Good afternoon, and welcome to Veer Biotechnology's conference call to discuss the company's Veer 5500 strategic collaboration with Estellus and positive Phase 1 data and 2025 financial results. As a reminder, this conference call is being recorded. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question and answer session. I will now turn the call over to Kiki Patel, Head of Investor Relations. You may begin, Kiki.

Thank you, Operator, and welcome, everyone. Earlier today, we issued three press releases, including a joint release with Estellas announcing a strategic collaboration with our PSMA-directed T-cell engager, VIR 5500, a second release reporting the Phase 1 VIR 5500 data that was presented at ASCO GU, and a third release reporting our fourth quarter and year-end earnings. Before we begin, I would like to remind everyone that some of the statements we are making today are forward-looking statements under applicable securities laws. These forward-looking statements involve substantial risks and uncertainties that could cause our clinical development programs, collaboration outcomes, future results, performance, or achievements to differ significantly from those expressed or implied in such forward-looking statements. Forward-looking statements include, but are not limited to, statements regarding the potential benefits of our collaboration with Estellas, that the closing of the Estellas collaboration is subject to the expiration or termination of the applicable waiting period under the Hart-Scott-Rodino Antitrust Improvements Act of 1976, the therapeutic potential of VIR 5500, our Pro X10 platform, our development plans and timelines, financial terms and milestone payments, and our cash runway and capital allocation priorities. These risks and uncertainties associated with our business are described in the company's reports filed with the Securities and Exchange Commission, including our forms 10K, 10Q, and 8K. Joining me on today's call from Beer Biotechnology are Dr. Marianne DeBoffer, our Chief Executive Officer, Dr. Mark Eisner, our Chief Medical Officer, and Jason O'Byrne, our Chief Financial Officer. Additionally, Dr. Johan de Bono from the Institute of Cancer Research in the UK is joining us for our prepared remarks to provide a clinical and investigator perspective. Let me briefly outline today's agenda. Marianne will start by sharing a high-level overview of the strategic collaboration with Estellus and discuss how VIR 5500 has the potential to be a best-in-class T-cell engager to address the significant unmet need in metastatic castration-resistant prostate cancer, or MCRPC. Mark will then review the phase one clinical data for VIR 5500 and he'll invite Dr. DeBona to walk through illustrative case examples. Mark will then summarize the broader data set and outline next steps for the program. Jason will cover the financial terms of the collaboration and provide an update on our 2025 financial results. And finally Marianne will close the call and we'll open the line for Q&A. With that I'll now turn the call over to Marianne.

Thank you, Kiki. Good afternoon, everyone. Today marks a pivotal moment for VIR biotechnology as we announce a landmark strategic collaboration with Astellas to advance the global development and commercialization of VIR 5500, our Pro-X10 dual-masked PSMA-targeting T-cell engager for prostate cancer. VIR 5500 is our most advanced immuno-oncology asset, and today we are sharing new phase one data that will be further presented by Dr. De Bono at ESCO-GU this Thursday, February 26th. Together, we believe these milestones positioned via 5500 for rapid advancement and allow us to move forward with both urgency and discipline. The collaboration we've announced with Astellas combines their deep global experience in prostate cancer with our differentiated T-cell engager powered by the Pro-X10 masking technology. Structurally, the collaboration is designed to accelerate the development of your 5500 across both earlier and later lines of prostate cancer, unlocking a significant market opportunity, while meaningfully de-risking our pipeline of cancer-immune therapies more broadly. Importantly, the new phase one data that we are sharing today show a compelling emerging safety and efficacy profile. While still early, these data increase our confidence that FEAR 5500 has the potential to be a best-in-class T-cell engager for the treatment of prostate cancer. And finally, today's update is also an important validation for the broader ProExTEN platform approach, which we believe can unlock opportunities to develop next-generation T-cell engagers in solid tumors. To understand the significance of this opportunity, it's important to consider the current landscape in prostate cancer. Prostate cancer remains a significant global health burden, representing the most common diagnosed cancer among men, with one in eight men being diagnosed in their lifetime. Despite significant progress in treatment, the five-year survival for patients with MCRPC is only 30%, with an estimated 100,000 MCRPC patients in the US and Europe. Across the prostate cancer continuum, there is a substantial and growing unmet need for novel solutions, capable of improving long-term disease control, as well as quality of life. T-cell engators, which activate the human body's own immune cells in situ to fight cancer, have transformed outcomes in several hematologic malignancies and there are multiple products on the market today. In solid tumors, however, use has been limited by toxicity challenges, including off-tumor activation and cytokine release syndrome. We believe FEAR 5500, powered by the Pro-Extend technology, has the potential to address these challenges. The Pro-X10 platform leverages a universal dual masking approach, which consists of a T-cell engager that simultaneously targets both the tumor antigen, shown here in blue, and CD3 on T-cells, shown here in orange, and the Pro-X10 masks in gray, which shield the T-cell engager through a unique steric hindrance mechanism. As you can see on the left side of the slide, the large hydrophilic polypeptide Xtend mosques surround and sterically hinder the CD3 and tumor-associated antigen binding sites. Upon reaching the tumor microenvironment, proteases cleave the lingers, here shown in pink, unmasking the active molecule precisely where it's needed. And once unmasked, the molecule can bind for tumor cells and T-cells, promoting targeted cancer cell killing. In healthy tissue, the Xtend mask remains intact, dramatically reducing interactions with normal cells and minimizing systemic T-cell activation and subsequent cytokine release. the dual masking approach is designed to reduce toxicity enabling higher dosing and a wider therapeutic window additionally the extant masks themselves provide an extended half-life of the molecules supporting optimization of dosing schedules for patients and as you'll see later in this call this hypothesis is translated directly into our VIR-5500 phase one clinical study results. In the trial, VIR-5500 affirmed early signals of a favorable safety and efficacy profile. Treatment with VIR-5500 also showed a dose-dependent anti-tumor activity as measured by PSA declines, radiographic resist responses, as well as PSMA PET responses. Well, let me turn to the collaboration with Aselas and why we believe they are the partner of choice for VR5500. First, Aselas is the market leader in prostate cancer. Xtendi remains the number one therapy globally in this space, having treated more than one and a half million men worldwide. This commercial success demonstrates deep experience in bringing important prostate cancer therapies to patients at scale. Second, Astellas has repeatedly proven its abilities to successfully co-develop blockbuster medicines with biotech partners. The examples on this slide highlight Astellas' ability to work collaboratively and successfully to translate innovation into market-leading therapies. Third, Astellas brings strong internal global clinical development and lifecycle management capabilities, operating across roughly 70 countries. Xtendi has benefited from robust lifecycle management, enabling multiple label expansions into earlier lines of prostate cancer. This ability to continually generate data, expand indications, and maximize long-term asset value is a key differentiator and an important capability, as we think about the future development opportunities. Here is a snapshot of the deal terms that we announced with Astellas today, whereby PeerBio and Astellas will co-develop and co-commercialize Peer5500 for the treatment of prostate cancer. The financial impact of these terms is substantial. The total potential in combined upfront and milestone payments is $1.7 billion. In addition, in the U.S., commercial profits will be split 50-50 between the parties, with VirBio having the option to co-promote alongside Astellas. And outside of the U.S., Astellas obtains exclusive commercial rights for Vir5500, while VirBio is entitled to receive sales milestones and tiered double-digit royalties on ex-US net sales. Global development costs will be shared between the parties with VirBio contributing 40% and Astellas 60%. Overall, this deal provides immediate capital and significantly reduces our near-term development spend while preserving substantial long-term economic upside. The collaboration can maximize the potential of Vir5500 through accelerated clinical development and global reach, thereby creating value and benefiting more patients. I now turn to Mark to walk you through the compelling VIR 5500 Phase 1 data that forms the foundation of this collaboration. Thank you, Marianne, and good afternoon, everyone.

