All right. Well, good morning, and welcome to the annual Citizens Life Science Conference. It's my pleasure to introduce the next presenting company, BioAtla. Joining us on the stage is the team from BioAtla, Jay Short, CEO, joined by Eric Sievers, CMO, Sherry Lydic, Chief Commercial Officer, and Rick Waldron, CFO. So welcome, everyone. I appreciate you guys being here. I never know who exactly is in the audience or who's listening on the webcast who knows the BioAtla story, So I always like to start off these discussions before we jump into details with maybe a two to four minute overview of what BioAtla is about.

Sure. I'm happy to give you a little bit of an overview. We're a clinical stage oncology company headquartered in San Diego, California. We have four clinical assets, clinical stage assets three are in phase two. too. We also have a fundamentally interesting and important conditionally active biologic platform that allows us to increase the therapeutic index of our therapies, meaning that we're able to increase potency while at the same time increasing safety. So that widening of that therapeutic window is fundamental and allows us to drug targets that otherwise would not be druggable without this technology. In addition, the company is in multiple active deal discussions, which we believe will allow us to advance at least a couple of our molecules into phase three together with partners. And so we're quite busy at the moment.

Great. So, you know, let's jump into, well, I guess before we jump into the pipeline, let's take just a step back as we think about kind of the conditionally active biologic space, right? You guys are one set of players. There are other competitors, you know, that you have that are all trying to, you know, in one way or another get these antibodies or ADCs to get activated at the tumor microenvironment. Based on the data that you've generated to date and even the competitor data as well as deals that are being done, right, in the space, can you maybe, you know, can you confidently say that the platform has been validated and now it's just a point of you know developing the right study you know to move forward and prove it or is it kind of still up in the up in the air and the platform still needs to be validated so first off the platform is mechanistically is different than any other group out there so and it has some significant advantages because it doesn't require an activation step and this means the kinetics are very good when it goes to the tumor it's able

to bind immediately when it leaves it won't attack a normal tissue target and that's why we refer to it as reversible so it's a fundamental difference and it widens the therapeutic window further it allows us to have higher potency in terms of validation and we think one of the greatest examples we've seen as Axel as our target we we know that and I think all of us know that there's been two other companies that went after this very important target. It's important because it's directly linked to MK-RAS mutations and lung cancer mechanistically. GAS-6, which is an activator of Axel, is one of the byproducts of MK-RAS mutations and that whole cycle is what causes tumor resistance. And so it's a really important target, not only for lung cancer but and a lot of other indications, but yet two companies failed to be able to build a drug that could show the risk-benefit, meaning that they had too much tox for the ability to treat the tumor. And here we've seen very strong data, what I would particularly point out is the overall survival. This is one of the areas and one of the main reasons that drugs fail in second-line non-small cell lung cancer is the lack of overall survival. they'll see some initial reduction in tumor size but then it's not sustainable and patients really do not survive and we're seeing very strong data going out over two years now 59% survival we haven't hit a median yet an overall survival and both you know I think two other companies have tried to take it into the they've taken it in the clinic but they failed on that so I think that's pretty black and white. I think the other quick example might be Epcam, Amgen worked very hard and diligently to try to get that important target, which probably represented on upwards toward 90% of all tumor types and couldn't make progress to get it to a dose that's really going to matter. We already have, even at a low dose, see three patients with double-digit tumor reduction, so we think we're on the path for seeing responses in the near term, and the safety is looking very encouraging at the moment. We'll let Eric talk about that in a few minutes, but those are just a couple quick examples. I think it's validated. We're on a very good path.

Excellent. So let's jump into the EPCAM program. We have some data coming out. First time we're seeing this data, if I remember correctly, at ESMO GI. You can correct me if I'm wrong, But, you know, can you kind of set the stage for us? What is it that you're looking for? What can help you kind of gauge that, you know, what are the metrics for that go-no-go decision going forward?

