Hello, I'm Robert Burns, a managing director at H.C. Wainwright, and I'm joined today by Dave Lennon and Dave Dornan, the President and CSO, respectively, of Whitehawk Therapeutics. Dave and Dave, thank you for joining us today. Thanks, Robert. Thanks for having us. Awesome. Why don't we just dive in? For those who may be unfamiliar with Whitehawk, can you please provide a brief overview of the company, its pipeline, and its platform, more importantly? Yeah, happy to do so, Robin. To do that, I'll share a couple of slides on Whitehawk today. We are—I'll start by saying there's some forward-looking statements here, some normal disclosures associated with that. Just to reorient everyone, we previously were known as AADI Bioscience and went through a transformation that we completed at the end of quarter one this year into Whitehawk Therapeutics. AADI Bioscience had been a small commercial-stage company that was working on an mTOR inhibitor. That product was actually sold to a Japanese pharmaceutical company along with the AADI Bioscience name and brand, and is now a wholly owned subsidiary of Kaken Pharmaceutical. That transaction net us $100 million, which we then, along with a PIPE raise for an additional $100 million, funded the acquisition and now development of an advanced ADC portfolio. We're working in antibody-drug conjugates against broad tumor populations with significant unmet need. We have a three-asset portfolio that we're rapidly bringing into the clinic over the course of this year, by the end of 2025 and early 2026. Whitehawk Therapeutics, as an ADC company, is very much focused on what we call established tumor biology. We have utilized tumor markers that are clinically validated and broadly overexpressed, thereby reducing the tumor target risk in our ADC portfolio. Second, we're focused on high-potential cancer indications. We think we have a broad opportunity to address a whole range of different types of cancers, including lung and ovarian cancer, other gynecological cancers, as well as a broad range of GI and other cancers, ultimately, with this portfolio. We do really think that this allows us to target broad patient populations that have significant commercial value. We are utilizing in our ADC portfolio a common ADC platform technology, so-called linker-payload technology.. This technology has really been engineered for greater stability, which allows for minimal off-target toxicity and an improved therapeutic index, hopefully building on what we've seen in this ADC field already and with the opportunity to deliver best-in-class efficacy in the indications of interest. I mentioned that all three of our programs are currently preclinical, but we anticipate filing INDs for all three by mid-2026. To talk a little more deeply about the portfolio itself, we utilize, as I mentioned, validated clinical targets. These are targets where there has been precedent data before. The first one of those is protein tyrosine kinase 7, or PTK7. This is an oncofetal pseudokinase with broad tumor overexpression, meaning that it's expressed early in embryonic development and then downregulated, but then co-opted by tumors to be overexpressed and utilize that growth and direction that is normally reserved for fetal development in the course of tumor progression. Ultimately, this is a broadly expressed tumor target that had precedent data from a Pfizer-AbbVie collaborative program called Cofetuzumab pelidotin that showed some really promising efficacy signal, but the platform utilized, being first-generation, had some limitations in terms of toxicity, and that program was discontinued. We look at this target as clinically validated with the opportunity now to come with the next-generation platform, which I'll talk about in a second. The second program is against MUC16. MUC16 is a really interesting tumor target because it's overexpressed in cancers of female origin. It is also then cleaved into the circulating biomarker called CA-125. MUC16 is the originating molecule for the circulating biomarker CA-125, which in gynecological cancers is a really important marker for clinical progression, widely utilized within the gynecological community to monitor cancer in those settings. We have a really interesting approach in targeting this molecule and also building upon precedent data the same way we are for HWK-007. With HWK-016, there was a Genentech program that showed some really promising efficacy signals in ovarian cancer. That program was discontinued due to side effects associated with first-generation molecules. In moving to our advanced platform, we think we can build on that efficacy signal and modify the safety profile for this target. Our third program is seizure protein 6, or SEZ6. SEZ6 is a CNS-limited protein that is often upregulated in cancers of neuroendocrine origin. These are cancers like small cell lung cancer and neuroendocrine neoplasias. HWK-206 is a targeted molecule which can specifically target these types of tumors and potentially lead to better efficacy for these patients. There's currently an AbbVie program, which is also targeted to this molecule, which is showing some promising early efficacy signals in small cell and neuroendocrine tumors. We think we have an improved approach to build upon that initial data with a best-in-class profile for this target. Ultimately, all three programs are built off of the same linker- payload platform, what we call the CPT113 