Welcome to the ALX Oncology Third Quarter 2025 Financial Results Conference Call and Webcast. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. Please note this conference is being recorded. I would now like to turn the conference over to your host, Jason Lettmann. Please go ahead, sir. Thanks, everyone, and welcome to our Q3 2025 results. I appreciate everybody spending some time with us this morning, and I'm looking forward to this update. On slide two here, before we start our presentation as housekeeping, here are our forward-looking statements for your review. On the next slide, slide 3 here, here is the agenda and our plan for today. We're going to be providing an update on our key accomplishments in the third quarter of 2025. Most notably, we are very excited to share with you the dataset that will be presented at SITC this weekend from a pre-planned analysis of our ASPEN-06 trial that showed CD47 expression as a key predictive biomarker for increasing durable clinical response with evorpacept in HER2-positive gastric cancer patients. Our goals for today are most importantly to share these detailed results with you as we believe this dataset now clearly validates the role of CD47 in HER2-positive cancers. We will then give you a sense of how this data now impacts our development strategy for evorpacept going forward. We will also be providing an update on our novel ALX-2004 EGFR-targeted ADC, which is now in the clinic. Today, we are also excited to be joined by Dr. Peter Schmid from Barts Cancer Institute in the U.K., who is a key opinion leader in breast cancer and investigator in our evorpacept phase II breast cancer study. He will be presenting his views on evorpacept data and its potential within the current treatment paradigm for HER2-positive metastatic breast cancer. Then our CMO, Barb Klencke will provide an update on our novel EGFR-targeted ADC, ALX-2004, which is currently dosing patients in our phase I trial. Now, on slide four, in the third quarter, we made significant advances in both evorpacept and ALX-2004 clinical programs. We again are excited to present the full data at SITC that is demonstrating the potential of CD47 expression as a predictive biomarker and highlight a clear opportunity to now identify patients who are most likely to achieve the greatest benefit from evo. As Barb will present in detail in her clinical section in this analysis, we saw that patients with high CD47 expression derived the greatest benefit across all key efficacy markers: response rates, duration of response, median PFS, and overall survival from evorpacept versus those with low expression. The data is very clear as the magnitude of benefit across many of these metrics was double or even triple those observed in the control arm, and also clearly compares very favorably with the large benchmark studies in second-line gastric cancer. Most importantly, these results support the potential to pursue a targeted oncology approach to additional tumor types with evo, and given the broad overexpression of CD47 in both solid tumors and heme malignancies, it gives us a real opportunity to really focus evo now as a targeted IL therapy. Our phase II clinical trial in breast cancer, which is designed to pursue a CD47 and HER2 biomarker-driven strategy based on this strong data, is on track to dose its first patient this quarter. As we've discussed, evo has the potential to represent the first and only option for metastatic breast cancer patients who overexpress CD47, which we know can lead to worse outcomes and a poor prognosis for these patients. With our second pipeline product, our novel EGFR-targeted antibody, ALX-2004, which is a highly differentiated ADC, we presented preclinical data and design of our phase I trial at the Triple Conference a few weeks ago. We're excited to announce today that we are currently enrolling patients in the second dose cohort, rapidly clearing the first dose cohort in this phase I trial. Turning to our financials quickly, we reported a total cash balance of $67 million, and that cash is expected to provide us runway into the first quarter of 2027, which positions us to achieve the value-enhancing data milestones for both ALX-2004 and evorpacept that we have coming next year. Now, turning to slide five, it has been very well established that CD47 is widely overexpressed across almost every type of cancer, and it is also clear that CD47 overexpression matters as it is clearly a negative biomarker for patients. When you look at research in CD47 over the last decade plus, it is a very strong foundation that CD47 is clearly a negative prognostic biomarker. What you can see here is a meta-analysis of 38 cohorts across 17 publications, which includes over 7,000 patients. There really is no question that CD47 is clearly associated with shorter survival and worse outcomes, and you can see on the right the wide range of tumor types where this has been established. Now, turning to slide six, and as a reminder that during our Q2 call just a few months ago in August, we presented the top line data which support that CD47 overexpression is a clear predictive biomarker for response with evorpacept in HER2-positive gastric patients. In this analysis, patients