Good morning, everyone, and welcome to today's conference call. My name is Adam Levy, and I'm Chief Financial Officer and Head of Investor Relations at Acrivon Therapeutics. This morning, we are going to share some exciting clinical data and provide other updates across our pipeline programs. Next slide, please. Before we begin, I'd like to remind you that certain statements made during this call may constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 and Section 21-E of the Securities Exchange Act of 1934 as amended. These statements involve known and unknown risks, uncertainties, and other factors that may cause our actual results, performance, or achievements to be materially different from any future results, performance, or achievements expressed or implied by such forward-looking statements. For a discussion of these and other important risk factors, please refer to the Risk Factors section of our most recent annual report on Form 10-K, quarterly reports on Form 10-Q, and other filings with the U.S. Securities and Exchange Commission, which are available on our website at sec.gov. Next slide, please. Leading the call today will be our Chief Executive Officer, President, and Co-founder, Peter Blume-Jensen. Peter is also the inventor of our AP3 platform. Mansoor Mirza will also be participating. Mansoor is our Chief Medical Officer and a highly accomplished clinician behind several guideline-changing therapies in the OB-GYN cancer space, including the recently introduced new frontline therapy for endometrial cancer. Next slide, please. We have an exciting agenda you see here. First, briefly, Peter will briefly review the company's foundational AP3 Generative Phosphoproteomics platform, and then we will proceed with reviews of the new clinical data we released earlier this morning for our lead program, ACR-368, and for ACR-2316. Finally, we will share highlights from our newest development candidate, ACR-6840, targeting CDK11. Following our presentation, we have a brief Q&A session. You may ask questions using the text box at the bottom of the webcast screen. With that, I'll now turn the call over to Peter. Peter, you're on mute. Thank you, Adam. We are super excited about presenting our data today, and thank you for joining this call today this morning. As you know, and we have previously shown, Acrivon is entirely centered around its predictive precision proteomics platform called AP3. The key concept is that rather than inferring from genetic alterations how a drug acts on a particular disease, we directly identify and quantify in an unbiased manner the global compound effects on the disease-causing signaling pathways in the intact cell. Specifically, we can measure how pathways are activated and inhibited by any compound, which is enabled by our cutting-edge mass spectrometry and computational science Generative Phosphoproteomics approach called CISR. CISR was recently introduced for the first time at the AACR NCI EORTC meeting in October last year. Acrivon stands for accurate or exact, and that is the concept or underlying concept of the method, which is that we directly identify how the drug acts on the proteins and the signaling pathways. This obviously enables identification of predictive biomarkers for drug efficacy, and also it's broadly applicable in R&D for indication finding. Endometrial cancer is an example of that. For drug discovery, that's how we generated 2316, our dual WEE1/PKMYT1 inhibitor. And also, we can identify and have published on that resistance mechanisms that are drug-induced, identify patient responders, for example, with our OncoSignature, and also we can use it for assessing and licensing candidates. We use it to drive our clinical and preclinical pipeline. Next slide, please. Our pipeline is shown here and is composed of potential first and best-in-class assets, including our phase II-B CHK1/2 potent selective inhibitor, and we'll talk about that in the beginning today, presented by Mansoor. We also have our phase I asset internally developed called ACR-2316, which is specifically designed to overcome resistance mechanisms and induce a potent tumor cell killing, and we'll show the initial clinical data with that agent. We're also going to disclose for the first time our preclinical cell cycle program development candidate as well as target. The target is CDK11, a master regulator of the cell cycle. Next slide, please. We have shown this as well before, but I just want to remind everyone that one of the key value propositions of our approach is the ability to identify sensitive indications prior to clinical entry. What you see here is on the left side, commercially acquired and repository-acquired patient tumor samples that we can screen with our drug-tailored OncoSignature predictive test. What is indicated in red is the proportion of patients. Each line is a patient sample that we will predict are sensitive. In other words, they're biomarker