Vir Biotechnology (VIR) Earnings Call Transcript

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DATE

Monday, Feb. 23, 2026 at 5:30 p.m. ET

CALL PARTICIPANTS

• Chief Executive Officer — Dr. Marianne De Backer
• Chief Medical Officer — Dr. Mark D. Eisner
• Chief Financial Officer — Jason O’Byrne
• Consulting Clinical Investigator — Dr. Johann de Bono

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TAKEAWAYS

• Astellas collaboration terms -- Total potential value of $1.7 billion in combined upfront, equity, and milestone payments; includes $315 million upfront ($240 million cash, $75 million equity at a 50% premium), $20 million milestone, and future development, regulatory, and ex-US commercial milestone payments totaling up to $1.37 billion.
• Profit-sharing and royalties -- Vir Biotechnology (NASDAQ:VIR) and Astellas to split US commercial profits 50/50; ex-US, Astellas holds exclusive rights with Vir Biotechnology entitled to tiered double-digit royalties and sales milestones on net sales.
• Development cost structure -- Global development costs shared 40% by Vir Biotechnology and 60% by Astellas; US-specific study expenses are split evenly, and Astellas covers 100% of ex-US study expenses.
• Phase 1 VR-5,500 safety and efficacy -- No dose-limiting toxicities observed across all cohorts; at maintenance doses of 3,000–4,000 micrograms per kilogram every three weeks, no Grade 3 cytokine release syndrome (CRS) occurred, with CRS limited to low grade (Grade 1 or 2, mainly fever); only 12% incidence of Grade 3 or higher treatment-related adverse events, mostly laboratory findings.
• VR-5,500 antitumor activity -- Dose-dependent PSA declines observed; at 3,000 micrograms per kilogram or higher, 82% of patients achieved PSA-50, more than 50% achieved PSA-90, and nearly one third achieved PSA-99; in 11 RECIST-evaluable patients at this dose range, five showed objective responses, with four confirmed.
• Durability of clinical response -- Durable PSA and radiographic responses seen in several patients up to 27 weeks (in the higher-dose cohorts); some individual case studies demonstrated complete responses with durability out to 12 months.
• Patient population heavily pretreated -- Study enrolled 58 patients, median of four prior lines of therapy (up to seven); 95% had prior taxane chemotherapy, 93% with bone metastases, 45% with visceral involvement, and 18% with liver metastases.
• Therapeutic index and dosing -- Dual-masking ProX10 (ProXTEN) platform enabled higher, less frequent dosing and widened the therapeutic window; prophylactic steroids or IL-6 blockade not required except in three patients at highest dose.
• Financial metrics -- 2025 R&D expense was $456 million, down 10% from $507 million in 2024; SG&A expense decreased 23% to $92 million from $119 million; net loss improved to $438 million from $522 million in the prior year.
• Cash position and runway -- Year-end 2025 cash, cash equivalents, and investments totaled $782 million, not including Astellas deal proceeds; company projects runway extending into 2028 based on current operating plan and planned partnerships.

SUMMARY

The call centered on the disclosure of a major collaboration between Vir Biotechnology (NASDAQ:VIR) and Astellas, featuring a combined $1.7 billion transaction value and a uniquely structured global development and commercialization partnership for VR-5,500 in prostate cancer. Management provided detail on VR-5,500's Phase 1 dose escalation results, where high-dose cohorts demonstrated substantial antitumor activity—particularly measured by PSA and RECIST responses—in a challenging, heavily pretreated metastatic castration-resistant prostate cancer population. The safety profile featured no dose-limiting toxicities and low rates of significant cytokine release syndrome, supporting both the promise of the dual-masking platform and the viability of a Q3-week regimen without routine steroid or IL-6 blockade use. Management revealed plans to rapidly progress late-stage mCRPC monotherapy and combination expansion cohorts in 2026, with a Phase 3 program slated for 2027.

