Thank you, operator, and welcome to today's Acrivon R&D and Investor Webcast. My name is Adam Levy, and I'm SVP and Head of Investor Relations at Acrivon. Joining on the webcast today from the company will be Peter Blume-Jensen, our CEO, President, Founder, and Chairperson; Kristina Masson, our Co-Founder and EVP Business Operations, and President of the company's research subsidiary, Acrivon AB, located in Medicon Village, Sweden; Rasmus Holm-Jorgensen, our Chief Financial Officer; and Eric Gamelin, our Chief Development Officer. We are also pleased that Dr. Ramez Eskander will join us on the webcast. He's currently running around at ESMO, but will be joining us shortly. Dr. Eskander is a leading gynecologic oncologist and assistant professor of Obstetrics, Gynecology, and Reproductive Sciences at the University of California, San Diego. Dr. Eskander has authored and co-authored many peer-reviewed articles, several book chapters, and is the co-editor of Gynecologic Oncology: A Pocket Book. He speaks frequently at annual medical conferences, and his work has been published in journals such as the New England Journal of Medicine, Journal of Clinical Oncology, Obstetrics and Gynecology, Gynecologic Oncology, and Clinical Cancer Research, among others. In two thousand and fifteen, he was awarded the Society of Gynecologic Oncology's John L. Lewis Jr. Presidential Award for Most Influential Scientific Paper. Dr. Eskander is the lead author on the two thousand and twenty-three New England Journal of Medicine paper on the use of pembrolizumab and chemotherapy in frontline endometrial cancer. As a reminder, during this call, we will make certain statements that are considered forward-looking statements within the meaning of the Private Securities Litigation Reform Act of nineteen ninety-five, including expressed or implied statements regarding our strategy, business plans, and objectives, the expected therapeutic and clinical benefits of our product candidates, and the potential of our platform and our product candidates, and progress in timing and execution of our clinical trials. Such forward-looking statements are not guarantees of future performance, and therefore, you should not put undue reliance on them. These statements are subject to numerous risks and uncertainties that could cause actual results to differ materially from what we expect. I refer you to the SEC filings on our website for a discussion of the risk factors that could cause our actual results to differ materially from those discussed today. We are excited today to share details and commentary on several important positive updates, as described in the press release we issued earlier today. You can access the press release from today, the slides we are reviewing, and the replay of this event by going to the Investor Relations section of our website. At the end of the webcast, we will have a Q&A session. To submit questions at any time, simply use the text bar at the bottom of the webcast screen. With that, I am pleased to hand the call over to Peter. Thank you so much, Adam, and welcome everyone. I am very, very excited to present today for you our recent data in endometrial cancer, and we'll get right at it. We have a packed schedule. As Adam mentioned, there are forward-looking statements as always, so please be aware of that. Here you see our agenda for today. I'll give a brief company overview and of the platform AP3 Acrivon Predictive Precision Proteomics. We will then go through the clinical data update on the prospectively designed registrational intent ACR368 phase II trial in endometrial cancer. We'll then give a brief status update on ACR2316, which is now cleared ahead of schedule for phase I. Finally, introduce our version two of the AP3 Interactome, which is our real-time computational science, machine learning-enabled platform, where we help store and analyze all our proprietary AP3 data. You can look at a comprehensive corporate deck on our website, acrivon.com. As you all know, we are a platform company, and we aim to transform precision medicine in the sense that we are founded on the two-decades-old concept of measuring and identifying perturbed dysregulated signaling that causes, is causally involved in disease, initially focused on oncology, but obviously with implications and applications outside. As we have already publicly disclosed, our next target will be in the autoimmune inflammatory area. So instead of looking more traditionally at genetic or transcriptomic alterations and association with disease and prediction of, or indirect inference and, and prediction of drug efficacy, we are directly identifying, with high-resolution mass spectrometry, the disease-driving pathways, and we can directly measure unbiased, how exactly any compound acts on that signaling network, regardless modality. It is at very high resolution. We are having a world-leading resolution at the moment, and have over one hundred and fifty thousand quantified mapped phosphorylation sites. And regardless mechanism of action, we have found that any compound, on average, will regulate statistically significantly about a third, phospho sites, and they are a measure of activity states of signaling pathways. And that is the differentiator from genetics and transcriptomics and other approaches to precision medicine. One can gauge and measure the activity state of what drives the underlying disease and directly match it with the drug mechanism of action. And Acrivon means exact or accurate and symbolizes that high-resolution ability to see exactly what a drug does. We can use it to optimize drugs, as we've done for ACR2316. We can use it to identify actionable predictive biomarkers, as we've done for ACR368, now in our registrational intent phase II trial. And we can use it to uncover resistance mechanisms and also do indication finding, which is how we identified endometrial cancer as a predicted particular sensitive tumor type. So with that, the applications are really, as I mentioned, listed here, so I will not really spend time on this. But we do think we are addressing some of the critical challenges in our industry, which is to identify compounds, especially in oncology, that are aiming for monotherapy clinical development, and hence aiming for the accelerated pathway. And you can see to the right the approach to that for each of these. And very importantly, the ability to identify patient responders obviously is the holy grail in precision medicine. All this is enabled by our machine learning-enabled AP3 platform, and very importantly, it has a lot of actionability. Here you see a snapshot of our pipeline. To the right, you have the catalyst that we have declared earlier this year. We've kept them for now, but hopefully this enables everyone to gauge our timeline progression here. Today, we are focused on endometrial cancer, for which we have a Fast Track designation for monotherapy in our Simon 2-stage Registrational Intent phase II trial. You can see our other tumor types, enrollment, and dosing is ongoing. We are going full speed in platinum-resistant ovarian cancer and bladder cancer as well. This is under one master guidance protocol, cleared by FDA, a year and a half ago or so. Further down, you see our dual WEE1 PKMYT1 inhibitor, specifically developed for superior single-agent activity and to achieve a very significant enhancement of the therapeutic index using our AP3 platform. We are now further ahead of schedule and have, the phase I activated. We have several sites activated as we speak, and, plan to have first in-human dosing in Q4 2024. And finally, as you know, we are applying the AP3 platform for both target validation and additional drug discovery programs. We have also, as we have listed earlier, always kept an option to initiate trials in squamous cell cancers, where there is proven durable single-agent activity of ACR368 as well. And Dr. Chung at Moffitt Cancer Center has initiated an investigator-initiated trial there in head and neck cancer. So let's jump right into it. We currently, this very moment, have a poster on exhibit, on display, being presented