Good morning, and welcome to the Shattuck Labs' third quarter 2023 earnings conference call. At this time, all participants are in a listen-only mode. Later, we will conduct a question and answer session, and instructions will follow at that time. As a reminder, this conference call is being recorded. We'll now turn the call over to your host, Conor Richardson, Vice President of Investor Relations at Shattuck Labs. Conor, please go ahead. Thank you, operator. Good morning, everyone, and welcome to the Shattuck Labs conference call regarding our third quarter 2023 financial results and recent business updates. The press release reporting our financial results was issued pre-market this morning and can be found on the investor relations section of our website, ShattuckLabs.com. During this morning's call, the Shattuck leadership team will provide a business overview of the third quarter of 2023, including clinical development updates. Speaking on today's call will be our Chief Executive Officer and Scientific Co-founder, Dr. Taylor Schreiber, our Chief Medical Officer, Dr. Lini Pandite, and our Chief Financial Officer, Mr. Andrew Neill. We will then open the call for questions following our prepared remarks. Before we begin, I would like to remind you that today's webcast contains forward-looking statements within the meaning of safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Such statements represent management's judgment as of today and may involve certain risks and uncertainties that could cause actual results to differ materially from those expressed in or implied by these statements. For more information on these risks and uncertainties, please refer to our most recent quarterly report on Form 10-Q for the quarter ended September 30, 2023, and our other filings with the SEC, which are available from the SEC's website or on our corporate website, ShattuckLabs.com. Any forward-looking statements represent our views as of today, November 9, 2023. With that, I will now turn the call over to Dr. Schreiber, our Chief Executive Officer. Taylor? Thank you, Conor. Good morning, everyone, and thank you for joining us today. We are very pleased that our lead clinical-stage product candidate, SL-172154, has advanced to a stage where we are able to begin sharing clinical data from both our hematologic and solid tumor programs. Importantly, we are also pleased to have observed our first responses and efficacy data across our clinical trials, including our phase 1b clinical trial in platinum-resistant ovarian cancer and our phase 1a/1b clinical trial in acute myeloid leukemia or high-risk myelodysplastic syndromes. We look forward to providing more details throughout the call. For the rest of the call, we will refer to SL-172154 as 154. This morning, we will discuss interim data from our phase 1b clinical trial of SL-172154 in combination with pegylated liposomal doxorubicin in patients with platinum-resistant ovarian cancer. In addition, we will discuss the encouraging data from our ongoing phase 1a/1b clinical trial in acute myeloid leukemia or higher-risk myelodysplastic syndromes that was described in an abstract released last week and will be presented at the American Society of Hematology Annual Meeting in early December. These data include dose escalation data for SL-172154 as monotherapy and in combination with azacitidine in primarily relapsed/refractory AML and higher-risk MDS patients. As a reminder, SL-172154 is a dual-sided fusion protein. It inhibits the CD47 checkpoint receptor and also directly activates immune cells by CD40 engagement. The CD47 landscape has evolved significantly over the past 18 months. Several advanced programs have encountered significant challenges with toxicity, including destructive anemia. These safety issues and the related clinical challenges have led to significant skepticism regarding the potential clinical utility of the CD47 pathway. We believe, however, that these safety issues are the result of the design of some CD47 targeted agents and are not inherent to the CD47 target itself. We believe that conclusions currently being drawn regarding CD47 as a pathway should be confined only to specific individual agents. We designed 154 to not engage Fc gamma receptors in order to avoid the anemias and other cytopenias that have plagued other agents in the class. Earlier this year at ASCO, we shared clinical data from our Phase 1a dose escalation clinical trial in platinum-resistant ovarian cancer or PROC patients. That data demonstrated that SL-172154 does not cause destructive anemia, and this observation remains true today. We remain encouraged by the safety and tolerability profile of SL-172154 to date. SL-172154 also differentiates from all other CD47 inhibitors through its CD40 agonist domain. This attribute of SL-172154 has already led to a differentiated pharmacodynamic profile in dose escalation studies and may contribute to improved response rates, accelerated kinetics of response, and durability of responses in our... Dr. Lini Pandite, our Chief Medical Officer, will expand on-... Okay. Okay. At a high level, our confidence is bolstered by the interim results of SL-172154 in combination with pegylated liposomal doxorubicin, which we will call PLD, in patients with PROC. As of October 31, 2023, we have observed an overall response rate of 27%, which, if it holds, would exceed the PLD monotherapy benchmark response rate of 4% in the Pfizer-sponsored JAVELIN Ovarian 200 trial. Lini will also highlight recent data from