• Jason O’Byrne detailed, The $75 million equity investment is priced at $10.36 per share, a 50% premium to Vir Biotechnology's 30-day volume-weighted average price as of Feb. 17, 2026.
• VR-5,500's clinical activity in liver metastases was illustrated with case examples showing rapid, deep reductions or complete resolution of metastatic lesions in patients otherwise resistant to standard therapies.
• Dr. Johann de Bono highlighted that, VR-5,500 resulted in pain disappearing following treatment in many patients as their disease regressed, emphasizing the drug’s potential benefit to quality of life in late-stage settings.
• The platform’s “plug-and-play” design reportedly supports seven additional preclinical candidates, with development candidate selection for the next asset targeted by early 2027.
• Operational efficiencies arising from the Astellas alliance permit Vir Biotechnology to redeploy resources toward its pipeline of masked T cell engagers beyond VR-5,500.
• Closing of the Astellas transaction remains contingent upon antitrust clearance under the Hart-Scott-Rodino Act, as stated by management.

INDUSTRY GLOSSARY

• ProX10 (ProXTEN) platform: Dual-masking technology that sterically hinders both tumor antigen and CD3 binding sites on T cell engagers, intended to reduce toxicity and permit higher dosing in solid tumor immunotherapy.
• PSMA: Prostate-specific membrane antigen, a target highly expressed in prostate cancer cells.
• PSA-50/PSA-90/PSA-99: Denote ≥50%, 90%, or 99% reduction in prostate-specific antigen from baseline, respectively, used as biomarkers for treatment response in prostate cancer.
• RECIST: Response Evaluation Criteria in Solid Tumors, a standardized set of rules for assessing tumor response to treatment through imaging.
• CRS (Cytokine Release Syndrome): An acute systemic inflammatory response characterized by fever and other symptoms, commonly associated with T cell immunotherapies.
• DLT: Dose-limiting toxicity; a treatment-related adverse event that prevents dose escalation in clinical trials.
• RECIP: An imaging-based response framework specifically for PSMA PET scans in prostate cancer, measuring changes in PSMA-avid tumor volume.
• TCE (T cell engager): A bispecific or multispecific antibody designed to link T cells to cancer cells, facilitating cytotoxic immune responses.

Full Conference Call Transcript

Joining me on today's call from Vir Biotechnology, Inc., are Dr. Marianne De Backer, our Chief Executive Officer, Dr. Mark D. Eisner, our Chief Medical Officer, and Jason O’Byrne, our Chief Financial Officer. Additionally, Dr. Johann 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 Astellas and discuss how VR-5,500 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 1 clinical data for VR-5,500, and he will invite Dr. de Bono to walk through illustrative case examples. Mark will then summarize the broader dataset 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. Finally, Marianne will close the call, and we will open the line for Q&A. With that, I will now turn the call over to Marianne.

Marianne De Backer: Thank you, Kiki. Good afternoon, everyone. Today marks a pivotal moment for Vir Biotechnology, Inc., as we announce a landmark strategic collaboration with Astellas to advance the global development and commercialization of VR-5,500, our ProX10 dual-masked PSMA-targeting T cell engager for prostate cancer. VR-5,500 is our most advanced immuno-oncology asset, and today we are sharing new Phase 1 data that will be further presented by Dr. de Bono at ASCO GU this Thursday, February 26. Together, we believe these milestones position VR-5,500 for rapid advancement and allow us to move forward with both urgency and discipline.

The collaboration we have announced with Astellas combines their deep global experience in prostate cancer with our differentiated T cell engager powered by the ProX10 masking technology. Structurally, the collaboration is designed to accelerate the development of VR-5,500 across both earlier and later lines of prostate cancer, unlocking a significant market opportunity while meaningfully de-risking our pipeline of cancer immunotherapies more broadly. Importantly, the new Phase 1 data that we are sharing today show a compelling emerging safety and efficacy profile. While still early, these data increase our confidence that VR-5,500 has the potential to be a best-in-class T cell engager for the treatment of prostate cancer.

Finally, today's update is also an important validation for the broader ProX10 platform approach, which we believe can unlock opportunities to develop next-generation T cell engagers in solid tumors. To understand the significance of this, it is important to consider the current landscape in prostate cancer. Prostate cancer remains a significant global health burden representing the most commonly 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 engagers, 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, including off-tumor activation and cytokine release syndrome. We believe VR-5,500 powered by the ProX10 technology has the potential to address these challenges.

