Greetings, and welcome to the Cue Biopharma update call. At this time, all participants are in a listen-only mode. A question- and- answer session will follow the presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference is being recorded. I would now like to turn this conference over to Mr. Dan Passeri, Cue Biopharma's Chief Executive Officer. Thank you, sir. You may begin. Okay. Thank you, and good afternoon, everyone. Just to remind you as we proceed through the presentation, we'll convey which slide we're on, and you can advance the slides directly. We appreciate your time and interest in our update call regarding our ongoing trials of CUE-101 as well as CUE-102, our initial representative drug candidates of the IL-2 based CUE-100 series. Joining me on today's call is Dr. Anish Suri, our President and Chief Scientific Officer, Dr. Ken Pienta, our Acting Chief Medical Officer, and Dr. Matteo Levisetti, our Senior Vice President of Clinical Development, and Kerri-Ann Millar, our Chief Financial Officer. This conference is being recorded and will be available on our website for the next 30 days. As a reminder, and as shown here on slide number 2, this presentation and overview may contain some forward-looking statements, and any forward-looking statements made during the call represents the company's views only as today, August 23, 2022. Our agenda for today's call is shown on the next slide. As an introduction, Anish will provide a synopsis of our progress to date, as well as describing our strategic and competitive positioning prior to turning the call over to Ken and Matteo, who will each provide a summary and status update of the data associated with observations from our ongoing phase I trials of CUE-101, as well as the recently initiated CUE-102 trial. Following Ken and Matteo, I'll provide an overview of our corporate strategy and additional pipeline expansions within the CUE-100 series. Kerri-Ann Millar will then provide a brief update of our financials, after which, I'll return for closing remarks and then open up the call for a Q&A session. With that, I'll now pass the call over to Anish Suri. Thanks, Dan. I'd like to start today's presentation by reminding folks of the genesis of our company's quest and the mission we seek to accomplish. Our mission is to address a very fundamental and consequential question for immunotherapy, which is, can we selectively and specifically activate antitumor T cells while avoiding the carpet bombing of the immune system to maximize efficacy and minimize toxicities? This is a very basic yet fundamental distinction from how others may be approaching the challenge of turning the immune system against cancers. To accomplish our objective, as shown in slide four, we envisioned exploiting the one unique marker of an antitumor T cell, which is the tumor-specific T cell receptor or TCR. We've engineered an innovative biologics platform termed Immuno-STAT that generates TCR selective engagers to deliver immune activating signals to tumor-specific T cells. The figure on the left in slide 4 depicts the core structure of an Immuno-STAT, which is essentially an antibody Fc-based biologic containing stabilized tumor peptide HLA molecules to selectively target tumor-specific T cells along with desirable activation signals that are consumed by those T cells. This framework provides a molecular basis for improved specificity for antitumor T cell activation while minimizing off-target toxicities due to systemic immune activation, which, by the way, continues to be a key impediment for many other broadly targeted immunotherapeutic approaches. On the right side of this slide, you can see a figure depicting the CUE-100 series, which is designed to selectively deliver IL-2 to tumor-specific T cells over irrelevant T cells, hence generating a therapeutic index for IL-2, which as of yet has been a challenge. We believe this is a superior approach for harnessing the fullest potential of IL-2, especially since the tumor-specific T cells are present in a very low frequency. Our current clinical candidates, namely CUE- 101 and CUE- 102, are derived from the CUE- 100 series and share the core IL-2 framework as depicted here. The next slide 5, summarizes the key and impactful takeaways that highlight the progress and clinical validation of our approach. Ken and Matteo will provide detailed insights into the clinical data and patient benefit that support the conclusions noted here. To summarize, we've engineered a novel biologics platform, Immuno-STAT, for selective targeting of antitumor T cell activation. As an initial drug construct, we chose to deploy IL-2 as the targeted activation signal. IL-2 is a well-characterized and validated therapeutic target but has suffered from significant safety liabilities due to lack of a therapeutic index. We have successfully generated a therapeutic index for IL-2 as evidenced by the fact that we have observed clinical activity between 1 mg/kg and 4 mg/kg and have dosed up to 8 mg/kg with no MTD. Most other IL-2 variants that are in the clinic have been dosed in the low microgram per kilogram range due to unwanted adverse side effects. Our first clinical candidate, CUE-101, targets