positive. Based on that screening across human tumor intended use process cancer tissues, we identified endometrial cancer as a particularly sensitive tumor type. Next to the right of that, you can see an example of how glowingly positive the three biomarkers in our OncoSignature are, and they are in the nucleus where they operate. They basically measure the active CHK1/2 activated drug signaling axis that the drug acts on, which drives the DNA repair essential for tumor spreading and growth. We can then obviously confirm this prediction by generating genetically non-modified PDX models, and we show that indeed a subset of them were particularly sensitive to the drug, just like we predict on the human tumor samples, and to the right, you can see that we could even predict which ones. Next slide, please. Just a brief summary of ACR-368. As I mentioned, it's a potent selective CHK1/2 inhibitor. It was exclusively licensed from Eli Lilly and Company, originally discovered by Array, now acquired by Pfizer. It has very importantly a balanced inhibition of CHK1 and CHK2, and we believe that's the reason it's the only replication stress-active CHK1/2 inhibitor or CHK inhibitor to date. You can see that the salt we're using in the clinic has an issued patent extended through 2037, and we hold all full unencumbered global rights to ACR-368. At the time of in-licensing, now after our own clinical trials, we know there's durable monotherapy activity in several high unmet solid tumor types. We have also uncovered an incredibly strong synergy, which we'll talk a little bit more about with anti-PD-L1. And finally, from all the patients treated to date, we have established what we consider a favorable manageable tolerability profile. It is really primarily transient mechanism-based hematological AEs and with a notable absence of those non-hematological AEs that are typically associated with, for example, ADCs and chemotherapy. So with that, I'll give the word to Dr. Mansoor Mirza, our Chief Medical Officer. Mansoor. Hi, thanks, Peter. Well, as Peter said, the ACR-368 OncoSignature is a tumor-agnostic biomarker test designed to prospectively predict benefit from ACR-368, a potent selective CHK1/2 inhibitor independent of genetic alterations. Screening with the ACR-368 OncoSignature across human tumor samples predicted endometrial cancer to be particularly sensitive to ACR-368. This trial is exploring the activity of ACR-368 in subjects with biomarker-positive endometrial cancer. Biomarker-negative endometrial cancer subjects are offered ACR-368 with ultra-low-dose gemcitabine given as a sensitizer. The study is an open-label phase II multi-center trial enrolling in 48 U.S. sites. Subjects with relapsed endometrial cancer with all histopathologies: serous, clear cell, carcinosarcoma, and high-grade endometrioid adenocarcinoma are eligible. All subjects must have received prior platinum-based chemotherapy and immune checkpoint inhibitor, and we allow up to three prior lines of systemic therapy. In arm one, subjects with biomarker-positive disease receive ACR-368 monotherapy. In arm two, biomarker-negative subjects receive ACR-368 with ULDG sensitization. Arm one is registrational intent. Arm two is exploratory arm. Next slide, please. At interim analysis, 36 subjects were enrolled in arm one, 16 arm two. Here, looking at the biomarker-positive arm one treated with ACR-368 monotherapy, we have observed an overall response rate of 39%. Please note final adjudication for a blinded independent central review is completed at the end of the enrollment. So at this point, we show the best of either BICR or investigator-assessed analysis. In addition to the fact that overall response rate is establishing itself around 40% in this all-comer population, we also observe an impressive disease control rate of over 80%. Next slide, please. We noted that in patients who received up to two lines of therapy, the overall response rate was 44% in the biomarker-positive population treated with ACR368 monotherapy. We also see a respectable overall response rate of 26% in the exploratory biomarker-negative population treated with ACR-368 with ULDG as a sensitizer. We believe this is due to the sensitizing effect of ULDG uncovered with the AP3 platform, and we have both preclinical and previous clinical evidence for this sensitizing effect. Of note, 10 milligrams per square meter of gemcitabine is only about 1% of standard dose and hence not having clinical activity on its own, as also agreed with FDA. Next slide, please. In order to further understand the contribution to observed response rate in biomarker-positive subjects, we looked at the response rate across endometrial cancer subtypes. Notably, we had observed that serous tumors showed a high proportion of ACR-368 OncoSignature positivity and generally higher OncoSignature biomarker levels, consistent with such tumors generally being G1/S deficient and CHK1/2-mediated S/G2-M checkpoint