Greetings, and welcome to the ALX Oncology Q4 2025 financial results call and webcast. At this time, all participants are in a listen-only mode. A Q&A session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. 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, welcome to our Q4 and fiscal year 2025 results call. 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 FLS slide in our corporate deck. With me today, we have Harish Shantharam, our Chief Financial Officer, as well as our Chief Medical Officer, Dr. Barbara Klencke. In terms of the first bit of news, we're delighted to announce today that Barb will continue leading our clinical efforts as our permanent Chief Medical Officer. Welcome, Barb. As many of you know, after joining in an interim capacity in September 2025, Barb has been absolutely instrumental in driving our development programs forward over the last five months. Barb, as many of you also know, is an incredibly experienced oncologist and drug developer, having served as Chief Medical Officer at Sierra Oncology and having senior roles at both Onyx and Genentech before that. We're beyond fortunate to add Barb during this critical inflection for the company and thrilled to welcome her permanently, and I'll 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. At the end, plan to open it up for any questions you may have. In general, our focus at ALX remains on execution. We have made great progress on both of our programs, Evorpacept and ALX2004 in 2025, and positioned ourselves to achieve significant catalysts from these programs in the coming 12-18 months. Our goal and vision for each is to advance both programs to a stage where they're ready for pivotal studies by end of next year. Execution has been strong over the last quarter, and I'm very pleased to report that our clinical development progress and timelines remain on track. In terms of Evorpacept or EVO, in 2025, we're coming off a year of massive amounts of data, really demonstrating the potential for Evorpacept across a variety of combos and tumor types, which well-informed our development strategy for EVO today. We've 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 evorpacept 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 state 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 I evorpacept and zanidatamab 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 and HER2 setting were largely restricted to CD47 overexpressers, 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 II ASPEN-09-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 activations 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. Given the broad overexpression of CD47 in both solid tumors and heme malignancies, it gives us a real opportunity to pursue focused development strategy for EVO in combination with anticancer antibodies and bispecifics. We're excited about our study in breast. We're also excited about the NHL data, which we recently shared in December, which furthers the findings of EVO in the heme malignancies. We are also ongoing partnering with Sanofi, and we are excited about what we're seeing across both of those studies, and Barb will go into both in more detail. In terms of ALX2004, turning to our ADC now, we are also very pleased with the clinical progress of ALX2004, 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 per kg dose now in the phase I trial. We are now expecting full ALX2004 safety data from the dose escalation cohort later this year in second half 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 million, 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 Barb to walk through some of the clinical data and findings and plans in more depth. Barb? Thank you, Jason. Well, let me start with some quick highlights of the strong results that we have seen with evorpacept in two HER2-positive breast cancer indications that we have reported on within the past three months. I'm referring now to slides 14-18 in our corporate deck. In the randomized phase II HER2-positive gastric cancer study, we saw impressive response rates with evorpacept when combined with a trastuzumab-based regimen in the subset of patients with HER2-positive overexpressing CD47 tumors. We've reported this data at the SITC conference in November of 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 3 x longer than that seen in the control arm. The median PFS was 18.4 months in the evorpacept arm and seven months in the control arm, with a hazard ratio of 0.39. Finally, the median overall survival was 17 months with evorpacept versus 10 months approximately 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 I/II study of evorpacept in combination with zanidatamab. 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 ENHERTU. We first reported data from this study at the San Antonio Breast Cancer Symposium back in December of 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 evorpacept plus zanidatamab 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 SOPHIA 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 had a median of six prior lines of therapy. Recently, in January of this year, we concluded the CD47 biomarker analysis from these patients. We recently announced that the responders were predominantly restricted to the patients who overexpress CD47. Full biomarker analyses from this trial will be presented at the ESMO Breast Cancer Conference in Q2 of 2026. The data from these two independent studies show the potential of evorpacept to drive very substantial benefit for patients with high CD47 expression. These extraordinary outcomes clearly validate evorpacept's mechanism of action and provide increased