Morning everyone, thank you for standing by. Welcome to the Context Therapeutics CTIM-76 phase I interim clinical data call. Please be advised that today's call is being recorded. I would now like to hand the call over to your host for today, Jennifer Minai, Context Chief Financial Officer. Please go ahead. Thank you. Good morning and thank you for joining us. Before we begin, I would like to remind everyone that during this call, we will be making forward-looking statements. Because forward-looking statements relate to the future, they're subject to inherent uncertainties and risks that are difficult to predict and many of which are outside of our control. Important risks and uncertainties are set forth in our most recent public filings with the SEC at sec.gov. We undertake no obligation to update any forward-looking statements, whether as a result of new information, future developments, or otherwise, except as required by law. Earlier today, we announced positive interim phase I data for CTIM-76 in advanced platinum-resistant ovarian cancer. For details on the company's pipeline updates, we encourage everyone to read today's press release and the associated materials, which will also be filed with the SEC. Additionally, the press release, a recording of this call, and our SEC filing will be made available under the investors and news section of our website. With me on the call today are Martin Lehr, Context's Chief Executive Officer, and Dr. Karen Chagin, Context's Chief Medical Officer. Marty will provide introductory remarks regarding Context's focus on T cell engagers in solid tumors, CTIM-76 antibody design, and clinical strategy. Karen will then walk through the CTIM-76 phase I interim clinical results and next steps for the program. We'll then wrap up with concluding remarks before we move to Q&A. With that, I'm going to turn the call over to Marty for opening remarks. Thanks, Jen. At Context, our mission is to advance high selective T cell engagers to address solid tumors where meaningful therapeutic options remain limited. Our approach emphasizes biologic selectivity, manageable safety profiles, patient convenience, and combinability, all with the goal of developing therapies that can ultimately move into earlier lines of treatment. Our lead program, CTIM-76, is a Claudin 6 bispecific CD3 T cell engager that is currently in phase I development and targets an estimated addressable U.S. patient population of more than 50,000 patients across multiple solid tumors, including ovarian and endometrial cancer. CTIM-76 is designated for high selectivity for Claudin 6 over related claudins, with a safety profile intended to support potent CD3 engagement without broad cytokine activation. Following up on today's update, we expect to report updated phase I interim weekly data later this year, potentially at a medical meeting. We also anticipate sharing initial Q3W data in the second quarter of 2027. Our second program is CT-95, a mesothelin-targeted T cell engager that targets an estimated U.S. population of more than 100,000 patients. Phase I interim data is expected in September 2026. Our third program is CT-202, a Nectin-4 x CD3 T cell engager that targets an estimated addressable U.S. population exceeding 125,000 patients. First patient is expected to be enrolled in this trial in the third quarter of 2026. Together, these programs underscore our strategy to advance highly selective next generation T cell engagers with the potential for best-in-class efficacy, a favorable safety profile, and broad applicability across solid tumors, while creating multiple clinical and data-driven inflection points over the coming year. Context is positioned to develop the next generation of transformative T cell engagers through a strategy that balances optimized monotherapy design with the potential for synergistic combination approaches. Our programs are engineered to deliver best-in-class efficacy while reducing the risk of cytokine release syndrome, or CRS, improving target selectivity, and maintaining favorable pharmacokinetics. Importantly, we believe these molecules can be advanced beyond monotherapy through rational combination strategies that leverage complementary mechanisms of action, non-overlapping safety profiles, and synergistic immunological effects. Based on these design principles, we see a significant opportunity to expand into earlier treatment lines using combination approaches such as T cell engagers paired with antibody-drug conjugates or PD-1 x VEGF therapies, with the goal of enhancing clinical activity while preserving safety and patients' tolerability. Turning now to CTIM-76, we are pleased to report that CTIM-76 met our internal goals for preliminary efficacy with a 29% response rate in 8th-line PROC and exceeded our expectations with regards to a very low rate of CRS and pharmacokinetics that support less frequent dosing. In fact, we think this data can get even stronger over time as we move into earlier lines of therapy where patients are less chemotherapy-experienced and will have more robust CD8+ T cell counts. In addition, we believe moving to dosing every three weeks, or Q3W, may further mitigate T cell exhaustion and potentially enhance treatment depth and durability. Now, stepping back a bit, ovarian cancer is reportedly the fifth most common cause of cancer in women. Patients whose disease returns less than six months after receiving platinum-containing therapy are referred to as having platinum-resistant disease, or PROC. Approximately 18,000 women with platinum-resistant disease are estimated to be candidates to start a new therapy each year in the U.S., with at least an equal number estimated in Europe. There are few treatment options for these women, and those that are in development are heavily concentrated around similarly acting topoisomerase-based antibody-drug conjugates. Therefore, an emerging unmet need in PROC is to identify novel therapeutics that can address ADC resistance or enhance ADC activity without introducing new toxicities or complicating patient treatment. Today, we are very excited to share encouraging interim phase I clinical data for CTIM-76. While we originally enrolled patients with a basket of Claudin 6-expressing tumors, including endometrial, testicular, and ovarian, we pivoted our attention to PROC. This decision was driven by high Claudin 6 expression in PROC and ease of PROC enrollment. In our trial, we found that about 75% of PROC patients are CLDN6-positive, and when positive, the patients tend to have high target density, thereby providing a naturally enriched patient population for CTIM-76. In baseline PROC patients, CTIM-76 demonstrated anticancer activity with a confirmed 29% overall response rate and early signs of treatment durability. Notably, 89% of the PROC patients in this phase I trial had received prior ADC therapy. Regarding safety, CTIM-76 has shown a favorable safety profile to date, including limited low-grade cytokine release syndrome, or CRS. We believe the safety profile