dependent. Accordingly, as shown here, the main contribution of the overall response rate in biomarker-positive subjects was from the serous subtype, showing a highly impressive confirmed overall response rate of 67%. Of note, we believe that ULDG might further sensitize these tumors, which will potentially further boost the response rate. Next slide, please. Here comes the most exciting key take-home message from the ACR-368 phase II data analysis. Consistent with the finding of high OncoSignature biomarker levels generally across serous subjects, we observed a confirmed overall response rate of 52% in the serous all-comer population with up to two prior lines of therapies, while in the non-serous population with up to two prior lines of therapy, the overall response rate was only 22%. While this is already very encouraging, please note that around half of the serous patients are biomarker positive and did not receive ULDG, which, as noted on the previous slide, we expect might further increase the activity of ACR-368 in the serous endometrial population. Next slide, please. At this interim analysis, the disease control rate and clinical benefit rate are also looking very promising. The disease control rate in the biomarker-positive population was 92%, and the clinical benefit rate at 16 weeks was 83%, while in biomarker-negative population, the disease control rate and the clinical benefit rate were 55% and 45%, respectively. Next slide, please. Serous endometrial cancer accounts for around 40% of all endometrial cancer deaths, and these outcomes have only moderately improved over decades. Only moderate benefit is seen from immune therapy with or without PARP inhibitors. There is also only limited benefit of targeted therapies. The HER2 population is only a small fraction of these tumors. Thus, the relapsed serous endometrial cancer is a huge unmet need. Peter, would you like to add anything here, please? Thank you so much, Mansoor. Yeah, I think that the key message is also that this aggressive subtype is underappreciated, and the contribution to mortality is, I think, very eye-opening. If we go to the next slide, please, we can look a little bit at numbers. Given that we here do not require a biomarker or any kind of tumor biopsy, this obviously opens up for an easy, more global entry. And so we are looking here at the U.S. and EU numbers and estimates based on various sources. And as you can see, as Mansoor pointed out, that the serous mortality accounts for about 40% of all deaths per year, which is about 20,000 deaths in the U.S. and EU combined, of which about 7,000-8,000 are in the U.S. alone. And the prevalence pool estimation is about between 55,000-60,000 patients. So we are talking about a very significant pool of patients here and the potential market opportunity that is relatively significant. The vast majority of patients progress to second-line therapy as well, especially after the new front-line therapy with IO and platinum-based chemotherapy that Mansoor and Dr. Ramez Eskander introduced and published in New England Journal of Medicine, and especially in third line, there's absolutely almost nothing to offer these patients. The response rate is between 10%-15%, and PFS about 2.5-3.5 months. Next slide, please, for Mansoor. Thank you. Thanks, Peter. In light of these promising results, an arm three has been initiated evaluating ACR-368 with ULDG in biomarker-unselected serous endometrial cancer subjects who have received up to two prior lines of therapy. The study is ongoing in 48 U.S. sites and being expanded to over 20 EU sites in France, Germany, Italy, and Spain. Arm three is potentially the fastest path to the potential approval. We are already well into enrollment in arm three. Next slide, please. Before we go to the next slide, I just wanted to, yeah, I think, Peter, you should take it here. I can take that. So in addition to our phase II studies, we have already submitted a phase III confirmatory trial protocol to the FDA on November 12, 2025. And this will be briefly introduced by Mansoor on the next slide. But the basis for the design is our in-house studies demonstrating extremely strong synergy with complete tumor regression and permanent immune memory despite repeated tumor cell injections in syngeneic immunocompetent mice shown here. Next slide, please. So this is a high-level design of phase III. It is planned to be double-blind placebo-controlled switch maintenance trial in advanced and/or recurrent pMMR endometrial cancer. The goal is to improve progression-free and overall survival by adding ACR-368 to anti-PD-1 in maintenance phase. Thank you. Next slide. Thank you. What you're seeing here is an overview of our Generative Phosphoproteomics AP3 platform. It is driven by our proprietary in-house generated data top-left. We have high-resolution mass spectrometry and are very computationally scalable, and this is the basis for our drug discovery and development