by our CMO and our radiologist from MGH, Dr. Jean-Marie Cuillerot and Bill Bradley. It is the interim data from the Registrational Intent phase II clinical trial in endometrial cancer that is on displays there, and that we are gonna discuss further today. This poster is available on our website as well as we speak. A real quick reminder of the platform deliverables, applications. These are all very importantly proven applications. Of course, one can argue that the bottom is the outcome of this and obviously being proven. We have identified predicted biomarkers. We have validated them based on our initial data several times in the ongoing trials. These are drug-tailored patient selection tests called OncoSignature test. We have an ACR368 OncoSignature test that is used for prospective patient selection, predicting individual patient sensitivity to the drug. We've used it to screen, and we call it AP3 indication finding, and that was how we identified endometrial cancer. We have many, many publications on uncovering resistance mechanisms. It's a very low-hanging fruit. And those resistance mechanisms that are drug-induced can be leveraged to optimize a drug for single-agent activity by simply building in, in addition to the on-target activity, also the ability to quench the dominant resistance mechanisms. And that's exactly what we did with 2316, hence achieving a very, very significant boost in potency and anti-tumor activity, resulting in complete regression across the tumor mouse models we have studied to date at much, much lower doses than the clinical comparators. And obviously, we identify a wealth of biomarkers. This is completely outdated now. I think we are at around thirty-five to forty thousand, statistically significantly regulated, PD markers in every single experiment, we run. And today, as I mentioned, we are gonna talk about the, performance of the OncoSignature in our ongoing trial and, about our 2316 asset and how we are applying that in the clinic. The platform is a two-step platform. We have pioneered the underlying two technologies. Mass spectrometry phospho-based phospho-proteomics is actually pioneered by Acrivon's co-founder, primarily Jesper Olsen, who runs the Novo Nordisk Foundation Center for Protein Research in Copenhagen and is a long-standing collaborator of ours, actually for many decades now... and we had the first compound proof of concept for, using such a method to identify overlapping and unique, predicted biomarkers, back in the days. We also pioneered the quantitative multiplex biomarker platform that is the AP3 on which the OncoSignature tests are run. This was done from 2010 to 2015. The team has worked together since 2010, just focused on this approach. And while it is an expert system, we have the original launch of a test was the prostate cancer test included under NCCN guidelines in 2015, which was a much more complicated eight-marker test. We have now leveraged all our lessons learned into simplifying this, so we are generating low-complexity tests. Typically, it's three-marker test, and as an example here, looking at pretreated tumor biopsies from high-grade serous ovarian cancer patients, where you see on the left, tumor epithelium in green, and on the right, the biomarkers in red. We measure them only in the region of interest. That makes it very accurate, and sensitive. And the three biomarkers, just to remind everyone, are built up the same way. They are function-based biomarkers. They are assembled, derived from this systems data, through a functional definition of three orthogonal biomarkers, that when they are all present, like is the case in this patient tumor, we can conclude the tumor depends. It's upregulated for the drug target signaling axis that the drug acts on, and it depends, in this case, on the CHEK1/2-mediated DNA repair. This is drug target activity. We measure here, this is very dedicated signaling and DDR, DNA damage repair, driven by CHEK1, CHEK2, not by other DDR target. It's a so-called consensus site for CHEK1, CHEK2, that correlates with and is required for that DNA repair. And this here is a so-called premature DNA replication driver. It's a protein that drives, forces cells through the cell cycle, hence necessitating the need for DNA repair to avoid a genomic catastrophe. When you disrupt that, you actually end up with that proapoptotic mitotic catastrophe that we see with such inhibitors. ACR-368 was in-licensed exclusively from Eli Lilly with worldwide rights. It was originally discovered by Array. It is very importantly, not only a CHEK1 inhibitor, but also a CHEK2 inhibitor, as far as we know, the only well-proven single agent potently active CHEK inhibitor to date that has been in the clinic. And we believe that this is what enables our approach with the current registrational intent trials. At the time of in-licensing, you can see some of the criteria that was the basis for in-licensing, which included, we wanted to see that there was durable monotherapy activity in solid cancers, and some of those data that were based on the Lilly-sponsored data are shown here. There's accordingly a huge drug safety database that we could lean up against. Remember, we got clearance in twenty-eight days from FDA for our registrational intent phase II trial in not only ovarian cancer, but also endometrial and bladder, the predicted tumor types. But the only thing that was missing was a method to identify the patient responders. Lilly had concluded in all their publications that there was a need for an alternative biomarker method beyond genetics-based methods. As mentioned earlier, we can use our AP3 platform and OncoSignature test for indication, screening, and finding. And again, each column here is each of the three biomarkers, one, two, and three. Red indicates the level of biomarker for each of these three, and when all three are elevated, we have the requirement fulfilled for believing that the tumor is dependent on the drug. And we had, at the time, back in the days, we showed Eli Lilly that we predicted that endometrial cancer would be a particularly sensitive tumor type. And we could even kind of predict the proportion of responders just based on commercially available tumor tissues, and you can see, call it a third here, based on, on this screen of commercially available samples. Each line is a patient sample. And we went on after this prediction. This is actually the real human tumors. There's an extreme addiction. Every single nucleus here in this tumor is upregulated for the CHK1/2 axis, and there's massive DNA repair going on. And we can verify that then in preclinical studies, in this case, we use patient-derived xenograft models, genetically non-modified, and we could show that indeed, a fraction were completely sensitive and others, less so to the drug, and could even show that we, in a blind and prospective design manner, could predict which ones are the responders. So based on all this and some recent developments in the standard of care for endometrial, especially high-grade, advanced stage endometrial cancer, we think there's a real opportunity that has opened up for a very attractive indication, and that is in the second line post-anti-PD-1. Our current target indication is high-grade, locally advanced or metastatic recurrent endometrial cancer, and it must have recurred after prior chemo and immune checkpoint inhibitor therapy. It is also completely irrespective of molecular, whether it's MMR, P53, or other alterations, and we're also agnostic to the subtype. There are four predominant subtypes: serous, endometrioid, clear cell, and carcinosarcoma, a very aggressive subtype of high-grade endometrial cancer. Based on the standard of care that has changed recently, driven by key opinion leaders like Dr. Eskander on our call and Dr. Mansoor Raza Mirza, PD-1, anti-PD-1 therapy has moved up frontline together with chemo, six cycles every three weeks, followed by 14 cycles of immune checkpoint inhibitor-only pembrolizumab or dostarlimab, and that is every six weeks. And the only way we now can assess the standard of care in second line is really