Good afternoon, and welcome everyone to the Prelude Therapeutics ESMO Presentation Conference Call. Today's call is being recorded and is expected to last up to one hour. At this time, I will now turn the call over to Prelude's Chief Legal Officer and Interim Chief Financial Officer, Bryant Lim. Please go ahead. Thank you, operator. Next slide. During today's call, we will make forward-looking statements based on current expectations, including statements concerning anticipated discovery, preclinical, and clinical development activities for our product candidates, the potential safety, efficacy, benefits, and addressable market for our product candidates, and clinical trial results for our product candidates, together with other statements regarding our plans, prospects, and expectations. Such statements represent our judgments as of today, are not promises or guarantees, and as you know, may involve risks and uncertainties that may cause actual results to differ from the results discussed in the forward-looking statements. Please refer to our filings with the SEC, which are available through the investor relations section of our website for information concerning risk factors that may affect the company. We undertake no obligation to update forward-looking statements except as required by law. During this call, we will also be referring to slides that are available through the webcast and also posted on the investor section of our corporate website under presentations and events. Also on this call are Kris Vaddi, Prelude's Chief Executive Officer, as well as Dr. Jane Huang, our President and Chief Medical Officer. We are also fortunate to be joined by Dr. Timothy Yap from MD Anderson Cancer Center, one of the investigators of the Prelude clinical study presented today. Dr. Hwang will introduce Dr. Yap in a moment, but first, let me turn the call over to Kris to kick things off. Next slide, please. Thank you, Bryant. Good afternoon, and thank you for taking the time to join us for this call to discuss the first-ever clinical data from PRT3789, a novel, first-in-class, highly selective SMARCA2 degrader, which is being studied as a potential therapeutic option for patients suffering from cancers with the SMARCA4 mutation. As some of you joining us today may be tuning into Prelude for the first time, I wanted to take a few moments to provide a brief overview of Prelude before I turn the call over to Jane, who will discuss the clinical results to date from our ongoing phase one study of PRT3789, which was the subject of an oral proffered paper session at the 2024 ESMO Congress earlier today. Next slide. Overall, as an industry, we've made tremendous progress in developing new medicines to treat cancer. Yet, despite all that progress, far too many patients are not candidates for precision or targeted medicines and still have no good treatment options other than chemotherapy. When we founded Prelude Therapeutics, we set out to change that. Prelude started as a discovery-stage start-up with a handful of chemists and biologists in 2016, and in the years since, we've evolved into a mature research and development organization led by a team of highly experienced scientists, clinicians, and executives with impressive track records of delivering practice-changing medicines. We're building a compelling pipeline of first-in-class or best-in-class precision medicines, anchored by patients' need and by using the best possible modality to selectively and potently target the mechanisms driving cancers. Next slide. Let me turn to our SMARCA portfolio. Several years ago, we recognized the need to develop better treatment options for patients who have dysregulated SMARCA pathways. That can result in highly aggressive cancers. So we initiated a comprehensive discovery and development program to identify highly selective molecules to address this important unmet need. SMARCA2, in particular, had been a target of intense interest in oncology field, but the discovery of molecules with the required level of selectivity and potency had been quite elusive. Our scientists at Prelude cracked that challenge. 3789, discovered by Prelude scientists, first from our program to enter the clinic, is a highly selective and potent IV SMARCA2 degrader and is the topic of our discussion today. We're excited to report the first clinical results with 3789. We believe these data represent initial proof of concept that selective SMARCA2 degradation can yield antitumor activity with acceptable safety profile in selected SMARCA4 mutated cancers. We're advancing the development of thirty-seven eighty-nine as monotherapy-... as well as in combination, to best position this molecule as the industry's first precision medicine treatment option for patients with a SMARCA4 mutation. We also announced recently that we received IND authorization for our second SMARCA2 regulator, PRT7732, potent, highly selective, and orally administered molecule. And I'm pleased to announce today that PRT7732 clinical study has been initiated. We see significant potential for both IV and oral programs, potentially in different patient populations, potentially in different lines of therapy, to help improve the standard of care for SMARCA4 mutated patients. As a third pillar to our SMARCA4 strategy, we're exploring utilizing a highly potent SMARCA2/4 dual