Good day, and thank you for standing by. Welcome to the Bicara Therapeutics first quarter 2026 earnings conference call. At this time, all participants are in a listen-only mode. After th e speaker's presentation, there will be a question-and-answer session. To ask a question during the session, you will need to press star one one on your telephone. You will hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please be advised that today's conference is being recorded. I would now like to hand the confe ren ce over to your first speaker today, Rachel Frank, Vice President of Investor Relations and Corporate Communications. Please go ahead. Thank you, and good morning, everyone. It's a pleasure to welcome you to Bicara Therapeutics' first quarter 2026 earnings call. Earlier this morning, we issued a press release highlighting results from the quarter in recent business progress. You can access the press release as well as the slides that we'll be reviewing today by going to the investor section of our website. Before we begin, please note that this call will include forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. Please refer to our most recent SEC filings for important risk factors that could cause our actual performance and results to materially differ from those expressed or implied in these forward-looking statements. Any forward-looking statement made on this call represents our views only as of today, and we disclaim any obligation to update any forward-looking statements. Joining us on the call today are Claire Mazumdar, Chief Executive Officer, Bill Schelman, Chief Medical Officer, Ryan Cohlhepp, President and Chief Operating Officer, and Ivan Hyep, Chief Financial Officer. I'll now turn the call over to Claire. Good morning, thank you for joining us today. The 1st quarter of 2026 set a strong foundation for the year ahead. We made measurable progress on the strategy we outlined earlier this year, with continued momentum behind our lead asset, ficerafusp alfa or FICERA, which we believe is a potentially best and first-in-class bifunctional EGFR-directed antibody combined with a TGF-beta ligand trap for the treatment of HPV negative first-line head and neck cancer. Our priorities remain focused on executing a strategic development plan for FICERA, preparing for commercial success by laying the foundation to capture a large and growing global market in head and neck cancer, and expanding FICER A's potential beyond our lead indication while maintaining financial discipline. To deliver on those priorities, we are building the team to match our ambitions as we transition from a clinical stage to a commercial stage organization. With that in mind, I want to share a few updates this morning. After several years as our Chief Medical Officer, David Raben has transitioned to a Senior Executive Advisor role, and Bill Schelman, previously Executive Vice President of Clinical Development, has stepped into the CMO role. David has been instrumental in shaping Bicara into the company it is today, guiding FICERA into pivotal phase III development and building the foundation of our clinical and medical organization. We are deeply grateful for his contributions and look forward to his continued partnership in his advisory capacity. Bill is well-positioned to build on that foundation. He joined us last fall as an experienced development and commercial stage leader and has quickly made an impact across our development programs. As we build toward commercial launch, we are thrilled to have brought on a proven leader to guide that work. Chris Sarchi joined last week as our Chief Commercial Officer, bringing extensive oncology, commercialization, and leadership experience. Chris will continue building out the team with additional hires across market access and commercial operations in the months ahead. In addition, we made a number of key updates in the first quarter. First, our continued execution has us on track to achieve substantial enrollment in FORTIFY-HN01 by the end of the year, positioning us for an interim analysis in mid-2027 for potential accelerated approval. With that progress, our belief in FICERA's potential to be both best and first-in-class in frontline recurrent and metastatic HPV-negative head and neck cancer has only strengthened. That conviction is grounded in FICERAS's differentiated mechanism, the depth and durability of response we have observed in our development approach. Recent developments in the competitive landscape are reinforcing this view. While the market has at times viewed peer timelines as ahead of ours, that picture is changing, driven by our own continued progress as well as the significant upsizing of a peer's pivotal trial. Together, these dynamics support our potential path to first-in-class. They also validate the strategic choice we made to develop FICERA specifically for HPV-negative patients, where the science, the unmet need, and the commercial opportunity align. Second, and