Good morning, and thank you for dialing in to today's conference call. I'm Jeanne Jew, Chief Business Officer of ALX Oncology. Today's call will focus on clinical data with Evorpacept, our next-generation CD47 myeloid checkpoint inhibitor from the ASPEN-05 phase I-A dose escalation portion of the trial in AML, presented at the American Society of Hematology Annual Meeting, or ASH, on December 12th. A slide deck for this webcast is available on our website in the Investors Events section. Dr. Abraham Fong, Senior Medical Director at ALX Oncology, will discuss the background and biological rationale for exploring evorpacept in combination with venetoclax and azacitidine in patients with AML. We are also privileged to be joined today by Dr. Harry Erba, Director of the Leukemia Program in the Division of Hematologic Malignancies at Duke University, North Carolina, who will discuss the initial dose escalation portion of the clinical trial data in patients with AML-administered evorpacept in combination with venetoclax and azacitidine. At the end of our remarks, we will open the line for questions. Dr. Jason Lettmann, our CEO, and Dr. Sophia Randolph, our Chief Medical Officer, will also be available during the question- and- answer session. Before we begin, we would like to remind you that today's presentation will include forward-looking statements based on our current expectations and beliefs. Such statements represent our judgment as of today and involve substantial risks and uncertainties that may cause actual results to differ materially from the results discussed in the forward-looking statements. I would like to introduce Dr. Abraham Fong. Abe? I will start by reviewing ALX's clinical pipeline, followed by a description of evorpacept's mechanism of action in combination with both venetoclax and azacitidine for the treatment of patients with AML, as well as the ASPEN-05 phase I-A trial design that was presented at the ASH 2022 meeting this year in poster number 4076. On slide number two, you can see that because of evorpacept's broad utility as a myeloid checkpoint inhibitor, we have multiple ongoing clinical studies in both solid tumors and hematologic malignancies, including head and neck squamous cell carcinoma, gastric and gastroesophageal junction cancer, urothelial cancer, breast cancer, myelodysplastic syndrome, acute myelogenous leukemia, and non-Hodgkin's lymphoma. All of these studies are designed to maximize the innate immune response against cancer by combining evorpacept with other established antitumor agents. We also have a new compound, ALTA-002, which is a SIRPα toll-like receptor agonist antibody conjugate that is currently in the IND-enabling phase. On slide number three, you can see that evorpacept is a CD47-blocking fusion protein that has been engineered with an inactivated Fc domain to minimize toxicity. Evorpacept effectively blocks the SIRPα/CD47 myeloid checkpoint, thereby promoting activation of macrophages. However, an additional pro-phagocytic signal on tumor cells is also required to maximally activate the macrophage, which can be provided by treatment with venetoclax and azacitidine. These are standard-of-care drugs for the treatment of AML. Preclinical experiments indicate that treatment of leukemia cells with these drugs leads to upregulation of the strong pro-phagocytic signal calreticulin on the leukemia cell surface. Evorpacept blocks CD47 on the leukemia cell, and in combination with calreticulin's engagement of the LRP1 on the macrophage, the macrophage's phagocytic activity is maximized against the leukemia cell. Because evorpacept's Fc domain does not engage the Fc gamma receptor on the macrophage, by design, normal blood cells are spared from CD47-targeted antibody-dependent cellular phagocytosis or ADCP activity. Evorpacept is designed to enhance the activity of targeted anticancer therapies with minimal hematologic toxicity. By inhibiting the myeloid checkpoint, the addition of evorpacept to venetoclax and azacitidine enhances the macrophage's AML-targeted phagocytic activity. On slide number four, we have previously shown that calreticulin expression on the surface of AML cells increases when cells are treated with venetoclax or azacitidine, which I'll refer to as Ven and Aza moving forward. In vitro phagocytosis assays demonstrate that evorpacept in combination with Aza, shown on the left-hand side, enhances the phagocytosis of AML cells compared to either agent alone. Similarly, on the right-hand side, evorpacept in combination with Ven enhances the phagocytosis of AML cells compared to either Ven or evorpacept alone. On slide number 5five we have previously shown that there is enhanced inhibition of leukemia growth upon treatment with evorpacept in combination with Aza and Ven, compared to the backbone combination of Ven and Aza alone in an in vivo