platform. This was part of our in-licensing strategy for this platform and has a unique architecture that provides for high linker payload stability and allows us to deliver a novel Topoisomerase I inhibitor payload, so-called advanced payload opportunity for each of these targets. Importantly, this platform has been tested in humans with two programs developed by our partner in China, DXC006 and DXC1002. These are programs that are currently in phase one dose escalation in China and demonstrating some early positive signals in efficacy and safety. Ultimately, our approach with our platform is really to engineer an improved therapeutic index for the ADC class. We have a proprietary TOPO-1 inhibitor payload, which really minimizes off-target effects and supports that higher therapeutic index that we're trying to generate with this next-generation approach. It's a highly stable, but still cleavable linker system. I think that's really important to note is that this kind of linker construct allows for low free payload release in circulation and really target release at the site of tumors and accumulation of the cytotoxic agent at the site of tumors. Ultimately, there are some tricks in chemistry that we have not fully disclosed yet, but really allow us to optimize the DAR ratio for these molecules and enhance the PK profile, which supports longer half-life of the ADC and ultimately optimal dosing for patients. Altogether, these effects—we are trying to drive that improved therapeutic index, which is shown on the right. First-generation ADCs have been really promising in their delivery of efficacy, but multiple of them have faced many limitations due to this concept of low therapeutic index, meaning that their minimally effective dose is very close to their maximally tolerated dose. Thereby, patients develop too many side effects for these molecules to be utilized regularly in patients. Ultimately, what we're trying to do with next-generation linker- payload constructs is widen that therapeutic index, lower the minimally effective dose, so more potent molecules, while increasing the maximum tolerated dose, meaning that we have a higher safety threshold. That's the promise of our CPT113 platform and each of the molecules that Whitehawk is trying to develop. As I mentioned, we have three programs that are currently in preclinical stage against each of these targets. We plan to deliver the first program, HWK-007, into IND in Q4 of this year. Shortly following that, by the end of the year, is HWK-016, and then by mid-2026, HWK-206. We really have three shots on goal here quickly into the clinic over the course of the next 12 months. As I mentioned, each of these molecules has precedent data being generated or that has been generated by prior molecules in various indications. Each of these markers is also expressed in other tumors that have not been tested yet, giving each of these programs a broad expansion opportunity to address a range of indications where there is still significant unmet need for an advanced ADC program. Ultimately, we believe we have a great value proposition and make a transformative impact for patients. As mentioned, we have clinically validated, broadly overexpressed tumor targets that we are coupling with an advanced ADC linker-payload technology. that really improves that therapeutic index opportunity. These are all high-potential indications, and we believe we have the opportunity to be first or second to market in each of these spaces with a high ability to compete from a differentiation perspective. I'm sure we'll talk more about that today. We mentioned where we're targeting our IND submissions already, and we have the team to execute upon that, folks like David Dornan, who joins me today as our CSO, with a deep ADC experience and multiple IND and clinical filings to date. Ultimately, we—sorry—ultimately, we anticipate our capital position to allow us to execute into 2028, which gives us sufficient runway to generate early clinical data from each of these programs through dose escalation and early expansion in our phase one trials. That's where we are today, Rob, at the high level, and happy to kind of go deeper and talk about questions you may have. Awesome. Thanks, Dave, for that overview. I guess before we get into your pipeline assets, one of the things that I find intriguing is that there are two—there's Hangzhou DAC programs, DXC006 and DXC1002. They're already in phase I development over there in China. And DXC006 is Anti-CD56- CPT113 target ADC. I think more investors are paying attention more to 1002 because it's a TROP2-targeted ADC. When we think about that landscape, obviously, you got Dato-DXd, and that initial data set, I think, can be extremely de-risking for your own portfolio assets. Is there any color as to when we might see initial data for that compound from your partner in China? Yeah, it's a great question, Robin. I would say that Hangzhou DAC has been an excellent partner to us. They've been working for over a dozen years on various ADC platform technologies. This is the most advanced platform technology that they've developed. Certainly, that data from DXC006 or 1002 could be highly informative to how the platform performs overall, as you say. It is a Dato company, it's not our programs, so I wouldn't comment on potential data release that they might have in plan. Certainly, we will look out for that, and that will be informative to what we