Greetings, welcome to the Cue Biopharma investor call. At this time, all participants are in a listen-only mode. A brief question and answer session will follow the formal 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. It is now my pleasure to introduce your host, Daniel Passeri, CEO. Thank you, Daniel. You may begin. All right, thank you. Good afternoon, everyone. As a reminder, this presentation and discussion is being recorded and will be available on our website for the following 30 days. Those listening may advance slides directly, and we'll notify you of which slide we're on and discussing. Joining me on today's call is Dr. Anish Suri, our President and Chief Scientific Officer, and Dr. Matteo Levisetti, our Chief Medical Officer. As shown here on slide two, this presentation and overview may contain some forward-looking statements. Any forward-looking statements made during the call represents the Company's views only as of today, June 14, 2023. After Matteo, I'll return for a brief summary prior to opening the call up to questions. First, let me provide some context pertaining to our accomplishments to date, our competitive market advantages and strategic corporate differentiation and positioning. As shown here in slide three, our focus and vision has been on translating what we refer to as nature's cues into protein therapeutics to realize the full potential of precision immunotherapy. Nature's cues is obviously where our company's name comes from. The data emerging from our CUE-101 trials is providing de-risking and clinical validation of our Immuno-STAT platform and protein engineering approach in general. The data continues to support our belief that we are well-positioned for clear competitive advantage and market differentiation. So when we refer to translating nature's cues into protein therapeutics, what we're referring to are the signals or molecular structures used in nature by our own immune systems to selectively regulate and modulate the immune system with specificity to maintain health. Anish will elaborate upon this central premise momentarily to provide context for the data you'll hear about from Matteo. We're pleased to be providing this update of what we consider to be clear in differentiating data, emphasizing our core competitive advantages. CUE-101's clinical data continues to support the clinical validation and the corresponding reduction of risk for the entire IL-2 based CUE-100 series, and importantly, appears to provide us with defined options for potential registrational trials and partnering opportunities. As Matteo will elaborate upon, CUE-101 appears to mechanistically complement and enhance the clinical activity of PD-1 blockade, that's through a checkpoint inhibitor, particularly in patients with low PD-L1 expression in the tumors, and that's evidenced by CPS scores less than 20. Historical data has demonstrated that anti-PD-1 therapy is less efficacious in those patients with CPS scores under 20. We believe that our platform has demonstrated the potential for significant market penetration by extending patient reach and enhancing clinical benefit, as demonstrated by expansion into patients with low CPS scores, expansion of progression-free survival duration, significant enhancement of overall response rates, and what appears to be a significant enhancement of median overall survival. You'll hear about these various metrics from Matteo momentarily. As such, we believe we're now well-positioned as a leading solution provider towards realizing the full potential of precision immune modulation. With that, I'm going to turn the call over to Anish, who will elaborate upon the underlying mechanistic principles that this entails. Thanks, Dan. I'll start with slide four, that highlights the unique opportunity that Immuno-STATs present to selectively activate tumor-specific T cells. It is important to remember that cancer-specific T cells are extremely rare, with a likely frequency of less than 0.01% of all T cells. To address the rarity of the cancer-relevant T cell repertoire, we engineered Immuno-STATs to selectively engage the T cell receptor, or TCR, expressed by cancer-relevant T cells. This property allows for an Immuno-STAT to selectively engage and activate tumor-specific T cells while sparing the greater than 99.9% of irrelevant T cells that are not specific for cancer antigens. The selective activation of the right T cell specificity is a seminal prerequisite for any subsequent or additional therapeutic interventions, including applications of checkpoint inhibitors. As shown on the next slide five, we developed the CUE-100 series Immuno-STATs to selectively target IL-2 to tumor-specific T cells. In principle, this approach applies to any given immune activation signal, including additional cytokines and/or cell surface receptors. The CUE-100 series has bivalent tumor peptide HLA molecules, along with four molecules of an attenuated IL-2 variant. The peptide HLA selectively binds to TCRs of tumor-specific T cells, which synergizes with the attenuated IL-2 molecules to induce anti-tumor T cell activation. The IL-2 on its own, in absence of TCR engagement, has been significantly attenuated to avoid the systemic activation of the much larger, irrelevant T cell compartment. The selective binding interaction with the right T cell results in the formation of a functional immune synapse and intracellular signaling, as shown on the right side of the slide. These are data sets generated as a part of a long-standing collaboration we've had with the laboratory of Dr. Michael Dustin, a pioneer and leader in understanding the molecular basis of T cell