Good day, ladies and gentlemen. Thank you for standing by. Welcome to iTeos Therapeutics conference call. At this time, all participants are on a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star one one on your telephone. You will then hear an automatic message advising your hand is raised. Please note that today's conference is being recorded. I will now hand the conference over to your host, Carl Mauch. Please go ahead. Thank you so much. Good morning, everyone, and welcome to the iTeos conference call to discuss the follow-up interim analysis from the phase II GALAXIES-Lung-201 study, assessing belrestotug, iTeos' anti-TIGIT, in combination with GSK's anti-PD-1 dostarlimab, in unresectable, locally advanced, first-line PD-L1 high non-small cell lung cancer patients. A press release summarizing the data became available on Saturday, September fourteenth, concurrent to the study's proffered paper session at the European Society for Medical Oncology Congress. This release, along with the slides of today's presentation, can be found on the News and Events section of the company's website at iteos.com. With me today are Michel Detheux, Chief Executive Officer of iTeos, and David Feltquate, Chief Medical Officer. Matthew Gall, Chief Financial Officer, Matt Call, Chief Operating Officer, and Yvonne McGrath, Chief Scientific Officer, will be available for the question-and-answer session. Before we start, I'd like to remind you that during this call, we will be making forward-looking statements, which can be found on slide two of our presentation. And with that, I would like to turn the call over to Michel. Thank you, Carl, and welcome everyone. We appreciate you joining today to review the interim analysis from our phase II GALAXIES-Lung-201 study. To start with slide 4, we are thrilled because the study, the largest phase II of a TIGIT antibody in lung cancer, has delivered all that we wanted to get for this interim readout. Here is what is important. First, for efficacy, we observe a clinically meaningful objective response rate at every dose of the belrestotug doublet compared to dostarlimab. We believe the consistent significant tumor reduction by the doublet and the 30% + difference in confirmed objective response rate at every dose compared to dostarlimab is a strong signal reflective of the unique profile of our TIGIT PD-1 doublet. Second, for safety, the doublet is showing a manageable profile, broadly consistent with the safety profile of approved IO combination. This phase II was designed as a dose optimization study in line with the FDA's Project Optimus, and it has enabled us to learn an incredible amount of data about our TIGIT combination with dostarlimab. And finally, we are seeing exactly what we wanted to see. This supports that every stage, preclinical, clinical, translational medicine, led to this meaningful differentiation of benefit by adding our TIGIT on top of a quality PD-1 backbone, which is exactly what we have with dostarlimab. Because of these interim results, we launched GALAXIES-Lung-301 in June, our phase III trial assessing belrestotug and dostarlimab against pembrolizumab, the current standard of care in PD-L1 non-small cell lung cancer. We anticipate presenting longer-term follow-up data, as well as additional ORR, safety, and ctDNA data from a more robust data set in 2025. As for GALAXIES-Lung-301, global enrollment is ongoing. Now, let me quickly remind you of the TIGIT mechanism of action on slide five. We continue to believe that TIGIT represents one of the most promising immune checkpoints. This is based on the potential of an anti-TIGIT antibody to modulate activity of multiple immune cells formed in the tumor microenvironment, as illustrated here. We are not only stimulating an antitumor response with activation of T cells and NK cells, as shown in the left panel, but with our active IgG1 isotype, we are stimulating additional antitumor mechanism, as illustrated in the right panel. Turning to slide six, what separates belrestotug from the competitive landscape is that we use our expertise in tumor immunology to select a unique TIGIT antibody in terms of affinity, potency, and activity. In phase I, belrestotug demonstrated that it efficiently binds to Fc gamma receptor at all dose tested as measured by T-reg depletion, and it was the first TIGIT to demonstrate monotherapy activity. These data were why we were able to strike such an amazing deal with GSK in 2021. For us, GSK's commitment to oncology and PD-1 inhibitor dostarlimab make them an ideal partner. As a reminder on slide seven, dostarlimab is the only PD-1 to ever go head-to-head with pembrolizumab in a randomized phase II study, demonstrating they are just as good as, if not better than, pembrolizumab. Having this strong PD-1 backbone sets us apart from the competitive field. With that, I'll pass it off to our new Chief Medical Officer, David Feltquate, to review the interim data set. Thanks, Michel. After joining only in August, this has been an incredible way