BioAtla at Citizens JMP Life Sciences: Strategic Partnerships in Focus

On Wednesday, 07 May 2025, BioAtla (NASDAQ:BCAB) presented at The Citizens JMP Life Sciences Conference 2025, providing a strategic overview of its clinical-stage oncology assets. The company highlighted the unique capabilities of its conditionally active biologic (CAB) platform, while also discussing financial sustainability and partnership pursuits. Despite positive clinical data, the focus on securing partnerships underscores the challenges of advancing to Phase 3 trials.

Key Takeaways

• BioAtla’s CAB platform offers increased potency and safety, positioning it favorably for growth.
• The company expects non-dilutive financing through partnerships, with cash sufficient to fund operations into 2026.
• Promising survival rates in KRAS-mutated non-small cell lung cancer were reported, with plans for a new trial in 2026.
• Active discussions for partnerships on ROR2 and CTLA-4 programs are underway, with confidence in securing deals.

Financial Results

• BioAtla ended Q1 2024 with $32 million in cash, expected to sustain operations into 2026.
• The company is pursuing non-dilutive financing through strategic partnerships.

Operational Updates

• EpCAM Program:

- Dose escalation study ongoing, with interim data to be presented at ESMO GI.

- Early signs of activity in colorectal cancer, with some patients showing extended periods without progression.

• Axle Program:

- Reported high one and two-year survival rates in KRAS-mutated non-small cell lung cancer.

- Plans to initiate a randomized trial against docetaxel in 2026.

• ROR2 Program:

- Updated data to be presented at ASCO, highlighting potential for accelerated approval in HBV-positive patients.

Future Outlook

• BioAtla is focused on advancing its programs through strategic partnerships.
• The company plans to explore combinations with PD-1 inhibitors in the EpCAM program.
• A randomized trial for the Axle program is planned, targeting overall survival as the key approval endpoint.

Q&A Highlights

• The CAB platform is validated by promising clinical data, especially in the Axle program.
• EpCAM’s potential as a pan-cancer drug could represent a multi-billion dollar opportunity.
• BioAtla is confident in securing a partnership deal within the year, supported by ongoing discussions.

Readers are encouraged to refer to the full transcript for a detailed account of the conference call discussions.

Full transcript - The Citizens JMP Life Sciences Conference 2025:

Rudy, Host: Alright. 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 Leidich, chief commercial officer, and Rick Waldron, CFO. So welcome everyone.

Appreciate you guys being here.

Jay Short, CEO, BioAtla: Thank you, Rudy.

Rudy, Host: I I never know who exactly is in the audience or who’s listening on the webcast who knows the Bio Atlas 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 Bio Atlas is about. Sure.

Jay Short, CEO, BioAtla: Us. 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 asset three assets three are in phase two. 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.

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.

Rudy, Host: Great. So, you know, let’s jump into well, I guess before we jump into the pipeline, let’s take it 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 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 and even the competitor date data, as well as deals that are being done, right, in the in the space, Can you maybe, you know, can you confidently say that the platform has been validated and now it’s just a 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?

Jay Short, CEO, BioAtla: 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, we think one of the greatest examples we’ve seen is Axle as our target. 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 MKRAS mutations in lung cancer mechanistically. Gas six, which is an activator of Axle is, one of the byproducts of MKRAS mutations and that whole cycle is what causes tumor resistance. And so it’s a really important target, not only for lung cancer, but in a lot of other indications. But yet two companies failed to show 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 a 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 a 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. We’re, seeing very strong data, going out over two years now. Fifty nine percent survival. We haven’t hit a median yet on 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 ninety percent 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 C 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.

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.

Rudy, Host: Excellent. So let’s let’s jump into the EpCAM program. We have some data coming out. First time we’re seeing, you know, 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?

Eric Sievers, CMO, BioAtla: Sure, so I want to emphasize this is 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 three hundred micrograms at the treatment dose every week. 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 F chem is an attractive target, it’s expressed so widely on adenocarcinomas 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 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.