disseminated mouse model of AML. This increased anti-leukemic activity correlated with improved overall survival of the mice. On slide number six, phase I-A part of the ASPEN-05 study design is shown. We will be discussing phase I-A dose escalation portion of the study that was presented yesterday at this year's ASH meeting. Patient cohorts were comprised of a mix of relapsed refractory or previously untreated high risk in AML in patients not considered suitable for intensive therapy. Patients were administered escalating doses of evorpacept in combination with standard dosing of venetoclax and azacitidine. In ASPEN-05, evorpacept doses ranged from 20 milligrams per kilogram once every two weeks, up to 60 milligrams per kilogram once every four weeks, reflecting similar exposure levels evaluated in the original first-in-human ASPEN-01 study. To discuss this trial, it gives me great pleasure to now introduce to you Dr. Harry Erba, who will speak about the use of evorpacept for the treatment of patients with AML. Dr. Erba is director of the leukemia program in the Division of Hematologic Malignancies and Cellular Therapy at Duke University and the current chair of the SWOG Leukemia Committee. He is internationally recognized as a leading researcher in hematologic malignancies, including AML. His clinical research focuses on the development of novel therapies for AML, as well as myelodysplastic syndromes, myeloproliferative neoplasms, and ALL. Today, we are honored to have him share his experience with the evorpacept in the ASPEN-05 study, as well as his thoughts around evolving approaches to AML therapy. Harry. Thank you, Abe. I'll begin with a brief disease background overview on slide number eight, providing context for the promising early results from the ASPEN-05 study. Acute myeloid leukemia, or AML, is a type of blood cancer for which we estimate there will be over 20,000 new cases diagnosed in the U.S. alone in 2022. AML is responsible for approximately 1.9% of all cancer deaths. AML is caused by mutations arising within myeloid progenitor cells, leading to their abnormal maturation and proliferation within the bone marrow. These leukemia cells suppress normal bone marrow function, causing cytopenias or low blood counts. At the time of diagnosis, patients with AML can be classified into lower or higher- risk groups based on the types of genetic abnormalities found within them. Patients are also evaluated for whether they are appropriate candidates for intensive chemotherapy or not based on their age and overall health status. As you can see, AML is primarily a disease of the elderly population with a median age at diagnosis of 68 years. Therefore, the incidence is rising as our population ages. In addition, the majority of these patients are considered too frail to receive intensive and potentially curative treatments. We currently manage these patients primarily with venetoclax combined with a hypomethylating agent such as azacitidine or decitabine. However, this regimen is not considered curative, and all patients will eventually relapse. With a five-year overall survival for all patients with AML of only about 30%, the field is in need of tolerable new therapies. Slide number nine shows some of the current available efficacy data within the AML patient populations that are similar to those that have been enrolled in the ASPEN-05 study. Frontline treatment with venetoclax and azacitidine in patients with previously untreated AML in the landmark VIALE-A randomized phase III study reported a complete remission rate of 36.7% and a median overall survival of 14.7 months. For patients with relapse or refractory AML after frontline treatment with Ven plus Aza, outcomes appear not as good. A small retrospective analysis has demonstrated limited activity with a median OS of only 2.4 months, indicating a clear area of unmet medical need. On behalf of the ASPEN-05 investigators in slide number 10, I'd now like to share preliminary results from phase I-A part of the study that were presented recently at the 2022 ASH annual meeting. In this study, we are evaluating the safety and preliminary efficacy of combining evorpacept, the CD47 blocking myeloid checkpoint inhibitor, with standard Ven and Aza in patients with AML. As shown on slide number 11, in the phase I dose escalation part of the study, we administered escalating doses of evorpacept together with standard dosing of Ven and Aza using a three plus three dose escalation design. The planned dose levels of evorpacept to be evaluated were 20 milligrams per kilogram every two weeks, 30 milligrams per kilogram every two weeks, and 60 milligrams per kilogram every four weeks. The primary objective of the phase I portion is to evaluate the safety and tolerability of combining evorpacept with Ven and Aza, and the primary endpoint is first-cycle