The ProX10 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 ProX10 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 XTEN masks surround and sterically hinder the CD3 and tumor-associated antigen binding sites. Upon reaching the tumor microenvironment, proteases cleave the linkers, shown here in pink, unmasking the active molecule precisely where it is needed. Once unmasked, the molecule can bind both tumor cells and T cells, promoting targeted cancer cell killing.

In healthy tissue, the XTEN masks remain 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 XTEN masks themselves provide an extended half-life of the molecule, supporting optimization of dosing schedules for patients. As you will see later in this call, this hypothesis has translated directly into our VR-5,500 Phase 1 clinical study results. In the trial, VR-5,500 affirmed early signals of a favorable safety and efficacy profile. Treatment with VR-5,500 also showed a dose-dependent antitumor activity as measured by PSA declines, radiographic RECIST responses, as well as PSMA PET responses.

Now let me turn to the collaboration with Astellas and why we believe they are the partner of choice for VR-5,500. First, Astellas is the market leader in prostate cancer. Xtandi remains the number one therapy globally in this space, having treated more than 1.5 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.

Xtandi has benefited from robust lifecycle management enabling multiple label expansions into earlier lines of prostate cancer. This ability to continually generate data and 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 Vir Biotechnology, Inc. and Astellas will co-develop and co-commercialize VR-5,500 for the treatment of prostate cancer. The financial impact of these terms is substantial. The total potential in combined upfront and milestone payments is $1,700,000,000.

In addition, in the US, commercial profits will be split 50/50 between the parties, with Vir Biotechnology, Inc. having the option to co-promote alongside Astellas. Outside of the US, Astellas obtained exclusive commercial rights for VR-5,500, while Vir Biotechnology, Inc. 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 Vir Biotechnology, Inc. 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 VR-5,500 through accelerated clinical development and global reach, thereby creating value and benefiting more patients.

I will now turn to Mark to walk you through the compelling Phase 1 data that form the foundation of this collaboration.

Mark D. Eisner: Thank you, Marianne, and good afternoon, everyone. I am pleased to walk you through the latest Phase 1 data for VR-5,500 that have been accepted for an oral presentation at the ASCO GU conference taking place later this week. This is the only dual-masked T cell engager under evaluation in prostate cancer and the emerging signals we are seeing reflect the potential of the ProXTEN masking platform to unlock the promise of TCEs for the treatment of solid tumors. As of the 01/09/2026 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 not required and were only explored in three patients at the highest 4,000 microgram cohort. Based on the emerging data for VR-5,500, 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 you 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. Ninety-five percent had received prior taxane chemotherapy. These are patients with extensive disease burden: 93% presented with bone metastases, 45% had visceral involvement, and 18% had liver metastases. Liver metastases are associated with rapid disease progression and poor response to existing treatment modalities. Approximately half of the study population was RECIST evaluable at 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 VR-5,500 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. 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 ProXTEN 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 RECIST-evaluable patients at these dose levels, five experienced objective responses. Four of these responders achieved confirmed responses, with one pending follow-up confirmation.

We are 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 treatment course. Finally, the depth of PSA declines is particularly encouraging. Eighty-two percent 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 would now like to invite Dr.

Johann de Bono to share his clinical perspective and discuss the real-world implications that illustrate the depth of responses we are seeing. Dr. de Bono is a world-leading physician and prostate cancer researcher who has fundamentally changed how the disease is treated. He has supported development of many breakthrough therapies, including abiraterone, cabazitaxel, enzalutamide, and olaparib. Dr. de Bono,

Johann de Bono: Thank you, Mark. The five case studies I am going to share with you, many of whom are my patients, demonstrate multiple impressive biochemical and radiological responses to this dual-masked T cell engager, VR-5,500, 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. VR-5,500 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 interleukin-6 levels remain low and relatively unchanged following treatment with VR-5,500 across these patients, with usually only Grade 1 fever being observed, which is really quite remarkable and different to many other T cell engagers we have studied that have resulted in cytokine release syndrome with hemodynamic instability requiring patient admission, vasopressors, and treatment with oxygen, etcetera, for respiratory compromise.

