Hello and welcome to the Medicenna Therapeutics fiscal Q3 earnings call. All participants are now in a listen-only mode. There will be a Q&A session at the end of the prepared remarks. 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. Thank you. 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 December 31, 2022. If you have not seen the press release, it is available on the investor page of Medicenna's website. Before we begin, I would like to remind you that certain statements and information shared during this call constitute forward-looking information within the meaning of applicable securities laws. All statements other than statements of historical facts shared during this call and that relate to the future operations of the company and other statements that are not historical facts, including statements related to the clinical potential, development, and tolerability and safety profile of MDNA11, preliminary clinical data, the clinical potential and development of MDNA55, partnering efforts, cash runway, the presentation of additional data and other milestones, and patent protection 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 events. Important factors that may cause actual results to differ materially from the company's expectations include the risks detailed in the Annual Information Form and Form 20-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. 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, the company does 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. Speaking on today's call will be Medicenna's President and Chief Executive Officer, Dr. Fahar Merchant, and Chief Financial Officer, Elizabeth Williams. I will now turn the call over to Fahar to begin. Fahar. Thanks, Dan, good morning, everyone. I'll begin by discussing the most recent news out of our phase 1/2 ABILITY study of MDNA11, our beta-only long-acting IL-2 superagonist. Earlier this morning, we announced that the phase I portion of the ABILITY trial advanced to a 6-dose escalation cohort where patients will receive a target dose of 120 micrograms per kilogram every two weeks. This is encouraging as it reflects that MDNA11 has a suitable tolerability profile in the end-stage cancer patients that have enrolled in the phase I study to date. The decision to advance to the sixth cohort was based on a review of the cohort 5 safety and preliminary pharmacodynamic data by our safety review committee, which consists of study investigators, key opinion leaders, and external advisors. With regards to safety, we are pleased to say that MDNA11 has been well-tolerated with no dose-limiting toxicities, dose interruptions, dose de-escalations, or treatment discontinuations due to safety issues. With regards to pharmacodynamics, we observed further increase in lymphocyte expansion in cohort five when compared to cohort four, which indicates that MDNA11's ability to stimulate an anticancer immune response had not yet plateaued. Collectively, this data suggests that we may be able to safely administer higher doses of MDNA11, which in turn could further enhance anticancer effects. To begin testing this hypothesis, cohort 6's dosing regimen includes 30, 60, and 90 micrograms per kilogram priming doses of MDNA11, followed by a further step-up to the fixed 120 micrograms per kilogram target dose I mentioned earlier. For comparison, participants in the fifth cohort received two 30 microgram per kilogram priming doses before stepping up to a fixed 90 microgram per kilogram dose. All doses are administered intravenously every other week. In addition to evaluating a higher fixed dose of MDNA11, the dosing regimen in cohort six has the advantage of getting participants to the 60 microgram per kilogram dose after only two weeks, as opposed to after four weeks. This was the case of cohorts five and four. This is important as the 60 microgram per kilo dose of MDNA11 has already led to tumor response, as presented last quarter at the SITC annual meeting. The data presented at SITC showed tumor control in five of 14, or 36% of evaluable patients treated with MDNA11 monotherapy. This included a confirmed partial response in a fourth-line metastatic pancreatic cancer patient treated at 60 micrograms per kilogram, demonstrating MDNA11's single agent potential in a notoriously difficult to treat cancer. We also observed encouraging signs of MDNA11's potential to drive durable clinical benefit as a patient achieving a partial response, so further deepening of tumor response on each of the two consecutive scans. While another patient with metastatic melanoma has maintained stable disease for more than one year and remains on study. These promising antitumor activity data were notably achieved in an extremely challenging patient population, with nearly 80% of patients having failed prior immunotherapy, including the pancreatic cancer patient achieving a partial response. The data are supported by PD results that show dose-dependent and multifold increases in anticancer immune cells with MDNA11 treatment, but not stimulation of Tregs or eosinophils. This is important as Tregs are associated with pro-tumor immune pathways, while eosinophils are associated with vascular leak syndrome, a serious life-threatening side effect of the only approved IL-2 therapy, Proleukin. Presented alongside these PD data were results demonstrating MDNA11's tolerability at the study doses as well as PK data that