Bill will speak to this in more detail, based on discussions with the FDA, we plan to initiate a study that will evaluate FICERA in combination with pembrolizumab as a loading and every three-week maintenance dosing regimen. This is an advancement that we believe has the potential to expand optionality for patients and providers and enhances the long-term commercial profile of FICERA. Just last Friday, a peer-reviewed manuscript was published in the Journal of Clinical Oncology detailing results from our phase Ib expansion cohort evaluating 1,500 mg of FICERA weekly in combination with pembrolizumab in frontline recurrent and metastatic head and neck cancer, data most recently presented at ASCO 2025. This publication is an important milestone that validates and adds to the growing body of scientific evidence supporting FICERA's differentiated mechanism of action and clinical benefit. It also provides the broader oncology community with a peer-reviewed view of the data underpinning our pivotal program. Lastly, with the completion of an oversubscribed public offering in February, built on an already strong cash position, we are well-positioned to invest in the opportunities ahead of us. As we look ahead to the next quarter and the remainder of the year, we're excited to share meaningful long-term follow-up data at ASCO in a few weeks. The data will further characterize FICERA's safety profile, along with the depth and durability of response driven by TGF-beta inhibition. These data span all three clinical doses tested in expansion cohorts, including the dose we're advancing in our pivotal trial. We are also continuing to enroll multiple phase Ib expansion cohorts to identify early proof of concept signals and inform FICERA's development strategy, both within head and neck cancer and across solid tumors. With that, I'll turn it to Bill to walk through our recent clinical updates and what to expect from us at ASCO this year. Thanks, Claire, and good morning, everyone. We have taken a deliberate and thoughtful approach to evaluating FICERA in patient populations with high unmet need and with the strongest biological rationale. This has included development in head and neck cancer, as well as other solid tumors, including metastatic colorectal cancer, cutaneous squamous cell carcinoma, and anal cancer. In that context, our recent disclosures have focused on clinical data from approximately 90 patients across three cohorts from our phase Ib study evaluating FICERA in combination with pembrolizumab in front-line recurrent or metastatic HPV-negative head and neck cancer. This patient population has particularly poor outcomes with limited treatment options and represents the vast majority of patients in this setting. The 1,500 mg weekly plus pembrolizumab cohort, which is the dose we are currently evaluating in the phase III portion of the FORTIFY-HN01 pivotal trial, was presented at ASCO last year and represents our most mature data set. With two years of follow-up, deep and durable responses were observed with a median duration of response of 21.7 months and a median overall survival of 21.3 months, more than doubling the overall survival observed with the standard of care pembrolizumab in HPV-negative patients. The 750 mg weekly plus pembrolizumab cohort supported the evaluation of the optimal biological dose of FICERA in the phase II portion of our ongoing FORTIFY trial and helped to inform selection of the 1,500 mg weekly as the OBD that is currently being evaluated in the phase III portion of the study. The data from these cohorts also reinforces our confidence in the interim analysis of overall response rate as the foundation for pursuing accelerated approval. The cohort evaluating 2,000 mg of the every other week plus pembrolizumab demonstrated that even at a less frequent dose, we see rapid and deep responses that are the hallmark of the FICERA clinical profile. The data from this cohort also helped inform our alternative dosing regimen study. Across all three phase Ib cohorts, the depth and durability of response observed underscore the central role of TGF-beta inhibition in FICERA's mechanism. By enabling tumor penetration, TGF-beta inhibition drives the kind of deep and durable responses that translate to long-term survival benefit. Taken together, the data presented to date affirm that FICERA has the potential to be a well-tolerated chemotherapy-free treatment option across the spectrum of disease burden, including in patients with large, bulky tumors and low CPS scores, where rapid and deep responses are particularly critical. As we look towards ASCO 2026, we will be presenting updated data across all three of these cohorts from the phase Ib study. We will provide three-year follow-up data from the 1,500 mg cohort, which will allow us to characterize the long-term efficacy from this dose compared to the standard of care. We will also share long-term endpoints from the 750 mg weekly and the 2,000 mg every other