Hello, and welcome to Medicenna Therapeutics' fiscal year 2021 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. Earlier today, Medicenna issued a press release providing financial results and corporate updates for the fiscal year ended March 31st, 2021. 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 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 analysis in Form 40-F of the company, and in other filings made by the company with applicable securities regulators from time to time in Canada and the United States. The reader is 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'll turn the call over to Dr. Fahar Merchant, President and Chief Executive Officer of Medicenna Therapeutics. Fahar? Thanks, Dan, and thanks to all listening or joining us on the call today to discuss our fiscal year 2021 corporate update. In addition to Dan, I'm joined by Dr. Mann Muhsin, our Chief Medical Officer, Dr. Kevin Moulder, our Chief Scientific Officer, Mina Merchant, our Chief Development Officer, and Liz Williams, our Chief Financial Officer. Fiscal year 2021 was Medicenna's strongest and most productive year yet, despite the unpredictable environment caused by the pandemic. We achieved key clinical, scientific, and corporate milestones that have left us well-positioned for sustained success. On today's call, we will review some of these recent accomplishments, give an update on the current status of our pipeline programs, introduce the new members of our executive team, and provide an outlook for fiscal year 2022 and beyond. Let us start with some of our accomplishments over the past year, beginning with our program focused on MDNA11, our long-acting IL-2 Superkine. Milestones in this program include the presentation of non-human primate data showing that MDNA11 selectively stimulates prolonged expansion of anticancer immune cells without causing unwanted side effects, such as the generation of anti-drug antibodies, hypotension associated with vascular leak syndrome, or cytokine release syndrome. We also presented additional preclinical data that further highlighted MDNA11's best-in-class potential by demonstrating its durable and potent therapeutic efficacy, both as a monotherapy and in combination with checkpoint inhibitors in murine tumor models. To prepare for the initiation of a clinical study in 2021, we completed our scientific advice meeting, which is similar to a pre-IND meeting with the United Kingdom Medicines and Healthcare products Regulatory Agency. During the meeting, the agency agreed that our CMC preclinical and phase I/II-A clinical plans would be appropriate for submission of an investigational medical product dossier for a first-in-human study with MDNA11 in the U.K.. We are on track to submit a clinical trial notification to the Australian Human Research Ethics Committee this quarter in order to commence the phase I/II-A clinical trial of MDNA11 in the third quarter of calendar 2021. Mann will provide more information on our MDNA11 clinical plans in the next few minutes. I'd now like to turn our attention to MDNA55, our IL-4 guided toxin targeting recurrent glioblastoma, or RGBM, the most common and uniformly fatal form of brain cancer. Throughout the past year, we presented updated data from our phase II-B trial in RGBM that demonstrated MDNA55's potential to change the treatment paradigm in a high unmet need indication. These data showed that amongst an all-comer population, a single MDNA55 treatment resulted in a greater than 100% increase in two-year survival compared to an eligibility-matched external control arm and a greater than 100% improvement in progression-free survival compared to what is achieved with approved therapies. Thanks in large part to the robust external control arm study we conducted, the substantial magnitude of the effect observed in the phase II-B trial, as well as the significant unmet medical need in RGBM, the FDA recommended we conduct a landmark phase III trial to support MDNA55's approval in this indication. This planned trial has an open label hybrid design that allows for two-thirds of the control subjects to be from a matched external control arm. This was truly pioneering recommendation by the agency and to the best of our knowledge, this groundbreaking design may be the first in oncology to include a substantial external control arm in a trial designed to support regulatory approval. I will talk more about this trial as well as a recent publication featuring our phase II-B data in a short while. I will say now that we remain in active discussions with potential partners to facilitate MDNA55's advancement. While the details of these conversations need to remain private at this point, we look forward to providing a more thorough update on these activities when appropriate. On the discovery and preclinical front, we also recently unveiled our bispecific Superkine platform, which we refer to as BiSKITs. These novel