All right. Well, good afternoon and welcome everyone. It's my pleasure to introduce Whitehawk Therapeutics, Dave Lennon, CEO, who'll be presenting for us. This is the Inaugural Life Sciences Conference. Inaugural only because it's our first time here in Miami, so thank you all for joining us, and thank you, Dave, for joining us. Yeah, for sure. A s well on stage. Appreciate it. I never know exactly who's in the audience and who's listening on the webcast, whether they know this story or not, so I always like to start off with maybe a two-four-minute overview. Sure. O f maybe what Whitehawk Therapeutics. is about before we jump into details. Yeah. Sounds great. Whitehawk Therapeutics, we've been in this incarnation of the company for about a year. We closed a transaction in March of last year that reset the company from a prior company called Aadi Bioscience, around a three-asset ADC portfolio that we in-licensed from WuXi Biologics. At that point, we also raised additional cash, and so we started the company with about $200 million in cash. We have $160 million as of the close of Q3, and we're using that money to prosecute these three ADC assets. The money takes us into early 2028, which gives us the opportunity to go into the clinic with all three assets and produce initial phase I dose escalation, as well as some expansion data, for each of those three assets, by which we've committed to delivering in the first half of 2027. We're entering now 2026, kind of with that momentum, having put the first two programs into the clinic. The first program is a PTK7-directed ADC called HWK-007. It's James Bond program, and it's enrolling very quickly now, as we approach dose escalation. The second program is a MUC16-directed ADC called HWK-016, which also entered the clinic recently and is also enrolling well, at that stage. That's most of our execution is focused on those two, but if it wasn't enough, we do have a third program going into the clinic in Q3 of this year. It's a SEZ6-directed ADC called HWK-206, and we will be enrolling that program in neuroendocrine and small-cell tumors later this year. Terrific. You're one of a few, a handful of, like, pure ADC companies a s far as I'm concerned. Maybe you can talk to us a little bit about, you know, the platform, if you will, or at least the critical components of, let's say, ADC development and what differentiates you from others in the field, like Sutro or Mersana got acquired, right? Sure, sure. And the like. Yeah, I mean, it's an exciting field because I think the prospect of ADCs is really built around all we've learned about chemotherapy over the last number of decades. Ultimately, ADCs, I think, are an opportunity to replace chemotherapy with more effective treatments that are more kinder to patients. Our platform is really based in it first and foremost on a topoisomerase 1-based inhibitor payload. We utilize that modality in terms of the development of ADCs, which has been, I think, a big movement in the field away from earlier generations of payloads like PBD or MMAE-based payloads that are kind of more of the approved payloads today. Certainly topo has kind of come into its own. A lot of folks are working on topos. The topo class can really kinda be defined by two main components or categories of payload within topoisomerase inhibitors. You have kind of exatecan and exatecan-like payloads, and then you have deruxtecan and deruxtecan-like payloads. Each of those have different parameters by which they operate. Exatecan tends to be more potent, but also comes with more toxicity, particularly on the hematological side effects versus deruxtecan and deruxtecan-like payloads, little less potent, but also less side effects. The challenge is: How can you generate linker systems that can control one or the other more effectively? We fall in the payload of deruxtecan type molecules, so we're generally looking at a safer profile, but we're always trying to then engineer how do we make them as potent as possible. That's really the underlying technology that we've developed, we think, really hits and threads the needle of delivering that potency with a much safer deruxtecan-like payload. That linker payload system is called CPT-113. We licensed it from a company called Hangzhou DAC that's based out of China. A scientist from ImmunoGen went back to China a couple dozen years ago now, or a dozen years ago now, and developed this technology that we think really is potentially best in class in terms of bringing a topo inhibitor payload with your antibody of choice. That linker system really, the main point of differentiation is one that delivers stability and, exposure of the ADC in circulation. It's really optimized to deliver and make available the payload at the site of the tumor in the most effective way possible. That's the core of the technology and what we can deliver. We've applied that technology across all three assets, so it's the same technology in all three cases, and we're really looking forward to kind of demonstrating what it can do in people. Terrific. Let's jump right into