Good afternoon, ladies and gentlemen. Welcome to the Shattuck Labs Fourth Quarter and Full Year 2022 Earnings Conference Call. At this time all participants are in a listen-only mode. Later we will conduct a question and answer session. Instructions will follow at that time. As a reminder, this conference is being recorded. I will now turn the call over to your host, Mr. Conor Richardson, Vice President on Investor Relations at Shattuck Labs. Conor, please go ahead. Thank you, operator. Good afternoon, everyone, and welcome to the Shattuck Labs Conference Call regarding our Fourth Quarter and Full Year 2022 Financial Results and recent Business Updates. The press release reporting our financial results was issued after market close this afternoon and can be found on the investor relations section of our website, shattucklabs.com. During this afternoon's call, the Shattuck leadership team will provide a business overview of the fourth quarter and full year of 2022, including clinical development updates for SL-172154, our lead program, and SL-279252. We will refer to these as 154 and 252 throughout today's earnings call. Speaking on today's call will be our Chief Executive Officer and Scientific Co-Founder, Dr. Taylor Schreiber, who will review our pipeline progress and upcoming key milestones, followed by our Chief Medical Officer, Dr. Lini Pandite, who will provide an update on our ongoing clinical activities. Our Chief Financial Officer, Mr. Andrew Neill, will review our fourth quarter and full year 2022 financial results and financial guidance. Dr. Schreiber will return to make some closing remarks, and we will then open the call for questions. 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 annual report on Form 10-K for the year ended December 31st, 2022, 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, February 23rd, 2023. I will now turn the call over to Dr. Schreiber, our Chief Executive Officer. Taylor? Thank you, Conor. Good afternoon, everyone, and thank you for joining us today. 2022 was an operationally focused year for Shattuck, and our clinical team did an excellent job of advancing 154, our lead clinical stage agonist redirected checkpoint or ARC product candidate. As a reminder, 154 is a SIRPα-Fc-CD40L ligand bifunctional fusion protein, which serves to both block the macrophage checkpoint molecule known as CD47 and also activates an important immune stimulatory receptor known as CD40. Linking these two functions within a single therapeutic differentiates 154 from all other CD47 inhibitors in clinical development. We are very pleased to have completed the phase I-A monotherapy dose escalation clinical trial of SL-172154 in patients with platinum-resistant ovarian cancer and achieved all of the primary goals of this first in human study, including the selection of a dose of SL-172154 to advance into our phase I-B combination cohorts, which I will describe in a moment. From a pharmacodynamic perspective, we believe that the clinical data generated through the course of the phase I-A trial has validated one of our central hypotheses in the design of the ARC platform and shown that SL-172154 was able to safely activate CD40 in a dose-dependent manner, including doses which saturated the CD40 receptor. One of the primary pharmacodynamic effects we observed in patients treated with SL-172154 was a rapid induction of interleukin-12, achieving high serum concentrations of IL-12 and a number of other cytokines widely believed to be important to support antitumor immune responses. We are looking forward to sharing these data at a medical meeting toward the middle of this year. In short, we are very pleased to have completed the goals of this study and to have selected the 3 mg/kg dose to move into the combination cohorts. As a class, in order to seek clinically meaningful efficacy, CD47 inhibitors rely upon combination regimens with another agent that provides a pro-phagocytic signal, such as a targeted antibody or ADC, or with an agent that causes immunogenic cell death. For this reason, we are pleased to have moved into the combination studies where objective responses are expected in both our ovarian cancer trial and our clinical trial for patients with acute myeloid leukemia and higher risk myelodysplastic syndrome. There are two combination cohorts ongoing in our phase I-B clinical trial in patients with platinum-resistant ovarian cancer. In the first combination cohort, one five four is being combined with a chemotherapy agent known as pegylated liposomal doxorubicin, or PLD for short. We selected PLD in combination with one five four for several reasons. First, PLD causes immunogenic cell death of ovarian cancer cells and was shown to enhance antitumor activity when combined with one five four in preclinical studies. Second, PLD is a standard of care in the platinum-resistant setting and is well known that patients treated