we have seen to date in late-line PROC is strongly supportive of developing CTIM-76 in earlier lines of therapy, including the maintenance setting and in platinum-sensitive disease. Before I hand the microphone over to Karen to walk through our exciting results in greater detail, I'd like to make a few comments on Claudin 6 as a target and on the molecular design of CTIM-76. Claudin 6 is part of the claudin family of tight junction proteins that serve to assist with cell adhesion. Claudin 6 represents a highly attractive immunotherapy target due to its unique biology and expression profile. Claudin 6 is an oncofetal protein that is normally expressed during embryonic development and is largely silenced or present at very low levels in healthy adult tissues, while its expression increases with disease progression. Importantly, Claudin 6 is a tetraspan membrane protein that does not readily internalize, making it particularly well-suited for a T cell engager approach. Achieving selective targeting is critical, as the antibody-binding region of Claudin 6 is highly conserved with other claudin family members, including claudins 3, 4, and 9, which differ by only a few amino acids. These related claudins are enriched in normal tissues, such as the ear and liver. As a result, precise selectivity of Claudin 6 is a key determinant of safety and underpins the design strategy for the CTIM-76 program. CTIM-76 is a T cell-engaging bispecific antibody that has been deliberately engineered to balance potency, selectivity, safety, and manufacturability. The molecule incorporates a highly selective Claudin 6-binding Fab arm designed to avoid off-target engagement with the closely related claudins alongside a functionally monovalent CD3-binding single chain fragment that mitigates aberrant T cell activation. CTIM-76 utilizes a silenced Fc domain to further reduce off-target immune cell engagement. Together, these design features support a potentially wide therapeutic window, enabling robust T cell-mediated tumor cell killing with minimal activation of circulating cytokines. The molecule is built on a stable IgG1 backbone, facilitating efficient and scalable manufacturing, and includes a fully humanized Claudin 6 and CD3 binding domains to support clinical development. We believe this optimized molecular architecture positions CTIM-76 to deliver meaningful clinical activity while maintaining a favorable safety and tolerability profile. I will now turn the call over to Karen Chagin, our Chief Medical Officer, to discuss the phase I study and data in more detail. Thanks, Marty. We began this phase I study in January of 2025, and we have made great progress since that time. The weekly dosing portion of the study discussed today enrolled CLDN6-positive patients with advanced ovarian, endometrial, and testicular cancers. Step dosing and steroid prophylaxis on cycle one, day one, our priming dose, and cycle one, day eight our first full dose, were incorporated from the start of the trial to mitigate cytokine release syndrome. We began dose escalation at the minimum anticipated biological effect level, or MABEL dose, of 22.5 µg administered every week, and we've escalated through 6- dose levels to date, enrolling a total of 21 patients. The 22.5 µg and 70 µg doses were deemed to be subtherapeutic, whereas the 560 µg dose exceeded target plasma exposures. We'll discuss the 560 µg dose in further detail on the next slide. The focus of today's update will be on active dose levels with full doses between 140 µg and 280 µg, which we refer to as Cohort 3, Cohort 3A, and Cohort 4. At these levels, we have 13 efficacy-evaluable patients, with nine of those being in platinum-resistant ovarian cancer. As Marty noted, we have increasingly focused on platinum-resistant ovarian cancer, given the high prevalence of Claudin 6 and the unmet need in patients with advanced disease. Constraints on the protocol emerged, most notably the 3+3 dose escalation design and the inability to backfill cohorts. To provide more substantial data in patients with platinum-resistant disease without a delay of a protocol amendment, we decided to add Cohort 3A to the protocol to incorporate additional patients with platinum-resistant ovarian cancer within the active dose range. We are quite fortunate that CTIM-76 exhibits ideal T cell engager pharmacokinetics, punctuated by exposure levels that meaningfully exceed our projections derived from preclinical studies. CTIM-76 demonstrated an estimated terminal elimination half-life of approximately 5.5 days. At doses of 280 µg and above, CTIM-76 exposure increased more than proportionally. At these dose levels, Cmax transiently exceeded the EC90, while Cmin remained substantially above the EC50 for up to one week following administration. At the 560 µg dose level, plasma concentrations exceeded preclinical projections and remained at or near the EC90 for prolonged periods of time. This exposure profile likely resulted in target saturation, excess T cell processing by the liver, and was associated with rapid T cell exhaustion. Accordingly, I halted further evaluation of CTIM-76 at doses of 560 µg and above. I'm happy to share that the Q3-week dosing portion of the trial has recently started. Based on a combination of pharmacokinetic efficacy and safety parameters, we selected 280 µg as the starting dose for Q3-week dosing and will explore additional doses on a Q3-week schedule throughout the second half of 2026. Q3-week dosing of CTIM-76 may optimize T cell activation and recovery through on and off cycling. As shown in our Q3-week dose simulation, doses of 210 µg and 350 µg maintained plasma concentrations above the EC50 for approximately 10 to 14 days. We refer to this as the CTIM-76 being on. Conversely, in the off setting, the subsequent decline in systemic exposure during days 15 to 21 may provide a pharmacologic washout interval, potentially permitting functional re-expansion and reinvigoration of the T cell compartment prior to the next dose. Extending the dosing interval may therefore improve patient convenience while also supporting more durable antitumor activity through preservation of a functional T cell population over the course of treatment. We'll move on into patient demographics and safety findings. As is typical for a phase I trial, we have a very heavily pretreated population. Overall, 69% of the patients that we enrolled had ovarian cancer, 23% had testicular cancer, and eight% of the patients had endometrial cancer. The median number of prior therapies in the all-comer population of 13 was six, with a range of 3- 16. Focusing on the platinum-resistant ovarian cancer population, we enrolled nine patients at our target dose levels of 140 µg - 280 µg. Claudin 6 expression was high in these patients, with a median H-score of 145. Because the trial permits the use of archival biopsy specimens, some samples may reflect earlier stages of disease rather than the contemporaneous tumor biology at study entry. We believe that Claudin 6 expression