Good afternoon and welcome to the Repare Therapeutics conference call. At this time, all participants are in listen-only mode. Please note that this call is being recorded. Following the presentation, we will conduct a question-and-answer session. If at any time during this call you require immediate assistance, please press star zero for the operator. I'll now turn the call over to Robin Garner, Vice President and Head of Investor Relations. Please go ahead. Good morning and thank you for joining us today to discuss the positive data from our Phase l MYTHIC Gynecologic Expansion Trial. I invite you to visit the Investors section of our website to view the webcast slides and today's press release regarding these data. As a reminder, a recording of today's event will be made available on our website later today. Before we begin, I'd like to remind you that management may make forward-looking statements during today's discussion. These statements are subject to risks and uncertainties that could cause our actual results to differ materially from those described in these forward-looking statements. The factors that could cause actual results to differ are discussed in our SEC filings, including our most recent annual report on Form 10-K and our most recent quarterly report on Form 10-Q. We undertake no obligation to update or revise any forward-looking statement for any reason. Today's presentation will begin with introductory comments by our President and CEO, Lloyd Segal. In addition to the Repare Leadership Team, we're fortunate to be joined by Dr. Brian Slomovitz, Director of Gynecologic Oncology at Mount Sinai Medical Center, who will discuss the current treatment landscape for gynecologic cancers. Everyone, as well as Steve Forte, our CFO, will be available for Q&A. To ensure equitable participation, we would kindly ask that you limit yourselves to one question and one follow-up. Let's get started. Thanks, Robin. Since 2016, our mission has been to bring practice-changing medicines to cancer patients who desperately need them, leveraging Repare's deep know-how in synthetic lethal biology to develop new and better treatment options. In the last eight years, we've entered the clinic with four compelling and proprietary programs, all of which have key catalysts in the next year. The focus of today's discussion, as you see at the top of this portfolio snapshot, is our most advanced combination of our PKMYT1 inhibitor, Lunresertib, and our ATR inhibitor, Camonsertib. I'll start with the headlines for today, the details of which will form the bulk of our presentation. In short, we have achieved proof of concept with our lunresertib-camonsertib combo in a well-tolerated, convenient new treatment alternative in gynecological tumors. We met clear and tangible unmet patient needs with compelling efficacy that we'll share. We're now set to get started on a randomized phase lll in endometrial cancer in 2025, with regulatory support from the FDA and EMA, including accelerated approval options in the U.S. We have a simple and straightforward set of COC obligations that we'll describe and a nice set of life cycle opportunities ahead of us, starting with platinum-resistant ovarian cancer that Phil will get to a little later. Today, though, we'll start with Dr. Brian Slomovitz to set the stage for the opportunity that we have overall in gynecologic tumors and with a specific focus in endometrial cancer, where he's uniquely positioned to provide a backdrop for the current journey of these cancer patients. Dr. Maria Koehler and Dr. Paul Basciano from our team will then walk you through the data and next steps, as well as our regulator-supported registration trial plans. We'll finish up with our Chief Commercial Officer, Phil Herman, who will walk you through briefly the immediate and longer-term patient and commercial opportunities. We'll then open it up to Q&A and do our best to get to as many questions as we can in the time we have. For clarity and consistency, I'd like to just take a quick moment to outline key abbreviations that we'll be using throughout today. We refer to our two lead programs, Lunresertib and Camonsertib, as Lunre and Camo. We've used some common abbreviations in gynecologic cancers, notably EC for endometrial cancer and PROC for platinum-resistant ovarian cancer, our two key tumors of interest today. We refer to our clinically proven biomarkers for Lunre-Camo as Lunre Biomarker Positive. These are the three genes for which virtually all patients have been enrolled and for which we plan to develop our products for, and those are Cyclin E1, PPP2R1A, and FBXW7. To level set everyone before we get into the program, I'd like to take a quick step back to highlight the strong mechanistic preclinical rationale that formed the basis for our Lunre-Camo strategy. On the left of the slide, you can see a simplified representation of the mechanism of action of Lunre-Camo. As you can see here, Lunre and Camo work synergistically to enhance CDK1 activation and kill cancer cells by driving them to premature mitosis in our biomarker-positive population, and the story of our three biomarkers and why we select for those patients are right here. On the right of the slide, you can see the strong mechanistic rationale was further supported by strong animal data showing complete regressions, all of which we've previously published. Based on that compelling preclinical rationale, we initiated MYTHIC, first to understand Lunre monotherapy activity and its potential. We then explored multiple combinations for which we established strong preclinical rationale prior to going to the clinic. Ultimately, we established safety, tolerability, and determined that the combinations were the best opportunity for efficacy with Lunre, starting with our Camo combination. We established regulatory support for an optimized RP2D and schedule representing the gold standard optimized approach in getting there. We also successfully mitigated some early anemia signals we saw in October of 2023 with a straightforward optimization of the schedule. We saw compelling early signals as well with FOLFIRI in combination with Lunre in colorectal cancer and powerful early signals in GYN tumors that catalyzed the phase ll-like enrichment cohorts we're sharing with you today in endometrial cancer and platinum-resistant ovarian cancer. These cohorts represent proof of concept for us to progress to our goal of registration trials starting next year. To sum up what Maria and Paul will explore in more depth, we share today what we believe is an effective, well-tolerated, convenient, differentiated option for EC and PROC, for which we'll launch a randomized EC phase lll trial next year. Across both indications, we saw efficacy in heavily pretreated patients and, moreover, as we'll show you, patients whose prognosis are worse given our selected biomarkers. We saw promising tumor responses and durable benefit. We saw a needed alternative to chemo and ADCs with better safety, tolerability, and convenience. We saw registration opportunities for both indications supported by our discussion with regulators in the U.S. and Europe. In sum, we saw a mirvetuximab-like opportunity for our biomarker-positive subset in both endometrial cancer and ovarian cancer. And while we've decided to put our initial focus and capital behind the EC opportunity where we saw greater unmet need, PROC represents the first of several life cycle expansions that Phil will describe later on. I'd like now to introduce our guest today, Dr. Brian Slomovitz. Dr. Slomovitz is Director of Gynecologic Oncology and Co-Chair of the Cancer Research Committee at Mount Sinai Medical Center in Miami. He is also a professor in obstetrics and gynecology at Florida International University, and he is the uterine cancer clinical trial leader for Gynecologic Oncology Group, as well as a board member of the GOG Foundation. I'll now ask Dr. Brian Slomovitz to share his perspective on the endometrial cancer and platinum-resistant ovarian cancer landscape. Hello, and Lloyd, thank you very much