activation. Importantly, this unique property of the Immuno-STAT molecular framework enables us to generate a therapeutic index for IL-2. The selective targeting and precision activation of only cancer-specific T cells is accomplished through stratifying patients based on tumor antigen and HLA expression. Through this approach, we are able to enrich for patients that are most likely to derive clinical benefit and respond to our therapy. As shown on slide six, the modular nature of the Immuno-STAT platform supports efficient expansion of our pipeline. CUE-101 is our lead clinical candidate that targets HPV-specific T cells in patients expressing HLA-A02, which is the highest prevalent HLA allele, approximately 45%- 50% of the population in the U.S. and Western Europe. CUE-101 is designed to activate HPV-specific T cells to attack and eradicate HPV-driven cancers, such as head and neck cancer, among others. Matteo will momentarily cover the rich clinical efficacy data sets from our ongoing monotherapy and combination therapy trials in recurrent metastatic head and neck cancer patients. These data sets not only provide clinical validation and de-risking of our platform, but more importantly, support registrational paths forward for seeking approval of CUE-101 as a differentiated and superior therapeutic option for patients suffering from recurrent metastatic head and neck cancer. CUE-102 is our second clinical candidate, which targets an epitope from Wilms' Tumor 1 or WT1, a well-known oncofetal antigen expressed by numerous solid and hematological cancers. CUE-102 is currently in dose escalation as a monotherapy in patients suffering from ovarian, pancreatic, colorectal, and gastric cancers. Matteo will also describe the highly encouraging clinical signals being observed already in the early stages of this trial. Due to the shared molecular features of the platform, CUE-101 and CUE-102 are 99% sequence identical, with the primary difference being the 9-10 amino acid tumor epitope, which is the targeting moiety for engaging a specific TCR repertoire. We believe the clinical de-risking achieved with CUE-101 has broad implications for the entire platform and provides significant regulatory and clinical development efficiencies. In support of this perspective, the FDA allowed the CUE-102 IND to proceed with no additional IND-enabling toxicology studies and allowed us to initiate the dose escalation at 1 mg/ kg, which saved us about 12 months when compared to the CUE-101 dose escalation that was initiated at 0.06 mg / kg. In summary, our data from the ongoing CUE-101 and CUE-102 trials has clearly demonstrated the differentiation of our approach for precision immune modulation of targeted disease-relevant T cells. We believe this strategy has enabled us to crack the code for IL-2, a validated cytokine of high interest for cancer immunotherapy. With that, I will now turn the call over to Matteo to describe our most recent clinical data and updates. Matteo? Thanks, Anish. The clinical data from the ongoing CUE-101 trial continues to demonstrate highly encouraging and robust metrics of clinical benefit for heavily pretreated recurrent metastatic HPV-positive head and neck cancer patients treated with monotherapy, and for newly diagnosed patients with recurrent metastatic HPV-positive head and neck cancer treated in combination with pembrolizumab. As shown on slide seven, data from the ongoing clinical trials with CUE-101 as monotherapy and in combination with pembrolizumab have provided clinical proof of concept in de-risking of our Immuno-STAT platform. The latest data generated to date in 2023 continues to support prior observations and further enhances our confidence in CUE-101 as a potential therapeutic for patients battling HPV-positive head and neck cancer. 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 expansion of targeted tumor-specific T cells directly in the patient's body. Recurrent metastatic HPV-positive head and neck cancer is a tough, incurable disease. The data we have observed throughout the monotherapy trial bolsters our position and enhances our confidence that CUE-101 is in fact stimulating the targeted cancer-specific T cells within these patients, resulting in demonstrable antitumor effects. Furthermore, and importantly, we continue to observe an evolving pattern of enhanced survival in the monotherapy trial. We believe this enhanced survival is due to the persistent expansion of tumor-specific T cells, given CUE-101's mechanism of action, especially in the tumor microenvironment. As shown on slide eight, CUE-101 demonstrates well-behaved and consistent pharmacokinetics with low interpatient variability at the recommended phase II dose of 4 mg/kg. The exposure pattern is consistent throughout multiple cycles of treatment without any attenuation of PK parameters, supporting the premise that there is no evidence of clinically relevant immunogenicity. Regarding its pharmacodynamic or PD profile, CUE-101 treatment also results in a consistently observed sustained increase in natural killer cells, or NK cells, a positive attribute associated with an anti-tumor response, as NK cells are known to induce potent tumor killing. Importantly, we have also consistently observed only a slight and transient increase in regulatory T cells. Regarding the intended PD effect, i.e., activation of targeted tumor-specific T cells, we have observed, as shown on the middle panel, robust expansion of tumor-specific E7-reactive T cells in the peripheral blood of patients as early as one week after administration of CUE-101. Paired and post-treatment biopsies demonstrate an increase in