may be prognostic. Accordingly, lower observed H-scores, including the minimum value of 25, may underestimate true target expression at the time of treatment. Overall, these data suggest that Claudin 6 expression was generally high across the platinum-resistant population that was enrolled in this trial. I do specifically want to call out just how treatment experienced this ovarian population was. The median number of prior therapies was seven, with a range of 5- 16. All patients had received VEGF inhibitor, and all but one received an antibody drug conjugate. The majority of patients received mirvetuximab. Others did receive Topo-based ADCs or topotecan. Relevant to the mechanism of action of CTIM-76 as a T cell engager, most patients had received pembrolizumab, reflecting the ever-changing treatment landscape. Other key baseline characteristics that have been known to influence therapeutic outcomes include high tumor burden and liver metastases, both of which were observed in our patient population. Seeing CTIM-76 in such a treatment-experienced patient population gives us hope that our data can improve over time as we enroll patients who are earlier in their treatment journey. CTIM-76 relies on healthy T cells, we expect enrolling patients who are earlier on their treatment journey will enhance the quality and number of immune cells, leading to durable responses over time. Turning our attention to safety, CTIM-76 has demonstrated a safety profile that is consistent with the expected mechanism of action of T cell engagers and supports continued clinical development. Adverse events generally occurred with the first or second dose and were predominantly low grade, with the majority of events being reported as Grade 1 or Grade 2, and these events were reversible with standard management. There was a very low rate of Grade 1 cytokine release syndrome that we will discuss further on the next slides. Cytokine release syndrome, also referred to as CRS, is an on-mechanism side effect of T cell engagers. We thought it might be helpful to benchmark the CRS profile of CTIM-76 with other approved or well-known T cell engagers in development. For CTIM-76, CRS at target dose levels has been limited to Grade 1 to date, whereas the benchmark TCEs have considerably greater rates of Grade 1 CRS and also have seen Grade 2 and even some Grade 3 events. The promising CRS profile of CTIM-76 may be attributed to Claudin 6 being restricted to tumor in its expression and also to our CRS mitigation strategy, which has included steroid prophylaxis and step dosing. This CRS profile potentially offers Context a range of exciting developmental opportunities, including moving into earlier lines of therapy, outpatient administration, and combination trials in the future. Over the next several slides, I will walk through the waterfall, spider, and swimmer plots that encapsulate the preliminary efficacy findings for CTIM-76. Shown here is the waterfall plot illustrating the objective responses in patients enrolled at the target dose levels of 140 µg- 280 µg. We observed tumor reduction across multiple patients and lesions, providing evidence of effective T cell engagement with activity that appears approximately dose proportional across evaluated cohorts. Importantly, cytokine release syndrome to date has been limited and manageable, with patients typically experiencing only low-grade transient symptoms consistent with the expected mechanism of action of T cell engagers. Taken together, the combination of meaningful tumor shrinkage, emerging signals of clinical efficacy across indications, and a controlled CRS profile reinforces our confidence in the CTIM-76 dose escalation strategy and supports the evaluation of higher doses of CTIM-76 in the Q3-week portion of the trial. The spider plot shows the evolution of anti-tumor responses over time. I do want to mention that Cohorts 3 and 4 initiated enrollments almost a year ago, which provides us with a longitudinal perspective on patients who were dosed in those cohorts of 140 µg-280 µg. Cohort 3A, which dosed at 210 µg, started enrollment in February 2026, so that longitudinal data is a bit more limited. Among ovarian patients at target dose levels, nine patients have been enrolled with seven RECIST evaluable and two patients who are pending their first scan. In platinum-resistant ovarian cancer, the confirmed overall response rate was 29%. The confirmed best response, which is a combination of our partial responses and our patients with stable disease, was 57%. Together, this data support an emerging response signal with weekly dosing. I wanted to highlight a few important observations. First, in addition to the confirmed partial responses, you can see in multiple examples that patients have had continuing anti-tumor activity over time, which is exemplified by patients who have sustained stable disease. The second observation is that when we did see patients progress after having a response, it was almost always a new lesion that was associated with a rapid increase in the number of exhausted T cells. Lastly, there were no discontinuations for ongoing treatment-related adverse events, which again highlights the favorable safety profile of CTIM-76. The swimmer plot shows the evolution of anti-tumor responses over time. To reiterate, the 140 µg and 280 µg dosing cohorts have had a chance for more follow-up as they opened last year. We have several patients who have been on drug for more than six months in those cohorts. The 210 µg cohort was only recently enrolled, so the data is more limited. As of the cutoff date, seven patients remained on treatment, and we will continue to collect follow-up data for those patients. I do want to highlight a remarkable patient that you can see at the top of the swimmer plot. This is a patient with testicular cancer. It is a 35-year-old gentleman who presented with a very aggressive disease and a very high alpha-fetoprotein level, which is a biomarker for testicular cancer. Typically, for patients who present as this patient did, you would anticipate that they would be on salvage chemotherapy for less than two months. However, within the first two weeks of dosing, alpha-fetoprotein levels for this patient had dropped precipitously. Fast-forwarding at the patient's six-month scan, a small new lung lesion was noted. Per our iRECIST criteria, the patient was able to remain on study while they awaited a follow-up scan to confirm progression. Upon confirmation that that lung lesion was still there, the treating physician recommended that the patient stay on treatment due to his ability to tolerate CTIM-76, and additionally, because that new lung lesion had not grown. To date, the lung lesion remains stable, and the patient continues to derive clinical benefit per patient and investigator. I also wanted to share an example of the activity that we've been observing with CTIM-76 in ovarian cancer. This is a 53-year-old female with metastatic platinum-resistant ovarian cancer. As is typical for patients