Good day, and thank you for standing by. Welcome to the Xilio Therapeutics conference call. At this time, all participants are in a listen-only mode. Please be advised that today's conference is being recorded. After the speaker's presentation, there will be a question-and-answer session. To ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. I would now like to hand the conference over to Scott Young, Vice President of Investor Relations. Thank you, Operator. Good morning, everyone, and thank you for joining today's call to discuss our masked T-cell engager programs and collaboration with AbbVie. The press releases reporting these updates can be found on the Investor Relations section of our website. Before we get started, I'd like to remind everyone that statements we make on this conference call will include forward-looking statements. Actual events or results could differ materially from those expressed or implied by any forward-looking statements as a result of various risks, uncertainties, and other factors, including those set forth in the risk factor section of our SEC filings, including our most recent Form 10-Q and any other filings that we have made or may make with the SEC in the future. In addition, any forward-looking statements made on this call represent our views only as of today and should not be relied upon as representing our views as of any subsequent date. We specifically disclaim any obligation to update or revise any forward-looking statements. Following the completion of this call, a replay will be available on the Investor Relations section of our website. Joining today's call are Dr. René Russo, our President and Chief Executive Officer; Dr. Uli Bialucha, our Chief Scientific Officer; and Chris Frankenfield, our Chief Financial and Operating Officer. With that, I'm pleased to turn the call over to René. Thank you, Scott, and thank you all for joining us. We have several exciting updates to share today. First, we are pleased to announce the next phase of Xilio's tumor activation platform technology, expanding our internal pipeline with three novel masked T-cell engagers for solid tumors. The team has been hard at work on these programs for the last 18 months, applying our clinically validated tumor activation technology and capabilities to three T-cell engager targets for solid tumors: PSMA, CLDN18.2, and STEAP1. All three of these targets are clinically validated and show exciting promise that we believe can be further enhanced by our proprietary masking technology. Second, we are pleased to announce a multi-program collaboration with the team at AbbVie to advance multiple masked immunotherapies, including T-cell engagers. T-cell engagers, or TCEs, represent an important breakthrough approach in immunotherapy. TCEs have demonstrated meaningful clinical activity and led to multiple approved products to date, primarily in hematologic malignancies. TCEs are bispecific antibodies engineered to simultaneously engage two targets: CD3 on T-cells and a tumor-associated antigen, or TAA, on cancer cells. This dual binding creates a synapse that bridges the immune system's T-cells directly to the tumor cells, leading to cancer cell destruction. Historically, many promising solid tumor targets have been considered undruggable with TCEs due to their presence on healthy tissues, which creates significant toxicity concerns and has limited this class primarily to hematologic malignancies. Our masking approach seeks to address this major limitation by enabling tumor-selective activation of the TCEs and thereby significantly improving the therapeutic window, which allows us to pursue previously intractable targets. In addition, we have built a novel TCE format that further enhances the potency of our masked TCEs by incorporating a co-stimulatory signaling domain. The addition of co-stimulatory signaling is designed to promote more sustained T-cell killing of tumor cells, potentially leading to more durable responses. We've developed two different proprietary formats for masked T-cell engagers that we call ATACR and SEECR. Both formats include conditional half-life modulation designed to enable potent localized T-cell activation and tumor cell destruction, as well as an improved therapeutic index by maximizing tumor exposure and minimizing peripheral activity. The ATACR format, which is designed for speed and simplicity, is a bispecific molecule consisting of a T-cell engager with a masked CD3 targeting domain. The SEECR format, which is built for enhanced activity and further differentiation, is a trispecific molecule that builds on the ATACR format by adding a co-stimulatory signaling domain designed to further enhance potency and T-cell activation. In both the ATACR and SEECR formats, we have the ability to mask the CD3 targeting domain, the TAA targeting domain, and the co-stimulatory domain in the SEECR format as needed. We will discuss each of these formats in more detail, including our preclinical work to date and how we intend to apply these formats to our wholly-owned T-cell engager programs currently underway. With that, I will turn the call over to Chris to provide an overview of the collaboration announced earlier this morning with AbbVie. Thanks, René. We're thrilled to announce that we've entered into a collaboration license and option agreement with AbbVie to develop novel tumor-activated immunotherapies, including masked T-cell engagers. As you know, AbbVie is a global leader in developing and