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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 2 here before we start our presentation of housekeeping here are our forward-looking statements for your review. So 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 data set that will be presented at SITC this weekend from a preplanned 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. So our goals for today are most importantly to share these detailed results with you as we believe this data set 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 ALX2004 EGFR-targeted ADC, which is now in the clinic. Today, we are also excited to be joined by Dr. Peter Schmidt 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 4. In the third quarter, we made significant advances in both evorpacept and ALX2004 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 our 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 compare very favorably with the large benchmark studies in second-line gastric cancer. Most importantly, these results support the potential to pursue 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. And 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. And 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. So we're excited to announce today that we are currently enrolling patients in the second dose cohort. We're 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 ALX2004 and evorpacept that we have coming next year. Now turning to Slide 5. 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. So 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. And what you can see here is a meta-analysis of 38 cohorts across 17 publications, which includes over 7,000 patients. And 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 6. 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 vivo. And 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. And 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. Now as you can see on Slide 7 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 and 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. And again, this is a second-line plus gastric population, which has historically been a very tough cancer to treat. So 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 2 years, which is more than triple the control. The median PFS was over 18 months in the evorpacept arm versus just 7 months in control with an impressive hazard ratio of 0.39. And then 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 data set 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 2 programs. First, driving evorpacept into ASPEN-Breast, which is our study investigating patients post in 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. ALX2004 also remains on track and continues to proceed very well. We dosed our first patient in August of 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 catalysts for ALX in 2026. And as you can see here on Slide 9, 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, ALX2004, 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. So 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 has broadly overexpressed on cancer cells as a means of abating 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 since 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 the 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 a 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. 90 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 IHC3+ staining in at least 10% of the tumor cells was present in 48% of these 90 patients. The expanded results of this preplanned 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 rate 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 avorpacept CRP arm versus 25% in the control arm. And in the subgroup by CD47 expression level, evvorpacept 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 avorpacept arm in both the CD47 and CD47 -- in 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 3x 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 are 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 7 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 look 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. And 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 ENHERTU 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 Ib/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 6 prior lines of therapy. In 9 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 MARI2'etuximab. Moving to Slide 21. We've now demonstrated in these 2 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 us 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 derisked by the 2 positive data sets in 2 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 2 examples of trials with immunotherapy agents he is a global lead investigator on the pembrolizumab KEYNOTE-522 study and the atezolizumab IMpassion130 study. With that, I turn this over to you, Peter.