showed dose-dependent increases in exposure that remained consistent with repeat dosing, suggesting a lack of an anti-drug antibody response. Those interested in reviewing any of these data in detail can find both SITC presentations on the event section of our IR website. Collectively, we believe ABILITY's early results demonstrate how MDNA11's carefully engineered design positions the superkine as a potentially best-in-class, long-acting beta-only IL-two therapy. We believe the key design features of MDNA11 can provide cancer patients with clinical benefit while avoiding the PK and safety shortcomings that plague Proleukin. ABILITY's data to date supports this hypothesis, which we plan to continue exploring with several important readouts from ABILITY expected over the coming months. The first of these readouts is anticipated later this quarter and will include initial antitumor activity data and high-level PD findings from ABILITY's fifth dose escalation cohort, alongside updated data from cohorts one through four. As in earlier cohorts, cohort five enrolled difficult to treat patients unresponsive to prior treatments. The same will be true for cohort six, as each dose escalation cohort utilizes similar inclusion criteria. We do, however, plan to take a different approach to enrollment for the phase II expansion portion of the trial, where the objective will be to not only demonstrate safety in approximately 40 patients, but importantly evaluate the efficacy of MDNA11 in patients with less advanced cancer and tumor types that are most likely to benefit from our IL-2 Superkine. Rather than enrolling patients with a dozen or more disparate tumor types, which has been the case with the phase I portion of the ABILITY study, the phase II portion will only focus on two or three different cancer populations that better reflect MDNA11's target addressable population. As we look towards the identification of MDNA11's optimal regimen and ABILITY's phase II expansion phase, we are optimistic on the trial's outlook. Having shown an ability to achieve enduring tumor control in a challenging patient population, we expect that MDNA11's demonstrable durability of response, which is a major challenge with approved immunotherapies, could be further enhanced with optimal dosing regimen and in a population of patients with better initial prognosis. Our current projections have us reporting data from ABILITY's sixth and potentially the final dose escalation cohort together with early antitumor activity data from the phase II dose expansion cohort in the Q3 of this calendar year. We anticipate reporting early data from the trial's combination arm evaluating MDNA11 plus Keytruda in the Q4 of this calendar year, providing us with multiple near-term opportunities to de-risk MDNA11 and demonstrate its potential as a vital component of cancer immunotherapy. Shifting gears, I would like to provide a brief update on MDNA55. The top-line results from the single-arm phase 2B clinical trial of MDNA55 in patients with recurrent unresectable glioblastoma, a uniformly fatal form of brain cancer, have been published in the peer-reviewed journal Neuro-Oncology, which is the official publication of the Society for Neuro-Oncology. These results showed that the trial met its primary endpoint with median overall survival in the primary and supportive analysis populations, exceeding predefined success criteria and key historical benchmarks. These promising results helped us to align with the FDA on an innovative open label hybrid design for a potential pivotal trial. I'm also happy to mention that the World Health Organization has approved the international non-proprietary name for MDNA55, which will now be referred to as bizaxofusp. Looking forward, we continue to pursue bizaxofusp's further development and potential commercialization through external partnership, as we have stated consistently in the past. This will allow us to enable bizaxofusp's advancement while maintaining our internal focus and resources on MDNA11 in our BiSKITs program, which was a subject of a key patent issued earlier this year. This new issued patent extends protection into at least 2039, with claims on methods of treating cancer with an IL-2 Superkine in combination with checkpoint inhibitors such as an anti-PD-1 inhibitor, which is being advanced in the combination arm of the ABILITY study, and for BiSKITs such as MDNA223, which comprises an IL-2 Superkine linked to an anti-PD-1 antibody. With checkpoint inhibitor patents due to start expiring in 2028, we believe the data from ABILITY's combination study, as well as MDNA223's IP, could be an important tool to facilitate collaborations or partnership with leaders in this space. With that, I'd have Liz review our fiscal Q3 financial results. Liz? Thanks, Fahar. I'll begin today by reminding those listening that all references made during this section of the call are in Canadian dollars unless otherwise stated. As of December 31st, 2022, Medicenna had cash and cash equivalents of CAD 36.2 million. Based on our projections, our current cash resources are sufficient to fund our operations through the Q2 of calendar year 2024. This cash runway is expected to take us through several important clinical readouts and the completion of the ABILITY study, including both the monotherapy and combination expansion phases designed to assess MDNA11's efficacy in relevant patient populations. Net