commercializing oncology therapies, and we believe their commitment to investing in next-generation cancer immunotherapies makes them the ideal partner for this type of collaboration. In addition, this collaboration will not only allow us to accelerate the next wave of innovation, leveraging our platform technology for masked T-cell engagers, but also enable us to advance multiple wholly-owned programs that Uli will describe shortly. Under the collaboration, we'll be advancing two initial programs leveraging our proprietary tumor activation platform. The first program is a masked T-cell engager program for an agreed-upon initial target and backup target. This is structured as an option program, where we'll advance discovery and development up to an IND data package prior to opt-in by AbbVie. The second program is for a masked antibody-based immunotherapy. This is structured as a licensed program, where we would advance discovery through early preclinical development and then hand off to AbbVie for further development. During the first three years of the collaboration, AbbVie can also nominate up to two additional masked T-cell engager programs. In terms of the financials, we'll receive $52 million in upfront payments, including a $42 million cash upfront payment and an equity investment by AbbVie of $10 million in our common stock, which closed yesterday. We're also eligible to receive up to $2.1 billion in contingent payments, which include option-related fees for the masked T-cell engager programs and development, regulatory, and sales-based milestones across all programs. Finally, we're eligible to receive tiered royalties ranging in the mid to high single digits on annual global net product sales. We anticipate the upfront payments from our AbbVie collaboration will extend our cash runway into the first quarter of 2026. This marks not only our third collaboration with a major pharma company, but also another important step forward in our commitment to leveraging our differentiated discovery engine to seek to develop transformative treatments for people with cancer. We look forward to working with the AbbVie team to maximize the potential for our platform in tumor-activated immunotherapies. With that, I'll turn the call over to Uli to provide an overview of our newly unveiled internal masked T-cell engager programs. Thank you, Chris. We're excited to share with you today the work that we've been doing for the last 18 months or so, applying our masking approach to T-cell engagers. We believe that these molecules have the potential to deliver meaningful clinical benefits to patients with a favorable safety profile. From our view, T-cell engagers are particularly well-suited for the masking approach, considering they are potent immunoagonists that have traditionally been limited by toxicity. As René mentioned, we have developed two formats of masked T-cell engagers, which we refer to as ATACR and SEECR. Regardless of the format, each of our masked T-cell engager molecules incorporates a tumor-associated antigen, or TAA, targeting domain, a masked CD3 binding domain, and a half-life extension domain. The TAA targeting domain is responsible for binding of the molecule to a tumor-associated antigen expressed on cancer cells. The CD3 targeting domain binds to CD3, which is a component of the T-cell receptor complex present on all T-cells. The half-life extension domain is a protein scaffold that enables antibody-like half-life in circulation and prevents rapid clearance when present. The SEECR format builds on our ATACR format by adding a co-stimulatory domain to the molecule that is designed to further enhance its potency. The co-stimulatory domain is a signaling molecule that provides additional co-stimulatory signaling to T-cells and results in enhanced T-cell activity. I'll also note that both formats are compatible with masking the TAA binding domain should a chosen tumor-associated antigen require it. All of these components and format design choices work together to optimize the therapeutic index of our T-cell engagers. First, our CD3 mask is optimized to prevent T-cell engagement in healthy tissue, greatly limiting potential for tumor toxicity, and we believe it is best in class. Second, our highly efficient and clinically validated masking technology allows for selective activation of the molecule in the tumor microenvironment, focusing the molecule's effects on the tumor cells to result in potent T-cell-mediated cancer cell killing. Third, our molecules are designed to lose the half-life extension domain following activation, enabling rapid clearance and systemic circulation and thereby contributing to limited peripheral activity. The first three targets that we are pursuing for our masked T-cell engagers are PSMA, CLDN18.2, and STEAP1. I'll note upfront that all three of these targets have seen clinical validation with systemically active, non-masked T-cell engagers in the clinic. However, toxicities, including Cytokine Release Syndrome, or CRS, as well as on-tissue, off-tumor toxicities, have been challenging to date. PSMA is a prominent prostate cancer antigen and has recently seen some exciting proof of concept with masked T-cell engager approaches, which support our belief that masked TCEs have significant therapeutic potential. For PSMA and CLDN18.2, our first two ATACR programs, we have decided to only mask the CD3 domain and leave the TAA arm unmasked. Given the lineage-restricted expression pattern of PSMA