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Greetings, and welcome to the ALX Oncology Holdings Inc. Fourth Quarter 2025 Financial Results Call and Webcast. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. As a reminder, this conference is being recorded. I would now like to turn the call over to your host, Jason Lettmann, Chief Executive Officer. Thank you. You may begin.

Thank you, and welcome to our Q4 and fiscal year 2025 results call. We appreciate you all spending some time with us this morning. As usual, we will be making forward-looking statements during the call, so please refer to our FOS slide in our corporate deck. With me today, we have Harish Shantharam, our CFO, as well as our CMO, Dr. Barbara Klencke. And in terms of the first bit of news, we are delighted to announce today that Barbara will continue leading our clinical efforts as our permanent Chief Medical Officer. Welcome, Barbara. As many of you know, after joining in an interim capacity in September 2025, Barbara has been absolutely instrumental in driving our development programs forward over the last five months. Barbara, as many of you also know, is an incredibly experienced oncologist and drug developer, having served as CMO at Sierra Oncology and having senior roles at both Onyx and Genentech before that. We are beyond fortunate to add Barbara during this critical inflection for the company and thrilled to welcome her permanently. I will turn the call over to her later today to walk through some of our clinical updates. In terms of the agenda and the goals for today, we will review our key Q4 2025 and year-to-date accomplishments referencing our press release and corporate deck available on our website. Then, at the end, we plan to open it up for any questions you may have. In general, our focus at ALX Oncology Holdings Inc. remains on execution. We have made great progress on both of our programs of vorpercept and ALX 2004 in 2025 and positioned ourselves to achieve significant catalysts from these programs in the coming 12 to 18 months. Our goal and vision for each is to advance both programs to a stage where they are ready for pivotal studies by the end of next year. Execution has been strong over the last quarter, and I am very pleased to report that our clinical development progress and timelines remain on track. In terms of evorpicept, or EVO, in 2025, we are coming off a year of massive amounts of data really demonstrating the potential for evorpocept across a variety of combos and tumor types, which well informed our development strategy for EVO today. We have treated over 750 patients with EVO to date and are now highly confident where the drug works and, most importantly, where it works best. The MOA of combining EVO with antibodies and bispecifics has been well validated in the clinic and will pave the way for us going forward. Importantly, CD47’s key role as a biomarker for increasing durable response with avoricept in HER2-positive gastric cancer patients was further strengthened and validated by additional data in November at the SITC meeting. Here, we shared further data from our gastric study demonstrating a transformative benefit for patients both in terms of durability and PFS. In addition, we recently shared top-line data from the phase 1 of vorprecept and zanidatumab breast cancer trial, which is now a second dataset validating the role of CD47 and its importance as a biomarker. The follow-up analysis of this trial from the HER2-positive cohort showed that the responders to this combination treatment in a post-in-HER2 setting were largely restricted to CD47 overexpressors, which is a similar finding that we had in our gastric study. Full biomarker analysis from this trial is expected to be presented at a medical conference in Q2 of this year. These findings taken together strengthen our confidence in the ongoing phase 2 ASPEN-9 breast trial, where we will evaluate patient responses by CD47 level to further define the predictive potential of this biomarker among patients with HER2-positive disease that have progressed following in-HER2. We launched the study last year and continue with site activation globally at a strong pace. We remain on track with our clinical timelines here and expect to provide top-line data for 80 patients from this study in mid-2027. As shifts to the treatment landscape occur in breast cancer, EVO has the potential to provide both a best and first-in-class option for the 50,000 patients in the second-line-plus breast cancer setting. EVO is also poised to be the only therapy that can address CD47 expression in this large patient population. Overall, the results for EVO from these two HER2-positive cancer trials support the potential for us to pursue a targeted oncology approach to additional tumor types with EVO. And given the broad over CD47 in both solid tumors and heme malignancies, it gives us a real opportunity to pursue a focused development strategy for EVO in combination with anticancer antibodies and bispecifics. We are excited about our study in breast and also excited about the NHL data, which we recently shared in December, which furthers the findings of EVO into heme malignancies. We are also ongoing partnering with Sanofi and we are excited about what we are seeing across both of those studies, and Barbara will go into both in more detail. In terms of 2004, turning to our ADC now, we are also very pleased with the clinical progress of ALX 2004, which, as you know, is our novel and potentially best-in-class EGFR-targeted ADC. We cleared the first two dose cohorts and continued to progress development per plan with the 4 mg/kg dose now in the phase 1 trial. We are now expecting full ALX 2004 safety data from the dose-escalation cohort later this year in the second half of 2026. The potential of these two novel therapies, coupled with our substantial progress on their respective clinical programs, contributed to the successful completion of our recent financing of $150,000,000, which we closed a few weeks ago. With our newly strengthened balance sheet, we now have the opportunity to deliver more robust and meaningful data readouts in both of our ongoing clinical programs as reflected in our milestone updates here. Our mission again is to have these two programs ready for a pivotal phase study by the end of next year, and we believe we can do so with continued focus on execution. I will now turn it over to Barbara to walk through some clinical data and findings and plans in more depth. Barbara?