might expect to see from our programs. Okay, that's completely fair. Why don't we then focus on your lead asset, HWK-007, the PTK7 targeted ADC? From a broad high-level overview, how should investors be thinking about the market opportunity for this compound? Because it seems to me that PTK7 is widely expressed across a variety of solid tumors. Yeah, I think that's the real opportunity here with PTK7. What I would say first and foremost is it is one of the most broadly overexpressed tumor targets that's available. You can think about it very much in line with the commercial opportunity of a TROP2 or a Nectin-4 or a HER2 in terms of its potential to impact a lot of patients because they do have expression on up to 60%-70% of all cancer patients at some point in their disease. The other point we really like to think about with PTK7 is that when it is expressed, it's often expressed at a moderate to high level. That's really important because that consistency of moderate to high expression, we know can potentially, or at least we know from other markers, can potentially lead to a greater chance of response from patients. That is another dimension of PTK7 we think is really important, that moderate to high expressing patient is one who will benefit potentially from a PTK7-directed ADC. When we think about this, those are really two important aspects of the overall opportunity. In the short term, we do want to make sure, though, that we also say, "Where do we have data?" We have data in lung cancer, in ovarian cancer, and in triple-negative breast cancer from Pfizer-AbbVie’s prior program. That already establishes an opportunity and a huge opportunity from a commercial perspective, let alone where else we can go in terms of GI cancers and other cancers down the road. Yeah. Obviously, I would assume then that those are going to be the three high-yield indications that you're initially going to go after to consider it so de-risked. There are some other high-level expressive ones like prostate and neck. Those will be secondary, if I see what you're saying correctly. Yeah, I think that's right. I think we haven't decided exactly which indications will be a first focus. But we do believe that the clear opportunity here is to demonstrate the differentiation from the precedent molecules and the opportunity to build on those, which will allow us to translate the impact of our platform and extrapolate that into further indications. It's kind of a right-to-play kind of approach that we like to take, which is that we validate the potential of the molecule on those precedent indications like lung cancer and ovarian cancer, and then we build in the future into other high-expressing PTK7 high-expressing cancers. Okay. Yeah, that's completely fair. One of the other things that I noticed from the preclinical data that we've seen is that it appears to indicate that it has superior activity relative to that first-generation Pfizer compound. I also note that there are two other competitor compounds, one coming from Zymeworks and the other one from Day One Biopharmaceuticals that they call next-generation ADCs. I want to get your thoughts on those competitor compounds and how HWK-007 is differentiated from them. Yeah. HWK-007 has, we think, some pretty great activities. Maybe I'll turn it over to David at this point to talk a little bit about the profile of HWK-007 from a potency and safety perspective and what we think the potential is there. I'll come back and comment a little bit on the competitive landscape. Okay. Yeah. No, happy to do that. As Dave mentioned, right, from the platform perspective, we have this aspect called a carbon bridge site-specific conjugation. Dave flashed up a figure that basically showed a carbon bond linking between two, essentially, that they were just linkers to payloads, if you will. What that essentially chemistry does is it enables the stability of the linkers to be conjugated onto the antibody. Importantly, there are other aspects that we have not described publicly at this time, but there were things that we have done that improve hydrophilicity, which, of course, topoisomerase I inhibitors are generally hydrophobic in nature. You have to do a few different chemistry plays to try and increase the hydrophilicity of it. We have done that. Also, we have a cleavable peptide sequence that we believe is fairly novel for our field. All in all, as Dave said, the goal of being able to optimize those three aspects, so basically the cleavability of the linker, the hydrophilicity, as well as, of course, the stability of even the conjugation using this carbon bridge, essentially, those three things are what are key to basically having an ideal PK profile, enhancing tolerability, and importantly, efficacy, because now you have more available ADC to get to the tumor. As we've mentioned before, right, it's all about how do you enhance the therapeutic index. I will say that even so, like bystander effect, which is, of course, the ability to kill target antigen-negative cells that are nearby target antigen-positive cells, like in the tumor, that is also something that this platform has been optimized as well to accomplish. That's why we believe our platform has the greatest potential. And then, Dave, if you wish, I can just allude a little bit on the competitor molecules, if you want. Yeah, sure. I'll start. Yeah. So I'll start and you can then. Like you mentioned, Day One. Day One uses