loss for the quarter ended December 31st, 2022 was CAD 1.1 million, or CAD 0.02 per share, compared to a loss of CAD 4.8 million, or CAD 0.09 per share for the quarter ended December 31st, 2021. The significant decrease in net loss for the quarter ended December 31st, 2022 compared with the quarter ended December 31st, 2021 was primarily a result of a non-cash gain of CAD 3.7 million related to the change in valuation of a non-cash warrant liability associated with the August 2022 financing. Research and development expenses of CAD 2.9 million were incurred during the quarter ended December 31st, 2022, compared with CAD 2.9 million incurred in the quarter ended December 31st, 2021. Research and development expenses were consistent quarter-over-quarter. General and administrative expenses also remain consistent quarter-over-quarter, with CAD 2 million incurred during the quarter ended December 31st, 2022, as well as during the quarter ended December 31st, 2021. 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 hand the call back to Fahar for closing remarks. Thanks, Liz. Before opening up the call for Q&A, I'd like to first thank all those who have supported the progress we spoke about today, including our employees, partners, investigators, shareholders, and clinical trial participants. I'd like to also emphasize how our recent progress has us set up for an exciting calendar year ahead, with crucial milestones anticipated throughout 2023. The first of these milestones is expected later this quarter, which is when we anticipate reporting high-level PD findings from ABILITY's first five dose escalation cohorts and an update on antitumor activity. In cohorts one through four, MDNA11 displayed promising signs of monotherapy activity as well as safety, PK, and PD profiles that position it as a potentially best-in-class IL-2 therapy. The key objectives of cohorts 5 and 6 are to confirm if MDNA11's immunologic activity can be enhanced with higher doses and whether these higher doses will be adequately tolerated. Based on what we see in additional readouts from ABILITY's dose escalation phase, we will select the optimal dose and schedule for the trial's phase II monotherapy expansion and combination arms. The phase II component of the study will be specifically designed to assess MDNA11's efficacy in patients that are similar to its target populations. We therefore believe that the readouts anticipated from the phase II portion of the trial, which are expected in the third and Q4 of calendar 2023, may represent significant de-risking events for the MDNA11 program. With encouraging signals of efficacy already observed in the extremely difficult to treat patients during the trial's dose escalation, we are optimistic about the ABILITY study's outlook. We look forward to its continued progress and to providing periodic updates along the way. With that, we will now begin our Q&A session. Operator. Thank you. The floor is now open for questions. 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. Once again, that is star one to register a question at this time. The first question today is coming from Charles Zhu of Guggenheim. Please go ahead. Good morning, everyone. Thanks for hosting the call and for taking the questions. First one from me. If I recall, dose cohort 5 was also the first when you instituted the new requirements around baseline lymphocytes. To what degree might the enhanced lymphocyte stimulation or PD markers you're observing be influenced by this higher baseline? How do you think about that relative, you know, due to the higher doses of MDNA11 you're evaluating? Thanks. Thank you, Charles. That's a good question. Certainly, as you know, we set a threshold for lymphocyte counts in this particular study. We clearly are seeing that, and we've seen mostly from previous studies with Proleukin, where a high baseline lymphocyte count generally results in better patient outcomes. The key thing here is, although that's something that's been demonstrated historically, we certainly do not have as much data with our therapy and our therapeutic regimen that we use with MDNA11. Needless to say, we have, I think if you recall, between the first three cohorts where the doses were below 60 micrograms per kilogram, we still saw patients with stable disease, including a patient that continues to be treated in cohort two, who started at 10 micrograms per kilogram, where the lymphocyte count or the baseline lymphocyte count, was not necessarily set at 1,000 per microliter. It may be a sort of a threshold that's maybe more relevant for Proleukin or other IL-2-based agents. Certainly, as far as we are concerned, although we feel that you can get to the threshold, lymphocyte count or a higher lymphocyte count or expansion to occur, we certainly haven't seen any consistency in the data that we have so far. Nevertheless, we expect that as we enter into sort of the phase II portion of the study, where we have patients with higher or sort of less heavily pretreated healthier patients, more likely that we have patients with higher lymphocyte counts. It's a bit premature right now to come to any conclusions based on the data we have on only 14 patients so far. We are encouraged to see that even a patient who started at less than 1,000 lymphocytes per microliter continues to be on study for now 15 months. That's quite encouraging. Got it. Great. Thanks for taking the