I'm pleased to walk you through the latest Phase 1 data for VIR 5500, which have been accepted for an oral presentation at the ASCO GU conference taking place later this week. This is the only dual-mask T-cell gauger under evaluation in prostate cancer, and the emerging signals we are seeing reflect the potential of the ProXtend masking platform to unlock the promise of TCEs for the treatment of solid tumors. As of the January 9th, 2026 cutoff, we enrolled 58 patients with advanced metastatic castration-resistant prostate cancer in weekly and every three-week monotherapy dosing regimens. Importantly, all dose escalation cohorts have cleared the dose-limiting toxicity period. Our dose escalation strategy leveraged insights from our broader TCE platform, enabling us to advance efficiently from very low initial flat doses through step-up dosing with the highest Q3-week maintenance dose of 4,000 micrograms per kilogram. Throughout this escalation, prophylactic steroids, or IL-6 blockade, were now required and was only explored in three patients at the highest 4,000-microgram cohort. Based on the emerging data for VR5500, our development focus is now centered on doses at or above 3,000 micrograms per kilogram, given once every three weeks. These dose levels are where we are seeing the clearest clinical signals. Here we see the baseline characteristics for patients enrolled in the study. Participants were heavily pretreated, with a median of four prior lines of therapy, and some receiving up to seven. 95% had received prior toxin chemotherapy. These are patients with extensive disease burden. 93% presented with bone metastases, 45% of visceral involvement, and 18% of liver metastases. Liver metastases are associated with rapid disease progression and poor response to existing treatment modalities. Approximately half of the study population was resistive valuable baseline, enabling assessment of radiographic responses alongside PSA and biomarker responses. This slide summarizes the emerging compelling efficacy and safety signals across the study. Overall, the VR5500 data show a favorable safety and tolerability profile with no observed dose-limiting toxicities. Cytokine release syndrome events were limited and predominantly low-grade, representing fever only. Importantly, we did not observe grade 3 CRS events at the dose levels of 3,000 micrograms per kilogram and above, reinforcing the potential of the pro-extend dual masking platform to widen the therapeutic index of our T-cell engagers. We observed a clear dose response relationship for efficacy. At Q3-week doses at or above 3,000 micrograms per kilogram, the data showed deep and consistent PSA declines. In 11 resisted valuable patients at these dose levels, 5 experienced objective responses. Four of these responders achieved confirmed responses with one pending follow-up confirmation. We're also seeing emerging evidence of durability, with several patients maintaining PSA and radiographic responses with continued therapy up to 27 weeks, though many in the higher-dose cohorts remain early in their shooting course. Finally, the depth of PSA declines is particularly encouraging. 82% of patients achieved PSA 50, more than half achieved PSA 90, and nearly one-third reached PSA 99. These are meaningful results for late-line metastatic castration-resistant prostate cancer patients, especially patients with visceral disease and liver metastases who represent the poorest prognosis population. To bring these data to life at the individual patient level, I'd now like to invite Dr. Johan de Bono to share his clinical perspective and discuss the real-world implications that illustrate the depth of responses we're seeing. Dr. de Bono is a world-leading physician in prostate cancer research who has fundamentally changed how the disease is treated. He has supported development of many breakthrough therapies, including apiriduron, cabastitaxel, enzalutamide, and alaparone. Dr. De Bono?

