Greetings, welcome to the Cue Biopharma Investor 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 the conference over to Dan Passeri, Cue Biopharma's Chief Executive Officer. Thank you. You may begin. All right. Thank you very much, and good afternoon, everyone. As a reminder, this presentation and discussion is being recorded and will be available on our website for the next 30 days. Also, please be aware that the slides accompanying today's update may be advanced directly by those listening in on the call, and we'll be notifying you, as we proceed through the presentation. Joining me on today's call is Dr. Anish Suri, our President and Chief Scientific Officer, Dr. Matteo Levisetti, our Chief Medical Officer, and Kerri-Ann, Kerri-Ann Millar, our Financial-- Chief Financial Officer. As shown on slide number two, this presentation and overview may contain some forward-looking statements, and any forward-looking statement made during this call represents the company's views only as of today, August 9, 2023. On the next slide, which is slide number 3, it just outlines the agenda for today's call. I'll begin with a brief summary, followed by Anish. Anish will provide you with some background context pertaining to our approach and resulting developments regarding the Immuno-STAT platform, with a brief synopsis of associated competitive advantages pertaining to the observations from our ongoing clinical trials. Following the background provided by Anish, Matteo will then provide an update on observations from our ongoing clinical development regarding mechanistic insights, having corporate development implications for our ongoing corporate strategic positioning. Both Anish and Matteo, during the presentation, will be providing updates with some of the data and slides having been previously presented and discussed on prior calls. The repeat of that data is meant to provide context and continuity in our foundational premise, but also serves to reinforce the consistent and steady progress forward, demonstrating the realization of our foundational vision to enable precision immunotherapy, helping to transform the treatment of cancer. Following, Matteo, Anish will return with a brief overview of our preclinical pipeline developments, and then, that'll be followed by Kerri, who will provide an overview of our financials for Q2 and going forward, going forward guidance. I'll then return for concluding remarks, and we'll open the call up for questions. I'm now gonna turn the call over to Anish. Anish? Thanks, Dan. As noted in slide 4, the foundational premise and vision for our therapeutic platform has centered on harnessing the natural signals or nature's cues that the immune system utilizes to guide its effective functions, including recognition and destruction of malignant tumor cells. We believe this approach provides us with a significant advantage by exploiting what evolution has already refined, which is the Herculean task of creating molecules and signaling pathways that lead to balanced immune responses. Most importantly, these signals or nature's cues have been fine-tuned and optimized to provide protective immunity while preserving the safety of the host. Using these underlying principles of selectivity, we have engineered and now clinically validated a new class of bispecific T-cell engagers, termed Immuno-STATs, for the selective modulation of disease-relevant T cells while sparing the broad, non-specific immune activation or carpet bombing of the entire immune system. For oncology applications, we've been able to deliver natural immune activation signals, such as the cytokine IL-2, selectively to the tumor-specific T-cells. This property enables us to create a meaningful therapeutic index to exploit the promise and potential of targeted immune activation in the patient. The same principle can be applied to any other cytokine or immune modulation signals. To the last point, we have published several key papers in top-tier journals demonstrating the modularity and breadth of our platform. As Matteo will discuss in detail shortly, we now have exciting insights from recent clinical data that we believe provide very strong support and validation for our biologics platform. Further, we believe that these data position us to exploit the breadth of our platform modularity to address patient needs in many cancers, and I will comment more on this as we discuss our pipeline and potential for expansion into indications with significant market potential. Okay, the next slide, slide 5, provides a conceptual framework for maximizing the success of cancer immunotherapies. By deploying Immuno-STATs, we have the potential to solve a significant and fundamental challenge, which is the selective activation of the rare population of T cells that express T-cell receptors, or TCRs, specific for tumor antigens. In contrast, many of the current standard of care therapies utilize a blunt sledgehammer approach to activating the immune system with little to no consideration pertaining to the specificity of the T cells being activated. These approaches, as now evidenced by extensive clinical data from modalities such as bispecifics, checkpoint inhibitors, or untargeted cytokines, result in suboptimal efficacy along with toxicities. We believe our approach not only demonstrates greater efficacy over standard of care, more importantly, appears to achieve these outcomes