IL-2 to HPV specific T cells to attack HPV-driven cancers such as head and neck cancer. Our clinical experience with CUE-101 highlights several important findings for our technology platform. Our molecules are well-tolerated with no evidence of systemic IL-2 toxicities, such as vascular leak syndrome or cytokine storms. They exhibit drug-like properties, including favorable PK, on-target PD signals, and monoclonal antibody-like manufacturability to support desirable cost of goods. We have demonstrated clinical efficacy as monotherapy in late-stage cancer patients that have failed numerous prior therapies, including checkpoint inhibitors. Ken and Matteo will describe these signals in detail, including an emerging benefit in overall survival. The observed clinical benefit is supported by mechanistic signals demonstrating T cell infiltration, which catalyzed our ongoing neoadjuvant trial in head and neck cancer. We have evidence prolonged benefit and antitumor activity in patients remaining on therapy for long periods, which underscores the extended kinetics for evolution of a beneficial immunotherapy response, as also noted previously by others. Lastly, early data from our first clinical experience in combo with a checkpoint inhibitor supports the potential for significant expansion of patient benefit. All these metrics will be described in greater detail in the ensuing clinical discussion. Importantly, since the core IL-2 framework is conserved across the CUE-100 series, we believe the clinical de-risking obtained by CUE-101 has essentially de-risked our entire platform. The recent IND acceptance for our next clinical candidate, CUE-102, targeting Wilms' tumor 1, or WT1, underscores the strategic advantages of platform de-risking accomplished by CUE-101. The FDA accepted the CUE-102 IND with no requirement for preclinical talks and has authorized us to initiate the trial at 1 mg per kilogram, a dose that has demonstrated clinical activity in the CUE-101 trial and is a significantly higher starting dose than the 0.06 mg per kg starting dose for CUE-101. These metrics highlight the resource, time, and operational efficiencies gained by the platform de-risking by CUE-101. To end, we believe the modularity of our platform, coupled with the clinical validation, positions us to generate a rich repository of therapeutic molecules targeting many cancers. As one evaluates the potential of IL-2 for cancer immunotherapy, we believe our platform has cracked the code for selective targeting of this cytokine to the tumor-specific T cell repertoire. Dan will address this in context of our corporate growth strategy towards the end of today's presentation. With that backdrop, I'll now pass the call to Ken for the clinical update. Ken? Thanks, Anish, and good afternoon to all listening to this call. We're excited to be presenting our updated data from the ongoing CUE-101 phase I trial as both a single-agent monotherapy and third line and beyond head and neck cancer, as well as the encouraging emerging early data from the combination study with pembrolizumab in first-line patients. As previously and consistently stated, we believe CUE-101's mechanism of action, as evidenced by the ongoing data generated to date, provides effective and tolerated dose levels enabling selective stimulation of tumor-specific T cells. Recurrent head and neck cancer is a tough and curable disease. The data we have observed throughout the monotherapy trial enhances our confidence that CUE-101 is stimulating cancer-specific T cells in a subset of these patients with a resulting antitumor effect. Furthermore, and more importantly, we continue to observe an evolving trend of enhanced survival. While this data is still maturing, we are encouraged by the observations to date. Clinical observations beyond overall response rate and median overall survival continue to bolster our confidence in the antitumor effects of CUE-101. For example, we have observed patients experiencing tumor reduction after prolonged periods on drug where no RECIST-based objective response was initially observed by imaging. This observation, consistent with observations made by others, demonstrates the kinetics of T cell antitumor activity that manifests over a longer period of time. This pattern can be seen in the tumor measurements plotted out on slide 6 for a patient receiving CUE-101 at 2 mg per kg, where we can see that the first several months appear to demonstrate tumor growth even beyond the 20% threshold used by RECIST criteria. However, we... Based on the overall clinical status, the patient was continued on treatment after we changed the protocol to allow this. After approximately 6 months, the tumor began to shrink, and the patient remains on therapy 14 months after starting treatment with CUE-101. The data presented on slide 7 from a patient treated RP2D of 4 mg per kg demonstrates stable disease lasting close to 12 months and ongoing with sustained reductions of cell-free HPV DNA, a biomarker that may reflect disease activity in patients with HPV-positive cancers. In fact, this is a test that is increasingly being used by experts to guide treatment in these patients. This may represent a pattern