with metastatic platinum-resistant ovarian cancer, there are multiple lesions in the peritoneum. As these CT scans demonstrate, there are also multiple lesions in the liver, which traditionally have been hard to treat. The patient had received five prior lines of treatment, including mirvetuximab, pembrolizumab, olaparib, and experimental therapy as well. The patient came on study and was treated with their priming dose of 70 µg on cycle one, day one, and was then followed with 140 µg on cycle one, day eight, and every week thereafter. CA-125 is a biomarker for ovarian cancer. This marker declined by 95% over the first four months of treatment. In fact, even if you look at the first priming dose of 70 µg, that dose resulted in a marked drop in CA-125 levels. The patient achieved a confirmed partial response that deepened over time, with an ultimate decrease in target lesion diameter of 85%. Notably, there was a disappearance of a peritoneal target lesion altogether. The patient was able to remain on treatment for 162 days before progressing due to the emergence of a new lesion. The emergence of this new lesion was in fact coincident with decreasing CD8 T cells and a sudden rise in the percent of CD8 T cells that were TIM-3 positive, which is a marker of T cell exhaustion. We look towards our Q3-week dosing in the second half of 2026, we believe that this may help to maintain the CD8 T cell population and reduce T cell exhaustion over time. T cell exhaustion is a hot topic within the clinical community. We thought it might be helpful to provide a case study to delve into this a little bit further and ponder the potential implications for CTIM-76 development. T cell exhaustion is a critical determinant of response durability and frames the rationale for moving from weekly dosing to three-weekly dosing. In this slide, we're comparing two patients who had similar baseline tumor burden and similar Claudin 6 H- scores. This enabled us to relatively compare the attribution of dose levels, 140 µg for the dose on the left and 280 µg for the patient on the right, to tumor response and T cell exhaustion over time. Across both patients, markers of T cell exhaustion, which again, in this case, we are looking at the percentage of TIM-3 positive CD8 T cells, increased in a dose- proportional manner over time, paralleling tumor biomarker rebound. The notable difference is that the 280 µg dose resulted in almost double the level of T cell exhaustion over time as compared to the 140 µg dose. As we have seen in the prostate space with T cell engagers targeting KLK2, PSMA, and STEAP1, there have been reduced markers of T cell exhaustion and improved efficacy when the dosing interval was expanded. It's our hope that with less frequent dosing, patients can stay on CTIM-76 for longer and at higher doses. Now, let's pivot into framing how today's data presentation overlays with the current and future ovarian cancer treatment landscape. Platinum-resistant ovarian cancer represents a significant market opportunity with a high unmet medical need, particularly in a biomarker-defined population, where treatment options remain limited. Approximately 75% of patients with platinum-resistant disease are CLDN6-positive. Yet there are currently no approved therapies specifically for treating this population. Across the U.S., Europe, and Japan, this represents an estimated global population of approximately 42,000 CLDN6-positive patients. Importantly, Claudin 6 exhibits meaningful target overlap with several established and emerging antibody drug conjugates, including folate receptor alpha, CDH-6, and NaPi2b, which creates the potential for rational combination strategies moving forward. Beyond the post-ADC setting in platinum-resistant ovarian cancer, we see broader opportunities to advance CTIM-76 into earlier lines of therapy, as well as into additional solid tumors characterized by Claudin 6 expression, which includes, but is not necessarily limited to, endometrial cancer and non-small cell lung cancer. Collectively, these factors support CTIM-76 as a potential monotherapy, as well as a combination backbone in biologically defined patients with substantial unmet need. Here we illustrate the estimated patient population and the potential evolution of CTIM-76 within the ovarian cancer treatment paradigm, particularly focused on the platinum-resistant setting, as well as focusing on the U.S. In the United States alone, ovarian cancer accounts for approximately 21,000 cases annually, with a substantial proportion of patients eventually progressing to platinum-resistant disease, where treatment options are limited, and outcomes remain poor. As patients advance through later lines of therapy, including post-platinum and post-ADC settings, there's a clear need for novel mechanism-based approaches. We believe that CTIM-76 is well-positioned to address this gap, initially as a monotherapy in later-line platinum-resistant ovarian cancer and over time, potentially in combination with ADCs, bevacizumab, or chemotherapy. Looking long term, as clinical experience and dosing strategies mature, CTIM-76 may move earlier in the treatment continuum, supporting a broad and flexible use case across multiple lines of therapy in a patient population with a high unmet need. The ovarian treatment landscape is changing with the emergence of ADCs and other treatments. There is currently one approved ADC, and many others are in phase III development. To a lesser extent, the recent approvals of KEYTRUDA and LENVIMA in combination with paclitaxel. On this slide, we introduce our initial product development strategy for CTIM-76 in platinum-resistant ovarian cancer, highlighting both the near-term monotherapy opportunity and long-term combination potential. In the later line, platinum-resistant setting, where patients have exhausted platinum chemotherapy and frequently progressed following ADC-based therapy, CTIM-76 is well-positioned as a differentiated monotherapy option, supported by its emerging efficacy and manageable safety profile. Importantly, as we look ahead, the therapeutic window of CTIM-76 may also enable combination strategies in earlier lines of treatment, including those combinations with ADCs, bispecific targeted agents, or chemotherapy. Over time, we believe this flexible development approach could allow CTIM-76 to become a backbone therapy in ovarian cancer. CTIM-76 is uniquely positioned within the competitive landscape for platinum-resistant ovarian cancer with what we view as a compelling and differentiated clinical profile in a heavily pretreated patient population. Unlike several comparator programs that have been evaluated in earlier line settings, CTIM-76 is being studied in patients who are heavily pretreated, including a substantial proportion with prior ADC exposure. Despite this, CTIM-76 has demonstrated encouraging anti-tumor activity to date, alongside a manageable safety profile consistent with the T cell engager mechanism. Importantly, the program is designed to address known