with PLD have an objective response rate in the range of 10%-12% from multiple phase III clinical trials. Thus, this was a mechanistically driven combination strategy where we do not expect difficulty determining the contribution of 154 in the regimen due to the known low response rates of PLD as monotherapy. The second combination cohort in ovarian cancer is the result of a collaboration between Shattuck and ImmunoGen. ImmunoGen received accelerated approval for an antibody drug conjugate known as mirvetuximab soravtansine, which targets an ovarian cancer antigen called folate receptor alpha, or FRα for short. The initial approval of mirvetuximab is for a biomarker-selected subset of platinum-resistant ovarian cancer patients whose tumors express high levels of FRα. The objective response rate is 31.7% for those patients. In preclinical studies, we demonstrated that combining 154 with mirvetuximab potentiated antitumor activity not just for ovarian cancer cells that express high levels of FRα, but also for tumor cells that express medium and low levels of FRα. This is a mechanistically driven combination where the contribution of 154 is expected to be observed both in terms of improving overall response rates and response duration across the spectrum of FRα expression. If successful, this could more than double the proportion of patients who benefit from mirvetuximab. We are excited about the opportunity in ovarian cancer for 154, we are also pleased to be well underway in our clinical trial of 154 in patients with AML and higher risk MDS. Many listeners will be aware, AML and higher risk MDS are among the indications where CD47 blocking antibodies first demonstrated clinical activity and where the first approvals based on overall survival may soon occur. Over the second half of last year, our clinical team initiated both the monotherapy dose escalation and an azacitidine combination dose escalation cohorts, and we remain on track for our clinical data milestones in the first half of this year. Although we acknowledge that the objective response rates for the 1st generation of CD47 inhibitors has contracted in this patient population over the past couple of years, we are excited about the opportunity that opens for agents like SL-172154, which provides the important component of CD40 activation in addition to CD47 blockade and which improved antitumor immunity in preclinical tumor models in published head-to-head studies at in comparison to CD47 blocking antibodies. Let us now turn to our SL-279252 program, a PD-1 Fc OX40L ligand bifunctional fusion protein. We have completed the multicenter open-label clinical trial evaluating the safety, tolerability, pharmacokinetics, antitumor activity, and pharmacodynamics of SL-279252 in patients with advanced solid tumors and lymphoma. After enrolling PD-1 inhibitor-experienced patients to the 12 mg/kg and 24 mg/kg cohorts, we did not observe an overall response rate of 20% or greater, which was our target to justify further clinical development, and thus we have made the decision to discontinue the SL-279252 program. The clinical data generated from patients treated with SL-279252 suggests that OX-40 stimulation in this setting was insufficient to overcome the resistance mechanisms in place in patients who have already failed a PD-1 inhibitor. I would like to take this opportunity to thank the patients and their families for participating in our study. As always, we remain focused on delivering novel therapeutics which will benefit patients experiencing cancer with high unmet medical need and look forward to the combination data in our ongoing clinical trials with SL-172154 in the coming quarters. With that, I will now turn the call over to Dr. Pandite, our Chief Medical Officer, who will provide you with more detail on each of these studies, the emerging data illustrating how 154 is a differentiated CD47 inhibitor, and will also provide you with guidance to the various clinical milestones that are coming over the course of 2023. Lini? Thanks, Taylor, and good afternoon. 2022 was a year of high operational focus, and I'm pleased with the execution of our clinical programs and the continued progress we have made. Our clinical focus is on the advancement of 154, our differentiated CD47 inhibitor and CD40 agonist with clinical data coming this year from each of 3 different clinical studies. As Taylor mentioned, we have now completed our multicenter open-label dose escalation phase I-A clinical trial intended to assess the safety, tolerability, pharmacokinetics, antitumor activity, and pharmacodynamic effects of intravenous administration of 154 as monotherapy in patients with platinum-resistant ovarian cancer. As a reminder, in this trial, we reached a maximum administered dose of 10 mg/kg, and we did not reach a maximum tolerated dose. As you will recall from the last quarter, we did not see any evidence of