dose-limiting toxicities. Eligible patients for phase I-A part of the study included a mix of adults with either relapsed, refractory AML or previously untreated higher-risk AML who were considered not suitable for intensive therapy and had a baseline ECOG performance status between zero and two. Response assessments were performed by the investigator using the modified ELN 2017 criteria. Slide number 12 summarizes the baseline characteristics of the 14 patients enrolled in the phase I dose escalation portion as of the data cutoff date. 11 patients, or 79%, had relapsed refractory disease with disease progression after one or two prior regimens, including nine that had previously been treated with Ven. There were three patients with previously untreated AML, and all three had a TP53 mutation. In addition, two of these patients, or 67%, had therapy-related disease or AML resulting from prior cancer treatment, which is another subgroup with poor prognosis. Together, these poor prognostic baseline characteristics reflect a difficult- to- treat population enrolled in the phase I part of this study. The initial safety data from the phase I-A study on slide number 13 indicate that evorpacept was generally well-tolerated in combination with Ven and Aza. All patients experienced an adverse event on study treatment, with three patients experiencing an event considered possibly related to evorpacept. The most common evorpacept- related adverse event was low-grade vomiting, which occurred in two or 14% of patients. The other evorpacept-r elated adverse events included nausea, cytokine release syndrome, and metabolic acidosis, which occurred in one or 7% of patients each. There were no evorpacept- related cytopenias reported. The maximum tolerated dose of evorpacept was not reached, and the maximum administered dose was 60 milligrams per kilogram every four weeks. The most commonly observed grade three or higher adverse events were febrile neutropenia, which occurred in six or 43% of patients, anemia and liver enzyme increase, which occurred in five or 36% of patients, and pneumonia, which occurred in four or 29% of patients. There was 1 dose-limiting toxicity in the 60 milligram per kilogram every four-week cohort of grade three cytokine release syndrome, which resolved. There were no evorpacept- related grade five events. Together, these initial data support the safety of combining Evorpacept with standard dose Ven and Aza. On slide number 14, you can see that we observed a decrease in bone marrow blasts in all patients treated to date, including those with both previously untreated AML and relapsed refractory AML, regardless of prior exposure to ven and across all dose cohorts. Among the 13 patients overall that were evaluable for ELN response in slide number 15, the overall response rate was 54% or seven out of 13. In the 10 patients with relapsed or refractory AML, there were four patients with responses, including two among the two patients with no prior ven treatment, both of which were CRI, and two out of the eight patients that had received a prior therapy containing ven, both of which were morphologic leukemia-free state. Among the three patients with newly diagnosed AML, all three achieved a response, including one with a complete response, one with a CRI, or complete response with incomplete hematologic recovery, and one with MLFS, or morphologic leukemia-free state. As previously noted, all three of these patients had a TP53 mutation. In slide number 16, data from the ASPEN-05 study indicate that initial responses occurred as early as the first one or two cycles of treatment. As of the data cutoff date, four of the patients that had achieved a response remain on treatment with ongoing responses, including two in the previously untreated AML group and two in the relapsed, refractory AML group. The median survival follow-up time to date on this study is 4.2 months. The preliminary pharmacokinetic analyses in slide number 17 indicate a dose- proportional pharmacokinetic profile with evorpacept that is consistent with results from prior studies. Preliminary pharmacodynamic studies demonstrate robust CD47 occupancy on AML blasts, both within the bone marrow and in peripheral blood. These results support the use of a once- monthly dosing schedule of evorpacept in combination with the 28-day cycle of Ven and Aza. In summary, on slide number 17, evorpacept is a CD47 blocker designed to maximize the innate and adaptive immune response against cancer cells. In patients with AML, preliminary data from the ASPEN-05 phase I study indicate that evorpacept can be safely combined with Ven and Aza with no maximum tolerated dose reached during dose escalation and an adverse event profile that appears similar to the published Ven and Aza backbone. We observed robust CD47 target occupancy in both bone marrow and peripheral