In addition to this absence of a requirement for prophylactic steroids or tocilizumab in this trial, very few subjects have required treatment with steroids after receiving this drug, VR-5,500. This is really quite important since steroids are immunosuppressive and can limit immunotherapy with T cell engagers and tumor activity. So this dual masking by limiting CRS has major advantages. Now let us go through these five cases in turn. Case study one demonstrates complete resolution of multiple, approximately 14, liver metastases 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, olaparib, lutetium-PSMA, and abiraterone.

This man had substantial disease burden, many liver metastases, diffuse bone disease, poor prognosis disease, seen on the PSMA PET imaging as shown on the left side of the slide. This gentleman received VR-5,500 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% PSA decline and, importantly, marked improvement in his tumor pain.

Now what is really noteworthy here is that liver metastases are often resistant to therapy and associated with poor prognosis, including resistance to hormonal therapies and often other therapies too, and in my practice these patients are very hard to treat. 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 RECIST response in multiple large liver metastases, 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 VR-5,500 monotherapy resulting in major shrinkage of his liver lesions by 50%, measurements being shown here on the slide. The patient had a 94% PSA fall as well as his partial response radiologically, and he remained on treatment after 10 courses. Again, such responses in liver lesions are particularly impressive with a single-agent T cell engager and underscore the broad potential of this agent as monotherapy to really impact outcomes from this challenging disease.

Let us move now to the next case. Case study three. This 70-year-old man had a durable RECIST, PSMA PET, and 90 response lasting more than eight months. He had peritoneal and abdominal wall lesions as can be seen on the scan, and essentially had complete resolution of these lesions on PSMA PET scan, a complete metabolic response, and, as I said, a 90% PSA decline, maintaining an excellent quality of life while on therapy. Let us now turn to the fourth case. This is a gentleman who is a farmer who had been off work because of his symptoms.

What has been amazing is that he had resolution of his pain, and he was able to go back to work. That is very powerful. A 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 us turn to the matched tumor biopsy data from the same patient on the left, which we believe is compelling evidence for VR-5,500's mechanism of action and potential. The duplex PSMA/CD3 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 ProXTEN-masked T cell engagers to engage the immune system to drive antitumor 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 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.

Here we start seeing durability, really, even with lower doses of drug. Overall, I have 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-masked 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.

Mark D. Eisner: Thank you, Dr. de Bono. Your clinical perspective on these patients treated with VR-5,500 is invaluable as we continue to advance this program. Turning back to the full study population, the safety profile of VR-5,500 remains favorable. The table on the left displays treatment-emergent adverse events for all patients treated with weekly and every-Q3-week dosing. The emerging safety profile supports a wide therapeutic index. We have 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 VR-5,500, and the second patient discontinued 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 1 and 2. The Grade 3 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 tumor-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 micrograms 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. In the Grade 1 events, there was 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 one. 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-week regimen. Responses were observed early, with some patients demonstrating deep declines as rapidly as cycle one, day eight.

What is striking here is the depth and consistency of the PSA responses, displayed in the table on the right. Additionally, radiographic RECIST 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 RECIST responses, supporting clinically relevant antitumor activity. This is an exploratory analysis evaluating the concordance of PSMA PET total tumor volume as assessed by RECIP criteria with PSA declines and RECIST responses. RECIP is an imaging-based response framework developed specifically for PSMA PET scans in prostate cancer. RECIP 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 VR-5,500 significantly reduced PSMA-avid tumor volume. These reductions correlated with both PSA responses and RECIST responses, providing further evidence of the drug's targeted activity against PSMA-expressing tumors. This slide presents radiographic response data for the 11 RECIST-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 are seeing a 45% objective response rate, or ORR, which includes four patients with confirmed responses and one patient awaiting a confirmatory scan. We are seeing a 64% disease control rate.

Patients with partial RECIST responses are also showing deep PSA declines with PSA-90s. It is worth noting that we are seeing these deep RECIST responses in patients with challenging disease characteristics, including those with liver metastases. What you are looking at on this slide is a spider plot illustrating the change of RECIST SLD, or sum of the longest diameters, over time at the 3,000 micrograms per kilogram or higher Q3-week dosing level. We are starting to observe RECIST responses that persist over time and are concordant with deep and sustained PSA responses. The higher-dose cohorts are continuing to mature. This swimmer plot gives us a longitudinal view of durability.