molecules, which are fusions of two complementary Superkines or a Superkine and an antibody such as a checkpoint inhibitor, have the potential to address critical unmet needs, such as the treatment of cold tumors that do not typically respond to current immunotherapies. We recently presented some very exciting early data from this program at AACR, which Kevin will discuss later in this call. Now, alongside our scientific and clinical accomplishments, we also achieved notable corporate milestones during fiscal 2021, such as our listing on Nasdaq and the strengthening of our board by the addition of Dr. Jack Geltosky. This corporate momentum has continued into fiscal 2022, as we recently added Mann and Kevin, two highly talented immuno-oncology experts, to our management team. As I will tell you in a few moments, our ability to recruit such ideal candidates was due in large part to the clinical and scientific milestones I just mentioned, which showcased the best-in-class and first-in-class potential of our assets, together with the power and versatility of our Superkine and BiSKITs platforms. I will now let you hear from these team members, starting with our Chief Medical Officer, Dr. Mann Muhsin. Mann, please go ahead. Thank you, Fahar. Good morning, everyone. Today, I'll be talking about the MDNA11 program. First, I'd like to introduce myself and explain exactly why I'm so excited to be part of the Medicenna team. I joined Medicenna earlier this month and have deep expertise in immuno-oncology and IL-2 specifically. I've conducted more than a dozen clinical trials sponsored by multiple industry leaders including AstraZeneca, Hoffmann-La Roche, Merck, Novartis, Eli Lilly, Johnson & Johnson, and Bayer. I've also designed, executed, and led clinical development programs and oncology trials for a variety of biotech companies, most recently working at Nektar Therapeutics prior to joining Medicenna. One of the primary drivers behind my decision to come on as Medicenna's CMO was MDNA11's robust preclinical data set, which demonstrates the molecule's best-in-class potential and clearly differentiates it compared to approved therapies and competing IL-2 variants in development landscape. As those of you familiar with the IL-2 space likely know, recombinant human IL-2, while approved for the treatment of metastatic melanoma and renal cell carcinoma, has some major shortcomings. These shortcomings stem from the fact that recombinant IL-2 targets the trimeric receptor, which includes CD25. Stimulation of CD25 leads to the activation of Tregs, which inhibits antitumor immune response and is associated with unfavorable prognosis in patients with various types of cancers, as well as causing extreme toxicity, which necessitates the dosing of patients in intensive care units. Additionally, the dosing is required every eight hours for nine days due to recombinant human IL-2's poor pharmacokinetic properties. What I find so exciting about MDNA11 is not only that it can overcome these shortcomings, but how it overcomes these shortcomings. Using the Superkine platform, Medicenna has engineered MDNA11 to have dramatically increased affinity for the CD122 subunit of the IL-2 receptor, while having reduced affinity for the CD25. This is significant as stimulation of the CD122 is key for the activation of the cancer-killing immune cells that are vital effectors of IL-2 therapy. Additionally, the inclusion of human albumin in the molecule improves the molecule's half-life and bioavailability in the tumor tissue. Its fusion to a second protein, in this case, albumin, is a key point of differentiation for MDNA11 compared to competing IL-2 variants, many of which rely on pegylation to improve half-life. In general, pegylation requires a complex manufacturing process that is well known to not only affect product consistency but can also unintentionally mask the active site of the protein and reduce its efficacy. We have robust preclinical data sets demonstrating how MDNA11 enhanced affinity for CD122 and reduced affinity for CD25 positions it to be best in class. This data set shows that compared to competing IL-2 programs, MDNA11 is able to preferentially stimulate cancer-killing effector T and NK cells as opposed to Tregs. Thanks to this high selectivity, the molecule has also shown impressive efficacy, both alone and in combination with checkpoint inhibitors in preclinical tumor models. Additionally, non-human primate studies indicate that the molecule does not cause vascular leak syndrome or cytokine release syndrome, as has been seen with other programs. It was these best in class properties of MDNA11 that led me to realize the power of the Superkine platform and ultimately drove my interest in joining Medicenna. Now that I've told you a little bit of how I got here, let me talk about the plan moving forward. We're currently in the process of advancing MDNA11 into phase I/ II-A clinical trial in Australia