with both confirmed HER2 positivity and CD47 high expression had a dramatic response to evorpacept as compared to those in the control group who did not have evo. As you can see here on the ITT population, we saw a strong response of a 41% ORR in the evo arm versus 27% ORR in the control arm. If you look at the data now in patients that clearly have CD47 high expression, there is a magnitude of benefit for those patients where we had an ORR of 65% in the treatment arm versus 26% in control with a nominal p-value of less than 0.05. As you can see on slide seven, and what we're very excited to share with you now and at SITC later today, this strong ORR benefit with evorpacept in combination with TRP in CD47 high patients was also reflected and translated well to DOR, PFS, as well as survival, as it's clear that patients who overexpress CD47 and retain HER2 expression is driving the effect here. This is very important as this clearly validates evo's dual mechanism of action. Again, this is a second-line plus gastric population, which has historically been a very tough cancer to treat. In addition to the ORR benefit, which had a delta of almost 40% versus control, the median duration of response here for those patients is over two years, which is more than triple the control. The median PFS was over 18 months in the evorpacept arm versus just seven months in control with an impressive hazard ratio of 0.39. We were also pleased to see these gains further translate to a benefit to overall survival where we saw a median OS of 17 months with evo versus about 10 months in control and also a strong hazard ratio of 0.63. Barb will walk through this data in more detail, and the full dataset will be shared at SITC here soon. What is clear is that this data shows the potential for evorpacept to drive really substantial benefit for these patients with high CD47 expression. On the next slide, this just shows the focus set of milestones that we're driving to now. In summary, we're laser-focused on these two programs. First, driving evorpacept into ASPEN-Breast, which is our study investigating patients post HER2 and again focused on CD47 high and understanding the impact of that biomarker. We continue to execute well against the milestones that we've communicated in the past and are anticipating first patient in Q4 of 2025 with interim data expected Q3 2026. ALX-2004 also remains on track and continues to proceed very well. We dosed our first patient in August 2025, and we continue to expect initial safety data first half of 2026. Turning to the next slide and in summary, before I hand the call over to Barb, we had a strong quarter both in terms of execution, continued tight discipline around our capital, and are excited about the key value catalyst for ALX in 2026. As you can see here on slide nine, this is a snapshot of our current clinical pipeline. As we have communicated previously, we are pursuing a focused development strategy for evo in combination with anticancer antibodies given the consistent proof of concept that we have seen in various clinical studies with different monoclonal antibodies, and this data here today further builds on that. In addition to our HER2-positive breast cancer program with a CD47 biomarker-driven approach, ALX-2004, again our EGFR-targeted ADC, continues to progress well, and we are also very excited about our partner program with Sanofi SARCLISA in multiple myeloma, which is now in dose optimization phase. Next, we'll turn this over to Barb, who will take over and provide more details on the evorpacept CD47 biomarker data presentation coming here at SITC. Barb? Thank you, Jason. I will start by describing evorpacept's mechanism of action. CD47 is broadly overexpressed on cancer cells as a means of evading the immune detection, and it does so by sending a don't-eat-me signal. Evorpacept is a fusion protein, and it's designed to block that signal. Evorpacept's Fc region is engineered to be inactive, and hence it's particularly effective when given in combination with an anticancer antibody such as Herceptin. The active Fc domain on the anticancer antibody can then trigger very effective phagocytosis, which otherwise would have been suppressed by the CD47 signal. Slide 12 shows that evorpacept's approach to blocking CD47 is different from the conventional approach pursued by other CD47-targeted agents. While CD47 is overexpressed in cancer cells, it is also expressed in healthy cells such as red blood cells. The conventional approach to block CD47 with an antibody that then also binds to macrophages through an active Fc has caused significant toxicities in some patients, and thus this approach has largely failed. In contrast, the evorpacept approach using an inactive Fc spares normal cells, and our safety database in more than 750 evorpacept-treated patients confirms the safety of this approach. Slide 13 shows the design of the ASPEN-06 gastric study that Jason has introduced earlier. We enrolled 127 second-line or third-line HER2-positive gastric cancer patients, all of whom had received prior HER2-directed therapy. Patients were randomized to evorpacept, trastuzumab, ramucirumab, and paclitaxel, or the TRP alone. The primary endpoint was