Excellent. Good afternoon, everyone, and welcome to the JMP Securities Hematology and Oncology Summit. It's my distinct pleasure to welcome BioAtla as the next presenting company. Presenting for the company is Jay Short, co-founder and CEO. The rest of the team is actually joining us as well. You know, Sheri is here, Rick, Bin, and Eric as well. And so, they may jump in with some of these questions. But Jay, great to see you. You know- Great... I never know exactly who is in the audience and how much they might know of the BioAtla story, so love to start these firesides off with maybe a three to five minute overview of what the company's about. Oh, that'd be great. Yeah, I'm happy to do that. The company is based and headquartered in San Diego. We do have a contract operation in Beijing, but we're a U.S. company. And we're focused on solid tumors, treating solid tumors, which represent over 90% of all the cancers. And but we do this with a novel technology, that platform that we developed and pioneered at BioAtla, and it's referred to as Conditionally Active Biologics, or CABs. And I think what often people confuse or don't understand is that these are not masked drugs. These are not pro drugs. This is a unique mechanism, and the key features of it are that it, when it goes into a tumor microenvironment or against a cancer cell, it's able to see epitopes that are unavailable on normal cells, and even if that's the same receptor that you're targeting. The reason for that is because it's a pH difference. All cancer cells are acidic, and they're acidic because in order to be able to continuously divide, they have to duplicate their DNA, the lipids in their membrane, and all of these other proteins. In order to... And as a consequence of that constant synthesis, they run the glycolytic pathway, which at the end secretes lactic acid from the cancer cell, and that's why all cancer cells are acidic. Because of this unique feature, whereas normal cells are alkaline, so our CAB antibodies will only attack these cells if they're acidic, and also all cancer cells are acidic. So this gives you an advantage of widening the therapeutic index, the therapeutic window, which gives you the opportunity to not only increase safety by eliminating on-target or attacking normal cells, it also allows you to improve efficacy. And we think we see both of those characteristics in our clinical data to date, as well as obviously in our preclinical data. So we have three drugs at Phase II and one at Phase I, and they include two ADC antibody drug conjugates, one immuno-oncology drug, and also our first T-cell engager. Hopefully that gives you a little sense of the company, and a lot going on. Terrific. Well, let's jump right into it. You guys had a really nice data update just yesterday. You hosted a KOL event, and it's all surrounding BA3011 data in non-small cell lung cancer. And so, you know, investors can obviously listen to the webcast to get all the details, but could you maybe, you know, review the highlights of this data for us, and importantly, help put it into context, maybe relative to other investigational ADCs? Yeah. Happy to do that. And it's... So this is our AXL antibody against the AXL receptor, which is a tyrosine kinase receptor. It's a tumor driver. So you see these AXL receptor expression increasing as the tumor progresses and becomes more resistant. And so we actually tested a very late-stage group of patients. All of our patients, the median had three prior lines of therapy, so we're testing basically a fourth line of therapy. In addition, AXL's expression is highly correlated with poor survival, so it's a very poor prognostic indicator. So these patients, as we had Professor Dr. Carl Gay speaking from MD Anderson and talking about his research in the area, and he really talked about how tumors become resistant to really almost every therapy type, whether it be chemotherapy and so forth, in the, as you increase the level of AXL expression. And we've seen efficacy against all levels of AXL expression cells. But in addition, interestingly, we saw activity against ones that even if only 1% of the cells, the tumor. Let's say you take the tumor, and 1% of the cells in that tumor express AXL, we saw partial responses even in those particular tumors. So the point is that we saw an ORR rate of around 33% in one set and 28% across all PD-1 resistant tumors. So this activity in this fourth line really matches what a lot of other companies are showing in second and third line. And any trial that we would go forward with either would be a second or third line. We are obviously going to move up from our current fourth line therapy. So we think we're competitive already, and we're in a difficult line, and we're also in AXL, all AXL-positive tumors. And so I think the data is, I think, very compelling. ... I think one of the, you know, benefits, right, that you had highlighted outside of efficacy is also the safety, the safety aspects. Can you comment, you know, in terms of, you know, what you found from a safety perspective as well? Yeah, and I think I would like Eric, our Chief Medical Officer, to respond to this. And I think, Eric, it would also be good perhaps if you just touch on the lack of on-target tox as well, if you don't mind. Sure. Thank you, Jay, and thank you, Rennie, for the question about the overall tolerability. In the slide that you have in front of us, it illustrates that it was really quite good. So just to reiterate what Jay was saying, we've designed the conditional binding in such a manner that we're not targeting AXL as it's expressed throughout the gut and on normal tissues. And other sponsors have attempted using ADCs targeting AXL that doesn't employ the conditionally binding technology. High-level constipation is observed in those experiences, and we're grateful that we're not seeing high-grade constipation with ours. And our thesis is, it's because we're not injuring the gut with the delivery of the auristatin payload to normal cells. As I go through the