and CLDN18.2, as well as our highly efficient CD3 masking approach, we believe this is the best design. I'll note here, however, that both the ATACR format and the SEECR format for our masked T-cell engagers are fully compatible with a dual-mask design that incorporates masking of the TAA arm should a chosen target require it. Overall, our aim for the PSMA ATACR molecules is to go fast while further improving the masking efficiency relative to other molecules in development. We believe a best-in-class CD3 mask has the potential to further improve the therapeutic index of T-cell engagers, enable higher dosing, and ultimately potential for enhanced activity. Moving to CLDN18.2, this is a tumor-associated antigen with broad therapeutic potential, considering its high expression in several GI cancers as well as lung cancer. Our aim is to also develop CLDN18.2 using our ATACR format, and we believe a masked TCE targeting CLDN18.2 could be first in class. Finally, for our third internal program, we are pursuing STEAP1, a promising tumor-associated antigen expressed in prostate cancer as well as subsets of colorectal and lung cancer. We're developing our TCE for STEAP1 in our SEECR format, which includes an additional co-stimulatory domain. As demonstrated by our preclinical data, co-stimulatory signaling potentiates enhanced T-cell expansion and fitness compared to standard non-masked T-cell engagers, both in vitro and in vivo with excellent PK and tolerability. STEAP1 in our SEECR format is essentially a trispecific molecule that combines T-cell receptor stimulation with potent co-stimulation in a single molecule, something that we believe is only achievable in a tolerable manner using our tumor-activated or masked design. Now for some data on the ATACR format molecules. We developed our initial PSMA ATACR molecules and also produced an analog of Janux Therapeutics, JANX007. As you can see on the left-hand side in this in vitro T-cell tumor cell co-culture assay, JANX007, which is shown in the blue color, shows a difference in potency between the masked state in the open triangles and the activated state in the filled triangles, showing JANX007 behaves like a masked TCE. However, we also see that in our ATACR design, it demonstrated a broader window between the masked state and the activated state, which we believe indicates that our masking solution is very effective and could ultimately contribute to an even better therapeutic index, particularly at high exposures immediately following dose administration. This has the potential to further reduce the incidence and severity of CRS, or Cytokine Release Syndrome, which, as we know, can be a serious adverse event commonly associated with immunotherapies, and this could ultimately position us to deliver higher doses with the potential for more durable PSA declines and improved activity as a best-in-class molecule. On the right-hand side of the slide, we show that our ATACR format is highly active in vivo, driving robust anti-tumor activity with excellent tolerability. We also confirmed that activity is tied to proteolytic activation of the molecule in vivo as a non-activatable form of the molecule where we replace the cleavable linker with a non-cleavable linker, which shows negligible activity. Together, these data indicate the ATACR format enables tumor-activated, high-potency T-cell engagement with broad applicability across TAA targets. Switching gears to look at our SEECR format, recall that this incorporates co-stimulation alongside CD3 and TAA arms. One of the first things we wanted to understand was whether incorporation of co-stimulation into our masked TCEs in the SEECR format indeed provides benefit. To this end, we built a repeat stimulation in vitro assay that assesses the ability of the T-cell to elicit serial killing of tumor cells and thereby allows us to assess durability of the T-cell response. What we saw was that the first time these T-cells encounter tumor cells, we see a similar type of response between a regular non-masked T-cell engager and a SEECR molecule. Both molecules are able to induce killing of tumor cells by T-cells. However, by the second time the same T-cells encounter tumor cells, the regular non-masked T-cell engager is already less potent. By the third time, we don't see any activity from the standard non-masked T-cell engager, and the T-cells are exhausted. This is in contrast to what we see with T-cells treated with the SEECR molecule. Here, the T-cells continue to kill tumor cells effectively over multiple rounds, supporting that co-stimulation in the form of the SEECR format enables more durable T-cell responses. This is very much in line with our understanding of the immunology of co-stimulation, allowing for these cells to expand further, more durably, and remain less exhausted. Next, we wanted to confirm that the benefits observed with the SEECR format in vitro also translated in vivo, and the short answer is they do. On the left-hand side here, we show that T-cell influx into the tumor is significantly enhanced with the SEECR format compared to a standard non-masked T-cell engager. We also see that the tumor-infiltrating T-cells continue to proliferate at a higher rate with SEECR. Perhaps most importantly, on the right-hand side, we show that this translated into enhanced potency. The SEECR molecule clearly outperformed the non-masked T-cell engager. In fact, we saw frank regressions in the majority of animals treated with the SEECR