and the United Kingdom, followed by expansion to the United States. We have chosen to begin the trial in these countries rather than United States for two reasons. First, starting in these countries allows us to begin the dose escalation portion of the trial at doses that are closer to therapeutically effective doses. Second, the United Kingdom and Australia have a relatively higher prevalence of checkpoint inhibitor naive patients compared to the United States, which may help with study enrollment. We continue to make good progress towards initiation of our trial as we wind down our GLP toxicology studies and are in the process preparing the regulatory package for submission in Australian agencies. This submission is expected by end of June. Additionally, we have chosen a CRO for the trial, and site selection is already underway in Australia. Initiation of the trial is expected in the third quarter of calendar 2021. With regards to trial design, we plan to begin with a dose escalation MDNA11 monotherapy phase, which will then be followed by a dose expansion phase. This dose expansion phase will evaluate both MDNA11 monotherapy as well as MDNA11 in combination with a checkpoint inhibitor. Another key element of the trial design is the planned collection of pre and on-treatment biopsies, which will allow us to collect valuable biomarker data that may speak to the MDNA11's mechanistic activity in humans. Looking ahead, we expect to provide a preliminary update on any available safety PK/PD and biomarker data by the end of this year. The first set of monotherapy efficacy signals from the trial are expected in the first half of 2022. Switching gears now, I would like to ask Fahar to speak briefly about our phase III-ready MDNA55 program. Thank you, Mann. As I mentioned earlier, MDNA55 is an IL-4-guided toxin targeting recurrent glioblastoma. Findings from the phase II-B trial evaluating MDNA55 in RGBM were recently published in the peer-reviewed journal, "Clinical Cancer Research." These findings indicate that early determination of progression-free survival with the modified RANO criteria employed in the study may be a strong surrogate for overall survival in RGBM. These results supplement previously presented findings showing an 81% tumor control rate based on modified RANO and a median overall survival of 15.7 months, which represents a greater than 100% improvement when compared to a well-balanced external control arm. As a reminder, the patient population included all MDNA55-treated trial participants with high IL-4 receptor expression and participants with low IL-4 receptor expression that received a high dose of MDNA55 treatment. We believe these positive modified RANO PFS and overall survival data bode well for the outcome of the planned phase III trial, which has overall survival as a primary endpoint. As I mentioned earlier, this planned trial utilizes an innovative open label hybrid design that allows for two-thirds of the control arm subjects to be from a well-matched external control arm. This design will reduce the cost and timelines associated with completing the trial by reducing the overall number of subjects needed to achieve the primary endpoint, which will be based on a one-to-one analysis of the MDNA55 treatment arm versus the pooled control arm. To ensure a near contemporaneous external control arm, we can include patients treated for RGBM over the past five years, as there has been no substantive change to the RGBM standard of care during this timeframe. We believe the FDA's recommendation to proceed with this first of its kind trial leaves MDNA55 well-positioned for success. The numerous benefits offered by the trial's hybrid design, together with our robust clinical data set, continue to drive our partnering discussions around the MDNA55 program. These discussions remain ongoing, and we look forward to providing an update on their status at the appropriate time. With that, I will now hand it over to our Chief Scientific Officer, Dr. Kevin Moulder. Thank you, Fahar. I'm very excited to be speaking on the call today. I would like to start by introducing myself to those listening since I, like Mann, am also a recent addition to the Medicenna management team. I joined Medicenna with over 30 years experience in drug discovery and development in several fields such as protein design, antibody technology, autoimmune disease, and immuno-oncology. This includes my time at Biogen, where I ran a predictive medicine department. My time as CSO at F-star Therapeutics, where I established the company's bispecific antibody technology and led the translational efforts to identify the program's first clinical lead. My time as Chief Development Officer at Tusk Therapeutics, where I directed the development of an anti-CD25 antibody. This antibody showed anti-cancer activity that stemmed from its ability to deplete Tregs while preserving IL-2 activity on effector T