to begin my future at the company. I spent twenty years developing IO therapies, including the combinations of Yervoy and Opdivo, and these are the kinds of data that I like to see. Okay, to ground us, let's begin with the overview of the trial design on slide nine. As you can see, GALAXIES-Lung-201 is a phase II open label randomized study designed to assess the efficacy and safety of novel immunotherapy combinations, including belrestotug and dostarlimab in patients with PD-L1 high first-line non-small cell lung cancer. The study design has several purposes, including dose optimization in a randomized setting, assessment of contribution of components, and in time, the comparison to other standards of care, including pembrolizumab, for which we plan to share data in 2025. Now, to enroll, it was required for patients to have PD-L1 tumor-positive score of 50% or higher, no actionable driver mutations, and they needed to be a current or former smoker. Patients were randomized to open cohorts to receive PD-1 monotherapy or immunotherapy combination treatment until disease progression, intolerable toxicity, or death. With our phase III in mind, we prioritize enrollment in the arms shown in the center, which assessed dostarlimab versus three different doses of belrestotug in combination with dostarlimab. This enabled us to generate contribution of component and dose optimization data early in the program. With this data in hand now, we have initiated enrollment in every arm in the study and look forward to presenting a broader and more mature data set in 2025. Now, the primary endpoint is investigator-assessed unconfirmed objective responses per RECIST 1.1 criteria, and the secondary endpoints were investigator-assessed PFS, OS, and safety. As of June seventh of this year, that was the data cutoff. The modified intention-to-treat patient population had at least 5.6 months of follow-up. For clarity, I want to explain what we mean by modified intention-to-treat. As you may recall, in May 2024, earlier this year, we announced a qualitative statement on this data set, which was based on an interim assessment taken in March. That analysis included the first 30- 32 patients in each of those four cohorts that had to have a minimum of three months follow-up. To provide a more balanced and more complete analysis of each cohort for presentation at ESMO, we took a data cut from the exact same patient group, but now with longer follow-up, and that was the data lock that occurred on June seventh. That was two point six months after that initial. So three months of follow-up, the initial two point six there, that's where the 5.6 months comes from. So all patients have had at least five point six months. Now, this cut was taken, the enrollment in the study also allowed us to continuing enrolling patients to select cohorts. And so there has been more patients that have been treated, and we'll discuss a little bit about safety for full transparency when I'm going over the overall safety slide. One thing I can tell you, though, is that there were no new deaths, no new categories of adverse events for those additional patients. Okay, so we move to slide 10. You can see the baseline demographics and disease characteristics, which were considered balanced between cohorts, with the exception of a lower number of patients with ECOG performance status of one in the dostarlimab monotherapy cohort, so dostarlimab is a better performing group than these other combination cohorts, and this is important because that's a prognostic marker. One last thing to note is how well-balanced each cohort was with PD-L1 greater than or equal to 90%, because that's a known positive predictive marker for the activity of checkpoint inhibitors. Now, I want to direct your attention to slide 11. Here you can see why we are so excited by this data. For the primary endpoint of ORR, the unconfirmed ORR ranged from 63%-77% for the combination cohorts, compared with 38% in the dostarlimab cohort. Similarly, with confirmed objective response, it ranged from 59%-63% in the doublet cohorts, compared to 28% in the dostarlimab cohort. To take a closer look on the next slide with waterfall plots, it becomes visually clear that not only are the number of responses, but also the depth of response, is much greater from the doublet at each dose compared to dostarlimab alone. Again, we're seeing meaningful impact on tumor reduction at every dose. And as Michel noted earlier, we're not aware of any other TIGIT PD-1 combination data set in this setting that demonstrates such consistent deep responses. Additionally, we want to highlight that a number of patients from the dostarlimab cohort achieved durable, stable disease, just shy of the 30% tumor reduction response threshold, indicating further benefit beyond the estimated response rate. This builds upon the momentum that dostarlimab has created and making and establishing that this has meaningful clinical benefit across a range of tumors, including non-small cell lung cancer, and