treatment-emergent adverse events that is illustrated on this slide, we're gratified to see relatively low rates of Grade 3 events. The way this chart was constructed, we are not seeing Grade 4 events in this range. The overall treatment-emergent adverse events of any grade, of any relationship, really lead with fatigue, diarrhea, constipation, decreased appetite. These are very commonly seen with cancer therapeutics and are very manageable in the clinic. Just sticking with this program, you know, I think another thing that came out at the event yesterday was the recent FDA guidance that you received. And, you know, I think you outlined the potential for a registrational study. There were two paths. Can you provide us some additional detail, you know, and kind of next steps? How do you decide between the two paths, and, you know, when do you think this begins? Well, we'll start off, and maybe Eric will add to this. But I think it's the first part of the question of what do we want to finish before we jump into that registrational trial. Because we saw a very good activity at even as low as 1% of the cells expressing AXL, in other words, 1% TMPS score, in a way, consistent with other ADCs, we don't believe that a biomarker is going to be required. Keeping in mind, the biomarker is simply using an immunohistochemical assay, so it's an arbitrary level of detection. So even if it says that you can't detect it, that doesn't mean that AXL is not expressed on those cells below that. And so we believe that we will be moving target-agnostic, meaning that we will not require the immunohistochemical assay to determine which patients to apply the medication to. So with that in mind, we do need to provide a tiny data set to the FDA before we can jump into that. What's nice about it, though, is this recruits very quickly because there's no requirement for a biopsy or any other additional testing. So we'll have that, I think, relatively quickly, and we'll provide that data, and that will position us for then moving forward on the registrational trial. What I like about it, of course, before we had about 30% of the lung cancer patients were positive for AXL by that assay. So here's a situation where you're increasing the market size by over threefold by simply not requiring that biomarker. So in general, that's the part we're going to do. We're finishing off, and then that'll position the company for the registrational trial. In addition, of course, we've mentioned that we're under discussions across all of our Phase II assets and some of the other, actually even preclinical assets, from a partnership, and we intend to forge one partnership or collaboration this year. And if it happens to be AXL, we're not guiding which one it'll be, but 'cause it depends on the economics and so forth. If it happens to be that, we would love to put that registrational trial in together, mutually with that partner. But we'll see where we are when we provide that data to the FDA. We'll see where those discussions are. From a standpoint of how do you make a decision then based on this really quite unique feedback that we got from the FDA? The second line, I think, was very, I would say, expected. You have a docetaxel control. It happens to be open label, which surprises a lot of people, and the main reason of that, it's so difficult to blind it because the treatment is very difficult to blind, so they tend to just do that open label. But the thing that I think was really unique, and I give our team a lot of credit for really putting that forward to the FDA, and I'm very appreciative of the FDA giving us a green light of going forward, but with a randomized blinded trial in the third line. And why would you consider third line? Well, first off, if you're target-agnostic, your market now in third line becomes just as big as it used to be in second line with the biomarker. So now you have a bigger market. The other thing is, you really don't have competition in the third line. It's a major unmet need. And in second line, you have four or five players, you know, all trying to get ahead in second line. So you could make the decision, if you're a very large pharmaceutical company, say, "I still want to go after second line," especially given the strength of the data we have in AXL in this fourth line study and AXL-positive patients. But the other way to go, you know, and this may be more whether it's my decision versus a joint decision with a partner, you know, the third line is quite compelling. And I think we can, with a blinded study, it'll be quite competitive. So yet to be determined which way we'll go, but we really like the fact that we have this freedom to go second or third line and target-agnostic. ... Got it. I know that, you know, I kind of focused on the most recent data, but, you know, maybe transitioning to 3021, your ROR ADC, I believe you recently received some encouraging, really some encouraging data in both melanoma and head and neck. Can you just quickly give us a quick snapshot of that data? Yeah, and, You know, it actually, if you think about why did this study take so long, I thought it took a long time, and the reason was, is because we were using a biomarker again, and, the percentage of the patients in melanoma was on the order of 5%-10%. Well, because it was taking a long time, we said, "Okay, let's not do that. Let's go target agnostic on this. There's data supporting in the literature that you may not need a biomarker for this, especially an MMAE ADC." And we pulled that out, and guess what? We got 2 PRs immediately with TmPS equals zero, without a biomarker. And so now we have a total of, We have one CR, three PRs out of eight patients. Pretty remarkable data, in addition to two stable disease patients and two, and only two PDs. So we're. We've already re-enrolled all the patients for completing that study, so we're in the process of getting scans, and we'll be able to report out on that early next year. So very exciting. And then also in the head and neck, we've. Now, we have only