cells. Advancements in its development subsequently prompted the acquisition of Tusk by Roche. At Medicenna, I will be applying my knowledge from these experiences as we work to leverage the power of the Superkine and BiSKIT platforms to advance first and best-in-class assets towards the clinic. These platforms are powerful and versatile drug development tools. My desire to work with them was a key factor behind my decision to join Medicenna. I'd now like to give a brief overview as to how these platforms work. I'll start with the Superkine platform, which works by enabling the enhancement of natural interleukins through a process known as directed evolution. During this process, subtle changes are made to interleukins to modulate their desired properties, ultimately resulting in a library of tunable Superkines designed to address the underlying mechanisms of a particular disease. Select Superkines can then be engineered to further improve properties such as half-life, as in the case of MDNA11, or to add new capabilities, such as the ability to deliver a payload of a cell-killing toxin specifically to cancer cells, as in the case with MDNA55. The natural progression of our Superkine platform eventually led to the creation of our BiSKIT program, which we unveiled in March. BiSKITs are highly versatile and powerful molecules that consist of a Superkine fused to a second anti-cancer protein, such as a checkpoint inhibitor or a second Superkine. By combining molecules in this fashion, we can create immunotherapeutic agents that incorporate two synergistic mechanisms of action and overcome the shortcomings of currently available therapies. At the AACR meeting last month, we presented data on one of these assets derived from our BiSKIT platform. The asset is designed to overcome the shortcomings of checkpoint inhibitors. As you may know, checkpoint inhibitors are designed to target tumors by enhancing the activity of cancer-fighting immune cells. However, many tumors have immunosuppressive microenvironments that limit the efficacy of these therapies. Such tumors are referred to as being immunologically cold, and it was with these tumors in mind that we designed MDNA19-MDNA413. As we discussed during our AACR presentation, MDNA19-MDNA413 consists of a super antagonist. It is designed to work via two complementary and synergistic mechanisms of action, targeting both IL-2 and IL-4/IL-13 signaling. I'll focus first on the IL-4/IL-13-mediated mechanism of action. The molecule was designed to modulate this signaling activity by selectively binding the IL-13 receptor alpha subunit on the cells of the tumor microenvironment. This leads to a disruption in the IL-4/13 signaling, ultimately the inhibition of an M2a polarization of tumor-associated macrophages. This is significant as blockade of M2a macrophage polarization mitigates the pro-tumor effect of immunosuppressive microenvironments. Mitigating these effects can effectively turn a cold tumor hot, thereby making it susceptible to destruction by anti-cancer immune cells. With regard to IL-2's signaling, MDNA19-MDNA413 works in a manner very similar to MDNA11, preferentially targeting CD122 to enhance the activity of cancer-killing effector T and NK cells. This IL-2-driven agonist action complements the IL-13-driven antagonist activity I just mentioned, making MDNA19-MDNA413 a potential anti-cancer agent with the potential to effectively target cold tumors that are often resistant to current available therapies. This potential was demonstrated in our recent AACR presentation, and while I won't go through the full data set, here are a couple of key points I'd like to highlight. First, the molecule effectively enhanced signaling in cancer-killing effector T and NK cells and reduced activation of pro-tumor Tregs. This was evidenced by a 209-fold and 90-fold enhancement in CD8 to Treg and NK Treg ratios in vitro, respectively, when compared to native IL-2. Second, the molecules selectively bound and inhibited both IL-4 and IL-13 signaling via the IL-13 receptor Alpha 1 subunit, which is normally associated with the pro-tumor effects of M2a macrophages, while showing reduced affinity for the IL-13 Alpha 2 decoy receptor subunit. Compared to long-acting Fc fusion of IL-13, the molecule was approximately 240 times more selective for the Alpha 1 subunit compared to the Alpha 2 subunit. This selectively led to notable functional outcomes, as MDNA19-MDNA413 was able to potently inhibit IL-13/IL-4 signaling pathways and mitigate the polarization of M2a macrophages in vitro. Taken together, these results show how the BiSKIT platform can effectively combine the enhanced immune signaling properties of multiple cytokines into a single bifunctional compound. In the case of MDNA19-MDNA413, this resulted in a novel molecule with the potential to enhance the power of the immune system to address critical unmet need. Looking forward, I'm eager to lead the continued