our phase 1a/1b clinical trial, evaluating 154, both as monotherapy and in combination with azacitidine in patients with relapsed/refractory higher-risk MDS and AML. We completed the dose escalation portion of this study in the second quarter of 2023, and these data will be presented at the upcoming ASH annual meeting in December. We have initiated two different frontline dose expansion cohorts, where 154 is being combined with azacitidine in patients with previously untreated higher-risk MDS or TP53 mutant AML. We are very pleased with the momentum in this trial, and enrollment has proceeded very quickly, which we attribute to the high unmet need for these patients and our investigators' enthusiasm regarding the differentiated profile of 154. We look forward to sharing an interim update from the frontline dose expansion cohorts in conjunction with ASH next month. With that, I will now turn the call over to Lini, who will dive into our clinical programs and provide an update on recent clinical data and activities. Thanks, Taylor, and good morning, everyone. 2023 continues to be a year of focused operational execution. I'm grateful for the relentless efforts of our team, our participating investigators, and most importantly, the patients themselves that have enabled this progress. As Taylor outlined, I will first provide an update from our phase 1b trial investigating 154 in combination with PLD in patients with platinum-resistant ovarian cancer, and then provide some color on the data in last week's ASH abstract from our phase 1a/b trial, investigating 154 in combination with azacitidine in patients with AML and higher-risk MDS. Let's start with our ongoing phase 1b combination clinical trial of 154 in patients with platinum-resistant ovarian cancer. As of the data cutoff date of October 31, 2023, 16 patients with platinum-resistant ovarian cancer have been enrolled into this study. These patients have a median of 1.5 prior lines of systemic therapy. SL-172154 plus PLD had an acceptable safety profile, which was consistent with the safety profile of the individual agents. For SL-172154, the most common drug-related adverse event was infusion-related reaction, mostly grade 1 or 2. As of the data cutoff date of October 31, 2023, 11 patients were evaluable for efficacy. We observed three partial responses, one confirmed partial response, and two unconfirmed partial responses. As of November 9, 2023, both patients with unconfirmed partial responses are still on study and have not reached the date of confirmatory response assessment. Four patients had a best response of stable disease, and four patients had progressive disease. As of the data cutoff date of October 31, 2023, the disease characteristics of the patients enrolled in this trial are similar to the characteristics of the patients enrolled in the Pfizer-sponsored JAVELIN Ovarian 200 trial, which is a recently published randomized trial that included a PLD control arm. In the JAVELIN trial, the overall response rate for patients treated with PLD monotherapy was 4%. Additionally, to date, a higher proportion of patients enrolled in our trial have bulky disease measuring over 5 cm in diameter and pretreatment with bevacizumab, both of which are poor prognostic factors. We expect to complete enrollment of the expansion cohorts this quarter and to provide additional response and response durability data from the full cohort by mid-year 2024. Overall, we are encouraged by the emerging data from this combination cohort and look forward to updates with more patients and longer follow-up. We are also continuing enrollment in our phase 1b trial of 154 in combination with mirvetuximab soravtansine in platinum-resistant ovarian cancer. Enrollment and dosing are progressing quickly. We expect to report initial combination data from this trial mid-year 2024. Let us now turn to the progress we have made in our phase 1a/1b clinical trial in AML and higher-risk MDS. In this trial, we are evaluating the safety, tolerability, pharmacokinetics, antitumor activity, and pharmacodynamic effects of 154 as both monotherapy and in combination with azacitidine, the current standard of care. As described in our ASH abstract, 37 adult patients with primarily relapsed/refractory AML or high-risk MDS have received 154 as monotherapy or in combination with azacitidine. These patients had a median of 2 prior lines of therapy. There are 19 patients in the monotherapy cohort and 18 patients in the combination cohort as of the data cutoff date of May 25, 2023. In this trial, 154 had an acceptable safety profile as a monotherapy and in combination. For 154, the most common drug-related adverse event was infusion-related reaction, mostly grade 1 or 2. Monotherapy responses have not been reported with CD47 targeted agents in heavily pretreated relapsed/refractory AML patients. Consequently, we were particularly encouraged by a monotherapy response in a heavily pretreated relapsed/refractory TP53 mutant AML patient. This patient had a rapid response to SL-172154 monotherapy, achieved a morphologic leukemia-free state, and was subsequently taken to allogeneic transplant and remains leukemia-free. Additionally, in other patients, we also observed antileukemic activity in the form of blast count reductions. We also enrolled several previously untreated TP53 mutant high-risk MDS patients in the dose escalation portion of our trial. These data are included in the ASH abstract. As of the data cutoff date of July 10, 2023, antitumor activity was observed