looking at the prior second-line standard of care, which was pembrolizumab and lenvatinib, where there was a control arm in that New England Journal of Medicine study published by Vicky Makker et al. And that would tell us that the best chemo performance standard of care there is about 15% response rate, with a PFS of about just under four months. In the third line, we have the original everolimus paper that showed just about 10% and even shorter PFS. So we believe that an attractive target product full profile would be the achievement of about 25% or higher response rate, with a lower bound above 20% and a duration of response of approaching six months. Just to remind you of our trial, which is shown here, you can see here we have our Simon 2-stage design for OncoSignature-positive patients. About a third of the three tumor types, endometrial, ovarian, and bladder, are positive for the biomarkers, and they get single-agent ACR368 therapy in our registrational intent trials. We have the OncoSignature negative, where we used our AP3 platform to uncover a way, a method to sensitize an unknown proportion of patients to ACR368. We see an OncoSignature upregulation. We have presented poster data on that from animal models, rodent models, cell lines at the TRI meeting and ACR last year. We now are using that to give a very, very low dose of gemcitabine together with ACR368, to explore in a phase 1b/2 trial what proportion might be sensitized. At the April Corporate R&D event, we had a total of 18 safety-evaluable patients, and those that were efficacy-evaluable for RECIST 1.1, defined as having had at least one on-treatment scan, was 10. We're now more than double the patients, but it's not so much the patient numbers as, as the fact that we now have very statistically significant conclusions to draw on our trial. Very importantly, as a control for us, you can see the prediction done years ago in our preclinical human tumor sample screening is holding up here. We have about a third of patients that are OncoSignature-positive. We, as I mentioned, have the enrollment of ovarian and bladder continuing, and we will update on that at a future date. The demographics and subject disposition is shown here for the 35 safety-evaluable patients. You can see that the median age is about mid-sixties. We have in that still relatively limited number, we are pleased to see that we also have representation from Black and African Americans and Asians. And we have a good coverage of most subtypes histopathological subtypes. And very importantly there is a requirement for having had progressed on prior anti-PD-1 therapy. There was one that was ineligible for that therapy, as you can see, but otherwise, all have had it. And I think that's what we need to say about this. So here is some of the key results summarized, and again, we are comparing with the progress and maturation since the April R&D event, which is really just a few months ago. It is a little unusual to have a subsequent interim update so soon thereafter, but it is really because the data are starting to come together very nicely that we wanted to share that publicly. Our prospective OncoSignature is now further validated with a segregation between the OncoSignature-positive and the OncoSignature-negative responders with a p-value on third decimal. At the time, if you remember, we had also a p-value on segregation in both ovarian and endometrial combined, but actually, at the time, we did not quite have statistical significance yet for the endometrial cancer only. We also now have, very important, the overall response rate we reported then, 60%, is holding up very well, I should say. And we now have a lower bound of the confidence interval that's really starting becoming very meaningful, even though it's a small patient number of 30.4. But very importantly, it's the 23 patients total that we are able to assess the performance of the OncoSignature on, not just the 8 patients, and it's a combined dataset that allow us to make conclusions about p-values. Also, all the responders are still on therapy at the time of data cutoff, and as you can see, the duration of response has not yet been reached, you'll see that on later slides, and is now currently six months versus about two months at the R&D event. Here you see the deep responses in a waterfall plot of the endometrial cancers patients that are OncoSignature-positive. These are all confirmed responders, which means they've had at least two on-treatment imaging scans that showed a RECIST response, and each scan is with about two months between each other, and so you can see on the right that the responses tend to occur early... and are durable, and we are looking very much forward to update you on the duration of response at a later time point. Here you have a little more deep insight into the different types of patients in these, amongst these OncoSignature positive. It's maybe a little busy, but column one is the histological subtype represented in the OncoSignature positive. We have the MMR status in column two, we have the P53 status in column three, and we have the best overall response on the last prior line in column four, and then we have the best overall response in the current trial here. And as you can see, we have a good representation of different subtypes. We have, so far, which is very consistent with the frequency, about 75%, maybe up to 80%, are pMMR versus dMMR, and we think that's pretty well represented here. You can see four pMMR patients here. Obviously, our OncoSignature is agnostic to MMR and molecular status, so we expect it to work equally well, and we actually have a complete confirmed responder in the, that is dMMR, in the OncoSignature negative. We'll show you that later. So it's agnostic to that, but we think this is simply a reflection of a frequency, as is the fact that there's more P53 mutated than wild type tumors here represented as well in the responders. And most strikingly, as you can see, we have three progressive disease as best response. Not only have they progressed on prior PD-1, but the best response was actually progressive disease for three of the five patients. One was stable disease, and only one was a PR, and these are the ones that we see our responses in. So durable responses in patients who all have progressed and where most of them had a best overall response of PD. Most of them are pMMR and P53 mutant, consistent with prevalence, and importantly, our OncoSignature is independent of molecular and histological subtype. Here you can see a little more details for each of the eight patients, and you have here the best overall response and last prior line, and you can see what they were. Where it says, chemo only here and with Doxil here, those patients have had prior PD-1, and you see the prior lines here. So there's only one resistant response amongst the six patients with a best overall response data from last prior line of therapy. Here's an example of the responses. Some of these are very well-established tumor here, tumors here. You're looking images from our centralized readers. Here you see the inferior vagina, where you see it's very established tumors here that we are having clinical activity on. And again, the responses tend to occur very, very rapidly overall. In the exploratory phase 1b/2 arm of this trial in the three tumor types, we are seeing signs of sensitization by ultra-low dose of gem. And again, remember, the recommended phase 2 dose that we declared five months ago or so, at 10 milligrams per square meter, is about 1-1.5% of standard doses of gemcitabine. So it is ultra-low doses of gemcitabine, and our data, AP3-based data, suggests that we have a sensitization to ACR368. With that, you can see we are achieving what we think is an initial disease control that is a reflection of that. In fact, if we didn't have low-dose gem, we think these would pretty much be completely non-responsive to ACR368 alone, based on all the data we have. We also have, as I mentioned, a complete confirmed responder, and we have an unconfirmed PR, as well, and then we have six stable disease, on this and