Thank you, Jason. Let me start with some quick highlights of the strong results that we have seen with avorpicep in two HER2-positive breast cancer indications that we have reported on within the past three months. I am referring now to slides 14 to 18 in our corporate deck. In the randomized phase 2 HER2-positive gastric cancer study, we saw impressive response rates with the vorapicep when combined with a trastuzumab-based regimen in the subset of patients with CD47 tumors. We reported this data at the SITC conference in November 2025. In this subset, the response rate was 65% in second- and third-line gastric cancer patients compared to 26% in the control arm. This is a delta of nearly 40%. The median duration of response was also quite impressive. It was more than two years, and more than three times longer than that seen in the control arm. The median PFS was 18.4 months in the avorpecep arm and seven months in the control arm, with a hazard ratio of 0.39. And finally, the median overall survival was 17 months with evorpazep versus approximately 10 months in the control arm, with a hazard ratio of 0.7 in this subset. In summary, this randomized study established the potential for CD47 to become an important predictive biomarker. In parallel, we worked with our partners at Jazz to evaluate the CD47 expression in patients enrolled in the phase 2 study of aborpicep in combination with zanidatinib. As a reminder, this study enrolled HER2-positive breast cancer patients who had progressed on prior HER2-directed therapies, all of whom had received prior in-HER2. We first reported data from the study at the San Antonio Breast Conference back in December 2024. As you can see on slide 22 in our corporate deck, at that time, we reported that in the nine late-line patients with confirmed HER2 expression by central assessment, the response rate with the vorpocept plus anadaptinib was a remarkable 56%. The duration of response at that time ranged from 5.5 to nearly 26 months, and the median PFS was 7.4 months. These data compared very favorably to benchmark data such as the data from the SOFIA trial, a predominantly second- and third-line HER2-positive breast cancer trial, which produced a response rate of 22% for margetuximab, whereas this data was obtained in patients who had a median of six prior lines of therapy. Now recently, in January, we concluded the CD47 biomarker analysis from these patients. We recently announced that the responders were predominantly restricted to the patients who overexpressed CD47. Full biomarker analyses from this trial will be presented at the ESMO Breast Cancer Conference in 2026. The data from these two independent studies show the potential of avorpicept to drive very substantial benefit for patients with high CD47 expression. These extraordinary outcomes clearly validate avoricep’s mechanism of action and provide increased confidence for our ongoing phase 2 breast cancer study. Before I provide an update on our ongoing phase 2 breast cancer study, I also want to highlight the results that we have seen so far in the hematologic malignancy setting. These data are summarized on slide 13 in our corporate deck. In three separate cohorts of indolent non-Hodgkin’s lymphoma patients, we see very high complete response rates relative to published CR rates in relevant benchmark studies. The most recent study was presented at ASH in December. These were in treatment-naive, first-line indolent lymphoma settings. These patients received evorbicep combined with Rituxan and Revlimid, known as the R-squared regimen. They achieved a complete response rate of 92%, which is almost double that seen with R-squared alone. These data are entirely consistent with the two studies of evorpocept with Rituxan or R-squared in previously treated indolent lymphoma patients where the CR rates were also extremely robust and more than double the CR rates enveloped in relevant benchmark studies, as you can see on the slide. Together, these five datasets strongly support the potential of a vorpa set to enhance macrophage-driven ADCP when combined with an Fc-active anticancer antibody. These data give us high confidence for our ongoing study in HER2-positive breast cancer. Let me now provide some quick updates on that study. The design of the study is provided on slide 23 of our corporate deck. As a reminder, in this study, we evaluate avoricep in combination with trastuzumab and single-agent chemotherapy in a single-arm design enrolling HER2-positive metastatic breast cancer patients who have progressed on in-HER2. Following the strong validation of CD47 as a predictive biomarker of benefit with avoracep plus anadaptinib, we have now decided