Thank you, Mark. The five case studies I'm going to share with you, many of whom are my patients, demonstrate multiple impressive biochemical and radiological responses to this dual-mass T-cell engager, Vir5500. In sufferers from metastatic and heavily pretreated prostate cancer, I serve these men in my clinics and have witnessed their experiences and symptomatic improvements on this agent. In advanced metastatic prostate cancer, many subjects experience significant pain, especially bone pain. VIR 5500 resulted in pain disappearing following treatment in many patients as their disease regressed. reduction in such pain is incredibly important to these men that we serve critically i believe that the data from this trial show that the dual masking approach works at minimizing cytokine release syndrome also known as crs we are reporting multiple amazing responses with little clinically significant crs in fact circulating intrusion six levels remain low and relatively unchanged following treatment with Vir5500 across these patients, with usually only grade one fever being observed, which is really quite remarkable and different to many other T-cell engages we have studied that have resulted in cytokine release syndrome with hemodynamic instability requiring patient admission, vasopressors, and treatment with oxygen, et cetera, for respiratory compromise. In addition to this absence of requirements for prophylactic steroids or tozolizumab in this trial, very few subjects have required treatment with steroids after receiving this drug, Virft 500. And this is really quite important since steroids are immunosuppressive and can limit immunotherapy with T-cell engages antitumor activity. So this dual masking by limiting CRS has major advantages. Now let's go through these five cases in turn. Case study one demonstrates complete resolution of multiple, approximately 14 liver metastasis after nine weeks of therapy with a 99% PSA fall. Really very impressive. This was a 63-year-old man who had received most standards of care treatments, including taxanes, olaprib, the PARP inhibitor, and abiraterone. This man had substantial disease burden, many liver mets, diffuse bone disease, poor prognosis disease seen on the PSMA PET imaging, as shown on the left side of the slide. This gentleman received Vrp500 at 800, 1,500, and 3,000 micrograms per kilogram step dosing regimen dosed every three weeks. And he had a stunning response with complete resolution of all the liver lesions and near complete resolution of the bone disease, as you can see in these images. The patient achieved a partial radiographic response with a 62% reduction in the sum of the longest diameters and the 99%, as I said, PSA decline and importantly marked improvement in his tumor pain. Now, what's really noteworthy here is that liver metastasis are often resistant to therapy associated with poor prognosis, including resistant to hormonal therapies and often other therapies too. And in my practice, these patients are very hard to treat and seeing such remarkable responses in late-stage heavily treated prostate cancer is really quite amazing, really unprecedented maybe even. In the next slide, case study two, we see here another significant resist response in multiple large liver metastasis again in a 75-year-old man with large bulky disease in the liver, as seen on the CT imaging on the left, with three courses of treatment with VIR5500 monotherapy, resulting in major shrinkage of his liver lesions by 50% measurements being shown here on the slide. This patient had a 94% PSA fall, as well as his partial response radiologically, and remained on treatment after 10 courses. Again, such responses in liver lesions is particularly impressive with a single-agent T-cell engager, and underscores the broad potential of this agent monotherapy to really impact outcome from this challenging disease. Let's move now to the next case, case study three. This 70-year-old man had a durable resist PSMA PET and PSA 90 response lasting more than eight months. He had pelotonin and abdominal wall lesions, as can be seen on the scan, and essentially had complete resolution of these lesions on PSMA PET scan with a complete metabolic response and as I said a PSA fall of more than 90 percent maintaining an excellent quality of life while on therapy. Let us now turn to the fourth case. This is a gentleman who's a farmer who had been off work because of his symptoms. What's been amazing is that he had resolution of his pain and he was able to go back to work. That's very powerful. The 63-year-old man with diffuse lesions in the bone and lymph nodes with prior exposure to multiple prior lines of therapy, including an actinium-based PSMA radiopharmaceutical, had a complete radiographic response by week nine, accompanied by a 99% PSA fall, as you can see on the right in the slide here, with PSA resolution to nearly undetectable levels, as you can see here down to 0.005. Now let's turn to the matched tumor biopsy data from the same patient on the left, which we believe is compelling evidence for VIR 5500's mechanism of action and potential. The duplex PSMA and C3 IHC for these biopsies at baseline on the left and post-treatment on the right show what this drug induces. You see on the left extremely dense PSMA positive tumor architecture and no meaningful T-cell infiltration. At week five, you now start seeing a major increase in T-cell abundance and a significant eradication of PSMA-positive tumor cells. This overall illustrates the ability of pro-XT and mass T-cell engagers to engage the immune system to drive an anti-tumor immune response. Let us now turn to the last subject. Here we see a complete response with three weekly 1,000 micrograms per kilogram with approximately 12 months of durability in response. This is a 77-year-old man with more than 20 bone lesions and lymph node involvement who actually received a lower dose of B500 with step dosing of 300, 600, and 1,000 micrograms per kilogram given every three weeks after the step dosing. This patient, as I said, had a complete radiographic response by week nine with resolution as you can see on the scans of his bone lesions and his PSA becoming undetectable. He experienced clinical benefits with diminished pain and actually, in fact, is regularly going to the gym while on drug. And here we start seeing durability, really, even with lower doses of drug. So overall, I've shown you five very impressive case studies from the trial overall, showing the potential for impressive and durable disease control in many patients with this dual-mass T-cell engager. I will now pass back to Mark to review the results of the trial overall.