limitations of other approaches through precise Claudin 6 selectivity and controlled CD3 engagement, which we believe may support both efficacy and tolerability. While the dataset remains early, we believe these attributes position CTIM-76 favorably relative to other emerging therapies and support of continued development as a differentiated option in a high-unmet-need biomarker-defined population. Now I will transition to Jen, who will share her concluding remarks Today is just the beginning. Over the next 12 - 18 months, Context expects multiple anticipated value-creating milestones across our pipeline. For CTIM-76, we expect to share updated weekly dosing data later in the year. This is expected to be followed by Q3W cohort data in the first half of 2027, which will inform subsequent dose expansion and phase I-B development activities. In September 2026, we anticipate sharing preliminary phase I data for our CT-95 program. Finally, we expect to dose the first patient with CT-202 in a phase I trial shortly, which is on track for preliminary data in 2027. Collectively, these milestones reflect a steady cadence of clinical execution across multiple programs and support our expectation of several meaningful readouts in the near term. Importantly, these development plans are underpinned by a cash runway extending into mid-2027, positioning the company to advance its portfolio through many of these key clinical and strategic milestones. We are incredibly excited about the prospects for CTIM-76. Today, we demonstrated clinical proof of concept for our Claudin 6 T cell engager with early signals of anti-tumor activity observed in a heavily pretreated patient population. We believe CTIM-76 has the potential to be a best-in-class Claudin 6 targeted TCE, representing a meaningful commercial opportunity. Importantly, the program's developing safety profile and pharmacokinetic characteristics support exploration of alternative dosing schedules that may enhance patient convenience and combinability. Looking ahead, we believe CTIM-76 is well-positioned to advance not only as a monotherapy in platinum-resistant ovarian cancer, but also in combination regimens and potentially in earlier lines of therapy, including platinum-sensitive and maintenance settings. Before we conclude, I would like to take a moment to recognize and sincerely thank the patients who have participated in our clinical trials and their families, as well as our clinical investigators and site staff. I also want to acknowledge the exceptional dedication of our team at Context Therapeutics, including both current and former employees, whose unwavering focus on disciplined execution has been central to advancing our programs on behalf of patients. We are also grateful to our board of directors for their continued guidance and support and to our investors for their sustained confidence in our strategy. At Context, we remain deeply committed to our vision, mission, and values, and we look forward to continuing to deliver meaningful progress in the periods ahead. With that, operator, let's go ahead and open the call for Q&A. Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. One moment please, while we compile the Q&A roster. Our first question comes from Biren Amin with Piper Sandler. Your line is now open. Hi, guys. Thanks for taking my questions and congrats on the data update. You enrolled some pretty late-line patients in the ovarian cancer cohort and still reporting an encouraging response rate. For the next Q3W dosing cohort, what efforts is the company making to ensure you're enrolling patients that meet your inclusion criteria of prior therapy but also are not very late-line patients where you give patients better odds to respond with CTIM-76? Thanks. Thanks, Biren. This is Marty speaking. As you noted, we had two confirmed partial responses observed in our platinum-resistant ovarian cancer patients. It's not lost on us that in both of those patients, they had received five prior lines of therapy. These patients also demonstrated higher CD8 + T cell counts compared to more heavily pretreated individuals. By focusing on enrichment in the fourth-line or fifth-line PROC population and mitigating T cell exhaustion through a Q3W dosing regimen, we believe future studies, including the Q3W, will have the potential to yield even stronger results. We believe that happens functionally in two ways. The first is a natural evolution of the trial. When you start a trial with an experimental therapy that is entirely unproven, you typically, and as you should from an ethical standpoint, start at the end of the line. I think we have demonstrated that we have a drug that's active and that is very well-tolerated. I think that will naturally lift the patient population. I think also moving to Q3W, which will enable us to move increasingly into smaller academic centers in the community, will help us naturally move into earlier lines of patients. Finally, what we could contemplate is a formal protocol amendment to limit the number of therapies over time. We have a lot of levers to pull to make sure that we start getting patients who have better CD8+ T cell counts out of the gate. Maybe a follow-up. J&J, with their KLK T cell engager in prostate cancer, also noted T cell exhaustion with weekly dosing, but they also reported, I think, loss of TCF1 expression could potentially lead to exhaustion of T cells. Have you looked for loss of TCF1 expression in this cohort? That's the first question on the exhaustion side. For the Q3-week dosing schedule, I understand, moving forward with a 280 µg dose, have you modeled out the 420 µg, in terms of the EC50, with the Q3-week dosing? Thanks. Appreciate it. Two questions. The first is looking at correlatives, and you are correct. J&J with pasritamig, this is the data presented at ESMO in 2025, really showed elegantly that there was a clear correlation with exhaustion and frequent dosing. In fact, they highlighted a patient who, in prostate cancer, initially had a response with weekly dosing with regards to PSA 50, had a rapid rise in PSA, and interestingly enough, when they moved to Q3W, the PSA levels dropped. That got people really excited about the idea of less frequent dosing. You are correct, TCF1 is an important marker. We look at many markers, and one of the things that we are considering is in the update later this year, sharing some of that data. At a high level, there's actually three markers we tend to focus on, and these are markers that you look for in the CD8 + T cells. You're correct, TCF1 is one that relates to T cell reprogramming. You also look at CD69, which is a marker of T cell activation. In our case, we like TIM-3 positive, which is a marker of exhaustion. You could also look at Tg and other markers. Looking at those trends over time and seeing if you can increase the activation and reprogram ability and decrease the exhaustion with less frequent dosing, I think will be really important. With regards to the 420 µg dose, you are correct. It's