without compromising patient safety. Slide six provides additional details into the design and functional attributes of our lead clinical candidates that are derived from the IL-2 based CUE-100 series. As noted here, Immuno-STATs are selective engagers of TCRs, of tumor-specific T cells, and deliver functional IL-2 signals to those very T cells. The CUE-100 series architecture is composed of two natural signals. One is the stabilized peptide HLA complex, or pHLA, that selectively binds to only the tumor-specific T cells. Note that the specificity is driven by the T cell epitope, shown in yellow, that is a tumor-specific peptide sequence. The other natural signal is an affinity-tuned IL-2 molecule that cooperates with TCR signals to fully activate T cells into potent killers of tumors. This functional cooperation of concurrent TCR signals and IL-2 signals is bespoke to nature's selective design and hence results in exquisite specificity. The generation of a therapeutic index for the right tumor-specific T cell over all other irrelevant T cells is further supported mechanistically by the elegant live cell microscopy experiments conducted by Dr. Michael Dustin's lab at University of Oxford. Dr. Dustin is a member of the National Academy of Sciences and is a pioneer in describing the molecular details of T cell activation. As shown here, the engagement of the Immuno-STAT with the antigen-specific T cells, that is, the T cell bearing the right T-cell receptor, results in formation of an immune synapse and TCR clustering and activation, as shown in green. When the same Immuno-STAT engages an irrelevant T cell, no such effect is noted. Before I pass the call to Matteo, I'll summarize our key highlights and accomplishments, as shown in slide 7. To note, we have developed a novel first-in-class biologics platform and have treated over 80 patients thus far, with evidence of anti-tumor efficacy and tolerability. Importantly, we've had patients in our trials that have continued to receive drug for up to two years, underscoring the durability of the clinical activity and the tolerability profile. We have demonstrated monotherapy activity in late-stage head and neck cancer patients that have failed several lines of prior standard of care therapies, including checkpoint inhibitors. Matteo will elaborate on the significant survival signal we are observing in our monotherapy patients. In the front-line setting, where anti-PD-1 therapy is approved, we have combined our Immuno-STATs to demonstrate a greater than doubling of the overall response rate. The overall survival data for these patients is continuing to mature. Importantly, in patients with low CPS scores, which reflects the level of PD-ligand expression in the tumor, we have seen an even greater increase in response rate over anti-PD-1 therapy alone. It is well recognized that patients with low CPS scores constitute a significant population and are notably less responsive to checkpoint inhibitor therapy. One possible explanation for the significant increase in responses in CPS low patients may pertain to the observation that Immuno-STATs increase the targeted T cell population and also engage T cells in the tumor tissue, which may alter the tumor microenvironment to be more permissive to immune attack against the cancer. Looking forward, CUE-101's maturing clinical profile in both the monotherapy and combination trials provides us with a range of potential long-term development and strategic, strategic opportunities. We also believe that the clinical data with CUE-101 have validated and de-risked our broader platform. To that end, the FDA acknowledged that the clinical and safety data from CUE-101 provided sufficient confidence to allow the acceptance of our second IND with CUE-102 without the need for additional IND-enabling toxicology studies, and allowed us to start the CUE-102 monotherapy dose escalation at the clinically active dose of 1 mg/kg. The latter point shortened our dose escalation in patients significantly and saved us approximately a year in clinical development timelines. We believe these unique regulatory advantages are a significant accomplishment and differentiating feature for our biologics platform. From a platform modularity perspective, the core IL-2 framework remains conserved between different CUE-100 series Immuno-STATs. The primary difference is at the level of the tumor antigen specificity or the pHLA part. For example, CUE-101 and CUE-102 are 99% sequence identical, except for the tumor antigen T-cell epitope, hence providing a very modular framework for development of distinct therapeutic molecules against a wide range of cancers. Lastly, from a manufacturability and cost of goods perspective, Immuno-STATs are manufactured using established and conventional CMC protocols for monoclonal antibodies and Fc fusion proteins. Our yields are similar to monoclonal antibodies in grams per liter, and GMP stability has been impressive. For example, CUE-101 has a shelf life that goes north of three years, which is comparable to or better than most monoclonal antibodies. With that synopsis, I will now pass the call to Matteo to provide the most recent clinical update for CUE-101 and CUE-102. 