week data sets. These data will provide the most comprehensive look at FICERA in front-line recurrent and metastatic HPV-negative head and neck cancer to date, including durability of outcomes not seen with other investigational agents targeting EGFR in this setting, a key differentiator and a signal of FICERA's best-in-class potential. Additionally, the strength and consistency of these results across cohorts further de-risk our pivotal FORTIFY-HN01 trial. Another key aspect of our ASCO update is that we'll further characterize the role of TGF-beta in head and neck cancer. TGF-beta inhibition is the defining feature of FICERA and what sets it apart from other EGFR-directed therapies. Our translational data has shown consistent TGF-beta inhibition across all FICERA doses, confirming the mechanism behind tumor penetration and immune activation, with the strongest inhibition at the 1,500 mg weekly dose and the 2,000 mg every other week dose. We'll also look to show how tumor penetration driven by TGF-beta inhibition translates into depth and durability of response that leads to long-term outcomes for patients. Alongside the clinical story we'll continue to build at ASCO, we're also focused on optimizing how FICERA is delivered to patients. As previously mentioned, based on discussions with the FDA, we plan to initiate an alternative dosing study in the third quarter of this year. This study will enroll approximately 150 to 200 patients and will evaluate the efficacy of FICERA on a 12-week loading phase, followed by an every three-week maintenance phase regimen. All patients will receive 1,500 mg weekly of FICERA plus pembrolizumab for 12 weeks and will then be randomized to either continue 1,500 mg weekly of FICERA plus pembrolizumab or transition to 2,250 mg every three weeks plus pembrolizumab. The primary endpoint will evaluate progression-free survival. In designing an alternative dosing regimen, our priority is to preserve FICERA's potential best-in-class profile while creating practical options for patients and providers. We expect to seek accelerated approval for FICERA with the 1,500 mg weekly dose from the FORTIFY-HN01 study, running this randomized study in parallel will allow us to potentially have results from this study in time for a potential approval, creating a compelling path for early adoption of this streamlined regimen. Additionally, this addresses an important need for patients, providers, and payers, specifically by providing treatment options that will reduce clinic burden, improve quality of life, and support long-term adherence. Critically, this dosing strategy is shaping how we are thinking about life cycle management and FICERA's opportunity beyond frontline, recurrent, or metastatic head and neck cancer. With that, I'll turn it over to Ryan to discuss the potential market opportunity and what's ahead for the rest of the year. Thank you, Bill. Turning to the broader opportunity, we have strong conviction in the differentiated profile FICERA has shown across our clinical program compared to other investigational agents in head and neck, and the development strategy we built around that profile is designed to deliver against the full opportunity a head. Head and neck cancer is a significant and fast-growing global market projected to reach more than $5 billion in global sales into the 2030s. HPV-negative patients represent a large majority of patients in the frontline recurrent metastatic setting, and HPV status is known at the time of diagnosis, which means that HPV testing is not a barrier to care. Across major markets, there are roughly 50,000 annually incident patients, including approximately 18,000 in the U.S., where we plan to launch initially. The unmet need in this population for a therapy that drives deep, durable, and clinically significant benefit while sparing chemotherapy and improving quality of life is what makes the rigor of our clinical data and the discipline of our development strategy matter. It is also why we continue to invest in the medical and commercial infrastructure required to deliver FICERA to patients. This includes the commercial leadership team we have been building, with Chris now leading our commercial efforts, including the pre-launch evidence generation and field readiness work required for a successful oncology launch, and we look forward to having him on the road with us at ASCO and beyond. While the frontline recurrent metastatic setting is our initial focus, the opportunity for FICERA in head and neck cancer is much larger. Given our conviction in FICERA's potential to be both first and best in class, we see clear space to own and lead a broader segment of the head and neck cancer landscape. The locally advanced setting, in particular, represents another large market with clear biologic rationale for FICERA and a meaningful opportunity for expansion. As we think about that opportunity, we have initiated two investigator-initiated sponsored studies in