Sure. So I want to emphasize this as an interim look at an ongoing dose escalation study, first in human, phase one, very standard study design where we've dose escalated through cohorts of patients. We're now treating at a treatment dose of 300 micrograms at the treatment dose every We plan to continue dose escalating per the rules of the trial as far as we can go as long as it's acceptably tolerated. We mentioned earlier that Epcam is an attractive target. it's expressed so widely on adenocarcinomas that, you know, that would include non-small cell lung cancer, triple negative breast cancer, colorectal cancer, pancreatic cancer, the list goes on. So any glandular tissue making EPCAM is really within our target. The, what we're seeing to date, we'll get into in the Congress, but we're setting expectations that roughly 25 to 30 patients will be discussed at this Congress. We'll talk about the safety that we're seeing and then the level of activity. We've recently noted that we have a patient that is over a year without progression and then one that is now over eight months without progression, both with colorectal cancer. And, you know, just to help remind us, so this is not a CAP, right? this is a bispecific or it's a cab okay and it's in fact a double cab so we say it's a dual cab and what that means is that it's conditionally binding on the t-cell arm the CD3 as well as the epcam and so what that does is it multiplies the conditionality Jay do you want to speak a little more to that yeah I can mention it I mean in our preclinical studies because the tumor targeting arm which is the epcam that receptors on the tumor cell and then we have the cd3 receptor on the t cell so you so on many antibodies you'll see it's a you know a homodimer so one arm can bind and

then it can still attack the tumor both arms bind attacks the tumor in this case you have to have the epcam binding and on the tumor cell and you have to have the binding to the cd3 on the t cell and only if you get both of those binding do you get it and do you get it correctly so if you added in selectivity you can just a simple way to think about it if I got tenfold selectivity on one arm and I got tenfold selectivity on the other arm I'll get a hundredfold selectivity that multiplies how good the selectivity is and we see in this in our animal testing that we're approximately two hundred fold a selectivity based on this so it's fundamentally differentiated even from our other calves in terms of how potent this is and we think that's a pretty powerful opportunity. And given its broad spectrum of expression, both on tumor cells and on normal cells, you really need a technology like this if you expect to turn that into a drug. And that's what Amgen didn't have back in the day. Got it.

And if everything goes well, according to plan, kind of what are the next steps, right? You mentioned this is an interim look. Do we then kind of wait for, you know, a recommended phase two dose, and then, you know, what's the path forward? Is it monotherapy? Do you evaluate combo? How does this, you know, kind of continue down the clinical development paradigm?

Yeah, so we're obviously looking for responses. We'll be gratified to see them when they occur. You know, I have no sense of exactly when that's going to occur, whether it's at 300, at 900, or higher in terms of microgram dosing. We contemplate the use of combinations where a PD-1 inhibitor might be added to really enhance the T-cell function and prevent T-cell exhaustion. Those are considerations that we're making, as well as what indication. I thought that the very recent report from Amgen that tarlatimab had a survival benefit is very good for other T-cell engagers in the clinic because it shows that in the lung environment, the T-cell engager can create that immune synapse in small cell lung cancer. And so I'm particularly intrigued with non-small cell lung cancer and, of course, colorectal cancer with 100% EPCAM expression. That makes it very straightforward without the need for a companion diagnostic.

I will add that in the animal modeling data as a monotherapy, which is the way we really think it will work in that setting, it's about 200 micrograms was what the modeling suggests. So there can be error around that, but we kind of feel like 300 micrograms is really the first level that we have a shot of starting to see the PRs. Based on the guidance of that, we think this can work quite well as a monotherapy. I mean, obviously, we can do future combinations as long as we maintain the safety that we're currently seeing. But I think it's a pretty exciting opportunity given other T-cell engager companies that are seeing excitement across this field. But to do it with Epcam is a whole other level, and that's because it's such a broad pan-cancer opportunity.

And just remind me, we should be expecting to see, you know, 300.

Yeah, I think 300, we should have some scans on that, yeah. By the data update? I'm hoping, yeah.

And hopefully, we'll see something encouraging, since already at subtherapeutic levels, we're starting to see hints of activity.

Yeah, if we see some good, stable disease, maybe we see it in a PR. We'll have maybe three-plus patients on that particular dose level, so we'll see.

So I want to bring Sherry into this discussion because, you know, Epcam as a target, I think a lot of investors have largely, you know, call it dismissed it, right? Because you brought up several other companies that have tried and failed. What is the potential market opportunity here? How should we be thinking about that?