confidence for our ongoing phase II breast cancer. Before I provide an update on our ongoing phase II 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 the treatment-naive first-line indolent lymphoma setting. These patients received evorpacept 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 evorpacept 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 in relevant benchmark studies, as you can see on the slide. Together, these five data sets strongly support the potential of evorpacept to enhance macrophage-driven ADCP when combined with an Fc active anticancer antibody. These data give us high confidence for our ongoing evorpacept 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 evorpacept in combination with trastuzumab and single-agent chemotherapy in a single-arm design, enrolling HER2-positive metastatic breast cancer patients who have progressed on ENHERTU. Following the strong validation of CD47 as a predictive biomarker of benefit with evorpacept plus zanidatamab, we've now decided to enlarge the current phase II study to up to 120 patients from 80, to increase the number of HER2-positive patients with CD47 overexpression. We are updating the primary endpoint to a response rate endpoint 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. ENHERTU has now been approved as first-line therapy, the treatment landscape for the second-line and subsequent therapies has really 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 ENHERTU therapy. 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-ENHERTU setting. Based on the activity that I've described to you for the evorpacept across a number of settings when combined with an anticancer antibody, we believe that evorpacept 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've initiated work on developing a companion diagnostic for CD47 expression. With respect to enrollment in the ongoing phase II trial, we're making good progress. While we're still early in the enrollment curve, the site activations remain globally on track. We're pleased to see that investigator interest in the study remains strong, and 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, ALX2004, 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've leveraged historic learnings to develop ALX2004, our EGFR-targeted ADC, which was designed by our internal team of world-class protein engineer experts. The preclinical data set 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 non-human primates. The antibody, matuzumab, has a unique affinity-tuned epitope whose binding to EGFR is not affected by mutations in the binding domain for these, for the other approved EGFR antibodies. In creating this ADC, we combined this antibody, the matuzumab 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 ALX2004 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- 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're currently enrolling patients in our third dose cohort, having initiated dosing initially at a robust dose of 1 mg per kg, then escalating to 2 mg per kg, and subsequently to 4 mg per kg, based on seeing no DLTs at the prior dose levels. We believe that the 4 mg per kg dose, our current dose level, could potentially now be at the lower end of the therapeutic dose range. As a reminder, we're 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 I trial, we'll 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 now provide data from the dose escalation portion of the ongoing phase I study in the second half of this year. With that, let me hand this over to Harish. Thank you, Barb, and good morning, everyone. 2025 was a year of strategic prioritization and clinical validation for ALX, highlighted by the progress we made on our lead program, evorpacept, and the clinical entry of our first ADC, ALX2004. In terms of financials, we finished the fourth quarter of 2025 with cash equivalents and investments totaling $48.3 million before strengthening the balance sheet from our equity financing we closed earlier this month in February. The net proceeds from the offering were $140.4 million 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 operating expenses through the first half of 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: one. the full biomarker analysis readout from our phase I/II trial, evaluating evorpacept in combination with panitumumab in advanced HER2-positive breast cancer patients will be presented at the ESMO Breast Cancer in May of 2026. Two. the ALX2004 safety data from the dose escalation phase of the trial is anticipated in the second half of 2026. Three. the readout on evorpacept top-line data from 80 patients from the ongoing phase II ASPEN-09-Breast trial is anticipated middle of 2027. With respect to the latest quarterly financials, the GAAP net loss was $22.8 million for the three months ended December 31, 2025, or $0.42 per basic undiluted share, as compared to a GAAP net loss of $29.2 million for the three months ended December 31, 2024, or $0.55 per basic and diluted share. The decrease in year-over-year spend can be primarily attributed to lower co- 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 II trial in breast cancer for evorpacept and the phase I trial for ALX2004. Moving forward, the clinical spend will be largely driven by these two trials, partially offset by reduced spend in evorpacept legacy trials that are winding down. With that, let me hand the call back to Jason. Jason? Thanks, Harish. As we discussed, we're coming off a very strong 2025, where we had a incredible amount of data with evorpacept really demonstrating our path forward. We're also very pleased with the progress on ALX2004. We