essentially the Multitude platform. Their play is something called a T1000 moiety. What they're—it's a self-immolative part of the linker, if you will. Essentially, they're using it to try and overcome the hydrophobicity of exatecan. It's a very, very smart chemistry play. Their platform uses regular cysteine conjugation. With that in mind, traditional cysteine conjugation does have limitations too. You can have, of course, deconjugation caused by retro-Michael reactions and things like that. You may get some payload that could essentially fall off. The reality is, sure, it's a smart platform. It's good what it is, as it says. It's advertised what it does. Relative to our platform, we've got more—we have more optimization involved from end to end, from antibody all the way through linker to payload. I think you mentioned Zymeworks. Zymeworks, they actually were one of the few as well that actually tried to find their own exatecan-like molecule. Their payload itself is dialed back on potency. They're essentially enhancing the hydrophilicity. I think their idea was, of course, to just help improve PK, plus the stability and such alike. From what we know from their molecule, which was a biparatopic one, it was being proposed to AACR. You know, obviously, we're big fans of biparatopics because of our SEZ6 group. We believe that they potentially can enhance internalization. That was seen in Zymeworks' AACR poster. There was some curious data that they had AACR that looked like it did not really enhance in vivo efficacy. For whatever reason, it was a very minor increase relative to a monoparatopic antibody. Nonetheless, that's just hopefully a high-level comparison across the platforms. Yeah, certainly. Appreciate that. Yeah, Rob. David, I think that's right. The thing I always like to step back and say is PTK7 has a huge space. There are multiple—we're not competing for a single indication or a subset of patients. There are lots of opportunities for potentially multiple parties to be in this space. As David points out, we think there are limitations to the platforms that are involved as being somewhat just maybe earlier versions of that next generation, that next generation wave, and not fully optimized in the right spaces. I think one of the things I would point out, right, is the T1000 platform from Multitude is actually being utilized across a number of programs. I think we've seen the first clinical data off of that platform from OnCusp recently at ASCO. Some of the things that we noted that are just questions in our mind is, I think, first is kind of maximum tolerated dose on that platform seemed to be limited at around 5 mg per kg. You also saw some intriguing safety cases of ILD in the ovarian population, which we thought was kind of unusual. Now, maybe it's a one-off. It was only a couple of patients. That was a little bit striking in that patient population. That may or may not carry through to other platforms, but there will be other data to read through on the Multitude T1000 platform. Similarly, on Zymeworks, they've had a couple of different shots with that platform. They've taken forward and later discontinued. I think there was a biparatopic HER2. I think there was a NaPi2b. There are probably learnings, I think, that folks could draw from kind of the progress of those prior molecules in the Zymeworks platform about where their therapeutic index may land in terms of the approach they take. Overall, what I would say is that I think that if you think about step changes in that therapeutic index opportunity, certainly both of those molecules improve upon first generation, but we do not think they are fully optimized to take advantage of that really higher—that real benefit of the risk-benefit opportunity that CPT113 platform that we have been licensed provides. Yeah. No, no, no. That makes a lot of sense. I am definitely curious as to how the data sets are going to evolve over time. One of the other things that I wanted to sort of touch base on with you, obviously, when we looked at the first-generation PTK7 targeted agents data set, obviously, we saw this massive differential between the effective response rates in the moderate-high population and the low population. We saw that as well in the first-generation folate receptor alpha program, right? Now, as we look towards the second-generation folate receptor alpha programs that are coming about, some of these assets don't seem to have as much of a delta between objective response rate in moderate-high versus low. I wanted to get your thoughts as to how HWK-007 will—what it will demonstrate in that lower expressing population. I don't know if you've ran that preclinical experiment, but I wanted to get your thoughts there as well. It's a great question, Robert. I think there's a couple of things. Biomarker expression is actually much more complicated than we make it out to be, especially since often what we're measuring is IHC-based analytical methods, which have a lot of variation and are uniquely tuned for each tumor target. What that means is a high-expressing PTK7 population versus a high-expressing MUC16 population may be very different in terms of the absolute expression of the marker because they're all graded on a relative scale. The IHC is tuned to generate kind of that differentiation. You can have markers that say they're high, medium, and low, but the actual variation may be very small. You can have markers that are