this. And exactly how we are gonna leverage this, we have different ideas about, and I'll talk a little bit about that, later. The safety profile, very importantly, as I mentioned, is, first of all, established on the basis of a huge robust safety database from Eli Lilly, and now we have had several hundred patients treated ourselves, and, we think it's very encouraging. We see only transient, reversible, typical mechanism-based DDR hematological adverse events. These are the ones that tend to be reversible and is simply a reflection of that we have dividing myeloid precursor cells in the bone marrow that do have a synchronized dependency on DNA repair. So it is, in essence, a PD marker, but very importantly, they are reversible. In stark contrast to chemotherapeutic chemotherapeutics and ADCs, where we have more long-lasting, irreversible myelosuppression. Also, we have a notable absence of the typical neuropathies and liver toxicities and, of course, pneumonitis and other things that have been seen with ADCs. And so we are very pleased with that. This is on the basis of encouraging usage of G-CSF together with the ACR368 dosing every fourteen days. That makes it easy to do, and it is mandated to give a prophylactic G-CSF in the combination arm. We have conducted a third-party blinded KOL market research that really seems to underscore the enormous opportunity for ACR368. And you can see some numbers here. It is a tumor type of increasing incidence, it's estimated to be about 1-3% per year. And the prevalence is very, very significant, just under a million patients in the U.S., about 68,000 new cases every year. And it is the high-grade that accounts for absolute vast majority of endometrial cancer deaths each year. The second line now represents a high unmet need. It's based on the market research and looking at mortality of about 13,000 every year, et cetera. It is estimated that the new cases for high-grade recurrent endometrial cancer is about 30,000 per year, and 90% or so of those are believed to progress to second-line therapy. We talked about the recent frontline approval of anti-PD-1 with chemo, followed by an anti-PD-1 only, which has reduced or almost eliminated because of the label is for all comers, pMMR and dMMR, Pembro and lenvatinib is second-line option, which means you're left with chemo. Once you've been on anti-PD-1, you typically, based on this market research, will wanna wait towards nine months before you would try to put them on again. Of course, there's variation in that thinking. And as I mentioned, based on the Vicky Makker trial control arm, chemo control arm, in the New England Journal of Medicine that led to the approval of pembro and lenvatinib in second line, we have a bar here of about 15% with PFS of 3.8 months. Here are just some quotes, and you can see that on our, R&D deck here that I'm presenting now on our website. I will not go through in detail, but in general, there has been, a positive reaction to a blinded profile of ACR368. This was a blinded market research. Nobody knew what drug we were talking about, nobody knew the company, nobody even knew it was a DDR inhibitor, but we simply presented blinded, or the third party did a profile based on the emerging data in a hypothetical fashion. These are some of the responses which include that, over 60% response rate, "I hope such a compound really exists." Obviously, "FDA likes biomarker-driven approaches in precision medicine." "There's a significant gap in second line," and, "There's still a huge unmet need." With that, I'll pause and give the word to Dr. Eskander to discuss briefly, the changing standard of care, and how he sees the big picture in the next coming years. Dr. Eskander, please. Of course. Thank you, Peter. I just wanna make sure you can hear me okay. Yeah. Wonderful. So as was already alluded to, the treatment landscape for the management of endometrial cancer is quite dynamic and continues to evolve as a reflection of our understanding of the disease. This image was really developed, a schema I put together to show the changes in the treatment landscape. And on the very left, we take a patient from symptoms to diagnosis, and subsequently surgical intervention. In patients who are diagnosed and have what is currently classified as advanced stage or metastatic disease, the therapeutic options, standard of care include chemotherapy plus immunotherapy, whether the patients are mismatch repair proficient or deficient, based on both the NRG-GY018 and RUBY clinical trials with U.S. FDA approvals. Also, opportunities for chemotherapy alone in certain patient populations, and then in addition to that, chemotherapy plus trastuzumab in appropriately selected populations that are HER2 positive. Now, unfortunately, with these therapeutic interventions, we see a benefit, and that benefit is clinically relevant, statistically significant, but we also see patients suffer from disease recurrence, particularly those with aggressive histologies and advanced stage metastatic disease at diagnosis. So if we follow the paradigm, we see patients diagnosed with disease recurrence while on maintenance therapy. And as was already alluded to by Peter, we live in a world where IO exposure in the frontline setting is gonna become exceedingly more common. And in patients who have had prior immunotherapy, which is the lower panel on the figure, we can see that lenvatinib and pembro is no longer an option for these patients. We're relegated to single-agent chemotherapy with an objective response rate of 15% or less, and a median progression-free survival of approximately 3.8 months, reflected in the KEYNOTE-775 study by Vicky Makker, or potentially an anti-HER2-directed ADC if they're HER2 3+. And that is a small proportion of the population. If we look at all of these endometrial cancer patients, HER2 3+ is on the order of approximately 15%, maybe generously 20%. We have a gap in our therapeutic landscape, an unmet need to address in the treatment of patients who progress after prior checkpoint in the adjuvant or metastatic setting. If they did not have prior immunotherapy exposure, of course, that opens up the opportunity to lenvatinib or pembrolizumab, or chemotherapy plus immunotherapy if the chemotherapy-free interval was greater than 6-12 months. Of course, that progression at that point, we again see patients who have limited therapeutic options for which we prioritize clinical trials or novel drug development, because cytotoxic chemotherapy has exceedingly poor response rates. I'll pause there. Peter, I'm more than happy to answer any questions. Thank you so much. And is it too early to tell, Dr. Eskander, what the how many of the patients will now get the prior IO, especially also in the PMMR group? Based on our market research, it seemed to be that it will be a seemingly smaller fraction, because of the broad label there, but do you have any insights into different doctors' usage and We're seeing more and more utilization of patients with advanced stage disease, chemotherapy plus immunotherapy, irrespective of MMR status. I'm here at ESMO, as you alluded to. The KEYNOTE-B21 data was just presented in the adjuvant setting. That is a broader population, but even in that clinical trial, we see the Stage Three completely resected appears to be advantageous. And I apologize, the applause is from the auditorium next to me. But more importantly, in the dMMR, we see again a dramatic benefit with IO, and some of those patients will still recur and have IO exposure. So the utilization and incorporation of immunotherapy in the frontline, I imagine, for the advanced stage patient, is gonna continue to grow. We're gonna see greater uptake, which is gonna be reflected in our need to develop novel strategies to fill that gap. Because lenvatinib and pembrolizumab is no longer an appropriate subsequent therapy because these patients have had prior IO, of course, which was not investigated on that. Thank you so much. With that, I will move on to the next slide and naturally transition to a possible development path for ACR368 in endometrial cancer. Obviously, we