blood AML blasts across all dose levels evaluated. The maximum administered dose of evorpacept on this study was 60 milligrams per kilogram every four weeks. Phase I-A study population enrolled was heavily enriched for patients with poor- risk AML features including TP53 mutations, therapy-related AML, and relapsed refractory disease after prior Ven treatment. Within this poor- risk population, we have observed encouraging evidence of anti-leukemic activity with objective responses and blast clearance. Thank you for your attention. I will now hand the presentation back to Jeanne. Jeanne? Thank you, Dr. Erba. That concludes our prepared remarks. We'd like to open the line for questions. Operator? The floor is now open for your questions. To ask a question at this time, please press star one on your telephone keypad. If at any point you'd like to withdraw from the queue, please press star one again. You will be provided the opportunity to ask one question and one further follow-up question. We will take a moment to render our roster. Our first question comes from the line of Li Watsek from Cantor Fitzgerald. Please proceed. Hey, good morning. Thanks, guys, for taking my questions. I guess the first question is for Dr. Erba. Can you just put this data into context for us, maybe just compare to some of the benchmarks that you referred to? What do you think about the contribution of ivosidenib, given that it's a triple? Maybe just help us understand how to untangle that. Good morning, thank you for that question. You know, we have to consider that this is a preliminary look at for only 14 patients with a mixture of previously untreated and relapsed refractory disease. I do think in these 14 patients there's some really very encouraging enticing data. Let's first start with the three patients who were previously untreated. They all had a TP53 mutation. We would expect with Aza/Ven alone about a 50% response rate and a very short duration of those responses. In these patients, all three responded, although one of them being just a morphologically leukemia-free state, clearly showing the biologic activity of this triple combination. It's hard to... It's impossible to say that three out of three responses is any different than a 50% response rate in a very, in a larger study. Again, very encouraging. The fact that two of these were still ongoing, so imagine that they were the two CR patients at the time of data cutoff, also very encouraging, because we know that these remissions can be very short duration. In the other patients, in the 11 patients with relapsed refractory disease, I think the most exciting data that I saw was in my own patients that I treated on this study. So for example, there was a patient 78 years old who had Aza/Ven. He had P53 mutated disease, a very complex monosomal karyotype. After two cycles of Aza/Ven, he achieved a complete remission. After the third cycle of Aza/Ven, he relapsed with over 50% blast. It's a very slowly marrow. It wasn't soft. Immediately after recovering from that cycle, without any further chemotherapy, he went on a study. He ended up getting the exact same combination of Aza/Ven, but this time with a single dose of Evorpacept. That's all that was different. 21 days later, his marrow was clear of leukemia. To me, in a phase I study, this is the kind of observation that gives me the greatest hope that this drug is clearly going to be adding something to Aza/Ven. I would have no reason to believe that after cycle three Aza/Ven, he had relapsed, and then just giving him the exact same drugs again, he would have a response unless there was something there that added to the efficacy of the regimen. Again, in summary, only 14 patients, a very early look at the data, but those are the kinds of observations that make me quite excited about moving ahead with Evorpacept. When you combine that with the safety, I think it's very encouraging. We did not see, for example, in these patients, you'll see anemia. I mean, they have AML, so of course there'll be anemia. You have to be there. You have to be there to taking care of these patients. We did not see the kind of acute drops in hemoglobin after the infusion of evorpacept that had been seen with magrolimab. We wouldn't have expected it based on the mechanism of action of evorpacept, but it was also very reassuring not to see it clinically. Right. Maybe just a short follow-up on your comment about duration of response. I guess, what would you like to see from the triplet? Is it, is there any plan to get these patients to transplant after remission? Yeah. That's a great question. There's clearly the plan to get them to transplant. That's really the only curative option in this population, especially with TP53- mutated disease. Very few patients end up getting there. If you think of it this way, of the 11 patients who went