degraders as payloads on novel antibodies through our partnership with AbCellera, to create a novel class of precision ADCs, which we believe will further expand the reach of this novel mechanism to target even broader population of patients who may or may not have SMARCA4 mutation. We will be reporting our initial preclinical data on this approach at the EORTC meeting or triple meeting in October, just over a month. Beginning with this update that we're providing today, Prelude has a number of additional key catalysts coming in the next several quarters, and we look forward to keeping you updated on our progress. Equally importantly, I'd like to acknowledge sincere gratitude, all the investigators and patients who have participated and partnered with us in these studies. Next slide. With that, I'm now going to turn the call over to Dr. Huang and Dr. Yap, so they can provide more context on SMARCA4 mutated cancers, discuss our goals with the study, walk you through today's interim data in-depth, as well as provide you with our thoughts on how we plan to advance the program to the next milestones for patients. Jane? Thank you, Chris, and good afternoon, everyone. I'm pleased to be able to give you a recap of the first clinical results from Prelude's Phase I trial of PRT3789, presented earlier today at ESMO by Dr. Robin Guo of Memorial Sloan Kettering, on behalf of investigators. However, before I do that, we are very fortunate that one of our investigators, Dr. Timothy Yap of MD Anderson Cancer Center, was willing to participate in the first part of our call here, in between his many commitments at ESMO, to share his perspectives on the current standard of care and prognosis for SMARCA4 mutated patients. Dr. Yap, thank you so much for taking the time to share your expertise. Dr. Huang, you're very welcome, and thank you for the opportunity to speak today. It's always a privilege to be part of a trial evaluating and very exciting new first-in-class agent, especially one that is targeting such a challenging and hard-to-treat cancer. And to that end, I prepared a few thoughts that I hope will help your audience interpret the data shared today and put these data into relevant context. First, it's, of course, important to note that this is a completely new mechanism of novel biology and uncharted territory. Also, it's important to appreciate the context of what SMARCA4 mutations mean for the prognosis of patients. These mutations appear in up to 10% of all non-small cell lung cancer and up to 5% of all cancers broadly. When it shows up on the NGS test report that I see as a treating physician, the only thing we can tell patients currently is that their cancer may be more difficult to treat than others. The prognosis for these patients historically has tended to be very poor. For patients that have a SMARCA4 mutation, even with aggressive chemoimmunotherapy in a frontline setting, you can only expect on average 20% of lung cancer patients to respond to treatment. As typical, once these patients relapse, the expected response rate goes down even more. That's important because that relapse refractory population is really the population of patients we were enrolling onto this study. Second, with a first-in-class therapy, the primary goals in a phase one dose-escalation study are establishing safety, pharmacokinetic profile, and pharmacodynamic activity. Safety is especially important when the target of the drug is a new mechanism addressing a fundamental cellular process like chromatin remodeling. In this case, we know that selectivity is critical, and demonstrating clear evidence of selective degradation of SMARCA2, but not SMARCA4, is another important objective because of the synthetic lethality approach with this agent. Achieving high levels of SMARCA2 degradation at safe doses will ultimately allow us to use this approach for patients with SMARCA4 mutations. Finally, in first-in-class Phase I trials, we obviously hope to also see signs of early clinical activity as monotherapy, as we approach doses where you would expect to see target engagement. In this case, synthetic lethality of cancer cells induced by selective SMARCA2 degradation. In this aggressive disease phenotype, stable disease, tumor shrinkage, and responses should all be clear signs of activity. And again, what we are seeing here are promising early signals, and as investigators, we look forward to the data to come as dose escalation continues, and we're now getting closer to the optimal biological dose. We will also be interrogating the potential for combination therapy and better understand the biomarker profile of patients who are responding to therapy. In fact, I'm pleased to be presenting an in-depth update at a plenary session of the upcoming triple meeting, the Molecular Targets Meeting, back here in Barcelona on October 2024, and I hope to see all of you there. I hope this additional context is helpful, and thank you again for the great opportunity to engage on behalf of all of the investigators and, more importantly, on behalf of the patients we serve. Back to you, Dr. Huang. Thank you, Dr. Yap. Now, let's dive into PRT3789. First, I wanted to acknowledge and thank the study patients, families, investigators, coordinators, and healthcare staff at each study site for participating in PRT3789-01 and advancing novel therapies