high, medium, and low, and the variation is very high. You can also have them at different levels of expression, right, in terms of absolute expression overall. I think it's very hard often to compare from marker to marker without kind of normalizing for all of those factors of that. Now, with all of that said, getting off the soapbox of why IHC might not be the best way to think about this, it is the situation we have today. Certainly, for PTK7, we do see that gradation across expression, at least in the early program. We'll see in the clinic what that means for our molecule. We do believe that our antibody starts with higher affinity or really a slower off rate, which should improve internalization, and particularly also in low-expressing cells, which may be beneficial ultimately to the efficacy that we see in those low-expressing patients. That's still to be proven. I think what is important here is also to think about the long-term prospects of how we think about expression. Ultimately, my belief is that doctors—and our belief at Whitehawk—is that doctors are going to want to find the drug that is most likely to give their patients a response. Expression profiling for tumor markers will start to become standard practice in the future as more ADCs and other modalities that utilize tumor markers become more prevalent in the regimens of choice for different indications. What we think that'll drive is a situation where doctors are going to select the molecule they use, not based on whether it's broadly applicable, but whether it's specifically applicable for that patient. We do think that biomarker expression and characterization of biomarker expression throughout a clinical development program is really important. That molecules that try to go for all comers and dilute their efficacy on their low expressors actually are hurting themselves in terms of their development profile overall. That's our view. I think one also held by just common sense, but also physicians who say, "Hey, I want to give my patient the best chance. And if you're a high PTK7 expressor, you're more likely to respond to a PTK7 ADC." Yeah, no, that's completely understandable. Since 007 is going to be in the clinic later this year, talk to me a little bit about the trial design, whether you're going to eliminate that low-expressing population, whether it's just going to be the moderate-high, and what are the sort of go-no-go signals you're going to be looking for to advance that program into later phase development? Yeah. At Whitehawk, we're very disciplined about our capital allocation, but also about how we think about moving programs through milestones. Our approach, as I mentioned, is one where we think the best thing we can do to generate differentiation is show that our molecule performs better in indications where we have precedent data and where there are clear competitors. Our initial phase one trial for PTK7 is likely to be focused in lung cancer and other gynecological, ovarian being one area of cancer where we have data already and where we have a number of competitors to demonstrate kind of the therapeutic bar that we expect to see. Typically, when we look at lung cancer today in biomarker-positive patients, we're seeing kind of 40% as the minimal bar for differentiation. We believe that's achievable with PTK7-directed approach. In ovarian cancer, that's often 50% now or higher overall response rate and some of that initial data. In terms of our phase one design, we will be very focused on generating information in those patient populations that prove out that hypothesis and demonstrate an ability to kind of beat the bar from an efficacy perspective and be competitive. If we don't achieve that, then we need to pivot and move on to other things. I think biomarker expression will be part of that strategy for sure. I think we're still working through a view on the data available to say what the right cutoff might be for that. That may be something we do retrospectively in the context of a phase one trial where we're still exploring exactly where this can be, the product can be most effective and at what expression level that happens. Okay. Last question for me on 007. I do not know if you've disclosed this already, but what is the DAR for that compound? David, do you want to talk about our DAR approach? Yeah, sure. The DAR of that molecule is six. That is what we optimize just based upon numerous parameters preclinically as well as manufacturing. DAR optimization is always an interesting topic that we could probably talk about, but I know you have other questions. Certainly, to say that methodical methods were put in place and criteria to select optimal DAR for the target. Okay. All right. Thank you for that. While we shift gears now to 016, obviously, MUC16 is a highly sought-after target. Several different approaches have been advanced, including bispecific, cell therapy, other ADCs, even monoclonal antibodies. I wanted to get your senses to how you view this competitive landscape with all of the different modalities that are going after this target. Yeah. It's a great question. I think that MUC16 is one of those targets because it was a circulating biomarker in the blood, CA-125, has been around for quite a long time, and people have thought about how to utilize it as a therapeutic moiety or target. When we think about oncology modalities, I do think that there's plenty of opportunity for competitors when