suggestive of a pathologic CR. Taken together, these data build our confidence in the therapeutic potential of CUE-101 and in the potential path forward for a registration study as a monotherapy in patients that have failed prior chemotherapy as well as checkpoint inhibitor therapy. We plan to present additional data at an upcoming medical meeting. I'll now turn this over to Matteo to talk more about this and our other data. Matteo. Thanks, Ken. The goal in our CUE-101 monotherapy study was to first prove safety for this first in-man biologic, and second, to prove that we could demonstrate antitumor activity. In addition to the data just described by Ken, we have observed in our 20 treated patients at the recommended phase II dose in our monotherapy trial, 1 PR and 7 patients with durable stable disease for an overall clinical benefit rate of approximately 42%. The next slide 8, shows a patient with a PR and their supporting pharmacodynamic metrics. This heavily pretreated patient has completed 17 cycles of CUE-101. You can see in the 2 upper right panels that the patient demonstrated a 9-fold increase in cancer-specific T cells but did not demonstrate an increase in the general CD8 positive T cell population, which might cause unwanted side effects, including immune-related adverse events. The patient also demonstrated a transient and modest increase in Tregs that returned to baseline by day 15. The patient demonstrated a sustained increase in NK cells, a positive attribute, for an antitumor response, as the NK cells may assist in tumor killing. We observed similar pharmacodynamic effects across many patients. On the lower right portion of the slide is a graph showing a rapid decrease in circulating cell-free HPV DNA corresponding with the decrease in tumor burden observed by imaging. We have made the same observation with several other patients who have demonstrated antitumor activity and continue to monitor cell-free HPV DNA as a possible predictive biomarker. The next slide 9, conveys our ongoing survival swimmer plot for the 20 patients dosed at the recommended phase II dose of 4 mg per kilogram. We have taken the liberty to draw a median overall survival line at 8 months, which is reflective of the median overall survival observed in both the KEYNOTE-040 and CheckMate 143 trials of pembrolizumab and nivolumab in second-line patients. As any experienced oncologist understands, the survival with third-line treatment is expected to be less as the disease has further developed and become more unstable. Our evolving data continues to support the premise that treatment with CUE-101 is clearly trending to increase survival in the third-line setting for patients with head and neck cancer. This data has encouraged our principal investigators, and they are aligned with our position that this potentially provides us with a promising path forward to a registrational trial. The demonstration of monotherapy activity bolsters our belief that we should see complementary mechanistic effects in combination with pembrolizumab. As a reminder, the data from patients treated in monotherapy clearly supports that CUE-101 increases the number of antigen-specific T cells. It is likely that these T cells will have greater freedom to kill with inhibition of the PD-1 pathway, a major mechanism used by cancer cells to prevent immune-mediated killing. Slide 10 demonstrates the spider plot as shown at ASCO this past June of first-line patients treated in the dose escalation cohorts of the ongoing study. Early data and signs of activity of CUE-101 in combination with pembrolizumab are encouraging. With 1 patient each in cohorts 2 and 3 experiencing a confirmed PR and an additional 2 patients experiencing durable stable disease. We are continuing to expand patient enrollment at the recommended combination phase II dose and look forward to presenting additional data at an upcoming meeting. Slide 11 shows the patient from cohort 2 demonstrating a decrease in all 4 of their target lesions, including 2 liver lesions. I want to emphasize that this is not just shrinkage in lymph nodes, but shrinkage of visceral tumor disease. To any oncologist, this is a significant and meaningful response. This patient has also demonstrated a clearing of their circulating cell-free HPV DNA, which is ongoing. As mentioned before, circulating, tumor DNA continues to be developed and used by our principal investigators as a potential surrogate for response. As shown in slide 12, the patient with a confirmed partial response from cohort 3 also demonstrated reductions in all 4 target lesions, including 2 parenchymal lung lesions and clearing of their circulating cell-free HPV DNA. We are excited by the preliminary data in this ongoing combination study, along with maturing data from our monotherapy and neoadjuvant studies, and look forward to presenting additional data at upcoming meetings. I am also happy to report that we have treated our first patient with CUE-102, which targets Wilms' tumor 1-positive tumors in a trial that is enrolling patients with advanced colorectal, gastric, pancreatic, and ovarian cancers. As shown on slide 13, CUE-102 and CUE-101 share 99% amino acid sequence