objective response. Importantly, because there can be loss of HER2 expression following prior HER2-directed therapy, we wanted to look beyond the HER2 status as diagnosed on archival tissue. Based on the known mechanism of action for evorpacept, our drug is not going to work as effectively if HER2 is not overexpressed on the cancer cell surface. To this end, ctDNA was obtained at baseline in all patients, and in addition, 48 patients underwent biopsy either at study entry or at some point following their prior HER2-directed therapy. In total, 95 patients, or 75% of the enrolled population, were confirmed as having retained HER2 positivity by either the ctDNA or on fresh biopsy. Ninety of these 95 patients were evaluable for CD47 expression in tumor cells using either archival tissue or where available a fresh biopsy sample. High CD47 expression based on a cut point of IHC 3+ staining in at least 10% of the tumor cells was present in 48% of these 90 patients. The expanded results of this pre-planned exploratory analysis of efficacy by CD47 expression level in patients who retained HER2 positivity is the focus of the data that I will review with you today. Slide 14 shows the objective response rates in key subsets. As we've previously reported, in the 95 patients who retained HER2 positivity, we see a robust response rate of 48.9% for the evorpacept TRP arm versus 25% in the control arm. In the subgroup by CD47 expression level, evorpacept produced a response rate of 65% compared to 26% in the control arm amongst patients with the high CD47 expression levels. The response rate in the control arm was consistent across CD47 expression levels and lower than that in the evorpacept arm in both the CD47 high and CD47 low groups. Moving to slide 15, I'm now displaying the duration of response in these same subgroups. Again, we see the potential of CD47 expression as a powerful predictive biomarker for evorpacept benefit. The duration of response in all HER2-positive patients irrespective of CD47 expression was 15.7 months for evorpacept plus TRP compared to 9.1 months for responders in the control arm. In the CD47 high group, the duration of response was three times longer for patients in the evorpacept trastuzumab RP arm compared to the control, with a median duration of response of 25.5 months versus 8.4 months. In the CD47 low group, evorpacept TRP had a median duration of response of 11.2 months compared to 12 months for TRP. In slide 16, we're now showing the progression-free survival in patients with confirmed HER2 positivity and high CD47 expression. The hazard ratio is 0.39, with a median PFS of 18.4 months for the evorpacept trastuzumab RP arm, which is more than double the seven months seen in the TRP alone arm, again suggesting the potential for CD47 expression as a powerful predictive biomarker for evorpacept benefit. Slide 17 shows a similar pattern of longer survival observed in the HER2-positive CD47 high evorpacept arm. Median overall survival was 17 months compared to 9.9 months for the control arm, with a hazard ratio of 0.63. All of these data being presented at the SITC Conference this week are based on mature follow-up. The median follow-up for survival, for example, was 25 months. Slide 18 shows some of the various cut points that we examined for CD47 expression based on the range and strength of IHC testing. As shown here, we looked at the median, we looked at medium or high-intensity staining defined as IHC 2+ and 3+ in at least 10% and in at least 25% of tumor cells. We also looked at high-intensity staining or IHC 3+ in tumor samples with 5% or more or 10% or more of cancer cells expressing that high-intensity staining. The prevalence of CD47 high across these ranges from 40% to nearly 60% of HER2-positive patients, depending on the cut point. The key takeaway from this slide is that we see consistent improvements in response rates, PFS, and OS in the evorpacept treatment arm irrespective of the cut point for CD47 expression. On slide 19, I'm showing a cross-trial comparison of our evorpacept efficacy data in patients with retained HER2 positivity and high CD47 expression relative to benchmark trial data in HER2-positive gastric cancer. With the usual cross-trial comparison caveats in mind, evorpacept data directionally compares very favorably to recent HER2 data from the DESTINY-Gastric04 study in the second-line setting. In that trial of nearly 500 patients published earlier this year in the New England Journal of Medicine, those patients required confirmation of HER2 status by fresh biopsy following a trastuzumab-containing regimen, and they randomized these patients to ENHERTU or to RP as a control arm. As effective as ENHERTU was in the second-line setting in that trial, our second and third-line evorpacept data generated in patients with high CD47 expression, a known negative prognostic biomarker, appear much better. Turning our attention now from gastric cancer to HER2-positive breast cancer, slide 20 introduces a phase I-B/II trial in HER2-positive breast cancer patients conducted by Jazz that evaluated the safety and efficacy of evorpacept plus zanidatamab in patients who progressed on prior HER2-directed therapy. These patients were heavily