Okay, got it. Perfect. All righty, let's get started, everybody. Welcome to the next session of the Piper Sandler Healthcare Conference. My name is Kelsey Goodwin. I'm one of the senior analysts here. I have the team from Whitehawk in the room with the President and CEO, Dave Lennon, here next to me. Welcome. Thanks for joining.
No, thank you, Kelsey. It's a pleasure to be here.
Of course. Thank you. Yeah, let's start with, for investors that are less familiar, let's start with a quick one- to two-minute summary of Whitehawk and where we stand kind of heading into 2026.
Sure. So Whitehawk is a company that was formed through the in-licensing of a three-asset ADC portfolio from WuXi Biologics that we initiated in December of last year and completed that transaction earlier this year and relaunched as Whitehawk. We're developing these ADCs in a number of solid tumor indications with our first programs going into the clinic this quarter. So our first two programs are submitting INDs in this quarter.
Perfect. In terms of the programs that you brought in, maybe just walk us through the platform that designs them, what differentiates that approach, and why you think these are differentiated.
Yeah, so the ADC field is one that has been continually evolving over the last really two decades. The biggest advance, I think, has been the transition from prior, largely tubulin inhibitor-based platform payloads into the topoisomerase class of ADCs. And we're part of that evolution. What people have come to understand is how you attach that topoisomerase inhibitor to the antibody that you're using within your ADC is really important. And generating stability in that platform, the proper release of payload in that platform, good PK characteristics in the circulation are all some of the important characteristics that end up defining a great ADC. What's different about our platform and what's unique is that we've designed and have chemistry and engineering that allows us to really generate high-stability ADCs which limit free payload release in the circulation.
That effect limits the side effect profile that's typically associated with topoisomerase-based ADCs, allowing us to hopefully achieve better potency with less side effects, which, of course, is always the goal with cancer therapeutics.
Great. And in terms of this platform, so you brought in three specific targets. Have we seen other programs from this platform elsewhere with different targets?
Yeah, the program was developed by a company, or the platform was developed by a company called Hangzhou DAC, based out of China in Hangzhou. They, as former ImmunoGen scientists, really brilliant scientists from a chemistry perspective, who developed this linker payload technology. And they have an asset they're developing in China called DXC006. It's a CD56-based ADC that is currently in dose escalation studies in Chinese patients. And we look, hopefully, to see data from that program sometime in 2026.
Okay, perfect. And then maybe before we dive into each of the specific targets, I guess high level, when you were bringing in these programs, what kind of targets were you looking for? Which ones did you think you'd have high success with?
Yeah, so the ADC field is very crowded, and there's often a crowding around targets that are successful. So if you look at HER2 or HER3 or TRP-2, there are literally dozens of follow-on programs that quickly are developed behind those. So when we look for our markers, the challenge is always finding that threading the needle between novelty and competition that exists within the marker space. And what we try to do is pick markers where we like to say they were validated but not inundated. So validated in the sense that there were programs proceeding against those targets that started to show some efficacy. But the targets weren't so competitive yet that we couldn't see our way to being first or second to market. And that's how we selected the targets that ended up being part of our portfolio.
Okay, perfect. In terms of one of your lead assets, 007, PTK7 targeted ADC.
Our James Bond program.
Yeah. Tell us about this target and what we know about this target from other programs?
Sure. Yeah, I mean, it's a classic example of our strategy, so PTK7 previously had been a target utilized by a program called Cofetizumab Pelidotin, which was being developed by Pfizer and AbbVie a number of years ago. Initially, they had developed it in non-small cell lung cancer, ovarian cancer, and triple-negative breast cancer. That program showed some early promising efficacy signal, but the asset itself had some issues with class-related toxicities of its payload, which was a tubulin inhibitor MMAE class of payloads, and so it's a classic example of a molecule showing some good initial efficacy, but the first-generation ADC not being able to actually deliver fully upon the promise because of the side effect profile, so we're really excited about that validation of the target, and that's what we built this program off of.
Okay, understood, and so that is working towards an IND. Maybe have you shared anything preclinically or anything you can share about what gives you confidence that this is a differentiated program?
Yeah, so we are submitting an IND for that program this year. We'll present preclinical data more fully in the first half of 2026. But what we really are excited about are kind of three aspects of our technology and its application here. So one is the targeting antibody itself. So the antibody is a high-affinity antibody to PTK7. It performs better when utilizing the same payload than cofetizumab pelidotin. So we know that it's actually more potent of an antibody or more effective as an antibody. It's also attenuated. So we attenuate the FC portion of the antibody to ensure that we don't get non-specific uptake of the ADC, which we think should lessen some particular side effects sometimes associated with topo-based ADCs. The second point that underlines our technology is the bioconjugation approach, which improves stability, which I mentioned before.