it, the PTK7. You know, ADC. Tell us a little bit about the target. You know, you always have this tension between, like, going after an established target, you know, and trying to have a better, you know, therapeutic profile versus going after one that's not established that, you know— Yeah. Hasn't had much success, right? You're kind of first— Right, first, yeah. First to the market, right? Yeah. Tell us about it, its expression, and why you think, you know, this— Yeah. Could be successful. PTK7's really interesting protein. It's expressed in young embryos and important in development. It's downregulated in adult tissues. It gets upregulated or co-opted by tumors who are looking to generate migration and other kind of forms of metastases that tumors go through, and PTK7 becomes an important player in that biology of a tumor. It's expressed in up to 70% of all tumors. If you have cancer, there's a 70% chance you're probably expressing PTK7, which makes it one of the most broadly overexpressed tumor targets that people have yet to go after. Really an exciting proposition because it can treat not just one cancer, but multiple types of cancer. That's really where expansion potential comes from this target and why you're seeing a number of people now kind of pile into the PTK7 story. We've been on this from the beginning because we really thought it was one of these high potential targets that was yet to be exploited. The reason we think it is high potential, and there is some validation behind it, because there was a Pfizer and AbbVie program that previously ran against PTK7. With an earlier payload, some of those previous generations I mentioned earlier delivered some really interesting response rates, anywhere from 20%-40% overall response rate, depending on expression and indication, but was really indicating validation for non-small cell lung cancer, for ovarian cancer, potentially for triple negative breast cancer. A number of opportunities, high potential opportunities where there's really unmet need. We have this target that's expressed broadly. We have some initial data from Pfizer that suggests you can go after this target, and it'll generate some responses in cancer patients. Now we're taking kind of the next step with a better approach to deliver against PTK7- positive tumors. You mentioned Pfizer. I think AbbVie as well may have had, you know. Yeah. There was a co-development. Okay. So. But they discontinued development. They discontinued it largely for safety, right? Okay. Some part of the challenge with that, those prior generations was the payload and linkers weren't always as stable. They could generate a lot of side effect profile, and ultimately, these were discontinued because of payload-related toxicities of that program. Okay. As of now, all we have is preclinical data to go on. Right? To kind of evaluate this therapeutic. Can you maybe talk us through Whitehawk's kind of established way of evaluating preclinical models and, you know, what kind of efficacy or what do you wanna see? Right To kinda hit that go, no-go decision. Right To advance to the clinic? Well, there's a number of parameters you can look at in the design of these molecules. The first one we look at is targeting of the antigen itself. How good is the antibody you're utilizing in finding PTK7 within the patient's body? We really look for high affinity antibodies that not only can identify the tumor, but also can be well internalized. We've designed our PTK7 with a very slow off rate. It actually, when it finds the tumor, it stays on the tumor, and that improves internalization of the ADC itself, where it can then go on and kill the tumor cell. That targeting approach, we think is, you know, the first component that's really important. The second component really is then how are you linking your payload to the antibody itself, bioconjugation approach. We use an approach that generates super high stability, and so we look at stability of the ADC in circulation in animals to determine, are we releasing the payload prematurely, or is it actually getting to the tumor? Our ratios of payload release are at 0.01% on a molar basis. This is 10x-100x more stable than most typical ADCs that are out there. We talked about payload earlier, delivery of that payload and release of that payload at the site of the tumor is important, and we look for that in terms of the potency that we see in animal models. We've been able to demonstrate potency down to about 1 mg/kg on average in animals, which directly translates into kind of the human dose you need for a minimally effective dose. We think our threshold for efficacy is around 1 mg/kg, and we anticipate being able to dose in our clinical trials starting at a higher rate than that. We should already be in our effective dose range when we translate that preclinical data that we've seen, that targeting approach, that stability in the linker, the payload that we've had, to human clinical trials. Just to put a bow on, you know, the James Bond part of the pipeline, clinical data, when do you think, you know, it's gonna be