in combination with azacitidine in two of four response-evaluable patients with previously untreated TP53 mutant high-risk MDS. We observed one complete response in a treatment-related TP53 mutant high-risk MDS patient, who remains on study, and one marrow complete response in a patient who was taken to bone marrow transplant. Two patients had best response of stable disease, one of whom was taken to transplant. Overall, we are encouraged by the growing body of data that validates the unique mechanism of action of 154 and its therapeutic potential to address the unmet needs of patients with AML and higher-risk MDS. Our data continue to show evidence of CD40-driven pharmacodynamic activity, both in peripheral blood and bone marrow. We believe that CD40 activation and the resulting involvement of the adaptive immune system is important in these heme indications and may provide significant improvement to CD47 blockade in terms of both improved response rates and durability of response. We look forward to presenting the complete data of the dose escalation portion of the trial in relapsed/refractory patients at the ASH meeting and sharing initial data from the frontline expansion cohorts during a company-sponsored event around the time of ASH next month. With that, I will now turn the call over to Mr. Neill to discuss our financial update. Andrew? Thank you, Lini, and good morning, everyone. As Conor mentioned at the outset of the call, the full financial results for the third quarter 2023 are available in our 10-Q and earnings press release, filed pre-market this morning. I would like to focus on a few key points from our disclosures. We continue to be well-positioned financially. As of September 30, 2023, our cash and cash equivalents and investments were $101.1 million. In the third quarter of 2023, our research and development expenses were $24.2 million, as compared to $18.9 million for the third quarter of 2022. In the third quarter of 2023, our general and administrative expenses were $5.1 million, as compared to $6.6 million for the third quarter of 2022. Our net loss for the third quarter of 2023 was $27.5 million, or $0.65 per basic and diluted share, as compared to a net loss of $24.6 million, or $0.58 per basic and diluted share for the third quarter of 2022. Based on our current operating and development plans, we reiterate our financial guidance. Shattuck believes its cash and cash equivalents and investments will be sufficient to fund its operations through year-end 2024, beyond results from its phase 1 clinical trials of SL-172154. This cash runway guidance is based on our company's current operational plans and excludes any capital that may be received, proceeds from any business development transactions, and/or additional costs associated with clinical development activities that may be undertaken. With that, I'll hand the call back to Dr. Schreiber for final comments. Taylor? Thank you, Andrew. In the third quarter of 2023, we made excellent progress across the four different ongoing expansion cohorts in our PROC, AML, and higher-risk MDS trials. We expect several additional milestones and clinical updates through the end of this year. For data updates, we expect to first present complete data from the dose escalation portion of our Phase 1a/1b clinical trial of SL-172154 in relapsed/refractory AML and high-risk MDS patients at the 65th ASH annual meeting. We also plan to present initial data from the frontline TP53 mutant AML dose expansion cohort and the frontline higher-risk MDS dose expansion cohort, combining SL-172154 with azacitidine in the fourth quarter of this year during a company-sponsored event following ASH. For clinical program milestones, we expect to complete enrollment in the frontline higher-risk MDS cohort in the fourth quarter of 2023. We also plan to complete enrollment of our phase 1b dose expansion cohort of 154 in combination with PLD and PROC in the fourth quarter of this year. Should the initial results gathered in our heme and solid tumor studies hold as the size and maturity of these cohorts increase, 154 would have first-to-market potential among CD47 agents in PROC, as well as both AML and high-risk MDS. These are all areas of significant unmet medical need, with multiple opportunities for accelerated development and subsequent registration-directed studies. Taken together, I believe the combination of our experienced team, transformational science and protein engineering, as well as financial resources, puts us in a strong position to move beyond our next set of milestones and into 2024. Before we conclude today's call, I would once again like to thank our patients and their families, the entire Shattuck team, our investors, and the many people who have been supportive along the way. With that, we are happy to take questions. Operator? Thank you. If you have a question, please press star one on your telephone keypad. If you wish to remove yourself from the queue, simply press star one again. One moment, please, for your first question. Your first question comes from the line of Jonathan Miller of Evercore ISI. Your line is open. Thanks so much for taking the question, guys, and congrats on getting to some real clinical data here. I'd love to start on the PROC study and ask a little bit more detail about the baseline characteristics of these patients. Obviously, these are platinum-resistant, but can you give a little bit more granularity on what other variety of agents these patients have seen in their prior lines