question. Thank you. The next question is coming from Matt Biegler of Oppenheimer. Please go ahead. Hey, guys. Thanks for the update. I'm curious, Fahar, based on the preclinical data, do we expect to plateau out on lymphocyte count in cohort 6? I guess another way to ask the question is how do we know when we're at the recommended Phase II dose? I have a follow-up. Right. Thanks, Matt, here. That's a good question again. I must say that you're right on spot when you talk about the data from preclinical studies. Certainly what we have, the way we have projected dosing regimens and selecting the different doses in different cohorts is given mostly by extrapolating from data we have from non-human primate studies. Based on the safety windows that we saw in non-human primates, as well as where we saw the threshold occurring in non-human primates, I would say that the current dosing regimen that we are enrolling patients in, which is the cohort 6 at 120 micrograms per kilogram, is pretty much close to where we are expecting this to plateau. As you know, we saw pretty impressive results at starting at cohort four at the 60 micrograms per kilogram dose. So far we've had, as you know, the data we have shared is on just seven patients that have received more than 60 or 60 micrograms per kilogram or higher. Based on the data we have so far, it seems like we are seeing pretty impressive clinical activity. Add to that, the fact that we are continuing to see increases in lymphocyte count at 90 micrograms per kilogram as reported today, we believe that when we get to 120 micrograms per kilogram, we should be pretty much on par with the upper limits of dosing, where we had from non-human primates. So far, the trends from non-human primate data are predictive of what we are seeing with the lymphocyte counts with other expansion of CD8 T cells, NK cells, so being consistent. We believe that we are pretty much close to that upper limit, and we do not expect that we will necessarily have to go to a sort of next higher dose. We already have promising data from the 60 micrograms. We have data from 90 and 120. We have three sets of data or dosing to pick from, in view of the fact that we've met the safety burden with both the 60 and 90 micrograms and since we meet the same safety burden at the 120. Generally, across the board, we feel pretty comfortable that above 60 onwards, we should be having a therapeutic activity that's more than adequate for MDNA11. Obviously, we want to make sure that before we enter the phase II portion of the trial, we need to make sure that we can confirm that by testing the higher doses as well. Right. Right. That makes sense. Okay. Maybe just a quick follow-up on, I'm sure you're aware Proleukin was effectively sold to Iovance, a few weeks ago. I'm just kind of curious on your view of that transaction and kind of what that means for the field and if, you know, in the future there's any opportunities to combine with other therapeutic modalities outside of checkpoint inhibitors? Thanks. Right. Again, a really good question, Matt. That really was an indication as to how large the potential opportunity is for molecules such as MDNA11. If you recall the data from Iovance, with the presented at SITC, clearly indicated that in the phase II setting where they were using Proleukin, the toxicities were clearly there. They were obviously not desirable. It's not surprising that Iovance is also looking to develop a much safer version of IL-2. I believe that the potential for IL-2, particularly MDNA11, where we have the selectivity for boosting NK cells and CD8 T cells and not Tregs, becomes really important because after going through a sort of a long process of isolating your T cells from the patient and then having to expand them through ex vivo manufacturing and then reinfusing the T cells, that itself, I think, as you know, is a long process, and you want to make sure that you have the best quality of T cells that you're infusing into the patient. The good thing about a molecule such as MDNA11 is that, as you know, it does not do a good job of stimulating your immunosuppressive Tregs. This is exactly what we want, is from a manufacturing perspective, make sure that you are able to boost the population of CD8 T cells and NK cells, not Tregs, which unfortunately is not the case with Proleukin because it will boost the population of Tregs. When you insert or re-infuse the T cells, you want to continue to expand those T cells selectively, not expand your Tregs. This is again, where MDNA11 has its distinct selectivity and therefore distinct advantage. We believe that this particular Iovance transaction sets the stage clearly for all other T-cell-based processes or CAR T-based processes, et cetera, where not only would a drug such as MDNA11 be ideal for manufacturing purposes, but more importantly is to then stimulate those T cells in the patient without boosting your Treg population. That's, I think, an important industry or important opportunity to exploit, and I think MDNA11 is really well suited for that purpose. Very cool. Thank you guys for the question. Thank you. The next question is coming from David Martin of Bloomberg. Please go ahead. Good morning. I've got a couple of questions. The first one is just a clarification. When you were speaking, Fahar, I think you said that we'd get PK/PD and initial efficacy results for cohort 5 in the first calendar quarter. In the