Good afternoon, ladies and gentlemen, and welcome to Marker Therapeutics conference call. At this time, all participants are in listen-only mode. Later, we'll conduct a question and answer session. Instructions will be given at that time. As a reminder, this conference call is being recorded. It's now my pleasure to turn the call over to Mr. Tony Kim, Chief Financial Officer at Marker. Mr. Kim, please go ahead. Thanks, operator. Welcome everyone, and thank you for joining us this afternoon for our clinical program and technical operations update call. With me today are Peter L. Hoang, our President and Chief Executive Officer, Dr. Juan Vera, our Chief Scientific and Chief Operating Officer, and Dr. Mythili Koneru, our Chief Medical Officer. This afternoon we issued a news release that you can find on our website at markertherapeutics.com which includes a summary of initial results from the safety lead-in portion of our phase II AML trial, as well as updates on our new manufacturing process and an overview of our near-term clinical plans. Before we begin, as a reminder, we will be making forward-looking statements regarding our financial outlook, in addition to regulatory, product development, and commercialization plans and research activities. These statements are subject to risks and uncertainties that may cause actual results to materially differ from those forecasted. A description of these risks can be found in our most recent 10-K on file with the SEC. I would now like to turn the call over to Peter. Good afternoon, everyone, and thank you for joining us today. Marker Therapeutics is off to a strong start in 2022, and we've made considerable progress in advancing our phase II AML trial. In just a moment, I'll be making a few remarks about our company's progress and providing an overview of our plans for the remainder of 2022. I'll then hand off the call to Mythili Koneru, who will walk through the initial results from the safety lead-in portion of our ongoing phase II AML trial. After that, Juan Vera will provide an overview of the T cell manufacturing improvements that we're currently implementing, and I will wrap up the call with several important pipeline updates and a summary of key milestones. We will open up the call to questions. Moving to the first slide, as you know, our clinical team has been hard at work advancing our phase II AML trial investigating MT-401, our lead multi-TAA specific T cell product candidate. Today, we're excited to announce encouraging initial results from the safety lead-in cohort. MT-401 demonstrated a strong safety profile with no SAEs or neurotoxicity observed. While we're presently working with small patient numbers, we were extremely pleased with the outcome. Of note, MT-401 generated an objective clinical response in a patient with measurable residual disease. MRD is a form of active disease in AML that is generally considered to be a precursor to frank relapse. This patient converted to MRD negative status after receiving treatment, meaning that patient's disease was no longer detectable and the patient was no longer at high risk of frank relapse. We're also excited to share details on our improved new T cell manufacturing process, which will be implemented with MT-401 in the phase II AML trial and other products in development. Beyond the significant process improvements we announced and implemented at the beginning of last year, Marker has continued to refine and improve its multi-TAA specific T cell manufacturing processes. We're pleased to announce that our development team has been able to achieve a number of additional process improvements, which we have already reviewed with the FDA. Our new manufacturing process is designed to deliver a more potent product, bolster tumor killing, and be manufactured in only nine days. This is of particular significance to MRD positive AML patients who have a high likelihood of frank relapse and negative outcomes. With this reduced manufacturing time, we can potentially treat more MRD positive patients during their short therapeutic window. Today, we're also announcing the expansion of our pipeline and additional company-sponsored clinical programs, beginning with pancreatic cancer, our first trial evaluating a multi-TAA cell therapy for the treatment of solid tumors, as well as a new trial in lymphoma. We plan to file INDs for our second multi-TAA specific T cell therapy candidate, MT-601, by year-end and initiate clinical trials in these indications in 2023. We're also excited to expand our AML trial with MT-401-OTS, a scalable off-the-shelf therapy with the potential to match patients to treatment in under three days. Looking ahead, we plan to develop additional off-the-shelf products in lymphoma and ovarian cancer with the goal of significantly improving patient access to promising cell therapies. With that, I'd like to turn the call over to Dr. Mythili Koneru, who will provide further details on our phase II AML trial. Thanks, Peter. I'll be discussing the safety lead-in results and analysis of the phase II AML trial. I'd like to provide an overview of the phase II AML study. The trial plans on enrolling approximately 180 patients, 120 in the adjuvant group, and 60 in the active disease group, which comprises of patients with frank relapse in a separate subgroup of MRD positive patients post-transplant. The primary endpoint is relapse-free survival for the adjuvant group and complete remission and duration of complete remission for the active disease group. The trial also encompasses a safety lead-in with six patients, which has since been completed. Next, I'll be focusing on the results of the safety lead-in patients. The purpose of the safety lead-in was to test safety for patients using a new