in oncology. Next slide, please. Targeting SMARCA4 mutated cancer by selectively degrading SMARCA2 is an exciting new area of unexplored cancer biology, and Prelude is leading the field with the industry's first highly selective SMARCA2 degrader. Cancer cells with deleterious SMARCA4 mutations become highly dependent on SMARCA2 for survival, and selectively degrading SMARCA2 induces synthetic lethality in SMARCA4 deficient cancers. Patients with SMARCA4 mutations are typically not eligible for other targeted therapies and are currently treated with standard of care chemotherapy or immunotherapy. Next slide. As Dr. Yap referenced in his opening remarks, SMARCA4 mutations in non-small cell lung cancer is associated with a very poor prognosis for those patients. In the multicenter retrospective analysis presented by Alessi et al., looking at 1,285 patients with non-small cell lung cancer receiving standard first-line chemoimmunotherapy, the median progression-free survival was 2.7 months, and overall survival was 8.1 months. Approximately 22% of these first-line SMARCA4 mutated patients responded to frontline chemoimmunotherapy versus approximately 39% in non-mutated patients. And as we've heard from Dr. Yap, the population of relapsed refractory non-small cell lung cancer patients that we are evaluating in our phase I study would otherwise anticipate an even lower response rate to standard of care treatment. There's significant unmet need for a new treatment option to serve these patients. Next slide, please. PRT3789 is a highly potent IV SMARCA2 degrader with a selectivity for SMARCA2 that is 1,000-fold over SMARCA4 in cellular assays. In preclinical models, in vivo, as previously published and reported, PRT3789 was found to have tumor growth inhibition and regression. The selectivity for SMARCA2 degradation is particularly important, in that it is believed that high selectivity over SMARCA4 is necessary to confer a favorable safety profile. Now, I'm pleased to share what Dr. Guo from Memorial Sloan Kettering, on behalf of our investigators, presented at ESMO earlier today. Next slide. This Phase I dose escalation study enrolled solid tumor patients with any type of SMARCA4 mutation. Patients received PRT3789 IV once weekly. This preliminary experience reports on patients who have been treated in escalating doses from 24- 376 mg, and some backfill cohort patients who had SMARCA4 Class 1 mutations. In this early cut of the phase I data, 65 patients were safety evaluable. Patients had a median number of 3 prior treatments, with approximately half of the patients with non-small cell lung cancer. In terms of Class 1 mutations, 34 patients had Class 1 mutations by next-generation sequencing, an additional 7 patients had loss of SMARCA4 protein by IHC. As of the data cutoff, 21.5% of patients remain on treatment, and only 1 patient discontinued treatment due to an adverse event considered unrelated to study drug. Next slide. PRT3789 was generally well tolerated, and there were no study drug-related adverse events or dose-limiting toxicities. 65 patients were safety evaluable, and listed here are all of the treatment emergent adverse events. PRT3789 was generally well tolerated. There were no drug-related SAEs or DLTs.... Of all grade adverse events, nausea, decreased appetite, and fatigue were the most common, and nausea occurred in 24.6% of patients, and decreased appetite and fatigue occurred in 18.5% of patients. As expected, with a potent degrader with high tissue penetration, the observed PD effect is more prolonged than the PK half-life. Additionally, with increasing doses of PRT3789, the degradation of SMARCA2 also increased in the PBMCs, with a degradation sustained out to cycle 1, day 8 pre-dose, exceeding the plasma half-life of the molecule and reaching greater than 75% degradation at higher doses. PRT3789 showed selective SMARCA2 degradation in the clinic, with minimal observed effect on SMARCA4 levels. We're continuing dose escalation to determine if we can further increase the target engagement. At the time of this analysis, there were 46 efficacy evaluable patients with at least one post-baseline scan. Of the 26 non-small cell lung cancer or esophageal patients with at least one post-baseline scan and were evaluable for efficacy, seven had tumor shrinkage. RECIST-confirmed partial responses were observed in three patients, two who had esophageal cancer and one with non-small cell lung cancer. Clinical activity was observed in patients with both Class 1 and Class 2 SMARCA4 mutations. Of note, there was a positive correlation between tumor shrinkage with having a higher level of sustained degradation. Enrollment is now into dose cohort 9 at 500 mg IV Q week. Next slide. If you recall from the Alessi paper, for patients with a SMARCA4 mutation, patients have poor outcomes with frontline treatment, with an overall response rate of 21.9%, a median progression-free survival of only 2.7 months, and the overall survival of only 8.1 months. In second-line and beyond, it would be expected that the response rate would decrease. In our study, in this heavily pretreated patient population, in addition to the confirmed PR, as I mentioned, additional patients have demonstrated clinical benefit as measured by prolonged SD, including one patient who has been on study for more than a year. The