identity. This enabled us to significantly decrease the development time and cost of CUE-102, as we were not required by FDA to repeat IND-enabling toxicology studies for CUE-102. We were also able to initiate the phase I dose escalation study at 1 mg per kilogram, the dose at which we observed clear signs of biologic activity with CUE-101. As slide 14 shows, and as mentioned just a moment ago, we are performing the CUE-102 dose escalation study in colon, gastric, pancreatic, and ovarian cancer patients. This design offers us the ability to do monotherapy expansion studies in all or any of the indications being evaluated in the dose escalation phase of the trial. This trial is actively accruing and will be open at 15 sites around the U.S. I will now turn the call over to Dan to talk more about our pipeline. Dan? Yeah. Thanks, Matteo. As just described by Anish, Ken, and Matteo, we've made significant progress towards the establishment of CUE-101 and by implication, the entire CUE-100 series as a breakthrough therapy for stimulating a patient's immune system against cancer. To remind you that's stimulating the immune system directly in the patient's body. As we continue to progress forward with CUE-101 and CUE-102 as our lead programs, we also have the potential to rapidly expand our pipeline and productivity, as conveyed in the schematic shown on slide 15. However under the current market conditions where capital is constrained and resource prioritization is paramount, we've streamlined our operational footprint and taken prudent measures to foster a focused and strategic prioritization of clinical development and those activities associated with pipeline development fostering strategic partnership. Our core approach is to validate and de-risk the IL-2 based CUE-100 series through the emerging data and associated metrics from our ongoing, 101 and now 102 clinical trials and position ourselves with greater leverage for retained value creation for our shareholders. We have promising preclinical data from our KRAS program, which is an extremely important target, covering a broad set of cancers, with expanded allele coverage into HLA-A*03 and HLA-A*11, and have preserved this clinically important program for potential strategic partnering, to be catalyzed by our emerging data from our CUE-101 trial and our CUE-102 trial, as well as a possible registration submission in CUE-101. We have also positioned ourselves for enhanced productivity and efficiencies with the development of a CUE-100 series derivative, which referred to as Neo-STAT, entailing a stabilized molecule as the MHC, HLA binding pocket where the epitope fits in, that's been stabilized for covalent chemical attachment of an identified cancer epitope. This will allow for the manufacturing of each allele framework, for example, HLA-A*02, HLA-A*03, HLA-A*11, et cetera, with an empty binding pocket, whereby the epitope may be subsequently attached chemically rather than made as a single fusion protein. This will provide us with cost savings, production efficiencies, and greater flexibility for epitope selection and combination, such as in the case with tumor instability and heterogeneity. Furthermore, we envisage that Neo-STAT may be an enabling innovation to realize the potential of personalized cancer immunotherapy, where one could sequence the tumor and identify particular epitopes and chemically attach those to a Neo-STAT. While we are currently prioritizing and strategically focusing internal efforts on the development of our CUE-100 series drug candidates for treating cancer, we're also actively engaged in strategic discussions with third parties to further develop CUE programs outside of oncology, including the CUE-400 series for treating autoimmune disease. These activities aim at ensuring optimal use of our internal resources on our most advanced programs while augmenting and enhancing our capacities with third-party relationships to further develop promising assets beyond our core focus. I'm now gonna turn the call over to Kerri, who will provide a brief overview of our current financials, and I'll then return to briefly provide some closing summary remarks prior to opening the call up to questions. Thanks, Dan. Turning now to slide 16, I'd like to provide a brief update on our financial results for the three months ended June 30, 2022. The company reported collaboration revenue of approximately $26,000 and $2.7 million for the three months ended June 30, 2022 and 2021 respectively. Research and development expenses were $9.6 million and $8.8 million for the three months ended June 30, 2022 and 2021 respectively. The increase was primarily due to an increase in laboratory and drug substance manufacturing costs, as well as clinical expenses related to our CUE-102 phase I dose escalation clinical trial that was initiated during the second quarter of 2022. General and administrative expenses were $3.8 million and $4.3 million for the three months ended June 30, 2022 and 2021 respectively. The decrease is due primarily to a decrease in stock-based compensation and professional and consulting fees incurred during the second quarter of 2022 as compared to the same period in 2021. We