pretreated with a median of six prior lines of therapy. In nine patients confirmed to retain HER2 status by central assessment, the response rate was 56%. The median duration of response for that group ranged from 5 months, 5.5 months, to nearly 26 months, with the median not reached and the median PFS being 7.4 months. These data compare favorably to benchmark data, including, for example, the SOPHIA trial, a predominantly second and third-line HER2-positive breast cancer trial, which produced a response rate of 22% for margetuximab. Moving to slide 21, we've now demonstrated in these two studies the potential of evorpacept to engage the innate immune response, validating the mechanism of action of evorpacept given in combination with anticancer-directed antibodies in both HER2-positive breast cancer and in HER2-positive gastric cancer. This gives a strong conviction of evorpacept's potential and its path forward in the HER2-positive breast cancer setting, which we'll talk about next. Slide 22 describes briefly the opportunity that we see for evorpacept in breast cancer, which now has a high probability of success, having been de-risked by the two positive data sets in two different HER2-positive settings. A CD47 HER2-positive biomarker-driven approach with evorpacept enables a highly targeted strategy, potentially addressing the high unmet medical need in the evolving breast cancer landscape, which includes patients who have now progressed on ENHERTU. It is now my distinct pleasure to introduce Dr. Peter Schmidt, a professor of cancer medicine and center lead at the Center of Experimental Cancer Medicine at Barts Cancer Institute. He's a well-known global lead investigator on multiple ongoing phase III trials in metastatic and localized breast cancer. Just as two examples of trials with immunotherapy agents, he's a global lead investigator on the pembrolizumab KEYNOTE- 522 study and the atezolizumab and IMpassion130 study. With that, I turn this over to you, Peter. Thank you, Barb. The treatment options for patients with metastatic HER2-positive breast cancer are currently undergoing, I would almost say, a dramatic change. We obviously have seen a very active drug moving initially into second and third-line treatment with trastuzumab deruxtecan, but everyone is aware of the data that now placing T-DXd increasingly in the first-line setting. I think that's where the drug will ultimately end up. That is fantastic from a patient perspective. We have a very powerful new first-line treatment option. The challenge that comes out of this is there is no standard of care for patients who have been treated with trastuzumab deruxtecan. The sequence we had previously that patients would get a treatment called TPH, first-line with trastuzumab, pertuzumab, and second-line T-DXd, and the third-line other options, that's just been turned upside down. At the moment, there are a number of options we can choose from, but none of those options have actually been specifically approved and tested in patients with prior T-DXd therapy. The options we have to choose from are tucatinib with trastuzumab in combination with capecitabine. T-DM1 is still an option. Some investigators, some clinicians may give chemotherapy and trastuzumab. HER2-TKIs play a smaller role and are increasingly less and less being used. Of course, we're also hoping we have other HER2-targeted therapies. There is a significant unmet need for patients with HER2-positive breast cancer who have progressed on or after T-DXd. I can see that evorpacept has a possibly exciting role to play, and it has demonstrated activity in patients post trastuzumab deruxtecan in combination with other HER2-targeted agents. If you look at what we would hope to see in such a situation, our challenge is to bring in new agents that can overcome the resistance to T-DXd. The need for agents in the HER2-positive breast cancer space at this point is to find novel agents, ideally bring a different mechanistic approach to target HER2. We can see for evorpacept, it has a different mode of action by killing cells via enhanced ADCP versus the classic payload-based ADCs or other drugs we are currently using. The second thing we want to achieve is we want to have a drug that obviously has demonstrated activity post HER2-directed treatments after ADCs and after monoclonal antibodies. The elephant in the room here is always trastuzumab deruxtecan. Now, we've seen from the data in the gastric study, but also in some of the HER2 pretreated breast cancer studies, that evorpacept has shown activity post trastuzumab in gastric cancer and following up to four or more lines of patients with HER2-positive breast cancer who had prior HER2 treatment. We would like to have a treatment that can supplement and enhance the current standard of care rather than replace the backbone treatment. If you look at the way how evorpacept works, it is really designed to work synergistically alongside the key therapies and the key backbone, obviously, for HER2-targeted therapy is trastuzumab or similar antibodies. We are keen to have a drug that's safe and safe from the ADCs. We had to learn over the years that ADCs have quite substantial possible toxicity, which is obviously