we think about immunology-directed approaches like a CAR T or a bispecific versus cytotoxic-driven approaches like ADCs versus potential other kind of combinations in the future. There's clearly play for both. Certainly, often immunologically-based approaches provide that opportunity for durable responses that all patients would like to achieve. The immune system does not always cooperate in terms of generation of that. You do need cytotoxic agents. I think one of the wonderful things about ADCs is that opportunity to replace systemic dumping of chemotherapy into a patient's blood for treatment of their cancer with highly targeted and postal ZIP code-directed cytotoxic therapy to their tumor. The reality is that chemotherapy is still the most utilized form of treatment for patients with cancer. ADCs have a huge opportunity to replace that regardless of what happens with other areas and different modalities that might target the same moiety, in this case, MUC16. That is the first point I would make. I think there is plenty of opportunity between modalities. I think the second thing I would say about MUC16 is that the problem with a lot of MUC16 approaches in the past has been that they targeted that CA-125 circulating portion, which made actually the execution against this target more complicated than it needed to be because the biological molecules, you kind of can get your molecule stuck in the blood and not get to the tumor, which happened, we think, with the prior Genentech program in the ADC field. Our approach is a targeted one. It's one being utilized by a couple of other players, not in the ADC field. It is an approach which targets the membrane-bound portion of MUC16. It's smartly designed to find an epitope that is below the cleavage site of the protein on the surface of the cell, thereby bypassing all of that circulating MUC16 or CA-125 and still getting to the tumor onto an epitope that is highly present there. We think this approach bypasses a lot of or has been developed based on an understanding of a lot of precedent data for this target and is really promising because now we can combine that biomarker circulating in the blood to identify patients who are enriched for MUC16 expression on the site of their tumor, but bypass the circulating CA-125 to get our drug to the site of the tumor. Interestingly, the thing about MUC16 is for some patients, it's the most highly—when we talk about absolute expression, it's actually one of the most highly expressed tumor targets that is out there, higher than HER2, which is also a highly expressed tumor target in certain types of cancers, and really has that potential then to be a very effective target for a lot of patients. Yeah. I completely get what you're saying there. I guess one of the things I'm sort of curious about as well is the data that we saw from the Regeneron compound 401. Obviously, it's being evaluated in phase two in combination—either it's monotherapy or in combination with an anti-PD-1. I want to get your thoughts on that program specifically. Also, let's assume that the Regeneron compound comes to market. How do you see the potential sequencing? Do you think that you could give a MUC16 targeted ADC post this MUC16 bispecific? I wanted to get your thoughts as to how you see that landscape specifically playing out. Yeah. I think the question that comes up, and David may have also had some comments on this, is what is the mechanism of progression on these tumor-targeted therapies? Generally, the data that we're seeing consistently shows that it is not loss of tumor marker that drives progression. It is loss of or ineffectiveness of the relevant payload or relevant modality. In the case of Regeneron, if their T-cell engager moiety progresses or doesn't work in that situation, we wouldn't expect that to lead to downregulation of MUC16. Certainly, a MUC16 targeted agent like ADC could still come after that and be effective, at least in theory. That obviously has to be borne out in practice. That's consistently what we're seeing so far is that patients progress mechanistically against the modality, not necessarily due to loss of target. David probably has more experience with this than I do, so. Any comments, David? Yeah. I mean, I do think that I view them like they're orthogonal mechanisms, right? The office regenerative molecule is bringing in, obviously, T-cells in theory to the tumor microenvironment to try and obviously kill the tumor. Even when you think about sequencing them or how you could do it, the fact that they're orthogonal, you could consider them, well, you don't have to be too far apart to give alternative different treatment options. Coming in with, we'll say, a topical inhibitor in any other IO right now, like a PD-1, for example, if Regeneron was combined with PD-1, then there's data to support that there's a synergy there with immunogenic cell that goes by, obviously, the topoisomerase inhibitor from the ADC. I think all options are on the table there when it comes to being able to combine potentially down the line. Obviously, not at the same time, but certainly, as you said, sequencing, certainly on topic of an orthogonal mechanism. Yeah. One of the things that you mentioned before with regard to 016, well, your MUC16 in general is this potential for an antigen sink. How exactly does 016 actually mitigate that? How do you get around that problem for that cleaved MUC16 that's in the blood? Yeah. It's