ended the quarter with approximately $66.1 million in cash and cash equivalents and working capital of approximately $60.7 million. Importantly, we took proactive steps to decrease the company's office and lab footprints and restructured specific functions which will afford us significant cost savings that can be allocated to our clinical programs. We believe our cash and cash equivalents as of June 30th, 2022 will allow us to support the development of our Immuno-STAT platform, including the clinical development of CUE-101 and CUE-102 through the third quarter of 2023. I'll now turn the call back over to Dan for closing remarks. Dan? Yeah. Thanks, Kerri-Ann Millar. As you've heard on this call, we continue to execute and make significant progress towards further advancing our lead and representative candidate CUE-101 towards a potential path for registration. Through the clinical development of 101, we've clearly demonstrated the ability to selectively target and activate defined antitumor T cells while not compromising patient safety. As seen on slide 17, we have successfully executed and continue to execute on defined strategies providing risk reduction and validation of the CUE-100 series and its derivatives. As such, CUE-101, which is targeting the HLA-A*02 allele, has clearly demonstrated tolerability and single-agent activity, and remind you with no maximum tolerated dose emerging from the dose range of 0.06 mg/kg all the way up to 8 mg/kg. We've seen clear evidence of pharmacodynamic effect on targeted tumor-specific immune cells, that is, T cells as well as natural killer cells. Obviously, the properties that we want to see in the immune compartment. Clinical activity demonstrated from 1 mg per kg to 4 mg per kg, with 4 mg per kg being our recommended phase II dose. Clear evidence of antitumor activity, which we've gone through some of these data showing sort of a prolonged effect having to do with the kinetics of stimulating the immune system, the immune system then dynamically interfacing with cancer. Clear evidence of that antitumor activity manifested as a confirmed PR, seven durable long-standing stable disease with one potential pathologic complete responder that Ken reviewed. We appear to be providing a survival benefit. This obviously needs to be determined as to what the median overall survival is, but it is clearly trending in a positive direction, and we believe it'll provide us with a potential path forward for registration. CUE-101 in combination with pembrolizumab is showing encouraging early signs of activity, which we look forward to presenting further details at an upcoming medical meeting later this year. CUE-102, the IND was accepted at 1 mg per kg starting dose, and we consider this to be a major achievement, basically underscoring the quality of the supportive data, but also kind of underscoring the risk reduction and validation that we believe we've achieved with the data emerging from the CUE-101 trial. Any evidence I should say that emerges in the 102 trial of clinical activity will be a further catalyst for validation and value creation regarding the platform's analog nature and modularity. Just to remind you, Wilms' tumor 1 is expressed in a significant range of tumors representing a very significant market potential in multiple tumor types. We believe those two programs add significant validation and value for our shareholders, and then coupled with Neo-STAT representing kind of a derivative of the 100 series as a next generation construct providing scale and flexibility, one that allows us to address tumor heterogeneity, but also just as importantly, it should substantially decrease our cost of goods and provide us with flexibility that we may even be able to go into personalized medicine. Again, to remind you, the attachment of the peptide is in the HLA pocket. That's a covalent attachment. We have attractive preclinical proof of concept data supporting that premise and look forward to providing you with updates as we continue to progress. We're positioned very well strategically and anticipate several important milestones throughout the coming year, including the potential of a registration path for CUE-101 as a monotherapy. These milestones as conveyed on the next slide include CUE-101 monotherapy with a median overall survival data by end of year, clarifying, and this is the potential start of registrational trial in the second half of 2023. CUE-101 plus pembrolizumab combination, the preliminary overall response rate data reading out in the second quarter of next year, 2023. The 102 monotherapy data, which we've just recently initiated. Data from the dose escalation will be reading out mid-2023. To remind you, that is a major significant market opportunity, so any evidence of clinical activity will represent a significant, prospective value increment. Also and importantly, as we focus our efforts and resources on the clinical development of CUE-101 and CUE-102, we believe that further clinical data sets will catalyze significant business development and corporate development opportunities for pipeline expansion. We look forward to providing further details on these trials at an upcoming medical