vendor for a reagent in the manufacturing process. Three patients treated with products manufactured using legacy reagent and three additional patients treated with products manufactured using the new reagent for a total of six patients. One patient had MRD positive disease, while the other five patients had active disease. The primary endpoint was safety, and the secondary endpoint was efficacy. No patient had any dose-limiting toxicities. Now, regarding efficacy, the MRD positive patient became MRD negative after infusion of MT-401. No objective responses were seen in the other, in any of the other patients. We were able to move forward with opening the rest of the phase II study in July 2021. Next, I'd like to highlight some of the characteristics of the patients enrolled in the safety lead-in. Regarding the patient demographics, the median age was 52. The patients were heavily pretreated with a number of prior therapies, as indicated on the slide. The patient's donors included matched related, matched unrelated donors, as well as haploidentical. The patients had a variety of genetic mutations and abnormalities, as indicated. The patient with measurable residual disease was patient 107-010A, who I will focus on next, since the patient converted to MRD negativity after infusion of MT-401. In the next slide, I'll discuss patient 107-01A details. This patient was a 43 year-old Hispanic male with AML. The patient had five prior lines of therapy and had a haploidentical donor. The patient also had a C-KIT mutation and RUNX1 genetic abnormality. Regarding the T cell composition and phenotype of the product for patient 107-01A, you can see by flow cytometry on the left that the product has a mixture of CD4 and CD8 T cells. They are predominantly effector memory cells. The panel on the right indicates that the product is comprised of more than 3,000 T cell clones, unlike other T cell therapies that only use a single TCR transgenic clone. Regarding the disease assessment, the patient's percentage MRD was measured using RT-PCR. Prior to MT-401 infusion, the patient had presence of MRD positivity around 0.8%. After infusion of MT-401, the patient's MRD percentage by PCR decreased compared to baseline, except at week 18, where there was an increase. At the time, it was unclear if that was a true spike or a reflection of the assay. However, the answer to this will become more clear when Dr. Juan Vera discusses some of the biomarker data associated with this patient. By week 32, the patient showed no evidence of MRD by peripheral blood. With that, I will pass it to Dr. Vera to discuss the very interesting immunomonitoring data for this patient in more detail. Juan? Thank you, Mai. Indeed, we were very pleased when we observed this clinical response, and the first question we wanted to ask was: What is the persistence of the infused T cell product, and can we see those cells expand and persistent in vivo after infusion? In the next slide, what we see is just that. Allow me to orient you here in this slide here. We're seeing an overlay between the levels of MRD and the frequency of antigen-specific T cells detected by interferon gamma ELISpot collected from peripheral blood. As you can see, there is an inverse correlation between the frequency of these antigen-specific cells and the level of disease burden, demonstrating this way the persistence and expansion of this infused product. Now, if we go to the next slide, we wanted to ask a very important question, and is: Can our therapy induce the recruitment of the endogenous immune system through a phenomenon that is called epitope spreading? A phenomenon that has been reported to be present in multiple of the Baylor studies and associated as a landmark of clinical efficacy. In this particular slide, we're looking at that phenomenon of epitope spreading. What we can see is the amplification of T cell response from the endogenous compartment, with a recognition of targets for antigens that are expressed in AML but are not present within the infused product. Again, here we see an inverse correlation between this immune response and the levels of MRD. What we have so far is basically that the administration of this product that has a broader spectrum of specificity can in fact restart the host immune system, amplifying this response as we see epitope spreading, a phenomenon that is very important, especially when addressing a complex target such as cancer cells. Again, this is something that is very important, and I will come back to this in just a moment. Now, if we go into the next slide, we can see that when we look into the tumor, we saw evidence of T cell infiltration. This influx of T cells had an inverse correlation with the levels of disease burden, clearly highlighting the interplay between the T cells and the cancer cells. In the next slide, we can see that when we look at the peripheral blood and put deep sequencing, evaluate the alpha beta TCRs, we can actually observe an amplification in vivo of specific alpha beta TCR clones that were present within the infused product, demonstrating in this way the in vivo expansion and persistence of the product that we administered to the patients. Now, if we go to the next slide, I would like to change gears slightly and concentrate now on the tumor. Although the MRD is able to provide us a black and white view in terms of the level of disease burden, we wanted to address the question of what is the constitution of the antigens present within the tumor? As you can see here in this slide on the right-hand side, we can address just that question by using RNA-Seq from tumor samples. Now in the next slide, you basically see an overlay between the levels of MRD and the target antigens present within the tumor. You