patient depicted here is representative of a classical patient with SMARCA4 mutations, poorly differentiated histology, and aggressive disease. In this patient with a confirmed partial response, you can see tumor shrinkage in liver lesions and lymph nodes. This patient was treated at 283 mg and is ongoing on the trial. Next slide. In summary, these data represent initial proof of concept that selective SMARCA2 degradation can yield antitumor activity in selected SMARCA4-deficient cancers and is generally safe and tolerable. So what comes next for PRT3789? Monotherapy dose escalation continues. We're now at dose Cohort 9 at 500 mg IV once weekly, with backfill cohorts continuing to enroll. We are enriching the backfill cohorts for non-small cell lung cancer in esophageal cancer patients with Class 1 mutations. We intend to confirm the biologically active dose for PRT3789 as monotherapy by year-end. We're also very pleased that this trial was accepted for plenary presentation by Dr. Yap at the upcoming EORTC-NCI-AACR Symposium on October 24th, back here in Barcelona. One of our other key priorities is further characterizing the activity of PRT3789 in Class 1 / 2 mutations, and the backfill cohorts will allow us to hone in on those patients with the Class 1 mutations at our selected optimal biological dose. Docetaxel combination cohorts continue to enroll, and we look forward to sharing data on that combination at a future medical meeting. Finally, we are pleased to be partnered with Merck to interrogate the potential combination of PRT3789 with Keytruda. That phase II trial is on track to commence in the second half of 2024. Next slide, please. Equally as exciting, we are pleased that the Phase I trial for PRT7732, our highly selective oral SMARCA2 degrader, has initiated following recent IND authorization. For those of you not familiar with our oral SMARCA2 degrader program, I'll just quickly highlight that this is a distinct molecular entity with unique properties relative to PRT3789. It's also highly potent, and the selectivity is greater than 3,000-fold over SMARCA4 in some models. Due to its unique chemical structure, PRT7732 has good oral bioavailability across species and has a projected low milligram once daily human dose based on preclinical models. Similar to PRT3789, our goal will be to rapidly test PRT7732 as monotherapy to determine the recommended dose and population of patients to select for further clinical development. We look forward to sharing more about this new program in the months ahead. I'll now turn the call back to Chris for some closing remarks. Chris? Thank you, Jane. Next slide, please. So before opening up the line for questions, I'd like to offer a few additional remarks related to our progress to date and where we might expect to go moving forward. As you can see from the data that Jane has just presented, we're making good progress with PRT3789 towards testing our hypothesis that highly selective degradation of SMARCA2 can make meaningful differences for patients whose tumors harbor a SMARCA4 mutation. We are continuing our dose escalation to arrive at an optimal biological dose to advance into larger backfill cohorts of homogeneous population of patients with loss-of-function SMARCA4 mutations. In addition to monotherapy studies, we're advancing two combination studies, one with docetaxel and the second with Keytruda as part of our recently announced collaboration with Merck. Both of these combinations have strong preclinical rationale. Finally, we've initiated our first study with our oral SMARCA2 degrader, seven seven three two. We look forward to providing a number of updates over the coming months across these programs as we continue to drive forward, beginning with Dr. Yap's plenary session presentation in October at the Triple Meeting. We're honored that Dr. Yap was able to join us today to provide his perspective. As a note, Dr. Yap needed to head back to the conference for the prior commitment. With that, next slide, please. Our team is standing by to take any questions you may have. Thank you. As a reminder, to ask a question, you will need to press star one one on your telephone. To remove yourself from the queue, you may press star one one again. Please stand by while we compile the Q&A roster. Our first question comes from the line of Reni Benjamin of Citizens JMP. Hey, guys. Thanks for taking the questions, and thank you for the update and congrats on the preliminary data showing monotherapy activity. I have a couple of questions. You know, just to maybe start off, so look, I understand that it's pretty early to be focusing on ORR, given that it's a dose-ranging study. But can you give us maybe some additional color in terms of, you know, the patients where you saw a pharmacodynamic effect? I think there are 11 of those. Did you see a corresponding increase in tumor shrinkage, you know, corresponding to increased levels of enzyme being degraded? And maybe related to that, did you see more responses in the loss-of-function mutant patients versus, you know, the non-loss-of-function mutant patients? I think, Jane, you mentioned in your prepared remarks you were seeing, you know, responses in both types. Then I have some follow-ups. Yeah, thank you. You know, we also are really excited about seeing the early responses. We do believe this proves