destructive anemia, which we attribute to the design of the Fc portion of 154 and the absence of binding to Fcγ receptors. We expect to report the full data from this dose escalation portion clinical trial mid-2023. Following the completion of phase I-A dose escalation clinical trial and selecting a dose, we advanced to enrolling patients in our phase I-B clinical trial of 154 in combination with liposomal doxorubicin in patients with platinum-resistant ovarian cancer. This multicenter open-label trial is intended to evaluate the safety, tolerability, pharmacokinetics, antitumor activity, and pharmacodynamics of 154 in combination with liposomal doxorubicin. We expect to report initial combination data from this trial mid-2023. I'm also very excited to share details about our new collaboration with ImmunoGen. We have initiated enrollment in a phase I-B trial to evaluate the safety, efficacy, and pharmacokinetics of SL-172154 in combination with mirvetuximab soravtansine in patients with platinum-resistant ovarian cancer. As Taylor mentioned, we believe that SL-172154 may broaden the activity of mirvetuximab beyond just folate receptor alpha high expressers, and thus we intend to enroll patients across a broader range of folate receptor alpha expression, including those with high folate receptor alpha expression defined as 75% or greater, medium folate receptor alpha expression defined as less than 75%, but greater than or equal to 50%, and low folate receptor alpha expression defined as less than 50% but greater than or equal to 25% expression of folate receptor alpha. We expect to report initial combination data from this trial in the second half of 2023. Let us turn our attention to the progress we have made in our phase I-A/1-B clinical trial in patients with 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. As a reminder, the first part of this trial is a parallel staggered monotherapy and combination dose escalation in which we expect to enroll a heavily pretreated, relapsed, refractory patient population. Enrollment in the monotherapy cohorts of this trial has progressed consistently and as planned. Importantly, we dosed the first patients in the azacitidine combination cohort in the fourth quarter of 2022. Initial data from the dose escalation portion of this trial as both monotherapy and in combination with azacitidine are expected in the first half of 2023. After we complete the dose escalation portion of this clinical trial, we intend to evaluate 154 in a front-line patient population setting in TP53 mutant AML and front-line higher risk MDS. With that, I will now turn the call over to Mr. Neill to discuss our financial updates. Andrew? Thank you, Lini. Good afternoon, everyone. As Conor Richardson mentioned at the outset of the call, the full financial results for the fourth quarter and full year ended December 31st, 2022 are available in our earnings press release and in our annual report on Form 10-K. Today, I would like to focus on a few key points from our disclosures. We continue to be well-positioned financially. As of December 31st, 2022, we had cash equivalents and investments of approximately $161.3 million. In the fourth quarter of 2022, our research and development expenses were $21.9 million compared to $16.2 million for the fourth quarter of 2021. For the year ended December 31, 2022, our research and development expenses were $82.9 million as compared to $56.6 million for the year ended December 31, 2021. In the fourth quarter of 2022, our general and administrative expenses were $4.8 million compared to $4.6 million for the fourth quarter of 2021. For the year ended December 31, 2022, general and administrative expenses were $21.1 million as compared to $18.7 million for the year ended December 31, 2021. Our net loss for the fourth quarter of 2022 was $25.4 million, or a loss of $0.60 per basic and diluted share, compared to a net income of $7.8 million for the fourth quarter of 2021, or $0.19 per basic share and $0.18 per diluted share. Our net loss for the year ended December 31, 2022 was $101.9 million or $2.41 per basic and diluted share as compared to $45 million or $1.07 per basic and diluted share for the year ended December 31, 2021. Based on our current operating and development plans, we reiterate our financial guidance for 2023 and beyond. We expect our existing cash and cash equivalents and investments to be sufficient to fund our planned operations into the second half of 2024. We remain committed to operating with strong financial discipline, including in our ongoing clinical programs, and given our projected rate of cash burn, we believe we are in a healthy position as it relates to our balance sheet and expected clinical data readouts for our 154 clinical trial in 2023. With that, I will now hand the call back to Dr. Taylor Schreiber for final comments. Taylor? Thank you, Andrew Neill. As you have just heard, 