are having a registrational intent with our ongoing phase 2 trial based on prospective patient responder identification and prediction of sensitivity, and aiming for the accelerated approval here in this trial. We are already thinking of potential confirmatory trial strategies and have several options. We think that, I'm just at high level mentioning a couple of them here. Obviously, we are evaluating options to potentially move towards a broader label, more towards frontline. Given the data that I showed to you just earlier, you can see that the high unmet need group of pMMR patients, which is the majority fraction in particular, is where we have great efficacy, but also in the dMMR. So this could potentially open up for a randomization in the maintenance phase of a frontline, where we could compare the effect or benefit of pembro versus pembro plus ACR368 during the fourteen cycles every six weeks after that. That would probably be based on a every three-week regimen of ACR368. There is very, very strong data, and high-impact papers from rodent models showing the synergy between DDR inhibitors, specifically ACR368 and PD-1 therapy, which basically show upregulation of PD-1 by DDR inhibitors, upregulation of cGAS-STING pathways, and double-stranded breaks inducing a significant immune reaction. That has been proven in multiple preclinical studies. Another one that's maybe more straightforward is I showed you that there is some benefit from the ultra-low dose of gemcitabine 10 mg per square with ACR368 in the OncoSignature-negative patient. Remember, the OncoSignature is drug-tailored for response prediction for single agent. It was the AP3 platform that uncovered that sensitization, so it's a fraction of them. But if they indeed do get some increased disease control with stable disease and a few rare responders, that actually can become meaningful in a confirmatory setting, potentially also in an all-comer where we would bring in that fraction of patients that are converted to more sensitive with ultra-low dose gem that are originally OncoSignature negative, and potentially also some of the OncoSignature positive that clearly benefit from the drug but currently don't have responses, they might get deeper responses based on the sensitization with ultra-low dose gem. More to come on that in the future. Beyond our three lead indications, endometrial, ovarian, and bladder cancer, and I mentioned already that we'll update on ovarian and bladder at a future date, it has also, very importantly, ACR368 shown activity in human papillomavirus squamous cell cancers. There were data from the MD Anderson from head and neck cancers, where there is an unenriched overall response rate of 19%, with a duration of response single agent of 7 months. And we also have an orphan drug designation for anal cancer based on the data, with duration of response of 12 months there in that more rare tumor type. All of these are of increasing incidence. Very importantly, the estimates are now about 50 to even 60 thousand new cases per year in the US. And they include a vast majority of oropharyngeal head and neck, some upper esophageal cancers, and basically cervical cancer and anal cancer is obligate HPV positive, so a very significant opportunity. And as I mentioned, Dr. Christine Chung, almost two years ago, reached out to us, expressing a very strong interest in beginning an investigator-initiated trial. She will be testing ultra-low dose gem in both HPV positive and negative patients with squamous cell cancers of head and neck post anti-PD-1, so we have PD-1 here again, and she has also the site activated there, so we think this represents a high unmet need tumor type and would be an attractive option for a next Acrivon-sponsored trial with ACR-368. So with that, I'll go over to our next part of this update, which is about our internally developed ACR-2316, potent novel dual WEE1/PKMYT1 inhibitor, which was really completely enabled by the AP3 platform. We call it phenotypic SAR, structure-activity relationship, the way we can optimize compounds by-... building into one molecule through our co-crystallography, our rational structure-based drug design, the ability to quench what we see the drug inducers of resistance mechanisms inside the intact cells using our AP3 platform. And that is how we aim to improve the therapeutic index, which we believe we have done with ACR2316. And as I mentioned ahead of schedule, we had an update in at the April R&D event, where we moved our IND filing from Q4 to Q3, and as you can see now, we have further accelerated our timelines, and we have already activated the first clinical sites for this exciting asset. Just a reminder, that the mass spectrometer-based phosphoproteomic step up front, the way we can profile drugs and optimize them, is a streamlined approach based on structured analysis, all machine learning-based. The most important are the bottom here. We can directly look at the drug-regulated up- and down-regulation of activity state of signaling networks and kinases based on consensus motif analysis, substrate motif analysis, meaning how much substrates are phosphorylated up and down by a drug. We can also take our proprietary in-house data and triage them against publicly available data and functionally annotate the drug mechanism of action, and have done so richly, and that is now built into our AP3 interactome to allow for very, very rapid turnaround. We have terabytes of terabytes of data now on many, many DDR inhibitors, both internally developed and both approved and clinical stage assets. I'll show a little bit of that towards the end with a demo version, where we have blinded substrates, but show some of the key players in our AP3 interactome. I will give the word to Kristina Masson, my co-founder, who runs the Lund Medicon Village subsidiary, where we have all our drug discovery and mass spectrometry-based phospho proteomics going on. Kristina? Yes. Thank you. I hope you can hear me. Yeah. I will give a brief summary of ACR2316, our very exciting and internally discovered clinical candidate. So the design of this molecule was enabled by AP3, like Peter just said, with a purpose to overcome limitations of current WEE1 and PKMYT1 inhibitors. And we do so by achieving superior single-agent activity, high selectivity with minimal adverse events, and streamlined clinical development by applying a drug tailor oncogenomic approach for indication selection and target engagement-based dose optimization. We achieved a very potent molecule with superior anti-tumor efficacy and complete tumor regression across preclinical models, and this is really enabled by potent WEE1 inhibition, and also the balanced inhibition of PKMYT1 to overcome potential resistance. Importantly, we also applied our AP3 technology to measure, with high-resolution mass spectrometry, all drug-regulated signaling pathways, meaning activity. As an example, to the right here, this cluster shows a massive on-target activation of CDK1 and 2, and also PLK1, which is essential for driving cells into the mitotic catastrophe, and thereby contributing to the strong profile of this molecule. The high selectivity was enabled by co-crystallography and structure-guided design to limit adverse events, to be mechanism-based and transient. On the next slide, we show you that it translates across cell-based models. Thank you. Here, we see that the potency of 2316 is very superior, both across human tumor cell lines and in PDX ex vivo tumor models. The left panel is showing you genetically non-selected cell lines, truly a random panel of different indication cell lines. What is noticeable here is that 2316, in orange, is pretty much basically a log scale more potent than benchmark WEE1 and PKMYT1 inhibitors in all of these models. On the next slide, most key here is that it translates to anti-tumor activity in vivo. We've done a number of tumor-bearing mouse model studies with different dosing regimens, and we're just showing you a snapshot here. But the key message is that 2316 causes complete tumor regression at doses much lower than any other clinical comparators. We