see that the profile of these antigens have a very similar pattern to the one that we observe with the levels of MRD. In the next slide, you see that there is in fact a correlation between the level of these target antigens and the frequency of these antigen-specific T cells, demonstrating that in fact these T cells are providing an immunological pressure that is forcing the cancer cells to adapt and change. Now, if you look in the next slide, this is something that I consider very, very interesting. We wanted to ask the question, what happened next, if we look at the architecture of the tumor to antigens that are not present to the infused product, and in this case we're looking at Proteinase 3. Proteinase 3 is an antigen that it is present on the tumor cells, but again, it does not constitute part of the specificity of the infused T cell product. What you see here in this figure is that over time you see an increased proportion of Proteinase 3 that then peaks at week 18 and then rapidly decline by week 24, which it happened to coincide with the decline of week 18 to 24 for the levels of MRD. Now, if you go to the next slide, you basically see that by week 12 there is a remarkable amplification from the epitope spreading, that it was a spike and it was generated by the administration of our product that it is responsible for the subsequent decline in the Proteinase 3 tumor subsets. Taking all this together, what it means is that the administration of the T cell product provide an immunological pressure that is forcing the cancer cells to adapt and change. As these cancer cells are trying to adapt and change, the architecture of the antigen and the compositions within, it starts to drift. As presented here, you see that the cancer cells have a predominant expression for one particular antigen, as the cancer cells are trying to escape this immunological pressure. It's precisely in this point of tumor invasion when the recruitment of the endogenous immune system becomes so valuable. It's this what is responsible for the subsequent control of the attempts of the tumor to escape. Really this highlights a feature that it is in particular unique to this type of therapy. Right? Now, if you go to the next slide, you can see this pattern highlighted very clearly. When you see that when you monitor the antigen expression profile within the tumor, you see that this changes over time. This particular feature highlights the importance of, one, infusing a product that has a broader spectrum of specificity, while two, allowing the recruitment of the endogenous immune system, avoiding in this way the mechanisms employed by the cancer cells to escape. Again, I think that this particular feature is what makes this therapy very different to everything else that is out there. With that, let me hand over to Mai to provide some of the clinical summaries. Mai? Thank you, Juan. To summarize the safety leading results of the phase II AML trial, I'll begin by mentioning that no dose-limiting toxicities, cytokine release syndrome, or neurotoxicity were noted. It was consistent with the safety data that was seen in the phase I/II Baylor studies in over 150 patients. Also, the immunomonitoring data indicates that the evidence of the epitope spreading after infusion of MT-401, showing the breadth of the immune response seen in the patients. Lastly, the results support further investigation of MT-401 in AML patients, particularly in MRD-positive population. Now with that, I'll pass it back to Juan to discuss the T cell manufacturing process improvements. Juan? Thank you, Mai. Indeed, we're very excited about the clinical progress that we see by our team. In particular, we're recruiting patients in the ongoing AML study. As our clinical team was very efficiently recruiting patients into the study, I can tell you that the research team was not standing still. I can report today a significant development in the manufacturing process that, in my opinion, has the potential to transform the company. I will get to that in just a moment. Before, please allow me to level set and provide a general overview of what we have reported externally so far. If you go to the next slide, this shows a parallel of the process that we licensed out of Baylor to the process that we are currently using in the clinical study and which is implemented in those clinical results that Mai just went over just a moment ago. The thing to note here is that we have already significantly improved this manufacturing process. As shown in the next slide, these improvements resulted in a significant reduction of the in vitro culture time by half, a significant reduction in the number of interventions, which resulted in a final product with a superior phenotype. Finally, a product with a better spectrum of antigen specificity as shown there in panel B. The question that we asked to our scientific team was, is this the best we can do for the product platform? Is this the best that we can do for our patients? The answer is we can do better. As shown here in the next slide, I'm very happy to present a new manufacturing platform that is far more sophisticated than what we have so far. This manufacturing platform, as illustrated here in this slide, can be initiated with an integration of a simple combination of ingredients that after only nine days of in vitro expansion, allow for the collection of the product. This significant advancement will cut the in vitro culture time by half, allowing an increase in the throughput of production. In addition, this is a process that is far simpler compared with the previous manufacturing process. What about the characteristics of this final product? Now, if we look in the next slide, we see a comparison in the level of