the locally advanced setting and continue to enroll additional cohorts that will inform our expansion strategy, including a cohort of patients in frontline recurrent metastatic HPV negative head and neck cancer with CPS less than or equal to one as well as a cohort of patients with frontline recurrent metastatic HPV positive head and neck cancer with heavy history of smoking. Beyond head and neck, we believe there is a strong biologic rationale to expand FICERA's pipeline and the potential into a solid tumor types with significant unmet need. We have already shown proof of concept in indications such as cutaneous squamous cell carcinoma and anal canal cancer, reinforcing our conviction in FICERA's broad applicability across TGF-beta driven tumors. Building on that foundation, we are currently enrolling patients in a phase Ib expansion cohort evaluating FICERA both as a monotherapy and in combination with pembrolizumab in patients with third line plus metastatic colorectal cancer. TGF-beta is implicated in metastatic disease and resistance to current treatments, providing a biologic rationale for evaluating FICERA in this setting. This is also a challenging setting. Patients are very sick, often progressing rapidly through prior lines of therapy. With the treatment landscape d i CRC continuing to evolve, we are taking a measured approach with a high bar for what would warrant further investment. As the data mature across these cohorts, we will continue to make thoughtful decisions about where FICERA can deliver the most differentiated value and how we allocate our resources accordingly. With that, I'll turn it to Ivan to review the financials. Thanks, Ryan. Earlier this morning, we reported detailed first quarter 2026 financial results in our press release. I'll summarize a few highlights here. Our total operating expenses for the first quarter of 2026 increased compared to our first quarter of 2025, driven by clinical operations and development expenses associated with our ongoing pivotal FORTIFY-HN01 study, including increased manufacturing and development costs. We also saw an increase in personnel-related costs, including stock-based compensation, as we have grown our workforce primarily in support of clinical operations and development functions. Consistent with the first quarter, we anticipate continued increases in operating expenses for 2026, reflecting increased investment in our clinical operations, particularly for the pivotal FORTIFY-HN01 study with the interim analysis expected in mid-2027 and parallel study, as well as an increase in SG&A as we invest in early commercial and medical infrastructure to support the potential launch of FICERA. We ended the first quarter of 2026 with $539.8 million in cash, cash equivalents, and marketable securities. Bolstered by an oversubscribed public offering in February that generated $161.8 million net proceeds and meaningfully strengthened our balance sheet, which provides cash runway into the first half of 2029 and allows us to invest thoughtfully in areas we believe will deliver future clinical and commercial success. With that, I'll now turn the call back over to the operator for questions. Operator? 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. In the interest of time, we do ask that you please limit yourself to one question. Please stand by while we compile the Q&A roster. Our first question comes from Eric Schmidt of Cantor. Your line is open. Good morning. Thanks for taking my question. Maybe one in terms of what to expect at ASCO in a couple of weeks' time. Can you provide us with any benchmarks for three-year outcomes data, landmark data in HPV negative head and neck? Then you mentioned looking at the role of TGF-beta as well. Does that mean that we're gonna see some correlations between PD and response rates? Thank you. Thank you for your question, Eric. The question was relating to a preview of the ASCO 2026 datasets. As we highlighted during the call, there are two separate abstracts that were accepted as behalf of ASCO. One is focused on long-term follow-up in terms of the three expansion cohorts in frontline recurrent and metastatic HPV negative head and neck, with the most mature dataset being the 1,500 mg one you were alluding to, which will have three years' worth of median follow-up. In that one, we really hope to speak to the so-called immunotherapy tail driven by the TGF-beta durability. In there, if you look at prior precedents, pembrolizumab in all comers delivers about a 20%-25% three-year overall survival, while it's believed to be about 15%-20% in the HPV negative subset from real-world datasets. The other abstract is focused on looking at depth and durability of response but from the TGF-beta inhibition. We'll continue to speak to what we believe is FICERA's defining hallmark, that TGF-beta inhibition is driving this depth of response that's ultimately leading to far superior durability than other investigational agents and leading