reconfirms our confidence in the quality of our PD-1 partner. We move to the next slide. I want to draw your attention. Again, looking at combination arms, we see clusters of patients with tumor reduction greater than 60%. With the dostarlimab monotherapy spider plot, you'll notice that that cluster is closer to the 30%. And again, that's consistent with what we described for the waterfall plots, which is this greater tumor reduction.... common cohorts. As a reminder, the minimum follow-up for this interim data set is 5.6 months. Further follow-up is required to better characterize the durability of the clinical benefit with the combination at each dose level, and we look forward to seeing these data in 2025. Wrapping up clinical activity, we've cut this data many ways, and everything we've looked at is trending in a positive direction. We want to point out that the benefit of randomized studies is treating patients under similar conditions. The magnitude of the ORR from the doublet at each dose is well beyond any historical single-agent pembrolizumab benchmarks. We're in the process of generating the pembrolizumab control arm data, which we believe will further enrich this already robust data set. We're also investigating changes in circulating tumor DNA, ctDNA, and data from that is on slide 14. This is an emerging on treatment predictive biomarker, specifically for the detection of molecular response in non-small cell lung cancer. So what is circulating tumor DNA, and why do we think it's relevant in our evaluation of the doublet? At a high level, tracking circulating tumor DNA reduction is an additional measure of the impact of a therapy on a patient's tumor burden. It allows us to better understand if a patient is responding to a therapy by observing reduction in circulating tumor DNA at an early time point. In this study, it was done at week seven. Additionally, high baseline levels of circulating tumor DNA are often associated with worse prognosis, greater tumor burden, and more aggressive disease. This data is additive and supports our conviction because there is growing evidence to suggest that reduction in circulating DNA is associated with better survival outcomes in non-small cell lung cancer patients. As for our data, once again, there's a clear trend in median circulating tumor DNA reduction and greater reduction in circulating tumor DNA from baseline by the doublet compared to dostarlimab monotherapy. We believe based on the circulating tumor DNA data, we are seeing a clear picture indicating to us that the 400 mg and 1,000 mg cohorts are having the greatest molecular response. Turning to safety on slide 15. Overall, belrestotug plus dostarlimab demonstrated a safety profile broadly consistent with what we've observed from approved IO combinations. Specifically, there's an increase in immune-mediated adverse events associated with the combination treatments compared to with dostarlimab alone. Now, the most common treatment-related adverse events were skin and subcutaneous tissue disorders that occurred in about half of the population, and endocrine disorders, which occurred in about a quarter of the population. It should be noted that the majority of these treatment-related adverse events were low-grade events and were considered manageable. Now, there were three treatment-related deaths on study. Two occurred in the belrestotug 100 mg cohort and one in the belrestotug 400 mg cohort. All these events were immune-related, and they were specifically one case was pneumonitis, one case was hepatitis, and one was a myocarditis, yeah. Lastly, the most common treatment emergent adverse events leading to discontinuation were skin and subcutaneous tissue disorders, as well as pneumonitis. Of these discontinuations in the combination cohorts, a quarter of them were for low-grade skin and subcutaneous disorders. We want to... All the data re-reporting is specific to the modified intention-to-treat population, which had the minimum of 5.6 months follow-up. Since this cut was taken, the enrollment in the study has significantly expanded. For those additional patients that have been treated but have had shorter follow-up, we can report no new grade 5 treatment-related adverse events, and no new categories of adverse events have been observed. One thing to point out, over the course of the study, as the teams at iTeos and at GSK have been reviewing data, speaking with investigators, we recognized there were opportunities to improve the detection and management of adverse events, and all these lessons are being implemented in the phase III GALAXIES-Lung-301 study. So this gives us confidence that the safety profile will continue to improve. Moving to slide 16, if we look at immune-mediated safety in more detail, specifically treatment-related, immune-mediated adverse events, skin and subcutaneous tissue disorders were the majority across all doublet cohorts. These events, again, were considered generally manageable with oral and topical steroids, and we're also