conference later this year. We'd like to thank our employees and clinical principal investigators whose dedication to our mission, through their commitment and professionalism, allows us to continue progressing our goal of helping patients in need. We'd like to thank our Board of Directors for their support and guidance. We want to thank our shareholders who provide us with the essential resources to continue this important work developing promising immunotherapies for patients. Most importantly, we wanna thank the patients who are participating in our trial and their families for their courage and willingness to be part of a clinical study, allowing us the opportunity to assess and determine the potential therapeutic benefit of our promising drug candidates. I'd like to thank you very much for your attention and interest. I'd now like to turn the call back over to the operator for questions. At this time, we'll be conducting a question- and- answer session. 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 to remove your question from the queue. For participants using speaker equipment, it may be necessary for you to pick up your handset before pressing the star keys. One moment while we poll for questions. Our first question comes from the line of Stephen Willey with Stifel. You may proceed with your question. Yeah, good afternoon. Thanks for taking the question, and thanks for the update here. With respect to the updated CUE-101 data, do you have a median duration of treatment at this point? I think it looks to be about two months just in terms of eyeballing it, but just wanted to know if that's correct. Can you just broadly speak to post-study therapy that these patients may or may not be receiving following discontinuation of CUE-101? I guess your confidence that post-study therapy is not impacting this extended OS time that you're seeing off treatment. I just have a quick follow-up on CUE-102. Okay. Thanks, Steve. Ken, you wanna take those questions? Yeah. Hi, Steve. The median therapy is 2 cycles, meaning half the patients got 2 cycles and came off. I would just point out that that's, you know, basically the same as we see with second line checkpoint inhibitors. It really comes down to what do those patients do as far as overall survival because the progression-free survival just doesn't correlate as you know. As far as follow-up therapies, we're still collecting that data and really don't have that to report yet. We do know some patients that are doing quite well off all therapies. We just don't know that data yet. Sorry. Okay. Just on CUE-102, I know the dose escalation portion and presumably expansion is requiring WT1 antigen positivity. Is this just kind of like a binary yes, no type of assay that's, I'm guessing IHC based, or is there some kind of graded expression that a patient- Um- needs to have in order to be eligible? Yeah, it is IHC based and it is graded. Our sort of minimal requirement is that 1% of the tumor cells are expressing WT1. Okay. I'll hop back in the queue. Thank you. Thank you. Our next question comes from the line of Reni Benjamin with JMP Securities. You may proceed with your question. Hey, good afternoon, guys. Thanks for taking the questions, and congrats on the progress. Thanks, Reni. Maybe just starting off, can we talk a little bit more about the biomarker data that you generated with the? I see the circulating, or sorry, the HPV DNA, you know, going down considerably, and then, you know, but the tumor shrinkage is occurring, but not clearly as much. And I think you may have called that a pathological CR. I'm not too sure if I understand how well that's being correlated. Can you talk to us a little bit about that? You know, would you use that going forward? And what other sorts of biomarker activities are you planning for these studies, both with 101 and 102? Okay. Ken, do you wanna take the first part of that and then have Matteo cover the second one? Essentially what we're seeing is that we have several patients with durable stable disease. As you know, with the immunotherapy types of therapies, the IO type therapies, you often can see sort of a stabilization of disease that could be scar, it could be fibrotic tissue, could be inflammatory tissue. Early on, we had the patient at 1 mg per kg who had stable disease, and we ended up going to the operating room and seeing, you know, that patient has remained off therapy for now 14 months or 19 months. Then the data that we've been getting from these ongoing cell-free DNA assays, which didn't really exist when we started the trial, was that several of our PIs have started to follow virtually all the patients with cell-free DNA to try and get some insight into their disease, especially when we, you know, we don't know when somebody has an increase in their tumor, if that's more iRECIST, is that an inflammatory change that we should be following? What's their cell-free DNA doing? Is that going up or going down, suggesting it might be more inflammatory? Or with these stable disease patients, do they have any active tumor left? The data, you know, I talked about with this one patient has very stable disease. The tumor is either just sitting there or