reported on two patients, but they were two PRs, two out of two, and in that particular case, we also got a TmPS equals zero patient. So, you know, you take the ROR2 data, and that's just adding on to our belief that target agnostic's the way to go, as we see with AXL as well, and aligned actually with all other ADCs. But we're very, I think, I think it's very promising what we're seeing in ROR2. Not quite as mature as the data set in AXL, but we're also seeing very, very encouraging safety with ROR2 as well. Excellent. So, switching gears again to 3071, the anti-CTLA, the CAB that's the anti-CTLA antibody. Yeah. You guys have an R&D Day coming up. I believe it's on the 13th. Would love to know, you know, any sort of an update you can provide on that, and I guess even more importantly, what can we expect at that R&D Day? Well, I think I'm gonna... There's a very specific things we would like to see from this data, and, and I can tell you we're doing a data cut this week, so we'll have a all together, have a fresh look at some of the latest, greatest. But, Eric, why don't you maybe lay out some of the expectations we would like to see that we think would allow this to be a transformational therapy going forward? Sure. Thank you, Jay. So if we think about CTLA-4 blocking technology, well, there are two approved agents, and, you know, this has been established for 20 years. There's a lot of excitement among oncologists to employ CTLA-4 blockade, but what stops them is safety. Particularly, high-grade, life-threatening colitis has been exceptionally challenging for the existing agents. And so our strategy is to use the conditional binding technology so that we limit the blockade of CTLA-4 in a low tumor pH environment, and largely avoid blocking CTLA-4 in normal tissues. And that, and the thesis is that by avoiding blocking CTLA-4 in normal lymph nodes, we might see lower colitis, lower pneumonitis, lower hepatitis, et cetera. And these are the issues that really challenge physicians using these agents. So that's how we see this. If you see the new agents in CTLA-4, I put them into two broad categories. One category is changing Fc and modifying the function of the antibody from that regard. The second strategy is some effort to limit the blockade of CTLA-4 in normal tissues, either using masking or caging technology, as other sponsors are using. I want to emphasize that for BioAtla, we're not using masks or cages. There's no proteolytic cleavage. There's no prodrug involved here. This is simply a part of the CDR. It's characteristic of the binding region, and those are the properties that we've built in to the antibody. So it's a normal antibody that simply binds its target in a low-pH environment and avoids binding at a higher pH. I think- Jay ... I'd add, I'd add, if you look at Ipilimumab or, you know, some of the you know, the kind of standard of care out there, you know, if you look at them at, let's say, on the order of 3 mg/ kg in combination with PD-1, you really can't get beyond 12 weeks of therapy. It's just too toxic. Patients come off, and frequently, they fall off before that. So the idea is, can we maintain patients on this drug? It's recruiting T-cells, it's very effective, and potentially far more powerful than PD-1 at treating a tumor, but you've got to keep them on therapy, and so you need that safety. You need to eliminate the colitis, and you need to maintain that efficacy and potentially improve it, 'cause if you can maintain it, you're likely to improve that efficacy. So, this is what we're giving the first snapshot of and out of our Phase I data. Obviously, it's got the dose escalation parts. We won't have... You know, it's probably on the order of approximately 20 patients, but it'll be- it will give us our first sense of, how things are rolling in that space, so we're looking forward to next Wednesday. Excellent. And if that wasn't enough, you also have, as you mentioned in your intro, a T-cell engager bispecific. And obviously, you know, bispecifics are continue to be, right, like quite the, quite the rage, just as ADCs are. Would love to, you know, kind of, get your take on the advantages of a, of a CAB approach, you know, and how this might impact the therapeutic window. Well, it's a big challenge, you know, I think for these T-cell engagers, because if you have any target on normal cells, you're really activating with the second arm against using the CD3 receptor. You're engaging that T-cell against those normal cells. So you really don't want that. You have to have something very specific. And so that I think that's important. So you could imagine easily enough that you put the CAB selectivity on the tumor-targeting arm, you say, "Okay, good, you're not doing that." But what we've done is we've put the CAB on both the T-cell engager part, the CD3 arm, as well as the tumor-targeting part, and what you get is the product of those two selectivities. So if you have 10-fold selectivity in each arm, you're bringing a 100-fold to it, and what we've said is we're over a 100-fold with this EpCAM target. And that's really important, because EpCAM is on a ton of normal cells. It's an extremely validated target, but you really can't afford to go after your normal cells. It's just gonna be too much to deal with. And so, it's in dose escalation now, and it's moving forward, and we know that this is an exceptionally potent drug. And we're very excited to look forward, and we think we're on track for reporting out all of the Phase I data and hopefully kicking off the Phase II study next year as well. So I think there's a lot of enthusiasm around it, like you're expressing, Rick. Yeah. You mentioned during when we were talking about kind of the path forward and the FDA correspondence, pursuing one or more strategic collaborations. And I guess, you know, there are many different flavors in which a strategic collaboration, you know, can, can occur. You know, can you talk a little bit about, you know, what, what it is that you would prefer? What would be the, you