development of MDNA19-MDNA413 as well as our broader BiSKIT program. We expect to declare our first lead candidate for the program in the fourth quarter of calendar 2021. With that, I'd like to hand off the call now to our CFO, Liz Williams, who will present our financial results for the fiscal 2021. Thanks, Kevin, and good morning, everyone. Before I begin, I would like to note that all references to dollar amounts are in Canadian dollars unless otherwise noted. I'm pleased to report that over the past fiscal year, Medicenna was able to establish and maintain a strong financial foundation while advancing our pipeline of cytokine-based immunotherapies. Medicenna had cash equivalents, and marketable securities of CAD 40.4 million as of March 31st, 2021. These funds provide the company with sufficient capital through late 2022 based on its current plans and projections. Net loss for the year ended March 31st, 2021, was CAD 17.3 million, or CAD 0.35 per share, compared to a net loss of CAD 8.3 million or CAD 0.26 per share for the year ended March 31st, 2020. The increase in net loss for the year ended March 31st, 2021 compared with the prior year, 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, as well as no reimbursement under the grant from the Cancer Prevention and Research Institute of Texas in the current year period. Research and development expenses of CAD 10.9 million were incurred during the year ended March 31st, 2021, compared with CAD 5.9 million incurred in the year ended March 31st, 2020. The increase in research and development expenses in the current year is primarily attributable to higher CMC costs associated with GMP manufacturing of MDNA11 for the planned phase I/II-A clinical trials, increased discovery and preclinical expenses associated with GLP compliant MDNA11 IND-enabling studies, as well as discovery work on the BiSKIT platform, increased regulatory costs associated with preparation for the end of phase II meeting for MDNA55, as well as regulatory activities associated with preparation for the initiation of a phase I/II-A clinical trial for MDNA11. Finally, no reimbursement of expenses with respect to the CPRIT grant in the year ended March 31st, 2021, compared with CAD 1 million in the year ended March 31st, 2020. General and administrative expenses of CAD 6.5 million were incurred during the year ended March 31st, 2021, compared with CAD 2.4 million during the year ended March 31st, 2020. The increase in the expenditures year-over-year is primarily attributable to increased directors and officers liability insurance premiums due to our Nasdaq listing, as well as higher legal fees and listing expenses in the current year period due to activities associated with the Nasdaq listing, filing a shelf prospectus in both Canada and the United States, qualifying our common shares with the Depository Trust Company, and other current corporate initiatives. 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 hand the call back over to Fahar. Thanks, Liz. Before we move on to the Q&A, I'd like to emphasize how proud I am of our team for all that they have accomplished over the past fiscal year. They showed a tremendous amount of talent and dedication amid the pandemic, which enabled us to generate strong clinical and pre-clinical data across our pipeline. This has left us poised to achieve a steady cadence of value-creating milestones over the next year as we work to drive our sustained growth, most importantly, improve the lives of patients. With that, we'll now open the lines for questions. Operator? Thank you. If you would like to ask a question, please press star one on your telephone keypads. 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 is from Matt Biegler with Oppenheimer. Please proceed. That's close. Hey, thanks, guys. Thanks for the questions and welcome to the new members of the C-suite. Fahar and Mann, appreciate the details on the planned phase I. Maybe if we could just get a little bit more granular. Have you actually nailed down or agreed upon with Australia or U.K. a start dose yet? Based on pre-clinical models, how long do you think into dose escalation it might take us until we get into a therapeutically active range? Right. Thanks, Matt. Thanks for calling in. Appreciate the question that you've asked. Clearly, I'll pass it on to Mann so he can elaborate a bit more. Suffice it to say that, as I mentioned earlier on, that we had positive meetings with the MHRA regarding the CMC, the pre-clinical, as well as the clinical plan. Therefore, that has been reviewed, and we've received comments and incorporated those in our dossier that we're preparing right now. With respect to dosing and et cetera, I'll pass it on to Mann. Perhaps you can elaborate a bit more. Mann? Thank you, Fahar. At this point in time, we won't be disclosing our first human dose or give you projections regarding how many escalations would we need before getting into