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 8, 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 and curable 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 effect. Furthermore, and importantly, we continue to observe an evolving pattern of disease control and 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 previous webcasts, I'd like to review the data on slide 9, as it is very important to understand the mechanistic differentiating features of CUE-101, including its effects on NK cells and tumor-specific T cells in the blood and the tumor microenvironment. In clinical trials to date, CUE-101 demonstrates well-behaved and consistent pharmacokinetics with low interpatient variability at the RP2D 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-102 treatment also results in a consistently observed, sustained increase in natural killer cells or NK cells, a positive attribute associated with an antitumor 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., the activation of targeted tumor-specific T cells, we have observed, as shown in the middle panel, robust expansion of tumor-specific E7-reacted 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. We believe this invasion of T cells into the tumor transforms the tumor microenvironment and plays a key role in the clinical activity observed with CUE-101 monotherapy, as well as that observed when combined with a checkpoint inhibitor. In addition to the favorable PK and PD just described in patients with advanced HPV positive head and neck cancer, we're also observing a spectrum of patterns of clinical benefit in patients that have failed prior checkpoint inhibitor treatment. As we have shown before, and now on slide 10, various patterns of clinical efficacy are observed with CUE-101 monotherapy. As shown on the left, 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 Q 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 partial response, and HPV cell-free DNA remained undetectable for the majority of time on treatment. Patient B, who just completed 24 months of treatment, 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 6. 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 at some point have a 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. 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. As shown on slide 11, the current median overall survival observed in the 20 patients treated at the recommended phase II dose of 4 mg per kg is approximately 14 months. The observed median overall survival of 14 months in patients treated in the third line and beyond is notable when compared to the historical median overall survival of approximately eight months observed in patients treated in the second line trials, in the second line, CheckMate 141 and KEYNOTE-040 trials of nivolumab and pembrolizumab, respectively. As any experienced oncologist understands, the survival with third-line treatment is expected to be less as the disease has further developed and becomes 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. Based upon the strength of this data, we plan to meet with FDA to define a registration path for CUE-101. As indicated on slide 12, I will now provide an update on the ongoing trial of CUE-101 in combination with pembrolizumab in first-line patients with recurrent metastatic head and neck cancer. Pembrolizumab is approved for the treatment of first-line patients with recurrent metastatic head and neck cancer that have tumors with CPS scores greater than or equal to 1%. CPS is a measure of PD-L1 expression in the tumor. As shown on slide 13, the distribution of PD-L1 expression observed in the KEYNOTE-048 study population shows that approximately 50% of CPS-positive patients have CPS values of one to nine, and the other 50% have CPS values greater than 20. Subgroup analysis of the KEYNOTE-048 study has shown that patients with CPS of 1 to 19 have lower overall response rates, lower median progression-free survival, and lower overall survival compared to the patients with CPS of greater than 20 when treated with pembrolizumab alone. As such, there is a clear need to expand the therapeutic reach for low CPS patients and to improve outcomes for all patients treated with checkpoint inhibitors. The next slide, slide 14, shows the current overall response rate of 44% observed in first-line patients treated with the CUE-101 and pembrolizumab, as discussed on the June 14th earnings call. Since that call, we have observed two additional patients with confirmed responses. As shown on the waterfall plot on this slide, the patient with the prior unconfirmed complete response has had a subsequent scan confirming the complete response, which I will describe in detail momentarily. In addition to the confirmed complete response, six of the first 16 evaluable patients treated at the RP2D of CUE-101 and pembrolizumab have experienced partial responses, now with all six confirmed. Partial response is defined as a reduction of tumor burden of greater than 30% of 30% or greater. An additional two patients that have experienced greater than 20% reductions in the sum of target lesions remain on treatment. The confirmed overall response rate of 44% observed in patients with CPS greater than or equal to one, treated with CUE-101 in combination with pembrolizumab to date, compares favorably to the historical response rate of 19% observed with pembrolizumab monotherapy in the KEYNOTE-048 study. Notably, four out of eight, or 50% of the combination patients with low PD-L1 expression, i.e., CPS scores of 1 to 19, experienced objective responses, which is greater