molecule, whereas with a standard non-masked T-cell engager, at these matched dose levels, we only saw minimal anti-tumor activity. Again, we believe this is due to the unique design of SEECR incorporating the co-stimulatory domain alongside potent CD3 and TAA engagement. To round out this section, here's how our pipeline of masked T-cell engagers is currently taking shape. We are advancing PSMA and CLDN18.2 in our ATACR format and STEAP1 in the SEECR format, with a cascade of development candidates starting later this year, and we're excited to be advancing additional targets in collaboration with AbbVie. I'll note that we're maintaining optionality on the specific format chosen for our masked immune cell engagers and may advance any of our targets in either ATACR or SEECR format, depending on whether speed or further differentiation is most desired. I'd now like to turn it back to René for closing remarks. Thank you, Uli. As you heard from the team this morning, we're incredibly excited to be embarking on this next stage of Xilio, applying our unique masking technology to T-cell engager targets for solid tumors with three newly announced internal programs and in our collaboration with AbbVie, which is our third collaboration with a major pharma partner. AbbVie is a well-recognized global leader in oncology therapeutics, and this partnership with the AbbVie team allows us to accelerate the expansion of our technology platform to next-generation immunotherapies, including masked T-cell engagers. In addition to the milestones that Uli laid out for our masked T-cell engager programs, we continue to look forward to multiple clinical and preclinical milestones across the Xilio pipeline in 2025 and beyond. With that, let's open the call for questions. Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. One moment for questions. Our first question comes from Michael with Morgan Stanley. You may proceed. Good morning. Thanks for taking the question, and congratulations on all the progress and the deal as well. Maybe just I want to talk a little bit about the ATACR and SEECR platforms. Looks like SEECR is more potent based on the data you shared with us, but just curious how you decide which indications to go after with which platform, and Uli touched on this a little bit, but just curious, or would it make sense that more potent molecule would in general be better or not necessarily? Thanks. Yeah, thank you, Mike. Appreciate the question. The way we are sort of thinking about this is in each cell Engager program, we will initiate on the ATACR format, and then if we feel that, given the target and the competitive landscape, that speed and efficiency in getting there quickly with a simple design is the right approach for that target, then that is ideal, right? Simplicity is always ideal when that is all you need. However, at any point in time, if we believe that additional differentiation is needed or enhanced activity with that co-stimulatory signaling, SEECR is built on ATACR, so it just continues forward. We do have some flexibility in how we approach this. Based on what we know right now, we believe that taking that ATACR approach, speed, and simplicity is the ideal strategy for our first two programs, PSMA and CLDN18.2, but that is flexible, right, as the landscape evolves and as we see our data. Let me turn it over to Uli to kind of go deeper on that. Thanks, René. Yeah, from our perspective, both of these formats have their place in applying to the targets of our pipeline. I will just point out one thought we've had on SEECR in particular is we do, of course, recognize that certain tumor indications are traditionally less inflamed, maybe really more susceptible to having co-stimulation on board, and then there are other tumor types where T-cell engaging modalities have seen some early promise. We are going to maintain very open-eyed as we apply these formats to our targets going forward. Makes sense. That's super helpful. Maybe just a quick follow-up in terms of your cash runway. Looks like you've been able to extend it into 1Q of next year. Just if you can, the deal with AbbVie, maybe talk about what the next potential milestone there might be, maybe the size and trigger, just trying to get a sense of when that might roll in. Thanks. Yeah, thanks, Mike. That's correct on the cash runway. It is now into Q1 of 2026, and that includes just the upfront $52 million for this deal. There was a lot of reasons why doing this partnership made a lot of sense for us, and we're excited about it. One of those is that ongoing milestones, right, do continue to support the company with an ongoing capital infusion, and so that is an important piece of these programs going forward. We're not disclosing those details of how that's broken out, but I think it is a key component of why this makes a lot of sense for us. I'll turn it over to Chris if he wants to add anything. Thanks, René. Yeah, Mike, as René mentioned, part of what's really compelling here is both for the T-cell engager programs in this collaboration as well as the antibody-based program, there are meaningful milestones as those progress. As she said, we won't guide to those, but I would say there's a number of those, particularly as you advance to the IND for the option-based programs, and then there's meaningful opt-in fees for those as well. Got it. Thank you. Yep, great. Thank you. Our next question comes from Marc Frahm with TD Cowen. You may proceed. Hey, thanks for taking