Thank you so much for your attention. Thank you, Dr. DiBono. Your clinical perspective on these patients treated with Vera 5500 is invaluable as we continue to advance this program. Turning back to the full study population, the safety profile of Vera 5500 remains favorable. The table on the left displays treatment-emerging adverse events for all patients treated with weekly and every Q3-week dosing. The emerging safety profile supports a wide therapeutic index. We've seen no dose-limiting toxicities to date with grade 3 or higher treatment-related adverse events in only 12% of patients. Most of these are laboratory abnormalities. We had only two patients discontinue treatment due to an adverse event. The first patient experienced spinal cord compression that was due to his underlying disease and not attributable to Vera 5500, and the second patient due to treatment-related blurred vision. The bottom half of the table on the left displays treatment-related adverse events at the highest doses of more than 3,000 micrograms per kilogram Q3 week. As you can see, the AEs are mostly grade one and two. The grade three and higher events are listed at the bottom, but primarily consisted of neutropenia and tumor flare, which are indicative of immune-mediated engagement. We observed two events of treatment-related blurred vision with unclear pathophysiology and nonspecific MRI findings that improved toward baseline visual acuity. Overall, limited CRS was observed in high-dose cohorts of 3,000 microgram per kilogram and higher. The bar graph on the right shows cases of CRS by dosing cohort. As you can see, all cases were low-grade, either grade 1 or 2, with no grade 3 CRS. And the grade 1 events were only fever, treatable with antipyretics. We did not require prophylactic steroids or anti-IL-6 therapy overall. In the highest-dose cohort of 4,000 micrograms per kilogram, we did evaluate pre-dose steroids in cycle 1. This slide highlights the strength of the dose-response relationship across the doses tested. The waterfall plot illustrates all patients who had an evaluable PSA. Each bar represents an individual patient, with the dose cohorts indicated at the bottom and CRS shown by the green and white colored markers. Across the entire dose range, increasing doses generated deeper and more consistent PSA declines. At doses of 3,000 micrograms per kilogram and above, PSA responses were rapid, pronounced, and durable, with responses confirming at subsequent time points. CRS severity remained low-grade at the higher doses, with no grade 3 CRS observed. This slide presents PSA data for patients treated at or above 3,000 micrograms per kilogram in the Q3 weekly regimen. Responses were observed early, with some patients demonstrating deep declines as rapidly as cycle one, day eight. What's striking here is the depth and consistency of the PSA responses displayed in the table on the right. Additionally, radiographic resist responses were concordant with PSA responses in evaluable patients. In other words, patients with the deepest PSA responses, PSA-90 and PSA-99, often had confirmed resist responses, supporting clinically relevant antitumor activity. This is an exploratory analysis evaluating the concordance of PSMA PET total tumor volume as assessed by RZIP criteria with PSA declines and resist responses. RZIP is an imaging-based response framework developed specifically for PSMA PET scans in prostate cancer. RZIP can detect treatment effects earlier because it tracks PSMA-avid tumor volume, not just anatomical size changes. This is especially useful in prostate cancer where PSMA levels reflect tumor activity. Higher doses of VIR-5500 significantly reduced PSMA-avid tumor volume. These reductions correlated with both PSA responses and resist responses, providing further evidence of the drug's targeted activity against PSMA-expressing tumors. This slide presents radiographic response data with 11 resist evaluable patients treated at our highest Q3-week dose cohorts of 3,000 micrograms per kilogram or above, showing best changes from baseline in sum of longest diameters. We're seeing a 45% objective response rate, or ORR, which includes four patients with confirmed responses and one patient who is awaiting a confirmatory scan. We are seeing a 64% disease control rate. Patients with partial resist responses are also showing deep PSA declines with PSA 90s. It's worth noting that we're seeing these deep resist responses in patients with challenging disease characteristics, including those with liver metastases. What you're looking at on this slide is a spider plot illustrating the change of resist SLD, or some of the longest diameters over time, at the 3,000 microgram per kilogram or higher Q3-week dosing level. We're starting to observe resist responses that persist over time and are concordant with deep and sustained PSA responses. The higher-dose cohorts are continuing to mature. This swimmer plaque gives us a longitudinal view of durability. Here, we're also looking at patients treated at 3,000 micrograms per kilogram or higher at Q3 week. In this graphic, you'll see markers indicating PSA 50 and PSA 90 responders. resist responses, and grade one or two CRS events. Each bar represents one individual patient, and importantly, we have multiple patients staying on treatment for at least six months. Patients achieving deeper responses, both PSA and resist, are also the ones remaining on therapy longer. As shown, CRS is largely limited to grade one and to early cycles, after which it falls off, allowing patients to continue on therapy with good tolerability. This slide presents VIR 5500's early clinical profile with other clinical stage T-cell engagers currently in development for the treatment of prostate cancer. While cross-trial comparisons have inherent limitations and are not head-to-head studies, in the table, we compared VIR 5500 against each program's recommended or go-forward dose. Based on the early numbers, VIR 5500 is exhibiting a highly active profile with deep PSA responses and markedly lower rates of high-grade CRS and treatment-related AEs, despite the majority of patients not receiving prophylactic steroids. Importantly, our every three-week dosing schedule for VIR 5500 may enable administration in the outpatient zone, representing a potential advantage in treatment convenience and broader clinical adoption. Overall, the combination of potent anti-tumor activity and favorable safety profile underscores VIR-5500's potential as a best-in-class T-cell engager for the treatment of prostate cancer. The totality of the data we've shown you today has enabled us to select a preliminary dose to take forward in the late-line MCRPC expansion cohorts. Importantly, we do not plan to use prophylactic steroids or anti-L6 agents with this dose. With Q-week and Q3-week dose escalation complete, our program is now positioned to transition into expansion cohorts. Our initial focus areas include late-line MCRPC monotherapy, first-line MCRPC in combination, and metastatic hormone-sensitive prostate cancer in combination. We expect to initiate these dose expansion cohorts in the second quarter of 2026. We plan to continue dose optimization in parallel to address the goals set out by the FDA Oncology Center of Excellence's Project Optimist and support advancement into phase three development in 2027. These next steps reflect our confidence in VIR 5500's clinical profile and the strength of the collaboration with Estellus, which enables broad and accelerated development across all disease stages. Now, I will turn the call over to Jason.