a proof of concept for this as a mechanism and pathway. In terms of the degradation levels, there are two components to the degradation levels, both depth of degradation as well as duration of the degradation. We show that when we're looking at the area under the curve, that combines both components, that we are seeing increasing depth and duration with increasing dose. Of the patients that had the higher AUC, more than 40%, they were more likely to have a response. In terms of your second question about the responders, the three responders were loss of function patients. They had known loss of function, and so that does corroborate our preclinical hypothesis that these patients will be most likely to benefit. The additional patients in the Class 2 type, or type of SMARCA2 mutations likely have additional loss of function mutations, and those are why we enrolled all SMARCA4 mutations into the trial so we could further characterize those patients. Got it. Just sticking with the response for, you know, another question. It seems like when I'm looking at the plot, at the interim clinical activity in terms of response rates, we're seeing a couple of lung cancer patients who look right at the borderline of a PR. Can you talk a little bit about the remaining patients on the study and whether we might see a deepening of responses, you know, or if all these patients have progressed since? Yeah, certainly there, there will be one patient that helps us understand this biology well, which is the patient at 80 milligrams, who was on study for more than a year. They are planning to dose escalate, and so we get more clarity as to whether or not that dose escalation can lead to further deepening of the response. And as I mentioned, we are trying to get patients as we dose escalate into that area where they have prolonged duration of SMARCA2 degradation. And yes, those patients that seem to have some sort of tumor shrinkage were the ones that had the longest depth and duration of tumor of SMARCA2 degradation. So as a follow-up, in terms of next steps, can you talk a little bit about the learnings from this study that might help you identify appropriate patients going forward? For example, did you notice any sort of differences in SMARCA2 expression levels from responders to non-responders? And, you know, when, you know, is that something that you might, you know, add to the enrollment and further evaluation? Yeah, not, not specifically SMARCA2 expression. We are still gathering more information around that in the tumor tissues, as we get more tissue biopsies. We are learning more about the different variability that we see in peripheral blood of the SMARCA2 levels, and understanding the depth and duration that we need to achieve to see those responses. Maybe I can just add to that. As with dose escalating, then that, you know, we expect to, again, as Jane said, given the increasing exposure that we're seeing, we expect to see further reductions in PD, you know, AUC of PD, and, that's typically associates with, you know, better response. So we hope to see that. Got it. And then my final question just has to do with RECIST criteria definitions. I thought that, you know, the definition for stable disease encompassed kind of changes between, like, a 29% decrease, right? Like, right up to the, right up to that PR level of 30%, up to, like, a 20% increase in tumor size, which, you know, then when I look at this chart, there would be about 16 patients or 62% clinical benefit rate. Did I mess up my definition or calculation? No, you're absolutely right. Because this is preliminary data, we wanted to characterize what we are seeing in terms of activity, but it would be premature for us to be calculating clinical benefit rates until we're at our recommended phase II dose, and so but you are absolutely correct. There are many patients that are benefiting beyond what we would expect for a second-line population. Just recall, front-line populations, progression-free survival is 2.7 months. If you look at our swim lanes, you'll see that patients are doing better than that. Got it. And if I can just squeeze one last one. In the plenary session that you mentioned at AACR, that will be at the triple meeting that'll be coming up, should we be expecting, you know, just data from all 65 patients and, you know, what you have from the backfill cohorts, just longer follow-up from these patients? What can you just give us some color there? Yeah, we're planning to give additional color around the biomarkers, around the degradation, as well as an additional data cut with additional patients as they reach that, efficacy evaluable. As you probably know, the scans are every six weeks, and so you do have to wait some time before the safety evaluable become efficacy evaluable. Excellent. Thank you very much for taking the questions. Thank you. Thank you. Our next question comes from the line of Jeff Hung of Morgan Stanley. Thanks for taking my questions. Can you just talk about the nature of the three treatment-related grade three plus adverse events? Like, you know, when they presented, how long they lasted, and whether it was dose dependent, and then I have a follow-up. Yeah, you know, the Grade 3 adverse events, you mean the specific ones that are leading to- Everything that... Yeah. Treatment-related? Yeah, you know, they're