driven by the payload as it is ultimately targeted chemotherapy. The safety profile of evorpacept is very different to what we know and seems to be much more favorable compared to some of the ADCs. Finally, having immune therapy agents that can really drive what we see sometimes in HER2-positive breast cancer, this long tail as clinicians often go on about, that is what ultimately patients need to have a long-term benefit in survival. We feel that there is an immune component to that. We know already that there's a small percentage of patients who have very, very long survival on HER2-targeted therapy. Enhancing that immune effect by giving a CD47-targeted drug can possibly increase the tail for patients, at least that is at least my hope. If you look at CD47 as a selection strategy, and again, I think that is really important for this program, is that we're not going into this blindfolded. We actually have a very powerful biomarker. And as you have seen from the gastric data, it's a very clearly better signal for this concept in patients with high CD47 expression. Now, as you can see, there's a number of breast cancer studies that have looked into this. And I'm not going to go into each of those trials and the scoring methods in too much detail. The bottom line is about 1,000 patients. And they're relatively consistently showing a CD47 high expression rate of around 50%. Fifty-four percent is the average if you go through those trials. That is a substantial proportion of patients and actually allows us to drive that program forward without having a target group that is ultimately too small to select for clinical trials. There are a couple of preclinical data I think are really interesting. Preclinical data, you may say it is a little bit nerdy, but I think it is really helpful for us to understand the biology. If you look at this slide on the left side, you see the CD47 expression in HER2-positive breast cancer cells compared to HER2-negative cells. Green means low expression. Red means high expression. This black or blue color is moderate expression. It is very obvious to see that we have a higher percentage of CD47 expression in HER2-high DCs. If you move to the right side of the slide, again, probably even more important for what we're aiming for, is this compares the CD47 expression in primary disease on the right side and in recurrent disease, so pretreated disease, on the left side. Again, it's very obvious that we have more positivity, CD47 positivity in tumors and therefore in patients who have prior HER2 treatment and have recurrent HER2-positive breast cancer. This is exactly the target population we're aiming for. If you then look at emerging data and again, cell line-based data for cell lines that were treated with trastuzumab deruxtecan. As I said earlier, this is the new standard of care in the first-line setting. Our prediction for the future is all patients will have T-DXd pretreatment. We have to focus on patients who have resistance to T-DXd. As you can see here in orange, these are cells that have been T-DXd pretreated, in purple, DM1, and then in white is ultimately control. It shows the percentage or the number of CD47 positive cells. As you can see, very, I think, impressively, is that we have a markedly higher expression of CD47 within cell lines that were prior exposed to trastuzumab deruxtecan. That is the target group we're aiming for. The target population is very clearly a substantial population of patients with HER2-positive breast cancer. The population is probably even bigger in patients who have prior CD47 pretreatment. It also may be one of the ways these tumor cells evade the ADC treatment effect and therefore maybe have a really fantastic opportunity for us to target this clinically. Now, the clinical trial that is ongoing, the ASPEN trial you're very much aware of, is in my opinion, it serves one key focus. As a clinician, I've asked that question before. I'm keen to see this move forward into a phase III as quickly as possible because we know it works. We know what the target population is. We know there's a huge need post T-DXd. What we don't know exactly is how to do the statistics for a phase III trial by having the exact response rate, PFS, and other endpoints, which we obviously need to do to size up and design the phase III trial properly. This trial, therefore, is a non-randomized phase II trial in patients with HER2-positive metastatic breast cancer with measurable disease with prior treatment with trastuzumab, duruxicab, and are then offered treatment with evorpacept in combination with trastuzumab and patients of physician's choice chemotherapy. Very pragmatic design. This is the real world out there. What we want to learn from this trial is really how the response rates are in patients who are ctDNA positive for HER2, but also what the duration of response, PFS, overall survival is in patients with CD47 high, but also CD47 low tumors to get further confirmation from the biomarker data we have already obtained from gastric cancer, which ultimately allows us to fine-tune the phase III design going forward. Thanks, everyone. I would like to pass back to Barb, please. Thank you, Peter. Let me wrap up this section with