Excellent. All right. Welcome, everyone, to Jefferies Healthcare London Conference 2025. My name is Roger Song, one of the senior analysts covering biotech in the U.S. It is my pleasure to introduce our next presenting company from Whitehawk and the CEO, Dave Lennon. Dave, welcome. Thank you. Thank you, Roger, for the introduction, and thank you to Jefferies for hosting us here in London. I'm Dave Lennon, President and CEO of Whitehawk Therapeutics. As a reminder, a statement made on today's call will include forward-looking statements representing our views only as of today, November 18, 2025. At Whitehawk, we're advancing a differentiated portfolio of next-generation antibody drug conjugates, or ADCs, that can target a broad range of cancer indications. I'm excited to share with you the progress we've been making on our portfolio today. Whitehawk was founded initially on three cornerstones: a differentiated science, proven leadership, and an execution-focused mindset. We began by in-licensing a three-asset ADC portfolio that we believe positions us to unlock high-potential indications across a number of targets, including PTK7, MUC16, and SEZ6. Targets that are clinically validated but not yet so competitive that we can't see a way through to be first or leading in each of these targets. We believe each of these targets has the potential to generate the same level of clinical impact as targets for approved ADCs like HER2, TROP2, and FR-alpha, but where we have the opportunity to lead. By leveraging clinical validation, we know we have druggable targets, and because these targets are broadly overexpressed, we can apply them to a number of high-potential indications. We believe in the next generation of ADCs will be born from a marriage of validated targets like the ones in our portfolio with differentiated and optimally engineered linker payload technology. That's why underlying each of these programs is our advanced ADC technology platform, and this with an advanced ADC architecture that's based on novel topo-1 inhibitor payload and highly stable linker chemistry, which is designed to improve therapeutic index. I'll go more into the details on that technology in a moment. That's the scientific backbone, but equally important is having the right team to carry it forward. Whitehawk is led by a management team and board comprised both of leaders with deep ADC experience and a track record that reflects operational excellence and M&A success. I'm also proud of the top-tier investors we've assembled to share the conviction in our portfolio and approach. When we transitioned the company earlier this year, we recapitalized from insiders while gaining support from New Biotech Specialist Fund. Finally, as a boldly pragmatic organization, we are lean, focused, and execution-minded. Capital efficiency is a core part of our DNA. We ended this past quarter with over $160 million in cash, which gives us runway into 2028 and enables us to report on anticipated key clinical data milestones for all three programs. Now let's dig into the science behind Whitehawk. At its core, Whitehawk's portfolio is an optimized next-generation ADC architecture engineered for selective tumor delivery, modality-leading stability, and optimized topo-1 inhibition for maximal tumor killing while minimizing potential toxicity. While many ADC companies say they are differentiated, let me highlight what makes our platform truly distinct. First, tumor targeting and effective antibody design. We select high-affinity antibodies that ensure precise tumor recognition and sustained target engagement. We test our antibodies versus reference MABs from prior and current ADC programs to ensure best-in-class tumor targeting. Additionally, our antibodies have been engineered with an attenuated FC region to minimize nonspecific ADC uptake and avoid ADC internalization by certain types of normal cells. Together, these attributes improve tumor specificity and support a wider therapeutic window for Whitehawk ADCs. Building off our advanced targeting approach, we have spent a lot of time on the often overlooked step in ADC design, bioconjugation, or basically how linker payloads are attached to the antibody. This is where Whitehawk chemistry really stands apart. The field has seen value in moving to ADCs that utilize the new class of topoisomerase inhibitors as payload, but interestingly, we estimate that more than 95% of new topo-1 ADCs in clinical development today still use an older bioconjugation process defined by single-chain partial spike-specific bioconjugation. It's a mouthful, but the single-chain bioconjugation process breaks disulfide bonds that normally hold antibody-heavy and light chains together. There are four paired bonds and eight cysteines that end up being freed up when those bonds are broken. Most ADC developers use single-chain linker payloads onto those cysteines to form a typical DAR 8 topo-1 ADC. Single-chain bioconjugation is simple but inherently unstable. First, the removal of the normal disulfide bridges between antibody chains makes the whole antibody component of the ADC less stable. Second, once the ADC is exposed to conditions in the circulation, each single-chain linker payload conjugation is subject to attack and cleavage in conditions in the blood, releasing free payload into the circulation. Payload that is no longer targeted to the tumor and can circulate and damage normal tissue. In essence, the standard process used by our competitors is fragile, prone to free payload release that may lead to high rates of class