and clinical development. As you can see, we have a data portal. It is absolutely essential for AI to have structured standardized data. We are able to convert multimodal data, whether it's imaging or crystallography or other types of data, into structured data that are amenable for AI. With that, we are able to have data going into our AP3 interactome, which is an integrative database for all data to date across many, many drugs, where we house all data on how drug acts on pathways, where we have in-licensing candidates, et cetera. We also have an AP3 CISR predictor, and that is a so-called CISR that we have invented that allows us, at a global level inside a cell, to assess how pathways are activated and inhibited by a drug. And based on that, we can actually design drugs based on desirable pathway effects. And that opens up for all the applications to the right. So using our platform, next slide, we generated as our first fully internally developed molecule, the oral dual WEE1/PKMYT1 inhibitor, potentially best and first-in-class agent with our platform approach. It was designed for superior single-agent activity, and we've shown in head-to-head studies that against existing WEE1 and PKMYT1 inhibitors, that there is a very, very potent tumor cell killing and complete regression across tumor mouse models. It is a potent activator of not only CDK12, but also importantly, PLK1, and designed for such to ensure a very strong proapoptotic mitotic catastrophe resulting in tumor cell death. It was also designed for relatively short elimination half-life combined with selectivity to have a quote-unquote "hit-and-run" effect so that we have the inevitable mechanism-based myelosuppression being very transient and the bone marrow can recover quickly, and that has allowed us to establish, as we'll discuss in a second, two weekly oral dosing regimens already. We're also going to talk about the AP3-based indication finding, and we have seen already clinical activity in AP3 predictor solid tumors, excitingly including small cell lung cancer and squamous non-small cell lung cancer, despite we have just completed or are in the midst of dose escalation studies, so the patient numbers are still small. Next slide, please, Mansoor. Thank you, Peter. So a total of 33 patients are dosed in these two-weekly dosing schedules in the ongoing phase I monotherapy dose escalation study. Two-weekly dosing regimens are 160 milligram daily, three days on, four days off, and 240 milligrams daily, two days on, five days off. They are established and the tolerability profile is encouraging. Based on the strong scientific rationale of Cmax driving tumor cell killing and the observed transient neutropenia, we have initiated a biweekly, two days on, twelve days off schedule as well. We are including enrichment of cancer types predicted sensitive by the AP3 platform, including such not previously shown sensitive to WEE1 inhibitors currently in clinical development, like squamous non-small cell lung cancer and small cell lung cancer. Next slide, please. Just briefly, a demographic overview of escalation study. Subjects are generally heavily pretreated. Three-fourths of the subjects have had prior immunotherapy and had been on other experimental agents. Next slide, please. We have seen an overall very favorable tolerability profile, limited to mechanism-based transient adverse events, mainly neutropenia. We did not observe grade 3 or higher non-hematological adverse events. Importantly, in the established three days on, four days off weekly schedule of 160 milligrams, no grade 4 toxicity were observed. In the two days on, two days off, five days off weekly schedule, of 240 milligrams, one subject had grade 4 neutropenia. Next slide, please. Clinical activity observed at dose level 120 milligrams and above, with tumor shrinkage in 9 out of 20 available patients. You will see the next slide for the waterfall plot, including small cell lung cancer, squamous non-small cell lung cancer, two tumor types, which have not shown sensitivity to previous clinical WEE1 and PKMYT1 inhibitors. These are the three examples of activity: endometrial cancer, Müllerian tumor at 120 milligram dose level, who had progressed after prior platinum-based chemotherapy, tamoxifen, second-line pembrolizumab, lenvatinib, had confirmed partial remission for 42 weeks. A squamous non-small cell lung cancer subject receiving 200 milligram, who had progressed after prior lines with platinum-based chemo, durvalumab, followed by three other immune therapies, had a partial remission, which recently confirmed on a subsequent scan after TET extract, and that patient is still on treatment. A small cell lung cancer subject at the established 160 milligram weekly dosing regimen, who had progressed after cisplatin, durvalumab, second-line tarlatamab, and multiple organ radiation therapies, for example, to brain, to pancreas, had partial remission of 50%, which further deepened