continue to advance through dose escalation and are looking forward to significant catalysts across both programs over the next 12-18 months. Our focus internally remains on execution, and that's what we will plan to do going forward. Again, very happy to remain on track in terms of the execution across both studies. With that, I will now open the floor to any questions. Thanks again for your time this morning. Thank you. If you'd 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'd 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 Bratzel with Piper Sandler. Please proceed with your question. Hi. Good morning, guys. Thanks for all the updates, and thanks for taking the questions. Just some follow-ups from me on evo. I think initially we were expecting an interim look at ASPEN-09-Breast this year, but it does sound like that's off the table in favor of the 80-patient readout next year. Could you just confirm, you know, is that correct? Barb, I know you covered this in the prepared remarks, but just hoping you could talk some more to the rationale behind, you know, the upsizing to 120 patients, the change in the primary endpoint, and just, you know, talk to how that informs on the regulatory strategy. Maybe just secondarily, you know, what kind of feedback are you getting from investigators on the biomarker approach? Just, you know, what do you expect to see on enrollment trends in ASPEN-09-Breast? Thank you. Great. Thanks, Ali. I appreciate the question. I'll let Barb take the second question. I think on the first question, that's correct. We're guiding towards 80 patients, full data from those 80 patients in mid next year. I think, yeah, from our perspective, our goal internally and externally as well, is to communicate full, robust data. I think, you know, at that point, we should have, you know, I think, 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's essentially all comers, so guiding to the 80, we think, makes the most sense because we are confident at that point we'll have real fulsome data, you know, across both the CD47 high population as well as the other buckets that we'll be looking at as well. That's the plan. It's an open-label study. We have an opportunity to share earlier if we think it makes sense, as well as talk to regulators earlier. The current plan is mid-2027. On your second question, Barb, do you wanna take that? Yeah. Hi, Ali. Yes, addressing the interim, Jason just did that. Upsizing, again, Jason hinted at that really just wanting to ensure really robust numbers of patients in various segments, various subpopulations. We'll have patients who can be confirmed HER2 positive in this setting by ctDNA or not. We'll have patients whose tissue has evidence of overexpression of CD47 or not, and we just wanna make sure that we have robust numbers. I think the most important thing for this study, 'cause I really am coming into this study with a lot of confidence that this is gonna work, but what we really want to know is what is 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. I think we just wanted to make sure that we had enough patients who are CD47 overexpressing that we can do that. In terms of the primary endpoint, it's always been a response rate endpoint trial. I think in the two studies that we talk about, the gastric and the zanidatamab combination, it's really been pretty remarkable just how powerful CD47 is as a predictive biomarker. I've just moved that up to the primary endpoint. Response by HER2 status will still be an important key secondary endpoint. Just really feeling like the CD47 is going to be the most powerful predictor of response. That's the justification for changing the primary endpoint. You asked about the investigators' perception of the study with a biomarker selection strategy. I think they're very excited about it. To have the ability to find a population for whom the therapy is going to really provide substantial benefit, and what we've seen in all of our prior studies that I talked about today, lymphoma, gastric, breast cancer, we're seeing these remarkable response rates, and we're also seeing durability, that's really both the two endpoints together are really providing transformational benefit. The ability to find a selected patient population where the treatment outcome can be so robust, I think is very exciting to investigators. Finally, you asked about the enrollment trends. Well, it's early. You know, we had our first patient in in January, so site activation is going extremely well. We're still early on the enrollment curve, but I anticipate with the amount of enthusiasm that we're hearing from investigators, I just got an email this morning from one who was thrilled to have, their site opening up. Yeah, we're excited about this study, as are the investigators. More to come later when we actually get to the point of releasing specific information. Super helpful. Thank you. Thank you. Our next question comes from the line of Li Watsek with Cantor Fitzgerald. Please proceed with your question. Good morning. This is Daniel Braun for Li Watsek. In addition to the update on the ASPEN-09-Breast study, it also looks like you've moderately pushed out the safety data for ALX2004. Can you give us some color on the underlying reasons for that, please? Thank you. Sure. Happy to. Thanks, Daniel. I think, you know, as Barb mentioned, and we highlighted in our comments, both studies remain on track, and the execution has been strong. I think the change post-financing here has just been to ensure that we're communicating robust data. You know, I think if you look at what we'd have this quarter, next quarter versus towards the end of