And then the third component is really the business end of the program itself, the payload that we're utilizing and the release profile of that payload. The payload here is very similar to DXd in its properties. And so in many ways, because we've combined it with a more potent antibody, better linker, we're able to generate that potency, but we should anticipate seeing a much cleaner side effect profile from this program. And that's what we think will make it best in class.
Okay, understood. In terms of the target PTK7, maybe just remind us, what tumors is that relevant for, and how are you thinking about lead indications for this program?
In some ways, with PTK7, I'd be better off telling you what it doesn't get expressed on because PTK7 is actually the most broadly expressed tumor target that's really yet to have an approved mechanism against it or approved ADC against it. So it's present in 70% of all tumors. It is consistently expressed from early onset of the tumor through metastases and progression of the tumor. You do not lose PTK7 expression. So it's kind of an ideal tumor target, and then it's really not expressed on normal tissue at all, which makes it a really great ADC target for us because we're not going to hit other tissues with our ADC. Ultimately, we're initially starting in lung cancer, ovarian cancer, and endometrial cancer, which are high PTK7-expressing tumors, but this is a tumor target that can go also into head and neck cancer, colorectal cancer.
It was originally cloned as a colorectal cancer gene, and ultimately, anywhere within the GI tract, as well as a variety of other tumors, also express PTK7, so really, one of the most, really just to reiterate, a broadly expressed tumor target that has a lot of potential.
In terms of moving it into a phase one study, how do you think about what that would look like and also what you would need to see to kind of advance into one of those indications?
Yeah. So we're really excited because the profile of our HWK-007 anticipates that we will be at a starting dose initially that we think could be effective already. And so we'll be starting at a relatively high dose or above our minimally effective dose, which could allow us to accumulate information very early in the dose escalation. So that's a great starting point for us. And we anticipate enrolling patients in dose escalation and backfill cohorts that'll give us some signal in terms of where to go with the three indications I mentioned. What we do anticipate is in a competitive field like non-small cell lung cancer, typically what you're seeing now is 35%-40% ORR as an early benchmark for efficacy within that non-small cell wild type or EGFR mutant population.
And then on the gynecological side, both ovarian and endometrial, typically about 50% is the bar we'd like to see in our early phase one studies to continue to progress those programs. So those are the internal bars we set and are based on kind of what some of the latest generation of products are showing. We do think we can beat those, and we're really confident on our approach.
Okay, got it. In terms of just emerging competitors, how do you kind of see the field shaping up over the next few years?
I mean, 2026 is the year of PTK7 because, as sometimes happens, there's a lot of interest in this target that was, I think, initiated at the Pfizer data I mentioned earlier, but people had to rethink it because it was a negative outcome for that product. So not as easily of a fast follower. But now we're seeing two to three years later, a number of companies come out of the woodwork, so to speak. We thought we were unique, but not so much. But it is going to be a competitive space. So a number of companies have started programs. So Day One and Lilly are the kind of leads on the PTK7 side, started programs this year. But also we had recent announcements from Kivu Bioscience as well as IDEAYA that they've started their PTK7 or are starting their PTK7 shortly.
And then Sutro themselves talked about a dual payload-based PTK7 ADC that they're planning to file in late 2026, early 2027. So really, 2026 is the year of PTK7. It'll be really interesting to see what develops.
Yeah, no, that's super interesting. Looking forward to 2026 in that case. Shifting gears to HWK-016, the MUC16-targeted ADC. Maybe walk us through this target, the rationale for choosing this target, and why maybe this platform is particularly well suited against this target?
Yeah, sounds good. I have no clever name for this target. Just 016, MUC16. Really interesting target because MUC16 is what we like to say is a super expressor in gynecological cancers. So in ovarian cancer, for example, is often expressed 3 to 10 times higher than HER2, FRα, CDH6, NaPi2b, anything you can mention in that space. So with HWK-016, we have a great starting point of a highly expressed tumor target on the surface of gynecological cancers where we're initially focusing our phase one program. The trick with MUC16 has always been, as highly expressed as it is, it's cleaved at the surface of the cell. And so MUC16 gets released into the circulation as the circulating biomarker CA125, which is the most commonly utilized biomarker, blood-based biomarker in gynecological cancers.