Thank you, Mark. Let me first summarize the economic structure of the Estellus collaboration. In the U.S., we will co-develop and co-commercialize Veer 5500 under a 50-50 profit-sharing arrangement, with Veer Bio retaining the option to co-promote alongside Estellus. Outside the U.S., Estellus will hold exclusive commercial rights, and Veer Bio will receive milestones and tiered double-digit royalties on net sales. Global clinical development costs are shared 40% by Veer Bio and 60% by Estellus. Expenses related to U.S. specific studies will be shared by BeerBio and Estellus 5050, while Estellus will cover 100% of any expenses related to ex-U.S. specific studies. We will receive combined upfront and near-term payments of $335 million, excluding certain payments to Sanity. That amount includes a $315 million upfront, comprised of $240 million in cash, and $75 million as equity investment. The $75 million equity investment is priced at $10.36 per share, a 50% premium to VeraBio's 30-day volume-weighted average price as of February 17, 2026. Further, we are entitled to a $20 million manufacturing tech transfer milestone expected by mid-2027. The collaboration includes up to an additional $1.37 billion in development, regulatory, and ex-U.S. commercial milestones. The total potential in combined upfront and milestone payments, excluding certain payments due to third parties, is $1.7 billion. Closing of the Estellus collaboration is subject to the expiration or termination of the applicable Hart-Scott-Rodino Act waiting period. We are pleased with the terms of the agreement and see Estellus as the partner of choice in prostate cancer. The agreement offers a capital-efficient structure that de-risks our development spend while potentially expanding the number of patients who may have access to beer 5,500. Moving now to our year-end results, we are pleased to report that our multi-year focus on financial discipline and prioritization has led to continued improvements in performance.

Let me highlight a few key financial metrics for 2025 compared to 2024.

R&D expenses for 2025 were $456 million compared to $507 million in 2024, a $51 million or 10% reduction. SG&A expenses decreased to $92 million in 2025 from $119 million in the prior year. This represents a 23% decrease in SG&A spend compared to 2024. This net reduction is primarily achieved through previously announced cost-saving initiatives. Our net loss for 2025 was $438 million compared to $522 million in 2024. Turning to cash, our 2025 net change in cash and investments was approximately $314 million. This amount includes a $64.3 million initial cost reimbursement payment received from Norgeen in December. We're starting in 2026 with a strong financial position of approximately $782 million in cash, cash equivalents, and investments, not including the upfront cash and equity we will receive through the Estellus collaboration. Based on our current operating plan and including the net effects of the Norgeen and Estellus agreements, we anticipate Cash Runway extending into the second quarter of 2028, enabling multiple value-creating milestones across our pipeline. I will now turn the call back to Marianne to provide the closing remarks.

Thank you, Jason. Today's announcements mark major progress towards our goal of building a world-class cancer immunotherapy program, the vision we set out for our company just 18 months ago. We believe the data we have shared today for VIR 5500 validates the potential of the PRO-X10 platform, enabling more rapid advancement of our pipeline of differentiated T-cell engagers and positioning VIR-Bio to be a leader in immuno-oncology. We have a lot to look forward to across our pipeline. Our HER2 and EGFR programs use the same dual masking architecture and benefit from shared learnings. We plan to share phase one dose escalation data from our HER2 program in the second half of this year. The ProExtense platform's plug-and-play design also lets us rapidly engineer new mask T-cell engagers for high-value solid tumor targets, creating a sustainable pipeline of differentiated therapies. We have thus far developed seven preclinical programs and will progress to development candidate selection. by early 2027. As we conclude today's presentation, I want to return to what fuels everything we do at VeerBio, transforming patients' lives, especially people living with devastating diseases who are vastly underserved by current treatment options. The partnership with Astellas will not only allow for swift advancement of year 5500, but also positions as well for more rapid pipeline expansion. All this gives us further flexibility to consider how we develop our pipeline assets and continue to unlock earlier value for patients and our shareholders alike. And importantly, by combining VirBio's potential best-in-class T-cell engager with Astellas' global capabilities, we will bring complementary strengths to one of the biggest unmet needs in oncology. Together, we can move faster and maximize the potential impact of year 5,500 for people living with prostate cancer. I would like to close by sincerely thanking the patients, their families, and the investigators who have supported the development of this program. With that, I'll turn the call back over to Kiki to begin the Q&A session.

Thank you, Marianne. This concludes our prepared remarks, and we will now start the Q&A section. Joining me for the Q&A are Marianne, Mark, and Jason. Please limit questions to two per person so we can get through all of our covering analysts. I'll now turn it over to you, operator.

At this time, we will begin conducting our analyst question and answer session. For our analyst, please raise your hand to indicate you would like to join the queue if you have not done so already. Once you hear the operator announce your name, you can unmute your line and ask your questions. Please hold for a moment while we poll for questions. Your first question comes from the line of Paul Choi with Goldman Sachs. Please go ahead. Hi. Good evening, everyone, and

congratulations on the data as well as the deal. Two questions for us, please. First, And of course, either for Marianne or Mark, can you maybe comment on the range of PSA responses you've seen by prior line of therapies, particularly with regard to prior radiotherapy? Any details there would be helpful, both on the PSA 50s and PSA 90s. And my second question is, how do you think your data today potentially reflects on the probability of success for your other T-cell engager programs, and just, you know, what is your level of confidence that we can make a reasonable inference of higher probabilities of success for your other programs? Thank you so much for taking our questions.