the year in ALX2004, you know, it's really a step change in data we should have towards the end of the year, really fulsome data from the dose escalation phase. I do think that will allow us to be, you know, much more clear about what we're seeing. Ideally, you know, we'll be able to communicate where we think the expected dose or two doses will shake out and, you know, allow us to communicate that externally. Really the goal is to, when we provide updates, to make them meaningful and full, and I think that's, you know, that's the thinking behind, you know, that guidance. if I may follow up on this, is it safe to expect, you know, up to four dose levels to be to have been tested at the point when you make the disclosure? Yeah, I think that's reasonable. As you know, Daniel, we've went from 1 mg per kg to 2 mg per kg to 4 mg per kg, so we've doubled now twice. You know, we do think we're at the low end of the therapeutic window as is and continue to progress that study very well. I do think, you know, the fact that we've cleared 1 and 2 so rapidly without seeing DLTs is encouraging. Certainly now into 4, 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, congrats on the update. Yep, thank you. Thank you. Our next question comes from the line of Sam Slutsky with LifeSci Capital. Please proceed with your question. Hey, good morning, everyone. Appreciate the questions. I guess two for me. One is that for the AD patients in ASPEN-09, remind me what's the expected ratio of those with CD47 high versus low expression? On ALX2004, just on 4 mg per kg being at the lower end of the therapeutic dose range, I know looking at some of the other kind of EGFR ADCs that are using TOPO1, it seems like they're at either 4.8 mg per kg, Q3W or less in terms of dose. Curious on what's driving this difference in where the therapeutic range starts with your drug, or is it that you would just consider it that you have a wider therapeutic window, which hopefully leads to better efficacy versus others? Sure. Thanks, Sam. I'll take the first one and Barb can handle the second one on the range. In terms of the percentages, you know, what's nice about CD47 is it's 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, you know, that range to be roughly 40% up to around 57% of the population. 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. The literature would support that. I think it's important to run the study, of course, and see how that shakes out, but we're expecting to see a significant number of this population be CD47 overexpressers. Barb, do you want to take the question on therapeutic range with ALX2004? Exactly. Yeah. The highest non-severely toxic dose in primates was 20 mg per kg, which equivalent, well, it's potentially around 6.5 mg per kg in patients. You know, there's 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'll be data-driven. We'll start... There's, we're not, I would never think that we would double again. We're now in a range where smaller incremental increases will be pursued. We'll just have to see how things go in terms of the tolerability and toxicity that we see in patients. We do think somewhere in the range of, in the 4, 5, 6 mg, maybe a bit higher, because as you know, the non-human primate data, there really wasn't any severe toxicity. Maybe we can go just a little bit above the 6 mg per kg-7 mg per kg range, but we'll see. We'll provide further updates later in the year. That's 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 & Co. Please proceed with your question. Thank you. Good morning, Jason and Barb. A couple of questions on ASPEN-09 and one on ALX2004. On ASPEN-09, you know, as you're expanding the trial to 120 patients, I'm just trying to understand a little bit of logic behind it. Can you discuss, you know, what's the prevalence of CD47 high in post and HER2 patients, especially if you're defining 47 high as IHC 3 positive greater than 10%? You know, this expansion driven more by statistical power or, you know, you're concerned about lower than expected prevalence of the biomarkers? Sorry, that's a long question one. On the second one is when we start thinking about, you know, physicians' choice of chemotherapy, should we be concerned about, you know, subsequent ADC use in this post trastuzumab patients, that it can impact the CD47 expression? On ALX2004, you know, when the, with the safety data expected in the second half, how are you monitoring the interstitial lung disease and the skin tox? Sure. Those are great questions. Thanks, RK. On the ASPEN-09, in terms of CD47 expression post ENHERTU, you know, we think that the% should hold that I mentioned before. Roughly half of the population should, you know, be CD47 high. We did highlight in the past on our calls, a study, a recent study from last year that showed that, you know, patients who are exposed to ENHERTU overexpress CD47. We do think it's certainly possible that those numbers are higher in this population. We know that CD47 is a key mode of evasion post ENHERTU, we do think that is possible. Barb, do you want to take the next one on the various chemo options and how that may impact things? Well, what we know in terms of CD47 expression, it there is data in the literature that it rises after patients post ENHERTU. We don't have a lot of other data. Most of the data on CD47 comes from archival tissue from the time of diagnosis. The literature does support higher rates of overexpression post ENHERTU, which is absolutely perfect as our patient population. It's where there's an unmet need, and it's clearly the clinical setting that's the most wide open at this point in time. Personally, I'm not sure that I