a recommended phase II dose and hitting an MTD level. We will continue to provide frequent updates and progress towards initiation of the trial in Australia, dosing the first patient, and, as indicated earlier, we will be communicating early results from the available patient population dosed throughout this year by end of 2021. Thank you. Okay. Yeah. I'll also add to it that, of course, the discussions with MHRA, for instance, they were keen to make sure that the first cohort would get a dose that was close to therapeutically active, and that remains our plan. Once we have shared the protocols with the regulators and ethics committees, and those have been approved, we'll be much better able to disclose the dosing plan, in subsequent disclosures that come by. Okay? Gotcha. Okay. Maybe I could just sneak one question in then about the safety profile. Obviously, the IL-2 space in general, safety is a potential concern and kind of striking that right balance between safety and efficacy is kind of the holy grail, I think, as we see it. Are you using any, as you think about your phase I trial, are you using any lessons learned from your competitors, such as prophylactic hydration to reduce the risk of hypotension? Anything that you can kind of incorporate into the phase I trial that you think could lower any safety risks? Thanks. First, I'll just give my brief comments. Suffice it to say that of course, all the regulator agency ethics committees who are familiar with the ongoing studies with different IL-2 programs that are in the clinic at the moment. We'll always want to ensure that we had appropriate language and procedures, protocols, et cetera, to address those. That would be expected from any ethics committee, but I'll sort of also let Mann supplement that. Yeah, thank you, Fahar. It's a good question. Yeah, absolutely. All the above. We will use all the lessons learned from agents in the IL-2 landscape, all the lessons learned, all the adversities seen with this drug class. Myself worked on IL-12, high-dose IL-2, pegylated IL-2, and as you know, there is a cluster of adversities that we typically see with this drug class anticipated for all those agents, and we will typically follow the usual institutional guidelines and specific guidelines in managing toxicities seen with this drug class and in IL-2 in specific. Thank you. Great. Thanks, guys. Looking forward to the next 12 months. Thank you, and thanks, Matt Biegler. Our next question is from RK Ramakanth with H.C. Wainwright. Please proceed. Thank you. Good morning, Fahar and team. A couple of questions here. Dr. Muhsin, if you could help me kind of compare and contrast the MDNA11 program here versus the programs that are being run by Nektar, especially NKTR-214, so we understand how these programs here are situated against what's out there in the competition. Thank you. Right. Well, great. Thanks, really. Sort of from a mechanistic point of view, let me just bring. Then I'll let the further clinical aspects to be presented by Mann Muhsin. Just from a structural perspective, the way the molecule has been designed is such that we have, as you know, engineered into the molecule two different key characteristics. The first one being that we have knocked out the binding or inserted mutations that would block binding to CD25. Second of all, we have inserted mutations that dramatically increase the affinity for CD122 and therefore selectively stimulating effector T cells, NK cells, and NKT cells as well. That's the key aspect that's differentiated. Of course, the way we have approached this molecule with respect to how we extend the half-life is to use albumin fusion instead of pegylated approaches that you mentioned was the case with NKTR-214. We believe that that's a big differentiator because we know that albumin does extend half-life, as we've shown in our non-human primate data, but also that albumin tends to accumulate in the tumor as well as draining lymph nodes. That by itself also allows us to better localize our engineered IL-2 at the tumor site. I'll pass it on to Mann, who's obviously got a lot more experience with NKTR-214. Mann. Thank you, Fahar. On top of what Fahar indicated from mechanistic, from drug design and MOA, I cannot disclose much or anything to you about NKTR-214, but I can tell you about our compound. Of course, given that we don't have yet clinical data, but based on the preclinical data and animal models we've seen the drug being utilized on those in those animal models, it doesn't look like we will have issues related to cytokine release syndrome, vascular leak syndrome, or other toxicities seen in this drug class and become dose-limiting toxicities in some patients. Based on the data available so far, it doesn't look like it will be an issue that's similar to agents in this drug class that have this issue based on mechanistic and pathway drug class effect. Obviously, the data, the clinical data