a smattering of things, meaning, like, there was an AST and there was an elevation, there was a neuralgia, there was a constipation. So, you know, the adverse events leading to that are related. It's hard to determine right at phase one because you're still characterizing your drug. But in general, everybody tolerated the drug very well and was able to receive all of their doses. And most of the investigators felt that it was disease-related rather than drug-related. Just to clarify, so in terms of dose dependence, so were these at kind of, you know, at different doses, or were they all more at like, you know, higher than the lower doses? Or can you just talk about that, even if qualitatively? Yeah, it was across the different doses. You know, for instance, one of the disease-related ones was due to... There was some abdominal pain, and they had underlying GI malignancy, for instance, and so that happened at lower doses. Okay. And then, given that you haven't reached the MTD, can you just talk about where you think you are in the therapeutic window, and how are you thinking about dose response, you know, with the best tumor shrinkage coming from the patient that was on the lowest dose? Thanks. Yeah, so, that's something that others have asked in terms of, we believe that patient was exquisitely sensitive, and for a variety of different factors, there's many factors in the clinic that can affect your sensitivity and whether or not you have higher or lower SMARCA2 levels. We do believe that our goal is to recapitulate what was seen preclinically, is to deepen and prolong the duration of the SMARCA2 degradation. And you can see that on our box plot. That's what we tried to encompass both parameters. You can't see both parameters when you're just looking at you know, like, depth at one time point, and so that incorporates both. And as we increase the dose, we're seeing more consistent across all patients, that depth and duration of SMARCA2 degradation. Great. Thank you. Thank you. Our next question comes from the line of Peter Lawson of Barclays. Hi, good evening. This is Alex on for Peter. Thank you for taking our questions. I just wanted to ask around the degradation and your views on kind of the optimal degradation that you need here. It seems like you achieve about 60%-70% at the higher doses. Do you think you can get higher degradation, or you think that you've maybe reached a plateau here? No, you know, we think we can increase the duration as well as the consistency, and that's important because patients come in all flavors in terms of the amount of degradation you have, and you wanna drive it as high as possible, which is why we are continuing to dose escalate, so we don't leave any efficacy on the table. Great. And then, just a quick question on the safety profile. You had about 30% of patients had dose holds. Was this due to adverse events or any comments you can make around that? Yeah, you know, only four of those were thought to be related to drug, but even when I look at those four patients, I mean, and when I look at those, some of them were a smattering, like I said, of AST, mild increase constipation, neuralgia, so, not one consistent adverse event, which would be typical for a phase one dose escalation trial. Okay, great. And then just a final question, a quick clarification. For the data we see at the Triple Meeting, are we going to see some data at higher doses as well? Thank you. We will be doing a later data cut. We haven't done the cut yet, so, it's TBD as to which patients we'll be including. Thank you. Our next question comes from the line of Roger Song of Jefferies. Great. Thanks for sharing the data, providing those comments, and then thanks for taking our questions. A few quick ones from us. The first one may be related to the dose selection. So based on the PK/PD, how would you characterize the therapeutic dose, the starting point? And then how does this correlate with the clinical activity you have been seeing? Maybe more specifically, as you confirm the dose by the end of the year, should we expect you will select the one or multiple dose to moving to the next stage? Thank you. Yes. So in terms of dosing, like you said, we are continuing to dose escalate, and we're anticipating to get to that dose before the end of the year. By Project Optimus, you have to look in more depth at least two doses traditionally. So that'll be a discussion as we advance the registration type programs as to what doses we select. But we certainly will be in discussions with the FDA around that, and certainly we will pick the doses that have the best profile for both efficacy and safety. Got it. And then another clarification is: Among those fourteen patients still on treatment, how many of them are actually, right now it's PR and or stable disease? Of the patients that we have on our waterfall plot, the patients that have tumor shrinkage to continue, and we're very encouraged by the response and clinical benefit that we're seeing. As I mentioned, we have others that have stable disease that are continuing on as well. Some of these patients have not reached their first scan yet. Got it. Thank you. That's it from us. Thank you. I would now like to turn the conference back to Kris Vaddi for closing remarks. Hello, everyone. Thank you very much for taking the time today to join the call.