an interesting dose. We have modeled it out. We want to see if we can really explore a maximum dose to really take it to the edge of exhaustion but also produce the most pronounced response rate profile. From there, we'll use that data to guide what the two doses going forward will be in the phase I-B. The other thing we also have to balance is if we are getting earlier line patients who have better CD8+ T cell counts, you probably don't need to go in with a super heavy dose in those patients. We're looking at a spectrum of variables to guide us into what the two doses ultimately will be in the phase I-B. Again, we're targeting the start of the phase I-B directly in January 2027. Great. Thank you. Thank you. Our next question comes from the line of Li Watsek with Cantor Fitzgerald. Your line is open. Hey, good morning, guys. Thanks for the update. I guess in terms of the cadence of Q3W dosing optimization, when do you expect to perhaps finalize a going forward dose or doses? For Q3W, would you be able to amend the trial and potentially convert it to a registrational study? As far as cadence, as my colleague, Karen mentioned, Q3w is now open and enrolling patients. We look forward to enrolling over the course of the second half of this year, then immediately progressing into what phase I-B. The protocol does allow for seamless transition in that regard. Obviously, there will be a little bit of a lag until we present that data publicly, which is why we're targeting Q2, potentially at a medical conference, to present the Q3w data. As far as an amendment to accelerated approval, I think, generally speaking, and some people have heard me say this, CEO get into trouble when they start opining about accelerated approval, and what the FDA may or may not let a sponsor pursue. What I can share is that Context will take every opportunity it can, assuming the data is strong enough to support it, to pursue the fastest registrational path possible. There is a historical precedence in the PROC space for sponsors being able to pursue and obtain accelerated approval. It's certainly on the table. I think we want to have a lot more data points in our back pocket before we provide any formal guidance around that. Okay, great. As maybe a follow-up question to the KLK2 TCE from J&J, I'm just curious, do you guys have any sense in terms of what magnitude of efficacy do you hope to achieve by switching from QW to Q3w? Just how much do targets matter in the context of us thinking about the ratio to CTIM-76? Thank you. Yeah. It's quality of target and then what kind of data you can get. KLK2 is actually quite similar to Claudin 6. Both are tumor-restricted, if you go on the Human Protein Atlas, you will find that both targets are only found in the tumor. There are vanishingly few targets that have been identified to date, that have similar expression profiles. That usually makes for a really interesting and attractive cancer target. We always hoped that we could have OVO- CRS profile. While I can't speak specifically to J&J's KLK2, I can say, as my colleague Karen disclosed, we really focused on the protein engineering aspects of CTIM-76 to optimize the cytotoxicity but minimize broad cytokine activation. I think that does play a part here. As far as data and where things go, I do think things can get materially better from here. We do view the directional 30% response rate as a starting point. Could we get to 40% or higher response rates in earlier patients? I think that's absolutely on the table. We need to generate the data to prove that. I think that could change the value proposition for the drug. I think also similar to the pasritamig KLK2 story, that's a drug that has an excellent safety profile, really solid durability, but it had no responses, and people are really excited about that drug. I think we have at least that pasritamig profile right now. If you could fold in significant and durable tumor shrinkage over time, I think that would be a really optimal outcome for patients in the clinical community. Thank you. Our next question comes from the line of Matthew Phipps with William Blair. Your line is now open. Good morning. Congrats on the update. Thanks for taking my question. First, I was wondering, you had a patient listed as progressive disease but did have a 37% shrinkage in target lesions. Wonder if you'd give any details on that, and then maybe some additional details on what you saw at the 560 µg dose. You mentioned kind of exhaustion of T cells, but were there any other safety issues or anything else that led to discontinuing that dose level? Thank you. Yeah. We did have a patient, if you look on the waterfall plot, the patient that Matt is referring to is the third from the right. This was an ovarian cancer patient who had a 37% decrease in their target lesion. They actually had, in some cases, complete resolution of their non-target lesions. But at their eight-week scan, they had a new, very small lesion that was identified, and per protocol, the patient was deemed progressive disease. That was a site that does not follow iRECIST, it was not confirmed a month later, which is a shame because you can't rule out that it was pseudoprogression or something else. I think our takeaway from that patient is the 280 µg dose looks really exciting. Maybe if you look at that patient, you will see also some T cell exhaustion settling in a little bit early. Again, if we can optimize around that 280 µg dose and give less frequently, we should be able to flip some of these patients like that -37% PD patient that you referred to. As far as the 560 µg, I think there's a couple of important things to note. Again, starting with the CRS profile exceeded our expectations relative to even our upside case. At that 560 µg dose, target saturation was achieved. The drug was above the EC90 for a sustained period of time, which is something we never, and most TC companies do not want to do. At that dose level, target saturation was achieved. I think what's important to note here is we also didn't observe any meaningful CRS at that dose levels. Based on these findings, we believe the CRS profile is likely to remain favorable over time. Given, again, the strong interest generated by pasritamig, the KLK2 TC, we anticipate their similarly compelling CRS profile will continue to be well received. The one thing to note is that when you do saturate target, you have excess T cells floating around that have been activated, so they do have to get processed somewhere, and that organ that processes activated T cells is usually the liver. We did see some short-lived and quickly resolving liver enzyme elevations in those patients. That was really it. Again, still maintaining a low CRS profile, even at the dose that you saturate the target, gives us a lot of confidence that on a go-forward basis, that CRS profile that we're seeing. Participants, please stand by. Our next question comes from the line of Paul Jeng with Guggenheim. Your line is now open. Hey, thanks for taking the question and I