see complete regression, but also a nice dose response here in these two top left and middle models, and with 2316 in different color schemes. Yes. Thank you, Peter. And we also see complete regression at the bottom right model here, with multiple different dose levels. Thank you. That speaks to the therapeutic index expansion that we are achieving with this molecule. We can also come in an already established tumor, the top right model, causing complete regression with a little more than half the dose and a five on, two off regimen, compared to the highest tolerated daily doses of azenosertib used in this study here. And finally, at the bottom left is another example of complete cures. In this model, we stopped dosing at 24 and 26 days, and we achieved a complete cure in this three on, four off dosing regimen, in mice. So the key message is really that regardless of the dosing regimen, we see a very similar robust anti-tumor activity. And if we go to the next slide. Thank you. ACR-2316 has a very favorable preclinical safety profile based on our completed MTD, DRF, and GLP tox studies. It was well-tolerated and resulted in tumor regression in syngeneic mouse models at multiple dosing regimens, as I just showed you, and with very manageable and fully favorable AE profiles. Adverse events were mechanism-based, reversible, and transient, and I'd like to end on that we have a rationally designed molecule with a very superior profile, now IND-cleared. We believe that the broad therapeutic index observed across our preclinical studies using the planned dosing regimen is consistent with the target human exposure required for anti-tumor activity, with anticipated reversible and mechanism-based adverse events. With this, I'll give the word back to Peter. Thank you, Kristina. We have the basis for this statement is, of course, all the murine models, but also that exquisite selectivity and potency that we believe is essential to be able to not push the dose more than necessary in the clinic. In fact, our study design and being very biomarker-driven, our approach is to look at drug target engagement post-dosing, both in the escalation and expansion phase, so be able to maybe back off from an MTD dose. I want to quickly go back and point that out, that you can see here as an example, we have multiple doses that can cause complete tumor regression, just speaking to the expanded therapeutic index, which would really open up for that. Looking at drug target engagement, where we can translate the essential threshold for anti-tumor activity from our preclinical studies, could be the basis on which we optimize the dose aligned with Project Optimus in the phase I study, which you see a simple outline of here. It's a rather traditional dose escalation phase here. Very importantly, we are doing it in selective solid tumor types. We obviously have used our AP3 platform already to identify tumor types that we haven't yet disclosed that we think are very exciting solid cancer opportunities of high unmet need. And then we select two tumor types for the dose expansion. One, for example, could be at MTD, and another one minus one dose level. As I said, we can then look at drug target engagement and, of course, potential anti-tumor efficacy to really optimize the dose that way, streamlined. We have multiple sites already activated that are screening, and we are expecting first dosing imminently. We have our AP3-based indication has been ongoing for quite a while, and we have prototype OncoSignatures being developed. The dose optimization, as I mentioned, will be guided by drug target engagement. In summary, we believe we have a potentially best-in-class agent based on head-to-head studies of clinical benchmark comparators. I think also based on all our data, it's a very significant. It's actually the biggest IND package I've ever been involved in myself. We believe we met our program goals. We have superior single-agent activity. In fact, we see complete tumor regression, as Kristina showed, at doses less than one-third of maximally tolerated or possible to make with the clinical benchmarks, causing only tumor stasis. We haven't seen regression with those, despite much higher doses. We believe that is mechanistically driven by not only the very, very significant upregulation of CDK1 and CDK2, but also PLK1, which is essential for that mitotic execution. We, at the same time, also uncovered with our AP3 platform, we have a slide on that, we call it reciprocal quenching. We uncovered the dominant resistance mechanisms based on deducing the consensus sequences for what was phosphorylated in response to a WEE1 inhibition, and that happened to emanate from PK Mid-1. It makes rational sense based on the G2/M checkpoint, role of these two molecules, but we actually unbiased could uncover that with our AP3 approach. We talked about the importance of the selectivity and potency, and how we believe that leads to a hopefully favorable safety profile in the clinic. We have seen that in based on the GLP tox studies, we have seen that is indeed the case. And we also will use our drug target engagement and biomarker expertise to hopefully accelerate the clinical development aligned with Project Optimus. So with that, the last part will just be to further introduce our machine learning-enabled AP3 platform, and very importantly, the proprietary data we generate with our computational science-driven interactome, on which we're now at version two. Basically, the upgrade from the previous introduction we gave is that we now are able, by push of a button, available for all scientists here at Acrivon, we can pull out analysis across all our experiments to date, quantitative experiments, massive amounts of data, drug profiling, and we can plot drug-regulated activity states. We can look at what kinase substrates relations that are actionable. We can uncover predicted biomarkers, PD biomarkers, et cetera. And it is a huge database that is now extremely actionable, and we have obviously used it for indication finding for 368. We used it when we in-licensed ACR368. We've used it to generate the onco signature, and we've now used it also for to generate 2316. So with that, we believe we have the basis for a reiterative engine by which we can generate optimized, molecules, go through indication finding before we enter the clinic, so to, quote-unquote, "de-risk the clinical development," hopefully knowing what tumor types will be sensitive, and go in with, if needed, patient selection. If not needed, simply going in where we believe there's particular sensitivity in certain tumors. Here's just some snapshot examples with our demo version, where we have blinded, as this is very actionable. But basically, here's an example of 2316, where we see that robust activation of CDK1. I think this is across 20 experiment, where we, for example, can directly pull out in a second by push of a button. We see that 206 substrates, most of which are upregulated by CDK1. That means CDK1 is activated. That's the together with CDK2, the most upregulated kinases for this WEE1/PKMYT1 inhibitor. And this, of course, it very efficiently inhibit the inhibitory phosphorylations, threonine 14 and tyrosine 15 in these molecules. We release the activity, and you can see it leads to a massive upregulation of these substrates. All this here is pull-down menus, and we can go across experiments and choose specific conditions, et cetera. Some of the most powerful applications is the ability to generate sunburst. So it's very small here, and I apologize. I'll blow up these graphics elements on the next couple of slides. But we have this opportunity to do real-time quantitative computational analysis of our proprietary AP3 drug profiling data. As I said, integration of all the different conditions and experiments over a couple of years now. And what you're looking at here is an extract of a certain number of experiments. In this case, it's quantified in 22 experiments, what we're pulling out here. And you can see here the drug names. These are some of all the preclinical leads we generated as part of generating