tumor-infiltrating T cells and associated tumor necrosis. In addition to the favorable PK and PD just described in patients with advanced HPV-positive head and neck cancer, we are also observing a spectrum of patterns of clinical benefit. Three examples are shown on slide nine. Patient A experienced a durable partial response with an approximate 60% reduction in tumor burden evident at six weeks after the first two cycles of CUE-101, which lasted close to one year on therapy. Importantly, this patient also demonstrated a significant reduction in HPV cell-free DNA that coincided with the initiation of the PR. HPV cell-free DNA remains undetectable for the majority of time on treatment. Patient B, who remains on treatment at the present time for greater than 22 months, has had durable, stable disease, with tumor burden reduction of approximately 20% observed at week 48 and maintained to the present time. Notably, this patient has also had complete disappearance of HPV cell-free DNA in the blood since week six. The undetectable HPV cell-free DNA, which is an increasingly recognized biomarker of disease activity, is suggestive of a pathologic complete response, i.e., a potential cure in this patient, who we expect may have surgical resection of the lesion for histopathological analysis. Patient C has experienced tumor reduction after a prolonged period on drug, where no RECIST-based objective response was initially observed by imaging. In this patient, treated with CUE-101 at 2 mg/kg, we can observe that during the first several months on treatment, the tumor appears to demonstrate gradual tumor growth, even beyond the 20% threshold used by RECIST criteria to designate progressive disease. However, based upon physician discretion, taking into account the overall clinical status of the patient, the treatment was continued. After approximately six months on treatment, the tumor began to shrink, and the patient remained on therapy for greater than 18 months after starting treatment with CUE-101. This observation, consistent with observations made by others, demonstrates that kinetics of T-cell antitumor activity may manifest over a long period of time and may not adhere to the traditional RECIST-based criteria. The next slide 10, conveys our ongoing survival swimmer plot for the 20 monotherapy patients dosed at the RP2D of 4 mg/kg. This still-maturing swimmer plot for these 20 patients, dosed at 4 mg/kg, demonstrates increased survival, with a median overall survival currently approaching 14 months, compared to the historic reported survival of approximately eight months observed in patients treated in the second line in the KEYNOTE-040 trial of pembrolizumab. 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 demonstrates single-agent activity by durably expanding tumor-specific T cells with antitumor activity, resulting in what appears to be a meaningful increase in survival for patients with advanced recurrent metastatic HPV-positive head and neck cancer. The demonstration of monotherapy activity in these patients bolsters our belief that we should observe complementary mechanistic effects in combination with pembrolizumab. As a reminder, the data from patients treated in the CUE-101 monotherapy trial clearly supports that CUE-101 activates and expands the number of tumor-specific T cells. In the combination study with pembrolizumab, these activated T cells have greater capacity to kill cancer cells when coupled with inhibition of the PD-1 pathway, a major mechanism used by cancer cells to prevent immune-mediated killing. The following data is updated from our recent ASCO presentation, with additional data not available on the ASCO data cutoff date of May 15th of this year. As shown on slide 11, the current overall response rate is 44% in the 16 evaluable patients treated in combination therapy. As shown on the waterfall plot on this slide, one patient has experienced an unconfirmed complete response, which I will describe in detail momentarily. An additional six of the first 16 evaluable patients treated at the recommended phase II dose of CUE-101 and pembrolizumab have experienced partial responses, four confirmed and two pending follow-up scans. Partial response is defined as a reduction of tumor burden of -30% or greater. Additional patients, as you will note in the center of the plot, that have experienced greater than 20% reductions in the sum of target lesions remain on treatment. The overall response rate of 44% observed with CUE-101 in combination with pembrolizumab to date, compares favorably to the historical overall response rate of 19% observed with pembro monotherapy in the KEYNOTE-048 study. Notably, five out of eight, or 63% of the combination patients with low PD-L1 expression, i.e., a CPS score of 1-19, experienced objective responses, which is greater than the expected rate of approximately 14%. As showed on slide 12, pembrolizumab demonstrates lower efficacy in tumors with low CPS scores. Specifically, an overall response rate of approximately 14% was observed with CPS scores of 1-19, and an overall response rate of 23% was observed with CPS scores of greater than 20. In totality, our data suggests that not only does CUE-101, 101 enhance the response rate of anti-PD-1 inhibition significantly, it does so by substantially enhancing responses in patients that are traditionally less likely to respond. As shown on slide 13, the objective responses observed with CUE-101 and pembrolizumab are durable, as evidenced by a current median duration of response of greater than 35 weeks. Additional data on the patient with the unconfirmed complete response shown on slide 14, demonstrates