on study with relapsed refractory disease, if, you know, they may have already seen a transplant, gone through a transplant, or were never eligible for a transplant. These were older patients by and far. For example, my patient's 78 years old. We really are looking for a regimen that may extend the remission rates that we see with Aza/Ven, not only clear the marrow to get the patients to transplant. Thank you very much. Our next question comes from the line of Michael Yee from Jefferies. Please proceed. Hi. Thank you. Good morning. Following up on the prior question, I guess, two parts. One is, can you help us put into context this data set as it relates to other competitors, CD47s, which showed perhaps less activity in this setting? Is running a frontline AML study. The question is, how do I untangle the data set as compared to them showing no activity in prior Ven-treated patients? If it works in the first line, then this drug would be currently going to phase III in the second line. Maybe you could help untangle the confusion there for us. Thank you. I think that question is again directed at me. What I would say is, I also saw the presentation from MD Anderson by Naval Daver of magrolimab with Aza/Ven in the relapsed refractory setting. You're correct. I mean, he presented data showing not as much excitement there, not as much activity there as in the previously untreated patients. Our, you know, hope for this drug would also be to move it up front into the initial combination. Aza/Ven was never meant to be a therapy for relapsed, refractory disease, even though we use it there in patients who have had prior intensive chemotherapy. Patients who've already failed after Aza/Ven, you know, that's a very difficult population. Patients with about a 10%-15% response rate and a median survival of only, two to three months. That's a high bar to overcome. The only way to help those patients in the relapsed refractory setting, using an HMA backbone still would be to clear the marrow and get them to a transplant. That would clearly be what we would wanna do there. I think what it's exciting about our phase I study here with Aza/Ven and evorpacept, our goal is to move it into the upfront setting. If we could show high response rates, which you're seeing with Ven/Aza, but more durable responses and more patients being able to get to transplant, I think that would be, you know, a, a step forward. The competitor has the ENHANCE-2 trial in TP53- mutated disease where patients are receiving magrolimab with azacitidine alone versus Ven/Aza or intensive chemotherapy. I think that study there is hoping to show that the magrolimab itself with azacitidine might be better than just Ven/Aza. I would think, you know, as a leukemia physician, cancer doctor, you know, that the triplet may actually provide more benefit, especially in the previously untreated patients. Again, these are very early days, encouraging signs of activity and clearly the safety. The goal would be to move this into the upfront setting as quickly as possible, and I think our phase I study allows us to do that. Once we get to the best dose. We will be doing a dose optimization phase after this phase I dose escalation. Perfect. Thank you. Our next question comes from the line of Swayampakula Ramakanth from H.C. Wainwright. Please proceed. Thank you. This is RK from H.C. Wainwright. Dr. Erba, as you discussed today from the MAJIC study, if it with median follow-up of 4.2 months on these patient groups, you know, especially of those VEN-naive patients where you're seeing CR, you know, when at what point can you call them a VEN, you know, because with, you know, what sort of survival rate or several time would you want to see in these patients? What is the situation you think now for prior VEN- treated patients? Is there a reason to think about combining with the CD123 because Dr. Davar also was talking positively about pivekimab, at ASH, you know, a few days ago. Okay. Thank you for those questions. I'm gonna start with the first question. I think what you're getting at is the response rates are similar or better, what kind of duration of activity and survival would we hope to see with the addition of evorpacept? The median survival of the TP53- mutated patients in the VIALE-A trial and the phase I-B study of HMA+VEN was somewhere between five and six months. If that median survival were to increase even to nine months, eight or nine months, that would be clinically important. Now that doesn't sound like much, does it? Again, keeping in mind that the patients who are getting Ven/Aza are older patients, often they don't have the option of going to transplant. What most of my patients say to me is, "I just wanna live longer to see some event in their life." So any amount of time extra they can get would be a benefit, especially keeping in mind that