to enlarge the current phase 2 study to up to 120 patients from 80 to increase the number of HER2-positive patients with CD47 overexpression. In addition, we are updating the primary endpoint to response rate in patients who have high CD47 expression. A key secondary endpoint will track response rate by HER2 status informed by ctDNA. This way, we will be able to track response rates both by CD47 expression on its own as well as in double-positive patients informed by high CD47 expression and HER2-positive status. As in-HER2 has now been approved as first-line therapy, the treatment landscape for the second line and subsequent therapies has entered uncharted territory. The optimal sequencing of subsequent therapies is unknown. Several real-world evidence studies suggest that response rates and PFS or time to next treatment might actually be lower than expected with available regimens in patients who have failed in-HER2 therapy. So we see a notable gap in the understanding of the optimal sequencing of available therapies and really a large unmet need for effective treatment options in this post–in-HER2 setting. Based on the activity that I have described to you for the avorpus app across a number of settings when combined with an anticancer antibody, we believe that avoricep has substantial potential for benefit in metastatic breast cancer patients in this setting. Furthermore, a CD47 biomarker-driven approach in HER2-positive patients could enable a highly targeted patient selection strategy. To be ready for a prospective selected registration study in the future, we have initiated work on developing a companion diagnostic for CD47 expression. With respect to enrollment in the ongoing phase 2 trial, we are making good progress. While we are still early in the enrollment curve, the site activations remain globally on track. We are pleased to see that investigator interest in the study remains strong. We project being able to share meaningful efficacy and safety data, including response rate, biomarker results, and early durability trends by mid-2027. Now let me turn our attention to the second clinical program, ALX 2000 and 4, our EGFR-targeted antibody-drug conjugate. While EGFR is a validated target, developing an effective ADC has remained a significant challenge due to the narrow therapeutic window. We have leveraged historic learnings to develop ALX 2000 and 4, our EGFR-targeted ADC, which was designed by our internal team of world-class protein engineer experts. The preclinical dataset is particularly exciting as it demonstrates potent, dose-dependent antitumor activity in numerous models across a broad range of EGFR expression levels and relevant mutations such as those in p53, KRAS, BRAF, and others. EGFR-related skin toxicity and interstitial lung disease were notably absent in our GLP tox studies in nonhuman primates. The antibody, metuzumab, has a unique affinity-tuned epitope whose binding to EGFR is not by mutations in the binding domain for the other approved EGFR antibodies. In creating this ADC, we combined this antibody, the metuzumab antibody, with our proprietary topoisomerase I inhibitor linker-payload, which was selected for linker stability and for its robust bystander effect. Given the attention paid to both efficacy and safety in the design of this molecule, we believe that ALX 2000 and 4 is uniquely positioned to break new ground as a potential first-in-class therapy for EGFR-expressing solid tumors. Additional preclinical highlights can be found on slides 26 to 33 in our corporate deck. I would also refer to the comprehensive preclinical data that was presented at the triple meeting conference in October 2025 and more recently at the 2026 World ADC Conference. Finally, in terms of progress in the clinic, we are currently enrolling patients in our third dose cohort, having initiated dosing initially at a robust dose of 1 mg/kg, then escalating to 2 mg/kg, and subsequently to 4 mg/kg based on seeing no DLTs at the prior dose levels. We believe that the 4 mg/kg dose, our current dose level, could potentially now be at the lower end of the therapeutic dose range. As a reminder, we are enrolling only patients who have non-small cell lung cancer, colorectal cancer, head and neck cancer, or esophageal squamous cell cancer, as these are EGFR-expressing tumor indications. In this phase 1 trial, we will perform both the dose-escalation as well as the dose-expansion component. These data will then ultimately set the program up to advance into a registration study. We plan to provide data from the dose-escalation portion of the ongoing phase 1 study in the second half of this year. With that, let me hand this over to Harish.