my questions and congrats on today's updates. Maybe first off, just on the PSMA ATACR design, where you provided a little bit of data there, just what do you think about the design as driving that potentially wider therapeutic index versus the Janux molecule? Is it important differences in the underlying TCE? Is it affinity of the mask for the TCE, or is it really all about kind of the cleavage domain and how efficiently that gets cleaved? Yeah, thanks, Marc. Appreciate the question. I would say overall, right, all of the components of our technology platform kind of work together, right, to maximize the masking and also the efficient unmasking and really tuning that in. We have the benefit now of having been in the clinic with three different programs with our masking technology and each time been able to learn, go back, and kind of integrate the clinical learnings back into our design. I think we've really kind of nailed this, and the process has become much more efficient for us. I'm going to turn it over to Uli to kind of answer your question more specifically. Yeah, thanks for the question, Marc. What we have done over the last 18 months is really refine and expand our capabilities on masking pretty much any protein surface. That is supported by display libraries we've built, and the result of that has been finding a masking solution for our CD3 domain that we think is highly efficient. That is important because you need to tune in the right level of affinity, but then also the mask needs to come off post-cleavage. As René pointed out, we generally profile the entire molecule in multiple assay systems to ensure that we have fully locked down what we want to mask, but that release is efficient. I think here we have the benefit now of multiple cleavage elements that we've clinically validated to incorporate alongside, again, a best-in-class masking solution. Does that answer your question? Yep, that's helpful. Maybe just following up on Mike's question, just with unmasked, just naked TCEs for PSMA and STEAP1 in prostate cancer, we've definitely seen tolerability issues with both targets, but maybe a bit wider therapeutic index with STEAP1. Just that decision on using ATACR for PSMA versus SEECR for STEAP1, on the PSMA side, is the view that just SEECR is just too much and adding that co-stim kind of starts to overwhelm the benefits of masking, or do you just think the potency of a PSMA is just so good that you don't need SEECR? Yeah, from our perspective, as we noted, we keep that option open, but at this point in time, we've been really encouraged by what we've seen on PSMA ATACR. With regards to the co-stimulation, one of the reasons we're applying that in the case of STEAP1, as you know, some other molecules out in development, they're really designed to target only the top expressors via an avid binding scenario. We want to capture the full population of STEAP1 positives, and not just in prostate cancer, but ideally in subsets of cancer, including colorectal and lung. For that, we think co-stimulation might open up that broader patient population. Okay, that's really helpful. Thanks for taking the question, and congrats again. Thanks, Marc. Thank you. As a reminder, to ask a question, please press star one one on your telephone. Our next question comes from Laura Prendergast with Raymond James. You may proceed. Hey, guys. Congrats on all the exciting news today. I was hoping that you guys could maybe elaborate a bit more on how the mask interacts with the T-cell engager and how this might differentiate versus how some of your other assets do. I just want to clarify, does this updated cash runway include any of the milestones from the Gilead partnership? Thanks. Thanks, Laura. I'll take the second part, and then we can turn the first part over to Uli. The cash runway does not include any potential upcoming milestones from the Gilead collaboration. Those would be in addition to this Q1 2026 runway. Got it. Thanks. In terms of, I think you're asking exactly how the differentiation in the masking and maybe how it relates to our clinical stage molecules and what are some of those specific design features. I'll turn that back to Uli. Yeah, thank you, Laura. For our masking, when we start out with a project and wanting to mask a particular protein surface, what we do is we really look at that closely, take into consideration structural information, and then we design a path towards the mask that leverages the right display libraries and discovery approaches we have. What that means is that for an antibody that we want to mask, we know exactly what libraries to use in order to find a mask that has high affinity and blocks where that antibody would interact with its target. For the cytokines here, typically there have been multiple interactions that those cytokines need to engage with their target. There, again, we've used a combination of empirical and structure-guided approaches to find the right masking solution. All in all, in the case of these T-cell engagers, the anti-CD3 domain is an antibody-based domain, and so we could leverage a lot of our experience in masking antibodies over the years. Got it. Thank you. Thank you. As there are no more questions in the queue, I'd like to turn the microphone back to Dr. Russo. Thank you for the call today. We look forward to keeping you updated on our progress in the months ahead. Thank you. This concludes the conference. Thank you for your participation. You may now disconnect.