2022 was a year in which we were intensely focused on the execution of our clinical programs. We are pleased to be approaching key clinical data in 2023. As you heard from Lini Pandite, clinical updates from the 154 program, including complete data from the monotherapy dose escalation trial in platinum-resistant ovarian cancer patients and initial data in combination with liposomal doxorubicin also in ovarian cancer patients, are expected mid-year 2023. Additionally, initial data from our trial in patients with AML and higher risk MDS are expected in the first half of 2023. As you can see, we expect 2023 to be a data-rich year. We look forward to sharing those data with you. One of the cornerstones of Shattuck Labs has always been the expertise of our preclinical development and research and development teams. I must highlight the team's tremendous progress in 2022, leading to the promotion of Doctors Fromm and de Silva as chief scientific officers to head the ARC and GADLEN platform research and development efforts, respectively. Interest in harnessing the activity of gamma delta T cells in cancer has continued to build, and we believe our GADLEN platform is truly distinct from all other approaches currently in development due to its unique design features. During the fourth quarter of 2022, we highlighted two preclinical compounds from the GADLEN platform, one targeting the CD20 antigen that we are evaluating for development in autoimmune disease, and a second targeting the B7-H3 antigen for which we are evaluating for development in certain solid tumors. We look forward to providing further guidance on the GADLEN program as it continues to advance later this year. In addition to our progress in the clinic and in our discovery efforts, I would like to underscore that our financial position remains strong, and we continue to investigate other opportunities to monetize our portfolio to increase shareholder value. I want to thank everyone for participating in today's call. We believe that the combination of our experienced team, transformational science and protein engineering, as well as financial resources, puts us in an incredibly strong position to move beyond our next set of milestones in 2023. We will keep you apprised of our progress as we continue to execute our strategic and corporate objectives. With that, we would now like to open the call for your questions. Operator? Thank you, Dr. Schreiber. Ladies and gentlemen, at this time, if you have any questions, simply press star one. Just a reminder, if you are joining us today using a speakerphone, please make sure you pick up your handset before pressing star one. We'll take our first question this afternoon from Jonathan Miller of Evercore ISI. Hey, guys. Thanks so much for taking my question. I'd love to start with the 154 program. I know you were seeing some liver tox at higher doses. I'm wondering how that seems to be filling out as you move forward. Have you seen any grade three or any high-grade, I should say, liver tox in the 3 mg combo cohorts? Just to build off of that, how many patients in combo do you expect to be available in the initial release, especially in AML and MDS? Is it enough that we should expect to be getting a good ORR comp relative to other CD47s in these releases this half? Hey, Jon. Thanks for the question. Lini can provide you guidance on patient numbers coming up in all the cohorts. With regard to tox, the profile that we're seeing in all of the combination studies is similar to what we'd seen in the monotherapy dose escalation. With regard to the specific liver toxicity question, we're not seeing any evidence of any cumulative tox between the molecules, and 3 mg per kg was well-tolerated as monotherapy in that monotherapy dose escalation study as well. Looking good so far from that perspective. Also consistent profile from what we saw in the monotherapy dose escalation with regard to no evidence of cytokine release syndrome or destructive anemias. On the combination, Jon, with the AML MDS cohort, the patients that we're enrolling in the dose escalation are patients who have relapsed refractory disease. We expect in excess of 20 patients across the monotherapy and the combo cohorts by the middle of the year. Just to put this in context, the CD47 targeted agents, they have a benchmark in the frontline setting, in not treatment naive patients. These patients are relapsed refractory patients. We will be starting those expansion cohorts in the frontline setting as soon as we complete the dose escalation. Makes sense. Thanks so much. I'll have to circle back and queue. Thank you. We go next now to Marc Frahm at Cowen. Thanks for taking my questions. Maybe I'll ask similar questions, but we'll go to the Doxil combo 'cause that's the next presentation. Lini, if you can give an update on kind of the scope of that presentation that we're likely to see. Related to that, as we