learning adaptations we can do to further improve the management. Overall, immune-mediated adverse events were higher in the 1,000 mg belrestotug cohort as compared to the 100 mg or 400 mg cohorts. Specifically, immune-mediated adverse events of pneumonitis, myocarditis, and rashes were more frequent in the higher dose cohorts. One of the benefits of presenting this data at a major medical meeting has been to gain feedback from experienced practitioners, and I can tell you, a resoundingly common theme has emerged from these discussions. Specifically, this is clearly an active regimen, that people have confidence in the quality of dostarlimab as a very active anti-PD-1 agent, and that the safety we're seeing with the combination is acceptable and manageable given the benefit we are seeing. No one more than us is eager to see how these signals will translate to survival. And with that, I'm going to turn back to Michel. Thank you, David. As we said earlier, we continue to be very excited with the interim data set presented today. We believe this is the strongest data set ever generated for TIGIT in this setting, and we could not be more happier. Indeed, this data were critical in making the decision to launch our first phase III, GALAXIES-Lung-301. We will apply our data-driven mindset to rapidly growing and maturing data sets as we explore opportunities to expand our development strategy. As a reminder, this trial, initiated in June 2024, is a randomized, double-blind, placebo-controlled global study enrolling 1000 patients with PD-L1 non-small cell lung cancer. The primary endpoints of this study are progression-free survival and overall survival. In July 2024, we announced, we announced that the first patient was dosed in this trial, and we look forward to providing updates as we continue to progress. Collectively, we believe the combination of safety and efficacy data presented here today gives us confidence in our go-forward phase III dose of 400 mgs. Now, as a conclusion, we are very excited that this study delivered an interim data set that validates the potential of belrestotug on top of dostarlimab to improve treatment outcomes versus current standard of care. With this data, I want to remind you that we observed 60% confirmed overall response rate at every dose of the doublet, with a 30% difference to dostarlimab. With ctDNA reduction at the 400- and 1,000-mg cohorts, a promising signal for survival outcomes. Lastly, a safety profile broadly consistent with approved IO combination and a generally manageable immune-related adverse event. We are more convincing than ever that belrestotug is a unique TIGIT therapy, and when combined with dostarlimab, this doublet has the potential to clinically change patient outcome for the better in non-small cell lung cancer and beyond this indication. With GALAXIES-Lung-201, we anticipate a more robust interim data set from this trial, showing longer term follow-up data, which will provide an even clearer depiction of our doublet's potential to benefit patients. Before turning the call over to questions, we want to remind everyone that 2025 will be another year with defining milestones. For TIGIT, the TIG-006 head and neck data will be presented concurrent with the randomized GALAXIES-Lung-202 trial. And as I just said a moment earlier, we anticipate a more robust cut of data from the GALAXIES-Lung-201 study in 2025 as well. And with our cash position of over $700 million and runway through 2027, with this, we have the firepower to support the data and allocate resources to create value and improve outcomes for patients. In closing, today, it is an important day in the growth of iTeos and our TIGIT program, and I am very proud of what we have delivered through this collaboration with GSK. We thank you for taking the time to join us for this introductory overview. I would also like to thank the patients, the families, and the clinicians involved in this study. And with that, we will turn the call over to the operator. We look forward to your questions. Thank you very much. Thank you. Ladies and gentlemen, as a reminder, to ask a question, you will need to press star one one and wait for your name to be announced. To withdraw your question, simply press star one one again. Please stand by while we compile the Q&A roster. Our first question coming from the line of Brian Cheng with J.P. Morgan. Your line is open. Hey, guys. Congrats on the data, and thanks for taking our questions this morning. Can you comment on the performance of the belrestotug monotherapy here compared to historical pembro combo? And then, have you also done an analysis on those patients that have PD-L1 expression higher than 90%? Any color on the response there? I have a quick follow-up. Thank you. Yes, Brian. Let me start by the fact that, as you know, it's also including pembrolizumab arm, then we'll have the ability to compare directly our patient population with the performance in pembrolizumab, in the near future. David, you want to comment on the