ACR2316. What we are doing here is we are looking at that specific CDK1 phosphorylation site, tyrosine 15, which is the on-target for WEE1 and PKMYT1 inhibitors, but primarily WEE1. And what we see here is that in blue indicates downregulation based on the log2 scale, and red, upregulation. So you can see that when we compare here, we have lunresertib, Debio, azenosertib, et cetera. We have had a very, very interesting lead that we didn't pursue further for other reasons. But you can see the general message is we have a very deep inhibition of the phosphorylation of this inhibitory site, which is why CDK1 gets so massively upregulated. Here, we're looking at a standard time point and concentration for us, where we have a 70-90% drug target engagement, 60 minutes. And you can see here the deep, deep inhibition compared to the others. Here, we go in much more detail and look at all the different doses we have looked at. Again, you have the comparators here. I apologize you can't read it, and that's really not the point. It's... The point is to show that we have a very, very potent molecule. You can see the deeper blue in general across experiments and conditions, and it also is the case across different time points. And here you can see in a little more granularity, the deep. Here, we're looking at a sensitive cell here, and you can see that, we have that deep inhibition across all these experiments. And we can do that for all the 150,000 phosphorylation sites. We just pull out one here that's very, very important because that's a reflection of the on-target activity of WEE1 in this case. Here we have the knowledge graph for the different doses here, and we have for the different time points here. So in short, we are super excited about the actionability of this approach, and it enables us to rank kinases in intact cells. So this is a phenotypic way to generate drugs. The challenges with traditional drug discovery, structure-based drug discovery, is we've become extremely good at making very selective drugs for a target or targets, but understanding which targets are the most important to inhibit or activate to get a maximal anti-tumor response or a maximal anti-inflammatory response has not been possible in the intact setting, and that's what this method now opens up for with the AP3 platform, where we can phenotypically optimize a compound for the optimal target selectivity, balance potencies to quench resistance mechanisms, and get that very, very significant single-agent activity, and here, finally, just an example of, again, we can pull out the kinases that are most, in red, upregulated or blue, downregulated, and you can see again that CDK, either with the cyclins associated, CDK5 is also an important partner here, together with, of course, CDK1/2, and then we have PLK1 and... As one of the top three or four most upregulated kinases. And that is what drives that very, very significant SD2M accumulation. In our corporate deck, we've shown we have almost 100% accumulation in SD2M upon inhibition with this molecule. Very importantly, also, some of these kinases that we have optimized to inhibit here with this inhibitor, not by hitting the target, but indirectly through the pathway connectivity, are involved in resistance mechanisms to DDR inhibitors. So again, in one molecule, we have built in the ability to quench important kinases driving resistance to DDR inhibitors. And we have not revealed what that is, but plan to do so in our future upcoming publication. So with that, I'll just end on the financial highlights and be happy to take questions. Rasmus? Thank you. The Acrivon team and platform are very capital efficient. We have significant flexibility also from a finance perspective, with a strong cash balance and a runway into the second half of 2026. Following our $130 million pipe in April, we ended Q2 with approximately $220 million in cash, cash equivalents, and marketable securities. Back to you, Peter. Thank you so much, Rasmus. And so with that, I'll just give the key takeaway messages here in interest of time. I think I'll just go very quickly over these. Our interim registrational intent phase 2 data for endometrial cancer has shown a confirmed response rate of 63%, with a lower bound of the confidence interval above 30%, really solidifying endometrial cancer as our possible first indication for potential approval. We have statistically significant segregation, really further validating the OncoSignature patient selection method. It's now just substantiating what we showed in April. Again, we get third decimal p-values for this prospective patient selection, not retrospective analysis. This is prospective patient selection and a subsequent segregation analysis, which enable us to derive a nonparametric bootstrap p-value of 0.009. The endometrial cohort data are still maturing. We have still not yet reached a duration of response, but it's currently six months at time of data cut. We are actively evaluating potential confirmatory trial designs for potential future label expansion. We have now not only cleared the IND for 2316, but also have the first sites activated and screening patients for enrollment in our phase 1a/b study. The interactome, generating our proprietary actionable insights, which is fully algorithm-based, has been further developed to now integrate across all conditions and elements. We are now in a phase where we are applying more generative AI to that proprietary data set to further really be able to go beyond that 1% of the surface we are scratching currently. There's a massive amount of information here, and Rasmus just mentioned that we believe we have runway well into second half of 2026. So with that, I'll just end on that it's a modality-agnostic approach. We are in a small area of oncology now, but regardless mechanism of action, we can see and measure the drug-induced pathway effects of any modality inside a cell. And our next area for this approach is obviously gonna be outside oncology, where we don't have genetic alterations or associations to really guide our precision medicine predictions, so if you want a higher unmet need area for new precision medicine approaches. And with that, let's take questions, and I thank everyone for taking the time this morning. Adam? Yes, Peter. Our first question comes from Divya Rao, who works on the team with Mark Frahm at TD Cowen. Divya says, "Hi, team. Congrats on the data!" And actually, with an exclamation mark. Very nice. Thank you, Divya. We have two questions. One, if you could give us any color on the biomarker status of the 12 unevaluable efficacy, unevaluable patients, how is the biomarker positivity rate compared to that was previously determined using the tissue biopsies? And how many of these 12 patients are awaiting their first scan? Thanks. We are talking about the 35 patients versus the 23 patients. They obviously enrolled, and they are at different stages of the ongoing trial. I assume that's the 12 you're referring to, Divya. Thank you for your question, and thank you for the nice comment. You know, they are just like all the other patients. They are entering their first scan during the next two months. And that's... And some of them have been scanned. The data cut was end of July. That is all I can say about that at this time, and we'll obviously keep following the progression of this trial. and I think there was four OncoSignature positive and eight OncoSignature negative that are, of course, safety evaluable as well, together with the 23 efficacy evaluable, and I assume that's the 12 patients you're talking about. And the second question was what, Adam? How has the biomarker positivity rate compared to that was previously determined using the tissue biopsies? It holds up very, very, well. It's a very important control for us, and we showed on one of the first slides, and you have it on our website, that it holds up to be about that one-third of patients that are OncoSignature positive. Very good. Our next question comes from Joe Catanzaro at Piper Sandler. Joe asks, "For the three OncoSignature positive non-responders, anything notable