and to the Repare team for giving me this opportunity to present to you today and to talk about what my passion is, and that's to come up with better treatment options for our patients who suffer from these gynecologic malignancies. It's really an exciting time in the gynecologic cancer research world, and I'm super excited to make strides forward, and I do believe that this is one of the opportunities we have to, again, transform the standard of care and to do better for our patients. Endometrial cancer is, in 2024, here's an overview. It is, interestingly, the only gynecologic cancer that has a rising incidence and a rising mortality, and that's quite surprising. Historically, we referred to ovarian cancer as the silent killer. We're doing better with ovarian cancer treatment options, even though that represents an unmet need, and I'll talk about that in a little while. But it's frustrating with gynecological cancers because the death rate is actually going higher and the incidence is going higher. As we could see from the numbers here, there's about 68,000 new cases each year. We're relieved that two-thirds of those are early stage with a good prognosis, but the ones that are causing us trouble and the ones that we're seeing an increased rise in are these high-risk pathologies or these patients with advanced or recurrent disease. These are the women that we're seeing most of the deaths or recurrences due to this disease, which make up about 13,000 cases, 13,000 cases-14,000 cases each year. What this is showing here is that the number of endometrial cancer deaths is outnumbering those of ovarian cancer deaths, which, again, I'll highlight again, is quite frustrating and presents an area of opportunity as an unmet need that needs to be filled. This is a timeline of endometrial cancer treatment options. The first FDA approval came in the early 1970s with progestins, hormonal treatment for endometrial cancer. To me, what's been extremely frustrating is while we've had treatment options for patients with endometrial cancer over really the last 40 years, there hasn't been much progress with regards to FDA approvals and really ultimately coming up with the best treatment options for our patients. We use carboplatin paclitaxel as a standard of care chemotherapy. This is based on a study, GOG-209, comparing it to the standard of care at that time, which was very toxic. Carboplatin paclitaxel is actually more tolerable. But the response rates there are still modest, with a response rate of about 52%-53%. It's not until the TCGA data or the Cancer Genome Atlas data came out in 2013, which helped divide solid tumors into different molecular sub-classifications. More than any other solid tumor, the classifications for endometrial cancer were really well delineated. The classifications being those with POLE mutations, those with deficient mismatch repair, those with high copy number or p53 mutations, or those with no specific molecular profile. Based on those, we became better at coming up with treatment options for our patients, really dividing those that would respond to immunotherapy by itself versus those that are cold tumors. And we find that immunotherapies worked. However, they need another treatment as well. Staging has been upgraded in 2023 to help reflect these molecular classifications. Now we're in this era of antibody-drug conjugates, or ADCs, that are molecularly targeted. However, we know even with ADCs, there's plenty of unmet needs, plenty of area of opportunity, and we really don't have anything for our patients either before ADCs that represent really a great standard of care change and definitely not after ADCs, and there's still opportunity there to come up with better treatment options. This slide shows a summary of immunotherapy and how it was incorporated into the first-line management of this disease. This slide shows four studies that have been completed within the last two or three years and reported: GY018, RUBY, AtTEnd, and DUO-E. The top line reflects the data in the dMMR population or the microsatellite instability. The bottom line reflects those with proficient mismatch repair or those that are microsatellite stable. All the studies have the common theme: chemotherapy plus/minus immunotherapy agent, whether it be a PD-1 inhibitor or a PD-L1 inhibitor. We could see from the deficient mismatch repair that immunotherapy is impressive. There's about a 70% reduction, up to a 70% reduction in those patients with advanced or recurrent disease requiring first-line chemotherapy, a reduction with the addition of immunotherapy. However, the addition of immunotherapy in the proficient mismatch repair patients is not as promising, is not as significant. It does have an all-comer approval with pembrolizumab and dostarlimab. However, there still represents a great opportunity here for improvement. Of note, the tumors that are targeted by the asset that we're talking about are mostly in the pMMR category, again, filling in the area that there's an unmet need here. So the Lunre and Camo patients are all pMMR. This will help us moving forward as we come up with therapeutic options. Particularly, what we're looking for is non-therapeutic, I'm sorry, non-chemotherapy options to help come up with better treatment options for our patients. What do we do after chemotherapy, after immunotherapy? There's NCCN guideline treatment options, lots of chemotherapy on that list. A standard of care chemo, which has been the control arm of a lot of trials, is either weekly Paclitaxel or Adriamycin, doxorubicin, with modest response rates and definitely limited durations of responses. In addition, we're in this ADC era where ADCs have been shown to work, and we're doing a lot of studies with ADCs. The big problem, as I see it with ADCs, as I like to call it, like one and done. Once a patient gets an ADC, most of these are topo I or topoisomerase I kills or payloads. Once they get them, they're not eligible. There's no data on ADC after ADC or topo I after topo I. There definitely needs to be better treatment options in this setting. Maybe some of these treatment options can be an alternative to the chemo-based ADCs. Remember, antibody-drug conjugates, while they have less systemic side effects of some chemotherapies, they are still a chemotherapy that is being delivered direct to the cell, but they're also being delivered to those organs in the body that overexpress the proteins that are targeted by the ADC. How am I managing my patients? I get a lot of patients in the second and third-line treatment for second opinions. Really, a lot of it is based on the biomarker-based selection. What biomarker profile do they have that identifies targetable mutations that will come up with better treatment options that will enhance the efficacy and limit the toxicity in order to give patients a good treatment and to continue to enjoy their quality of life? One of the things that it's really nice in this era of our clinical trials is that it's a global effort. I'm the clinical trial lead for the GOG, as was mentioned, for endometrial cancer. We work hand in hand in a partnership with our European colleagues, our South American colleagues, our Canadian colleagues. We also have strong relationships with the South Korean colleagues and Japanese colleagues in order to come up with the best clinical trials that could yield better treatment options for our patients, and by doing it globally, we're really doing it in a more efficient time. One of the things that's important, those tumors, both in endometrial and ovarian cancer, that have the biomarker profile that is susceptible to this treatment have a worse prognosis. So when we look at those patients with the, we'll call it a Lunre biomarker positive versus biomarker negative, those with a biomarker positive do worse in this dataset than those that are biomarker negative. Further highlighting the opportunity here that by exploiting this pathway, by exploiting this pathway, we're not coming up with just a better treatment option, but we're also coming up with a better