a great question. One of the things that was seen in the Genentech program or hypothesized in the output of that program. What happened with that program is you really saw it was an MMAE-based payload. What you saw is a lot of a highly effective molecule at about 5.2 mg per kg, which for an MMAE-based payload is actually a very high dose. Typically, doses utilized are lower than that. One of the hypotheses that Genentech had was that actually they had to go to higher dose because so much was getting cleared in the blood. Like half of that amount was getting cleared in the blood. Really, their effective dose was closer to like 2.4 or 3 mg per kg when you think about what was getting potentially cleared through circulating CA-125 because there is a lot within the blood. What we've done with the HWK-016 molecule is actually pick an epitope, which is below the cleavage site of the molecule. You think about the protein sticking out of the cell. It gets cleaved at some point along that on the extracellular side of the cell. Our epitope is below that cleavage site. We've shown this in vitro and in vivo in animal models, there is no binding of HWK-016 to the CA-125 portion of MUC16. That allows us to bypass circulating CA-125. When we've tested that in animals that have been implanted with high-shedding tumors, we can demonstrate that the MUC16 antibody does not work, and we can demonstrate that our antibody works both in the context of our CPT113 platform, but also using the prior Genentech platform. There is really an opportunity here for the antibody just to be much more targeted to the site of tumor and be much more effective in those patients who are having high-circulating CA-125, which is the vast majority of progressive ovarian cancer patients and a lot of other gynecological cancers. Okay. This phase one program that you are going to initiate by the year end, I am assuming it is going to be targeted solely at the gynecological cancers. Any thoughts as to targeting other MUC16 targeted tumors? Because it is not just ovarian and other gynecological cancers that you could go after with this target. I want to get your thoughts there. Yeah. MUC16 is a really interesting molecule. It is overexpressed in a number of other cancers, particularly pancreatic cancer and some non-small cell lung cancers. There are large portions of patients who have that. I think given that, but at the same time, a lot of those patients don't express high-circulating CA-125. That may be tumor dynamics, etc. Part of our strategy here is to prove out the molecule's highly potent in those gynecological cancers to demonstrate that we have that before we take on the risk of going into these other unproven spaces and difficult to treat pancreatic cancer being a very difficult cancer to treat. It will be a second step in our program, but clearly an excellent expansion potential for those patients who have MUC16 positive cancers. Okay. While we shift to the last asset within your portfolio, at least the last asset that we know of within your portfolio. This is a biparatopic. This is your first biparatopic compound that you're actually developing. I want to get your thoughts as to the biparatopic approach in general, whether we could potentially see more biparatopics in your portfolio. Where do you think a biparatopic is best suited versus the monoparatopic ADCs? Yeah. It's a great question. There's a lot of science behind this. Maybe I'll turn it over to David to talk a little bit about his thoughts on this approach. Definitely one of his favorites. Okay. Most things in science, right, we should be designing them fit for purpose, right? Why do you need one tool versus another, right? Biparatopic versus monoparatopic fit in that kind of category, right? Ultimately, it just depends upon—a lot of it depends upon your target antigen, right? Because sometimes binding one site on a receptor is more than sufficient to drive internalization. Sometimes when you add another binding site, it actually does not increase much. Whereas in our case for SEZ6, this is a case where actually when you do bind two binding sites with one antibody, then you actually result in significantly enhanced internalization. I think like everything else in biology, as long as you are designing it for what the intended purpose was and what you are trying to achieve. In this particular case, as I said, for SEZ6, we identified that if you bind two independent sites on the molecule, you get greater internalization. That is not the same for every target. Every target behaves differently. That is why you just have to design what you are trying to do. Yeah. No, I completely hear you there. I think just to build on that, what we have seen is that that needs to translate into better efficacy. The first set of that is showing that in vivo. What we can consistently see is this antibody performs better than the AbbVie antibody in the preclinical setting when conjugated to the same payload structure. We think it is at least an initial step demonstrating that advantage. Now we'll look for that to translate either into better efficacy for patients in the clinic or better safety because there is also that potential to be a safer drug with a biparatopic approach utilizing lower doses. Obviously, we saw the ABBV-706 data at ASCO. I wanted to get your thoughts on it both from a small cell lung cancer perspective, but also a neuroendocrine tumor perspective. Yeah. I think