Here, we are also looking at patients treated at 3,000 micrograms per kilogram or higher Q3-week. In this graphic, you will see markers indicating PSA-50 and PSA-90 responders, RECIST responses, and Grade 1 or 2 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 RECIST, are also the ones remaining on therapy longer. As shown, CRS is largely limited to Grade 1 and 2 early cycles, after which it falls off, allowing patients to continue on therapy with good tolerability.

This slide presents VR-5,500'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 VR-5,500 against each program's recommended or go-forward dose. Based on the early numbers, VR-5,500 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 VR-5,500 may enable administration in the outpatient setting, representing a potential advantage for treatment convenience and broader clinical adoption.

Overall, the combination of potent antitumor activity and favorable safety profile underscores VR-5,500's potential as a best-in-class T cell engager for the treatment of prostate cancer. The totality of the data we have shown you today 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–IL-6 agents with this dose. With Q1-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 2026.

We plan to continue dose optimization in parallel to address the goals set out by the FDA Oncology Center of Excellence's Project OPTIMUS and support advancement into Phase 3 development in 2027. These next steps reflect our confidence in VR-5,500's clinical profile and the strength of the collaboration with Astellas, which enables broad and accelerated development across all disease stages. I will now turn the call over to Jason.

Jason O’Byrne: Thank you, Mark. Let me first summarize the economic structure of the Astellas collaboration. In the US, we will co-develop and co-commercialize VR-5,500 under a 50/50 profit-sharing arrangement, with Vir Biotechnology, Inc. retaining the option to co-promote alongside Astellas. Outside the US, Astellas will hold exclusive commercial rights, and Vir Biotechnology, Inc. will receive milestones and tiered double-digit royalties on net sales. Global clinical development costs are shared 40% by Vir Biotechnology, Inc. and 60% by Astellas. Expenses related to US-specific studies will be shared by Vir Biotechnology, Inc. and Astellas 50/50, while Astellas will cover 100% of any expenses related to ex-US–specific studies. We will receive combined upfront and near-term payments of $335,000,000, excluding certain payments to Sanofi.

That amount includes $315,000,000 upfront comprised of $240,000,000 in cash and $75,000,000 as an equity investment. The $75,000,000 equity investment is priced at $10.36 per share, a 50% premium to Vir Biotechnology, Inc.'s 30-day volume-weighted average price as of 02/17/2026. Further, we are entitled to a $20,000,000 manufacturing tech transfer milestone, expected by mid-2027. The collaboration includes up to an additional $1,370,000,000 in development, regulatory, and ex-US commercial milestones. The total potential in combined upfront and milestone payments, excluding certain payments due to third parties, is $1,700,000,000. Closing of the Astellas 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 Astellas 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 VR-5,500. Moving now to our year-end results. We are pleased to report that our multiyear 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 $456,000,000 compared to $507,000,000 in 2024, a $51,000,000, or 10%, reduction. SG&A expenses decreased to $92,000,000 in 2025, from $119,000,000 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 $438,000,000 compared to $522,000,000 in 2024. Turning to cash, our 2025 net change in cash and investments was approximately $314,000,000. This amount includes a $64,300,000 initial cost reimbursement payment received from Norgine in December. We started 2026 with a strong financial position of $782,000,000 in cash, cash equivalents, and investments, not including the upfront cash and equity we will receive through the Astellas collaboration.

Based on our current operating plan and including the net effects of the Norgine and Astellas agreements, we anticipate cash runway extending into 2028, enabling multiple value-creating milestones across our pipeline. I will now turn the call back to Marianne to provide the closing remarks.

Marianne De Backer: 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 eighteen months ago. We believe the data we have shared today for VR-5,500 validates the potential of the ProX10 platform, enabling more rapid advancement of our pipeline of differentiated T cell engagers and positioning Vir Biotechnology, Inc. 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 1 dose-escalation data from our HER2 program in the second half of this year.

The ProXTEN platform’s plug-and-play design also lets us rapidly engineer new masked 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 Vir Biotechnology, Inc.: 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 VR-5,500, it also positions us 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. Importantly, by combining Vir Biotechnology, Inc.'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 VR-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 will turn the call back over to Kiki to begin the Q&A session.