payload toxicities. Whitehawk's approach is truly unique. We add linker payloads to the monoclonal as carbon-bonded pairs. That is, two linker payloads that are covalently bound together are added at the exact location where disulfides on the monoclonals have previously been broken. This strategy re-bridges the native paired cysteines, replacing the disulfide bond with a new carbon bond in the linker. This carbon-bridge cysteine repairing method restores the antibody's more natural state, which we've shown enhances ADC stability beyond what is traditionally achieved in single-chain bioconjugation. Building on that, we also employ an additional bioconjugation step, linker hydrolysis, to lock the carbon-bridge structure of the ADC, further improving stability, reducing free payload release, and limiting potential payload toxicity. The third differentiator in the Whitehawk platform is a tumor-busting business end of our ADCs. First, we utilize peg-based masking to optimize hydrophobicity of our linker, supporting longer ADC half-life in circulation and optimal ADC dosing. We layer onto that a novel triple-peptide intracellular cleavage site that ensures a controlled release profile of cytotoxic payload only once the ADC is inside the tumor cell. Finally, we use a proprietary modified exatecan payload, which, unlike pure exatecan, which while extremely potent in topo-1 inhibition often leads to significant hematological toxicity, our modified version retains potency but with less toxicity, particularly in regards to the impact on the bone marrow. This heme-sparing profile helps address challenges like severe neutropenia that has emerged with exatecan-based and other topo-1 ADCs. When it comes to the next generation of ADC platforms, we often hear the sentiment that all topo-1 inhibitor ADCs can be lumped together, but in fact, this is far from the truth, and the platforms are not created equal. Let's take a look at how our platform stacks up against peers. Based on key pre-clinical measures of tumor potency, stability, and safety, our Whitehawk platform shows clear quantifiable advantages compared to average topo-1-based ADCs. Starting with tumor potency across xenograft models, our ADCs achieve tumor reduction at doses roughly 3-10 times lower than conventional topo-1-based ADCs. This increased potency translates to lower, minimally effective dose needed to achieve tumor regressions, hopefully in humans. Next, ADC stability, we consistently see 5-25 times lower levels of free payload in plasma versus other topo-1 ADCs. This advantage in stability is the function of our carbon-bridge cysteine repairing that I described earlier and other aspects of our novel chemistry, which sequesters payload in place until it reaches the tumor cell. And safety, because of the improved targeting, stability, and novel payload, we observe a 2-3 times higher safety margin in non-clinical models than typical topo-1-based ADCs. In other words, we believe we can dose higher and stay within a favorable tolerability window. When you put all that together, greater potency, marked improved stability, and a wider safety margin, it underscores the potential of Whitehawk to differentiate with this next-generation platform and the potential for powerful tumor killing and lower side effects in clinical trials. We're applying this platform to a number of targets, and it's comprised across three assets: HWK-007, HWK-016, and HWK-206. This slide highlights the cancer indications we've planned to pursue in a phase one dose escalation with focus on indications with established clinical precedent for each of these targets. You'll also get a sense of the numerous opportunities for expansion that we have with each of these programs. In essence, we have multiple shots on goal within our portfolio and multiple paths of success with each program. We are rapidly advancing our three assets into the clinic with HWK-007 and HWK-016, INDs expected this quarter, and HWK-206 to follow by the middle of next year. Let's take a look at each program in turn. Let's focus first on PTK7. This is one of the most intriguing and, I think, increasingly compelling ADC targets within oncology. PTK7 is an oncofetal pseudokinase that is normally expressed in embryonic development. It's turned off in adult tissues but then co-opted and reactivated by tumor cells in a broad range of cancers, as you can see here. PTK7 is one of the most ubiquitous tumor markers among clinically validated and emerging ADC targets. It's found in approximately 70% of solid tumors, making it the third most highly expressed tumor marker in ADC development today. We estimate that there are nearly 750,000 patients with PTK7-positive cancers in the US alone, underscoring its massive potential. Now, while there are no approved PTK7 ADCs, it has been clinically validated by a first-generation Pfizer AbbVie ADC called Cofetuzumab Pellidotin, or COFI-P. COFI-P demonstrated efficacy in initial phase one trials with responses across a range of tumor types tested, including ovarian and lung cancer, as shown here. Response rates were particularly robust in moderate and high-expressing subgroups with an ORR up to 46%. Despite these encouraging signals, COFI-P was ultimately discontinued, likely due to the side effects associated with the first-generation tubulin inhibitor payload used in this ADC. With our asset, we're taking this proven target and significantly upgrading the ADC design to our Whitehawk ADC platform. HWK-007 is our PTK7-targeted ADC that was designed to demonstrate the power both of