the time course of response in both target and non-target lesions, evidencing continual clinical improvement. The patient had a target disease burden of 7.5 cm, comprising a lesion at the base of the tongue and 2 lymph nodes, and non-target disease in bone, liver, and additional lymph nodes. A partial response was observed in the first scan at six weeks, and a complete response was observed in the tonsil lesion at 18 weeks. At week 42, a complete response was observed in all target lesions, followed by a complete response in all radiologic evidence of disease at 48 weeks. Two of the target lesions were lymph nodes, and they have reduced in size to less than 10 mm, i.e., the size of a normal lymph node, which, in addition to the other findings, meets RECIST criteria for a complete response. Slide 15 shows that all 16 patients treated to date at the RP2D remain alive as of the last follow-up for each patient. The current estimate of the median progression-free survival is approaching six months, which is double the median PFS of approximately three months observed with pembrolizumab monotherapy in the KEYNOTE-048 trial. The follow-up data on these first 16 patients, as well as new emerging data on additional patients treated with combination therapy, continues to strengthen, and we look forward to providing an update on the cumulative data at an upcoming oncology meeting. Key observations in patients treated with CUE-101 monotherapy in the third line and beyond include, as detailed on slide 11, demonstration of single-agent antitumor activity, evidence efficacy, evidenced by RECIST-based partial response and durable stable disease in third line and beyond recurrent metastatic head and neck cancer patients. A median overall survival benefit from survival follow-up in the RP2D cohort. As previously announced, the robust data on CUE-101's activity in monotherapy and in combination with pembrolizumab enabled the granting of Fast Track designation for the treatment of patients in both the first and third-line setting. The cumulative data from these ongoing trials with CUE-101 have provided us with clear evidence of target expansion of HPV E7-specific T cells, with antitumor activity as a single agent and as a complementary mechanism with checkpoint inhibition for what we believe will broaden patient reach and enhance efficacy of checkpoint blockade therapy. As such, we believe CUE-101, our first biologic therapeutic from our CUE-100 series, represents a potential therapeutic breakthrough for patients. Furthermore, we believe the data from CUE-101 has provided a de-risking and mechanistic validation for additional biologics from the IL-2 based CUE-100 series, beginning with CUE-102. As shown on slide 17, 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're not required by the FDA to repeat IND-enabling toxicology studies for 102. We're also able to initiate the phase I dose escalation study at 1 mg/k g, a dose at which we observe clear signs of biologic activity with CUE-101. As slide 18 shows, we are conducting the CUE-102 dose escalation study in colon, gastric, pancreatic, and ovarian cancers. This design offers us the ability to perform monotherapy expansion studies in any or all of the indications being evaluated in the dose escalation phase of the trial. Findings observed to date are summarized on slide 19. The study is actively enrolling patients in all four indications. The patient screening and enrollment rate continue to go exceedingly well, underscoring investigator enthusiasm and the need for effective therapies in WT1-expressing cancers. We have recently completed enrollment at 4 mg/kg. CUE-102 has been well tolerated to date, with no DLTs observed. Evidence of antitumor activity has already been observed in heavily pretreated patients, including reductions in target lesions, stable disease, and reductions in tumor markers in several patients. For example, a patient with gastric cancer that progressed on three prior lines of therapy, including a checkpoint inhibitor, has experienced a decrease in the sum of three target lesions of -25% as at week six and 12, and the patient continues on treatment. These early signs of clinical activity are particularly encouraging as they were observed at the doses of 1 mg/kg and 2 mg/kg dose levels, the scans on the 4 mg/kg dose cohort are upcoming in the next several weeks. We're encouraged by these early observations of monotherapy antitumor activity in these indications, where checkpoint inhibitors have been largely ineffective. We look forward to presenting additional data as they become available. I will now turn the call over to Dan. Thanks, Matteo, and appreciate the overview. As seen in the next slide 20, we believe our corporate positioning and competitive advantage are firmly established on solid foundational data, as exemplified by CUE-101, which, you know, represents the CUE-100 series and represents the far-reaching potential as a therapeutic breakthrough for our approach. To date, CUE-101 has demonstrated monotherapy single-agent activity in late-stage refractory and metastatic cancer patients. Again, with single-agent activity, and evidence of extending median overall survival in third line and beyond, refractory metastatic patients. To date, we're observing significant increase that is approximately a doubling in combination with checkpoint inhibitors, compared with historic checkpoint inhibitor monotherapy, even in low CPS scores, as Matteo laid out, evidencing our drugs' activation and expansion of cancer-relevant T cells. We've demonstrated favorable tolerability. We've treated greater than 70 patients to date with