Thank you, Paul. Really appreciate it. I'll start with answering your second question and then turn it over to Mark. So we really believe that the data we have showed you today validates our dual masking as steric hindrance approach, so really the pro-extend masking. You've seen that the lower systemic immune activation is reflected in limited CRS toxicity, very low incidence of high-grade treatment-related AEs, and very limited number of PSMA-target-related AEs, again, all very low-grade. Also, you saw that we can reach now a wider therapeutic window, so we are able, because of the mask, to those higher and less frequently. So we have actually selected a preference for every three week dosing. And then thirdly, you have seen that, you know, there's great concordance between PSA responses, resist responses, PSMA pet responses, it all, you know, shows too great on tumor engagement. So we think this all bodes really well for our other programs. Of course, every program is unique, But we have, I think, really here shown a validation for the technology. As to your question of range of PSA responses, especially with patients that have been exposed to prior radio ligand therapy, Mark, can you?

Yeah, very good question, Paul. So, first of all, we have a very heavily treated, pre-treated population with a median of four prior lines of therapy. The vast majority of patients have received taxanes. So we do think we have very strong PSA responses, particularly as we get into the 3,000 microgram per kilogram doses and above. You know, I direct you to case number four, the one that was presented by Dr. DiBono. This patient had received a radioligand treatment and actinium conjugated agent, PSMA targeted agent. That patient had a PSA 99 response and a complete response in the target lesions. And that patient also had evidence in the lymph node of PSMA decline in terms of expression and T cell abundance in the lymph node five weeks after treatment. So we don't have a lot of data yet in the post-RLT setting. We are continuing to look at those patients, of course, but at least in this one patient post-RLT, very, very promising results in this individual. In terms of other prior lines of therapy, it's difficult to say because the patients were just generally very heavily pre-treated, so we haven't been able to disambiguate any specific effects of prior line of treatment on PSA responses, but they do appear to be strong across the board,

particularly when we get to the higher doses. Yeah. I mean, the only thing I would add is we have two patients that were exposed prior to the STEEP TCE. So we have annotated those on the

slides if you would want to go and have a look. Your next question comes from the line of Corey Kasimov with Evercore ISI. Please go ahead. Hey, this is Josh Zaron for Corey. Congrats

on all the progress. And clearly, you guys have been busy executing here. So thank you for that. And the question here is, can you give us a little bit more color on what the next steps are before you and Estella's move to phase three? And are there plans for you and Estella's explore additional dosing schemes beyond the Q3 week? Thank you.

Yeah. Jen, thank you for that question. Is it Josh? Yes. Yes. Josh, thank you for the question. Mark, you want to take that?

Absolutely. So, yeah, we're very excited about the partnership with Estellas, and we're also very excited about the next steps of the program. So we do plan to get into, you know, we've selected a go-forward dose. We plan to get into expansion cohorts in Q2 very shortly in this year. We will be having, you know, late-line MCRPC, which is the population here, as a monotherapy. We'll have a combination with enzalutamide in the early-line toxin-naive setting. And we also will be doing some dose optimization in parallel to satisfy the goals of the Project Optimus to satisfy the FDA's requirements there. we will be working with Estellas. And I should also mention the combination of metastatic hormone sensitive prostate cancer and expansion cohort. So taken together with the expansion cohorts, with the dose optimization work, we expect to get into phase three in 2027 and to be well positioned

there. Yeah, this was exactly why we were so excited about entering into the partnership with Estellas. It allows us to accelerate the clinical development and also really broaden the potential on expanding the trials to reach more patients.

Your next question comes from the line of Rana Ruiz with Leering Partners.

Hi. Evening, everyone. Yep. Thanks. So, two questions for me. On the Astellas collaboration, I'm just curious, how are you thinking about unlocking resources for investing into the broader Pro-X-TEM platform and thinking about other solid tumor indications? And, you know, what sort of calculus will you do in terms of thinking about prioritizing certain programs over accelerating others? And my second question, with the larger cohort of patients evaluated on 5500, how does this evolve? You're thinking about where 5500 could be positioned within the sort of treatment paradigm in terms of line of therapy, combination versus monotherapy,

and thinking of the future yes thank you rhina um yeah as it relates to resourcing obviously teaming up with a with a world-class player in the prostate cancer field and astellas has entirely internal development capabilities that will help us tremendously and again accelerating of your 5500 program from a finance perspective also it allows us to divert certain expenses to our other programs and potentially accelerate those as well so we think that the collaboration certainly has a lot of benefits beyond just for view 5500 alone as to work to position 5500 you

Sure, absolutely. So, yes, so we are very excited about the progress we've made so far and the data that we've presented you to today, and we plan to really be able to address a broad range of patients with metastatic prostate cancer, including late-line MCRPC and a monotherapy, and these are the data we presented you today, a more early-line MCRPC in combination, And as you recall, we've been dose escalating in combination with ENZA in the frontline taxane naive setting already, and that's going well. And in addition, in metastatic hormone-sensitive prostate cancer in combination, so we really are very excited to continue to progress the program. And these are certainly three high-end met-need populations within the metastatic prostate cancer setting that we think we can address.

Your next question comes from the line of Mike Olds with Morgan Stanley. Please go ahead.

Good afternoon. Thanks for taking the questions, and congratulations on the data and the deal as well. Maybe just one on VIR 5500 and durability, I guess maybe just talk about your level of confidence there that some of this very strong early data that you're seeing can be sustained over a longer term.