to outsized overall survival benefit. Thank you. Thank you very much. Thank you. Our next question comes from Tyler Van Buren of TD Cowen. Your line is open. Hey, guys. Good morning. Congrats on the progress. Thanks for taking the question. Just wanted to ask a quick follow-up before my question, if you don't mind. A follow-up on Eric's question related to the ASCO data. I guess it's clear that we'll have three years of follow-up with the 1,500 mg dose, but since investors are asking, it would be helpful if you could just clarify how much follow-up we should expect with the 2,750 dose cohorts. We can obviously guess, but just clarity there would be helpful. Then, I guess my main question is related to the alternate dosing regimen of the 1,500 mg induction with the 2,250 mg maintenance. Do you think it's possible that that regimen could have improved durability than either 1,500 mg or 2,250 mg alone based upon exposure and the data you've produced to date? Thanks for your questions, Tyler. I'll answer the first question first, which is a question around the other two cohorts being presented at ASCO, which are the 750 mg weekly cohort as well as the 2,000 mg every two week cohort. Both of those have approximately 12 to 18 months' worth of median follow-up. We do plan to share longer-term follow-up datasets for both of those at ASCO in a few weeks. To help answer your question around durability of response in the maintenance setting, I'll pass that question over to Ryan. Thanks, Tyler, for the question. You know, in terms of the regimen, you know, again, the overall approach that we are taking there, as you mentioned, is we're initiating with the 1,500 mg weekly and then transitioning to a maintenance phase at 2,250 mg. A couple, I think, key tenets of that approach. One, you know, as you recognize from the data that we've presented thus far, you know, we see deep, rapid responses which are enabled by the 1,500 mg dose. You know, really being able to get a depth of response, you know, more than 80% of our patients are getting depth of response of 80% or greater, which we really believe is contributing to that durability. One of the things that the 2,250 mg every three weeks enables is an exposure profile that allows us to, I think, maintain that durability after we've received or achieved very meaningful reductions in tumor reductions. You know, keeping patients on from a tolerability perspective, you know, I think being able to bring people into clinic every three weeks rather than every week while maintaining exposures that maintain that durable response, we absolutely believe that, you know, this regimen potentially enables both a more durable as well as a better, a more tolerable profile. Thank you. Our next question comes from Stephen Willey of Stifel. Your line is open. Yeah, good morning. Thanks for taking the questions. Maybe just some color around the use of PFS as a primary endpoint in the dose optimization trial, just given that this is obviously an adventure of an endpoint, there's no control arm. Is there a formal non-inferiority margin that you need to hit? I guess just any color you can provide around kind of this formal notion of comparability would be helpful. Thanks. Thanks for your question, Steve. I'll actually answer the second part of your question first, around non-inferiority. This is actually not designed as a non-inferiority study. We got positive feedback from the FDA based off of our discussions. Based off of the sizing of the study, which we alluded to being, approximately 150 to 200 patients, it would have required far more patients as a non-inferiority study. The other focus, again, going back to Tyler's question, the other focus of looking at this dosing regimen is really, again, to ensure that we're maintaining the efficacy profile focused on depth and durability of response with the induction into maintenance dosing. The focus of the PFS endpoint was really to look at that, ensuring the durability is consistent between the two arms. The FDA was comfortable with PFS being that endpoint for that reason. Great. Thanks. Thank you. Our next question comes from Kelsey Goodwin of Piper Sandler. Your line is open. Hey, good morning. Thanks for taking my questions. I think you alluded to it in the prepared remarks, but for your competitor's frontline trial where they increased target enrollment by about 200 patients, I just first wanted to confirm, is there any read-through to Fortify in its trial size? Secondly, how do you think about the gap in timing now between FICERA and PETO? Thanks so much. Thank you for your that question, Kelsey. Just to highlight, we were alluding to the LiGeR-1 study, and you may have not seen on ClinicalTrials.gov that the page was updated to reflect enrollment of 700 patients, up from the original 500 in an all-comer study. I think that's consistent with feedback we've been hearing from investigators that they were planning to add additional HPV-negative patients. From