available and kind of what's the go/no-go decision at that point? Yeah. You didn't set me up for this, but you're asking me for the "view to a kill." There it is. I should've thought of that. I should've thought of that. We are currently enrolling those trials. We have, you know, a plan, and we've communicated our initial thought is to release data in first half of 2027. What we wanna do is generate a significant bolus of data so you can really understand the differentiation potential of the program and the platform overall. We anticipate having, you know, at minimum 20-30 patients enrolled at that point that we can read out for patients or for people in the first half. When it does read out, you know, obviously, if it's very good data, it applies to the rest of the portfolio, right? Sure. Because everything works. What if it's not as good, or you may have to go back to the drawing board? You know, how do you view then the rest of the pipeline? Yeah, I mean, I think there's definitely a read-through in terms of the platform performance, relative to each molecule. I think in the case that it's not performing the way we would want it to, we'd really have to understand what's on target potentially versus what's off target, and if there's any translation or missing translation we have within that, and we'd evaluate that from the beginning. I wanna say we're a very disciplined team when it comes to spending and this kind of decision-making. We keep our team super light. We're about 25 people today, executing against this program. We were started out of a transaction, and we are not beholden to the technology in and of itself. If it's not working, that's something we would, you know, take into account, but we wouldn't pursue something that we didn't think could be differentiated. That's really important for us for keeping good discipline in pipeline decision-making. Excellent. Let's switch gears to MUC16. Yeah, MUC16. You know, we've heard a lot about this target. There's a MUC family of targets. Sure. Right? Right away, you know, we start thinking about, is there homology between these? Right. Different MUC targets and stuff. It's a long-winded way of saying talk to us a little bit about MUC16. Yeah. Its expression, why are you going after it? Right. Mucin 16 is a protein that it's a highly glycosylated protein family. It's often associated with mucus. That's why they call it Mucin 16, or mucin in general. But MUC16 has been known to be highly expressed in the gynecological tract and massively overexpressed when it comes to ovarian cancer, and endometrial cancer, as well as some other cancers like pancreatic cancer, mesothelioma, and some non-small cell lung cancers. The really cool thing about MUC16, well, there's a couple cool things about MUC16. I have no clever name for it, but the industry or the community does because MUC16 is cleaved into a circulating biomarker called cancer antigen 125 or CA-125. CA-125 is like the most well-known blood-based biomarker in gynecological cancers. It's often used by gyn-oncs to measure progression of disease or response to therapy. MUC16 is the originating protein for that circulating biomarker. It generates some interesting biological choices that we can talk about in a little bit, but I think it also provides a great way to measure response to therapy in the context of developing a MUC16-directed ADC. It also happens to be the most highly expressed ovarian cancer target in the ADC field, and so it's 3x-10x more prevalent than FRα, B7H4, CDH6, claudin- 6, or any of the other ADC targets that are currently under development in the space. When we're attacking ovarian cancer, we start with this like massively overexpressed target. Even a low expressing ovarian MUC16 patient on an absolute basis is a high expressing FRα patient. We just start from a much greater point of absolute ability to address the tumor with a MUC16-directed ADC. Okay. When we are talking about this particular ADC, can you just take us through, you know, what's unique about it, right? The payload, the DAR, you know, the linker and the like. Also, is there any lessons from the history when people have gone? Sure. Either after MUC16 or one of the family members? One of the first things I can think of is— Yeah. If it's being cleaved, you know, would it— Right. Would your antibody potentially bind that cleaved product? Yeah. 