no vascular leak syndrome and notice no cytokine release syndrome, et cetera. Importantly, the manufacturing of the drug, it's based on an antibody-based design, so we have favorable cost of goods, highly manufacturable, and the drug is extremely stable. We've been really impressed by what we've observed to date. It has stability of greater than 36 months. As was just articulated, we've demonstrated, because of the modularity, significant regulatory advantages. We have Fast Track designation in both mono as well as in combination. The FDA authorized, because of this modular feature, they authorized the IND for CUE-102 to be principally based on the safety data from CUE-101, with no requirement for IND-enabling toxicology. We were approved to start the trial at a higher dose of 1 mg/kg, as stated, that's observed biologically active dose, saving significant time and cost. We're highly encouraged by both the enrollment rate of CUE-102 presently and the early signs of monotherapy clinical activity in multiple tumor types where checkpoint inhibitors have shown minimal effect to date. These indications represent greenfield opportunities and continued signs of clinical efficacy. Remember, this is just in the dose escalation portion. We've completed dosing at 4 mg/kg, but haven't had any scan data come in yet, so this data is highly encouraging. Continued clinical efficacy in these indications would represent a major market opportunity for CUE-102 to establish, in essence, a new therapeutic standard for WT1 overexpressing indications. We view the cumulative data as supportive of our central premise, namely, that the Immuno-STAT platform, and more specifically, the IL-2-based CUE-100 series, represents a therapeutic breakthrough by harnessing nature's specificity through targeting the T cell receptor, the TCR, enabling targeted delivery of cytokines such as IL-2 to disease-relevant T cells. In short, we believe we've demonstrated the ability to engineer biologics for precision immune modulation, addressing the pressing needs for more effective cancer therapies. We're pleased to provide you with this post ASCO update and believe we're now very well positioned to demonstrate the breakthrough potential of our platform for precision immune modulation in both oncology as well as autoimmune disease, which we didn't touch upon today, including CUE-401, which is currently partnered with Ono Pharmaceutical. I want to thank everyone for listening in, particularly our shareholders, for their support, and appreciate the ongoing interest in our important progress for developing these promising therapeutics for patients in need. I also want to thank our dedicated employees for their commitment and consummate professionalism. With that, I'm gonna turn the call over to the operator, open up for questions. Operator? Thank you. We will now 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 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 key. One moment please, while we poll for questions. Thank you. Our first question comes from Reni Benjamin with JMP Securities. Please proceed with your question. Good afternoon, guys. Thanks for taking the questions, and congratulations on this very nice update. Maybe just to start off, can you talk a little bit about what the average time to response is for these patients, both in the monotherapy as well as in the, in the combo? You know, we've got several unconfirmed sort of responses right now. Can you talk about when we might get the kind of the final read or the next scan, if you will, to confirm these responses? I have a follow-up. Okay. Yep. Thanks, Reni. Matteo, you want to take that? You're on mute. Matteo, you may be on mute. I'm sorry. Thanks for the question, Reni. The time to response for the patients treated in combination is sort of explicitly shown on slide 13 on the spider plot. Here, you know, we had two patients that have responses as early as six weeks, which is the first scan. The other responses occur really between 12, really around 12 to 18 weeks. Really sort of two sort of time frames of response. On that note, the transition to a complete response in this patient, you know, treated for close to a year now, is really a remarkable observation. That really speaks to, really an ongoing, durable, antitumor, immune response, in that patient. Regarding, the time frame, when we will have the follow-up scans on the two unconfirmed partial responses, the answer is really, four to six weeks. Those patients should get their subsequent follow-up scans. Just to follow up on that, Matteo, is there anything in particular, any learnings that you've identified regarding this patient that went from a PR to a CR? You know, would you predict, you know, that maybe some other PRs that you see might ultimately go to a, to a CR? I certainly think that's possible. You know, what's really remarkable about this patient's, you know, experience is the large burden of disease that they went into. Not only, you know, they joined went on trial with a large mass, you know, tonsillar mass and lymphatic and lymph node disease in the neck, but really distant metastatic disease, including bone and liver. Really a large burden of target and non-target disease. The individual spider plot sort of shows how the target disease completely responded first, and then ultimately, at 48 weeks, the non-target disease, again in bone and liver, are responding. Really a remarkable, you know, remarkable findings for this patient and, you know, kinetics, I think, again, that speak to the, you know, durable nature of the therapeutic effect. With regards to the other patients that are continuing