get towards the MIRV data set, just in your prepared remarks, Taylor, you mentioned the kind of approved response rate that a mirvetuximab has in the biomarker-selected population. Of course, the trial is gonna enroll a broader population. Yeah, how should we think about kind of interpreting that data as we get it, given that you know, it'll include patients who aren't approved for monotherapy plus, you know, some of your proposed benefit is really on durability, not as much on the response rate? Great. Thanks, Marco. Lini can handle that for us. With the Doxil, we are expecting, you know, something in the order of 10-20 patients by the middle of the year. We would be sharing data both on the safety as well as the efficacy. It'll be a mixture of that data, depending on the enrollment. And we expect that, you know, we would provide some guidance closer to the time as to what to expect by the middle of the year. To answer your question, the Doxil will be in the order of 10-20 patients. With the MIRV, looking at the MIRV data, Yes, I mean, with the MIRV is approved in the high expressor group, 75% or greater, and here we are enrolling patients with 25% or greater. We will be looking at the response by subgroup in those subsets. You know, at this stage, what we are doing with ImmunoGen is that we are partnering with ImmunoGen to see what would be an interesting response rate and durability of response based on their database. We will definitely be working with them to benchmark this, the data that we see, against the datasets that they have. By the end of the year, we would hope to have or expect to have about 40 patients to worth of data. Great. Thank you. Very helpful. Thank you. We go next now to Yigal Nochomovitz of Citi. Yeah. Hi. Thanks. I'm just trying to get a feeling for expectations for the combo studies with 154 and AZA both in the relapsed refractory setting as well as in the frontline setting. What do you generally believe is the efficacy bar for AZA by itself and with the addition of 154 in both the relapsed refractory AML and MDS as well as in the frontline setting in TP53 mutant, what might you expect to see with the combo above AZA? Thanks, Yigal. As Lini said in the initial portion of the trial, we're enrolling primarily venetoclax and HMA experienced subjects. Any activity in that relapsed refractory setting, I think would be helpful and perhaps provide some guidance toward what you might expect in the frontline setting. The first two cohorts that we expect to have data from in the second half of this year in the frontline setting are number one in the TP53 mutant AML patients. There, we believe that the expected effect, in terms of complete responses for azacitidine alone are in the range of 22%. We're looking for a combination complete response rate in the neighborhood of 40% or so. In the higher risk MDS cohort, this is where there continues to be a bit of blurriness, honestly, in the field as to what the expected effect size of azacitidine alone is. Some of the older studies place that complete response rate in the high teens. The more recent Takeda study with pevonedistat suggests that it could be as high as the low thirties. You know, we think it's best to cite the higher response rate as the benchmark. We're looking for a combination response rate somewhere in the neighborhood of 50% for complete responses. Okay. I'm not sure if you mentioned it in the prepared remarks, but just, can you just go through again the choice of the 3 mgs per kg for one five four in combo with the liposomal doxorubicin. What was driving that decision? Sure. It, it was driven by a few factors. First of all, on both the CD40 and CD47 binding sides of the molecule, we were looking to find a dose where full receptor occupancy and receptor saturation was achieved. That was achieved by that 3 mg/kg dose and that was visible both in terms of the receptor occupancy data and observation of nonlinearity in the PK profile. Beyond that, we were looking for a dose that led to maximal induction of the pharmacodynamic effects driven by CD40. Many folks are aware that with CD47 inhibitors, the only pharmacodynamic effect you see in a study like this is receptor occupancy. The observation of rapid margination of CD40 expressing cells from the peripheral blood post dose is a unique effect for 154 relative to any other agent in the space. That was maximal by the 3 mg per kg dose and maintained that maximal plateau up through the 10 mg per kg dose. The other primary pharmacodynamic effects were rapid induction of multiple cytokines including interleukin-12, IP-10, CCL2, CCL4, CCL22, and a number of others. Those cytokines also achieved a what appeared to be a maximal plateau by that 3 mg per kg dose, which did not escalate appreciably by the 10 mg per kg dose, but also importantly didn't decline. On all of those markers, 154, just was differentiated both from single acting