antigen specificity. On the left-hand side of this slide, we see the magnitude of antigen specificity from the Baylor process, the current process, and the new process highlighted in red, the new nine-day process. What is very obvious is that this new manufacturing process provides a product that is 4x more potent based on antigen specificity. If you look on the right-hand side, there is a further detail of three different manufacturing runs comparing the current process and the new nine-day process, showing that not only the final product has a greater magnitude of antigen specificity, but also the diversity of these cells is far superior. Allow me to provide a parallel of the evolution of this platform in a slightly different way. If you now look at this on the next slide, we see here the evolution of the manufacturing process from top to bottom, from the Baylor process to the current process, and in the bottom, the now more sophisticated nine-day process. In this case, on the x-axis from left to right, you have 22 different manufacturing runs. On the y-axis, you have the antigen specificity for PRAME, WT1, and NY-ESO-1, survivin. In this case, we have normalized the outcome to a simple binary result, meaning everything that you see in blue is the result of what we consider to be a product positive for an antigen, and everything that is white is considered a final drug product where we fail to recognize a specificity for a particular antigen. The first thing to notice here is that if you look at the pattern on the Baylor process, that you will clearly see that some of these result in manufacturing failures, and some of these products are specific only for one or few of those antigens. This pattern looks much better in the condition on the middle, where you have the current process, where the number of manufacturing failures is reduced and the number of antigen specificity within each of the manufactured products increases. However, if you look on the panel on the very bottom, you basically see how this new, simple, and enhanced manufacturing process that lasts only nine days results in a final drug product that is specific, the vast majority of the cases for the four target antigens. Probably the question that you're asking yourself at this point is what this means in terms of potency and killing capabilities. Now, if you go to the next slide, you see precisely that comparison. Here on the left-hand side, there is a comparison in the magnitude of antigen specificity of the current process and the new manufacturing that takes only nine days. As you can see on the left-hand side, the magnitude of antigen specificity is about 4x greater. In the figure on the right-hand side, you see the correlation between antigen specificity and killing, where you see a very direct linear correlation. Now, as you extrapolate the magnitude of antigen specificity for each one of these products, you can clearly see that the new manufacturing process will be capable of yielding a product that will be at least 4x more potent in terms of killing capabilities. To summarize this development, we have a new manufacturing process that yields a final drug product that has a greater magnitude of specificity. It also has a greater breadth of antigen recognition and has a greater killing potential. In addition to that, the short-term in vitro culture of nine days with minimal manipulation allows for a significant advantage in terms of manufacturing throughput that will clearly translate as we now enroll more patients in the AML study. With that, let me hand over to Mythili so that she can tell us how we're planning to integrate this exciting development into the clinical plan. Mythili? Thank you, Juan. This slide shows the phase II AML study schema in the post-transplant setting. Cohorts one and two refer to the safety lead-in portion, which has been completed and discussed earlier in this presentation. I would like to highlight that the MRD-positive patient from the safety lead-in received product using the current manufacturing process. We have since completed cohort three, which is also using the current manufacturing process with a higher dose of 200 million cells per infusion. This cohort has been completed and cleared since no dose-limiting toxicities were noted. We also have cohorts four and five, which we'll be looking at using the new manufacturing product at both 100 million and 200 million cells respectively. After cohorts four and five have been completed, we will reopen groups one, the adjunct group, and group two, the active disease group, shown in green and blue boxes respectively, using the new manufacturing process. I would like to highlight that the active disease group was further subdivided to include frank relapse and MRD positive patients in separate subgroups with approximately 30 patients each, to tease out the signal seen in each population. With that, I will pass it back to Juan to discuss some of the pipeline updates. Juan? Thank you, Mai. Now, as I mentioned earlier on, we're really excited about this new development and platform. I believe this development has the potential of transforming the future of the company. What I mean about that is that this new process not only has the ability to be manufactured in a very short and simple fashion while producing a product that is more potent, it also address perhaps one of the biggest obstacles out there in relation to adoptive T cell therapy. This is the individualized production of products to patients. The simplified manufacturing process now will allow the generation of a cell bank inventory that can be manufactured in advance, allowing in this way the benefit of pre-manufacturing and short time to deliver this product to the patients. If we