Yeah, absolutely. So we are very encouraged by the resist responses that we've seen, particularly those that have occurred up to 27 weeks, and the fact that we're able to confirm resist responses in patients. We're also seeing a accordance of resist responses with PSMA PET responses and DPSA responses, which we are also think is further evidence of the efficacy we can achieve. Also, the case studies that Dr. DiBono presented to illustrate patients with up to one year of durability, which represents the potential, I think, of your 5500. So taken together, we're really pleased with the emerging evidence of durability in the program.

Yep. Makes sense. Maybe just one more question from me, obviously, you're presenting the data at ASCO GU later this week. I'm curious if the data you shared with us today is the same that will be presented at the meeting, or are there any additional updates or data points we should be looking out for? Thanks.

Yeah, the oral presentation at ESCO-GU this Thursday by Dr. DeBrono, I mean, these oral presentations are rather short, so there won't be additional data, but it will be a subset of this data.

Great. Thank you, and congratulations again.

Thank you.

Your next question comes from the line of Phil Nato with T.D. Cowan. Please go ahead.

Good afternoon. Let us add our congratulations on the data and the Estelle's collaboration. Two from us. First, in terms of the go-forward dose, could you give us more information on what that dose is? And I guess in particular, was there a dose response in those doses above 3,000 micron like gram per kilogram uh q3w or how did you identify that that go forward dose and then second just clarifying question it sounds like um there's no grade three crs and doses above three thousand was there any below it didn't seem to be from one of the slides but we just want to

make sure we saw that correctly thank you yeah thanks for the question so in terms of the go forward dose we've done a lot of work on that integrating uh safety the efficacy psa psma had resist responses and so forth and we have selected a go forward dose you know as you can uh appreciate we have now a partner of stelis which we're thrilled to have on board and you know so we're not going to be communicating the exact dose today because that's that's a something that involves both both of us in the partnership but i can tell you we'll be in the 3,000 to 3,500 maintenance dose range in terms of dose response above out or above 3,000 I mean you can see clearly we showed you all the data for all the doses tested for PSA responses I think you can see there's a compelling dose response across all of those doses once we get about 3,000 there still is some dose response but primarily we're in a range where we're seeing very, very strong efficacy and a very strong therapeutic index. So we feel confident that we've identified a go-forward dose that really optimizes the therapeutic index moving forward. In terms of grade 3 CRS, about 3,000 mics per kilo in the go-forward dose range, we've seen no grade 3 CRS. We did observe one grade 3 CRS in an earlier dose cohort in a low-dose patient who had intra-panticipate dose escalation and had one episode of grade 3 CRS that recovered rapidly and the patient did very well. That's very helpful.

Your next question comes from the line of Edsler DeRoot with Berkley's. Please go ahead.

Thanks for taking the questions and congrats on this data set. Really nice to see. Just one question I had on the go-forward dose, just wondering if in the combination study that you've initiated, if new patients would be enrolled at these effective doses of greater than 300 micrograms per kilogram. And then also, is there an opportunity with this data in hand to maybe convert to a flat dose versus a weight-based dose in these patients, and whether you see this as a potential opportunity moving forward for the molecule?

Yeah, thanks. That's a good question. So, in terms of the go-forward dose in combination with enzalutamide, I mean, we anticipate that the dose should be consistent in the two populations. We are doing a, we're almost complete with a dose escalation in combo with the frontline MCRPC just to confirm that there's no issues there, but we do anticipate should be very similar or the same. In terms of flat dose, right now we do not have plans for a flat dose. I mean, it would be possible in theory, but we're still using the microgram per kilogram dose.

Your next question comes from the line of Joseph Stringer with Needham & Company. Please go ahead.

Thanks for taking our questions. Just to follow up on the deal with Estella for 5500, what might this mean for the rest of the oncology pipeline? Is there an opportunity for some of these programs to be standalone for beer, or do you see the long-term strategy here to seek partners or to partner these programs? And then the question for Dr. Debono, just based on these updated data, what are the read-throughs in your outlook, and where do you see potential for VIR 5500 in earlier lines of MCRPC therapy? Thank you.

Okay. Thank you, Joey. Yes, so the sell-outs deal, again, was a very strategic choice based on the fact that, first of all, the unmet need in prostate cancer is incredibly high. The landscape is evolving very quickly. We thought that time to market is, you know, utmost important. So we really were looking for a global partner with, you know, scale and with aligned incentives that would help us accelerate the program. And also, as I mentioned earlier, really allow us to really grow the pie, so to speak, and see how much value, how much more value could we bring to a broader subset of patients. And that's, you know, everything that our startup collaboration really delivers, while we can retain a significant portion of the value through the 50-50 profit split, the milestones and the ex-U.S. royalties and so on. For the rest of our pipeline, we are going to be very strategic and thoughtful in a similar vein. A lot depends, again, on the competitive landscape, on the size of the commercial opportunity and the indications about, you know, the financial needs to bring these indications forward. So we will be making very thoughtful choices on what to partner, how to partner, what to keep for ourselves 100%. Also, just to remind you that we have seven preclinical mask T-cell engagers, and for sure on the pre-clinical programs this is just too much for us to to move forward on on our own we will certainly be looking for partners there and because of the plug and play nature of the platform again you know it allows us to move actually pretty quickly in pre-clinical uh in pre-clinical uh research so um you know you you will be seeing that we will be looking for partners in some of those areas. The second question was related to read-through. Okay, Dr. De Bono is not available here during the Q&A, but Mark, do you want to take in?