CD47 inhibitors and lacked any of the toxicity or bell-shaped dose response effects that characterized prior CD40 agonists. All of that gave us confidence about this being the right dose to bring into combos. Great. Thank you. Thank you. We'll take our last question today from Zhiqiang Shu of Berenberg. Good afternoon. Thanks for taking the question. My question is related to your 252 program. Obviously, it's not surprising to see the discontinuation there, but I was wondering if you can talk about the learnings from this program, particularly around the PK/PD aspect to your 154. What, you know, the PK/PD from 252 is consistent with what you are observing in 154. Thank you very much. Sure. Thank you, Zhi. The trial cross comparisons here are, I think, quite valuable. With the 252 program, we've completed dose escalation through that 24 mg/kg dose. Compound continued to be extremely well-tolerated. Across that dose escalation, we saw a dose-dependent binding to CD4 cells expressing OX-40 and migration of those cells out of the peripheral blood post-dose. Again, from a TNF receptor agonist perspective, the tolerability and lack of any evidence of a bell-shaped dose response curve and the pharmacodynamic effects with both 252 and 154 are helpful in terms of validating one of the central hypotheses of the ARC platform that if you engage TNF receptors with a hexameric drug, you will not observe some of the toxicities and abnormal pharmacodynamic effects that prior antibody-based regimens have seen. That's an important finding from a platform expansion standpoint, again, both from the safety and the pharmacodynamic side. We're also learning, you know, some important lessons, I think, in terms of what OX-40 and what CD40 stimulation achieve in human cancer patients. When you look at the 252 data and you note that there, you know, there were no appreciable serum cytokine changes. The only cells that were migrating were those specific CD4 positive, OX40 positive cells. It was a much more immunologically quiet molecule, so to speak, in this patient population, whereas the CD40 agonist clearly, you know, all across the dose escalation led to, you know, very clear escalations in a number of cytokines. Infusion-related reactions have been much more common with that agent. The differentiation in biology between the two constructs paints a very clear picture that this is target-mediated activity that we're seeing here. You know, always hard to close down a program like this, but I think we've learned what we needed to learn from this molecule, and those learnings will benefit other compounds moving forward. Great. Thanks. Then maybe just quickly on GADLEN platform, you disclosed, I think, consensus last time that you have two preclinical assets. Can you talk about sort of the prioritization there and when we can see more data or more development from those two programs? Sure. The B7-H3 molecule is the one we're considering for development in oncology, and the CD20 is the one that we're considering for development in antibody-mediated autoimmune disease. You know, what we're seeking to achieve with the initial clinical study with the GADLEN platform is to select an indication where we believe it will be most likely that a GADLEN molecule will differentiate from CD3-based T-cell engagers, antigen-specific antibody molecules. You know, we've learned a lot about what gamma delta T cells rely upon to be fully activated. Just like alpha beta T cells, they require a T-cell receptor stimulus, which comes from the GADLEN molecule itself and the butyrophilin heterodimer, and they also require a co-stimulatory ligands to be expressed by their target cell. You know, a part of the exercise that is guiding the effort is looking at tumors that express B7H3 and trying to assure that patients that we might enroll early in a phase I dose escalation study are likely to express those signal 2 ligands on their tumor. That's on the tumor side and on the autoimmune side, you can have certainty actually that any B cell which expresses CD20 will also express a signal 2 ligand in the form of CD80 or 86. Those are some of the design principles that we have in mind for that phase I trial. We'll be providing more specific guidance as to exactly what that study is gonna look like in the short term this year. Great. Thanks, Taylor. Thanks, Zhi. 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. Thank you all for joining the Shattuck Labs Fourth Quarter and Full Year 2022 Financial Results and Business Updates Conference Call. We appreciate your continued interest in Shattuck, and we look forward to updating you on our milestones throughout the remainder of what we hope to be an exciting 2023. Thank you. Thank you again, ladies and gentlemen. That will conclude today's conference call. We just like to thank you all so much for joining us and wish you all a great remainder of your day. Goodbye