antibody engineering and our next-generation topo-1 platform. First, HWK-007 shows improved potency versus COFI-P. HWK-007 binds PTK7 with higher affinity, a slower off-rate leading to more durable target engagement and sustained delivery of payload to the tumor. Additionally, we've upgraded the ADC design with the Whitehawk topo-1 platform, and together, these changes lead to superior tumor killing across multiple pre-clinical models. For example, you can see that reflected in the xenograft data on the right. Across all dose levels, HWK-007 drives deeper and more durable tumor regressions compared to COFI-P. HWK-007 has all the attributes of the Whitehawk platform I described earlier: exceptional stability with low free payload release and favorable PK and safety margins. In short, HWK-007 ticks the important boxes that we believe will translate clinically into a potential best-in-class profile. Now on to MUC16. MUC16 is a glycoprotein with a low level of expression in normal human tissues and high level of expression in certain gynecological and other cancers. MUC16 is actually often better known once it is cleaved from the tumor as a circulating biomarker CA125, a biomarker for cancer screening and disease monitoring, particularly in ovarian cancer. MUC16 stands out as a particularly exciting target due to its super expression within gynecological cancers. As you can see on the left, in ovarian cancer, MUC16 is expressed at levels up to 10 times higher than other well-known ADC targets, including those for approved ADCs like folate receptor alpha and HER2, and is markedly higher in other tumor markers in development like CDH6, NAPPI2B, B7H4, and CLOTN6. This level of expression could translate into better selectivity, stronger efficacy compared to other ADCs in development. MUC16 expression also shows up at a high level in non-gynecological indications such as mesothelioma, non-small cell lung cancer, and pancreatic cancer, which represents potential expanse and opportunities beyond our initial focus. MUC16 is a clinically validated target, similar to PTK7, in ovarian cancer, including by Genentech's first-generation ADC DMUC4064. This program showed a promising response rate in a first-line ovarian cancer trial or, sorry, in a phase one ovarian cancer trial, but was discontinued due to limited therapeutic index. This was likely driven by two challenges. First, toxicities consistent with MAE class effects, but also by inhibition by binding to circulating CA125. This is known as an antigen sink effect. The phenomenon is depicted here. Antigen sink occurs when the MUC16 overexpressed on a tumor target is cleaved from those tumor cells and released into the circulation. The ADC binding to the shed portion of MUC16 protein in circulation is cleared from the patient rather than reaching the tumor. As is the case with DMUC4064, ADC efficacy can be dramatically hindered by this antigen sink effect. To overcome the antigen sink issue, our ADC targets the membrane-bound portion of MUC16 protein. This allows HWK-016 to bypass the antigen in circulation and get directly to the tumor. HWK-016 is the only known ADC that targets the non-shed portion of MUC16 in this way. Pre-clinical data shows that HWK-016 demonstrates superior tumor growth inhibition in vivo compared to the original Genentech program in a model where you have high circulating CA125 shedding into the circulation. That difference in the ability to suppress, we believe, will translate into a potential clinical benefit and a better therapeutic index for this molecule. Our development plans related to both of these programs at a high level focus on delivering clear differentiation that will establish our platform and for each of these individual targets as potentially best-in-class. We focus on generating well-characterized patient populations and ultimately enabling rapid expansion into additional indications based on this initial proof of concept. For HWK-007, we are focused on two leading precedent indications of lung and ovarian cancer that I showed you earlier, as well as additionally adding in endometrial cancer, which is one of the highest PTK7-expressing tumor types. Because PTK7 is upregulated across a broad spectrum of cancers, following proof of concept in these initial tumor types, we have the opportunity to expand into novel indications with potential for additional impact. HWK-016 will focus its phase one trial on ovarian endometrial cancers. We anticipate, given the expression profile combined with the advantages of our platform, that we will have the opportunity for a favorable side effect profile that could be used in combination, and we will look to further expand the benefit of HWK-016 into earlier lines of therapy in combination with standard of care in those indications. To set expectations early, I always say we have to earn the right to play from an efficacy perspective. Our initial approach is focused on exceeding the established efficacy benchmarks in these indications and delivering a potential best-in-class efficacy profile from these initial studies. We also want to make sure that we provide data once we have adequate patient numbers to draw meaningful insights. With that in mind, we expect to provide our earliest data readouts for both of these programs in early 2027 when data is sufficiently mature. Our third asset is HWK-206, and I won't spend a ton of time on this today. Just say we have a very interesting approach to a validated target called SEZ6, where we think we can best competition by establishing a