cells, in addition to that you might see from a peripheral perspective. I think we are achieving both goals with our MDNA11 program in terms of localization by virtue of the albumin, but also the selectivity towards CD122. That's, I guess, the key differentiator. Last, Mann, if he has got anything else to add. Thank you, Fahar. I think I want to emphasize on the albumin component of our compound. If we just learn from history, there is no tumor as desmoplastic as pancreatic cancer. The very only drug approved in this tumor type is Abraxane, which is nab-paclitaxel. It's a nanoparticle albumin-bound paclitaxel, which is able to accumulate and penetrate tissue and tumor as desmoplastic as pancreatic cancer. I believe albumin is a key component of the drug on top of the mutations and affinity to CD122 and the limited, if any, Treg activation. I think MDNA11 will enable us to grow the tumor types with huge unmet needs, tumor types that are in the middle of the immunogenicity spectrum that are not to be that responsive to IOs. That will give MDNA11 positive attributes that make it superior and best in class compared to competing agents in the IL-2 development landscape. Thanks, guys. Looking forward to year-end. Our next question is from David Martin with Bloom Burton. Please proceed. Yes. Good morning. My question's a competitive one as well. One of your competitors, instead of your approach of increasing CD122 and decreasing CD25 binding, has reduced binding to CD132. I'm wondering if you can talk about biologically what you'd expect out of your approach versus the reduced CD132 binding. In particular, they seem to think that the activation of the naive T cells and the NK cells might be the underlying cause of the toxicity, the vascular leak syndrome. Can you talk about what you've seen so far as far as VLS? Right. Answering your last question with respect to VLS, so far, at all the doses that we have tested in non-human primates going as high as 600 micrograms per kilogram, we haven't seen, either clinically or histologically, any signs of vascular leak syndrome so far. That's very encouraging, and it sort of consistently supports the hypothesis that the binding to beta is not the culprit here in terms of vascular leak. In fact, the same author of the work that you mentioned regarding the competitor has published in Nature the work with MDNA109, where you had clearly a higher affinity to CD122, and that publication demonstrated lack of vascular leak or lung edema in that paper, and clearly showing that having high affinity to CD25 was the cause of vascular leak. In a sense, we feel quite encouraged with those data and consistent with other approaches and other data that have been published to date, the CD25 is likely the more critical culprit in the vascular leak scenario. With respect to reduced binding through gamma C, clearly what you sort of end up doing is that you reduce the signaling and therefore proliferation of the actual cells, namely the effector T cells, to fight the cancer. On top of that, you prevent signaling and proliferation of naive CD8 T cells and also the same with NK cells. I must say that we believe that activation of NK cells is important in tumor control, and I will sort of pass it along to Mann Muhsin, who has obviously a much better understanding of the role of NK cells and naive CD8 T cells and why the approach that we are taking is the correct one. Mann? Thank you, Fahar. NK cells are a very important critical component of the immune surveillance in human immune system, and the human immune surveillance mechanism is key, and it's evolved to protect against tumorigenesis. The importance of the NK expansion in modulating the tumor microenvironment and to achieving some therapeutic effect in certain agents in tumor models. It's clearly shown that it does that immune surveillance, it modulates the tumor microenvironment without eliciting toxicity, and this has been established in tumor models and in publications as well. As Fahar indicated, last but not least, our GLP studies, the data we have seen so far from the MDNA11 show clearly those findings, and it's well aligned with the existing knowledge today, publications, and animal models that stimulation of CD122 will not result in that toxicity that is prohibitive of dosing in humans. As we all know, this is the basis of many IL-2 agents in the development landscape today. Thanks for the question. Thank you. That is it for me. Our next question is from Naureen Quibria with Maxim Group. Please proceed. Hi. Thanks. Good morning, and thank you for taking my questions. I guess the first one is, I'd like to just sort of drill down on what. Can you hear me? Yes. Okay. I'd like to drill down on what Matt asked earlier with regards to the biomarker data that will be presented or will be reported at year-end. Mann, you kind of rattled off quite a few biomarkers. Are there any specific ones that'll give you greater confidence in the drug's profile, and are there any benchmarks related to those specific biomarkers that we should focus on? Thanks for the question. Yes. The list I provided is the short list. We have an extensive list of biomarkers. Some of them are classical for the IL-2 pathways, and some of them are novel that we believe we will see some substantial effect or movement or ratio, like the example I gave about CD8 to Treg. At this point in time, it's hard to predict which one of them exactly moves to what level to make it significant. As you know, those markers could be variable from one patient to another. As a matter of fact, some of those markers, as you know, can be even variable within the same patient as they progress from one treatment to the next. It's hard to disclose specifically what markers will move at what level at this point in time. As indicated earlier, we will be absolutely providing you guys with a continuous update as we dose more patients and progress through the course of the study. Got it. That's helpful. Fahar, with respect to the same ABILITY-1 study, obviously you're planning to expand, you've mentioned beyond Australia to other jurisdictions, North America, U.K., Canada. I guess perhaps I missed it. Will you be planning on to have those other sites come online at about the same time, or is there a specific sequence in the regions that you plan to follow, have the study come online? Right. Yeah, good question. The key thing for us is that before the end of this year, we should have