both are just super exciting. I mean, the small cell data initially they showed was 60% ORR in that initial data, very highly potent molecule or tumor target in a very high unmet need indication. That we think is very exciting to validate this tumor target and provide a starting point, we think, for where we can build on and improve the overall therapeutic profile for those patients. Then recently, the neuroendocrine data, I mean, there's really nothing for neuroendocrine patients. Other than radiation therapy components, yeah. Yeah. I mean, and that's if you can find their tumor, right? This is really an opportunity, we think, to—it was a 40%-ish response rate that you saw with that, which is really a great response for those patients. Again, we think data that we can build on with our approach, with an improved approach in terms of targeting and the platform approach we have, which we think has certain advantages. I have seen the in vivo preclinical data where you showed greater binding as well as internalization relative to the ABBV compound. I did not see any efficacy data there, however. I wanted to have you run that head-to-head experiment against ABBV-706 from an efficacy in vivo perspective in xenograft models. What I can say, which is what I said before, is that when we conjugate, we really look at antibody performance as kind of the first differentiator. Certainly, when we look at antibody performance when conjugated to the same payload, we see greater efficacy in the approach that we have generated. Ultimately, ABBV-706 has a proprietary linker construct and novel payload, which is utilized both for their 706 molecule, but also their 400 molecule, which just recently was approved in c-MET-driven cancer. Certainly, we cannot compare those head-to-head per se. We are really confident, at least in our targeting approach being of an improvement upon that molecule. Ultimately, we will see where the clinical data sets out when we compare across platforms. Okay. When we look ahead, obviously, we got these INDs sort of coming back to back to back, right? First one is going to be 007, then 016, and then obviously 206. By middle of next year, pretty much all your program is going to be in the clinic, right? Talk to me a little bit about your war chest and what sort of operational runway that provides, as well as when can we expect to see additional preclinical data for these agents? Yeah. That's a great question, Rob. We've played things pretty close to the vest in terms of releasing data publicly. It is a hyper-competitive space. We know people would love to see all the data all the time. Our first goal is to get these programs into the clinic, get cleared with the FDA to start running our clinical trials. We will disclose more data. You can expect to see more data coming in 2026 from a preclinical perspective and details on our plans for more detailed plans around our clinical trials and biomarker strategy, etc. That's kind of the timing when you'll see that information coming. I think stepping back to the war chest question, the company started Q2 with approximately $185 million in pro forma cash in the bank to prosecute specifically against these assets after we completed all of the transactions to sell our prior asset and license this portfolio. We believe that gives us runway into early 2028. Our goal is really to generate a bolus of data that gives clarity around the potential differentiation and performance of each of our molecules before we go back to the market for additional monies to think about further development. We do believe that's probably an early 2027 event that we would think about release of data. It's because we don't want to drip data out per se. We want to come with a clear kind of view on what these products can do in a reasonably sized patient cohort. Yeah. I think that's an extremely judicial measure, especially because we've seen time and time again by smaller biotech companies leak data out in increments and then they get hammered on the market, right? Just because there's no way to. It always seems to get worse somehow, right? It always seems like the first one's great and the next ones aren't so great. We'll just come with the answer, hopefully. No, I hear you. Last question for me before I let you guys go. Obviously, it seems like there is a lot of potential behind this platform, right? And there's a lot of viable targets that you can go after. Is there anything else under the hood that we might not know about yet? And when could we potentially find out? Rob, that's not a question I'm going to answer today, unfortunately. Just to say, it is a highly competent and capable team. We have a great group of investors behind the company. We are continuing to think about how we can augment our approach while being judicious and focused on the execution that we have in front of us. Importantly, any one of these molecules shows positive efficacy, and it is really a positive for us. We have three opportunities to do that. Do we need more? Maybe, maybe not. We will come to that bridge when we cross it. All right. Sounds good. We are always ready to come to it, I guess, is what I should say. I certainly appreciate you guys taking the time with me today and for everyone else who is watching this. Dave, Dave, thank you again. Rob, thank you so much. I appreciate that H.C. Wainwright is hosting the call today. Awesome. Sounds good, gentlemen. Thank you so much. Sure.