'Cause then it becomes a sink, right? Cleavage and antibody sinks are a big topic and they are a real issue within the MUC16 case, and this has been the problem with MUC16 development. People have known about the target for a long time, have wanted to go after it 'cause such a high expressing target, and Genentech actually did that. They went after this with an ADC on two occasions. They used the same antibody each time, and that antibody was directed to the glycosylated cleaved portion of MUC16. Oops. The issue. Yeah. The issue you can obviously, you know, summarize or suggest is that, they formed an antigen sink. They had to dose that program extremely high, to overcome the antigen sink effect in the blood, almost 2x what you would actually typically dose that product at. Now, when they did that, and they overcame that antigen sink, they had great responses, 42% overall response rate in ovarian cancer in their phase I study at that dose, and really robust responses overall. It's a great target. The issue is when you dose that high with that particular product, you generated a ton of side effects. Particularly in the MMAE class, they had ocular toxicity, they had peripheral neuropathy, and other things which made that program not be able to move forward. Every time we show docs this, they're like, "Man, I wish I could get that kind of response for my patients." What we've done in this case is actually really been smart about the targeting, and we actually have designed an antibody that binds below the cleavage site of the CA-125 on MUC16. It bypasses all of that circulating antigen that's in the blood, and that allows us to actually target the tumor and get all of the ADC to the tumor. We can show that this is, you know, much, much better therapeutic modality than the prior Genentech program. We've taken the antibodies, comparing them head to head on the same linker payload. We massively outperform the Genentech program at a much lower dose. In vitro, we've shown we don't bind CA-125, and we can get around that. Now we can go after this super highly expressed tumor target with this targeting ADC, which bypasses circulating CA-125, and there's no competition for us on this target because others have not designed ADCs in this way. We have all the advantages I mentioned before about the linker payload is the same as PTK7, so we have stability, we have the heme-sparing payload approach, and we really think this is a potential best-in-class agent for the treatment of gynecological cancers. I asked this before, but I'm forgetting. What's the drug-antibody ratio in these molecules? Oh, we used DAR 6. Okay. Across all the programs. We found that's optimized for exposure and release of the payload for our construct. Okay. This is now in the clinic. Just again, wrapping a bow on this program, when do you think you'll have data here? What are you kind of looking for that go, y ou know, no-go decision from— Listen, it's a massive achievement for our team. Our side, I give all the kudos to our team for getting two programs into the clinics weeks apart. This one's enrolling as we speak. We'll have data in the first half of 2027. Okay. Thinking about go/ no-go decisions from a clinical I think go/ no-go decisions, I think when you're talking about gynecological cancers these days with ADCs, you wanna see a 50% overall response rate in those patients or better. That's kind of the standard out there. We think, you know, with the Genentech program having been at 40%, with us moving to a better targeting approach, a better payload linker system, that achievement of 50% should be quite reasonable, and potential for 60% or better overall response rate is possible. Excellent. In the last sort of six minutes we have left, the final program that you mentioned. Yeah. SEZ6. I've never heard of that target. Would love to learn more— Sure. About it. It's also a biparatopic ADC. Which I don't think I've heard of. I mean Yeah. I've seen the biparatopic antibodies. Sure. Not the biparatopic ADC. Can you talk to us about the importance of that as well? Yeah. This is a really cool target. SEZ6 is seizure protein 6. It's a CNS-delimited protein, so in the central nervous system. It's overexpressed in cancers of neuroendocrine origin. This is small cell lung cancer, and then a vast array of various tissues that develop neuroendocrine tumors. A rarer indication than the prior two I've mentioned, but still really an important and high unmet need. In the small cell space, you also have targets like DLL3 and B7-H3. Those are kind of the more common targets that people think of when they think of neuroendocrine targets. SEZ6 is a really interesting target because it's actually more highly expressed than either of those, and really quite clean in terms of its expression profile relative to normal tissues in those cancers. We think this is really a best-in-class target for small cell and neuroendocrine tumors. Part of the reason we think that is that AbbVie has actually been developing an ADC against this target that's shown some really good response rates so far, probably top of the class in terms of response rate, to therapy. The challenge with AbbVie's platform is it comes in that exatecan payload group. And it generates a ton of a large degree of toxicity. I shouldn't, like, it's not bad. I'm not talking bad. It's a really good product in terms of efficacy, but it comes along with a lot of Grade 3 neutropenia, hematological toxicity in general, nausea and vomiting, and other cytotoxic effects that reflect the potency of that payload. The challenge for us was how do we design a molecule that can deliver that level of potency or better, but take away a lot of those side effect issues that we think ABBV-706, which is the name of that program, is going to have. What we did