of therapy? And then maybe a little bit more open-ended, as we think about comping this program to other CD47 programs, which obviously have, well, have not been gathering the excitement that they once did, what is your expectation for being able to demonstrate in these patients that are responding, the impact of CD40 ligand outside of the molecule on the efficacy that you're seeing? Great. Well, good morning, Jon. Thank you, and thanks for the questions. Lini, why don't you go ahead and answer Jon's first question around the baseline characteristics of these patients and how they compare to JAVELIN? And, then I'll follow you with the second part. Thank you, Jon, for the question. Yes, these patients compare very well to the patients who were enrolled in the JAVELIN study. The majority of these patients, and that's 88% of these patients, had failed the frontline platinum-containing regimen and were resistant to frontline platinum. So 100% of these patients had received platinum. 56% of these patients had also received bevacizumab. These patients have also received PARP inhibitors. That number isn't in the slide deck, but the patients have received PARP as well. Great. Thanks, Lini. Pardon me. With regard to, you know, how 154 needs to show in these patients and how that compares to what's evolved in the AML and high-risk MDS space with other CD47 inhibitors. You know, so as most of the audience probably knows, this has been an evolving space over the last three years, and, you know, certain agents might have been discontinued in the AML and high-risk MDS space early on, purely for competitive reasons, under the assumption that magrolimab would be first to market and therefore, the commercial opportunity might have dwindled. Clearly, that's changed, and we certainly look forward to Gilead sharing more data around exactly what happened with ENHANCE and ENHANCE-2, you know, as part of their new commitment to increase transparency. It seems, however, as though, you know, many of these patients enrolled to the magrolimab arms may have discontinued earlier or may have had dose interruptions in a way that could have impacted the top-line readouts of that study, and hopefully we'll learn more about that. Regardless, 154 has to stand on its own two feet in this indication, and clearly we're encouraged by the differentiated safety profile, the lack of destructive anemia. And in preclinical models, you know, the activity of CD40 agonism translated to both improved response rates and improved response durability. And clearly in patients like this, improved CR rates, not just over the expectations of azacitidine alone, but over prior benchmarks with Aza plus drugs like magrolimab are important to exceed. And if and only if you exceed those CR rates, you then have an opportunity of seeing an improved duration of response and improved overall survival. And so that's what we'll be looking to see, and certainly share the first glimpse of that in proximity to ASH in December. And in the high-risk MDS population, we're looking to exceed the azacitidine benchmark in terms of complete response, which comes from the AZA-001 study of about 22%, by at least double. And in terms of the TP53 mutant AML cohort, where azacitidine alone delivers complete response rates in the low single digits, and the combination of AZA/magrolimab, we'll get more data, I hope, soon, but seems to deliver CR rates in the low 30s. And again, you know, we'll look to exceed that by a substantial margin. So, these are things that we have to show on our own, as the field hopefully learns more about the other agents that have been discontinued. Thank you. Your next question comes from the line of Joe Pantginis of H.C. Wainwright. Your line is open. Hey, everybody. Good morning. Thanks for taking the question, and nice to see the early data. Congrats as well. So maybe, Taylor, wanted to see if we could get or do some scenario analysis here, maybe start with the AML MDS study. What do you... Obviously, the expansion cohorts need to read out, but could you envision a say, more targeted path for initial approval, say, targeting TP53 or other focused mutation? And then also, can you provide any color with regard to the kinetics of the responses that you're starting to see in the AML MDS study? Sure. Thanks for the question, Joe, and good morning. So as you know, the one of the expansion cohorts is already specific to TP53 mutant AML patients, where, you know, even in the frontline setting, there is a very high unmet medical need. And, you know, there certainly would be an opportunity for an accelerated path there. You know, if we were to first hit a CR rate, you know, in excess of forty percent or so, I think that would be interesting and be a good indicator of what that could translate into in terms of duration of response, where we'll be looking to exceed, you know, something in the six-seven-month range as a benchmark. And those are readouts that we expect to come in the first half of next year, having fully enrolled that TP53 mutant AML cohort during the third quarter, and would be the basis for discussion with regulators about, you know, first, an incremental expansion of that study to confirm that data, and subsequently, what the registration-directed path could be there. But I do agree that there is a potential accelerated opportunity. In terms of the kinetics of response, I can comment on a couple data points that we have, and we'll certainly add to this soon. First of all, the relapsed/refractory AML patient