The challenge has been that this creates a problem for targeting MUC16 because you end up with antibodies that target circulating MUC16 in the blood rather than getting to the tumor. What we've done here is redesign the approach to targeting to actually go after the part of MUC16 that's retained at the tumor cell, which allows us to bypass circulating CA125 and get to the tumor more effectively. This is a unique design. There's no ADCs against MUC16 that utilize this approach or generally utilize MUC16 because it has been difficult to target otherwise.
Understood. In terms of the status, kind of where is it now? What are the guided timelines? And have we seen any preclinical data?
Yeah, we're basically on the same timeline between HWK-007 and HWK-016. So a couple of weeks behind. We're submitting an IND also in quarter four for this program, and look to start the clinical trial in Q1. We have not released preclinical data on this program yet, but would anticipate that in the first half of 2026.
Okay, got it. And then in terms of relevant cancer types, it sounds like you'll start in ovarian and endometrial. Is there any other tumor types this might be relevant for?
Yeah. Yeah, I mean, the natural place to start with MUC16 is those two indications. But there's also some really interesting segments like pancreatic cancer, mesothelioma, as well as about 40% of non-small cell lung cancers that express high levels of MUC16 and are quite particular in how they behave, which we think makes for a really interesting and unique proposition in terms of indication expansion in places where we really don't have ADC solutions yet. So that's an exciting proposition for us that once we demonstrate differentiation of this program and its effectiveness, we can go into those really sometimes very hard to treat cancers.
Understood. In terms of the competitive dynamics here, I guess what other emerging assets do we have against MUC16, and what have we learned from prior assets trying to target this?
Yeah, so again, that strategy of validated but not inundated applies here too. So Genentech actually ran a couple of programs against MUC16 back a number of years ago now, but they showed some really promising initial response rates, like over 40% response rate in ovarian cancer, but suffered from two issues. One is that circulating CA125 that I mentioned. Their antibody targeted that portion of the molecule. You may ask why? It's a very high affinity part of the molecule. It produces really great antibodies. But unfortunately, that also led to them being taken up in the circulation, and they had some side effects associated with the class of MME. So overall, some really promising efficacy signal from that early data. Since then, there's really been a dearth of MUC16 development for that because of the targeting issues.
There is another approach to targeting the membrane retained portion of MUC16 that's being taken by Regeneron with their TCE platform or TCE platforms in CD3 and CD28. And they have some early data showing some initial responses, and they're currently moving that program into a phase two. So we'll get some idea. Obviously, a different modality, but same targeting approach.
Understood. In terms of the lead programs in ovarian and endometrial, how do you think about the kind of market opportunity there? What's the unmet need?
Yeah, well, there's clearly an unmet need for new therapies. Certainly, you're seeing IO take a leading position within those, but second line and third line options for those patients are limited. There are a number of ADCs that are being developed within the ovarian and endometrial space, and it'll be interesting to see how that competition stakes out, particularly FRα, CDH6, and now NaPi2b, I think is the latest, to show some promising data within that space. So there's definitely intra-target competition that'll be developed. We'll have to see how each of those programs gets profiled over time, and that'll be part of what we'll be working on.
Understood. And for both of 007 and for 016, have you guided to when we might see initial data?
Yeah, so our commitment is to bring data around Q1 2027. We want to come back to the market and back to investors with a relatively comprehensive set of data for a few dozens of patients within each of those programs so that we can really be clear about the profile and how we want to take those programs forward.
Got it. And for 016, are you also anticipating that you're starting at an active dose?
We do, yeah.
Okay, understood. Shifting to HWK-206, your third asset. Tell us about this asset and the target.
Yeah, so the third asset's same investment thesis. So SEZ6 is seizure protein 6. It's a CNS transmembrane protein that's often overexpressed in cancers of neuroendocrine origin. So this is small cell lung cancer and high-grade neuroendocrine neoplasia. The validation here is a program from AbbVie called ABBV-706, which has shown some really promising data in small cell lung cancer and neuroendocrine neoplasia, but also has some challenges on its side effect profile. So high rates of neutropenia and other hematological toxicities associated with that payload. So here we're the second to market against this target. Really think we have the opportunity here to demonstrate a best-in-class profile from an efficacy and safety perspective, which is really important when we consider not just initial late-line usage, but moving into earlier lines of therapy, particularly in combination.
That's where we think this program, but our platform overall, should perform better when we think about a safer profile that can be combined with the likes of IO, chemo, anti-VEGF therapies down the road.
In terms of the ADC construct, I guess what makes 206 unique?