treatment option for those patients that have a worse prognosis. So not only is that important, but when we look at the data, it's important to note that we're not looking at historical controls in the whole population. We need to understand that this is a higher-risk population and that coming up with statistically significant improvements from standard of care may actually be more impressive than just the biomarker population, than the entire population, not just in the biomarker positive population. We could see from the data here, both in endometrial cancer and in ovarian cancer, the biomarker profile here portends a worse prognosis. I talked a lot about endometrial cancer. I want to touch base here on ovarian cancer. We know that this is sort of the natural history of ovarian cancer. Patients present with symptoms. We used to consider them to be symptom-free. That's not the case. They have symptoms that are just nonspecific symptoms. Then they get a combination multimodality chemotherapy and surgery, platinum-based chemotherapy. Maintenance therapy after chemotherapy includes either PARP inhibitors for those with homologous repair deficient disease or BRCA positive or BRCA mutated disease or bevacizumab if they don't have homologous repair deficiency or if they're homologous repair proficient. We learned that in my practice, maintenance therapy is extremely important because I believe it's not only the drugs, but it's the duration of exposure, which helps make a difference in the success in our treatment options. The median time to recurrence is 18 months. Those that recur after six months are considered platinum-sensitive. Chemotherapeutic options in the platinum-sensitive patients include platinum-based chemotherapy. But eventually, those patients that recur will eventually become platinum-resistant, and their treatment options are also limited, and we need to come up with better treatment options. I've talked about ADCs. There is a subset of patients who have alpha-folate receptor expressing tumors that there's an FDA approval for mirvetuximab in this setting, which is an alpha-folate receptor targeted ADC. But not only in those patients that recur after mirvetuximab, but in patients that don't overexpress, we need to come up with better treatment options. And again, there's an opportunity here in ovarian cancer to implement newer treatment options. Again, I think there's an opportunity here to meet the urgent needs of our patients, particularly with a chemo-free regimen. The Lunre biomarker status is linked to significant reduced median overall survival. It's potentially an attractive chemotherapy-free regimen. We feel that there's a comparable efficacy to the emerging ADCs. And even with this comparable efficacy, there's a role either before ADCs or especially after ADCs that represents an unmet need. We need to further study applying tumor selection, biomarker-selected populations, which in most of my trials, and I have about 20 trials that I'm running now through the GOG, most of them do have some biomarker selection incorporation in order to come up with a more targeted approach and better treatment options. In summary, endometrial cancer, there's no approved endometrial second-line therapy after previous immune checkpoint inhibitors with chemotherapy, and we desperately need that, and in ovarian cancer, existing therapies are insufficient to manage these high-risk biomarker-positive patients. Thank you for your time, and I look forward to the discussion. Thank you, Dr. Slomovitz. We are excited to share this data with you today. We will start with a look across our gynecological data, given the early signal we saw last year that catalyzed the enrichment cohorts. Paul will then walk you through the data in endometrial cancer, in platinum-resistant ovarian cancer. And I will provide some perspectives on the key mechanism in which Lunre and Camo acts and how this distinct mechanism of action results in a way that enables our planned phase lll studies. I will end with the go-forward opportunity in endometrial cancer and why we have chosen to focus on this initial clinical trial. Paul? Thanks, Maria. I'll start with a few slides summarizing the robust data package from over 50 patients in both endometrial cancer and ovarian cancer, all with the same fundamental biological drivers of disease. They're a starting point for our highly confident view of the overall activity of this novel combination. All our data throughout will be presented in the context of RP2D and optimized schedule, which is agreed upon with regulatory authorities and will be used for all future studies. Within this heavily treated phase l population, more than 70% of patients had tumor shrinkage, and more than 30% achieved a RECIST-defined response. As you can see, activity was seen in both ovarian in purple and endometrial in green, with endometrial cancer responses being particularly deep, including complete resolution of tumors, which is highly remarkable for these late-line patients. Here we show that across the two tumor types, regardless of the biomarker, Lunre plus Camo drives long-term clinical benefit and deep tumor size reduction. As expected, the PPP2R1A and FBXW7 genetic alteration groups are mostly composed of patients with endometrial cancer, while the vast majority of the CCNE1 tumors are ovarian cancer. There is clear activity of the combination across all of our biomarker-defined subgroups. Even where tumor shrinkage in the blue PPP2R1A subset seems a bit less, the duration of treatment on the left is not much different than the other groups. Across all tumor types, including gynecological tumors, we provide the overall safety. We showed these data across all tumors as it gives us a larger dataset from which we can draw conclusions. The data from patients with gynecologic cancers is highly consistent with what is shown here, as they make up a majority of this overall population of close to 70 patients. So just to stress that point, our endometrial cancer and ovarian cancer patient subsets look almost identical to what you see here. Critically, less than half of the patients had a reported grade 3 treatment-related event. The observation here is based on very long durations of treatment, with a median of 15 weeks and up to 49 weeks, sufficient to comprehensively characterize the early and late tolerability effects. Grade three anemia is comparable to other novel agents at less than 30%, and there were no grade 4 anemia events reported. Importantly, we do not see a decrease in platelets of any grade and have few patients with clinically meaningful decreases in neutrophils, showing that the injury to the bone marrow is light. We see no alopecia or hair loss, so common with platelet-toxic chemo, including emerging ADCs, and this is of great importance to many women receiving cancer treatments. Our diarrhea rate is low, and duration was generally short. Finally, we see some rash and mucositis related to Lunre, as expected and as we previously reported, and which patients and treating physicians consider acceptable and differentiated from chemo and ADC options. Supportive care was initially limited in this protocol, as is usual in phase l studies, to allow us to fully understand our safety profile. With our profile now firmly established in preparation for the pivotal study, we recently introduced consistent supportive care protocols, such as standardized mouth care, erythropoietin injections as needed to support red blood cell production in patients experiencing anemia, and the use of topical care, such as creams for rashes. We expect that these commonly used supportive care treatments, when used consistently, will further enhance our differentiated and favorable tolerability profile and should result in better patient acceptance of treatment, resulting in longer duration of treatment overall. We'll look now at the data in endometrial cancer in more detail. We report here the 27 patients treated with RP2D doses with endometrial cancer and who have at least one scan. This was a very poor prognosis