a brief breakdown of the addressable patient numbers in the core markets. As you can see, there are roughly 48,000 breast cancer patients in the second-plus-line setting who are HER2 positive. Of that, we believe that at least 60-80% of these patients will retain HER2 positivity following prior therapy. Of that group, 50-70% will have high CD47 expression. As Peter highlighted, there are a number of publications to support that CD47 overexpression in HER2-positive breast cancer patients will be upregulated post in HER2 treatment. We believe that this represents approximately 20,000 addressable patients who are both HER2 positive and CD47 high. If you boil this down and use conventional estimates on pricing, you get to roughly a $2 billion-$4 billion market opportunity. Again, just in patients that are CD47 high and HER2 positive, representing a significant opportunity for evorpacept. On slide 31, I now want to provide a quick update on ALX-2004, our EGFR antibody-drug conjugate program. As shown on slide 32, our company's first ADC, the ALX-2004 molecule, was a result of rigorous internal drug design process. Our goal was to create a best and potentially first-in-class drug designed to maximize the therapeutic window and to overcome the historic toxicity challenges that others have encountered in targeting EGFR with an ADC. With ALX-2004, we have optimized all three components to do this, including the payload, the linker, and the antibody to create a truly novel molecule against a very well-validated target. ALX-2004 uses metuzumab-derived EGFR antibody selected to minimize skin toxicity and to maximize the therapeutic window. Its binding epitope is distinct from the U.S. FDA-approved EGFR antibodies such as cetuximab and panitumumab. Additionally, ALX-2004 has a proprietary linker payload and total one inhibitor payload engineered to offer improved linker stability for on-target delivery of payload and enhanced bystander effect. At the recently concluded Triple Meeting in Boston in October, we presented preclinical data highlighting these elements in greater detail. Moving to slide 33, here are the preclinical data highlights. Both in vitro and in vivo animal models support impressive dose-dependent activity and a differentiated safety profile. Importantly, non-human primary toxicology studies did not demonstrate EGFR-related skin toxicities at clinically relevant doses. There was no evidence of payload-related ILD in the animals. This overall profile supports our conviction that this molecule could potentially demonstrate efficacy with a manageable safety profile in patients. Slide 34 shows a snapshot of the efficacy data from our in vivo models. ALX-2004 showed regression and tumor suppression across a panel of xenograft models representing a broad spectrum of cancer types and EGFR expression levels. Notably, ALX-2004 was effective in models harboring KRAS, BRAF, and p53 mutations. ALX-2004 shows excellent tumor suppression activity at doses as low as 1 mg per kg, given either once or once weekly times three, leading to complete tumor eradication in several of the models. These results confirm the broad applicability of ALX-2004 in targeting EGFR-positive cancers. Slide 35 shows the key findings from our six-week repeat dose with six-week recovery period in the GLP non-human primate tox study. All findings were minimal to moderate and fully recoverable. Thus, these data support the design of the ALX-2004 study and the likely safety margin for clinical use. Slide 36 highlights our clinical development plan. We are targeting EGFR-expressing tumor types, namely lung, colon, head and neck, and esophageal squamous cell carcinoma in this dose escalation and dose expansion trial. We dosed our first patient in August, and we have completed our first dose cohort at 1 mg per kg without any DLT. We are currently dosing patients in our second dose cohort at 2 mg per kg. We are on track to provide initial safety data from the phase I-A portion of the study in the first half of 2026. Our goal in this phase I-A, phase I-B trial is to identify the dose that optimizes safety and activity in tumor types which we believe have the highest potential for success. These data will then set up the program well to advance into a future registration study. With that, I turn the call back over to Jason. Thanks, Barb. Thanks again to Dr. Schmid for sharing his perspectives on the program as a KOL in the field. Q3 was a strong quarter, both in terms of execution and new data. What we're most excited about now is driving a targeted IO breakthrough in a first-in-class drug with evo, as well as we are very encouraged by ALX-2004's fast start in the clinic and building momentum. In sum, our CD47 blocker has been successful where no other has, both in terms of its manageable toxicity profile as well as activity, as we've now demonstrated efficacy in a randomized study. We've identified an actionable and predictive biomarker for response to evo in our gastric cancer study. This further reinforces the benefit we have seen in terms of DOR, PFS, and OS. This biomarker is on mechanism. Going forward, we're developing a CD47 biomarker. Therefore, it is really of no surprise to see that CD47 overexpression shows such a strong impact on our data. What this allows us to use is CD47 to select for patients in both current and future trials with the goal of replicating the results we have seen here with gastric cancer and demonstrating the same significant and transformational benefit for patients in our HER2-positive breast study. Again, there are no approved therapies for patients overexpressing CD47 and no options in late development to address this known path of evasion. We remain focused on delivering for them. In 2004, there are also no approved EGFR-targeted ADCs. Although clearly a validated target, there remains a substantial unmet need for these patients as well. ALX-2004 is off to a very strong start in the clinic. We believe also has the potential to redefine standard of care across a range of EGFR-expressing cancers. With that, I'll open up the floor to Q&A. Again, thank you for the time this morning. Thank you. We will now be conducting a question-and-answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two 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. Again, that is star one if you would like to ask a question. Our first question will come from Li Watsek with Cantor Fitzgerald. Good morning, ALX team. This is Daniel Bronder on for Li. This is an exciting update. We're curious to hear your thoughts on how to correlate the CD47 positivity that you showed on slide 30 with the kind of CD47 expression cutoffs that you showed in the gastric data on slide 18. What would you say is CD47 high in this context? How should we think about the patient population that would be matching that in your trial? Thanks, Daniel. Appreciate the question. So 30, just thinking about what we saw in breast or what we've observed in the literature versus gastric, is that the question? Yeah, basically, yeah. Okay. Yeah. It's a great question. I think it's one we've looked into. I think what we're really fortunate to have is a strong scientific basis behind CD47. What we see is really promising concordance across the two indications. If you look at gastric, it was roughly 50-50 in terms of the CD47 high group. I think then if you turn to the benchmarks, and again, this is where the strength of the science comes in, we see we have five different publications looking at the question of CD47 and specifically HER2 positive cancer. Again, what we see is strong concordance there too. If you add those numbers up, it's roughly half again. Five different studies supporting that around 50% of the patients will be CD47 high. Interestingly, those different publications use different clones, different methodologies, etc. I think that's what gives us such conviction that this is translatable not only to breast, but frankly, a broad range of tumor types. If I may, can I ask a follow-up question? Yeah, sure. How should we think about your companion diagnostic development? Are you doing that yourself in-house? Are you using the same kind of evorpacept construct, or are you using an independent antibody? Can you shed any light on that? Yeah, sure. I mean, I'll take it at a high level and then maybe ask Barb to weigh in on the path to a CDX. We've done the testing with a partner for the gastric study, planned to do the same in breast. Of course, as this data builds, and I think as we continue to understand the right cutoff and how this translates, we'll pursue further work. Barb, do you want to add to that? I would just say that the assay is an IHC. It's a research-use assay that was applied to the gastric data. Our ongoing or our soon-to-be enrolling trial in breast cancer, the 80-patient single-arm trial, will use the same research-based assay. We are working already with partners to think about the operationalization of the process prior to the initiation of a phase III trial so that we will be ready for a companion diagnostic, but again, via a partner. Great. Thank you so much for your time and answering my questions. Great. Thanks, Daniel. Our next question comes from Roger Song with Jefferies. Great. Thanks for taking the question. A very interesting data. Thank you for sharing this. Maybe related to the efficacy in the CD47 high population, do you have any data in your breast cancer trials with Jazz and any new data you can maybe give some comments on the CD47 high versus low? In terms of historical breast cancer, do we have any evidence for the CD47 high population, the traditional or the standard of care is performing less than the CD47 low population? Have you done any retrospective study as well? Because I know the benchmark is using the SOPHIA or any other CD47 HER2 chemo combo, but that's in the broad HER2 positive, not the CD47 cutoff. Thank you. Yeah. No, those are both great, great questions, Roger. Number one, in terms of the high versus low comparisons and the zani study and frankly, broadly, I think those are great questions. This data and the way in which it's rippling through our development plan is relatively new, as you know, Roger. I think we're really excited about what we're seeing. It's incredibly strong in terms of CD47 high and gastric. There's no question it's driving the effect in that study. The natural question is, where else is this working? I think whether