have any concern that different chemotherapy drugs will perform differently in patients who have CD47 expression when they're combined with trastuzumab. Our main focus on the mechanism of action is the combination of trastuzumab or some such antibody with an active Fc plus evorpacept. We certainly will look at the five different chemotherapy options across the different subsets to see if there's any major differences, but I'm not expecting to see really any much variability there. In terms of ALX 2004, you asked about how we might be monitoring for both ILD and skin toxicity. Patients do go through CT scans on a regular basis as per protocol. A lot of times that's 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're all very cautionary, meaning it's 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 non-human primate toxicology studies. We will monitor for it, but have a we have a low likelihood based on our NHP work. In terms of skin toxicity, certainly matuzumab was the antibody that we selected for, just for the lower skin tox that's been shown clinically in the early investigational use of that matuzumab antibody. That's obviously something that every time a patient is seen in clinic, they'll be examined and can report that. That'll be an early thing that we could pick up once we get into the various dose ranges. What else can I say about skin toxicity? Our prediction is that we're 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 matuzumab's safety profile, that gives us a wider therapeutic window. We don't, we don't expect to be too limited by skin toxicity. 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, than, based on the, you know, protein design that we have, with this agent. Thank you. Thank you both. To your last question, RK, just on the sample size. There was no change- Yeah. ... in the assumptions in terms of the percentages or efficacy. you know, there's been- Okay. no change there. I, the driver is really just to ensure that we have a very robust phase II and in a position to de-risk the phase III as much as possible. You know, the ability to flex up to 120 allows us to do that. Of course, as we mentioned, you know, it's an open- label study. If we see data that's, you know, even in the ballpark of the, you know, 56% we saw and the 60% we saw in the breast and gastric studies respectively, I think we'll have plenty of room to clear the hurdle. Again, I think the goal of this is to inform the phase III. Once we see a sufficient signal, that'll then, you know, I think, spur into action conversations with the regulators and moving quickly to a phase III. Yeah. Fantastic. No, thank you. Thank you very much. Thanks to both of you for answering in detail. Thanks. Thank you. Our next question comes from the line of Roger Song with Jefferies. Please proceed with your question. Hey, good morning, team. Thanks for taking our questions, and congrats on the updates. This is Nabil on for Roger. Question on the CD47 cut point. Maybe this was asked, but wanted to ask again, is that IHC cutoff for ASPEN-09 primary endpoint already locked in? Or could you maybe talk about those pre-specified decision rules we're using to select that cut point? Then on just the IHC evaluability, how do you guys handle, like, borderline cases with maybe, like, some insufficient tissue? Is that ever a thing that comes up? Thank you. Yeah, sure. Thanks, Nabil. The, the question on CD47 expression, I'd say what we know is that we would anticipate it to be different across different tumor types. We know gastric, you know, is as a baseline tissue type, expresses CD47 more highly than breast. Just as that is the backdrop, we expect it to be different. Again, encouraging with gastric was that it effectively didn't matter, meaning we could pick IHC 3, IHC 2/3 and continue to see a good response. I'd say the evo plus Zani study in breast informs that. I think we do have a, what I'd call a good estimate of how it could look. I think going forward, it'll be critical for us to run this study to really understand exactly where to set the cutoff. That's part of the goals of this current study that we're in the midst of, and I think that'll be informative. In terms of the missing tissue or different tissue types, we don't anticipate that to be a significant issue just because we're using, you know, tissue at time of diagnosis to base CD47. We expect CD47 to be relatively stable, and I think that should be pretty straightforward. Anything else to add on that, Barb, in terms of- No, I think it's- ... getting the tissue and how we... Yeah. Yeah. Everybody will be required to submit tissue. I think there is always an estimate in most trials that you might have some missing data. I wouldn't expect it to be unusual, so 10% or less. We anticipate being able to have measurable CD47 in nearly all patients, and it could be, it could be 100%, but I wouldn't be surprised if we ended up with a rare patient for whom the tissue just wasn't sufficient. That shouldn't be a problem. IHC is a very standard assay methodology, so easy to perform, et cetera. No major, no major risks there. Thank you. Ladies and gentlemen, that concludes our Q&A session. I'll turn the floor back to Mr. Lettmann for any final comments. Great. Thanks, everybody. Appreciate the good engagement and questions this morning. Again, exciting time at ALX. Here, a lot in front of us and continue to execute well. Looking forward to the next quarter here and the next year, where we have, you know, a lot of important milestones here to lay out. Appreciate all the interest and support. Thank you. Thank you. This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation.