Good day, and thank you for standing by. Welcome to the ALX Oncology's ASPEN-07 update to discuss evorpacept plus enfortumab in patients with advanced bladder cancer. At this time, all participants are in a listen-only mode. Please be advised that today's conference is being recorded. After the speaker's presentation, there will be a question-and-answer session. To ask a question, please press star 1-1 on your telephone and wait for your name to be announced. To withdraw your question, please press star 1-1 again. I would like to hand the conference over to your speaker today, Jason Lettmann, CEO. Great. Thanks for the intro, and thanks, everyone, for joining today. Thrilled to have a good group on the call and discuss our most recent results with evorpacept plus PADCEV in advanced bladder cancer here. So if you go to the first slide, just as a reminder, before we begin, I'd just like to remind everybody that today's presentation will include forward-looking statements based on our current expectations and beliefs. Such statements represent our judgment as of today and involve substantial risks and uncertainties that may cause actual results to differ materially from the results discussed in the forward-looking statements. So with that, on the agenda slide, we are going to kick it off here, just introducing what we're up to. I think many of you are aware of our program, evorpacept, and specifically what we're pursuing on the ADC front. With that, I'll hand it over to Sophia Randolph, our CMO, to walk through the mechanism as well as the scientific basis for the combination. And then, thrilled to have Dr. Sam Funt join us as well, who's been heavily involved as an investigator in the study, a KOL in the space, and will share his view of both the treatment paradigm as well as our data. And then we'll wrap it up and take questions. So if you go to the next slide here, slide four, this is just a reminder of who we are. Again, ALX is the CD47 leader developing evorpacept, which is both best in class and first in class now. We've treated over 500 patients to date, and we believe that our program is highly differentiated, and that's what's led to what we're seeing in the clinic, certainly on the safety front, but as we see a building cadence of efficacy, very excited about the profile across both solid and heme malignancies. Coming off the backs of the first randomized data here in the fall, which was our ASPEN-06 study in gastric, it was the first study to read out in CD47 in solid tumors, and we're very excited about that data. And of course, looking forward to full data coming here next month. We have nine clinical studies ongoing across various indications, both heme and solid, and again, really testing this concept across 3 major modalities: antibodies, checkpoint inhibitors, and ADCs, where we'll focus today. I mentioned some of the milestones that are upcoming. We're in the middle of a very exciting time for the company with several catalysts. We're coming off of AACR, where we had the NHL data ASCO last weekend with this bladder data. We have the full gastric data coming in July. And then certainly not last but not least would be ASPEN-03 and ASPEN-04 with over 300 patients randomized and head and neck towards the end of the year, Q1. So if you go to the next slide, again, this just highlights the development plan. I mentioned the gastric data that is now in phase two, and we're going to share that full data in July. The bladder data is where we'll focus today. We're also excited about the story in breast, both in what we're doing with Jazz, with zanidatamab, as well as with ENHERTU. With this story building within ADCs, I think the ENHERTU data is certainly of interest, and we're looking forward to sharing that and targeting Q4. And then last, we have the head and neck studies, which I mentioned. So on slide six, just a reminder of what we're targeting. We are targeting CD47, which is the don't-eat-me signal. It is the ultimate marker of self in a way in which cancer has been able to hijack that signal and essentially evade detection. Since the company's founding and to today, we are the only company with an inactive Fc. This is an important differentiator in that we block the don't-eat-me signal, but we do not target it the old-fashioned way, if you will. We use either an antibody or an ADC to provide that positive signal. And by bifurcating the signal is how we are able to more effectively target cancer. So if you go to slide seven, and again, this will be a reminder for many of you, but this is how we're differentiated. On the left are some of the key attributes and the molecular design of evorpacept. We have a very potent CD47 binder, again, with a dead Fc. We have a low molecular weight, which we feel helps on the solid tumor front, like we'll discuss today, and our PK is like an antibody. All of these things working together is what leads to very potent CD47 blockade. It also leads to less of a sink effect. We've been able to dose at levels far greater than the competition with an active Fc, which has, I think, led to this differentiated efficacy. And again, we have greater solid tumor penetration, and we've been able to dose alongside the backbone regimen, which is a key advantage as well. So that's really what's led to this story here. And I think with all the clinical data supporting this, it's been exciting. So slide eight is our vision for the molecule, again, both first and best in class, universal combination agent across these three classes: antibodies, ADCs, and checkpoints. In the middle, you can see the nine combinations that are currently in the clinic, and that's representative of a very substantial market. Roughly half of the U.S. oncology market is where we're playing. And today, we're going to focus on ADCs. We feel we've chosen well in terms of picking PADCEV or enfortumab and ENHERTU to focus, and I'm excited about the emerging story there. So on slide nine, again, this will be familiar for most of the investors here. ADCs is an increasingly crowded market. I think as time goes on, differentiation will be more and more difficult, certainly a meaningful space and an area of rapid growth, but also one that is very crowded. There's currently over 150 ADCs in development. The targets that are of high interest, like Nectin-4, are increasingly crowded. There's over 25 ADCs targeting Nectin-4 alone in the clinic. And this is where the combination story is important and what we think we bring. As differentiation lessens, combinations are going to be more important. And when you have a combination that is as safe as we are, we feel we can effectively combine with any Fc active ADC, of which there are many. So on slide 10, this is where we're going to focus today. This combination with PADCEV is a large opportunity. As a reminder, PADCEV is a very significant drug. Sophia and Dr. Funt will walk through this today. But PADCEV was driving significant sales in the second-line setting, and then up until recently, with their first-line approval, is now on pace to deliver over $7 billion in front-line sales. It's well reimbursed. It is the primary first-line treatment now for these patients, and that's why we think it's such an interesting combination story for us. So I'm going to turn it over to Sophia and Dr. Funt to walk through the treatment paradigm and mechanism here next. But as you can tell from slide 11, bladder is a significant area of unmet need. There's 17,000 patients in the second-line alone. And it's an area that, particularly in the second line, there's just few good options with PADCEV now moving to the front line. So with that, and on slide 12, I'm going to turn it over to Sophia to walk through the mechanism here. Okay. Thanks very much, Jason. And so now we're on slide 12, which has the cartoon of evorpacept in combination with PADCEV. And as you can see in the figure, and as Jason alluded to a little bit earlier, the mechanism here that we're invoking involves evorpacept and its ability to enhance the ADCP activity of the macrophage in a couple of different ways. Here first, by blocking that CD47 SIRPα myeloid checkpoint on the cancer cell, here we're using the active Fc gamma domain of enfortumab or PADCEV, where it engages the Fc receptor on the macrophage, fully activating it against that Nectin-4 expressing bladder cancer cell. The vedotin payload on PADCEV, and that's shown as the red circles, can also lead to a cytotoxic cell death of that cancer cell, allowing the release of neoantigens that will then activate the adaptive immune response. This is shown a little bit more on the next slide, slide 13, where again, over on number one, what we've discussed before about the enhancement of ADCP activity as evorpacept works in combination with this monoclonal anti-Nectin-4 antibody. But then on the right side in numbers two and three, you can see that evorpacept, also by blocking CD47 that's upregulated on these cancer cells, also blocks CD47 on the dendritic cell, and that can lead to that dendritic cell's activation. So as that enfortumab cytotoxic payload induces an immunogenic cell death, these neoantigens can be more efficiently presented to cytotoxic T cells by these now evorpacept-activated dendritic cells. So in this way, we have both the innate and the adaptive anti-cancer immune response in play. On slide 14, it is a little bit of preclinical data here to support this mechanism. In-house, on the left, you can see some of our in vivo data where evorpacept combination is shown with the ADC ENHERTU in a mouse model of gastric cancer. And you can see that we have this enhanced anti-tumor activity in combination compared to either agent alone. And then on the right side, on the in vitro side, when we look at the in vitro combination data of evorpacept with PADCEV or with ENHERTU, again, we're showing this enhanced phagocytosis compared to either agent alone. On slide 15, there is in fact a growing body of preclinical data, not only our in-house work, but also through others, supporting this mechanism for combining a CD47 blocker with an ADC. And we're excited to see that preclinical data set grow. Today, we'll hear now about our initial clinical experience in combining the CD47 blocker evorpacept with the ADC PADCEV in patients with locally advanced and metastatic bladder cancer. On slide 16, I'm very pleased to introduce Dr. Samuel Funt, who is director of the inpatient genitourinary oncology service at Memorial Sloan Kettering Cancer Center in New York. Dr. Funt is the director of the bladder cancer clinical trial operations at the cancer center and serves as a member on their data safety monitoring committees. Having led clinical trials now for well over 10 years, his expertise in bladder and testicular cancers certainly reflected in the over 60 peer-reviewed articles as well as NIH and Oncology Society research grants that he has been awarded in this area. Dr. Funt's research focus is on the development of personalized and effective cancer treatments, and particularly through understanding novel biomarkers, not only of therapeutic response, but also of resistance. We're very honored to have Dr. Funt today as a lead investigator on our ASPEN-7 study. He will discuss not only some of the current treatment landscape in bladder cancer, but also summarize the data from the ASPEN-7 evorpacept bladder trial that was presented earlier this week at ASCO. I'm going to turn it over to Dr. Funt. I think you're on slide 17. Thanks so much for the kind introduction. On slide 17, I listed my disclosures. Then on slide 18, just a bit in terms of the overview of the epidemiology of bladder cancer, there's approximately 84,000 new cases every year in the United States, the majority of them in men, the majority of them diagnosed at a localized stage, non-muscle invasive to be exact. There are definitely a meaningful percentage of patients that progress to locally advanced and metastatic disease, leading to approximately 16,000 deaths-17,000 deaths annually in the United States. It is the eighth most common cause of cancer-related death in men. As you can see there, also kind of shown is the incidence rate globally as well. Then on slide 19 is listed the pre-EV-302 readouts. So even going back further into 2014, all we really had was cytotoxic chemotherapy for patients with metastatic bladder cancer. But then over the last 10 years, there's just been explosive therapeutic development, first with PD-1 blockade and then with antibody drug conjugates and targeted therapy. But prior to the EV-302 readout for patients with newly diagnosed and untreated metastatic disease, the treatment paradigm was to give platinum-based chemotherapy to those patients that were eligible. And then in patients that were not progressing after platinum-based chemotherapy four to six cycles, we continued them on avelumab maintenance. And then after progression on chemotherapy, platinum-based chemotherapy, and PD-1 blockade, Padcev was the standard of care based on the EV-301 trial, which I'll show shortly. Patients progressing after Padcev, if they have FGFR3 alterations, could get erdafitinib or Balversa. Trodelvy has accelerated approval in the space. Then there's also single-agent cytotoxic chemotherapy that was used. Then just going to the EV-301 study on slide 20, which really led to the approval of enfortumab vedotin or PADCEV in patients progressing after platinum and PD-1, we can see here the confirmed overall response rate of 40.6%. And that's going to be important because it's going to serve as a bit of a benchmark for the upcoming data that I'm going to show. And again, this beat out single-agent investigator choice cytotoxic chemotherapy in this EV-301 trial with a hazard ratio for overall survival of 0.56 listed there. Or I'm sorry, 0.7, the hazard ratio for overall survival. This led to the full approval of enfortumab vedotin in patients after platinum-based chemotherapy and PD-1 blockade, again, with a confirmed overall response rate of 40.6%. But on the next slide on slide 21 shows the dramatic shift in the treatment landscape that occurred after the readout of the EV-302 study, which read out initially at the past ESMO meeting and was subsequently published in the New England Journal, and then led to the approval of the combination of PADCEV and KEYTRUDA, of enfortumab vedotin, and pembrolizumab in all previously untreated patients with metastatic bladder cancer, irrespective of platinum eligibility, whether they're cis-eligible or cis-ineligible. So this has become a standard front-line treatment now for newly diagnosed patients with metastatic disease. And then in the second line, we're kind of left in a situation where there's really a paucity of data to guide our decision-making in terms of what to do upon progression. We have platinum-based chemotherapy. We have other antibody drug conjugates, targeted therapy, and HER2, etc., that we could talk about. But it really kind of remains largely undefined in the second-line space. So that leads us to the current study, which was a phase 1 dose escalation study of evorpacept and enfortumab vedotin in patients with metastatic urothelial carcinoma. That's slide 22 was the title slide. And then slide 23 is the basic study design. We accrued patients with locally advanced or metastatic bladder cancer or urothelial carcinoma who had progressed after prior platinum-based chemotherapy and a PD-1 or PD-L1 inhibitor. And they were all treated with evorpacept at either a 20 milligrams per kilogram or 30 milligrams per kilogram dose every 2 weeks, along with the standard dosing of enfortumab vedotin at a starting dose of 1.25 milligrams per kilogram given days one,eight and 15 of a 28-day cycle, which was the dosing that was used in the EV-301 study. The primary objective was to look for dose-limiting toxicities and to establish a maximum tolerated dose. Dose escalation was examined in sequentially enrolled dose cohorts, again, at 20 milligrams per kilogram and 30 milligrams per kilogram. Investigator-initiated response was assessed per RECIST version 1.1. Moving to slide 24, which is the baseline characteristics of the 28 patients that were presented at this past ASCO annual meeting, is typical of a metastatic bladder cancer patient population with a male predominance. Listed there is the ECOG scores. These were primarily patients with disease starting in the bladder. As of April 3rd, we had enrolled 28 patients. As I said, 15 at the 20 milligram per kilogram dose and 13 at the 30 milligram per kilogram dose. The median age was 71. This was a patient population definitely with a certain percentage with visceral metastases. We saw approximately a third of patients have liver metastases, which is a known poor prognostic indicator for the disease. Again, all of these patients had progressed after prior platinum-based chemotherapy as well as PD-1 blockade, immune checkpoint blockade, and were therefore heavily pretreated. On slide 25, given the primary endpoint was the DLTs and the maximum tolerated dose, there were no DLTs that were observed in this study in the phase 1 dose escalation. We did not observe DLTs neither at the 20 milligrams per kilogram dose nor the 30 milligrams per kilogram dose. Listed here are treatment emergent adverse events that arose on therapy. Listed are the toxicities we saw that occurred in greater than or equal to 25% of patients. So you could see the side effect profile there. The maximum tolerated dose was not reached. Then on the next slide, slide 26, are the most common evorpacept-related adverse events occurring in greater than or equal to 15% of patients. These were mostly low-grade. The most common evorpacept-related adverse events were low-grade fatigue, nausea, transaminase elevation. In terms of the grade 4 evorpacept-related adverse events, we saw 2 patients with grade 4 neutropenia. Neither of those patients had febrile neutropenia. At the 30 mg/kg dose, we saw one patient with thrombocytopenia and anemia. Importantly, there were no treatment-related deaths on the study. On slide 27 is some of our pharmacokinetic data that was generated on the study, both at the 20 mg/kg and the 30 mg/kg dose. Overall, evorpacept exhibited a dose-proportional PK consistent with results presented previously by ALX. On slide 28 is an assessment of the initial activity of evorpacept plus enfortumab vedotin in evaluable patients. So in terms of the data that we presented at ASCO with 22 evaluable patients, there were responses in 13 of those 22 with an overall response rate of 59%. That is an unconfirmed overall response rate of those 13 responding patients. Seven of the responses were confirmed, and six were unconfirmed responses. ALX subsequently released a press release expanding the n from 22 to 26. And in those 26 patients, there were 16 responding patients, 8 of them confirmed, 8 unconfirmed, with 4 of those patients with unconfirmed responses remaining on treatment and 4 patients with stable disease. On slide 29 is a waterfall plot demonstrating decrease in change in the target lesions from baseline on treatment. As you can see, nearly all of the evaluable patients demonstrated anti-tumor activity and shrinkage of target lesions. On slide 30 is a spider plot really showing, again, this decrease in tumor lesions on evorpacept and enfortumab vedotin. And you can notice in a few of the spider plots that there were patients that went on to develop later responses. So initially had partial response and stable disease and went on to develop even deeper responses. So on slide 31 are our conclusions from the study that we recently presented at ASCO. And this study, the ASPEN-07 study, was the first study to our knowledge reporting data on the combination of CD47 blockade in combination with an antibody-drug conjugate. All the patients we treated had received prior chemotherapy and PD-1 or PD-L1 inhibition. There were no DLTs observed with evorpacept and PADCEV and no treatment-related deaths. No MTD maximum tolerated dose was reached. The maximum administered evorpacept dose in the study was 30 milligrams per kilogram every two weeks. Evorpacept exhibited dose-proportional PK, which was consistent with the prior experience at all the dose levels evaluated. There was promising initial clinical activity with an unconfirmed response rate of 59% versus that PADCEV benchmark that I showed from the EV-301 study with a confirmed response rate of 41%. So we feel based on these data that it's worthy of further investigation in this refractory patient population and in patients that are treatment naive or patients that have not had prior PADCEV, and also in patients that had had prior PADCEV and are now progressing and are looking to resensitize. So those efforts are currently ongoing. Thanks so much. Great. Thanks, Dr. Funt and Sophia as well. Really appreciate it. Excited about these results. And I think, as was pointed out, this is the first study of its kind to look at CD47 blockade with an ADC. And I think what we're seeing here is certainly encouraging. Still early days, of course, in the field as well as on this study in particular, still enrolling and accruing patients. Many of these patients are very early in terms of follow-up and scans. So an early data cut, no question, and one that we're going to follow up here closely. So again, a big thank you to Dr. Funt and all the investigators and certainly patients that participated here. And with that, we'll open it up to any questions. Thank you. As a reminder, to ask a question, please press star 11 on your telephone and wait for your name to be announced. To withdraw your question, please press star 11 again. Please limit yourself to one question, and you may re-enter the queue. One moment for questions. Our first question comes from Michael Yee with Jefferies. He may proceed. Hey, guys. Thank you for the question. Maybe just two. One for the doctor. I guess maybe just try to put into context thinking about activity in bladder cancer for response rates and what information here we have on durability, given that, I guess, Trodelvy has very high response rates but then failed on PFS and survival, I think, just a week or two ago. So maybe just try to put into context how to think about efficacy here and response rates versus what we just saw in the context of bladder cancer for Trodelvy. And then maybe for the company, I guess, what are the next steps here for bladder? And would that change if the gastric data next month is either positive or negative? Thank you. Great. Thanks. Dr. Funt, do you want to take the first one for us? Yeah, sure. Thanks for the question. I think I showed initially in terms of response rate with enfortumab alone after prior platinum and PD-1, kind of the benchmark from the EV-301 study of 41%. I think that's kind of what we were looking to compare to. But again, as Jason said, very early days, a lot of the patients are still on study. What we saw initially was promising. And so we just kind of need further follow-up in order to establish durability. I think, obviously, safety plays a major role and might have played a role in thinking about sacituzumab and those data that we just saw. And so obviously, there's more that goes along than just the response rate in terms of durability of response, safety profile, tolerability, and so forth. I'm not sure if that answers your question or you have anything more specific. Yeah. I guess I was thinking about, even though there's higher activity, that durability is important. And I think maybe Trodelvy kind of explored that. And so I was wondering if we have any durability or how to interpret durability here. That was the sort of the question. Yeah. We could also ask Jason and Sophia as well. I think we need more follow-up that this is pretty early data to establish durability. Yeah. Yeah. I think this is Sophia from the durability aspect of it. This particular data set at ASCO had a median follow-up of about 5.8 months. So just to echo, I think, what Dr. Funt was saying, it's still early in terms of evaluating this data set. It'll definitely need time to mature. So we do not have durability information on this database yet. But I think that's an important question. And it's definitely something that we would want to we will follow as the data set evolves. Got it. Okay. Good. And then the strategic or expanding question for Jason, how do you think about scenario planning here? And do things change if gastric is positive or negative next month? Thank you. Yep. Sure. Well, thanks, Mike. Appreciate the question. I think for us here, we're excited about the path forward. We had a great investigator meeting at ASCO on Sunday. I think the focus of that discussion was, well, both the data and your question. I think there's opportunity certainly to go at the front line. If you think about combining with PADCEV and this signal that we're seeing here and now adding pembro, which is the key component of our mechanism, and one in which we think we have a very strong signal there and head and neck. So I think that's very tantalizing. Of course, big study, big swing, and will require making a big bet. I do think we have continued to explore subgroups of that. So patients that we know can't tolerate or won't tolerate PADCEV, and how do you identify those patients and potentially target those as a subgroup of the front line? And then there's the second line piece, right? That's why I think we're keen to look at this PADCEV experienced population, enrolling patients there now to do so. And I think that'll provide a window into the opportunity in the second line. And I think, as has been highlighted today, there's just no good options for those patients. So that's how we're thinking about it. I don't know, Sophia, if you have anything to add or anything I missed. No. I think that's kind of the big picture is letting the data guide us, looking at enfortumab naive as well as enfortumab experienced patients. As those data sets mature and we get that data back, that'll have to guide us moving forward. Thank you. Thank you. Our next question comes from Christopher Raymond with Piper Sandler. You may proceed. Thanks. Yeah. Just two from me as well. I guess first, I want to understand maybe the dynamic with the confirmed and unconfirmed responses. I think in the deck here, you've got four more evaluable patients from the April 3 cutoff now with one more confirmed and two unconfirmed responses. Maybe can you first confirm whether any of the April 3 unconfirmed PRs were deemed to be not confirmed? And I guess maybe more of a general question on that is, with more than, I guess, two months now since April 3rd, why haven't the lion's share of these unconfirmed responses been confirmed? And then my second question, on the spider plot on slide 30, if you just eyeball the depth of response, and I know these are still small numbers, but it looks like you're seeing deeper responses at the lower dose. Actually, if you look at the response rate, you got a higher response rate at the lower dose with more CRs. Your 2 CRs are at the lower dose. I guess just if you're getting full receptor occupancy at both doses, but you expect better tumor penetration at the higher dose, wouldn't you expect these responses to be deeper at the higher dose? Thanks. Yeah. Thanks, Chris. Appreciate it. Good questions. On the confirmed versus unconfirmed versus unconfirmed, what we've tried to do here is just provide the most recent data and make sure that everybody knows where it sits as of the current response-evaluable patients. So as of today, that's the 16 responses that we have, 8 confirmed, 8 of which are unconfirmed. And then we have 4 of those that are on study as well as 4 stable diseases that I think we're encouraged by. And so if you look at what happened between the 2 data cuts, we certainly have had patients confirm. We had some go off study. And again, that's why we tried to provide the most recent data just to bring everybody up to speed. We did, between those 2 data cuts, we had an unconfirmed CR confirm, which was encouraging. When we look at, and this gets to your second question, when you look at sort of how those patients have progressing, we know we've seen several patients out beyond 20 weeks that have flipped to PR that were SD that flipped to PR relatively far down the road, which I think we're encouraged by. Again, this is all kind of signal reading here. All that taken together, I think, is encouraging. So yeah. Sophia, anything else to add there? No. Just again, I think the 26 patient, again, this is just a one-month difference there. It represents the most recent data that we have. So yeah, just what you said. We've tried to kind of be transparent who's still in play. And I think the other question you had asked was about some of the different dose levels and. Yeah. Dose response. Yeah. Exactly. The depth of the response. Yeah. So mostly, I think on the spiders, what you're seeing, again, that was as of the ASCO data cut. What you're seeing there is the impact of the sequentially enrolled cohorts. So the patients who were at the 30 mg/kg, it's just a more immature data set. So they haven't been on study as long. But really, from a PK perspective, both of those doses should be active. The idea there is that as you get into the tumor microenvironment, you really want to try to maximize that drug exposure, right, even beyond what you're seeing in the periphery. And so that's why we're still trying to push across our program, trying to push the 30 mg/kg exposure levels. But I think as we follow these patients out longer, you'll start to see that same contour that we're seeing in the 20 mg per kg spider plot, where you start to see that gradual decrease in tumor size over time. That seems to be a little bit of a hallmark of an IO-type agent. So definitely, we'll continue to follow these. But we do not see a difference at this point between the 20 and the 30. I think it's just a matter of immaturity of the data set of the second cohort. Okay. And then just if I can ask a clarifying question, the first one. So have any patients who were deemed unconfirmed responses as of April 3rd, have they flipped over on the second scan to not be confirmed? I'm not sure if you answered that. Yeah. I'm not sure if we're slicing and dicing the same way you are. But I think that the easiest way to look at it is just with the most recent review of those 26 patients. We've got 8 confirmed. So you can see, I guess, between April, we've picked up a confirmed. We picked up a couple of unconfirmed. And then there's some patients who are remaining on treatment. And we've tried to put down of those who are unconfirmed who is still remaining on treatment. And then the stable diseases obviously are still in play as well. Okay. Thanks. Thank you. Our next question comes from Sam Slutsky with LifeSci Capital. You may proceed. Hey. Good afternoon, everyone. Thanks for taking the questions. Just one for me. I guess looking at the waterfall plot, a couple of these stable diseases look like they're somewhat close to the partial response threshold. I guess, are any of those patients still on study where it's possible that they could convert to a PR at a later time point? Thanks. Yeah. We have several that are in that. Thanks for the question, Sam. We have, I'd say, several in that bucket. We have 4 SDs that we think are very much in play. And again, we've seen that play out elsewhere with patients that are many months on study, SD trending in the right direction, and flipping. And again, that's really encouraging for us. Obviously, we're developing an IO agent here. We've seen that trend elsewhere in gastric, for example. And so that's what we have an eye on here going forward. And we'll certainly provide an update on that once we get down the road here a little more and let things bake. But I think what we're seeing with the SDs in play is encouraging. And we'll be getting back to you all on that once we see how that shakes out. Thank you. Our next question comes from Li Watsek with Cantor. You may proceed. Hey, Greg. Thanks for taking my questions. I guess the first one is, can you talk a little bit about the patient characteristics from the study? How does that compare to the phase 3 EV-301 of PADCEV? And since you mentioned the treatment landscape has evolved during the trial, so just wonder if that might have impacted sort of the type of patients enrolled in the study? Yeah. Sure. I'll kick this over to Sophia and Dr. Funt. I think in our patients, we are seeing a patient population that is heavily pretreated. I think we also highlighted the rate of liver mets here, which is a negative prognostic. But Sophia, do you want to answer that more? Yeah. Dr. Funt, I mean, as you look at the demographics, do you have any thoughts that you want to bring up first regarding this versus EV-301? Well, I think we were very rigorous in enrolling patients that had progressed after prior platinum and prior PD-1. And there were patients that received additional lines of therapy as well. So I do think it was a heavily pretreated patient population. In terms of comparing it to the EV-301 data, perhaps a slightly higher proportion of patients with liver mets than in EV-301, which was closer to 22%, around 20% or so with liver metastases in that study. And then in terms of prior lines of therapy, I think overall, again, this was a heavily pretreated patient population. We do have more therapies available in bladder cancer than perhaps EV-301 when EV-301 was initiated, if that was your question. Yeah. And I think just to add, and the only other thing I could think to add on to that would be that certainly, and Lee, this may not be quite your question, but for the EV302, for example, that was not in play when we were enrolling this study. So the population here, as Dr. Funt outlined, all of these patients would have seen prior platinum and would have seen prior checkpoint inhibitor. And nobody would have seen prior enfortumab. So most consistent with that EV-301 population. Okay. And I have a follow-up. You mentioned that you might look at the PADCEV experienced patients. So I just wonder, is there a good rationale to use PADCEV plus evorpacept given that the signal you're seeing is from the naive patients? Yeah. It's an interesting idea here. And I think part of this rationale is that the way in which we're using PADCEV, right? So we're using PADCEV here as a way to identify those Nectin-4 positive bladder cells and bring them to an activated macrophage. So in a way, it's exploiting this ADCP activity in a way which really hasn't been exploited before. It's almost similar to our gastric cancer study where even though patients may have seen prior trastuzumab and have resistance to trastuzumab, in a post-trastuzumab setting, we're still seeing activity when we put that monoclonal antibody together with a CD47 blocker because we're now using this ADCP mechanism of action, which hasn't been exploited before. So I do think there is a rationale for looking at enfortumab experienced patients, again, making use of this ADCP mechanism of action. Thank you. Our next question comes from Bradley Canino with Stifel. You may proceed. Hi. Thanks for the event. And thanks for the question. One clarification first. I'd just like to know, you mentioned of the 8 unconfirmed 4 are remaining on treatment. So 4 have discontinued from treatment. What were the reasons for that? Was it progression? Was it toxicity withdrawal, etc.? And then second question to the doctor, this idea of re-challenging with PADCEV plus evorpacept. I guess, how should I think about interpreting those data when they might become available? What would you imagine to be the expectation for efficacy or clinical signs that you would see in a PADCEV re-challenge in patients if there's any of that available? Thank you. Thanks, Brad. Appreciate the question. For number one, on those four patients that are off study, I think it's a mix. But I'll let Sophia chime in as to whether it was a progression or PADCEV tolerability. I mean, we know patients we've lost due to PADCEV tolerability. But I'm not sure on the four. Yeah. For those specific four, I believe it was just due to disease progression. But I would have to go back and double-check. Yeah. And then thanks for question number two. I think given the treatment landscape shift to EV-pembrolizumab in the front line and thinking about treatment of those patients when they progress, I think there'll be some heterogeneity in terms of the patients that are progressing while on therapy and straight-through therapy versus those patients that come off for toxicity and then progress off of therapy. But I think there are now other options available for those patients. There are a percentage of patients with FGFR3 alterations that will be eligible to receive erdafitinib, so kind of a genomically defined patient population that might be about 20%-25% of patients with metastatic urothelial cancer. We now have approval for an HER2 pan-tumor for those patients with high HER2 expression based on immunohistochemistry based on the DESTINY study, a very small number of patients in that study. But that's an available option. But it's really hard to even estimate, even though it's approved, what the response proportion will be in bladder cancer because we just need more data. And then there's the sacituzumab data which has been brought up. And with the recent negative TROPiCS study, raises some concern about using that agent, although I think we have learned how to use it more safely now with prophylactic growth factor. But I think it's really hard. I don't think that there's really a good benchmark. I think that really some activity, and again, it would be just kind of conjecture, a response rate of 30%, 40% in the EV experienced patient population would be promising. But it would need to be confirmed in larger studies. Does that answer your question? It does. Thank you. Thanks. Thank you. Our next question comes from Swayampakula Ramakanth with H.C. Wainwright. You may proceed. Thank you. Most of my questions have been answered. I just have a quick question. I'm looking at the 30 milligram per k cohort. And just I was wondering about the lack of complete response in this cohort. Is it more of a timing issue, you think? Or is there some dose kinetics that we need to think about as well? Yeah. Thanks, RK. Okay. I appreciate the question. I think, as Sophia pointed out, these two cohorts were enrolled sequentially, right? And so we know that the 20 is more mature. And I think that is an important point. And as you mentioned, the CR, you can just see some of this on the spider plot. But we had one patient that just had very nice tumor shrinkage and got down to the 90%+ mark out 200+ days, right, on their primary or on their target lesion. And we disclosed in the press release, or maybe here, but we had 2 CRs, one of which was unconfirmed that we've since confirmed. And to your point, both were in 20. But we do not, again, expect there to be a dose difference here, 20 versus 30. The PK is right on top of each other. 30 is what we're using in the gastric study and have been using across the program. Given that we're seeing CD47 blockade down to 3 mg/kg, certainly feel we have both very active doses here. Perfect. Thank you. Thanks for taking that question, Jason. Sure. Thank you. Thank you. Our next question comes from Ting Liu with UBS. You may proceed. Hi. Good afternoon. I got two questions, if I may. So the first question is to Dr. Funt or Sophia. Still regarding the deeper response and 20 mg/kg versus 30 mg/kg that have already been discussed, it's understood that the data needs to be further mature. Just out of curiosity, does it have to do with less tox and also dose reductions? So maybe longer average duration of patients on full dose at 20 mg/kg. Then as a reference, I see the average treatment duration for PADCEV monotherapy in EV-301 was 5 months. Could you provide any color? How does the average treatment duration look like for the combo at respective doses? Thank you. Sophia, you want to take that one? Sure. Sure. So thanks for the question. And the short answer is we'll have to see. We certainly haven't had real issues with tolerability of the regimen. And I think that in a way, it does sort of speak to what you're asking, which is with a tolerable regimen, patients are able to stay on longer. And then you can actually see the benefit, the anti-cancer benefit coming out from a tolerable regimen. For the 30 mg/kg, patients just haven't been on long because it's a more recently enrolled cohort. So you can see from the ASCO data that Dr. Funt presented, at that point, we only had eight patients who were enrolled in that study into that cohort. So over time, as we continue to look at the tolerability, we don't anticipate any differences. But we certainly will follow that out. Hopefully, these patients will see that benefit, that clinical benefit from being able to stay on a tolerable regimen over time. And then I forget the second part of the question. I'm sorry. Oh, I haven't asked. Yeah. Thanks, Sophia. Yeah. So my second question is on the development strategy for evorpacept in bladder and then in this post-EV-302 time. So you did mention the rationale to test EVO plus Padcev still in the post-Padcev setting. Just wondering, would you also test EVO in combo with a different ADC or a different active drug in that second line? And then another alternative strategy you also discussed with us before is that having evorpacept plus Padcev and pembrolizumab in first line. So I have a question about that how do you coordinate the dosing schedule here since when Padcev and pembrolizumab alone dosing front line, they're in a 21-day treatment schedule. And then I believe Padcev is still on a different schedule where patients do get a break on the third week. So when you're adding every two weeks evorpacept into this regimen, does that mean that patients need to come to infusion center every week to receive something? Or you may coordinate this combo to a different schedule? Yeah. No, thanks, Ting. Those are great questions. So on the first, I think the beauty of the mechanism here is that we can combine with other ADCs. And as long as there is strong effector function, I think we can do so. And whether it's with Trodelvy or in this case with PADCEV or with some of the other ADCs in development, I think that's an option. And we spent a better part of ASCO meeting with potential partners with novel ADCs in development. And there's a lot of interest in us doing so. I think our strategy internally has been to let's pick the best, right? I mean, that's why we picked PADCEV, picked ENHERTU, and picked ADCs that are standard of care. But that's not to say mechanistically that we can't look elsewhere. And we think that that could make sense for us going forward. On your second question, Sophia, do you want to cover that one? I know we're almost at the end. Yeah. Yeah. Yes. We're at the end of the time. But the short answer is for the dosing that we actually have flexibility with evorpacept dosing. We have Q week, every other week, Q three week, and Q four week dosing. So we can actually match it in a convenient way to the partner drug. And we can follow up with you after that. But we do have that flexibility. Thank you. Thank you, everyone. Thank you. We have a few minutes left and would like to turn it over to Jason for any closing remarks. Great. Well, really appreciate the questions here. And again, a big thank you to Dr. Funt for taking time on a Friday to join us. Very excited about the potential, again, early days on this study, but excited about what we're seeing so far. And very much looking forward to next steps. So thank you again. And we'll be in touch. And hope everybody has a great weekend. Thank you. This concludes the conference. Thank you for your participation. You may now disconnect.