population characterized by heavy pretreatment, with nearly 60% having three or more prior therapies, including all patients having received prior platinum regimens and nearly 80% treated with immune checkpoint inhibitors, which are now a key part of the standard of care, as you heard from Dr. Slomovitz. These patients also were a high-risk group based on their advanced age with a median of 67 years and tumor features such as higher-risk histologies and 85% having a p53 mutation. This last part is critical, as p53 mutations define a subgroup of patients with the most aggressive endometrial tumors. You saw in Dr. Slomovitz's presentation the lower benefit of first-line therapy for patients with tumors defined as MMR proficient, which is the larger subgroup. All EC patients enrolled in MYTHIC trial had proficient MMR, offering an important solution for the expected poor outcomes for these patients. Lastly, you can see that most patients had PPP2R1A alterations, 22% had FBXW7, and 15% had CCNE1. This graph shows the time on treatment for patients with endometrial cancer. You can see the timing of RECIST responses and benefit observed in all histologies, including those considered very difficult to treat, such as carcinosarcoma. Patients with this histology are unfortunately excluded from many endometrial cancer trials, but were included in MYTHIC because we anticipated that Lunre plus Camo could bring benefit to these very high unmet need patients. The percentage of patients with endometrial cancer without progression at the six-month time point is 43%. This is similar to what has been reported for ADCs being developed in endometrial cancer, and importantly, the patients receiving ADCs generally had less prior treatments, including fewer receiving prior immune checkpoint inhibitors. The clinical benefit rate defined by RECIST response or reaching 16 weeks without progression is 48.1%. You can also appreciate here the unique pattern of benefit we see in patients treated with Lunre plus Camo. That is, there are patients who derive long-term clinical benefit who do not achieve response, seen most clearly in the longest-treated patients so far at the top of the graph, as well as patients who derive long-term benefit but do not have confirmed responses, such as a patient who's fourth from the top with the blue diamond, denoting an unconfirmed response happening late in their treatment course at 20 weeks. Looking at the entire endometrial cancer group, 70% of patients had tumor shrinkage, with 25.9% having more than 30% and achieving a RECIST response. 18.5% had confirmed responses, with the others described experiencing a definitive benefit that we expect to realize in a randomized study that Maria will expand on shortly. Responders here include one patient with a complete response, others having a partial response, and one other who had all of her measured lesions resolve. As you can see on the spider plot on the right, tumor shrinkage or stabilization was quite durable in patients with response durations of up to 30 weeks. The activity seen was observed across all three genotypes and across all the high-risk histologies, including carcinosarcoma. I'm now going to transition to platinum-resistant ovarian cancer, starting with our patient profile. We treated 24 patients with Lunre plus Camo. This likewise was a heavily pretreated group, with more than 50% having received our combination as fourth-line or later therapy, and all, per protocol inclusion criteria, were either platinum-resistant or ineligible. Nearly half had prior PARP inhibitor treatment. The majority were serous tumors, and the remainder were high-risk histologies, with all having p53 mutations. As expected, almost 90% of our ovarian cancer tumors harbored a CCNE alteration, with the remaining tumors harboring alterations of our other genes of interest. Here we show the time on treatment and timing of response for patients with platinum-resistant ovarian cancer. The percentage of patients without progression at the six-month time point is 45%. As shown in the table, the percentage of patients who had 16 weeks without progression or had a response defined by RECIST was 79%. The data will continue to mature as nearly 30% remain on treatment, and four patients recently started and did not yet have their first scan as of the data cutoff. Again, we see a unique pattern of benefit in patients treated with Lunre plus Camo, where some of the patients with long-term benefit do not have RECIST responses, and some patients with RECIST responses occurred late, including after the 16-week time point. Lastly, benefit was seen across serous, colored in green, and non-serous histologies shown in gray. And these histologies are often excluded from ovarian cancer trials, such as those for mirvetuximab soravtansine or CDK2 inhibitors. This again shows not only are we seeing benefit, but we are seeing benefit across the most difficult-to-treat patients. 75% of platinum-resistant ovarian cancer patients had tumor shrinkage, with 37.5% having more than 30% shrinkage and achieving a response. Four of these patients had a confirmed response, while five were unconfirmed. Of that group, two of the most recent ones are pending confirmation. While most patients had CCNE1 alterations, we documented a response also in a patient with an FBXW7 alteration. As you can see on the spider plot on the right, tumor shrinkage or stabilization was quite durable in patients, with response durations of up to approximately 64 weeks. Notably, the activity was seen across all genotypes and all histologies. I would like to summarize endometrial cancer and platinum-resistant ovarian cancer with respect to efficacy parameters in context of our distinctive mode of action. We see a consistent pattern of strong anti-tumor activity and clinical benefit in both tumors, and this guided our pivotal trial design. These are highly pretreated patients. More than 50% of patients who received MYTHIC treatment had received it as a fourth-line of therapy or more, with high-risk tumors defined by presence of p53 mutations, enrollment of adverse histologies such as carcinosarcoma, and the fact that these biomarkers, which, as you heard from Dr. Slomovitz, select for adverse prognosis. The patients are older, underwent frequent pelvic radiation and multiple surgeries, and have very advanced disease. The RECIST-defined response is highly encouraging at 26%-37%, but does not fully convey the full benefit of treatment, with approximately 45% of patients estimated to be progression-free at six months, which is the measure of benefit we will focus on for our pivotal trials. Our differentiated safety profile allows for long-term treatment in these patients. One established way to understand how effective the treatment is, especially for agents for which RECIST does not fully convey the benefit, remember the well-established benefit in CDK4/6 or immuno-oncology drugs or Avastin, is to compare it to the outcome of most recent treatment the patient received. The patient's own medical history serves as a control for what is being observed now. Here, we focus on patients with clear benefit from Lunre- Camo, those who received treatment for longer than five months. We then compared how long they received most recent prior treatment against the duration of treatment with Lunre- Camo. As you can see here, the duration of prior treatment was much shorter than treatment with Lunre- Camo. First, this isn't because these were slow-growing tumors. We know this because Lunre biomarkers select for patients with highly aggressive tumors. The aggressiveness of the tumors is supported by the short time they received the prior therapies. Most of these patients discontinued due to progression, and for most, prior treatment was either chemotherapy or ADC. As you heard, these tumors are chemotherapy resistant. Second, Lunre- Camo is a well-tolerated regimen. Patients received this combination for a long time. A few of the patients in the graph stopped the prior treatment due to toxicity, and the toxicity prevented