Thank you, Bob. The treatment options for patients with metastatic HER2-positive breast cancer are currently undergoing. I would also say, a dramatic change. We obviously have seen a very active drug moving initially into second and third line treatment with trastuzumab deruxticam, but everyone is aware of the data that now placing T-DXd increasingly in the first-line setting. And 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. But the challenge that comes out of this is there is no standard of care for patients who have been treated with trastuzumab, the sequence we had previously that patients would get a treatment called TPH, first line with trastuzumab, pertuzumab and second-line T-DXd and then third line other options has just been turned upside down. So at the moment, there's 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. So the options we have to choose from is tucatinib trastuzumab in combination with capecitabine. PD-1 is still an option. Some investigators and clinicians may give chemotherapy and trastuzumab HER2 TKIs play a smaller role and increasingly are less and less being used. But of course, we're also hoping to have other HER2-targeted therapies. So there is a significant unmet need for patients with HER2-positive breast cancer who have progressed on or after T-DXd. And I can see that well percept has a possibly exciting role to play that has demonstrated activity in patients post trastuzumab deruxtecan in combination with other HER2-targeted agents. Now 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. And we can see for evorpacept that 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 treatment after ADCs and after monoclonal antibodies. And at the out of 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 4 more lines of patients with HER2 breast cancer with 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. And again, 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 safer than ADCs. We have to learn over the years ADCs have quite substantial possible toxicity, which is obviously driven by the payload as it is ultimately targeted chemotherapy. And 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 immunotherapy agents that can really drive what we see sometimes in HER2-positive breast cancer, this long tail we as clinicians often go on about that is what ultimately patients need to have a long-term benefit in survival. And we feel that there's an immune component to that. We know already that there's a small percentage of patients who have very, very long survival on HER2 target therapy. But enhancing that immune effect by giving a CD47 targeted drug can possibly increase the tail for patients, 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%. So 54% is the average if you go through those trials. And that's 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. Now a couple of preclinical data, I think, are really interesting. Now preclinical data, you may say it's a little bit nerdy, but I think it's really helpful for us to understand the biology. So 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. And it's very obvious to see that we have a higher percentage of CD47 expression in HER2 high disease. If you move to the right side of the slide, again, probably even more important for what we're aiming for is this is -- this compares the CD47 expression in primary disease on the right side and in recurrent disease, of pretreated disease on the left side. And 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 scans. And this is exactly the target population we are aiming for. If you then look at emerging data and again, cell line-based data for cell lines that were treated with trastuzumab deruxtecan. And as I said earlier, this is the new standard of care in the first-line setting. So our prediction for the future is all patients will have T-DXd pretreatment. And we have to focus on patients who have persistent 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 controlled. And it shows the percentage or the number of CD47 positive cells. And as you can see very, I think, impressively is that we have a markedly higher expression of CD47 in cell lines that were prior exposed to trastuzumab deruxtecan, and that is the target group we are aiming for. So 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. But it also may be one of the ways these tumor cells evade the ADC treatment effect and therefore, may be 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, serves one key focus. So as a clinician, I have 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, and we know there's a huge need post T-DXd. But what we don't know exactly is how to do the statistics for a Phase III trial by having the exact response rate at PFS and other endpoints, which we obviously need to do to size up and design the Phase III trial properly. So this trial, therefore, is a nonrandomized Phase II trial in patients with HER2-positive metastatic breast cancer with measurable disease with prior treatment with trastuzumab deruxtecan 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. But what we want to learn from this trial is really how -- what the response rates are in patients who are ctDNA positive for IL-2, but also what the duration of PFS overall survival is and 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. Well, 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% to 80% of these patients will retain HER2 positivity following prior therapy. Of that group, 50% to 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 ENHERTU 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, we get to roughly a $2 billion to $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 ALX2004, our EGFR antibody drug conjugate program. As shown on Slide 32, our company's first ADC, the ALX2004 molecule was a result of rigorous internal drug design process. Our goal is 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 ALX2004, we have optimized all 3 components to do this, including the payload, the linker antibody to create a truly novel molecule against a very well-validated target. ALX2004 uses matuzumab-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 TPO 1 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, nonhuman primate toxicology studies did not demonstrate EGFR-related skin toxicities at clinically relevant doses, and 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. ALX2004 showed regression and tumor suppression across a panel of xenograft models, representing a broad spectrum of cancer types and EGFR expression levels. Notably, ALX2004 was effective in models harboring KRAS, BRAS and p53 mutations. ALX2004 shows excellent tumor suppression activity at doses as low as 1 milligram per kilogram given either once or once weekly times 3, leading to complete tumor eradication in several of the models. These results confirm the broad applicability of ALX2004 in targeting EGFR-positive cancers. Slide 35 shows the key findings from our 6-week repeat dose with 6-week recovery period in the GLP nonhuman primate tox study. All findings were minimal to moderate and fully recoverable. Thus, these data support the design of the ALX2004 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 milligram per kilogram without any DLT. We are currently dosing patients in our second dose cohort at 2 milligrams per kilogram. We are on track to provide initial safety data from the Phase Ia portion of the study in the first half of 2026. Our goal in this Phase Ia, Phase Ib 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, and thanks again to Dr. Schmidt for sharing his perspectives on the program as a KOL in the field. Again, Q3 was a strong quarter, both in terms of execution and new data. What we're most excited about now is driving a targeted IL breakthrough in a first-in-class drug with evo as well as are very encouraged by AOX2004'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, and 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. And again, this biomarker is on mechanism. Going forward, we're developing a CD47 biomarker, and therefore, it is really of no surprise to see that CD47 overexpression shows such a strong impact on our data. So 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. So we remain focused on delivering for them. In 2004, there are also no approved EGFR-targeted ADCs. And although clearly a validated target, there remains a substantial unmet need for these patients as well. ALX2004 is off to a very strong start in the clinic, and we believe also has the potential to redefine standard of care across a range of EGFR-expressing cancers. So with that, I'll open up the floor to Q&A. Again, thank you for the time this morning.[ id="-1" name="Operator" /> [Operator Instructions] And our first question will come from Lee Watsek with Cantor Fitzgerald.