it's the study with Jazz or our work with Sanofi or the other studies we have going with anticancer antibodies, we're very keen to understand that. I'd say what we know is we're seeing a 56% overall response rate in patients post ENHERTU that have seen a whole lot of HER2-directed therapy. To your point around the margetuximab comparator, it's well north of what you'd expect. Actually, there was recent data at ESMO that supports, again, a relatively low response rate. There was a real-world study that was sub-20% in patients in terms of ORR post ENHERTU. To see 56%, it's very strong. I think your question on CD47 high versus low is one we're in the process of understanding. Your second question on just benchmarking the data and what we see, Barb had weighed out the comparator in HER2 and the DESTINY-Gastric04 study. Certainly, if we were to line up the rainbow studies, to the best of our knowledge, the control arm is performing at par with benchmarks across a number of different studies. To your question, which again is a good one, those benchmarks we think are the best they're going to be, right? Because we know CD47 high is a negative prognostic, and we know that those patients should do more poorly. To clear those benchmarks and compare well, and then also be armed with the knowledge that those patients probably, if we were to select from those studies, the CD47 high-only patients, they would do even worse. Certainly, I think builds our conviction. Yeah, makes sense. Thank you. Thanks, Roger. As a reminder, if you'd like to ask a question, please press star one. We'll go next to Sam Slutsky with LifeSci Capital. Hey, good morning, everyone. Thanks for taking my questions. Just on the interim next year of both the EGFR ADC and the breast cancer program with evorpacept, curious on how many patients you're hoping to have in each of those data sets and then just how you view a win as you think about safety on the EGFR side and then just the delta of efficacy on the evorpacept side. Yeah, both great questions. Thanks, Sam. I'll take 2004, and I'll ask Barb to weigh in on the breast front. I think 2004, as you know, targeting EGFR, one of the most well-validated trodden targets in oncology. There's just no question that EGFR is effective. I think it's led to a natural question from investors and partners. That's, can you target this target with an ADC when you have a payload involved? As a reminder, again, I think we're very encouraged by what we see in the primate work. That tends to translate very well. So far, so good, right? To clear one mg per kg quickly, I think, is a strong start at already a relatively high dose. Now on to the next cohort, which again, I think is moving fast, is what you want to see. As we go into the next year, early next year, in terms of what we'll share, I think it depends, right? Which is the reality of a dose escalation study. I think our goal is to answer the safety question as best we can in a phase I and then put up data that will answer that. Again, the study is marching very well here. I think we feel real confident that if this continues, of course, we'll be able to share something going into early next year. On the breast front, in terms of benchmarks, Barb, do you want to weigh in on that one? Yeah, I think, Sam, thank you. I think you were asking what might our expectations be both for number of patients as well as the bar. The bar I'll start with, there's a lot of data with trastuzumab and chemotherapy, which really is the backbone upon which we add evorpacept in our trial. Chemotherapy trastuzumab at best will have about a 20% response rate. Interestingly, there was new data coming out of ESMO looking at the post-ENHERTU setting, and response rates continue to drop, not unexpectedly. As we noted, our trial will enroll all patients post-ENHERTU, where we do anticipate that CD47 overexpression becomes part of the mechanism of resistance. We attack that directly, and we anticipate having good outcome data in our evorpacept trial. I think the benchmark is going to be in the range of 15% response rates. Again, 20% might be the upper bound, but with the combination of the two things, the poor prognostic effect of CD47, as well as the evolving standard of care and the fact that there really is not anything that has shown up well post and HER2 really bodes well for us. What do we expect in our bar? I think doubling that would be nice, 35%-40%. Certainly, in our gastric data that I showed you in the gastric setting, did even better. We anticipate that the opportunity is there to do quite well, but I think we would be very happy with a 35%-40% response rate in our breast trial. Okay. Thanks. Thanks, Sam. This now concludes our question and answer session. I would like to turn the floor back over to Jason Lettmann for closing comments. Great. Thanks, everybody. Really, really excited to share this data with you. Continued good progress across both evo and 2004. Real positive update today. Again, appreciate the engagement and support and look forward to future updates. Thanks so much. Ladies and gentlemen, thank you for your participation. This does conclude today's teleconference. You may disconnect your lines and have a wonderful day.