look here in the next slide, we can basically see how this manufacturing process is completely scalable, and it speaks to the sophistication and the robustness of the manufacturing platform. Here you see that despite the fact that we use a small footprint such as a G-Rex 10 or a large culture device such as G-Rex 500, you see that the T cell fold expansion viability it is comparable, and you see a linear production of the material. This will enable the mass production of material up front, which then will be available to patients in need much faster. The way that this will apply in the clinic is something like this, as illustrated in the next slide. You basically will see that a number of donors, healthy individuals, will be collected to manufacture these products, which will be then expanded in large quantities, characterized and cryopreserved. At this point, this inventory will reside and be maintained in a cryo form, and at a moment of patient request, this product will be rapidly given to the patient in something that we believe will be in about 72 hours. If you look in the next slide, you see the combined benefit of this discovery. Basically, we see first of all, that a therapy can be given to patients much faster in just 72 hours. You also see the cost benefit by product scalability and also the ability of extending this product portfolio to other indications, not just hematologic malignancies, but potentially even solid tumors. Finally, the strategy that we're using of providing this product in the partially HLA match setting is a strategy that has been extensively being tested when using similar products such as bispecific T cells. Hopefully you can recognize that the combined value proposition here is significant, not just to the stakeholders, but more importantly to the patients. With that, I would like to pass over to Mai. Mai? Thank you, Juan. Next, I'd like to go over the off-the-shelf dose escalation study schema in patients with relapsed AML MDS. Eligible patients will be HLA matched with MT-401-OTS product based on a specific algorithm. The product will then be shipped to the site for administration. The dose escalation will have four cohorts. Cohort one and two look at single infusions of 50 million cells and 100 million cells, respectively. While cohorts three and four explore increased infusions at 100 million cells, with cohort three patients administered two doses and cohort four exploring four doses. Now each dose being administered is two weeks apart. This study, along with the extensive biomarker work entailed, will allow us to explore how cells are behaving at both increased doses and increased numbers of administration. The study will enable us to explore other indications as well outside of AML MDS, allowing us to create a platform. In this next slide, you can see that our off-the-shelf program expands our treatment capabilities. We started with one patient-specific MT-401 product that we are exploring in our phase II AML study, where each product is tailored to the patient. We then have extended into the off-the-shelf product, which will allow the administration of that product to greater than 100 patients and the ability to expand beyond AML to other heme malignancies and solid tumor indications. I will pass it back to Peter to discuss the pipeline further. Peter? Thank you, Mythili Koneru. Over the next 12 months, we plan to initiate three additional clinical trials. These will include a Marker-sponsored study in pancreatic cancer to build upon the results of the Baylor phase I study. This study will use our new six-antigen product, MT-601, and has already been granted Orphan Drug Designation by the FDA. In addition, we will start the first Marker-sponsored study in lymphoma, an indication in which Baylor observed particularly striking complete response rates and durability of remissions also using MT-601 in this trial. Lastly, we will initiate our first clinical trial with an off-the-shelf product, initially for patients with MDS or AML. We anticipate that this trial will be expanded into a number of additional indications, including both hematologic malignancies as well as solid tumors. Beyond these three new studies, our research team continues to develop a number of experimental approaches, including MT-1201, a twelve-antigen product, as well as a number of potential combinations with therapies that have been shown to be able to amplify T cell activity in cancer patients. We look forward to updating you on these programs as they progress. Looking to our plan for 2022, we have a very active year ahead of us. Our first goal is to fully implement the new nine day manufacturing process into our current AML study, which we anticipate will be done in the very near term. As Mythili indicated, our goal is to complete both the dose escalation cohorts for the new manufacturing process by Q3 and transition seamlessly into the enrollment of phase II patients in the Q4. Also, in the first half of this year, we expect that we'll be able to provide additional top-line readouts for those patients we have treated to date with the current 18 day process. Lastly, we will use this year to build our cell bank for the off-the-shelf program and complete IND-enabling work for the pancreatic, lymphoma, and off-the-shelf studies with INDs for those studies projected to be filed in the Q4. With that, I'd like to thank everyone for your time and attention today. As you can see, we're very excited about the clinical progress and the patient results that we observed in the safety lead-in period and the potential for our latest process improvements to generate a significantly more potent product. Operator, at this time, I'd like to turn the call over to any questions we've got from the audience. Thank you. Thank you. I'll be conducting your question and answer session. If you'd like to be placed into question queue, 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'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing star one. One moment please, while we poll for questions. Our first question today is coming from Joseph Catanzaro from Piper Sandler. Your line is now live. Hey, guys, thanks for the update here, and thanks for taking my questions. Maybe the first one for me. I know you walked through a lot of detail for patient 107, but wondering if there was anything distinct about the baseline product attributes that this responding patient received versus the non-responding patients, whether that be CD4 or CD8 composition or mixture of antigen-specific clones. Anything you could say along those lines. Thanks. Yeah. Thanks, Joe. That's a great question. Let me turn that over to Juan. Yeah. Thank you. In fact, our current characterization and the product composition that we have used in the clinic shows comparability in the analysis of the product that we have infused to these patients. What I'm trying to say to that is that from everything that we have done so far in terms of characterizing the product that we infuse, there is nothing unique or different to the product that we infuse to this patient with MRD compared to the product that was infused in the other patients in the clinical study. Okay, got it. That's helpful. Maybe sort of along a similar line, can you speak to the extent of any anti-leukemic activity you observed in those patients with frank relapse who didn't achieve objective responses and whether you saw a reduction in blast counts? Mythili? Yeah. Thank you for your question. I think we try to highlight the patients that we think was of importance, which is that MRD positive patient. As I mentioned in the call, the other patients, the five patients with frank relapse, none of them had any objective response. Okay, got it. Then maybe if I could just squeeze one last one in here. I think if I heard you correctly, Mythili, you said sort of reopen the main portion. I just wanna confirm that right now the main portion of the trial is currently paused until the new manufacturing process clears at either this 100 million or 200 million dose. Yes, that's correct. Currently we are focusing our efforts on cohorts four and five, which is the new manufacturing process at the 100 million and the 200 million dose. Once those are completed, we will reopen groups one and two, the adjuvant and the active disease groups, and continue enrolling in those groups. Okay, got it. That's clear. Okay, great. Thanks so much for taking my questions. Thanks, Joe. Thank you. Our next question today is coming from Kristen Kluska from Cantor Fitzgerald. Your line is now live. Hi, good afternoon. Congrats on these initial findings and for all of these accomplishments related to manufacturing. Maybe I'll start with a manufacturing-specific question. I think in the past, outside of length and time to take, you've also communicated that the previous round of manufacturing updates led to a 90% reduction in the number of required operator interventions. I was wondering how this process looks now, especially since the time was reduced by more than half, and how you also expect that these changes could help with costs. Juan? Thank you. Yeah, that's actually a great question. If you look at this slide here, the manufacturing process virtually has two main components of interaction. One is the culture setup, where basically the key ingredients are added into the culture, right? You can see it's basically the media, the raw material, the cytokines, and the peptides. From that point on, the culture basically is left undisturbed, virtually unmanipulated for the rest of the culture period, and then harvest at the end at day nine. I think that now you basically see a significant reduction on the number of interventions. As you mentioned, that will have a significant impact on the cost for many reasons. One of them, it would be the cost associated with the use of the facility and the cost associated with the time and personnel and the ability to use our current manufacturing facility to manufacture more products for the patients. Got it. Thanks for that. How are you thinking about the specific antigen expression for these models in totality outside of just this particular MRD plus patient who became MRD negative? For example, do you think or expect there could be any differences when looking at the profile of those at frank relapse or perhaps other patients who presented with different baseline characteristics? Yeah, that's actually a great question. Now, let me tell you that this is something that for us, you could probably recognize it was a significant amount of work for us to characterize in a lot of level of detail this patient with MRD, that we're definitely very excited about the clinical response. We're gonna be conducting a similar level of characterization in the rest of the patients in this study. Right? Now, I think that level of characterization will give us more information to trying to understand the differences that we see when we use this therapy in some of these group of patients. Definitely it's a great question and it's something that for us is on the table to address as we continue doing the characterization on the other group of patients. Great. Thanks. For the pipeline expansion, part of this decision of course is from some of the work we saw at BCM in addition to some of the implementations you've shown in-house. Just wanted to ask you there if you've seen any updated data or findings from some of the last updates. I think for pancreatic there was something like 31 