This is Daniel Bronder on for Lee. This is an exciting update, and 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? And 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?

Yes, basically, yes.

Okay. Yes. Well, yes, it's a great question. I think it's one we've looked into. I think what's really -- what we're really fortunate to have is a strong scientific basis behind CD47. And so what we see is really promising concordance across the 2 indications. So if you look at gastric, it was roughly 50-50 in terms of the CD47 high group. And I think then if you turn to the benchmarks, and again, this is where the strength of the science comes in, it's -- we see we have 5 different publications looking at the question of CD47 in specifically HER2-positive cancer. And again, what we see is strong concordance there, too. And if you add those numbers up, it's roughly half again. So 5 different studies supporting that around 50% of the patients will be CD47 high. And interestingly, those different publications use different clones, different methodologies, et cetera. And so yes, 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.

And if I may, can I ask a follow-up question?

Yes, 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?

Yes, 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, plan to do the same in breast. And then, 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. But 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. And then 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. [ id="-1" name="Operator" /> And our next question comes from Roger Song with Jefferies.

Very interesting data. 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? And then 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 HER2 chemo combo, but that's in the broad HER2 positive, not the CD47 cutoff.

Yes. No, that's -- those are both great questions, Roger. So number one, in terms of the high versus low comparisons in the zani study and frankly, broadly, I think those are great questions. So this data and the way in which it's rippling through our development plan is relatively new, as you know, Roger. So I think we're really excited about what we're seeing. It's incredibly strong in terms of CD47 high in gastric. There's no question it's driving the effect in that study. And so the natural question is where else is this working? And 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. So 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. And to your point around the margetuximab comparator, it's well north of what you'd expect. And 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. So to see 56% is very strong. And I think your question on CD47 high versus low is one we're in the process of understanding. And then your second question on just benchmarking the data and what we see Barb had laid out the comparator with ENHERTU in 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. And 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. And so 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. [ id="-1" name="Operator" /> [Operator Instructions] And we'll go next to Sam Slutsky with LifeSci Capital.

Just on the interims next year, 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 delta efficacy on the evorpacept side?

Yes, 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 Trode targets in oncology, there's just no question that EGFR is effective. So I think it's led to a natural question from investors and partners, and that's can you target this target with an ADC when you have a payload involved. And as a reminder, again, I think we're very encouraged by what we see in the primate work. That tends to translate very well. And so far, so good, right, to clear 1 mg per kg quickly, I think, is a strong start at already a relatively high dose and now on to the next cohort, which, again, I think is moving fast is what you want to see. So as we go into the next year, early next year in terms of what we'll share, I think it's 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. And again, the study is marching very well here. And I think we feel real confident that if this continues, of course, we'll be able to share something going into early next year. And then on the breast front, in terms of benchmarks, Barb, do you want to weigh in on that one?

Yes. 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. And 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. So 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 2 things, the poor prognostic effect of CD47 as well as the evolving standard of care and the fact that there really isn't anything that has shown up well post ENHERTU really bodes well for us. What do we expect in our bar? I think doubling that would be nice, 35% to 40%. We certainly in our gastric data that I showed you in the gastric setting did even better, and we anticipate that the opportunity is there to do quite well, but I think we would be very happy with a 35% to 40% response rate in our breast trial. [ id="-1" name="Operator" /> And this now concludes our question-and-answer session. I would like to turn the floor back over to Jason Lettmann for closing comments.