appreciate the nice and very comprehensive update today. My question is, was there any correlation that you saw between Claudin 6 H-score levels and the depth of antitumor activity you observed? I know there's some variability in the cutoff for Claudin 6 from other studies. Just wondering if you're contemplating any adjustments to the screening as you advance CTIM-76, or are you fairly comfortable with where you are? Thanks, Paul. Good question. We really didn't see a ton of correlations in our study. Claudin 6 is known to be prognostic, meaning that expression does increase with disease severity. It wasn't particularly surprising to us that enrolling really late-line patients, the patients had very high, very homogenous levels of Claudin 6. Given the homogeneity of the clinical population, it's pretty hard to draw conclusions there. With regards to the cutoff, we do use a very low cutoff, 10% of the cells being 1+ via IHC. It turns out, at least in the clinical population that we evaluated, it's rather binary. Patients either don't have Claudin 6, that's about 25% of the patient- Pardon me, ladies and gentlemen, please stand by. Your conference will resume momentarily. Please stand by. Your conference will resume momentarily. Marty, you may resume. Pardon me, ladies and gentlemen. Please stand by. Your conference will resume momentarily. Pardon me. Please stand by. Marty, you may resume your conference. Thank you. Sorry for those IT difficulties. To remind everyone, Paul's question related to any correlations that we may have seen. The only emerging correlation we've seen thus far, this is a classical one as it relates to immunotherapies, is that the patients who are earlier in the treatment journey tend to have higher CD8+ T cell counts. Those are the patients that responded best to our drug. Again, that's guiding us for future patient selection, giving us confidence that the data, as we enrich for that population over time, could get stronger. Great. Thanks. If I could have a quick follow-up. Just wondering to what degree the data you've shown today and are continuing to generate for CTIM-76 impacts how you're thinking about development for CT-95 or CT-202, specifically in terms of dose range and frequency. Are there any learnings that you could apply more respectively to the other programs and studies? Thank you. The answer is yes. I think, unfortunately, from a competitive intelligence standpoint, we can't share a whole lot. I think what we tend to focus on to guide decisions across the programs and leverage intelligence across the programs does relate to PK/PD. How does the exposure of the drug in blood over time impact the markers that we care about? We focus really on two areas. One, cytokines, so things like IL-2, IL-6, IL-10, interferon alpha, interferon gamma, TNF alpha. Looking at markers of T cell activation, exhaustion, and reprogramming. That's absolutely something we're doing, and we will increasingly over time, share the correlations that we're finding. Okay. Thanks very much. Thank you. Our next question comes from the line of Silvan Türkcan with Citizens. Your line is now open. Good morning. Thanks for taking my question. Congrats on this data. I just want to see if you could provide any more details on the one patient that was left to the patient that was previously discussed with ovarian cancer patient that had a 15% reduction in target lesion. It seems like this patient is stable as well. Just would more dose help here or maybe Q3 dosing? Do you have any data from the T cells from this patient about why the tumor reduction might have not continued, despite this patient clearly having mounting some sort of response, considering they also have CRS? Thank you. Yeah. I will say these are our most recent patients. The patient you're referring to is in the 210 cohort. We do see some trends in the study. Some patients who are rapid progressors tend to have exhaustion settle in quite fast. For others, and these are patients who had more durable responses, it's not until months, maybe five or six, that we start seeing exhaustion settle in. What we do want to do, and we'll be able to in real time evaluate, is moving to Q3W and seeing how those exhaustion and activation trends change over time. I think the one thing we're also thinking of is for some of these patients who had more moderate responses, could they deepen? That's really kind of two levers to pull there. One, a higher dose, moving to something like the 28, either 420, or the Q3W, where you can have less exhaustion of the T cells. These are all things that we'll be evaluating during the Q3W protocol. I think it would be interesting, assuming we have enough data points to contrast the Q3W experience with the QW, provide thoughts around that, and how that's informing future development strategies. Great. Thank you. Maybe a follow-up, if I may. Just looking at your safety profile, some of these combos that you are proposing, is there anything from your TAEs that would block any of these? It looks pretty good for a T cell engager here at this point. I think our safety profile, frankly, did exceed expectations, we don't see anything as limiting right now. I do think mechanistically, right, T cell engagers, you would anticipate, and this is shown in our TAEs, that you'll have low-grade ALT and AST elevations in directionally 40%, maybe 50% of your patients, because the T cells, as they get activated, get processed by the liver. I think looking at some of the ADCs that have a more profound impact on the liver, and in some cases even have liver toxicities, that's probably an area that would give us pause. If you look at the ADC space, there's many more ADCs that don't have that issue, than do. If you look more broadly in standard of care therapies, whether it is in the platinum resistant setting, that would be paclitaxel, doxorubicin, and bevacizumab, no immediate concerns there. We're really excited to explore those potential combinations, particularly as it relates to bevacizumab, since it does release an immunosuppressive break. No particular concerns in the platinum sensitive setting. Great. Thank you so much for taking my question. Thank you. Our next question comes from the line of Charles Zhu with LifeSci Capital. Your line is now open. Good morning, everyone. Thanks for taking the questions. Two quick ones from me. May have missed this, but did either one of your PROC responders occur in patients that had prior exposure to topoisomerase-based ADCs? Second question, you had two invaluable PROT patients that were still ongoing as of data cutoff. Have you been able to check, given that it has been two and a half weeks or so since the data cutoff and they should have received their first scan by now? Thank you. Yep. We haven't reported out ADC utilization by patient, for the specific reason that it's too soon to draw any correlations, and we've disclosed in this conversation that we have not seen any correlations to date. What I can share is that, of the nine ovarian patients, about 