about their background or their biomarkers and the degree to which they met the predefined thresholds? Thank you for the question, Joe. Not really. There is, of course, always tumor heterogeneity. The metastatic lesions that are the basis for the pre-treatment tumor biopsies do have heterogeneity, so all I can say is that we will never expect 100% response rate, as I've always emphasized. The OncoSignature approach is functional. We measure dependency on what the drug acts on. That mean we get, and we show, obviously, a very significant disease control rate now and response rate, but there will be some that don't benefit from the drug. There... These are very, very advanced cancers with a lot of metastatic lesions, and often what we see is that it can be another lesion-... other than the target index lesion that starts progressing, and suddenly that is the one that can pop up. So these are some of the things that can be behind this kind of observations, and there's nothing we can do about that. Tumors are heterogeneous. But nothing noticeable at this point. The actual lesions we measure are completely driven by our clinical decision-making, biomarker thresholds and which is run by our CDx partner. Thank you, Peter. Joe had a second part: On your strategy and earlier line strategy in endometrial cancer and combining with an anti-PD-1, you mentioned some data in the literature, but within the AP3 data you've generated with ACR368, has that told you that there's impact to immune relevant pathways in sensitive tumor cells? So there is a lot of very, very strong literature. Some of the references are on the bottom from MD Anderson, from other groups in very high impact journals that have delineated the multiple mechanisms in general for DDR inhibitors, but also very specific studies with ACR368, which is also known as prexasertib. And those studies are referenced in the bottom, some of the key studies. And as I mentioned, the findings there are three primary mechanisms: double-stranded break induction of significant immune defense upregulation, upregulation of PD-1 and PD-L1 with DDR inhibition, and also upregulation of the cGAS-STING pathways involved in interferon response and other things. So there's a wealth of data in preclinical models. I think that's kind of where we are now. In terms of thinking of expansion to potentially moving towards frontline in that pembro-only part of the frontline and then add ACR368 there, we do have some safety data from a prior study done by Jeff Shapiro at Dana-Farber, where this showed consistent with the non-overlapping adverse events from PD-1 therapy and ACR368, that doses seem to be well-tolerated, standard doses of those seem to be well-tolerated. That's kind of what I want to say about this at this time. Thank you, Peter. Our next question comes from Matthew Biegler of Oppenheimer. Matthew asks, "Remind us how you're dosing prexasertib. Is it continuous or an on-and-off schedule? And then maybe comment on the safety, in particular neutropenia, which has stumbled some of your competitors in the CHK1/WEE1 axis. What's unique about ACR368 that allows you to thread that needle?" And I'll mention there was another question on ADC safety as well that's related. Okay. Thank you for the question, Matt. Let me see here. ACR368 is dosed at 105 mg per square meter every 14 days as an infusion. That opens up for a long-lasting prophylactic G-CSF. Typically, it's done. It can be done in the home by the patient the next day, typically, and that is what is strongly encouraged for the single agent ACR368. G-CSF was used in the past investigator-sponsored trials. We are now encouraging it because of the ease by which it can be given together with the once every 14-day schedule for ACR368 at RP2D. And with that, we are controlling neutropenia and thrombocytopenia and anemia quite well. In fact, we think the safety profile is not only encouraging, it seems to be slightly better in terms of neutropenia being in the low double digits, and it's typically occurring in the first and/or second cycles, and then it, vanish out. That's a general picture of these. And it unless one gets the not-so-nice complication, which is, about, high single-digit%, febrile neutropenia, which has also been seen in the past studies and also tend to occur in the first cycles, you won't feel these transient reversible hematological AEs. And that is in contrast, I think that was the last part of the question, to the typically more long-lasting myelosuppression you see with chemotherapy, platinum for sure, taxanes, doxorubicin, et cetera. And also very importantly, the non-hematological AEs, everything from the keratopathies to the neuropathies, liver toxicities, pneumonitis, et cetera, that are seen. We do not see any of those, so it's really limited to the mechanism-based AEs. The explanation for that is that ACR368 is actually a very selective molecule. It's most potently inhibiting CHK1 and a slightly less potent inhibition of CHK2. And also importantly, while with other DDR inhibitors, one also tends to see GI tox. We, perhaps consistent with that, it's an infusible injectable. We do not really see GI tox with this molecule. I hope that answers your questions. Thank you, Peter. Our next question is from Lucas Shumway, who works with Etzer Darout at BMO Capital Markets: Have you discussed the ACR368 data with FDA as to how to approach these next steps? If not, when do you plan on having that dialogue? ... Thank you. That's a very important question. It is data-driven. We have a registration intent, Simon 2-stage design. We have obviously a very rich dialogue with the FDA. Not only did we get a clearance in 28 day for where we did get, I think as the only DDR company during Project Optimus, we got clearance for recommended phase 2 dose out the door. Not only did we get that in ovarian cancer, but also in the predicted tumor types, endometrial and bladder. We also got clearance to use our OncoSignature method for prospective patient selection based on the confidential data we shared with FDA, which is certainly unusual. All the PD-1, PD-L1 studies in the past started out with Merck and others using retrospective analysis, semi-quantitative measurements. We got the clearance because all our data were quantitative, blinded, prospectively designed studies in preclinical models, and also on actual pre-treatment tumor biopsies from past trials, and that opened the door to go that route. So with that, we also achieved Fast Track designations for endometrial and ovarian cancer, as well as a Breakthrough Device designation. And so with all that, we have a rich dialogue with FDA that means that we let the data speak, and it is really our decision for how we move over and advance the compound further in this trial. And we simply plan to cement the data a little more and then share the confidence interval bounds and the segregation with the biomarker and the data, safety data with the FDA when we want to accelerate this. We have not disclosed publicly when that is, but we're in continuous dialogue with the FDA. Yes, they are aware that this is a registrational intent, obviously, as we also have disclosed in our S-1 filing. There are several exchanges that were listed way back when we did our IPO in November 2022, that showed that there is a registration intent here. Thank you, Peter. Any more questions? That is all the time we have today, Peter. Okay, um- We- Go ahead. We thank you all again for participating, and Peter, any final words? No, I just want to thank everyone. It's first of all Dr. Eskander for joining this session. You are pioneering therapies for endometrial cancer. It's a very high unmet need and obviously an important mission. We want to thank you sincerely for joining this session. I want to thank all the people calling in. It's only six o'clock on the West Coast, maybe that's why Dr. Eskander went to Barcelona instead, so it's mid-afternoon and all the people on the East Coast. So thank you so much, and thank you for the great questions, and look forward to updating you in the future on the continuing ongoing trials. Thank you.