what we think is not viable tumor is just sitting there, like a scar, and their cell-free DNA is zeroed out. That suggests to us, based on the other patients that that may be a pathologic CR if we took that out. That is, you know, this whole area is evolving, especially in head and neck cancer. Our investigators are learning how to use cell-free DNA. It's not an accepted biomarker of response by the FDA by any means, but that's why we're trying to really figure this out and learn this. We are, you know, we don't have all the cell-free DNA back yet, the data, because it, you know, we do it in batches. We're very encouraged by it as a biomarker, as are all of our docs. We're gonna continue to follow that and use that as a potential. We are talking about with one of our investigators, in fact, about doing an adjuvant study, based on cell-free DNA responses in patients. I'll stop there and let Matteo talk about what we're doing with WT1. Thanks, Ken. I believe the questions have been well addressed at this point. I did wanna add one comment regarding the previous question on the WT1 assay. Although we do use a binary result for eligibility, I just would add that we're paying very close attention and tracking both the nuclear and cytoplasmic expression of the WT1 by grade so that we can correlate this data with potential patient outcomes. Sorry, just kind of sticking with this, you know, theme for a second. Are you seeing the converse occur in that, you know, once patients are, you know, kind of progressing or off the study, are you seeing HPV DNA, cell-free HPV DNA pick up in those patients as well, or do they consistently stay, you know, low all the way through? Good question. We don't have cell-free DNA on the patients after they come off study. We just are following them for survival and, you know, whatever therapies they've been on, et cetera. What we can see is in patients who do progress, their cell-free DNA actually will go up also. It roughly correlates with tumor burden. We, you know, it's dynamic, but that's why we're still learning about it as a biomarker. In people who are truly progressing, their cell-free DNA does go up into that. Yeah. I'd add as well, Ken, that, you know, this is an endpoint and a biomarker assessment that is gaining traction with FDA over the last 12-18 months, whereas it may be possible in the future to use it as a secondary endpoint and actually use it to inform decisions in adaptive trial design. It's really not there yet. That would be an opportunity in the future to introduce that biomarker to sort of accelerate or perhaps enhance decision-making in the next trial. Got it. Second question is, you know, when I look at the overall survival curves that you have, there are clearly, you know, those patients with durable SDs, some, you know, obviously with partial responses. There are those that clearly have progressed. I mean, they're surviving, right? I'm assuming that these that don't have a durable SD marker next to them, their tumors are growing. I guess the question I have is have you guys been able to investigate what sort of mechanisms of resistance might be occurring? As you think about that, what sorts of combination therapies are you thinking about that could maximize, you know, CUE-101's durability going forward? Well, the $1 billion question. It's a great question. We honestly don't know of the myriad of resistance mechanisms, which ones are at play. What I think has caught us certainly by surprise early on and caught all of our docs by surprise early on is these durable survivals in these patients that are even have come off therapy fairly soon. I think, you know, obviously, when we're increasing the number of cancer-specific T cells in the periphery and in the tumor itself, we're allowing for checkpoint therapies to work better. Certainly we've seen some, you know, early indications of potential antigen spread and which would suggest that combinations with, you know, further cytotoxic types of therapies that are going to increase neoantigen to be seen by T cells is certainly something that, you know, we'll consider in the future. As far as other mechanisms, you know, like HLA downregulation, et cetera, we just don't know yet. We don't have that data. Maybe Anish wants to comment on this, but you know, clearly we think there's gonna be synergies, the obvious ones with checkpoints as well as with chemo. Yeah. The only thing I'd add, it's a really important question, Ren. We have to look at these analysis. There has been, you know, all the way from operational resistance pathways because of the TME to cell types, to even the tumor intrinsically changing its immunogenicity profile, whether it is because of loss of HLA or loss of sort of components of antigen processing. We just need to sort of get a better grasp on this and that as a part of, you know, the ongoing analysis. Certainly, you know, in our sort of line of sight, we just need to gather the data. That will then dictate what possible other combinations can we bring in along with CUE-101 to further sort of extract even more benefit than with what we've already started to see. Got it. Just one final one for me. I probably missed this in the