2/3 have received mirvetuximab. The other 1/3 have received a topo-based ADC payload, either experimental or approved. Even within the mirvetuximab-experienced population, many of those patients got topotecan over the course of their treatment. The vast majority of our patients have been exposed to a topo-based payload of one form or another. For the two patients without scans as of yet, we want to provide that update later this year at an academic conference. As you know, cutoffs can sometimes be a moving goal. We set our cutoff to May 29th, do not move from that date. Understood. Thank you. Thank you. Our next question comes from the line of Emily Bodnar with H.C. Wainwright. Your line is now open. Hi, good morning. Thanks for taking the questions, congrats on all the progress. Maybe for the first one, can you kind of clarify your go-forward strategy? Are you initially planning to look at monotherapy in the post-ADC setting, or are you also planning to look at potential combinations in dose expansion? If so, what are kind of the initial targets that you're looking at? Maybe if you could comment a bit on the testicular cancer patients. In other Claudin 6 therapies, we've seen pretty good positive efficacy in testicular cancer patients. Curious why maybe you kind of saw less of that in your patients. Thanks. Yep. Two good questions, Emily. As far as a go-forward strategy, the most important strategy as of today is developing the drug as a monotherapy and advancing it as rapidly as possible to registration. From there, we are interested in combinations, a core goal for us as a company is developing all of the preclinical data to support exploration of those opportunities. That clinical exploration could happen as soon as the second half of 2027 and would obviously also be financing-dependent to fund that work. As far as testicular, you are correct. Some of our peers have had some nice data in testicular cancer. What we have found thus far working in testicular is it's a very challenging indication. It's incredibly unfortunate. These are young men dealing with hyper-aggressive cancer, who typically, as a function of getting an allogeneic stem cell transplant and progressing on that, are heavily compromised from a comorbidity standpoint. We just found it very challenging to manage these patients. We felt like a better strategy for us as of now was to pursue PROC for all the reasons my colleagues outlined earlier. Also, the PROC patients tend to have, you can see the ECOG scores of our patients there, much healthier and heartier relative to the testicular. Testicular is something we're very interested in but would probably be something we come back to at a later date. Thank you. Our next question comes from the line of Boris Peaker with JonesTrading. Your line is now open. Great. Thanks for taking my question. I just want to focus on the CRS. Just curious if there's a correlation between CRS onset or CRS in general and response. I guess the fundamental question around that is that you showed a fairly low level of CRS compared to other T cell engager. The question is, does that suggest that maybe you're leaving some potential efficacy on the table if CRS is part of the mechanism of T cell engager activity? Thanks, Boris. It's a great question. I think the best way to think about this is our understanding of CRS and clinical intervention to mitigate it is evolving. If you look back to some prior data updates from peer companies in 2023 and 2024, many of them noted that you had to have CRS to have a response. I think what we're increasingly seeing across the TCE space, not just KLK2, but we saw with some BCMAs and aggressive prophylaxis, that there is, in many cases now, examples where you don't need broad CRS to have a response. In fact, people are optimizing the development of their TCEs, just like we did, to select for TCEs that can induce cytotoxicity without broad cytokine activation. There's even next-generation CD3s that are not necessarily CD3 epsilon-focused like us, that will also have reduced cytokine activation. I think broadly, you're going to see across the board with TCEs, lower and lower CRS rates, which is reflecting why the clinical community is suddenly, I think the appropriate word is suddenly, because it's happened rather quickly, interested in this modality. Again, if you have low CRS rates and you can move to less frequent dosing, CAR T, TCEs, they were the domain of large academic centers. This profile for the industry with respect to TCEs enables sponsors to move in the community, that broadens the use case. It frankly, for patients, gets the drug into the hands of a much broader patient population to help them. I'm really, really excited by this. I'd love to say it's unique to us, but I think you're going to start seeing it popping up across the TCE landscape. Great. Thanks very much for taking my question. Thank you. Our next question comes from the line of Tanay Mehta with Rodman & Renshaw. Your line is now open. Hey, guys. This is Tanay on for Mike King. Congratulations on the updates. Thank you for taking our questions. On the PROC patient who achieved the two sequential partial responses before progressing at day 152, given that her TIM-3+ producing CD8 T cells were already rising before progression, was dose modification considered at that point, and does that inform how you'll redesign treatment criteria in the Q3w cohort going forward? Yeah, it's an interesting question. This goes back to the patient who, at the 140 µg dose, had a deep and durable response. Over time, we've gotten a lot of questions. Why did this patient at the 140 µg dose respond? This was a fifth-line patient. She actually had, if I have this correct, the highest number of CD8 + T cells in our trial. A lower dose produced a rather outsized response for that particular patient. We do, as we move into earlier lines of therapy, need to think critically about what the right dose is for that particular patient population. As we've been treating our patients, though, data continues to emerge, right? I referenced the pasritamig data earlier, where the patient with weekly dosing had a rising PSA rate, and then just by moving to Q3W, the PSA level dropped. I do think today it's a combination of dose and interval, and that's what we're optimizing the second half of this year, of 2026, so that we have two doses that we're really confident in. Hopefully, both are Q3W to evaluate in phase I-B. Great. Thank you so much. Thank you. I'm not showing any further questions in the queue at this time. I'd now like to turn the call back to Marty for closing remarks. Thank you. I just want to thank everyone for joining us today. It's obviously a very exciting day for all of us here at Context and a very important day for cancer patients, in particular, ovarian cancer patients. Thank you for your time, and we look forward to keeping you updated on our progress in the future. This concludes today's conference call. Thank you for participating. You may now disconnect.