was basically utilize a biparatopic approach for the antibody targeting. Biparatopics are antibodies that combine two different epitopes on the same molecule. What that allows you to do at the cell surface is actually concatamerize protein receptors, then they cluster, and they internalize much better. We've shown that we can bind better to the antigen, and we get better internalization of the ADC at the site of tumor. When we then taken that and compared it head-to-head to ABBV-706 monoclonal antibody, we can show we're 2x-3x more potent when you link them to the same payload. Okay. That allows us to achieve a better potency overall. Now when we switch to our payload, which is a little less potent, but much better safety, we actually get equivalent efficacy versus ABBV-706. We've developed a molecule now that's as potent as ABBV-706, but is gonna be much safer for patients on the hematological parameters in particular, and hopefully much more tolerable to take. Where that becomes really important when you start thinking about combination, 'cause ultimately, small cell's a really aggressive disease, as a neuroendocrine disease, and you wanna get into a position where you can combine it with chemotherapy, with IO therapy, and that's where we think the real advantage will lie with our HWK-206 program. Okay. As we, I think you mentioned it, but just to remind investors, this is likely getting into the clinic in the third quarter of this year? Yeah. We're on track for an IND submission this year. We'll start phase I in third quarter. In all cases, have you been able to start dosing, or at least for the two trials that are in the clinic, start dosing on the higher end of the dosing spectrum, or have you? Yeah, we haven't talked about our kind of dosing strategy explicitly. I can say a couple things. One is that we typically see potency of our molecules on average around 1 mg/kg in animal models. We think this is an important threshold for thinking about translation into humans. Generally, when you look in xenograft studies, you can translate one-to-one into humans. It's crazy that you can scale from mice to humans in these models. But, 1 mg/kg in mice indicates about a minimally effective dose that you might see in humans. We anticipate being effective at one mg/kg or better, and we've started both of our programs and plan to start the third program at doses higher than that. Okay. In kinda the last two minutes we have left, you mentioned the cash with three programs, you know, that are ongoing. How long does the cash take us out till? It takes us into early 2028. That, you know, we're looking at that data readout in first half of all three programs. That should give us plenty of time to think about where we're taking those programs next, our next raise, ahead of kind of running out of cash in 2028. Got it. It seems like, right, that investors can wait, and, you know, the clinical data is only coming out in the first half. I feel like there is a coming out party at potentially AACR. Yeah. One of these medical conferences coming up. Yeah. At least a review of all the data. We've talked about milestones kinda sprinkled throughout our talk. Maybe just as a final endpoint as investors are looking at the company, what are kinda the next milestones coming up over the next six to 12 months? Yeah. Even with the preclinical data? Yeah, for sure. We encourage people to pay attention to a couple things. Whitehawk's kinda been flying below the radar. Sorry, that's a bad one, but it's. Yeah, yeah. It's all right. We'll right. We'll figure it out. We're trying. Yeah. We are trying to kind of, that was purposeful. It's ADCs are a competitive space. We do plan to release preclinical data on all three programs in an upcoming congress this spring, and you can look out for that data, which will give you kind of potency, stability, PK, H&STD, all the metrics that people like to look at in terms of comparing preclinical profiles between assets. Those will all be coming out. We also encourage people to look out for a program called DXC006, which is a program running in China by Hangzhou DAC. If you remember, I mentioned them in the beginning. They are the linker payload company we licensed from. This program has the same chemical structure we utilize in our program. Slightly different bioconjugation, but we think it's a pretty reasonable read-through in terms of potency and safety profile for our linker payload system. They've discussed releasing data later this year at an upcoming congress. That'll be something for folks to pay attention to, and we'll certainly kind of help draw attention to that once that becomes available. Your clinical data across— Our clinical data, first half of 2027. You know, HWK-007 and HWK-016 kind of run pretty parallel, so it might be together, it might be separate; 206 is obviously about six months behind, but it's a smaller trial, and we'll have learned a lot by then, so you might see that towards the middle of 2027. Excellent. Dave, thank you very much for this, and appreciate you coming to the conference. Excellent. Thank you.