Rudy, Host: And you know, to help remind us, so this is not a cab, right? This is a bispecific or

Eric Sievers, CMO, BioAtla: 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 c d three, as well as the F chem. And so what that does is it multiplies the conditionality.

Jay, do you want to speak a little more to that?

Jay Short, CEO, BioAtla: Yeah, can mention it, I mean in our preclinical studies because the tumor targeting arm, is the EpCAM, that receptor is on the tumor cell, then we have the CD3 receptor on the T cell. So on many antibodies, you’ll see it’s a homo dimer, 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 the binding to the c d three 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 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. So we see in this in, our animal testing that we’re approximately two hundredfold a selectivity based on this. 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.

Rudy, Host: 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?

Eric Sievers, CMO, BioAtla: 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 three hundred, at nine hundred or higher in terms of microgram dosing. We contemplate the use of combinations where a PD one 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 Tarlatumab 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 straight forward without the need for a companion diagnostic.

Jay Short, CEO, BioAtla: I will add that in the animal modeling data as a monotherapy, which is the way we’re really thinking it will work in that, setting. It’s about two hundred micrograms was what the modeling suggests, you know. So there’s can be air around that, but we kind of feel like three hundred 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 we’re 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 another level and that’s because it’s such a broad pan cancer opportunity.

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

Jay Short, CEO, BioAtla: Yeah. I think 300 we should have some scans on that. Yeah.

Rudy, Host: By the by the data update at

Jay Short, CEO, BioAtla: I’m hoping. Yeah. Yeah.

Rudy, Host: And and hopefully we’ll we’ll see something encouraging since already at subtherapeutic levels, we’re starting to see hints of of activity as well.

Jay Short, CEO, BioAtla: Yeah. If we see some good stable disease, maybe we we see it in a PR, you know, we’ll have maybe three plus patients on that particular dose level. So we’ll see. But

Rudy, Host: So wanna 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?

Sherry Leidich, Chief Commercial Officer, BioAtla: Yeah, mean, so EpCAM, as Eric noted, is widely expressed across a number of different adenocarcinomas, breast, lung, colorectal. I think, 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.

Jay Short, CEO, BioAtla: As an example, it’s expressed one hundred percent of colon cancer tumors. One hundred percent. I mean that’s kind of very unusual for a cancer target. And multiple ones in the nineties plus percent.

Rudy, Host: Terrific. Look forward to seeing some of that data at ESMO GI. I want to switch gears to the Axle product, right, that you have in 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 kinda 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 and double blind, you know, or random studies.

Sherry Leidich, Chief Commercial Officer, BioAtla: Yeah, sure. So, yeah, we’ve seen unprecedented one and two year landmark survival in KRAS mutated non small cell lung cancer of sixty seven percent and fifty nine percent 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 forty percent and less than twenty percent. 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.

This is important because seeing this type of survival in two different indications, I think strengthens our conviction that MEKV 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.

Rudy, Host: 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 wrong. But when might the next update be that that we can take a look at this? And then also, I guess, more importantly, what are the next steps for this program? Right? Because we can continue to follow and 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,

Jay Short, CEO, BioAtla: we’ve had guidance that the trial from the FDA, that the trial would be against docetaxel kind of standard 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 Axle, but I think our we believe very strongly it’s gonna be a q two w one point eight mgs per kilogram.

That’s gonna be our dose. We’re seeing high safety. We’re seeing, I think, twenty five percent 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 smeared 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 indication 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. Epcam, we’re putting some basic price, small priority, maybe large priority on that one above all because we really wanna drive that. It’s very unique.

There’s low competition in multiple areas with that drug. So I’d say full pressure on driving that dose, getting to finishing the dose escalation, driving expansion, then right behind and with that is the actual activity. And with ROR two and with CTLA four, we’re focused on partnering and have active discussions there.

Rudy, Host: Yep. I’m gonna end with ROR two and CTLA four, but just going back to the the, you know, with MiKV, the the combination with docetaxel sorry. Not combination. Ran one last year. When do you think you might start that?