than the expected rate of approximately 14% with pembrolizumab alone. As such, CUE-101 appears to significantly enhance the response rate of anti-PD, of PD-1 inhibition, particularly in patients that have low PD-L1 expression, which represents approximately half of the patients eligible for treatment with a checkpoint inhibitor in the front-line setting. The next slide, slide 15, shows the overall response rates observed in subgroups of patients treated with pembrolizumab alone, according to CPS values in the KEYNOTE-048 trial, compared to the overall response rates observed with CUE-101 and pembrolizumab combination therapy. As shown, 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 to 19, compared to an overall response rate of 23% that was observed with CPS scores of greater than 20 in the KEYNOTE-048 study. For all patients with CPS scores greater than or equal to 1, an overall response rate of 44% was observed with CUE-101 and pembrolizumab, which represents a greater than doubling of the historical response rate of 19% observed with pembro alone. Notably, for patients with CPS scores of 1-19, an overall response rate of 50% was observed with CUE-101 and pembrolizumab, which represents a greater than tripling of the historical response rate of 14% observed with pembro alone. Furthermore, CUE-101 also appears to increase the response rate in patients with CPS scores greater than 20, with an overall response rate of 38% for CUE-101 and pembrolizumab, and a response rate of 23% for pembro alone. In totality, our data suggests that not only does CUE-101 appear to demonstrably enhance the response rate of PD-1 inhibition, but also that it does so by substantially enhancing responses in patients that are traditionally less likely to respond. This is particularly important since patients with low CPS scores, i.e., 1-19, represent approximately 50% of all patients that are eligible to receive pembrolizumab. Additional data on the patient with the now confirmed CR, shown on slide 16, 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 approximately eight centimeters, comprising a lesion at the base of the tongue and two lymph nodes, and non-target disease in the bone, liver, and lymph nodes. Partial response was observed at 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, in all radiologic evidence of disease at 48 weeks. The complete response was confirmed on scans performed at week 54. Two of the target lesions were lymph nodes, they have reduced in size to less than 10 millimeters, i.e., the size of a normal lymph node, which, in addition to the other findings, meets RECIST criteria for a complete response. The swimmer plot, shown on slide 17, shows that 16 of the 17 patients treated to date at the recommended phase II dose in the ongoing combination trial of CUE-101 remain alive as of the last follow-up for each patient. As an update, we just recently treated the 18th patient at the recommended phase II dose and have four additional patients in screening. Of note, nine patients remain on treatment, and to date, five patients have lived beyond 12 months, which was the median overall survival observed in patients treated with pembrolizumab alone in the KEYNOTE-048 study. The swimmer plot also shows an emerging trend of extension of progression-free survival in patients treated at the recommended phase II dose of CUE-101 and pembrolizumab. The follow-up data on these first 18 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 the November meeting of the Society for Immunotherapy of Cancer, also known as SITC. Key observations in patients treated with CUE-101 monotherapy in the third line and beyond include, as detailed on slide 18, demonstration of single-agent antitumor efficacy evidenced by RECIST-based partial response and durable stable disease in third line and beyond recurrent metastatic head and neck cancer patients, and a median overall survival benefit from survival follow-up in the recommended phase II dose 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 settings. The Fast Track designation will facilitate planned interactions with the FDA to define a monotherapy registration path. The cumulative data from these ongoing trials with CUE-101 have provided us with clear evidence of targeted 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 a reminder, shown on slide 19, 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 CUE-102, and we are also able to initiate the phase I dose-escalation study at 1 milligram, 1 mg/kg, a dose at which we observe clear signs of biologic activity with CUE-101. 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 20. The study is actively enrolling patients in all four indications. The patient screening enrollment rate continues to go exceedingly well, underscoring investigator enthusiasm and the need for effective therapies in WT1-expressing cancers. We are currently enrolling patients at 8 mg/kg and expanding the 2 and 4 mg/kg cohorts. CUE-102 has been well tolerated to date, with no dose-limiting toxicities 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 approximately minus 25%, seen on scans at weeks six, 12, and 18. The patient currently continues on treatment. These early signs of clinical activity are particularly encouraging as they were observed at the 1 mg/kg and 2 mg/kg dose levels, with the scans on the patients dosed at 4 mg and 8 mg/kg are currently pending. We are