to 67% on a subsequent scan after TET extract, but patient progressed due to non-target metastatic liver lesions. Next slide, please. Here you can see the waterfall plot of subjects treated at or above the active dose level of 120. On the left, you can see nine out of 20 subjects with tumor shrinkage, and on the right, initial tumor burden at the time of best response. Note, we had only one squamous non-small cell lung cancer and two small cell lung cancers and achieved two partial remissions and one stable disease of these AP3 predicted tumor types. Peter, would you take it from here? Yeah, thank you. I think you said partial remission. I think you meant partial responses, right, but on the next slide, please, you will see that we have, obviously, with these exciting data an opportunity to develop this compound further as an oral, given this remarkable activity in tumors that are really having extremely aggressive behavior and where chemotherapy and IO is the main standard of care upfront, and we also have an opportunity. We have the same strong synergy seen with ACR-368, also for ACR-2316 with IO, and we have completed phosphoproteomic profiling studies showing a remarkable synergy also with topoisomerase inhibitors, which is the main payload for most ADCs to date. This opens up for, together with a biweekly dosing regimen, for dosing regimen flexibility and combination opportunities to move more upfront line. Next slide, please. Adam. Thank you, Peter. I'd be happy to review briefly our new development candidates, our new preclinical cell cycle development candidate, ACR-6840. We're excited to tell you about this agent. It targets CDK11, a target well-suited for the AP3 platform, given multiple protein isoforms. We believe it is a potential first-in-class. CDK11, for those that don't know, plays a broad role in the cell cycle in contrast to other CDKs you may be familiar with in development. Part of these roles includes mRNA processing and splicing, as well as mitotic control. Our rapid work has resulted in several promising chemical series, and we are encouraged by the initial properties that ACR-6840 exhibits, including its selectivity and potency. In addition, preclinical anti-tumor activity has also been observed. You can see here on the bottom left a representation of the crystallography work we have done to identify ACR-6840, and on the right, a reminder that everything we do, including the discovery of this agent, relies and is driven by our AP3 platform, which Peter described earlier. On the next slide here, you see a snapshot of some of the work based on AP3 profiling of ACR-6840. A key finding is the downregulation of MCL1, a BCL2 family member protein, which is a recognized resistance mechanism for hematological malignancies. This provides for potential synergy with BCL2 inhibitors, suggesting it may be interesting to study the agent in hematological settings, and on the bottom left, we indeed observe induction of apoptosis in an aggressive AML cell line. Importantly, we are guiding to IND submission in Q4 of this year, and we look forward to further updating you as we make progress, and I'd ask Peter to make any further comments on this slide and on our exciting new development candidate, ACR-6840. I know. Thank you, Adam. Just looking forward to show more data in the future on that. Next slide, please. So this slide, you see a quick update of our financial highlights. And I would caution that these are approximate numbers based on a preliminary unaudited view of our financials as of the end of last quarter, ending 31 December 2025. Approximate cash and investments of $119 million. Importantly, projected runway still into Q2 2027, as we have been guiding, and you see the share count here on the right. Next slide, please. Peter. Thank you, Adam. So briefly here, the many take-home messages. Most excitingly, we have the update and the finding that serous subtype subjects, all comers, are showing a very high response rate in our ongoing phase II-B trial with ACR-368 of 52%. We are now excited about expanding that population into Europe as well and have selected already and submitted CTAs to more than 20 sites in four major countries there, as Mansoor discussed earlier. We think it's a highly compelling clinical profile, and especially also the fact that we're adding ULDG to sensitize further is an opportunity to potentially further boost the overall response rate. That's already very remarkable. The phase III trial design that Mansoor discussed earlier as well, and the protocol has been submitted to the FDA almost 60 days ago now, and there hasn't been any further comments, and that is based on that strong synergy with IO and to move up front line as a switch maintenance opportunity. ACR-2316, our fully internally developed molecule for which we have established two weekly oral dosing regimens, has shown a very favorable tolerability profile, primarily only limited to transient