submitted and secured approval from each of these three jurisdictions, namely U.S., Canada, and U.K., to start enrolling in this global phase I/II clinical trial. The sequence, it's basically going to be whichever comes through first, and we'll proceed along that basis. Therefore, unlikely that we have full control over that. Of course, that will be based on each of the territories' process of reviewing, namely ethics review and regulatory review. We will be submitting, though, most of these different applications at more or less the same timeframe. Nothing special in terms of which territory should come online first. Okay. That makes sense. Thank you. That's all for me. Our next question is from RK from H.C. Wainwright. Please proceed. Thank you. Good morning, Fahar and Mann. A lot of my questions have been answered. In terms of the BiSKITs program, what's the next thing that we should expect? Yeah. With BiSKITs, as you know, we did present some data at the AACR meeting in early first half of this year. It was really focused very much along the two fusion partners, namely MDNA413, which is the IL-4/IL-13 antagonist fused to our IL-2 superagonist. That program was the data that we shared with. The company is continuing to screen a number of different versions of BiSKITs that consists of different Superkines, but also different fusion partners. Those activities are continuing with respect to optimization of the specific linkers that we use, the specific cytokine or Superkine that we use, and also the orientation of the Superkines. That work is currently well underway. We are hoping to identify a lead candidate that is an optimized candidate before the end of this year, so that we can then start IND-enabling studies in 2022. That is our plan. The identification of a lead candidate has not been finalized yet. It will be done at the end of this year. Okay. Okay? Thank you for that. On the ABILITY study itself, would patients from Europe and U.S. be included, or do you need to do some additional work to get the regulatory filings started, both at the FDA and the EMA? Right. Yeah, sorry. Yeah. We are looking to U.S., Canada, and U.K. Those three territories, the filings will be identical with respect to all the work that has been done to date for the Australian submission. In that sense, we do not expect to have any additional work required for these different filings. The data that we have so far will be sufficient. Of course, if we have additional data from the Australian patients as they are enrolled, those would certainly be supplemented, if necessary. Otherwise, no, the package would be more or less identical other than the required geographical changes in how you submit the document. The content will be identical. Okay. Thank you for that. Thanks for taking my questions. Thanks. In the interest of time, we're going to ask each speaker to just ask one question. Our next question is from David Bautz with Zacks Small-Cap Research. Please proceed. Hey, good morning, everyone. Most of my questions have been answered, but, Liz, a question about spending. How should we think about R&D spending in the upcoming quarters compared to the current quarter? Our projected burn by quarter for the next sort of 18 months is about CAD 5 million-CAD 6 million per quarter. It will fluctuate up and down. This quarter, we did have some significant costs associated with the GMP manufacturing, and we do expect that that's split over the current quarter as well as our fiscal Q2, so ending September 30th. In the second half of the year, it will be a bit lower. Of course, the CMC cost will be replaced by clinical costs. That's our projection. About sort of CAD 3 million-CAD 4 million per quarter in terms of R&D expenses going forward. Okay, great. Appreciate it. Our next question is from Kumar Raja with Brookline Capital Markets. Please proceed. Hi. Thanks for taking my questions. With regard to the CTA review, where do we stand? What are your expectations there, like, do you have any updates there from the agencies? Also, are you able to screen patients while the CTA is being reviewed? Right. Good question. Yes, the application is under review. We are on target to enroll patients this quarter. Things are progressing well, and we will notify the markets as soon as we've enrolled our first patient. With respect to the second question regarding, I'll sort of pass it on to Dr. Mann. Thank you, Fahar. Yeah. We are in direct communication with our investigators in Australia. Now, technically for the screening and pre-screening activities, as you know, they won't happen without a patient signing the informed consent, which requires the full submission to be accepted, approved, and so forth. As Fahar indicated, we have every reason to believe and full evidence that we will continue as our timelines and projections and as our guidance to dose the first patient in the study by the end of calendar Q3. We'll provide updates as soon as we are able to. Okay. With regard to U.K. and U.S., you mentioned that you'll be moving forward with the application as and when possible. In terms of the clinical trials in these two jurisdictions, how are you thinking about leveraging data from Australia? Clearly with Australia, as I mentioned earlier, the study design is essentially the same design across the globe. The data, as we obtain the data, will be therefore used to supplement. We would be required to provide any additional evidence to the regulators if we have them at that time. That would be the normal course of business, and therefore we sort of follow the same regulatory guidelines with respect to any new data that is generated. That will certainly help with respect to dosing, and therefore we can continue with the dose escalation along the same basis once we have data from the earlier cohorts. That should translate into proceeding with the higher dose cohorts in those other territories as well. Okay, great. Thanks. We have reached the end of our question-and-answer session. I would like to turn the conference back over to Fahar for closing comments. Thank you, operator. Thanks again to everyone for joining us on the call, and also our loyal shareholders. We look forward to the continued advancement of our pipeline, and we'll keep everyone updated along the way. Thank you again. Take care, and bye-bye. Thank you. This does conclude today's conference. You may disconnect your lines at this time, and thank you for your participation.