Thank you, Barbara, and good morning, everyone. 2025 was a year of strategic prioritization and clinical validation for ALX Oncology Holdings Inc., highlighted by the progress we made on our lead program evaporposet, and the clinical entry of our first ADC, ALX 2004. In terms of financials, we finished the fourth quarter of 2025 with cash, cash equivalents, and investments totaling $48,300,000 before strengthening the balance sheet from our equity financing we closed earlier this month in February. The net proceeds from the offering were $140,400,000 after deducting for the underwriting discount and other offering expenses. Following the cash inflow from this offering, we believe the cash and investments on hand are sufficient to fund ALX Oncology Holdings Inc. operating expenses through 2028. With our newly strengthened balance sheet, we now have the opportunity to deliver more robust and meaningful data readouts in both of our ongoing clinical programs over the next 12 to 18 months. The key milestones we currently guide to include: number one, the full biomarker analysis readout from our phase 1/2 trial evaluating evorpocept in combination with danitatumab in advanced HER2-positive breast cancer patients will be presented at the ESMO Breast Conference in May 2026; number two, the ALX 2000 and 4 safety data from the dose-escalation phase of the trial is anticipated in 2026; number three, the readout on evorposet top-line data from 80 patients from the ongoing phase 2 ASPEN breast cancer trial is anticipated in 2027. With respect to the latest quarterly financials, the GAAP net loss was $22,800,000 for the three months ended 12/31/2025, or $0.42 per basic and diluted share, as compared to a GAAP net loss of $29,200,000 for the three months ended 12/31/2024, or $0.55 per basic and diluted share. The decrease in year-over-year spend can be primarily attributed to lower stock compensation, lower personnel and related costs, as well as lower preclinical costs following pipeline prioritization. Please refer to the press release for the detailed breakdown on the R&D and G&A operating expenses for the quarter. Operationally, our team is now singularly focused on executing the ongoing phase 2 trial in breast cancer for evorpoced and the phase 1 trial for ALX 2004. Moving forward, the clinical spend will be largely driven by these two trials, partially offset by reduced spend in evaporizat legacy trials that are winding down. With that, let me hand the call back to Jason.