patients treated and very clean safety with no CRS or neurotoxicity, and you had some efficacy data from 13 patients, but just wondering if there's been an update to either of those trials from BCM. Mythili Koneru, why don't I turn that over to you? Sure. Thanks, Kristen. The updates that were provided from Baylor, there are currently no further updates, but we will continue to have dialogue with Baylor and to determine additional information regarding overall survival, for example, in those 13 patients. In the meantime, we're obviously very eager to also move forward our MT-601 in pancreatic cancer to also further interrogate, you know, the addition of the antigen and potentially higher doses as well in a similar patient population. Both those efforts are continuing to move forward. Great. Thanks for taking the question. Thanks, Kristen. Thank you. Our next question today is coming from Matt Biegler from Oppenheimer. Your line is now live. Hey, guys. Thanks for the update. Congrats on the progress on the manufacturing side. Mythili, you may have just alluded to this, but I'm curious whether you can push the dosing with that new manufacturing process past that 200 million cell dose, and whether this is something that you're considering given, you know, what we've seen so far, which is a very strong safety profile. Yes, we're definitely interested in looking at, you know, the 200 million dose, and potentially higher. I think right now though, with the increased specificity, you know, 4x more potency, that we're essentially, even though it's the 200 million dose, we're essentially have already, theoretically bumped up the dose you can think of it because the cells that you're infusing, you know, have higher specificity to it. So essentially, the equivalency of using the old manufacturing process at that same dose and the new manufacturing process at that dose is essentially like administering a higher dose. So we're really excited about, you know, cohorts four and five and the capabilities, and then, assuming that the toxicity profile stays consistent, you know, moving that forward. Yeah. Matt, you know what I would add to that, Matt, is, if you actually look at the readings on the charts that we provided here with respect to the T cell expansion and the epitope spreading, what you'll notice is that, you know, the magnitude of the T cell expansion and the epitope spreading that we're able to detect here is many times greater than what you typically saw from Baylor. As we implement a product that, you know, by our best measure looks to be about 4 x more efficient in terms of tumor killing, I think that we wanna be cautious in terms of moving dose until we really understand, you know, what sort of efficacy profile we're seeing, you know, from just the manufacturing improvements. At the end of the day, like you said, you know, dose is always on the table for us. Yeah, that makes sense. I'll ask, maybe follow up with a controversial question, though, but given, you know, some of the early data in the relapse refractory cohorts, are you guys at all considering adding a cohort that studies preconditioning given that, you know, preconditioning with fludarabine is a pretty well accepted standard of care in cell therapy at this time? Thanks. I mean, given that we have seen in the MRD positive patient really good evidence of epitope spreading, you know, we would have concerns about adding preconditioning that would eliminate that phenomenon that we believe is very important in the technology in creating that durable lasting response. At this time, I think we have a lot of opportunity to expand what we're seeing in additional patient populations, and get additional biomarker information. I think our focus is there at this time and not necessarily preconditioning. Yeah, Matt, you know, from the perspective of that MRD positive patient in particular, you know, I pulled up slide 20 for you here. You know, the way that we look at this and the importance of the epitope spreading versus the expansion of just our T cells. If we look at the overall trajectories here, you know, I think that reasonable conclusion would be that, you know, you saw fairly extensive expansion of our T cells immediately after infusion, which, you know, leads to this fairly significant immediate decline in the tumor. When you see the tumor recur, in many ways, we think that, when we look at the antigen expression, it looks like a lot of that week 18 recurrence is being driven by, you know, the outgrowth of a tumor cell population that primarily expresses Proteinase 3. You know, it was the epitope spreading in this case that you see at week 12 that we think was able to to really, you know, put pressure and eliminate those T cells post week 18. You know, in many ways, you know, we look at this and we say, "But for the epitope spreading, this patient might not have been an objective responder." I think that for us, we're very, very cautious about impairing, you know, the phenomenon of epitope spreading. All right. Thank you. Thanks, Matt. Thank you. Our next question is coming from Tony Butler from Roth Capital. Your line is now live. Yes, thanks very much. Peter, your last comment is actually telling in a couple of ways, and I appreciate it a lot. If I go back simply to slide 11 and just look at disease assessment, and Mythili. This actually gets to two earlier questions in one. The patients that were frank relapsers, do you actually see any blast reduction even at similarly at week eight or 12, even if in fact, if we were to make an assumption that again, it's a clone that is very high in Proteinase 3. As an assumption for those other five patients, much like you see in week 18, could one say that you had some activity or no activity