treatment that have partial responses, I certainly wish them the best and would welcome complete responses in these patients. Got it. You know, just in regards to maybe the competitive landscape and the impact that it may be having on enrollment across both the 101 and 102 studies, can you provide just any sort of, you know, color regarding enrollment in the two studies? I think, Matteo, in your prepared remarks, you mentioned enrollment goes exceedingly well. You know, any sort of additional color would be great. Let me start perhaps with the CUE-101 trial. There's been a bit of a headwind enrolling patients in the first-line setting at many of our research centers that tend to be sort of tertiary referral cancer centers. What we hear from the investigators is that, you know, given the first-line and availability and approval of pembrolizumab, that they're seeing many less of these patients. They tend to be treated in the community with pembrolizumab and then are referred, you know, when they progress. Unfortunately, at that point, they've already been treated with a checkpoint inhibitor, and they're not eligible to enroll on the trial. There's other enrolling trials in the first-line setting that also serve as competition. It's a combination of, I think, those two or three factors. We, you know, our investigators continue to look for patients, and we currently have four patients in screening as of today. The CUE-102 trial has really been, you know, quite a different experience and one of the sort of fastest enrolling studies that I've been responsible for in a dose escalation setting. I think the factors here are multiple. We really have now investigators that are highly enthusiastic, and that's been driven by the observations we've had to date in the first two, three, first six patients treated. Where, for example, you know, a patient with advanced cancer disease has a durable reduction of 25%. We have another two patients with durable, stable disease at 12 weeks, and then another two patients with reductions in tumor markers. This, in addition to the many patients, you know, in these indications that these lines of therapy that are looking for options and treatments, we've actually evolved and have a wait list currently for slots that may open up. We're completing the DLT observation period for the 4 mg/kg, three patients in the next few days. We've started to backfill or expand the cohort at 2 mg/kg, where we've seen clear benefit, so that we could meet some of this patient, you know, demand to get on the trial. Perfect. Thanks for that. Congratulations. I'll jump back in the queue back some follow-up. Thank you. Our next question comes from Mark Breidenbach with Oppenheimer. Please proceed with your question. Hey, good afternoon, and thanks for this update. Really nice to see some of the responses deepening over time. So, a few questions from me. First, maybe it would be helpful if Matteo or Anish just provide some comment on the rarity of complete responses in head and neck cancer, sort of, what you would expect in terms of a complete response rate with single-agent pembro. Maybe a related question is, are you at all surprised that you're not seeing a better response rate in CPS-high tumors? It seems like we're maybe not seeing as much activity than we would expect with single-agent pembro in the CPS-high patients. Is that just a small numbers game or, you know, I'd appreciate your thoughts on that. I have one question on CUE-102 after you take these. Matteo, why don't you start and then if Anish needs to elaborate on any various aspects of it. Very good. The response to the complete response rate, I'll just be transparent here, is so low that I don't recall. I have to follow up on that. It's certainly less than 3% or so in the larger studies. I think you're right. So very, very low. What? Anish, just say you're right. I think you're right. It's about 3%-4%, low single digits, complete response rate with pembro alone. I think you're right. Yeah. Thanks, Anish. The question then, I believe, regarding CPS scores. To sort of summarize here, it's been recognized, okay, so in head and neck cancer, you know, both in KEYNOTE-040 and KEYNOTE-048, that there's been a trend for a better overall survival that's associated with higher PD-L1 expression, so CPS score is greater than 20, and that patients with lower CPS scores don't do as well. This observation has been done, has been seen in multiple different tumor types, including, you know, lung cancer. What's notable in our small number of patients is that we're seeing an overall response rate, okay, that's much higher than one would predict if one looked at the patients with CPS scores of 1- 19. We're seeing responses in, you know, 63%, so five out of the eight patients with low CPS scores. If you look, for example, in the data from KEYNOTE-048, for patients with CPS scores that are less than 20, the overall response rate was just 14%. This is really showing that the combination, that CUE-101 in its therapeutic effect, basically overcomes whatever it is that results in low CPS score having a lower probability of response or doing well. There was, I think, a question, I'm sorry, about high CPS. CPS high, and why we're not seeing maybe a better response rate in CPS over 20 patients. Yeah, Mark, I think. Yeah. Go ahead, Matteo. No, no, Anish, go. Yeah. Mark, our thinking here, if you think about the mechanism of action, the drug is intended to induce an expanded repertoire, likely inducing local information. We've actually published on this in clinical models. I think as the CPS high situation goes, one could imagine that there are existing