historical performance of pembro? Yeah, there, there were two quite right, the performance of relative to dostarlimab, relative to pembrolizumab, and then it was also PD-L1 greater than 90%. So I'll take the first one. Yeah, so overall, the data is of dostarlimab monotherapy is consistent with pembrolizumab in this population. So what, why do I say that? Well, the response rate of unconfirmed 37%, confirmed twenty-eight 28%, is on the lower end of what's seen for the range for pembrolizumab. But when you factor in durable, stable disease, and I think you saw that data in the waterfall plot and in the spider plot, there are many patients that were hovering around a 20%-29% tumor reduction. In fact, I can recall two patients that actually went to -32, then they went to -28. Then, you know, these are borderline responses. So in total, we're seeing activity that is quite comparable to what you see with pembrolizumab. And again, it bolsters our confidence that, like in other studies, like the PERLA study, that dostarlimab is as active as pembrolizumab. Now, you asked a question about anti-PD-1, the PD-L1 marker greater than 90%. We showed you the demographics that we have balanced across all these cohorts. But what we didn't show you is one of the analyses that we do when we parse out all the data. What we like to do is look at comparisons again, of each of the combos at each dose level relative to the monotherapy. And I can tell you across all those cohorts, it was a consistent finding of this net increase of about 30%. I don't have, off the top of my head, what was the actual response rate, and I think that was specifically what you were asking, but I can tell you the consistency was there. Great. And then, lastly, just on the timing for the next updates coming from Lung 201, when could we potentially get data on, you know, PFS, and also the data on the pembro monotherapy arm? Thank you. Hey, Brian, this is Matthew. There'll be a lot of data coming in 2025. That's been discussed. At this point, we're not guiding any further than you should get a lot of what you're looking for next year, and continue to maturity beyond. Okay. Thanks, guys. Thank you. And our next question coming from the line of Chris Raymond with Piper Sandler. Your line is open. Hey, thanks for taking the question. I've got two, actually, if that's okay. So just first on the question we've been getting a lot from folks over the weekend and today is, you know, points back to the experience of tiragolumab with efficacy degrading between the CITYSCAPE dataset and then phase II SKYSCRAPER. Can you maybe just talk about what gives you confidence, you know, this obviously it's a, it's a different phase II design with this dataset versus CITYSCAPE, but what gives you confidence that this phase II data will hold up in phase III? And then the second question is just moving forward in phase III. You mentioned, I think over the weekend, that you still need regulatory buy-in globally. Can you maybe clarify which agency this is and sort of what has to be done to begin enrolling sites? Thanks. Hi, Chris. Then for the first part of the question, what make us confident is that, as I said, this is the largest dataset ever produced for non-small cell lung cancer. We have more than 90 patients, which is being treated with the doublet, compared to 29 patients within CITYSCAPE. What makes us also confident is that we are comparing to one of the best PD-1 currently in use. And the last part is that we have also a pembrolizumab arm that will be available in the near future for direct comparison between the monotherapy and the doublet. David? Yeah, and one other thing I would add is, this is the best-in-class anti-TIGIT that's out there. You've probably seen some of the earlier data around T-reg depletion we published. You know, we have great confidence in the preclinical data that David Spigel showed in the background on the presentation. We have high confidence in this compound. Thanks. And just on the regulatory buy-in? So the regulatory process, we are in the final decision with the regulatory agencies. We've opened the studies in Japan, Korea, Panama, and South Africa, and we continue to expand. And Argentina, sorry, and we continue to expand the opening of sites globally. One thing I can say is there's nothing unusual happening. Every global study I've done, you work with regular process of, with health authorities, to open up your study, and that's exactly what we're doing right now. There's nothing happening now that is giving us pause. Great. Thanks so much. Thank you. Now, our next question coming from the line of Daina Graybosch with Leerink Partners. Your line is open. Hi, guys. Thank you for the questions. Hello from ESMO. I wanna understand more your dose selection. So a couple sub-questions in that. I wonder how much of that selection of the 400 mg dose was based on the dataset we got to see at ESMO, and what additional datasets you considered beyond the scope of what you've made public? And then the second