that is disclosed in the ASH abstract as a monotherapy responder, as Lini outlined, this was a tough patient. You know, they, they had failed 7+3, they failed FLAG, they failed venetoclax, and then they came on the study and had a response within the first cycle of 154 monotherapy. That's unusual for a patient like this, but it's consistent with the kinetics of response that we had observed with the preclinical equivalent of 154 in various models. I can also say that the confirmed responder in PROC, that response started at the very first 8-week scan, and that's also the case with the two unconfirmed responders in PROC, where at that first 8-week scan, they met that PR criteria. It appears that the kinetics of response to 154 are rapid, and, you know, that's helpful, especially when looking at initial data sets and trying to forecast how that might translate. Great. Thanks, Taylor. Thanks, Joe. Your next question comes from the line of Marc Frahm of TD Cowen. Your line is open. Hey, thanks for taking my questions, and congrats on the early response data today. Maybe to start off with, Lini, can you just explain the gap from the 16 who've seen drug and the 11? How many of those five are still on trial awaiting the first scan versus, you know, having maybe discontinued for other reasons? And then are you seeing any, you know, to the point of about half the patients have had PARP experience and half have not. I know it's small numbers, but any sense that maybe the efficacy is in one of those populations more than the other? Great. Morning, Marc. Thanks for the question. Lini, why don't you go ahead and take those? Lini, you might be on mute. Sorry, Marc, can you repeat the first question? I lost the connection. Oh, sorry. Yeah, the safety database has 16 patients in it today, and 11 are efficacy evaluable. Can you just explain the kind of 5-patient gap there? How many of them are waiting for their first scan versus maybe discontinued for other reasons? Yeah, all five are still on study. They are waiting for their first scan. ... Okay, and then of the responses you're seeing, any sense that maybe this efficacy is more or less in the PARP experience versus non-PARP eligible type of patients? At the moment, Marc, it's too early to kind of draw those conclusions. The first patient had received PARP. The first patient with the PR had received PARP inhibitors. The second patient, the next two patients, you know, have received Bev, so it's hard to draw any conclusions at this time. Okay. Makes sense. And then thinking forward to next year when we'll see the initial Merv combo data, you know, there's a couple different populations based on Merv expression level, or sorry, folate expression levels. Just can you kind of frame how big of a data set you're expecting to be able to provide and, you know, and the robustness you'll be able to look across those different expression levels? Yeah, we are expecting to enroll up to 70 patients. That 70 patients will include high, medium, and low. And we are working with ImmunoGen to benchmark what would be an interesting response rate and durability of response in each of those subgroups. Your next question comes from the line of Kaveri Pohlman of BTIG. Your line is open. Hi. Thank you for taking my questions. I'm Christian. I'm on for Cowen. So, you actually answered part of my question. It was just about the Elahere combo trial. I wanted to know what you guys would consider a meaningful RR, like, are you guys getting close to determining that, considering that this is enrolling folate receptor alpha, medium and low expressers? But beyond that, I noticed that Elahere's registrational trial required 100% of the patients to receive prior bevacizumab. So going forward, are there plans to also make this a requirement in that trial? Great. Morning, Christian. Thanks for the question. Lini, why don't you go ahead and take that question as well? Thank you for the question. So the trial was designed with the exact eligibility criteria as SORAYA. So all patients were required to have received bevacizumab, and that's how the trial was written. Got it. Thank you. And my next question is just about the PLD combo trial. Are you guys planning to use biomarker analysis to determine differences in responders and non-responders? And if so, are you planning to use this to take eligible patients in the future? Yeah, thanks, Christian. We are continuing to collect a variety of different biomarker data from these patients, some of which is similar to the data that was shared in our ASCO abstract earlier this year with regard to peripheral cytokine responses, margination of CD40-expressing cells, changes in the immunophenotype of both peripheral cells as well as through evaluation of pre- and on-treatment biopsies from these patients. We hope certainly that data may inform a patient selection strategy or a responder, non-responder analysis at a subsequent date. But we'll report on that as the size of the data set increases toward the end of the study. Got it. Thank you. That was helpful. Thanks for taking my questions. No problem. Again, if you would like to ask a question, please press star and the number one on your telephone keypad. Your next question comes from line of Yigal Nochomovitz of Citi. Your line is open. Yeah, hi. Thanks for taking the question. On PROC, I was just wondering if you plan to look at or if you already have looked at any correlation between the platinum-free interval for these patients and the degree of response. And then on