T cells already primed and ready to go, so that dependency may favor more in tilt in favor of sort of an existing reaction. In the CPS low, CUE-101 is clearly inducing a repertoire and local inflammation and sort of expanding that reach. Albeit, even if you look at the CPS high, right now, we're about two out of eight there, Mark, so that's about 25%. You know, there is an opportunity as the data continues to mature, that that signal comes through as well. That is at the ORR level. Ultimately, as you think about survival, as you think about the long-term, sort of patient benefit, that may still very much manifest. Okay, great. Then just quickly on CUE-102. I guess I'm left wondering if you're seeing any evidence of WT1 specific T-cell expansion in patients, especially the gastric patient you mentioned that had a 25% reduction from baseline on lesion sizes, and maybe the patients who achieved stabilization of disease. You know, any translational data to support or early observations from the scans? What specifically are the plans for additional data presentation from the CUE-102 trial? We haven't yet done the NEPD analysis. That we intend to do a batch analysis as we sort of get through the dose escalation. We certainly hope to be able to talk and present about that data. I will remind you from the CUE-102 preclinical presentations, that when we've looked at this both in human samples and A02 mice, that one or two induced a really robust expansion and burst of a high-frequency polyclonal repertoire of WT one reactive T cells. We confirmed that those were polyfunctional by interferon gamma, TNF alpha, and the granzyme B marker CD-107. We certainly are very excited to do this in a human patient samples. We just haven't gotten there yet. Okay. next data presentation from this trial? We'll be submitting an abstract for presentation at an oncology meeting later in the year. Okay, got it. We can hopefully see an update this year. Yes. Correct. Thank you. Yes. Thank you. Our next question comes from Stephen Willey with Stifel. Please proceed with your question. Yeah, good afternoon. Thanks for taking the question. Thanks, Steve. I guess, can you give us any, kind of updated thoughts around the potential regulatory strategy here for CUE-101? I know you've been kind of contemplating single agent, more later line salvage, and I think now you have this kind of growing body of combo data in the frontline setting in combination with pembro. I guess, when should we expect to kind of hear about go-forward decision, in what line of therapy? Do you think that 20 patients of frontline data, is gonna be sufficient to make that decision? Good, good question and important question. Steve, one of the reasons we haven't clarified earlier is what you just stated. We had the maturing monotherapy, which was more and more encouraging as the median overall survival continued. Clear evidence of single agent activity. We needed to see more data from the, you know, the 20 patient expansion to be able to assess what our options were. It's quite clear that we have the prospects of a registrational path for both third line and beyond, as well as now frontline with this data that's emerging. And again, 20. An evaluation of 20 patients, I would say what we're seeing right now, we're absolutely confident there's a registrational path there. What Anish just stated, for instance, about the high CPS scores, you can't really ascertain. We're expecting those numbers to actually, you know, kind of mirror what we're seeing in the low as we go forward, just 'cause the numbers are small. We're clearly, with the number of low CPS patients we're seeing, there's clearly a signal there that we're confident is real, just a matter of building that out. The direct answer to your question is, this is ultimately a board decision of strategic options. In lieu of the fact that with CUE-102, we're seeing single agent activity, I think the take-home message is this is a high-quality problem to have. We have a couple of registrational path alternatives, and we have the next asset, early stage, showing what looks like clinical activity, that if it continues to hold and manifest this type of data going forward, that represents a tremendous opportunity for us. I think what we would do is strategize an approach with the FDA, have that meeting, and decide, do we want to use that as a partnering package? You know, we have obviously a partnership with Merck presently. We haven't had discussions with the data yet. When we finish the 20 patients, we'll engage in that discussion. We have obviously, registrational paths that we could pursue ourselves or through a partnership, and then in lieu of 102. We have to assess, cost-benefit to our shareholders based on the market conditions, the quality of this data, the options that we have, and, we have some flexibility in what option we pursue. That's a high-quality problem. Okay. Then could you just remind us if Merck has any kind of right of first refusal on the, on the phase I data, or is this just a straight-up clinical supply collaboration? Yeah, it's a supply collaboration. They do not have a right of first refusal. They have a, you know, first look right. When we complete this study, we're gonna be going through that data, you know, in-depth with Merck prior to, you know, releasing that out publicly. Okay. Maybe just one quick question on CUE-102. I know that you're, I guess, on slide 18, you're suggesting that 4 mg/kg, which was the go-forward dose for CUE-101, and there's obviously a lot of sequence homology between the two. You're flagging that as a likely dose for monotherapy expansion. I'm just kind