will trump everything, and we'll keep you updated based on the clinical data obtained in the dose escalation portion of the program. Thank you, Fahar. Thank you. Thank you all. The one additional question, this is on the BiSKIT program. From what I understand, this is a balancing act between inhibiting a pro-tumoral activity and activating a pro-inflammatory response. In such a program, what sort of safety signals should we be looking out for, especially in your preclinical work and also when you get into the clinic in the phase I study? Yeah. Again here, clearly, it all depends on what components or what two bifunctional molecules become part of the candidate that goes into the clinic. As we said, we are currently conducting research to identify the best candidate, and we will disclose the best candidate towards the end of this year as a lead candidate. It's a bit difficult for us to predict as to which molecule will be the one that goes into the clinic at this time, and based on the key components of the molecule. For instance, if it contains the IL-2 super agonist, then of course, we'll need to incorporate the safety issues that are consistent with the IL-2 space. With respect to any other fusion partner, whether it's a checkpoint inhibitor, a targeted antibody, or an IL-4, IL-13 antagonist, that will then be based on those molecules' characteristics and potentially, we will obviously know a lot more once we've done some initial screening in non-human primate studies as to what safety signals we need to look at. It'd be premature for us to say anything at this time. One last question. This is on the MDNA55. I understand you can't really talk too much about ongoing discussions. Obviously, this has been a subject for you folks for a while now. What exactly are you looking for in the partnership, and what are the major discussion points at this time that you need to get through before you can sign an agreement? Yeah. It's difficult for us to present anything with respect to what the discussion points are. Of course, those, as you say, remain private and therefore, I can only say that we are in active discussions, and we will be able to provide an update as soon as the timing is appropriate. That's the plan going forward. Suffice it to say that we do have discussions going on, so that's all I can say for now. Thank you, Fahar. Thanks. Thanks. Our next question is from Jason McCarthy with Maxim Group. Please proceed. Hi, everyone. It's Dave on the line for Jason. Thanks for taking my question. With respect to MDNA11, would the ex-U.S. trials help guide the direction of U.S.-based trials, and do you think it's possible that data gathered from these trials could possibly help expedite the development process of the change to MDNA11 in the U.S.? Sorry, I didn't quite get the question. Could you sort of repeat it once more, please? Sure. The trials that are initiating outside of the U.S. for MDNA11, I was just asking if those trials would help guide the future direction of the U.S.-based clinical trial, and if you think data gathered from the ex-U.S. trials could help expedite the development process of MDNA11 here in the U.S. Yes, of course. Any data we gather from outside the U.S. will be part of the same protocol, and therefore, if any submissions that we make to the regulatory agency and as part of the protocol itself, we will make sure that there is a unified protocol that can be used globally. I will let Mann also supplement that, please. Mann? Yes, Fahar, it's confirmed. The data that we will be gathering from Australia will contribute to the overall program and will be combined with the data generated in U.S. and other regions, ex-U.S., and that will constitute the total efficacy safety data, the total sample size for the phase I and the phase II portions of the program. Thank you. Great. Thanks for the additional color. I appreciate it. Our next question is from Kumar Raja with Brookline Capital Markets. Please proceed. Fahar, thanks for taking my questions. Congratulations and welcome Dr. Moulder and Dr. Muhsin. First, maybe with regard to the characteristics of the patients you plan to enroll in the phase I trial, are there any particular histologies you guys are planning to target? Also looks like initially you are looking at checkpoint inhibitor-naive patients, but how are you guys thinking about patients who are resistant to checkpoint inhibitors as well as progressing on those? What are your thoughts on combinations with the checkpoint inhibitors? At what time point do you think you'll be able to move into that? Right. Thank you, Kumar. Good to talk to you today. I will ask Mann to respond to that question. Mann? Yes. Thank you, Fahar. Thanks for asking. The histologies and the patient population to be included in the phase I and the phase II portions of the program, we will be including patients who are resistant, who failed prior lines, failed checkpoint inhibitors, and