Heme, with respect to the frontline studies in TP53 and high-risk MDS, do you have any reason to believe or biologic hypothesis that the 172154 aza combo would be potentially more effective in one of these cohorts versus the other? Thank you. Sure. Yeah, good morning, Yigal. Thanks for the questions. As, as Lini mentioned, 88% of the patients enrolled to date in the PROC study progressed within the first six months of, of platinum. And so this is, you know, a fairly homogeneous, poor prognosis group with rapid kinetics of disease. And we really can't, as Lini alluded to before, the size of the data set is not large enough where we can try to distinguish between, you know, did it make a difference if the patient progressed on platinum within one to three versus three to six months? All that we can say is that all of these patients were rapidly resistant to primary platinum. and then, you know, with, with regard to whether, you know, there's, there's a difference in the subpopulations or, or TP53 mutant AML versus high-risk MDS in conjunction with azacitidine, you know, we, we-- we're looking forward to sharing more data there soon, with the frontline cohorts. And what I can say is that, you know, it's always been a little bit of a mystery why the TP53 mutant AML patients with some prior studies seem to do a bit better than the TP53 wild type patients, because otherwise, those are, are quite similar diseases.... And one of the hypotheses that's been out there in the literature is that, the TP53 mutant patients seem to have a higher mutational burden. Perhaps there were more tumor-infiltrating CD8 positive T cells, i.e., perhaps it was a more immunogenic tumor to start than some of the TP53 wild type patients. You know, part of the value proposition of adding a CD40 agonist to a CD47 inhibitor was framed around the expectation that some of those characteristics might be normalized because of the immune-activating potential of CD40. And so it's certainly something that we're looking at, and you know, a priori, we can't necessarily say that that would indeed be the case, but we'll be sharing data soon and following that over the next six to nine months. Okay. Thank you. You're welcome. Your next question comes from the line of Gil Blum of Needham & Company. Your line is open. Hey, good morning, and thanks for taking our question. So maybe just to focus here on the ovarian cancer, what would you gauge is a go, no-go decision on PLD plus 154? And how relevant is PLD these days and PROC? I mean, you face some enrollment challenges here, so I'd love your two cents here, and I have a follow-up. Yeah, good morning, Gil, and thanks for the question. I mean, I can tell you that when we first started this study, there were many investigators who only joined the study because of the Elahere arm, because, you know, as is highlighted by the JAVELIN study, PLD doesn't help very much in these patients. And, you know, it's now, it took us about as long to enroll the first five patients in the study as it has to now complete enrollment in the study. And, you know, perceptions can be changed by data, right? I think we're starting to see that 154 is adding something in both heme and solids, and certainly, people always seem to shy away from the word synergy, and we can't say that quite yet, but if these data hold, then that's what this will mean in the PLD setting. This is an all-comer population, and a response rate in excess of 25% in an all-comer PROC setting, non-biomarker selected, in and of itself could be meaningful, and could be very meaningful if it is accompanied by a duration of response that exceeds 5 months. Those are benchmarks that we will be looking toward as the data mature over the first half of next year. You know, similar to my comments on the TP53-mutant AML cohort in terms of what the next step would be, you know, we'd be looking at an incremental expansion of the current study, you know, somewhere between adding 20 and 40 patients or so, to confirm the results and to enroll those patients with our current momentum. That would be the basis then of a regulatory discussion for the first registration-directed study. Excellent. Very helpful. And my follow-on is, can we get a sense of the behavior of the non-responding patients with stable diseases, kind of, you know, in immune oncology, a lot of times you see these prolonged stable diseases. Thank you. Sure. It, it's too early to say too much. You know, as Lini alluded to, there were out of the balance of 8 patients, 4 had a best response of progressive disease and 4 had a best response of stable disease of varying lengths of time. I think we need to wait and see the full data set from the initial 20-patient cohort before we can make any assertions about whether those patients with stable disease had stable disease for longer than you would expect in a patient population like this. All right. Excellent. Thanks for taking our questions. Thanks, Gil. Thank you. This concludes the Q&A session of the call. At this time, I would like to turn the call back over to Taylor Schreiber, Chief Executive Officer of Shattuck Labs, for closing remarks. Thank you, operator, and thank you all for joining the Shattuck Labs third quarter 2023 financial results and business updates conference call. We appreciate your continued interest in Shattuck, and we look forward to updating you on our milestones later this year. Thank you. This concludes today's conference call. Thank you for participating. You may now disconnect. Have a wonderful day.