Jason?

Thanks, Harish. As we discussed, we are coming off a very strong 2025 where we had an incredible amount of data with evorbicept really demonstrating our path forward. We are also very pleased with the progress on ALX 2004. We continue to advance through dose escalation and are looking forward to significant catalysts across both programs over the next 12 to 18 months. Our focus internally remains on execution, and that is what we will plan to do going forward. We are very happy to remain on track in terms of the execution across both studies. We will now open for questions.

Thank you. If you would like to ask a question, please press 1 on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press 2 if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. Our first question comes from the line of Allison Marie Bratzel with Piper Sandler. Please proceed with your question.

Hi, good morning, and thanks for all the updates, and thanks for taking the questions. Just some follow-ups from me on EVO. So I think initially, we were expecting an interim look at 80-patient readout this year. So could you just confirm, is that correct? And Barbara, I know you covered this in the prepared remarks, but just hoping you could talk some more to the rationale behind the upsizing to 120 patients, the change in the primary endpoint, and just talk to how that informs on the regulatory strategy. Then maybe just secondarily, what kind of feedback are you getting from investigators on the biomarker approach, and what do you expect to see on enrollment trends in ASPEN breast? Thank you.

Great. Thanks, Allison. I appreciate the question. I will let Barbara take the second question. On the first question, that is correct. We are guiding towards 80-patient full data from those 80 patients in mid next year. From our perspective, our goal internally and externally as well is to communicate full, robust data. At that point, we should have enough patients to really understand where the study is headed. We certainly are trying to guide to ensure we have enough CD47-positive patients in this study. As you know, the enrollment is essentially all comers. So guiding to the 80, we think, makes the most sense because we are confident at that point we will have real, fulsome data across both the CD47-high population as well as the other buckets that we will be looking at as well. That is the plan. Certainly, it is an open-label study. We have an opportunity to share earlier if we think it makes sense, as well as talk to regulators earlier, but the current plan is mid-2027. On your second question, Barbara, do you want to take that?

Yes. Addressing the interim, Jason just did that. Upsizing, again, Jason hinted at that, really just wanting to ensure robust numbers of patients in various segments and various subpopulations. We will have patients who can be confirmed HER2-positive in this setting by ctDNA or not. We will have patients whose tissue has evidence of overexpression of CD47 or not. We just want to make sure that we have robust numbers. I think the most important thing for this study could really be the optimal cut point. We have to be able to have data that drives the proposed cut point. FDA will be very interested in that. We just wanted to make sure that we had enough patients who were CD47 overexpressing that we can do that. In terms of a primary endpoint, it has always been a response-rate endpoint trial. In the two studies that we talk about, the gastric and the adaptinib combination, it has been pretty remarkable just how powerful CD47 is as a predictive biomarker. So I have moved that up to the primary endpoint, and response by HER2 status will still be an important key secondary endpoint, but we feel like the CD47 is going to be the most powerful predictor of response. That is the justification for changing the primary endpoint. You asked about the investigators’ perception of the study with a biomarker selection strategy. I think they are very excited about it. To have the ability to find a population for whom the therapy is going to provide substantial benefit, and what we have seen in all of our prior studies that I talked about today—lymphoma, gastric, breast cancer—we are seeing these remarkable response rates and we are also seeing durability. The two endpoints together are really providing transformational benefit. The ability to find the selected patient population where the treatment outcome can be so robust, I think—

Our next question comes from the line of Li Wang Watsek with Cantor Fitzgerald. Please proceed with your question.

Sure. Happy to do. Thanks, Daniel. As Barbara mentioned and we highlighted in our comments, both studies remain on track, and the execution has been strong. The change post financing here has been to ensure that we are communicating robust data. If you look at what we would have this quarter or next quarter versus towards the end of the year in 2004, it is really a step change in data. We should have, towards the end of the year, really fulsome data from the dose-escalation phase, and I think that will allow us to be much more clear about what we are seeing. Ideally, we will be able to communicate where we think the expected dose or two doses will shake out and allow us to communicate that externally. The goal is to make updates meaningful and full, and that is the thinking behind that guidance.

If I may follow up on this, is it safe to expect up to four dose levels to have been tested at the point when you make the disclosure?

I think that is reasonable. As you know, we went from one to two to four, so we have doubled now twice. We do think we are at the low end of the therapeutic window and continue to progress that study very well. The fact that we have cleared one and two so rapidly without seeing DLTs is encouraging. Certainly now in the four, things continue to go well, and I do think getting to four doses as part of that cohort is definitely a reasonable expectation.

Great. Thank you so much, and congrats on the update.