them from achieving benefit from the treatment. We, along with our investigators, believe that we may have the right solution for this specific subset of endometrial cancer and platinum-resistant ovarian cancer. To build on this idea further, you can see here the time course of tumor shrinkage in both endometrial cancer and PROC for the five patients who came off trial with unconfirmed response. Confirmation requires two consecutive tumor measurements showing shrinkage of more than 30%. These patients profiled here had one tumor measure showing 30% reduction, even if they continued on trial with definitive tumor shrinkage. All these patients derived long-term clinical benefit from Lunre- Camo. Some did not have response confirmation because they had mild fluctuations of the tumor size around the 30% mark. Others had a non-target lesion progression, qualifying them as progressors. Regardless of the reason of not confirming the initial partial response, these patients benefited from treatment, some well beyond six months. The key takeaway here from our pivotal development is that these unconfirmed partial responses will definitely contribute to the primary endpoint, progression-free survival of our planned phase lll registrational trials. Importantly, FDA encouraged us to progress the accelerated approval data package via the randomized evaluation, where unconfirmed responses contribute to the decision, as the decision can be made in context of the concomitant assessment of the control arm. See the footnote below on the right, so that the hypothesis of worse outcome in control arm can be instantly confirmed. The FDA advice was extremely helpful to our eventual phase lll approach, you will see shortly. On this slide, we outline what we see as key points of differentiation between Lunre-Camo and the ADC as an up-and-coming modality. An obvious first difference is the convenience of dosing, with our oral regimen versus ADC being given by vein, requiring the patient to visit the physician's office. Expected lower frequency of overall high-grade toxicities in other areas, while Lunre-Camo would be the preferred option for patients. Lunre- Camo also shows, in general, fewer other toxicities that require intense and urgent attention versus ADCs, such as ocular toxicity, interstitial lung disease, thrombocytopenia, or neutropenia that present as an event frequently consequential or necessitating emergency attention. In short, we believe that this oral well-tolerated combination meets the key needs that Dr. Slomovitz noted in this high unmet need population. With that, I will sum up our observations overall and turn to our clinical path to registration. We have chosen endometrial cancer for a pivotal start in 2025 based on our desire to address second-line therapy. It is definitely an important patient need to have a chemotherapy alternative, especially for the well-defined biomarker subset with chemo resistance. Endometrial cancer is a large, growing, and global unmet need. European and FDA regulatory support with accelerated option for earlier registration in the United States, favorable competitive dynamics, and our belief that we bring this important new option to patients globally in the 2027-2028 timeframe. With that, I'm going to move into our pivotal trial plan. We secured the support of FDA and EMA for our pivotal plan in several steps and achieved three things enabled by the fast track designation. Number one, we agreed the RP2D and the optimized schedule, which was previously disclosed. We agreed the contribution of components upon an efficient trial that will be enrolling shortly, and which is expected to be done very quickly. And the key agreements on the trial design that I like to move to now were also established, including the accelerated approval option we thought. So here you see an overall overview of the endometrial clinical development plan, starting with a small randomized contribution of components trial with futility analysis after nine patients in each arm. This is a 40-patient trial for which the regulators, based on compelling biology and preclinical data, did not require testing of camonsertib alone in this population, given the significant body of data we had in the homologous recombination deficient population. We agreed with FDA that it's sufficient to provide the result of the COC study at the time of accelerated approval submission and obviously inform FDA on the outcome when completed. That is operationally extremely convenient and provides us with an efficient way to start the two-arm pivotal study thereafter. The eligibility criteria for the contribution of components trial and the study assessments are matching those for the planned phase lll trial for ease of interpretation. Finally, the contribution of components trial is now IRB approved, is being executed in more than 25 centers within the EndoMAP study throughout the Alliance Foundation Trials, and enrollment is anticipated to start after the holiday. For our pivotal trial, we are collaborating with the Gynecologic Oncology Group and the ENGOT group in Europe to execute the phase lll study in patients who are receiving second-line therapy and beyond. This approach can support both full approval as well as potentially accelerated approval in the U.S. Here you can see more details of our pivotal study design as agreed in principle with FDA and EMA. We are now in final protocol development time ahead of the end of phase ll meeting and protocol submission to both agencies in first quarter 2025. The eligibility you can see on the left. Progression-free survival will be the primary endpoint of the study, powered for a hazard ratio of 0.65 on this progression-free survival endpoint. For accelerated approval, FDA advice supports the use of response rate with support from the overall efficacy analysis in both arms. This is a key aspect of the design that they are limited on no existing data for overall response rate and progression-free survival data in the control arm. We noted previously the adverse prognosis and chemo resistance in this subset that has no relevant benchmark. We are indeed targeting the chemo resistance subset in an attempt to meet the most urgent need for those patients. Further, our tumor population includes carcinosarcoma, known to have progression-free survival of 1.7 months and overall response rate of 5% in recurrent setting. The fact that we had 20% of carcinosarcomas in the MYTHIC study definitely would affect the known benchmark for endometrial cancer commonly assessed in published studies. For more details on eligibility that I included on the left, I would like to note that we are going to select the tumors by the validated Repare's Partner Foundation Medicine NGS assay, which will form the basis for the eventual companion diagnostic. Now, I will orient you to our expected timeline to full approval and submission. The first step is the contribution of components study, which is ready to start enrollment after the holidays. The interim readout planned for accelerated approval will be based on randomized assessment of response with potential submission expected early in 2027, supported by the completed COC study. The interim analysis plan was discussed with FDA, and as usual, the full statistical analysis plan will be included in the phase lll protocol for the regulatory agencies to agree upon at the time of first quarter 2025 Type B meeting. At that time, we plan to discuss timing of NDA, accelerated approval process, full clinical development strategy, pediatric plans, and others. That sums up our clinical objective, regulatory support, and timelines. Phil Herman now will share the patient opportunity we expect to address and the commercial value we are targeting. Thank you, Maria. As you've heard from Lloyd and Maria, we have selected endometrial cancer as our lead indication for investment. We did so given a more favorable competitive landscape and meaningful commercial potential. Beyond our potential patient impact, what is exciting about our phase lll development plans is the potential for accelerated approval built into the design, offering a potential path for earlier market entry. As we have engaged with oncologists and patients, and as you have heard from Dr. Slomovitz, there is a clear high unmet need in second-line endometrial cancer and a desire for novel agents that offer a differentiated profile from that of chemo or ADCs with the chemo payload. We believe Lunre- Camo is well positioned to meet those needs. Recent approvals of ICI plus chemo in first-line endometrial cancer will lead to the majority of second-line patients having already received ICI and chemo. This creates a compelling opportunity for novel agents in second-line endometrial cancer, given chemo also offers limited efficacy with AEs, and there is little to no data for existing agents and patients who received prior IO. Across the emerging treatment options currently being evaluated for second-line endometrial cancer, we believe Lunre-Camo is well positioned to compete, offering a differentiated value proposition, including a biomarker-driven approach along with the convenience of oral dosing. Second-line endometrial cancer offers a meaningful commercial opportunity with a global potential that we estimate in the range of $900 million-$1.2 billion. We arrived at this range with the following assumptions in mind. Our biomarker population is roughly a third of the overall endometrial cancer population, and this equates to roughly 3,000 second-line endometrial cancer patients in the U.S. We also assumed a duration assumption of five to six months and a net pricing reflective of analog novel agents. This culminates in a global market estimated at twice the U.S. opportunity. We believe Lunre- Camo is positioned favorably to capture a meaningful share of the roughly $1 billion market potential that we see for endometrial cancer. Other Lunre combinations, including and in addition to Camo, offer the potential for a significant life cycle opportunity beyond endometrial cancer. Building off of the Lunre- Camo combination potential of roughly $1 billion, PROC, as you've heard earlier, offers an immediate de-risked life cycle opportunity. The overall ovarian cancer market potential is estimated at roughly $7 billion by 2030, of which our Lunre biomarker population represents roughly 29% or roughly $2 billion of that large overall ovarian market. Lastly, Lunresertib is being evaluated in combination with both FOLFIRI and with WEE1. These combinations could open additional life cycle opportunities in metastatic colorectal cancer, esophageal, and stomach cancers. A market potential of roughly $2.5 billion by 2030 is projected here. With that, I will pass the call to Lloyd for some concluding remarks. Lloyd? Thank you, Phil. To wrap up where we started today, we've achieved proof of concept with our Lunre- Camo combination and are set to enter phase lll trials in 2025. In endometrial cancer, we see the best path to approval and the greatest unmet need. Our registrational plans have been established with both U.S. and EU regulatory support. We intend to start with the endometrial cancer contribution of components trial early in 2025 and then begin our endometrial cancer phase lll pivotal trial in the second half of the year. We are excited to now be able to discuss these data and development plans with external collaborators, with clinicians, and potential financial and strategic partners as we look to begin executing in earnest starting in the new year. I would like to congratulate the team and our clinical collaborators for the tireless work that got us to this key inflection point. Above all, I'd like to thank our trial participants, their families, and support teams for helping make this outcome possible for a future generation of cancer patients. I would like to open the call to questions. Operator, please proceed. Ladies and gentlemen, we will now begin the question and answer session. Should you have a question, please press star followed by the number one on your touch-tone phone. You will hear a prompt that your hand has been raised. Should you wish to decline from the polling process, please press star followed by the number two. If you are using a speakerphone, please make sure you lift your handset before pressing any keys. One moment while we prepare the Q&A roster. Your first question comes from the line of Maxwell Skor from Morgan Stanley. Please go ahead. Great. Thank you. And congratulations on the update. I have one question for the KOL. Given your participation in, it sounds like, a range of clinical trials, what is your view on the individualized dosing schedule? And is it common to leverage this approach in the pivotal trial? And then lastly, if I could, one more. Based on my understanding, the mortality rate is higher among endometrial cancer patients, but the prevalence is also significantly higher. Could you just give us a sense of the percentage of these target mutations among second-line plus endometrial patients? Thank you. Thanks for that question, Max. Brian, I'll hand those off to you, and you can also pull on Maria if you want to bring some additional color. Yeah, no, thank you for that. I'll start the—and I apologize, I know there's a couple of points to the question there. But as far as the molecular profiling, I think in the second-line setting or greater, we'll probably see a higher proportion of the patients having this biomarker positive profile just because we know that this molecular signature portends a worse prognosis, not just a shorter duration of response, but a higher likelihood of recurrences and things like that. So given the percentage in earlier lines, the better patients, the ones that don't recur, will further concentrate the pool that have a higher biomarker proportion. As far as we think that the dose optimization was successful, we're satisfied now with the overall safety profile. I think the regulators, the FDA, was aligned with the plan that we have as far as the dose optimization. We're not changing the dose, only the scheduling. I think that it's going to be aligned with the, to your point, with the phase lll registrational trial. I'm comfortable with that. It's a similar approach that we've seen in some of the, not only in endometrial cancer, but in other gynecologic tumors that proceed with registration approval from PARP inhibitors and things like that. Maria, anything to add? No, we are getting a lot of questions on that. And just like Dr. Slomovitz mentioned, everybody is comfortable. The most important item is that the dose remains, and there are very clear and simple instructions when to change the dose. And actually, we are changing the dose to prevent the anemia rather than treat the anemia. So this is a very patient-friendly approach. Thanks, Maria. Thank you. Thanks, Dr. Slomovitz. Next question. Your next question comes from the line of Marc Frahm from TD Cowen. Please go ahead. Questions. One, just with the EndoMAP trial determining the contribution of components, do you feel like you need to see any of the early data response data coming out of there, kind of just making sure it's tracking in line with expectations before you actually dose the first patient in phase lll, or do you view these trials as kind of completely independent from each other? And then on that phase lll design, just the responses seem maybe a bit more prominent in the serous subtype, although I understand those patients maybe do maybe not quite as bad as some of the other subtypes. But can you speak to the decision to enroll a broad population versus maybe just focusing in on specific subsets of endometrial? So thanks for that question, Marc. And maybe I'll answer the first one, and Maria or Dr. Slomovitz can take the second. So the question in the first, Marc, is very simple. And the only purpose of the COC is just to satisfy in a really efficient and fast way the performance of Lunre alone versus a Lunre and Camo combo. So we're not looking for anything else. The futility is built in at nine patients on each arm. So, given that we need, I think it's three scans following that, the probability is even the best of cases we'll enroll more than nine patients, but not necessarily 20 in each arm. And the goal is just to get an answer rapidly. I kind of view it as a real belt and suspenders approach by the FDA that we expected and the street expected. And I think the key takeaway here is that this is at the lowest end of where the street was expecting we would have to do a contribution of components undertaking for the FDA. It wasn't even required by the EMA at all. And I note, as Maria covered earlier, we don't have to do any COC for Camonsertib given how much work we've done there. On the second question, I'll pass it off to Dr. Slomovitz. Yeah, hi, thanks for that. As far as the uterine serous, they're actually some of the more aggressive players. So again, I think as we get into later lines of therapy, we're going to see more uterine serous carcinosarcomas that portend a worse prognosis, even the poorly differentiated endometrioid histology. But in general, we wanted to leave it into a broad group in order to best determine the role of the therapy in the entire group of endometrial cancer patients. That's going to be weeded out, obviously, in the biomarker profile. Thanks, Dr. Slomovitz. Maria, did you want to add anything on that point? No, we have data, which we very carefully generated in all the subsets. We had a lot of discussion whether we should pre-select the patients and be sort of afraid of the more aggressive histology. And we made the decision not to be afraid, and it was the right decision because we do have multiple responses in carcinosarcoma and even clear cell. So it is all about the biomarker and less so about the histology. Plus, the unmet need is in these more aggressive tumors. Thanks, Maria. Let's go to the next question. Your next question is from the line of Joe Catanzaro from Piper Sandler. Your line is now open. Hey, guys. Thanks for taking my questions. Maybe first one for me on the planned phase lll and the control arm options. Maria, maybe you tried to answer it, and maybe you said there's no good benchmarks, but wondering if you could just speak to expectations of how those control arm options perform in this biomarker-selected population. And then with regard to the accelerated approval opportunity based on response rate, what is your understanding of the response rate delta that you would need to show to pursue that path? Thanks. And I may have a follow-up. Yeah, thanks for those questions, Joe. And what I'm going to do is I'm going to ask Dr. Slomovitz to answer the first and I think very important question, given how new the first-line standard of care is for endometrial cancer, what we expect for that population. And then I'll let Maria answer the questions on the trial design. Dr. Slomovitz? Yeah, no, thanks for that. And actually, the control arm here has been really based on control arms in previous trials, particularly KEYNOTE-775, which was looked at weekly paclitaxel Adriamycin. And that's what gives Len/ Pem its approval. I think in all else being equal, the response rates would be about 10%-15% and the progression-free survival about three to four, maybe even five months. But given this higher risk population, I would suspect that our response rates of the control arm would be about 10% and maybe about three months PFS. So definitely an area of opportunity that needs to be improved upon the unmet need. Thank you for that question. Thanks, Dr. Slomovitz. And Maria, in terms of Joe's question on the trial design, do you want to comment there? Sure. So we had a discussion with FDA on this topic, and we made an assumption consistent with what you heard from Dr. Slomovitz and consistent with what we are hearing from investigators who are actually surprised about the degree of responses that we see in our population. So we assumed about 10%, 10%-12% in the control arm. And then we would like to improve it at least triple. So the response rate needs to be in the range of 25, which is actually the range that we are seeing. So the delta for the response will be 15%-20% for the accelerated approval. It needs to be clinically significant. We are not planning to increase from 10%-15%. Okay, great. That's all helpful. Thanks for taking my questions. Let's get to the next question. Your next question comes from the line of Chris Shibutani from Goldman Sachs. Please go ahead. Hi, this is Kevin on for Chris. Congrats on the update, and thanks for taking our questions. Just a couple of quick ones, whether or not you looked at efficacy by dosing regimen and by background hemoglobin for the data update today. And then for Dr. Slomovitz, where do you see, as you look at the emerging profiles of ADCs here in an adverse event profile, how do you see that comparing to the profile that we see with this combination? Thanks. So why don't we, Maria, why don't you address the first question on just what we were seeing in terms of hemoglobin levels associated with responses? And then we'll turn the latter question to Dr. Slomovitz. Right. So just to clarify, the data that we presented were only in patients who are the candidates for the same profile as our patients for a phase lll study. So these were patients with optimized dose. We did present at ENA, which is in October. We presented an answer to this very question, whether the decrease in intensity of dosing, which means the incorporation of the one-week off in patients who have low hemoglobin at entry, matters. And to the best of our assessment, in context of a non-randomized study, we do not believe that there is any indication that the patients are losing efficacy. So the poster is available, but we do not believe that there is any detriment in efficacy because this is about the dose and the hit to the tumor in the right moment of the cell cycle. Thanks, Maria. And Dr. Slomovitz on the latter question? Yeah, that's a great question, Kevin. Thanks for that. One thing I want to say about ADCs, I like ADCs. I'm doing a lot of studies in ADCs. But one thing that people aren't realizing, it's not HER2 versus TROP2 versus B7-H4. It's the kill. Most of the ADCs have a TOPO1 kill. And they work pretty well. The problem is there's no data of TOPO1 after TOPO1. So most likely, the ADCs are going to be one and done. Now, I like this registrational strategy because it allows for one to three priors mandating HER2 ADC if there's three plus HER2, but also allowing for an ADC. So I don't really think that filling this unmet need is a comparison versus ADCs. It's an opportunity to, what if one of the first-line or adjuvant ADC trials works, we'll still need something here in the second line. So I'm not as concerned about that. Specifically about the AE profile, I think it's safe. This regimen seems to be safe. I like the dose optimization decreasing the anemia. The anemia is the number one AE seen here. Interestingly, no thrombocytopenia, which was. It's nice for our patients. Not really a direct head-to-head comparison, but there is the AE profile of ADCs is not benign. Obviously, they were worrying about the ILD that we see and other side effects. I think ADCs are an important part of what we're going to do for our patients in endometrial cancer. I'm not sure if they're going to be before or after this or even earlier lines, but I'm not worried about the head-to-head profile. Thank you for that. That's really helpful. Thanks. Take our next question. Your next question is from the line of Mr. Charles Zhu from LifeSci Capital. Your line is now open. Good evening, everyone. Thanks for taking the questions and for providing this update. Looking at the baseline characteristics of the phase lll eligibility criteria as well as the update right here, it looks like for the phase lll, you'll restrict it to one to three prior lines, but all patients would have had prior ICI and platinum. Could you comment based on the current data set and maybe also from Dr. Slomovitz's experience as well, by the degree to which some of these efficacy headline figures could potentially change as you move