what we have heard today is that, you know, there was potentially an imbalance in terms of HPV-positive versus HPV-negative patients in that particular study, given that there are no other HPV-positive studies in phase III. We haven't seen any read-through other than the fact that, you know, it continues to highlight what we've always highlighted, that FICERA has the potential to be both best and first in class. We've seen very strong execution of the FORTIFY-HN01 study, and those dynamics continue to speak to what we believe is a significant narrowing of the perception around FICERA and FORTIFY being second to market. In fact, we continue to believe in our potential first in class. That's great. Thank you so much. Thank you. Our next question comes from Bradley Canino of Guggenheim. Your line is open. Hey, good morning. Thanks, team. It's nice to be on the call. At ASCO, maybe just to drill into one of the doses, the lower 750 mg, which wasn't selected for the phase III. How do you look at that as really being able to support the TGF-beta hypothesis, given the exposure and coverage that it provides? Will that view only be in a subset of patients such as the responders? Just a quick second, given we're talking about the competitor trial and the upsize, where do you sit with expected timing of OS analysis for your phase III study today? Thank you. Thanks, Brad, for your question. Welcome to the team. To the first question around the 750 mg dose. That was, as you highlighted, a dose that we did not take forward in the pivotal phase III study. However, we do see significant TGF-beta inhibition. We know that from an EGFR receptor occupancy, we are fully saturating the EGFR locus. We've always thought of it as still superior than EGFR monoclonal antibody while showing slightly less TGF-beta inhibition. What you will continue to see at ASCO is that even in this patient population, the hypothesis that TGF-beta inhibition is driving improved depth and durability, will continue to speak to another strong data set that will reinforce the notion now in a total of 90 patients, that we have strong depth and durability data that will speak to outside overall survival benefit. Your second question was related Timing of OS analysis for your study. The timing for OS. Yes, I apologize. Timing of OS analysis. As we continue to guide to the interim analysis for potential accelerated approval, is slated for mid 2027, which is a look at overall response rates with six months of durability and likely a look at qualitative overall survival at that time. We do anticipate being focused on HPV negative patients only, that our event rates will happen more rapidly than those of our peers, and that the OS endpoint will come again more rapidly than anticipated. Great. Thank you. Thank you. Our next question comes from Judah Frommer of Morgan Stanley. Your line is open. Yeah. Hi, good morning. Thanks for taking the questions, guys. Maybe just broadening out the competitor conversation a bit. We saw some data from an OX40 targeting asset this morning, but I believe in CPS greater than 20. Maybe can you just remind us of kind of the breakdown of the epidemiology by CPS score and kind of, you know, what the advantages of a broader targeting asset in FICERA could be, and again, what timelines could look like versus this asset? Thanks. Thanks for your question, Judah. I do believe you're referring to an ENHERTU presentation that actually I believe is happening at the same time as our call. While we haven't had a chance to significantly look at the dataset, I can speak at a high level to those results. As you alluded to, the dataset from I believe a randomized phase II is focused on CPS greater than or equal to 20. These are considered the CPS high patients who typically do respond to pembro monotherapy. What we do know is that FICERA is being in the FORTIFY study, is being looked at in the CPS greater than or equal to one. As well, we have shown some strong results from our late line patients in CPS 0 and are currently looking at an open label CPS 0 cohort. In the CPS 1-19 category, we see strong response rates across all three of our cohorts between 50%-70%, really speaking to the TGF-beta inhibition going after the more immune, so-called immunosuppressive patients who are the CPS low. From an epidemiological standpoint, it's believed to be about 50/50 CPS 1-19 versus CPS 20 to greater, and 15% of the frontline market being the CPS 0. I think your other question was around just the competitive threat. What we believe we're hearing is that they're slating to start enrollment in the pivotal study later this year, with full enrollment scheduled to be 2029, so significantly later than our interim analysis for potential accelerated approval coming mid-2027. We do not- Thanks. See this as a competitive threat in terms of timing. Thanks. Thank you. Our next question comes from Reni Benjamin of Citizens. Your line is open. Hey, great. Thanks for taking