neutropenia. Initial clinical activity has been observed in our AP3 selected solid tumor types, importantly including very aggressive cancers like small cell lung cancer, squamous non-small cell lung cancers. And this oral targeted agent shows our activity despite being severely pretreated for these particular subjects that we show. We are now developing a biweekly oral dosing regimen, two days on, 12 days off, based on strong rationale for Cmax driving tumor cell killing and allowing the bone marrow to fully recover to potentially have a much, much higher Cmax and also for dosing regimen flexibility. Finally, we have just disclosed that our cell cycle program, preclinical cell cycle program, the targeted CDK11, a master regulator of the cell cycle, controlling global transcription, pre-mRNA splicing, especially of cell cycle genes and mitosis, and ACR-6840 is our first development candidate for this oral targeted agent. So it is our AP3 Generative Phosphoproteomic platform that's fueling all our drug development and clinical development. So with that, I will thank everyone and we'll be ready for a Q&A session. Thank you so much. Thank you, Peter. Audrey, our first question will be from Marc Frahm of TD Cowen, please. Marc, go ahead with your question. Maybe just if we can start with this, please think of kind of how the bar may differ for that, for the registrational endpoint arms in terms of serous versus the non-serous. And I guess, can you walk through the protocol design and how you'll, for the phase, the confirmatory phase III, how you'll treat your subtype? Thank you, Mark. I can start and then I'll give the word to Mansoor to finish up. It was a little difficult to hear everything, but I think I got it. So first, what the bar is for our new Arm 3, well, if the response rate holds up in our prospective trial that we are now enrolling up to 90 patients in, where we are going out in both the US and EU with a big number of sites and with anticipated completion of enrollment Q4 this year, if it holds up, and that, of course, we want to show in that prospective approach, then I think it's very competitive as a clinical profile in the second-line setting after the front line IO and platinum-based chemo in the patients that are not HER2/3 plus and also 2 plus where trastuzumab deruxtecan is given. In third line, as I mentioned, the bar is very, very low. There's basically not much that work in that setting. Regarding the protocol details, this is an all comer, no biopsy requirement, no biomarker requirement upfront. We are doing a retrospective biomarker assessment with the OncoSignature. Mansoor, anything to add? No, I think you made it very clear. I think this is a real unmet need, especially when you go to the second line and third line. We don't have any approved therapies, and single-agent chemotherapy has a very dismal response, and progression-free survival is about three months. So it's a very low-hanging fruit in that case. So I believe that if we keep up to the response to which I believe we will, also now we are adding ULDG to all patients, we probably will really change the outcome of these patients. Thank you. Thank you, Mark. Audrey, our next question will be from Roger Song of Jefferies. Roger, please go ahead. Can you hear me? Yep. Yes. Hi, Roger. Good morning. Thanks for the update and I think our question. A couple of follow-ups. In terms of the data, maybe I missed it, but did you show any durability data from your arm one or arm two and any updated safety data to date for that new data cut? And then in terms of the pivotal path, I just want to clarify, since you are enrolling the arm three for the biomarker unselected population, would that be the new registration or the initial approval pivotal cohort, or arm one still be the registration endpoint? Thank you. All great questions. Thank you, Roger. I can start. For arm ones and arms one and two, we did not show anything about durability or anything else as the focus was on the new update for arm three. I can tell you that that is still maturing and a lot of patients are on therapy, so we will obviously update on that at a later point. Arm one is registrational intent. The safety data was just summarized in a slide leading into it, but it's exactly as we've seen and updated at the last update. We see that mechanism-based transient hematological AEs and a notable absence of GI tox and long-lasting non-hematological AEs seen with other more severe agents. So that has not changed at all. So we did not update on that except give a general summary and confirmation that that's holding up. It's more than 1,000 patients treated, so we feel very certain that this will hold up also in the future. Regarding the arm three versus arm one, so we obviously, given that this is an analysis of the ongoing trial, we want to show that it holds up in a prospective trial now where we enrolled an all-comer serous group, and of course, if that holds up