Sure, so your question was about the potential in earlier lines of metastatic prostate cancer. So, yes, we definitely believe there is potential there. We are planning first-line toxin metastatic castration-resistant prostate cancer is an expansion cohort as addition to metastatic hormone-sensitive prostate cancer. So we are really looking across the metastatic prostate cancer landscape to help these patients who really need better treatments.

Your next question comes from the line of Patrick Trucchio with H.C. Wainwright. Please go ahead.

Thanks. Good afternoon and congrats on the data and the deal. I guess just a follow-up on the Astellas deal with VIR having an option in the U.S. to co-promote. What would that look like? And at what point in the development process would you be able to exercise that option?

Okay, thank you, Patrick. Yeah, so we have an option to co-promote alongside Astellas in the U.S. And, you know, up to a year before the start of our paper trials, we will be able to make that decision.

Great. And then if I could, just a follow-up question for Dr. De Bono. I'm just wondering, just based on the data that you've seen so far, how confident are you that this treatment could potentially move into frontline, and what would you need to see in order to give you that confidence?

Thank you, Patrick. So, unfortunately, Dr. De Bono is in time, so it's not available for this Q&A. He will be at the ASCOGU this Thursday, but maybe, Mark, you want to?

Yeah. So, yeah, I encourage everybody who can to attend this talk or to understand his perspective there. But for sure, we see potential across the metastatic prostate cancer landscape. we have generated, we think, compelling early data in the late-line MCRPC setting. We're currently enrolling patients in dose escalation in the frontline taxane-naive MCRPC setting. We would anticipate, based on what we've seen to date, that we should have an effective drug in that population, potentially. They do have lower disease burden overall, and we think our our mass TCE approach should work. And we will be generating those data. And as I mentioned before, we are also going to be looking at the metastatic hormone-sensitive prostate cancer setting as well. So that gives you kind of an idea of where we're heading.

Terrific. Thanks so much.

Thank you. Your next question comes from the line of Sean McCutcheon with Raymond James. Please go ahead.

Hey, guys. Congrats on the strong data, and thanks for the question. A couple from us. Given the seeming lack of strong dose response on CRS and lack of DLTs, how are you thinking about the limit on the higher end of the range of dose escalation, you know, whether that's saturating on enzymatic activity or otherwise? And the second question, you know, how are you guys thinking about the partnership with Astellas and optionality for combining VR3500 with other ARPIs beyond EMSA? Thanks.

Thank you, John. I will take your second question. Obviously, in partnership with Astellas, we will be determining our future combination strategy, which of course could be broader than just ARPIs, but that will be something I think that we will need to inform you about at a later time point. Your first question, what's related to the dose?

Yeah, so you're asking about dose response for CRS and efficacy, and what's the limit of the dose on the high end. So a couple of points there. I mean, our whole goal has been to maximize and optimize the therapeutic window to get the best possible safety with the minimum possible adverse events and CRS. So we've taken a careful look across the data set on all of the efficacy parameters and safety parameters, including PSA, including resist, including PSMA PET, all the safety events, CRS, et cetera. And we think we've gotten to a range in the 3,000 to 3,500 maintenance dose. And we have picked a specific dose there, which we can communicate in combination with our partner at a later date where we think we really optimize the therapeutic index and can move forward into expansion cohorts in Q2 of this year.

Your next question comes from the line of Alex Stranahan with Bank of America. Please go ahead.

Hey, guys. Thanks for taking my questions, and congrats on the really clean update here. Maybe first, just following up on an earlier question regarding durability, I'd be interested to hear your thoughts on how we could correlate PSA declines as maybe a leading indicator for what we could expect on PFS with longer follow-up and when you think you might be in the position to update the markets with that data. And then second, in the six patients with the evaluable PSA but not resist, assuming these will feed into the overall PFS analysis. Could you maybe talk about why we weren't – those weren't available at baseline and what your prediction might have been in terms of response, given many of them had fairly deep PSA declines, maybe on disease control rate or something else?

Thank you. So your first question has to do with durability and how do we think PSA declines will track with PFFs, right? So in general, I would say that the deeper PSA declines, particularly PSA 90s and PSA 99s, are associated with more durable responses. And we are very encouraged to see that we have some very deep PSA declines, PSA 90s and PSA 99s. In terms of radiographic PFFs, I mean, you're correct, we did not present those data at this update because, as you can see, the data, particularly for the high-dose cohorts, is still evolving, and the patients are still maturing over time.

So those data really aren't available yet.

And in terms of exactly when we'll present further data, I think that we'll just have to give guidance on that at a subsequent time point. Could you clarify, I wasn't quite sure I got the second question. Was that why were some patients not PSA valuable, or what was the question?

Well, I think there was six patients that had a PSA, like, out of the 17, six were not valuable for resist. I guess, what was sort of the—you couldn't get the scans at baseline. Was that kind of the driver there? And then, I guess, what would you sort of expect in terms of, you know, PFS for those patients?

No, thanks for clarifying. I appreciate it. So, yeah. So, in the 3,000 or above, we had 22 patients in the cohort. We had 17 patients who were PSA valuable. Two of those patients are just early at the time of the clinical cutoff. So we will get those subsequent PSA values, which they weren't part of the data set. So two out of five are early, and those are coming. Three out of the five discontinued early, so we will not have, you know, they won't be PSA valuable. And that's very typical for prostate cancer trials in a late-line setting, because these patients are quite sick with a very heavy disease burden. We have 11 patients who are resistive valuable, And among those, we had five responses, four were confirmed, and one is still waiting for the next confirmatory scan between week nine and week 18. So that one is coming in time.

That makes sense. Thanks, Mark. Congrats again. Thank you.

This concludes the call. Thank you for participating.