at all? I mean, it's actually really critical because if I take all these data, and I think this is what everyone's hinting at, if I take the entire data set and I put it together and I say, what can I take away? I don't know which patient to give this therapy to. I wanna know when the phase II trial opens again, how those physicians are going to treat incoming AML patients with what you're going to be able to tell them that, well, look, we've had some positive. We've had a positive response in an MRD positive patient. It's fantastic. How do they actually know that this will be the right patient for whom to give the appropriate therapy? Thanks a lot. Mythili? I mean, the early Baylor data does suggest that this therapy works in patients with frank relapse. The number of patients in the CTP Eden was very small. It was only six patients. It would be too early to say that, you know, there's a specific patient population that we should be targeting at this moment in time. Therefore, it is very critical moving forward that we look at both populations of frank relapser and MRD positive patients, which is why in the group two patients, we've subgrouped the patient population to look at and interrogate both sets of patients. Looking at the biomarker data, I think we have a really clear idea of how to move forward and interrogate those types of questions. I think it would be too early to say that there's a specific patient type that we would want to target at this moment in time. Clearly, it's worked in frank relapse. Clearly, it's working in MRD positive. We'd want to obtain more numbers of patients to treat to really identify what you're getting at. Yeah. I mean, if anything, I think that this data just corroborates some of the findings from Baylor ensuring the interplay between the T cells, the endogenous immunity, epitope spreading, and how that is affecting the disease burden. I agree with Mai. I think that it's probably too early to say that this therapy will work only in a subset of patients. When we look collectively at the data from Baylor, that's reasonable to believe that this therapy will work also in patients with frank relapse. Yeah. You know, Tony, you know, on top of that, I would say that, you know, when we look at the patients where we've seen clear clinical benefit, you know, those patients have been all across the board. You know, we saw a complete responder with a patient with severe extramedullary disease. We saw a patient who had extremely high blast counts, you know, 70%, see those blast counts get reduced to 40%, enabling him to move on to another therapy. I think that those cases underline the fact that the therapy, even as it was being manufactured with the Baylor process, was capable of generating objective responses for patients with frank relapse, even those with potentially very high blast counts. What I think that this data shows is now with our manufacturing process, we actually have the ability to hit MRD positive patients in a way that was never practical before. You know, even the guidance from the FDA on how to measure MRD positivity is relatively recent, you know, less than two years old. For us, I think that what this data set underlines is that we actually have identified another patient population that may actually be even more amenable given the lower tumor burden associated with these MRD positive patients. You know, that's why when you look at Mai's revised trial schema, you see that what we've done there is, you know, kept the trial design basically static, with the exception of dividing the active disease group into those patients that are frank relapse versus those patients who are MRD positive, particularly because today there is no treatment for MRD positive patients. You know, for- I appreciate. Yeah. Yeah. The way that we look at it. No, I appreciate that. Yep. Thanks, Tony. Peter, I'm sorry. One more question, though. No, I. Juan, this is back on manufacturing, Peter, to be fair, so that's why I'm asking Juan. Is the media that's utilized with serum? I just wanna be clear, and importantly, just forgive me for not remembering, what are the cytokines that are also added? I wanna be sure that what is actually dosed to the patient is absolutely free of any serum or cytokine. Yeah. Thank you for the question. I mean, let me go to this slide, and I have to apologize, first of all. I mean, I cannot go into all the details in the manufacturing, for intellectual property reasons. We have filed recently intellectual property, which I think is gonna be very important for the company, but we're also keeping some of these as trade secrets. Now, what I can tell you is that, we have worked closely with the FDA and received recent approval for this new manufacturing process, right? This is something that it really goes in line to be able to have a process that is not only suitable for the clinical study, but it's a process that will be suitable for future commercialization. Hopefully that is the way that the FDA is actually evaluating this new CMC package that it was put in front of them, right? I have to say that really this has been an enormous amount of work and really excellent performance by the company's quality group and regulatory group working with vendors to get to this point where everything that we actually have used, we basically have sources that are GMP-grade from multiple vendors, ensuring the highest quality as we use these materials in the GMP production. Thanks, Juan. Thank you, Peter. Thanks, Tony. Thank you. We've reached the end of our question and answer session. Ladies and gentlemen, that does conclude today's teleconference and webcast. You may now disconnect your lines and have a wonderful day. We thank you for your participation today.