Cue Biopharma, Inc. (NASDAQ:CUE) Q2 2023 Earnings Call Transcript
Cue Biopharma, Inc. (NASDAQ:CUE) Q2 2023 Earnings Call Transcript August 9, 2023
Operator: Greetings, and 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. [Operator Instructions] 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.
Dan Passeri: Hi. Thank you very much, and good afternoon, everyone. As a reminder, this presentation and discussions being recorded and will be available on our website for the next 30 days. Also please be aware that the slide accompanying today’s update maybe advance directly by those listening in on the call, and we'll 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 Millar, our Chief Financial Officer. As shown on slide number 2, this presentation and overview may contain some forward-looking statements, and any forward-looking statements made during this call represents the company's views as of today, August 09, 2023.
On the next slide, which is slide number 3, it just outlines the agenda for today's call, and I'll begin with a brief summary followed by Anish. Anish will provide you with some background context pertaining to our approach and result in 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, we'll 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 they will be followed by Kerri, who will provide an overview of our financials for Q2 and going forward guidance. I'll then return for concluding remarks, and we'll open the call up for questions. I'm now going to turn the call over to Anish. Anish?
Anish Suri: Thanks, Dan. As noted on slide 4, the foundational premise and vision for our therapeutic platform has centered on harnessing the natural signals on HSQs 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 on HSQs 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 nonspecific 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-STAT, we have the potential to solve a significant and fundamental challenge, which is the selective activation of their 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 sledge hammer 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 biospecifics, 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, but more importantly, appears to achieve these outcomes without compromising patient safety. Slide 6 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 P-HLA, 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 life cell microscopy experiments conducted by Dr. Michael Dustin's lab at University of Oxford. Dr. Dustin is a member of the National Academy of Science 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 immuno 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 on 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 frontline setting, where anti-PD-1 therapy is approved, we have combined our Immuno-STAT 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-STAT increased 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 opportunities. We also believe that the clinical data with CUE-101 have validated and derisked 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 per kg. The latter point shortened our dose escalation in patients significantly and saved us approximately a year in clinical development time lines.
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 Q12. Matteo?
Matteo Levisetti: 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 eight, data from the ongoing clinical trials with CUE-101 is monotherapy and in combination with pembrolizumab have provided clinical proof-of-concept and derisking 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 effect. Furthermore, nd 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 webcast, I'd like to review the data on slide nine, 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 milligrams per kilogram. The exposure pattern is consistent throughout multiple cycles of treatment without any attenuation of PK parameters, supporting the premise that there's new 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 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 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 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 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, 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 resist 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 2 dose of 4 milligrams per kilogram 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 a checkpoint -- in the second-line CheckMate 141 in KEYNOTE-040 trials of nivolumab and pembrolizumab, respectively. As any experienced oncologists understand the survival with third-line treatment is expected to be less as the disease has further developed it 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 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 of CPS values of 1 to 9, and the other 50% have CPS values greater than 20.
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Subgroup analysis of the KEYNOTE-048 study has shown that patients with CPS at 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 14 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'll 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% -- 30% or greater and 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 one 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-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 frontline 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 one 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 score is greater than or equal to one, 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 one to 19, and 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., one to 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 continued clinical improvement. The patient had a target disease burden of approximately eight centimeters, comprising a lesion at the base of the tongue in 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 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, and they have reduced in size to less than 10 millimeters, i.e., the size of a normal lymph nodes, 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 in 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 at 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 evidence by resist 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, enable 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 derisking 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 shared 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 1 dose escalation study at 1 milligram per kilogram, a dose at which we observed 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 in the need for effective therapies in WT1 expressing cancers. We're currently enrolling patients at 8 milligrams per kilogram and expanding the 2 and 4 milligram per kilogram cohorts, CUE-102 has been well tolerated to date with no dose-limiting toxicities observed. Evidence of anti-tumor 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 in three prior lines of therapy, including a checkpoint inhibitor, has experienced a decrease in the sum of three target lesions of approximately minus 25% and seen on scans at weeks 6, 12 and 18 and the patient currently continues on treatment.
These early signs of clinical activity are particularly encouraging as they were observed at the 1 milligram per kilogram and 2 milligram per kilogram dose levels with the scans on the patients dosed at 4 milligrams and 8 milligrams per kilogram 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?
Anish Suri: Thanks, Matteo. As discussed by Matteo, the clinical validation data with CUE-101 and 102 provides us enormous confidence to exploit the breadth of our platform to cover many cancers. As shown on Slide 21, the core IL-2 framework for each distinct immuno state remains constant. The primary difference between each molecule is that 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 derisking.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-STAT 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 immunostatus with HLA-A02, AO3, 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 102 which continue to generate data demonstrating patient benefit and evidence of durable clinical activity. We believe this validation positions us strongly to expand the 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 Pharmaceuticals to develop CUE-401as a therapeutic for many autoimmune disorders. CUE-401is a novel bispecific molecule for induction and expansion of regulatory T cells or Tregs. Many IL-2 mutein 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 induce Tregs as well as expand the pre-existing natural Tregs. Hence, we believe there's 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 on synopsis, I will pass the call to Kerri to review our financial data. Kerri?
Kerri Millar: 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 Pharmaceuticals 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 the remarks. Dan?
Dan Passeri: Yeah. Thanks, Kerri. So 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. Furthermore, in combination with existing standard of care therapies, such as checkpoint inhibitors, and Immuno-STAT may significantly expand patient reach and clinical efficacy. These developments could be transformational for the future of cancer immunotherapy. And our CUE-102 trial, we're very pleased to already observe metrics of anti-tumor activity in several patients in the dose escalation portion. Furthermore, an increased demand for patient access to our trial we believe, underscores the therapeutic platform's potential and 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 and 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 constant 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?
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