encouraged by these early observations of monotherapy antitumor activity in these indications where checkpoint inhibitors have largely been ineffective. We look forward to presenting additional data at the SITC meeting in November. I will now turn the call over to Anish. Anish? Thanks, Matteo. As discussed by Matteo, the clinical validation data with CUE-101 and CUE-102 provides us enormous confidence to explore the breadth of our platform to cover many cancers. As shown in slide 21, the core IL-2 framework for each distinct Immuno-STAT remains constant. The primary difference between each molecule is the T-cell targeting moiety, which is unique to the cancer specificity. In other words, these different Immuno-STATs are essentially analogs of each other. To that end, we believe that the clinical experience with our first clinical candidate, CUE-101, provides platform validation and platform de-risking. We believe this unique positioning has a read-through for the entire class of therapeutic molecules that can be developed using our technology platform, which provides a significant competitive advantage. The core advantage around platform modularity to enhance precision immunotherapy is also exemplified on this slide. As shown, we can easily swap tumor-specific T-cell targeting modules to cover many different cancers. CUE-101 serves as a beachhead that provides not only a registrational path for HPV-driven cancers, but also provides proof of concept for developing additional Immuno-STATs for different cancers by targeting shared tumor antigens, personalized tumor antigens, and/or neoantigens. This extensibility is highlighted by CUE-102, that targets Wilms' tumor 1 for multiple indications, and by preclinical validation of additional Immuno-STATs that incorporate important tumor targets such as mutated KRAS, MAGE, et cetera. The other aspect of platform modularity allows us to incorporate multiple HLA alleles to expand patient global patient coverage. We've already demonstrated this versatility by generating Immuno-STATs with HLA-A02, A03, A11, and A24 as examples. The next slide, slide 22, gives a snapshot of our current pipeline in oncology and autoimmunity. We remain focused on our clinical stage assets, that is CUE-101 and CUE-102, which continue to generate data demonstrating patient benefit and evidence of durable clinical activity. We believe this validation positions us strongly to expand our pipeline into additional indications, as mentioned. To that end, we have preclinically validated several different Immuno-STATs that can be progressed into clinical stage assets. We are currently engaged in strategic discussions to map the path forward for our oncology pipeline assets. Let me briefly comment on our autoimmune pipeline. Earlier this year, we announced a collaboration with Ono Pharmaceutical to develop CUE-401 as a therapeutic for many autoimmune disorders. CUE-401 is a novel bispecific molecule for induction and expansion of regulatory T cells, or Tregs. Many IL-2 muteins are being developed for enhancing the small subset of natural Tregs. In contrast to these muteins, CUE-401 is composed of an IL-2 variant and a TGF-beta variant. Both these cytokines together have been demonstrated to generate new populations of Tregs, also known as induced Tregs, as well as expand the pre-existing natural Tregs. We believe this dual mode of action differentiates CUE-401 from all other IL-2 mutein and holds the promise to reset immune balance. We continue to make very good progress with this asset and are actively generating data sets that support us moving forward towards an IND. We also continue to be engaged in discussions to further develop additional assets within our autoimmune pipeline. With that synopsis, I will pass the call to Kerri to review our financial data. Kerri? Thanks, Anish. I'd like to provide a brief update on our financial results for the three and six months ended June 30, 2023. As shown on slide 23, during the second quarter of 2023, the company continued to use its resources in a disciplined and efficient manner while maintaining a consistent level of overall spend when compared to the same period in 2022. Importantly, we reported collaboration revenue of approximately $1.4 million for the three months ended June 30, 2023, as compared to $26,000 for the three months ended June 2022. Revenue in the second quarter of 2023 was due to work related to the recent collaboration and option agreement with Ono Pharmaceutical that Anish just mentioned. As of June 30, 2023, the company had approximately $57.9 million in cash, cash equivalents, and marketable securities, compared with $66.1 million as of June 30, 2022. Our current cash position includes proceeds from the sale of shares of our common stock in July under the October 2021 ATM agreement with Jefferies. We expect our current cash position, cash equivalents, and marketable securities to fund operations through the third quarter of 2024. I'll now turn the call back over to Dan for closing remarks. Dan? Thanks, Kerri. In summary, we view the updated data from our ongoing trials with CUE-101 and CUE-102 to be foundational, representing breakthrough potential by enabling what we consider to be precision activation of the patient's own immune system to destroy cancer. In combination with existing standard of care therapies, such as checkpoint inhibitors, Immuno-STATs may significantly expand patient reach and clinical efficacy. These developments could be transformational for the future of cancer immunotherapy. In our CUE-102 trial, we're very pleased to already observe metrics of anti-tumor activity in several patients in the dose escalation portion. An increased demand for patient access to our trial, we believe underscores the therapeutic platform's potential in addressing the significant unmet medical need for these patients, especially since many of these cancers have largely been unresponsive to checkpoint inhibitor therapy. Our platform versatility and modularity also offers market expansion opportunities into additional indications and broad HLA coverage to treat global patient populations. We also believe the application of our platform in autoimmune disease, as Anish just touched upon, more specifically, CUE-401 holds blockbuster market potential as a possible treatment for a myriad of autoimmune diseases. We continue to make impressive progress forward with our partner, Ono Pharmaceutical, and we look forward to providing further details on this program later in the year. I want to thank everyone listening in, particularly our shareholders, for their support, and appreciate the ongoing interest in our important progress for developing promising therapeutics for patients in need. Speaking of, I want to thank the patients participating in our trials, as well as their families for support. I also want to thank our dedicated employees for their commitment and consummate professionalism for bringing these promising therapeutic candidates forward. With that, I'll now turn the call over to the operator and open up for any questions. Operator? Thank you. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press the star followed by the one on your touchtone phone. You will hear a three-tone prompt acknowledging your request. Questions will be taken in the order received. Should you wish to withdraw your request, please press the star followed by the two. If you are using a speakerphone, please lift the handset before pressing any keys. One moment, please, for your first question. Your first question comes from Ted Tenthoff from Piper Sandler. Please go ahead. Great. Thank you very much, and thank you for the update, and congrats on all the strong data to date. You know, you guys are presented with sort of a, a win-win scenario here, where, you know, you're seeing enhanced activity on top of Keytruda in frontline lung with 101 as well as monotherapy in later-stage patients. You know, what goes into the process throughout the rest of the year as you generate more data, and we're looking forward to that at SITC. What really is gonna go into that process? And even beyond the data, what other factors, whether they be strategic or financial, how does all that kind of come together to sort of chart your path forward? Thank you. Yeah, thanks, Ted. This is Dan. Appreciate the question. Yeah, it, it is a dilemma 'cause we have positive data on both fronts. More importantly, we're a platform company, not a head and neck cancer company, and we have limited resources. We're thinking on a very strategic level. This obviously has to do with our corporate development initiatives, partnering initiatives. What's the best strategy for developing both this particular asset and various scenarios, monotherapy, combination? We do plan to have a meeting with the FDA in the coming months. That will define possible registration path, and I think that would also be an asset for our strategic partnering discussions as well. We also have this data emerging from CUE-102 as a monotherapy in cancers that by and large, have not been responsive to checkpoint inhibition. If we can demonstrate that we're turning these, you know, cold, tepid tumors into, tumors into hot tumor, tumors, and expanding patient reach, that's gonna put us in a, an enviable position in terms of enabling, the application of checkpoints in cancers that have previously not been a-available. We're looking at all of this, obviously in a pragmatic, strategic manner. We're looking at various strategic scenarios, and we're in ongoing dialogue with our board, which ultimately, you know, is, is part of this decision process. I appreciate the question. It's an important one for us to continue to define and refine, and I think in essence, we're gonna have a decision tree based on pros and cons, based on capital access requirements, cost of capital, and our, our various alternatives on strategic partnering. All of these are, you know, they're good problems to have. We just have to address them head-on and in a timely manner, going forward. Great. Thank you. I'll hop back in the queue. Thank you. Thank you. Your next question comes from Ren Benjamin from JMP Securities. Please go ahead. Hey, guys. Thanks for taking the questions and congratulations on all the progress. Thanks, Ren. I have a couple of questions. Yeah, a couple of questions, maybe just starting off with the monotherapy study and the update on, on overall survival. Can you talk a little bit about, you know, what additional information is really needed from the study so that, you know, you can kind of, like, book the appointment with the regulatory body, have your discussion, and, and what would you consider to be a, you know, a trial design agreement win, if you will, you know, in, in terms of, you know, once you've had that meeting? Then I have a couple of follow-ups. Sure. I'm gonna ask Matteo to handle that question. Certainly. So thanks for the question. You know, as this data has matured in the cohort of 20 patients treated at 4 mg/kg, it's really strengthened now with an approximate median OS of 14 months, which really compares very favorably to that which was observed even in the second line setting at eight months. Component of the planned, you know, FDA interaction is to put forth a proposal for a registrational trial. We've developed a synopsis and design for that trial, and it's basically a randomized trial, most likely two to one randomization of CUE-101 monotherapy to sort of investigators' choice of three potential chemotherapeutic regimens. We have, you know, all of the details and statistical parameters defined. In our interaction with FDA, with regards to a win, it's really, we anticipate having, if you will, endorsements, quote, unquote, for a single registrational trial to support an approval, in late line patients. Got it. Then just switching gears, you know, 'cause I know we've talked in the past about the neoadjuvant study, the importance of the neoadjuvant study. I might have missed it in the prepared remarks, but can you, can you talk a little bit about kind of where we are, when we might expect to see any data, and, you know, how that program might ultimately move forward? Yep. Matteo, I think that's also you. Yeah, certainly. The neoadjuvant trial at Washington University is going very, very well, okay? The trial is currently enrolling patients in the second schedule, which is patients are getting 2 doses of CUE-101, you know, before treatment with curative intent, either surgery or chemo-RT. Important to note that this is an investigator-sponsored trial, and so the timing of, of, of sharing and presenting this data, you know, will occur, you know, as a, as a collaboration, you know, with, with, with the group there that, that hold the IND for the IST. We have seen, you know, some early data that looks very encouraging. We, we really feel that this will further, you know, our understanding of CUE-101's effect in the tumor microenvironment, since the, the, the analyses, and characterization of, of tissue-based TME, blood-based, immune markers, and even T-cell receptor presence in, in the tumor pre, and, and post-treatment, really is gonna be really an exciting data set to, to look at when it is, you know, presented with our collaborators. Got it. Then I guess just finally, as we think about, you know, CUE-101 sorry, CUE-201, I think, you know, going after WT1, You know, you mentioned on the call, a clinical activity that you've seen. Can you maybe provide some additional color on those responses and the tumors where you saw an impact? Maybe related to that, as you think about that program, you know, moving forward, you know, how should we be thinking about the ideal combinations and the potential to sequence with subsequent checkpoints? Thanks, thanks for the question. To begin, you know, the next steps are really to determine the recommended phase II dose. That is the primary objective of the dose escalation component. With regards to the activity that we're observing, okay, we have 4 cancer types here. As we've stated, we've seen now a reduction that's been sustained for over 18 weeks in a patient with advanced metastatic gastric cancer. We have several patients now that have stable disease confirmed up to 18 weeks, so across different indications. We look forward to presenting, you know, the formal analysis of what we've seen with regards to effects on tumors at the SITC meeting. With regards to where we'll be going, I think, once we establish, you know, the monotherapy activity, okay, in these various indications, that we'll certainly assess rational combinations to consider taking forward. Really importantly, I think, understanding, you know, that the unique biologies of different tumor types, okay, may really direct based on the data where it would make sense to combine CUE-102. We look forward to seeing that. Just as an example, you know, in colorectal cancer, it's, I think, you know, believed or pretty much accepted that a part of the resistance to checkpoint inhibitors and immunotherapy is born out of a, a dominant immunosuppressive environment. In that tumor type, it would make sense to consider combining with something that, that interferes with that immunosuppressive pathway. It could be a TKI, it could be a, another agent. That's where we'll be, be, be heading. For example, in gastric cancer, I think, there's been some activity with checkpoint inhibitors. There, there's, an approval in, in, in the HER2 positive subset of gastric cancer for pembro plus, HER2, targeting agent, that that may be a cancer, you know, indication where it would make sense, to combine with an anti-PD-1 or other checkpoint inhibitor. That's what I think we'll, we'll, we'll be considering. Terrific. Thanks very much for taking the questions, good luck. Thanks, Ren. Thank you. Your next question comes from Steven Willey with Stifel. Please go ahead. Hi, guys. This is Julian for Stephen. Can you guys hear me okay? We can hear you just fine. Thank you. Okay, great. Thank you. Thank you for taking my question. I have two questions on my end, starting with the CUE-101 plus pembrolizumab, the combination cohort. Do you think you guys will pursue specific target population