know, the best-case scenario, if you will, and is there a prioritization of which assets you're willing to, to partner right now? Well, for strategic reasons, we're not going to say prioritization. We're keeping that close to the vest, and 'cause we want to... We're looking at the economics of each one of these, and we think that each of these Phase II assets are very valuable. It's a kind of a case by case. We do think and keep a very close eye on North America and the United States, how our sharing goes in that. Are we gonna have a partner that's going to respect that? We do have, we are in discussions and have had reach-outs across all three of those Phase II assets. We've also have interest in, I'd say, territorial deals and so forth. The way you really in the end of the day look at it, we're going to look at what the partner is interested in, and we're gonna run. We're particularly interested in partners that can increase, you know, the NPV value, the IRR return on these things, and looking at, can some partner take us into first line earlier than we could do it on our own, for example? That would be quite interesting. If they are going to do a global deal, can they move us into the market faster, so our math looks better for the shareholders? You know, all of those kinds of decisions get weighed in and will be analyzed, and ultimately, the best scenario will be the ones we pick. The reason we say we want to, we're targeting at least one, we may, and we do up to two, the message there is we're gonna keep one ourselves, no matter what. We want one that's fully in our, in our control, and, and I think... But on the other hand, it's possible that you could see a blend, one that's global, one that's territorial deal, and we'll just take it case by case. But we think also timeline-wise, these data are the datasets that further those discussions, and so we hope over the next six to nine months that we'll be able to bring something, meaningful to the bottom line here. It's nice because we have runway into the second half of 2025, and I think that gives us time to really do the right discussions and get the right positioning. Got it. So maybe before we finish off in the next couple of minutes, before even talking about the upcoming milestones, you know, one of the questions that we typically get involves durability of response and, you know, and how we should be viewing these results in this patient population, and should we be developing strategies to enhance that response rate or durability of response? Just wanted to get your thoughts on it. Well, I think the only ones we've read out on durability response is AXL, at the BA3011 molecule. So, you know, we think, and not I would say we, I'd say, MD Anderson believes, Dr. Carl Gay, who treats these patients, says the duration of response we have is unprecedented in this line of patients. In addition, he's an AXL expert. He's one of the few people that's actually published on AXL and knows how difficult AXL patients are to treat, and he's looking at it and say, "Look, I didn't even expect responses. I'm seeing not only responses, I'm seeing durability that's meaningful there." Now, any study we would go forward with is an earlier line than the dataset we just provided. We would go at least to the third line, and, and we've given data on the fourth line, you know, three prior lines, and so we were treating the fourth line. So I think, he's quite enthusiastic, and, you know, he's probably the best spokesman I've seen on it, and here's a guy with one of the few people in the world that has the knowledge. And so I think, we will get an increased duration of response, very likely. One would expect it. And I'll give you a little bit of anecdotal data. Look at the combo data.... That effectively was, close to a fourth, four prior treatments. It just was the luck of the draw the way the patients came in, but we're treating almost a fifth line there. You can see that it was a little lower ORR, small, smaller numbers in the sense as 20 and 20. But the point is that that's almost indicating as you go to those earlier lines, you're gonna see improved responses, and you're gonna see improved duration of response. And there hasn't been any example that I know of that hasn't happened that way with ADC, so I'm expecting us to become very competitive in these earlier lines. Got it. And I guess in the last 30 seconds, these are the milestones that we have for you guys. Of course, you've already reported the lung cancer data, so we'll be taking that off. But if you had to kind of rank order it, you know, as to what might drive shareholder value the most, you know, would you give us a thought on that? Well, you know, they're all multi-billion dollar opportunities, each and every one of these. There isn't one here that isn't. I think what I like about BA3011 is that it's ahead, it's earlier. When you look at the math on that, that matters, right? But I think, what's interesting about the BA3071 is it could potentially go into every drug combination out there. Like, you know, the PD-1s are today, but here's a chance to be a more effective equivalent, 'cause it's T-cell recruiting as opposed to just activating what's already there. You're actually bringing new T-cells. You can't ignore that one. And of course, I think the longer term, if you can add a little time to it, I think your EpCAM has a shot. We don't know the data yet, but has the shot of being one of the first pan-cancer drugs, so that's really powerful. But, you know, we gotta have the data on that one. But I... All of them matter, and I think ROR2 has much to explore. Wish we had the funds to go after triple-negative breast cancer with that one, but I think a partner will, and much excitement there as well. So there's not a bad asset here at all, and all of them matter. But hopefully I've touched a few points on that you were- You got it. Yeah, no, thank you very much. Really appreciate it, Jay and team. Appreciate the update, and thanks for joining us. Thank you. Appreciate it.