Kiki Patel: 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 will now turn it over to you, Operator.

Operator: At this time, we will begin conducting our analyst question-and-answer session. For our analysts, 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.

Paul Choi: Hi. Good evening, everyone, and congratulations on the data as well as the deal. Questions for us, please. First, either for Marianne or Mark, can you maybe comment on the range of PSA responses you have 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. 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 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.

Marianne De Backer: Thank you, Paul. We really appreciate it. I will start with answering your second question and then turn it over to Mark. We really believe that the data we have shown you today validates our dual masking-of-serum approach—so really the correct masking. You have 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. We are able, because of the mask, to dose higher and less frequently. We have actually selected a preference for every-three-week dosing.

Thirdly, you have seen great concordance between PSA responses, RECIST responses, and PSMA PET responses, which all show great on-tumor engagement. We think this all bodes really well for our other programs. Of course, every program is unique, but we have, I think, really shown a validation for the technology. As to your question of range of PSA responses, especially with patients that have been exposed to prior radioligand therapy—Mark?

Mark D. Eisner: Sure. Very good question, Paul. First of all, we have a very heavily pretreated population with a median of four prior lines of therapy. The vast majority of patients have received taxanes. We do think we have very strong PSA responses, particularly as we get into the 3,000 microgram per kilogram doses and above. I would direct you to case number four, the one that was presented by Dr. de Bono. This patient had received radioligand treatment, an actinium-conjugated, PSMA-targeted agent. That patient had a PSA-99 response and a complete response in the target lesions.

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. We do not have a lot of data yet in the post–radioligand therapy 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 is difficult to say because patients were just generally very heavily pretreated, so we have not been able to disambiguate any specific effects with 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.

Marianne De Backer: The only thing I would add is we had two patients that were exposed prior to a PSMA TCE. We have annotated those on the slides that you would want to go and have a look. Your next question comes from the line of Cory Kasimov with Evercore ISI. Please go ahead.

Josh Schimmer: Hey. This is Josh Schimmer on for Cory. Congrats on all the progress, and clearly you have been busy executing here, so thank you for that. The question here is, can you give us a little bit more color on what the next steps are before you and Astellas move to Phase 3? Are there plans for you and Astellas to explore additional dosing schemes beyond the Q3-week? Thank you.

Marianne De Backer: Yes. Josh, thank you for the question. Mark, do you want to take that?

Mark D. Eisner: Absolutely. We are very excited about the partnership with Astellas, and we are also very excited about the next steps of the program. We have selected a go-forward dose. We plan to get into expansion cohorts in Q2 very shortly this year. We will be having late-line mCRPC, which is the population here, as a monotherapy. We will have combination with enzalutamide in the early-line, taxane-naive setting. We will also be doing some dose optimization in parallel to satisfy the goals of Project OPTIMUS, to satisfy the FDA's requirements there. We will be working with Astellas. I should also mention the combination in metastatic hormone-sensitive prostate cancer in expansion cohorts.

Taken together, with the expansion cohorts and the dose optimization work, we expect to get into Phase 3 in 2027, to be well positioned there.

Marianne De Backer: This was exactly why we were so excited about entering into the partnership with Astellas. It allows us to accelerate clinical development and also really broaden the potential and expand the trials to reach more patients. Your next question comes from the line of Ronny Gal with Leerink Partners. Please go ahead.

Analyst (Leerink Partners): Hi. Good morning, everyone. Thanks. Two questions from me. On the Astellas collaboration, just curious how you are thinking about unlocking resources for investing into the broader ProXTEN platform and thinking about other solid tumor indications, and what sort of calculus will you do in terms of prioritizing programs over accelerating others? My second question: with the larger cohort of patients evaluated on VR-5,500, how does this evolve your thinking about where VR-5,500 could be positioned within the treatment paradigm in terms of line of therapy, combination versus monotherapy, and thinking of the future?

Marianne De Backer: Yes. Thank you, Ronny. As it relates to resourcing, teaming up with a world-class player in the prostate cancer field—and Astellas has entirely internal development capabilities—will help us tremendously in again accelerating the VR-5,500 program. From a finance perspective, it also allows us to divert certain expenses to our other programs and potentially accelerate those as well. We think that the collaboration certainly has a lot of benefit beyond just for VR-5,500 alone. As to where to position VR-5,500—Mark?