biparatopic approach to targeting this target, as well as combining that with our platform. As I've outlined for you today, Whitehawk is differentiating as a next-generation ADC developer. We've selected validated targets with clear clinical precedent, but with room for leadership in high potential indications. With one of the most stable and selective ADC platforms in the field, we have optimized ADC architecture with engineering advantages like our carbon-bridge cysteine repairing technology that will enable us to lead the next wave of topo-1-based ADCs. Behind this science, we have the team and the capital to execute, and we're moving quickly into the clinic over the course of this quarter and look forward to updating you on our progress as the year goes on. With that, I'll end my prepared remarks. Excellent. Dave, a couple of minutes, maybe we can do a couple of questions. First one, very intriguing, this technology platform. You give us a lot of technical kind of explanation why you are so differentiated on the linker payload, etc., so all the conjugation. Understanding you are entering the clinic and we're going to see data kind of in a couple of years. When we can start to see proof of concept from this platform? I remember you are licensing this drug from China partners. So are they also doing this in clinical? Also when we maybe actually see some data, and so far, have you seen anything? Yeah. So it's a great question. As you mentioned, we license this technology. We have a partner in China called Hangzhou DAC, who is developing this platform on different targets within China. We understand that they have a phase one ongoing that should report data by sometime within 2026. We should see data ahead of our own data from that program. What do you want to, what will be considered as a very good positive resource to your program? Yeah, I think, yeah, it's different targets. What I always like to point people to is the fact that when you look across platforms, doses and side effect profiles tend to be consistent based on the underlying linker payload technology. When you look at read-throughs from other programs, I always encourage people to look at dose and side effect profile as the clear pieces which should be consistent between platforms. That's what I would encourage people to look for in that program. The target there is a target called CD56, which hasn't been validated previously, so it's unclear exactly what they'll show with regards to efficacy against that target, and that could be a target issue. I think dose and safety will give you a sense of the profile that we expect to have also. Any specific AE given the topo? I think you also say you are proprietary topo one. So any specific AE you would like to kind of general? I think the general class AEs for hematological toxicity is the kind of biggest problematic class AE that you see with topo-based payloads. You have about a third of ADCs which are pure exatecan, which is quite a potent topo inhibitor, but also quite a toxic one. You see a high rate of grade 3 toxicities on the heme space, particularly neutropenia. A number of folks pursue DXD or DXD-like programs, about a third of programs are that structure. We are similar to that profile, which side effects you're looking out for with the DXD programs are less about hematological toxicity, although those exist, but also reducing ILD because that's a problem with the DXD-related programs. Then about a third of programs are truly novel, and it's always a question mark exactly what to look for in each of those programs. What I would say is that what we think we really have the opportunity to do with our payload is really a heme-sparing payload, which also reduces ILD because of the FC attenuation that we've actually introduced into our antibodies. Maybe the lead program, clinical program, the PTK7. I understand you have a couple of players already developing that, discontinued, but they also have a couple still ongoing. What do you want to see from them to give you some benchmark? Yeah, it's a great question. I think within PTK7, I think it's a space you'll see really heating up this year. There's a number of programs that were announced even in the last couple of weeks for new competition within this space. It really is a hot target overall. As I mentioned, we think we have this really unique linker chemistry, which gives us the opportunity, we think, to be best in class. Of course, what we're looking for from other players is validation on the target, what their actual profile looks like. As I said, everyone's kind of going to be reporting data within a pretty small window of that, so that'll sort out as it comes. Question? Yeah. Just one other question. As you know, all the ADC payloads usually do not go into the cancer. Does your new linker payload technology, do you expect, or do you have evidence that this payload is more confined to the cancer? Yeah. What we look at is really free payload release in the animal models that we test within that to look at the ratio that's sitting at the cancer versus getting to other places. What we see is a really much stronger biodistribution to the tumor and much reduced kind of free payload available that would hit normal tissues and create that imbalance in that side effect profile. We do think that we have a molecule that is very much cleaved intracellularly, is not released extracellularly, and does do an excellent job in terms of potency, which we think is really important in those models. Sounds promising. Thank you. Yeah. Thanks. Yeah. Thanks.