question is, we all know Merck took 200 mg dose forward, and they ran into issues with toxicity and discontinuation, apparently contributing to a lack of benefit overall when they combined with chemotherapy in an early phase setting. And I wonder what gives you confidence of this dose in combination with chemo or beyond, and might you end up picking a different dose for those combinations? Thank you very much. Yes, Daina, then we have multiple datasets, including our dose expansion in phase I, but also additional data from TIG-006, our partners in head and neck and non-small cell lung cancer when we evaluate the triplet with chemotherapy. Obviously, the most important dataset is the 201, and David, do you want to comment on the dose selection? Yeah. Daina, it sounded like you specifically wanted to know what was the data that we observed that had us land on 400. Yes. As you know, you look at the totality of data. That includes everything from safety, efficacy, pharmacodynamics, things like this. As we reviewed in this presentation, the data we had basically indicated that from a safety standpoint, the lower doses were generally more tolerable than the higher. We also saw from an efficacy standpoint, the middle and higher doses seemed to have more activity. These are trends, right? We're about to talk high slopes here. When we look additionally beyond the traditional responses, looking at circulating tumor DNA as an indicator, there appeared to be a little bit more of an effect, again, with those middle and higher doses. In total, it was telling us that, you know, in the middle was the preferred dose. That was the dose we were expecting going into the phase II. The data really just confirmed what our underlying expectations would be. The chemotherapy combination question? Yeah, as Michel was pointing out, so you're asking specifically around Merck and their combination with chemo, what they've seen, and I can't speculate on what's happening there. I can tell you what we know about our drug. Where we've looked at initially in a phase I, a combination with chemotherapy, it's been well tolerated, no signals outside of what you would have expected with chemotherapy and a combination with IO. As well as I told you, we're learning lessons in doing that randomized phase II about management guidelines, how we frame the protocol, and advice to investigators on how to do this, and we think we're optimizing that and continuing to improve the profile. We also believe that compared to Merck, which is, I would say, looking to a co-formulation, our co-administration of the two drugs is helping us to a better management of the safety profile. Yeah, and I can give you a concrete example. So early in the program, the protocol-defined follow-up on certain laboratory parameters to look for early safety events needed to be tweaked. So we weren't following, troponins and looking for early myocarditis, which we all know when you can find it early, then the patient that died of myocarditis, it probably would have prevented if we had done it. We implemented that in the study, and that also is gonna be done in 301. Another example, we had a rule that we were very conservative. Any grade three rash, a patient had to discontinue from the study. Well, as we all know, other than for exfoliative rashes, you hold drug, you give steroids, patients get better, and you retreat them. That didn't happen here. That was one case, but it's indicative of a lesson we learned. We made a modification. All that's gonna be applied to 301. That's why we think we're gonna even have a more improved safety profile. That's very helpful. Maybe one follow-up. I suspected the ctDNA played a role, and it is quite compelling that it's so responsive. But what specific validation do we have in lung cancer, that this is correlated or even associated with clinical benefit, particularly also with IO therapy? Yeah, as you know, there's been some data published, but there's still ongoing work, and what we really need are larger randomized studies that are doing that, right? So the results are not 100% conclusive. However, the totality of the data, you talk to investigators, people who work in this, and there is a general belief that this data is suggesting that this may predict long-term outcomes. So that, to us, was an important data point to incorporate into how we were thinking about this. Thank you. Thank you. And as a reminder, ladies and gentlemen, if you have a question, please press star one, one. And our next question coming from the line of David Nierengarten from Wedbush Securities. Your line is open. Hey, thanks for taking the questions. Most of them might have been asked, but a little bit of a follow-up on dosing and dose selection. I believe in the past, and also with Tira in the past, it seems that, you know, the TIGIT, anti-TIGIT antibodies achieve saturation and pretty soon in dose escalation, but others have, and you have escalated beyond that. Could you just comment on, you know, if receptor occupancy isn't the