Yeah, I mean, so Epcam, as Eric noted, is widely expressed across a number of different adenocarcinomas, breast, lung, colorectal. I think, you know, as you know, it's also widely expressed on normal tissue. So a dual-cab is really something that we think will be differentiated and we'll be able to take this to market. So it could potentially be, given its expression, given what we can do with a dual-cab, could be a pan-cancer drug across the adenocarcinomas that Epcam is widely expressed. So clearly a multi-billion dollar opportunity if we're able to really bring this forward.

As an example, it's expressed 100% of colon cancer tumors. 100%. I mean, that's kind of very unusual for a cancer target. And multiple ones in the 90s, plus percent.

Terrific. Look forward to seeing some of that data at ESMO GI. I want to switch gears to the Axel product, right? that you have in development. The KRAS mutant non-small cell lung cancer data look really impressive. And I think in your most recent deck, you guys announced results yesterday. Your deck is updated. So I'd urge investors to kind of take a look at that. You've shown kind of historical overall survival curves. You've shown, you know, what your current survival curve looks like. Could you maybe, you know, talk us through that and kind of help set expectations with the caveats that, you know, obviously cross-trial comparisons, you know, need to ultimately be proven out in double-blind, you know, randomized studies.

Yeah, sure. So, yeah, we've seen unprecedented one- and two-year landmark survival in MKRAS-mutated non-small cell lung cancer of 67% and 59% respectively. And to put this into context, if you look at previous studies In patients who have MKRAS, non-small cell lung cancer, treated with docetaxel, you're seeing one- and two-year landmark survival of less than 40% and less than 20%. So a substantial survival benefit that we're seeing over the long term. I think it's also important to note that we're seeing a similar type of survival benefit in sarcoma, subtypes of sarcoma, which we just included in our corporate deck. And this is important because seeing this type of survival in two different indications, I think, gives us, strengthens our conviction that MECV is actually improving the natural history of the disease and is allowing patients to live considerably longer, despite what they might receive after. So, I mean, you know, this is, we're excited about it. We believe that it's differentiated from what standard of care agents that are currently available on the market can do, as well as potentially investigative agents as well.

Now, can you just take us through the, it's an ongoing study you're following. There are patients still on therapy and living longer, I believe, just correct me if I'm But, you know, when might the next update be that we can take a look at this? And then also, I guess even more importantly, what are the next steps for this program, right? Because we can continue to follow and maybe do three-year landmark and things along those lines. But what, you know, what can you do to either, A, you know, move it forward yourself or trigger a potential partnership opportunity?

So we've had guidance that the trial would be against docetaxel kind of standard of care in second line plus therapy. What we would hope to do is add a few patients randomizing against docetaxel as kind of a preparation for that phase three trial. In parallel, though, we are in discussions with several partners around this asset. And so we think that it's likely that that one may be advanced together with somebody, but we'll see. And then I think that from there, we have quite a bit of data in Axel, but I think we believe very strongly it's going to be a Q2W 1.8 mg per kilogram. That's going to be our dose. We're seeing high safety. We're seeing, I think, 25% confirmed response rate. But really, the thing that ultimately gives you approval in this space is the overall survival. And that's wildly differentiated. And as Sherry said, we've just mirrored the same type of activity in soft tissue sarcoma across multiple types with the axle as well there. And to see that happening in two different indications really gives us increased confidence that we're dealing with something very important and powerful. And I think that's kind of our base plan. And Epcam, we're putting some basic, small priority, maybe large priority on that one, above all, because we really want to drive that. It's very unique. There's low competition in multiple areas with that drug. So I'd say full pressure on finishing the dose escalation, driving expansion, then right behind and with that is the actual activity. And with ROAR2 and with CTLA-4, we're focused on partnering and have active discussions there.

I'm going to end with ROAR2 and CTLA-4. But just going back to the, you know, with MICV, the combination with docetaxel, sorry, not combination, going against, right, when do you think you might start that?

Well, I think our target is to have that data in the first half of 2026. and our runway will allow us to get to that end point and a little beyond. And hopefully, we're believing that we'll be dropping a deal in before that happens, and so we'll go much further.

And when we look at the landscape, right, we have KRAS inhibitors, the landscape is changing, right? And we think ultimately better for patients.

But as you guys look at it, where do you see this, you know, kind of potentially fitting fitting in is it ultimately in combination is it you know what straight up against docetaxel in the worst of the worst patients how do you think about it i would just start off and let eric finish this but i just want to point out that we're not seeing a lot of overall survival uh good results that ultimately require the full approval okay there's uh i think from a comparator standpoint, this is very strong. And you may not have so much competition when it comes to that ultimate overall survival standpoint as a monotherapy. Clearly, there's opportunities as in combination with safety. But Eric, you can put a finer point on all that.