press release, it kind of indicates only PK/PD, and the efficacy will be an update for cohorts 1 through 4. Just confirming, are we getting efficacy data for cohort 5 in Q1? I did not realize. Thanks, David, for that particular question. Yes, let me sort of correct that. If the press release did not mention that, then apologies. Yes, the intent is for us to release the PK/PD, but also the tumor activity data from cohort 5, before the end of this quarter. Okay. Thank you. Um. Thanks. Another clarification. With the patients with higher baseline lymphocyte counts in cohort 5 and 6, you had anticipated that by using that inclusion criteria, that you would get healthier patients. And yet you're saying that cohort 5, cohort 6 are still very six-sick patients, and you'll only start getting healthier patients in the dose expansion. Is that correct? By selecting based on higher baseline lymphocytes, you didn't get healthier patients in 5 and 6? It's not, as you know, healthier patients is based on a healthier immune system. Certainly, in cohorts 5 and 6, you end up with patients with sort of a baseline lymphocyte count that is higher than what we enrolled in cohorts 1, 2, and 3. From that perspective, certainly, what we want to try and simulate is obtain or realize that in cohorts, in the expansion cohorts, we will be looking at patients that have gone through fewer lines of therapy, and therefore, we expect that those patients enrolled in that expansion cohort will likely have higher lymphocyte counts. It's in a sense for us to provide that information, to gather that information so we are better able to foresee what to expect going down the road. Remember one thing about patients that have gone through multiple lines of therapy. It's their lymphocyte count, primarily from their immune health perspective. Then again, there are a host of other issues that we need to take care of or worry about. Remember, in the dose escalation portion of the study, where we are is really treating about 12 different type of tumors in this particular portion of the trial. Trying to sort of come up with some kind of homogeneity or minimizing the variability is the point here with sort of trying to stabilize and using 1,000 lymphocyte counts per se. Nevertheless, patients would have, as you know, gone through so many different type of therapies, some focused on immunotherapies, others with different kinds of chemotherapies as well. We have a very diverse patient population in the dose escalation phase, where not only are we dealing with different tumor types, but also different therapies that patients have received. Patients' health is not only determined by the immune count, but also from other prognostic factors. Age is a good example, for instance. That also we cannot obviously restrict from that perspective, but there is a host of variations that we take into account. The focus really now is planning for the dose expansion phase of the study and identifying two or three different tumor types that are most likely to be beneficial to the patients. These patients certainly will not be end-stage patients. Therefore, we expect the patients to be more homogeneous than we were in the phase I dose escalation part, where even if you have a lymphocyte count standardized, we still are dealing with 12 to 15 different tumor types. It's a sort of a combination of different far too many parameters in the dose escalation portion that we cannot really predict what would happen. Nevertheless. Okay. It's very encouraging to see that, in cohort six we were able to show promising data above the 1,000 lymphocyte count. Okay. Just one last quick question. With the new priming schedule, you say you get to the 60 dose faster. Can you remind me when your dose cohort that dosed at 60, did you go right to 60, or did you start at 30 and went to 60? No, we started at 30, and there were 2 doses of 30 in the cohort 4, and then went to 60. It took 4 weeks before we got to, 60. In this case, we'll get to 60 in 2 weeks. You're pretty comfortable that they'll be able to tolerate getting to 60 that fast? Well, that's the objective, and that's why we had a safety review committee, to make that final call. Okay. Okay, that's it for me. Thanks. Thank you. The next question is coming from RK of H.C. Wainwright. Please go ahead. Thank you. Good morning, Fahar and Liz. A lot of my questions have been answered. When you get to phase II, I was just wondering, you know, among the four indications that seem to be the ones that you're looking at, during this stage of development, you know, how would you order them, or would you consider just taking the pancreatic and the melanoma as the indications to go forward? Yeah, we haven't decided specifically on the tumor types so far. I think we continue to review the data. We certainly will be collecting more data from cohort five, cohort six as well as historical data that we've seen so far from the first four cohorts. We are working closely as to what indications to pursue it in the dose expansion, and we will provide an update as soon as we have had received feedback and guidance from our clinical advisors, KOLs, et cetera, based on the growing body of evidence from the current study that we are conducting. Nothing's been etched in stone at this moment. Okay. One last question from me. Any update on the BiSKITs program? Because we didn't hear much today. Yeah. The BiSKITs program, since our last set of data we presented at a conference late last year, we continue to advance that particular program. We certainly are continuing to optimize the design of the molecule and generating more in vitro, in vivo studies and characterizing that molecule further. We will, as we get an opportunity to present data at additional conferences or submit a publication, we will be providing more evidence and more data at that time. Okay. Thank you. Thank you for taking my questions. You're welcome. Thank you. Thank you. The next question is coming from Catherine Novack of Jones Research. Please go ahead. Hi. Good morning. Thanks for taking my question. Just a couple from me. One, you know, in terms of the phase II cohort data or phase II data in the Q3 of 23, I'm curious, does that mean that, you know, you've settled on a phase II dose, given that I imagine that you'll have to start enrolling that before the 120 micrograms per kilogram dose cohort has finished reading out? You know, do you anticipate, you know, further dose finding work in the expansion phase? No, we will not be doing any further dose-finding studies during expansion phase. We will establish what we call is a provisional recommended phase II dose that will be executed and implemented in the dose expansion phase of the study. That's the plan, and we expect that we'll have some early data by the end of Q3 this year. Okay. Can you give any additional color, maybe on the kind of efficacy data we'll see from cohort 5? You know, how many patients, what kind of follow-up? Have you gotten any additional paired biopsies in this quarter or in this cohort? Yeah. We will be providing more data, as we plan to do that at the end of this quarter. This will allow us to share with you all, the patients that have been enrolled in cohort 5, the type of tumors they had, the number of lines of therapy they had, as well as the PK/PD and of course, tumor response data. We'll be presenting all that together as a complete set of data, including data from patients in earlier cohorts that are still on the study. Okay. Then in terms of patients that are still on the study, I believe at the last update, there were three still on study. Any update on that? Yes. That will be when we present that update at the end of this quarter on those 3 patients, plus the patients in Cohort 5. We will be able to share all that information, including the data from more recent scans, from not only Cohort 5, but also from the earlier cohorts as well. All right. Thanks so much for taking my questions. You're welcome. Thank you. The next question is coming from David Bautz of Zacks Small Cap Research. Please go ahead. Hey, good morning, everyone. Fahar, I'm curious why you aren't restricting the patients for cohort 6 to certain tumor types. I understand you haven't decided exactly what you're gonna look at in the phase II expansion cohort. I'm curious why you aren't limiting it to even the ones you're considering for phase II. Well, I think, the key thing here is, of course, the range of tumor types we've already treated is, as I said, about a dozen or so. Trying to generate data on three different tumor types in a cohort of maybe three or six patients is unlikely to provide you with certainly any trending data. Obviously what we are trying to do is try and enroll more patients that would potentially fit the profile for the dose expansion. We're not sort of change the protocol right now. We either have instructed the sites to only limit it to one or two or three different tumor types. It's too early. I would say that the purpose of dose expansion is to do that exact same, as the idea in the dose expansion is to really have adequate number of patients, in those 2 or 3 different type of tumors, rather than having to make a decision based on 3 or 6 patients. Okay, that makes sense. Real quick, when you present this updated data later on this quarter, will that be at a scientific conference, or is that gonna be through just a press release? Well, as I said, the data from cohort five will be presented at the end of this quarter. With additional data that comes through, it's likely that we'll present at a scientific conference. We will at that point, depending on when the scientific conference takes place, we should have more data on cohort 6, potentially even early data on the dose expansion, but that remains to be seen. Okay. Sounds good. Thanks for taking the questions. You're welcome. Thank you. At this time, I'd like to turn the floor back over to Dr. Fahar Merchant for closing comments. Thank you. Thank you very much, all of you for joining the call today. Really appreciate the support, the patients that have participated in the clinical trials, as well as the families, and the investigators that have been patient with the clinical study itself, and of course, all our shareholders, employees, etc., that have been supporting Medicenna's progress. We look forward to providing with all of you some additional updates, as we said, at the end of this quarter, as well as at the end of Q3. In between, hopefully at a time when there's a conference before the end of Q3, we will provide additional updates. Look forward to providing those additional data in the coming weeks and months. Thank you all for joining today's call. Ladies and gentlemen, thank you for your participation. This concludes today's event. 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