once the disease comes back after Ven/Aza, at least at this point in time, the options are incredibly, you know, limited, with a few targeted therapies. So, extending that five to six -month median survival, I think would be a real advantage. If we can do this without adding toxicity, which our phase I study clearly, in my mind shows we're not adding toxicity, then I think that would be a step forward. Okay. Now, the second part of your question again, Oh, boy, I talked too long the first time, so remind me of your second question. No, this is Dr. Davar's pre-presentation where he was saying... Oh, yes. the feedback. Yeah. Yes. No, thank you. Thank you for my-- I'm actually an investigator on that study as well. Okay. -it, it's an interesting thought of combining a targeted chemotherapy with it. I'll be, you know, as an investigator on that study, I find it actually harder to tease out the added benefit of the anti-CD123 antibody drug conjugate to Ven/Aza than what we're seeing in this study. Just because of the nature of how these two studies were done, and the population that was treated. The blast reductions in our previously treated patients with the venetoclax, I think is very, very encouraging. It was hard for me to, in the anti-CD123 ADC study, to really get an idea of the contribution of that antibody. To get to your question about a combination, as Abe actually pointed out earlier, some of the initial work with this drug was done with in combination with antibodies against solid tumors. I think that would be a very interesting combination to explore with Evorpacept. In other words, using that antibody to target the surface of the cancer cell and then as a eat me signal, if you will, but also combining with the evorpacept to block the SIRPα CD47 interaction. I'm certain those kinds of studies will be done in the near future. Interesting, interesting thought on the combination route. I'm not sure the anti-CD123 antibody that was discussed would be the best drug to use, but clearly, one of them, any of the antibodies targeting CD33 or CD123, would be interesting to combine with this one. Perfect. Thank you very much for your answers, Dr. Erba. Thank you. Our next question comes from the line of Bradley Canino from Stifel. Please proceed. Hi, it's Bijan on for Brad Canino. Congrats on the data. Given the early efficacy you're seeing in the newly diagnosed group, we're wondering when we can expect a more fulsome data set? Abe? Yes. The next steps for the ASPEN-05 study are to await the dose optimization results from the ASPEN-02 study, which is our study in MDS. This is done to increase the efficiency of dose finding. We anticipate those results to be available in 2023, and the decision on the ASPEN-05 to follow shortly thereafter. Got it. Our final question comes from the line of Adam Evertts from LifeSci Capital. Please proceed. Thank you. Good morning. A question for Dr. Erba. For, patients who have failed first- line Ven or Ven/Aza, would you ever retreat them with venetoclax, maybe even after, a stem cell, transplant? And what type of outcomes would you expect there? That's an excellent question. You know, in an area where we don't have many, many options for this patient population, the answer to that question will become yes, and but it will depend on the situation. What stands apart about the patients we saw here is they were treated immediately after failing Aza/Ven. However, the question you ask is it possible to see, you know, Aza/Ven treatment working a second time in a patient who wasn't refractory to it the first time but actually relapses after it? I've actually seen that in my own patient population, and that's been, you know, published as well, that you will see some patients responding again. For example, I just finished treating a woman who's 55 years old, so younger, with TP53-mutated disease, received decitabine Ven, got into remission, and got a transplant. Then a year after the transplant, relapsed. Used the exact same regimen again and again with two cycles as the first time, got into remission, and was able to get to a second transplant. Yeah, in answer to your question, you can re-treat them with a Ven-based regimen or using Ven with intensive chemotherapy and see responses. What distinguishes our patient data set is that we saw those responses in people who were refractory to the Aza/Ven and then responded. Fantastic. Thank you. Mm-hmm. That concludes today's questions. I would now like to turn the call over to Dr. Randolph for closing remarks. Thank you. Thank you all for participating. If there are no more questions, we'd like to extend our appreciation, especially to Dr. Erba. Thank you for your valuable insights. Thank you. Have a great day. Thank you, ladies and gentlemen. This does conclude today's call. Thank you for your participation. You may now disconnect.