the questions, and congrats on the progress. As my question is mainly focused around the phase Ib expansion cohorts and the early proof of concept signals, can you just maybe provide more color on each of those expansion cohorts, kind of why we're going after CPS less than one and those patients with heavy smoking? Same thing with the CRC. What is that high bar that you're hoping to achieve when those results come out in the second half? Thank you. Thank you for the question. You know, I'll start with the other cohorts. You know, you'd mentioned CPS less than one and also the, the heavy smokers. You know, I think what we had saw in dose escalation is we actually saw some pretty significant responses in those patients who had CPS 0. In fact, one patient in particular had a complete response there. As you go back to kind of the fundamental biology of our molecule of EGFR and TGF-beta, you know, there's a lot of biological support for the synergy associated with those two mechanisms being given together and also in combination with a, with a PD-1. That was, you know, biology that we wanted to probe and again, exploring a population. You know, as Claire had alluded to in the last response, in terms of an epidemiological perspective, about 15% of patients are CPS less than 1, so it's a meaningful population, and again, a biology that's supported by our molecule. In the heavy smokers, you know, I think it goes back to our view when we looked at our dose escalation data retrospectively, there was a responder population with an HPV positive. All of those patients who responded were heavy smokers. In that case, you know, we saw people who had a history of smoking of 20 pack years or greater who responded. Again, of our three responders there, two out of the three of them were complete responses. Our view is that, you know, there's likely a component of smoking that's driving the biology there, even more so than the HPV-positive infection. Again, an area that we wanted to probe as we think about those expansion opportunities within the head and neck population. CRC, you know, I think honestly, it's an evolving, you know, target. You know, we continue to look at the landscape. We've seen datasets out from other agents of recent. I think the other thing, not only is it relative to the competitive landscape, but also our own internal. You know, we had mentioned activity in cutaneous, anal canal. There's good opportunities for this molecule in the locally advanced setting of head and neck. As we evaluate the various opportunities, you know, there are, I think, are ample opportunities to develop, FICERA across a range of different tumors and more broadly in head and neck cancer. That really is the bar, is, you know, where we think we're gonna have the most meaningful impact, and that's where we're gonna end up, you know, investing our capital. Can I just follow up with, you know, when we might see some of the data for We know when the CRC data's coming out, but maybe from these other cohorts, when might we see those data? Again, we've not provided specific guidance on that. Again, we'll provide, you know, greater clarity in terms of timing for that in future updates. Great. Thank you very much for taking the questions. Thank you. Our next question comes from Jeet Mukherjee of BTIG. Your line is open. Great. Thanks for taking the question. Just looking ahead to your loading and maintenance regimen, just as you talk to your investigators, how do they think about a 12-week weekly regimen followed by once every three weeks versus just a pure once every two week regimen from Pido there? Is there any preference that they have generally between one or the other? Obviously, safety and efficacy being, you know, the primary point there, but just was curious if there's any preference there between the two regimens. Then just coming back to ASCO, are we looking to have updated data be a part of the abstracts, or will they be reserved for the conference presentation? Thank you. I'll take your first question there. You know, as we have talked with investigators and the broader, you know, community, I think there's a real focus on that initial therapy and the rapidity and the depth of, you know, that initial therapy. I think even if you look at, you know, the historical treatment paradigm, we continue to see a fair amount of chemotherapy used, and that is largely being driven by the desire to have very rapid responses. In terms of that trade-off of, you know, being able to go to every two weeks at the outset versus being able to get rapid deep responses, the preference continues to be that rapid deep response which the weekly regimen gives. Again, you know, I think, you know, as you think about the overall administration schedule and transitioning to every three weeks at the 12-week mark, I think the view there is a willingness to get faster, better efficacy quick, and then be able to go to a more convenient maintenance regimen over time. To