and we don't need a biopsy and the enrollment is very rapid and the easy opportunity for a global reach without requirement for tumor biopsy, then of course, we would be able to potentially prioritize that over arm one, but until we see that, and given that we have a nice, actually very nice enrichment and competitive profile, we think for arm one, we want to keep that going as well since that is of registrational intent as well. So right now we see it as "two shots at goal." So thank you. Got it. Thank you. Thank you, Roger. Our next question will be from Lee Watzek of Cantor Fitzgerald. Lee, please go ahead. Hey, good morning, guys. Thanks for taking our questions. Very interesting data. So maybe a question for Mansoor, wondering if you can put the data into context for us. Now we're seeing more such ADCs moving into endometrial cancer in second line. I mean, especially in serous subtype, looks like you have very strong signal here. So maybe just comment on just based on the data, where do you think 3, 6, 8 could fit in in the context of some of the ADC competition? Yeah, thank you, Lee. That's a very good question. The field has moved extensively and you can see how the ADCs are entering the field. What we are seeing is that most of the ADCs have response rates of about 30%-40%. If you don't talk about T-DXd, which showed in HER2/3 plus 84% response rate, that's a small population, 8% of serous carcinomas. And in 2 plus, it was also only 20%. But 2 plus, you have comparable to our drug response rates, if we may have a trans-trial comparison, which is the other interesting drug, which until now we see is the folate receptor from Genmab. And the thing is that these drugs are covering whole spectrum. In serous cancer itself, we don't have anything which can cover serous cancer altogether. And if we hold that and if we have a 50% response rate, we definitely have quite a huge population after first relapse in the second line. And even further, much more population in the third line after second relapse where ADCs have already been there. We will be capturing that area. If you understand that ADCs, if you have given, these are mostly Topo I, and if they are already given in first line or second line, you don't have anything left. The third line is completely, I'm sorry to use the word hopeless with what we have today. So I think we have a huge unmet need in serous endometrial cancer to work on. Peter, do you want to add something? Yeah, I just want to add that obviously we have a very different tolerability profile and safety profile versus ADCs. So I think that's important to mention with a comparable response rate, if not better, that the tolerability profile is also very, very differentiated from ADCs. Thank you. Maybe a second question is, can you just share some of the feedback from the FDA in terms of how much you'll need to enroll for the confirmatory trial to support a potential AA here? Peter? We have submitted the protocol and design and had a phase II type B meeting, sorry, last year, mid last year, and so where we presented a high-level overview of the trial design. So we haven't shared numbers there, but it's the typical phase III confirmatory trial design with the placebo-controlled arm, as Mansoor showed, and we are talking about many hundreds of patients, obviously. And we haven't. Thank you, Lee. We haven't received any further comments. Thank you, Lee. We're over time now. We have time for one more quick question from Ted Tenthoff of Piper. Ted was not able to dial in, so I'm going to read his texted question, Peter and Mansoor. What are the most promising cancer types for ACR-2316? Thank you. I can take that. I think seeing small cell lung cancer, the median survival there is something like 13 months after chemo, platinum-based chemo upfront and immune checkpoint inhibitor and potentially T-cell engager, you're really out of options. So seeing that with an oral targeted agent being so active in two out of two patients, we have activity, one stable disease and one very deep target lesion response. Now this patient was extremely heavily pretreated with radiation on three major organs, including pancreas and brain, as Mansoor mentioned. So seeing that is obviously very, very exciting and is predictive with the AP3 platform. So that is one very exciting opportunity. As is, I would argue, squamous non-small cell lung cancer in this case, and even more heavily pretreated patient where we have now also confirmed PR. So, I think these are for sure two tumor types that are of great interest to us, especially also with the opportunity, as I mentioned, combined with both Topo I and also IO. Thank you. Thank you, Peter. We're over time now, so that will conclude our Q&A. Peter, would you like to make any concluding remarks? No, I just thank everyone for joining our call this morning, and looking forward to update you on data, more data in the future. Thank you so much and have a great day.