The uniqueness of 206 is really around our targeting approach. 206 uses a biparatopic antibody towards the SEZ6 target. Biparatopic antibodies are antibodies that combine two different epitopes on a single molecule. What that allows in the context of a cell is the concatenation of molecules at the surface of the cell, simple side-by-side clustering of receptors, which improves internalization. This molecule binds better, internalizes faster, and therefore we think will deliver better performance than AbbVie's program or other SEZ6-directed antibodies.
In terms of where this program stands, what's the status of it and what's kind of the guided timelines that you've given so far?
We're currently in IND enabling work for this program. We plan to submit the IND mid-2026 and start the clinical trial in the second half of next year with potentially early dose escalation data around the same time as the first two programs.
Okay, got it. In terms of the lead indications for 206, I guess how do you think about designing the phase 1 trial and what's kind of the benchmark, the market opportunity? How do you think about that?
So neuroendocrine really centers around small cell and neuroendocrine neoplasia. The benchmark for small cell these days is around 50%-60% ORR in initial dose escalation studies, and for neuroendocrine, anything above 30% would be good for those patients. They have very limited options and a lot of progression. The nice thing about SEZ6 relative to some of the other categories, or other markers in the field, like DLL3 or B7-H3, is it's expressed at two to four times the rate of those markers. And so we have a better starting point in terms of marker expression to compete with not just ABBV-706 molecule, but the other programs that are coming into this space.
On that, I guess, who else is entering this space? How is this market, kind of, how do you expect it to evolve over the next few years?
Yeah, so you definitely have the DLL3 ADCs. Well, first DLL3 TCE has performed relatively well within the context of small cell and kind of set a new paradigm for treatment for a number of those patients in the second line setting. And certainly, DLL3 ADCs are coming behind that. So Zai Lab and IDEAYA have programs that are in phase one against DLL3. And then you add B7-H3, the lead being from the Daiichi Sankyo program being there, but multiple competitors also in that space, AZ, GSK, others. And so this can be quite a crowded space quite early because small cell is not small. It's not as big as non-small cell for sure.
And so we think that, again, we can be best in class, but we also think the advantage here might be in the neuroendocrine space where we have better expression, less competition, and an opportunity to improve upon a relatively lower bar that's been seen in those patients.
I guess what is the competitive dynamic in that setting?
It's more limited right now. People haven't focused on it as much, and we haven't really yet seen the data from the B7-H3 and DLL3 ADCs in those indications.
Okay, understood. And that one was IND mid-2026 and then starting the trial second half?
You got it.
Okay, perfect. Maybe just remind us where you stand in terms of cash runway and then just remind us the catalyst lineup?
Right. So we have cash through early 2028, which should be almost a year before we would or after we would present our initial data across all three programs. We start this quarter with $163 million that was part of the financing we did back in December of last year, as well as the sale of our prior asset that we had at that time, so we're in a great position to not have to raise money again until we have those inflections. Over the course of 2026, we'll obviously communicate around our IND filings and patient recruitment, preclinical data expected in the first half of the year against all three programs, and then the clinical data as we said in Q1 2027.
Understood. In terms of additional BD, are these the three main programs you want to move forward, and are there opportunities to partner them further?
We always have to do what's in front of us and make sure we get that right. So executing plan on these programs is priority one, two, and three for the organization. Obviously, a program like PTK7, which has such broad potential and really multi-billion-dollar opportunity, is always potentially an attractive partnering asset, but it's not core to our philosophy at this point.
Understood. And then maybe just in our last few minutes, final thoughts heading into 2026, kind of the year, how we've shaped the year of 2025 and what investors can look forward to.
Yeah, I mean, we're really excited about this transition we're about to make from preclinical into a clinical stage company. We just brought on our CMO this week, a former very experienced oncology developer, Margaret Dugan, who joins us from Schrödinger. Margaret and I previously worked together at Novartis for a number of years on oncology development, so we're really excited to be making that transition both from an asset perspective, but as importantly from a talent perspective in terms of building out the company.
Ultimately, investors can expect to see that clarity of logic of preclinical data, how the platform and assets work together with the targets to generate a differentiated profile at that preclinical stage, and how that's going to transition into our demonstration of differentiation from the indications we select, which we think is the foundation of that earning the right to then expand into higher risk into other indications where there isn't yet validation for ADCs.
Understood. And then for 2026, it sounds like an execution year getting all three of these programs into the clinic. But will we see also the preclinical data from all three? Will those be at a conference potentially, or?
Yeah, I would look for the first half conference for that data, preclinical data.
Okay, perfect. All righty. With that, we will wrap up. Thank you guys so much. Thank you for joining me.
Thank you. Thanks for having us.