your second question, Jeet, which I believe was about whether the data presentation will have more mature data than the abstracts, that is correct. There will be more data provided during our presentation than what was provided in the abstracts. Thank you for your question. Thank you. Our next question comes from Boris Peaker of Jones Trading. Your line is open. Great. Thanks for squeezing me in. Just to follow up on a prior question when we're talking about every two week dosing, every three week maintenance dosing. In addition to potentially satisfying FDA's Project Optimus requirements, how important do you see this dosing from the commercial perspective, and kind of competitive perspective? I'll answer your first question around Project Optimus and then pass it over to Ryan. Just to highlight, Boris, we have satisfied Project Optimus by choosing the 1,500 mg dose weekly as opposed to the 750 mg dose weekly within the FORTIFY-HN01 study. This is a separate parallel clinical study that is looking at moving this new alternative dosing regimen into a potential ultimate label. To your second question around the commercial uptake, I'll pass it over to Ryan. Yeah. In terms of, you know, from a differentiation perspective, you know, efficacy remains the key parameter for differentiation, you know, consistent, I think, with most oncology molecules. Again, that's why, you know, we continue to initiate with 12 weeks of weekly therapy to maximize efficacy, deep, durable, rapid responses. And again, we think that that will be the key that's gonna drive differentiation and the initial, you know, share uptake between ourselves and competitor molecules. Being able to also maximize and optimize for schedule once you get out to that 12-week maintenance phase, we, you know, believe that we'll be creating a regimen that has the ability to not only compete, but to differentiate and be best in class from an efficacy, tolerability, and from a convenience perspective, really, you know, being able to, you know, fully optimize the profile across all three dimensions. Great. Thanks for taking my question. Thank you. Our next question comes from Joe Catanzaro of Mizuho. Your line is open. Hey, everybody. Thanks so much for taking my questions. I actually had one as well on this maintenance trial that you've sort of, I think, touched on. Wondering if you could speak to the quantitative difference in exposure at steady state, if any, between 1,500 mg weekly and 2,250 mg every three weeks. You know, it sounds like you need those longer-term efficacy metrics, but wondering if the argument could be made on sort of equivalent PK and safety between those two regimens. Thanks. I mean, again, from an overall exposure perspective, what we are looking to accomplish there, the 2250 mg, essentially, we're looking for exposures that are comparable to what you've seen at 750. Again, why we look across the various datasets to really get to, I think the regimen that we have gotten to. We're looking at the strength of the data across all of our various cohorts. Again, I mean, I think the key here is starting at the 1500 mg, getting that rapid deep response, and then being able to maintain those exposure levels to maintain the durability of response. Okay, great. Thanks so much. Thank you. Our next question comes from Richard Law of Goldman Sachs. Your line is open. Hey, guys. Good morning. Based on that accelerated approval timeline, I believe you mentioned in the past that only a small clinical team will be unblinded to review the interim phase III results and management will still be blinded. When will management team become unblinded, and when should we expect to see the data as well? Does it mean that the unblinded clinical team will file the BLA without management seeing what's in there initially when filed? Richard, I think you're Just to understand your question, the study is a blinded study. We have an interim for potential accelerated approval in mid 2027 that will be based on response rates with six months' worth of follow-up as well as qualitative overall survival. Like any company, there will be, you know, the data cut will be done, the data lock will be done, and then, our team within Bicara will submit the BLA. There are no oddities to that process. There's no separate unblinding with a different team and then where I thought that was the case before. No. There is an IDMC, like in many cases, that will allow us to submit, and th en we w ill move to the B icara team. Okay, thanks. Thank you. I'm showing no further questions at this time. I'd like to turn it back to Claire Mazumdar for closing remarks. Thank you for joining us today and for your continued support of Bicara. We're focused on the work ahead for the program and, most importantly, for the patients we're working to serve. We look forward to seeing many of you at ASCO in a couple of weeks. This concludes today's conference call. Thank you for participating, and you may now disconnect.