Thank you. Our next question comes from the line of Samuel Evan Slutsky with LifeSci Capital. Please proceed with your question.

Good morning, everyone. I appreciate the questions. Two for me. One is that for the 80 patients in ASPEN-9, remind me what is the expected ratio of those with CD47 high versus low expression? And then on 2004, on 4 mg/kg being at the lower end of the therapeutic dose range, looking at some of the other EGFR ADCs that are using topo 1, it seems like they are at either 4.8 mg/kg Q3W or less in terms of dose. Curious on what is driving this difference in where the therapeutic range starts with your drug, or is it that you would just consider that you have a wider therapeutic window, which hopefully leads to better efficacy versus others?

Thanks, Sam. I will take the first one, and Barbara can handle the second one on the range. In terms of the percentages, what is nice about CD47 is it is really well studied in the literature, and this specific question around CD47 expression has been well documented. We know in our gastric study that about half of those patients that were confirmed HER2-positive were CD47-high, and we looked, as you recall, across four different cutoffs and showed that range to be roughly 40% up to around 57% of the population. So a really substantial percentage. We also know from the literature that percentage is relatively consistent in breast. Again, we expect the cutoff and the expression profile to be different, but the patients that have CD47 high we expect it to be around half, and the literature would support that. It is important to run the study to see how that shakes out, but we are expecting to see a significant number of this population be CD47 overexpressors. Barbara, do you want to take the question on the therapeutic range with 2004?

Exactly. The highest nonseverely toxic dose in primates was 1 b, which is potentially around 6.5 mg/kg in patients. There is definitely variability on that, but that was one way for us to think about where we might be able to get the dose to. I think it will be data driven. I would never think that we would double again. We are now in a range where smaller incremental increases will be pursued. We will have to see how things go in terms of the tolerability and toxicity that we see in patients. We think somewhere in the range of the fours, five, six mg, maybe a bit higher, because, as you know, in the nonhuman primate data, there really was not any severe toxicity, so maybe we can go just a little bit above the six to seven range, but we will see. We will provide further updates later in the year, but that is the allometric scaling in terms of where we think we might start to see some toxicity.

Okay. Thanks.

Thank you. Our next question comes from the line of RK with H.C. Wainwright. Please proceed with your question. Thank you. Good morning, Jason and Barbara.

A couple of questions on ASPEN-09 and one on 2004. On ASPEN-09, as you are expanding the trial to 120 patients, trying to understand the logic behind it. Can you discuss what is the prevalence of CD47 high in post–in-HER2 patients, especially if you are defining CD47 high as IHC 3+ greater than 10%? Is this expansion driven more by statistical power, or are you concerned about lower-than-expected prevalence of the biomarkers? On the second one, when we start thinking about physicians’ choice of chemotherapy, should we be concerned about subsequent ADC use in this post-trastuzumab setting that it can impact the CD47 expression? And then on 2004, with the safety data expected in the second half, how are you monitoring the interstitial lung disease and the skin tox?

Those are great questions. Thanks, RK. On ASPEN-09 and CD47 expression post in-HER2, we think that the percentages should hold that I mentioned before. Roughly half of the population should be CD47 high. We did highlight in the past on our calls our recent study last year that showed that patients who are exposed to in-HER2 overexpress CD47. We think it is certainly possible that those numbers are higher in this population. We know that CD47 is a key mode of evasion post in-HER2, so we do think that is possible. Barbara, do you want to take the next one on the various chemo options and how that may impact things?