prepared remarks. I remember, you know, we were talking about a neoadjuvant study for quite some time, and primarily what had gotten me most excited about it was the ability to have, you know, biopsy samples kind of before and after and the like. Just wanted to get an update as to what was happening with that study. I'll make a few comments, and then I'll probably turn it over to Matteo to add on. That study is going quite well at Wash U, Ren. We've actually already recruited our first couple of patients. We've got the biopsies in place. We've got plans in place to get a composite batch analysis going, as soon as a few more patients are recruited. That's in locally advanced head and neck cancer. Matteo, please feel free to add more to it from your lens. Thanks, Anish. That's really quite accurate. We've treated a bit more than a few, and we look forward to sharing the data in the future when it becomes available. All right. Thanks, guys. Okay. Thank you. Thanks, Reni. As a reminder, if you would like to ask a question, please press star one on your telephone keypad. One moment while we pull for questions. Our next question comes from the line of Mark Breidenbach with Oppenheimer. You may proceed with your question. Hey, guys. Good afternoon, and thanks for taking questions. Just a couple from me. First, with respect to upcoming interactions with the FDA, is the plan right now to have the end of phase I meeting in conjunction with the availability of MOS data from your phase I trial? When can we kind of expect to hear their perspective on regulatory path forward? I guess I'm also just wondering why there looks to be kind of a gap between the availability of the MOS data and the potential start of a registrational study. That's one question for me. The other one is just with respect to the CUE-102 trial. Does this protocol include a paired biopsy collections? You know, I know that wasn't something that was included in the head and neck study. I'm just wondering if any changes have been introduced so we have more translational data from the CUE-102 patients. Okay. Matteo, do you wanna take that? Yeah, sure. I can start with the question regarding the interaction with the regulatory agency. As we just covered here, we anticipate having mature median overall survival data by the end of the year in the 20 patients dosed at the recommended phase II dose. We have designed a phase III trial that we plan to present to FDA in the context of a subsequent registrational trial. We're beginning to do preparations for such an at-risk trial and anticipate that we could begin to open that trial, which would be a global multi-regional trial, sometime later next year. Did you wanna comment? You do the biopsies as well in the WT1 trial? Yeah. Um- We have. You know, you're absolutely correct. We have made in the protocol paired biopsies optional. We've had a lot of productive conversations back and forth with investigators, and we recruited some that are keenly interested and capable of arranging those. We hope that in the tumor indications that we're enrolling in the 102 trial, we'll have the opportunity to get paired biopsies, perhaps, in anatomic locations in these indications that may be, if you will, more facile and amenable to biopsy. To your question, it is an optional procedure at this point. Whereas in the neoadjuvant trial, by design, we have an opportunity to examine pre- and post-dose biopsies as a component of the patient's interventional standard of care in the setting of locally advanced cancer that's undergoing a resection with curative intent. Okay. Just going back to the regulatory question, I just wanna be absolutely clear. We wouldn't hear until 2023 regulatory feedback with respect to what a registrational trial might look like in head and neck cancer. Is that correct? I think that's correct, and I would say early 2023. You know, of course, some of the interactions will really depend upon the timelines granted by FDA. But in this setting, we're confident that requesting a Type B meeting request, given where we are in the development, that FDA would agree and be collaborative, so as not to deny the potential of the development for this drug and this unmet medical need in third line patients and beyond with head and neck cancer. Okay. Thank you so much. Yeah, this is Ken. We certainly, I think, the end of 2023 is, you know, our conservative estimate. We know what that trial we want that trial to be. You know, as soon as we get the data, we'll be ready to go and hopefully be able to launch sooner at this point. Got it. Ladies and gentlemen, we have reached the end of today's question- and- answer session. I would like to turn this call back over to Mr. Daniel Passeri for closing remarks. Okay. Thank you very much. I wanna thank the research analysts for questions very helpful and instructive. I just wanna thank everyone for listening in and your ongoing interest and support of our activities in bringing these very promising therapies to patients. Thank you very much. Take care, and we look forward to providing updates throughout the year. Take care. This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation. Enjoy the rest of your day.