of wondering if you think that there's a rationale for maybe trying to push to eight again with this asset. Thanks. Yeah, that's an important question. We've actually had some debate internally. I don't mean to speak for Matteo and the clinical team, but, you know, the general consensus is, you know, based on what we've seen to date, and the number of patients that we've had in screening, we're looking at the prospects of continuing up. We might as well survey eight, but also concurrently expand at, you know, two and four, because those patients are available. That's the current thinking right now, Stephen, is just continue expanding out this survey to define the therapeutic window and the optimal dose. All right. Thanks for taking the questions. Yeah. Congrats on the update. Thank you. Appreciate it. Thank you. Our next question comes from Ted Tenthoff with Piper Sandler. Please proceed with your question. Great. Thank you very much, and congrats on the encouraging update. A lot of questions answered here. I wanted to get a sense when it comes to CUE-102, you know, what are the potential cancers here where you could be applying that target without Wilms' tumor antigen? Does this data now, in terms of multiple positive, you know, readouts with varied targets, does it give you confidence to move forward with other constructs such as I know we've talked about KRAS in the past, things like that. Is there a reason to sort of accelerate on the pipeline, or should we be thinking about this more focusing on the assets that you currently have? Thanks a ton. Thanks, Ted. Important question and no easy answer. It's really resource availability and prioritization. Again, the good news, Ted, is we have multiple options that are presenting with our first drug, now our second drug, and obviously by extrapolation, you know, KRAS, you know, MAGE, all of these have potential to be really important asset classes. We simply don't have presently the resources to build this pipeline out to the degree we would desire to. Partnering our strategic alternatives is gonna be part of our overall thought process. The registrational strategy for 101 is clearly going to play a role in what we can do with the remainder of the platform. We're eager to define the next clinical candidate, but we also have to be, you know, prudent of maintaining control of cash burn until we have some additional capital coming in through, you know, a support from a partnership. That's the overview. Makes a lot of sense, Dan. Thanks, and congrats. Yeah, really appreciate it. Thank you. Thank you. Our next question comes from Reni Benjamin with JMP Securities. Please proceed with your question. Hey, guys. Thanks for taking the follow-up. I guess just building upon a couple of the other questions that were asked earlier. In terms of business development, Dan, you know, what do you need to see to maybe start having talks with other PD-1 or even PD-L1 players? You know, ideally, at least based on your low CPS data that you're starting to generate, you know, there could be kind of multiple plays being made here, especially going after cold tumors. As I think about that, what kind of, I look at CUE-102, I know we're focused on monotherapy dose escalation, but if I take CUE-101 as kind of the poster child, likely CUE-102 is gonna be used in combination. How are you thinking about potential different combination partners with CUE-102 and expanding a BD repertoire, if you will? Yeah, great question. You know, obviously, I think if you look at the landscape, what we've learned from this, first of all, it's a very confused sector just because of all the companies that were pursuing various aspects of this, just, you know, IL-2, for instance. We held off on a concerted BD initiative until we felt we had convincing data sets that clearly differentiated, and we feel we're presently there. The matter of CUE-102, other checkpoint inhibitors, et cetera, I think the attractive feature is these indications, presently do not have, you know, approved checkpoint inhibitors covering these sort of broad indications, which gives us what I refer to as a sort of greenfield opportunity. I think looking at various checkpoint players that have approvals in other indications that may look at this as a key strategic move for market expansion makes a lot of sense. I think what we want to do is define that landscape, look at strategic capabilities, what would be the most attractive partners in different indications, and pursue it accordingly. We've been very thoughtful about this, and it's a really important question that you asked, and, you know, we've been looking at it strategically. I think the good news is, in these indications, if we're now, you know, generating data that supports the premise that we're turning cold into hot tumors, where checkpoints will now work, in a, you know, more effective manner, that opens up a lot of opportunity for us. Important issue for us to really think through deeply. Thanks for taking the questions. All right. Thank you. There are no further questions at this time. I would like to turn the floor back over to management for closing comments. Sure. Thank you. Again, I want to thank everyone for listening in. We appreciated the opportunity to provide this update. We continue to make good progress. Most importantly, we're thrilled to see the additional benefits that the patients are deriving from these studies. I want to thank everyone for your time, and we look forward to providing updates on an ongoing basis. Thank you. This concludes today's teleconference. You may disconnect your lines at this time. Thank you for your participation.