best measure, is ctDNA the best measure, or are there other measures of tissue penetration or other things that we should be, or other biomarkers that you might reveal later that we should be looking for? Thanks. Yeah. So I'll take that sort of part by part. So you mentioned about receptor occupancy, and it's true, we've seen this with other IO agents, that at lower doses, you can achieve that. And that's receptor occupancy and circulation. Now, as we know, it's about also getting enough drug into tissues, and there you commonly need greater exposure to achieve that. We don't have direct data on that, right? So our inferences is we need to be higher than that. Then we look at the data, and we try to understand, are there hints in the data that are telling us that higher doses will achieve potentially greater outcomes? So what, what do we know about that? Well, we've looked at the response data, and you can see there it's a slow slope, but it's a gradual rise across the doses. We just discussed circulating tumor DNA, where it wasn't as gradual, right? That when you both mono and a hundred mgs had activity, but when you got to 400 and a 1,000, you had more activity. It's possible that the two mechanisms of action that are at play with this drug, one of which being T-reg depletion, it's important to have higher doses, and that is why we're seeing that effect. And again, that would be not only in circulation, but a tissue penetration goal that we're trying to achieve. And again, we have confidence that with the data we have, we've made the right choice. Thank you. Thank you. And our next question coming from the line of Eva Fortea-Verdejo with Wells Fargo Securities. Your line is open. Hi, guys. Thanks for taking our questions. Two quick ones from us. The first one on efficacy. What's driving the difference in confirmed and unconfirmed responses? Is it just time? And how many of these patients with unconfirmed responses are still in the trial and could ultimately get confirmed? And the second one is on safety. Are discontinuations happening early on treatment? And did you provide any color on those interruptions in the different dose cohorts? Thanks. Sure, I can take that. So I'll start with the efficacy. So you're pointing out what are the differences and what do we know about the patients that were unconfirmed and confirmed. So to recap from the data slide, there were three patients in the monotherapy that were different from the confirmed, unconfirmed, one in the 100 mgs, two in the 400, and four in the 1,000. And as you know, right, there really are two categories of reasons for this. Either patients haven't had their last scan was an unconfirmed response. They just they haven't had the data lock. They didn't have the time for a follow-up, so it's pending. Or people had initial unconfirmed response, so then on some scans, they didn't have it. As an example, for that last category, if you look at the data from the spider plot on slide 13, and you look at the monotherapy cohort, and I apologize, I know there's a lot of lines intersecting, but if you look on there, it's actually incredible. You'll see just in that zone, there are two patients that go to about - 32% reduction, so they had an unconfirmed response, and then the next scan, they went to - 28, - 25. The next scan was about - 25 again. The next scan, they went on study for many months, and they keep just missing the response. So that's unconfirmed responses. We have to call them that, but they're quite frankly getting benefit. They're durable, stable disease. So again, with more follow-up, we'll have more clarity on some of these other things. But it points to, I would say, the general meaningfulness around the similarity between these two findings. And again, overall, even with the confirmed response we're seeing with the combination, this is well above the historical pembrolizumab benchmark of 40%-45%. Now, you mentioned safety, and you're asking about discontinuation timing. So we've looked at this, and I can tell you across the different cohorts, you see some patients discontinuing early within the first month or two. You see some continuing a few months later and some that occur later. There actually is a pattern there. And I can tell you, working on other IO agents, that's similar to what you see. Obviously, the frequencies can be different with different IO agents, but what we're seeing here is consistent with what we've seen with other IO therapies. Then you asked about dose interruptions. And you're right, we didn't report that there. There are approximately about 25% of patients that have had dose interruptions, and then they get back started on treatment. Next questions. Thank you. As a reminder, ladies and gentlemen, if you have a question, please press star one, one. We'll give it a moment. All right, I see there are no further questions in the Q&A queue at this time. Ladies and gentlemen, that has been our conference for today. We thank you for your participation, and you may now disconnect.