earlier in line of therapy? And to what degree could this also be offset if you're moving from, let's call it, 78% receiving prior ICI to 100% receiving prior ICI? Thank you. Thanks for that question, Charles. I'm going to hand that to Dr. Slomovitz to give us his perspective. Yeah, no, thanks for that. And it's an important question. We do feel, based on FDA approvals, that checkpoint inhibitors are effective in all women with endometrial cancer, right? In the deficient mismatch repair group, clearly, the single agent act of checkpoint inhibitors in the second line on the KEYNOTE-158 study was 48%. In the first-line trials, the RUBY trial was as low as a hazard ratio of 0.28 when given with chemotherapy. In the pMMR as well, we have broad indications from RUBY and from GY018 allowing for pembrolizumab and dostarlimab to be given to all comers, all types of endometrial cancers, including the pMMR in the first-line setting. Right now, for those patients that don't receive IO in the first-line setting, we rely on the data from, I mentioned earlier, KEYNOTE-775, which demonstrated an overall survival advantage when compared to, again, the control arm here, weekly paclitaxel or Adriamycin. I think it's a good point of what the efficacy will be when it goes from 70% or so to 100% or so. It's never going to go to 100% of usage because there are patients who do have contraindications, autoimmune disease, as far as they can't get immune checkpoint inhibitors. But in general, I don't foresee the numbers, the effectiveness going up any higher with more widespread use just because a lot of the people who aren't getting it now are the pMMR subgroups. And we've also seen that comparing it to ovarian cancer, there wasn't an immediate uptake of PARP inhibitors and BRCA-mutated ovarian cancer patients. That took a while. So I see as the uptake does get higher, though, I don't see a difference in efficacy. Thank you. Thanks, Dr. Slomovitz. Let's take our next question. Your next question comes from the line of Ben Burnett from Stifel. Please go ahead. Hey, great. Thanks so much. And congrats on these data. I wanted to ask about the contribution of components trial that's being contemplated here in EndoMAP. It looks like there's, if I read the slides right, there's an interim futility analysis. I guess, what are the mechanics here and when will futility be assessed? Yeah, so I can take that one. Thanks for the question. It's really straightforward. And this is just a trial that the FDA has asked us to do to answer a very simple question, which is, can we be certain that the Lunre-Camo combo has a distinct efficacy profile from Lunre alone? We knew from almost two years of monotherapy work that we just didn't see a signal. We had one responder, and I think it was close to 60 patients on monotherapy at RP2D. So what the futility is designed to do is just look at nine patients on each of Lunre alone and Lunre plus Camo, and just answer the question, do we see separation? And although the futility is at nine patients, because we need three scans for all the patients, we're likely to enroll something north of nine and south of 20 in each arm to get our answer. But based on our phase l, I think we're highly confident that this will be a small and really efficient trial to answer a really straightforward question from the regulator. Okay. That's super clear. Thank you for that. If I could just squeeze in one other question. So just around the toxicity profile that you outlined in, I believe it's slide 23, clearly achieved what you set out to achieve. You've lowered grade three anemia substantially. Just curious, when there was grade three anemia, looks like one way that was managed was through dose modifications. Any color around that? Were both drugs modified, or was the approach to modify one agent versus the other? So again, yeah. Maria, why don't you go ahead? We can answer this really briefly in the time we have. So the main modification, the whole concept of the dose optimization was to prevent the anemia, as I said before. So the main mechanism of doing it was to incorporate the break to give the marrow recovery. We incorporated it either if the patient started with low hemoglobin or if the patient started with high hemoglobin, but the hemoglobin dropped very fast, like 2 grams, then the patient got the break. So it was not really about one drug or another. It is about the synergistic effect because the anemia in ATR is very low. It's only 11%. And the anemia in PKMYT1 is like 3%. So it's not about each of the drugs. It is about the combined effect of the drug. It works better in the tumor, but it also causes the marrow tox. But I want to just pull the lens back. Thank you, Maria. And just make the most critical point here, which is that with the optimized dosing, as we've discussed earlier, we didn't see any meaningful change in the overall efficacy, but we've brought the anemia rates down to something on the order of 27% and have derived an overall tolerability safety tox profile that, as Dr. Slomovitz and others have noted, is incredibly competitive and demanded by these women who want alternatives to chemo, which comes with black box warnings and real tolerability and accessibility challenges. So I think we've put to bed any question about anemia. And we've drawn praise from the regulator and from our clinical collaborators for how we did it in a really elegant way. Very clear. Thanks so much. Thanks. Next question. Your last question is from the line of Mr. David Martin from Bloom Burton. Your line is now open. Yes. Thanks for taking my questions and congrats on the data. I may have missed it, but linked to one of the earlier questions, in these expansion cohorts, did you see differences in response rate and PFS among the patients who received prior checkpoint inhibitor or not? David, I love it. Thank you for asking the question that we can answer most simply. No, we did not. Okay. And second question, quickly, if I could. Have you identified any other factors that influence the response or not to the combo in the expansion cohorts that you could take into phase lll as far as inclusion criteria? Again, not really. And I think that while we were satisfied with the total number of patients we have here, it's still on the order of 50 total patients, roughly half in each of endometrial and PROC. So there's only so much slicing and dicing you can do. But I think we have the story incredibly clearly here, which is that we have in front of us now a combination that has met a clear proof of concept. We're beating the current second-line standard of care. We've got a differentiated safety profile with competitive emerging therapies. And we're ready to move it into a registrational phase lll trial. As Dr. Slomovitz and others have said today, there's just this urgent and growing need for better therapies for these patients. And we don't see the need to slice and dice this endlessly because the high-level answer is, I think, very obvious. And we're excited to move ahead. Yeah, thanks. There are no further questions at this time. So I'd like to turn the call over to Lloyd Segal for closing remarks. Sir, please go ahead. Again, thanks for extending a little bit of time today. We've gone over the hour we had, but I am just thrilled for the part of the team and above all for the patients that we have been aiming to prove we can serve with this combination, and we're excited to turn the page to be a registrational company aiming to deliver this important Lunre-Camo combination in endometrial tumors starting next year. I want to thank Dr. Slomovitz, who's actually in the U.K., and it's late at night for him. He has been, and we hope will continue to be a core advisor along with the group at GOG in getting started in this trial work and delivering with a company now focused on an NDA in the 2027-2028 filing timeframe. I thank you all for taking the time with us and wish you a good evening. Ladies and gentlemen, this concludes today's conference call. Thank you very much for your participation. You may now disconnect.