Jay Short, CEO, BioAtla: Well, I think our target is to have that data in the first half of twenty twenty six, and our runway will allow us to get to that end point and a little beyond. So and hopefully, we’re believing that we’ll be dropping a deal in before that happens and so we’ll go much further.

Rudy, Host: Got it. And when we when we look at the landscape, right? We we have, you know, KRAS inhibitors, we have the landscape is changing, right? And and we think ultimately better for for 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?

Jay Short, CEO, BioAtla: I would just start off and let Eric finish this, but I I just wanna point out that we’re not seeing a lot of overall survival, good results that ultimately require the full approval. Okay? There’s, 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 in combination with safety. But Eric, you can put a finer point on all that.

Eric Sievers, CMO, BioAtla: Well, I see our approach as orthogonal and absolutely could be combined. We haven’t been combining with adagrasib or sotorasib 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 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 I think, you know, these results, these survival data speak for themselves and obviously we would need to prospectively confirm that in randomized pivotal study against the standard of care docetaxel. But unlike the other agents, the survival endpoint has been particularly challenging as we saw from the ODAC with Amgen and sotorasib in the code break study not being interpretable for overall survival or clinical benefit.

Rudy, Host: 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?

Eric Sievers, CMO, BioAtla: I think quite clearly, we put out a poster in December, what was called the Hot Topics in Non Small Cell Lung Cancer It’s available on our website. We put all of our presentations there and we saw very clear survival benefit amongst the patients that got the Axle 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 and so that’s the moment we realized we found our target population biologically defined using mutated KRAS, the genotype.

Sherry Leidich, Chief Commercial Officer, BioAtla: And I would just add that we see, we continue to see a high correlation of Axle and MKRAS expression. So mechanistically there’s evidence there that makes sense as to why we would see what we’re seeing.

Jay Short, CEO, BioAtla: Got it. And we have an internal control, I mean we’ve compared our overall survival with the non MKRAS versus MKRAS and it’s it’s definitely differentiated. You can see responses in the non MKRAS 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.

Rudy, Host: So in the last, call it two and a half minutes that we have left, I wanna talk about partnerships because Mhmm. 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 and the CTLA four? I think you have some updated data coming out at ASCO regarding your Roar asset.

We’d love to kinda Yep. That’s set expectations and probably end with, what do you think the chances are that a that a deal gets done this year?

Jay Short, CEO, BioAtla: Well, think the chances of this deal getting done are very high. We’re very confident that we’re gonna do it. And, because of the stage of the discussions, I also think that, leaning on war two just for a moment, I think this differentiated activity in HBV positive patients really differentiates from the pack. 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 $750,000,000 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 gonna make some good progress there. Some of that data, it 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 that there’s some discussions in that area.

So I feel pretty strongly that we’re gonna we’re gonna move a partnership here, with non dilutive capital and we’ll keep driving here. So I don’t know if that answers your question No. Any, but we’re pretty pretty excited about it.

Rudy, Host: I like the confidence of a a deal happening.

Jay Short, CEO, BioAtla: It’s based on the stage of those discussions. Yeah. Perfect. You never have a guarantee, but I feel if anything is likely, that’s pretty likely.

Rudy, Host: So thirty seconds left. I asked Rick just regarding the cash position you guys reported yesterday. How long does that, you know, kinda take you? And I won’t speculate on on how long it you know, if you got a deal done, how long that takes you, but how about with the existing case?

Jay Short, CEO, BioAtla: Well, we know it goes in the February, but maybe Rick, you can provide a little color on the what’s happening in the upcoming quarters at a general level.

Rick Waldron, CFO, BioAtla: Finished the first quarter at $32,000,000 in cash. And as Jay just mentioned, that in itself is sufficient to carry us into 2025.

Jay Short, CEO, BioAtla: ’20 ’6.

Rudy, Host: ’20 ’6,

Rick Waldron, CFO, BioAtla: excuse me, ’26 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.

Rudy, Host: Excellent. Well, thank you guys very much. I really appreciate the update. Appreciate it. Thank you.

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