What we know in terms of CD47 expression, there is data in the literature that it rises in patients post in-HER2. We do not have a lot of other data. Most of the data on CD47 comes from survival tissue from the time of diagnosis. The literature does support higher rates of overexpression post in-HER2, which is absolutely perfect as our patient population. It is where there is an unmet need, and it is clearly the clinical setting that is the most wide open at this point in time. I am not sure that I have any concern that different chemotherapy drugs will perform differently in patients who have CD47 expression when they are combined with trastuzumab. Our main focus on mechanism of action is the combination of trastuzumab or some such antibody with an active Fc plus avorpazep. We certainly will look at the five different chemotherapy options across the different subsets if there are any major differences, but I am not expecting to see much variability there. In terms of ALX 2004, you asked about how we might be monitoring for both ILD and skin toxicity. Patients go through CT scans on a regular basis as per protocol, and a lot of times, that is where initial phases of interstitial lung disease may be detected. You do want to detect it before it gets too symptomatic, and having scans to watch for their cancer progression or response, that should be picked up. There are guidelines in the protocol. They are all very cautionary, just because this class of agents has in the past caused—you know, the payload itself has been associated with ILD—but we did not see any evidence of that in our nonhuman primate toxicology studies. We will monitor for it, but we have a low likelihood based on our NHP work. In terms of skin toxicity, certainly metuzumab was the antibody that we selected for the lower skin tox that has been shown clinically in the early investigational use of that metuzumab antibody. Every time a patient is seen in clinic, they will be examined and can report that, so that will be an early thing that we could pick up once we get into the various dose ranges. Our prediction is that we are not going to see skin toxicity at the lower doses. Certainly, cetuximab and panitumumab are known to have quite a bit more skin toxicity. If you were to do a cross-trial comparison of safety data from the approved antibodies versus metuzumab’s safety profile, that gives us a wider therapeutic window. We do not expect to be too limited by skin tox. It allows us to move up higher into the dose range, similar to the question that maybe Sam asked earlier about maybe having a wider therapeutic window for this agent based on the protein design that we have with this agent.

Thank you. Just on the sample size, there was no change in the assumptions in terms of the percentages or efficacy. There has been no change there. The driver is really to ensure that we have a very robust phase 2 and are in a position to de-risk the phase 3 as much as possible. The ability to flex up to 120 allows us to do that. Of course, as we mentioned, it is an open-label study. If we see data that is even in the ballpark of the 56% we saw and the 60% we saw in the breast and gastric studies respectively, I think we will have plenty of room to clear the hurdle. The goal of this is to inform the phase 3. Once we see a sufficient signal, that will then spur into action conversations with the regulators, moving quickly to a phase 3.

Fantastic. Thank you very much. Thanks to both of you for answering in detail.

Thanks, Nabil. On the CD47 expression, I would say what we know is that we would anticipate it to be different across different tumor types. We know gastric, as a baseline tissue type, expresses CD47 more highly than breast. With gastric, it effectively did not matter, meaning we could pick IHC 3, IHC 2/3, and continue to see a good response. The pre-Eval-plus-any study in breast informs that. We have a good estimate of how it could look, and going forward, it will be critical for us to run this study to really understand exactly where to set the cutoff. That is part of the goals of this current study that we are in the midst of, and I think that will be informative. In terms of the missing tissue or different tissue types, we do not anticipate that to be a significant issue, just because we are using tissue at time of diagnosis to base CD47. We expect CD47 to be relatively stable, and I think that should be pretty straightforward. Barbara, anything else to add on that?

No. I think everybody will be required to submit tissue. There is always an estimate in most trials that you might have some missing data. I would not expect it to be unusual. So 10% or less. We anticipate being able to have measurable CD47 in nearly all patients. It could be 100%, but I would not be surprised if we ended up with a rare patient for whom the tissue just was not sufficient, but that should not be a problem. IHC is a very standard assay methodology, so it is easy to perform, etc. So no major risks there.

Thank you. Ladies and gentlemen, that concludes our question-and-answer session. I will turn the floor back to Mr. Lettmann for any final comments.

Thanks, everybody. We appreciate the good engagement and questions this morning. It is an exciting time at ALX Oncology Holdings Inc. out in front of us, and we continue to execute well. We are looking forward to the next quarter and the next year where we have a lot of important milestones to lay out. We appreciate all the interest and support. Thank you.