moving forward? Like, because you guys mentioned a lot about how this combination improves low CPS, you know, low CPS score population even better compared to, let's say, high, for example. Do you think there will be any potential signal indication that you guys would be targeting specific population? That's related to CUE-101. Regarding CUE-102, can you please provide a little more color on enrollment dynamics and maybe possibly additional comment on, like, how many patients have been enrolled so far? If possible, maybe additional color on, like, data disclosure, data update at CC. That's all on my end. Thank you very much. Thank you. I think the first question had to do with stratifying with CPS scores. Yeah, I, I can, if, but, I'm, I'm, I'm happy to, to, to, to take. Yeah, go ahead. Thank you for these, these two great, great questions. You know, with regards to CUE-101 and pembrolizumab, and the data that we're observing, right, where we have a really meaningful tripling of response rate in the CPS low population. Also, we have about 1.6 times increase in the CPS high population. The way I think we're thinking about this, this is actually really a win-win for any patients that are being treated in the first line setting with a checkpoint inhibitor such as pembrolizumab. You know, if you actually look at the data, on the low population, you know, it's, it's less than one in five patients that benefit or have a response. So i- if we can push that up to 50%, that's fantastic for, for the patients. Then even in the CPS high population, you know, we're, we, we have a clear benefit o- of, of improving the activity there. So I think where, where things stand now, pembrolizumab is, is approved in the first line for treating any patients that are CPS greater than or equal to 1%. And it's not clear that, that, that stratification really would, would, would be needed or, or, or specific targeting since really all of these patients appear to benefit more from the combination. With regards to CUE-102, the enrollment is, you know, in my experience, been, you know, close to the fastest for a dose escalation phase I advanced cancer study. As I mentioned before, this is really born out of the remarkable enthusiasm of the investigators. I think also it underscores the large unmet need of patients with, you know, advanced disease in these four indications. Regarding the numbers of patients, I think, you know, we anticipate presenting the initial data on approximately 20 patients or more at SITC in November. The data that we'll be presenting at that time is the initial observations on the safety and tolerability of CUE-102 monotherapy. We, we have already and, and we'll, we'll fill out more, some preliminary pharmacokinetic data from the dose escalation patients, characterize the clinical course that's been observed, and also share any correlative data sets that we have available at that time. As, as I'm sure you know well, we're, we're working very actively with, with several different vendors that are gonna help us, do, the, the correlative analyses, and, and we hope to have some of that data to share at SITC as well. Thank you very much. Thank you. Thank you. Ladies and gentlemen, as a reminder, should you have a question, please press the star followed by the one. Your next question comes from Peter Allard with Oppenheimer. Please go ahead. Hey, guys. It's Trevor. Hi, Trevor. Thanks for taking the question. Excited to see the SITC updates. Looking ahead to 2024, can you guys discuss some of the additional data that we might see throughout the year there? Yeah. On 2024, obviously, we'll have resolution from our FDA discussions, what the strategy is on CUE-101, and also clarity on our strategic decision on what indication, what line, you know, front line, third line, both. In 2024, we should have also the decision of whether we're partnering CUE-101, and with whom, what structure. CUE-102, as Matteo just articulated, we, we have, you know, a very enviable position. We have multiple cancers. We're seeing early activity and dose escalation. Just to reiterate what Matteo conveyed during the call, we're seeing activity at the 1 Mig and 2 Mig dose level, so we also have the scans for four and eight. We'll be providing at SITC. Going into 2024, it's gonna be a pretty exciting year just from a standpoint of prioritizing. Obviously, in this current financial climate, we have resource requirements that we're gonna have to address, so most likely through strategic. We also have data from CUE-401 that is emerging. We'll have clarity by end of year going into 2024. We consider that to be a, a really important transitional year for us. I think it's gonna be a, a year of multiple milestones that will be clearly defining by the end of the year, as well as pipeline expansion decisions. Okay. Yeah, appreciate it. Thank you. At this time, there are no further questions. Please proceed with your closing remarks. Yeah, I want to thank everyone for your time and interest in our continued progress. We're clearly making very good, steady progress as we move forward, and we're looking forward to SITC and providing you with further updates as we continue developing for the remainder of the year. Wish everyone a pleasant remainder of the week. Again, thank you for your interest, and take care. This concludes your conference call for today. You may now disconnect your lines. Thank you.