in certain cases, they're resistant. The tumor types are yet to be fully disclosed, but I can tell you in general, we will follow the tumor types that have the highest likelihood of response and have a higher probability of success based on the high-dose IL-2, based on the PROLEUKIN, based on what we know about the IL-2 activity in the immunogenicity spectrum. This patient population will be naive as well as previously treated, but we won't be accepting heavily pre-treated patient population. As you know, this is a safety first part of the study, is a safety-focusing arm that will evaluate the dose and toxicity. We have to be mindful of that. In regards to the checkpoint inhibitor part, yes, we will be having a checkpoint inhibitor arm in the study, of course, after clearing the dose testing monotherapy part of the program as well and seeing the activity before combining it with the checkpoint inhibitor, ideally PD-1 and PD-L1. Thanks for asking. In terms of the U.K. trial, when do you think it will come on board, and how do you plan to coordinate with the Australian trial? Just to let you know, as you know, we will be starting off in Australia, and the same protocol will apply to the U.K. From a timing perspective, of course, as we generate some initial data and prepare the IND dossier for submission to MHRA, those will be sequential. Filing and submitting the package to the FDA as part of an IND package. These will all follow after we have started enrollment in Australia. Timing is not confirmed per se, but we will provide guidance as we advance with the enrollment in Australia first. Okay. Maybe finally, in terms of dose escalation based on the animal models, how are you thinking that how quickly can you dose escalate? Thanks. Mann, maybe you can answer that. Sorry, if you could repeat the question, I didn't get the second part of the question. No, I'm asking how quickly you think you can dose escalate based on the data from the animal models? Thank you. Thank you. As Fahar indicated, and we also articulated in the call, we will not be starting from subtherapeutic doses or low doses. It will be an accelerated sequential dose escalation that will allow us to choose intermediate doses, deescalate, and in some cases, also, we could skip a dose level based on the availability of safety PK data and others. I don't anticipate we'll have multiple escalations. I do anticipate that we will get into our recommended phase II dose relatively quickly. I'm confident the drug will deliver a favorable safety profile, superior efficacy profile to competing agents in the landscape, and certainly compared to high-dose IL-2. Thanks for asking. Okay, thanks so much. Our next question is from David Bautz with Zacks Small- Cap Research. Please proceed. Hey, good morning, everyone. Thanks for the update this morning. In thinking about the development pathway for the MDNA413 bispecific molecule, do you eventually think you'll end up testing that in combination with a PD-1 molecule, or would that more likely stay as a monotherapy? Right. Good question, David. The key aspect is that, of course, as you know, we have different modalities with respect to the BiSKITs program itself, and one of them we demonstrated was the MDNA19-MDNA413 as a potential candidate. That's not really etched in stone as that being the molecule that will take ahead. It could be a molecule that has a fusion to a checkpoint inhibitor, for instance. Until we've done some additional studies, identified the lead candidate, and studied these molecules, either in a monotherapy setting or also in a combination setting, once we have that data, we will be able to judge further as to what will be appropriate combination partner or if we even need a combination partner. That's still to be determined, so that's a bit too early at this moment. Okay. Do you foresee the company presenting any additional preclinical data on either MDNA11 or the BiSKIT program later this year? We are obviously looking forward to certain conferences that are on our horizon as to potential places where we would present additional data on MDNA11. This will be preclinical, as well as additional data on our BiSKITs pipeline. We look forward to updating these different programs that we have ongoing, and hopefully, there will be those presentations before the end of the year. Okay, great. Thanks for taking the question. Thank you, David. We have reached the end of our question and answer session. I would like to turn the conference back over to management for closing remarks. Well, thanks again to everyone for joining us on the call. We look forward to the continuous advancement of our pipeline and discussions along the MDNA55 partnering activity as well, and we'll keep everyone updated along the way. Thank you very much, and goodbye. Thank you. This does conclude today's conference. You may disconnect your lines at this time, and thank you for your participation.