Well, I see our approach as orthogonal and absolutely could be combined. We haven't been combining with adagracib or sodiracib or the revolution medicine drugs, but certainly could be done but we got a bit of a head start now we have data showing a remarkable three-year overall survival no no median overall survival yet with continued follow-up eight patients continuing in long-term follow-up regardless of a variety of different treatments they've received so so i think you know these results these survival data speak for themselves And, obviously, we would need to prospectively confirm that in a randomized pivotal study against the standard of care dosetaxel. But, unlike the other agents, you know, the survival endpoint has been particularly challenging, as we saw from the ODAC with Amgen and Sotiracid and the Code Break study not being interpretable for overall survival or clinical benefit.

And correct me if I'm wrong, Eric, but my understanding is there's a very, very high selectivity to mutant KRAS versus those that are wild-type KRAS patients. Has that already been determined in your study?

I think quite clearly we put out a poster in December at what was called the Hot Topics in Non-Small Cell Lung Cancer Meeting. It's available on our website. We put all of our presentations there. And we saw a very clear survival benefit amongst the patients that got the Axel ADC who had the mutated KRAS compared to the wild type. So the wild type, you know, of people who got the ADC is tracking right along where docetaxel would be. But ours has a plateau and a survival benefit. it. And so that's the moment we realized we found our target population biologically defined using mutated KRAS, the genotype.

And I would just add that we continue to see a high correlation of axil and MKRAS expression. So mechanistically, there's evidence there that makes sense as to why we would see what we're seeing.

Got it. And we have an internal control. I mean we've compared our overall survival with the non-MK RAS versus MK RAS and it's it's definitely differentiated. You can see responses in the non-MK RAS group but when it comes to overall survival it's like black and white. And mechanistically it's very logical. So we're hitting the mechanism that's the driver.

So in the last call it two and a half minutes that we have left I want to talk about partnerships because it's not only a way to help you extend your cash position I'll end with Rick at the end regarding cash position but extend your cash position but then also get you know additional external validation you know and the like how are you thinking about partnerships especially with you know the the ROAR asset and the CTLA for I think you have some updated data coming out at ASCO regarding your ROAR asset So we look to kind of help set expectations and probably end with, what do you think the chances are that a deal gets done this year?

Well, I think the chances of a deal getting done are very high. We're very confident that we're going to do it. And because of the stage of the discussions, I also think that leaning on ROR2 just for a moment, I think this differentiated activity in HPV-positive patients really differentiates from the PAC. It's something that's poorly served with EGFR agents, and this is a large but niche area, kind of in the half a billion to $750 million area. If we focus in second line, HBV positive, you can have a more modest trial and opportunity for accelerated approval. That's attractive to people, and so we think we're going to make some good progress there. Some of that data was first revealed in March, so that's kind of new, but it's making an impact. And then, of course, I think the actual safety does lend itself for people that like to think about combination therapies, already have a drug that can fit in. So we know there's some discussions in that area. So I feel pretty strongly that we're going to move a partnership here with non-dilutive capital, and we'll keep driving here. So I don't know if that answers your question, but we're pretty excited about it.

I like the confidence of a deal happening.

It's based on the stage of those discussions. Yeah, perfect. You never have a guarantee, but I feel, if anything, it's likely this pretty likely.

So 30 seconds left. I asked Rick just regarding the cash position you guys reported yesterday. How long does that kind of take you? And I won't speculate on how long, if you get a deal done, how long that takes you. But how about with the existing cash?

Well, we know it goes into the first half of 2026, but maybe, Rick, you can provide a little color on what's happening in the upcoming quarters at a general level.

Yeah, we finished the first quarter at $32 million in cash, and as Jay just mentioned, that in itself is sufficient to carry us into 2025. 26, excuse me, 2026 by itself. But it's always been the strategy of the company to develop its programs in partnership with corporations, major corporations. And we're in active discussions right now. And, of course, that will be non-dilutive financing to be able to carry these programs forward. Well, thank you guys very much.

I really appreciate the update. Appreciate it.

Thank you.