Mark D. Eisner: Sure. Absolutely. We are very excited about the progress we have made so far and the data that we have presented to you today. We plan to address a broad range of patients with metastatic prostate cancer, including late-line mCRPC as a monotherapy—these are the data we presented to you today—earlier-line mCRPC in combination, and, as you recall, we have been dose escalating in combination with enzalutamide in the frontline setting already, and that is going well. In addition, we plan combination therapy in metastatic hormone-sensitive prostate cancer. We are very excited to continue to progress the program. These are three high unmet-need populations within the metastatic prostate cancer setting that we think we can address.

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

Mike Ulz: Congratulations on the data and deal as well. Maybe just one on VR-5,500 and durability. Talk about your level of confidence that some of this very strong early data that you are seeing can be sustained over the longer term.

Mark D. Eisner: We are very encouraged by the RECIST responses that we have seen, particularly those that have occurred up to 27 weeks, and the fact that we are able to confirm RECIST responses in patients. We are also seeing a concordance of RECIST responses with PSMA PET responses and deep PSA responses, which we also think is further evidence of the efficacy we can achieve. Also, the case studies that Dr. de Bono presented illustrate patients with up to one year of durability, which represents the deep potential, I think, of VR-5,500. Taken together, we are really pleased with the emerging evidence of durability in the program.

Mike Ulz: Makes sense. Maybe just one more question for me. Obviously, you are presenting the data at ASCO GU later this week. Is the data you shared with us today the same that will be presented at the meeting? Are there any additional updates or data points we should be looking out for? Thanks.

Marianne De Backer: The oral presentation at ASCO GU this Thursday by Dr. de Bono—these oral presentations are rather short—so there will not be additional data, but it will be a subset of this data.

Mike Ulz: Great. Thank you, and congratulations again.

Marianne De Backer: Thank you.

Operator: Your next question comes from the line of Phil Nadeau with TD Cowen. Please go ahead.

Philip M. Nadeau: Good afternoon. Congratulations on the data and the Astellas collaboration. Two from us. First, in terms of the go-forward dose, could you give us more information on what that dose is? In particular, was there a dose response in those doses above 3,000 micrograms per kilogram Q3W, or how did you identify that go-forward dose? Second, just a clarifying question. It sounds like there is no Grade 3 CRS in doses above 3,000. Was there any below? It did not seem to be from one of the slides, but we just want to make sure we saw that correctly. Thank you.

Mark D. Eisner: Thanks for the question. In terms of the go-forward dose, we have done a lot of work on that, integrating safety, efficacy, PSA, PSMA PET, RECIST responses, and so forth, and we have selected a go-forward dose. As you can appreciate, we have now a partner, Astellas, which we are thrilled to have on board, so we are not going to be communicating the exact dose today because that is something that involves both of us in the partnership. But I can tell you it will be in the 3,000–3,500 microgram per kilogram maintenance dose range.

In terms of dose response at or above 3,000, you can clearly see we showed you all the data for all the doses tested for PSA responses. There is a compelling dose response across those doses. Once we get above 3,000, there still is some dose response, but primarily we are in a range where we are seeing very, very strong efficacy and a very strong therapeutic index. We are confident that we have identified a go-forward dose that really optimizes the therapeutic index moving forward. In terms of Grade 3 CRS above 3,000 micrograms per kilogram in the go-forward dose range, we have seen no Grade 3 CRS.

We did observe one Grade 3 CRS in an earlier dose cohort in a low-dose patient who had an intra-patient dose escalation and had one episode of Grade 3 CRS that recovered rapidly, and the patient did very well.

Philip M. Nadeau: That is very helpful. Thank you.

Operator: Your next question comes from the line of Etzer Darout with Barclays. Please go ahead.

Etzer Darout: Great. Thanks for taking the questions and congrats on this dataset. Really nice to see. One question I had on the go-forward dose: in the combination study that you have initiated, will new patients be enrolled at these effective doses of greater than 3,000 micrograms per kilogram? 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 do you see this as a potential opportunity moving forward for the molecule? Thank you.

Mark D. Eisner: Thanks. Good question. In terms of the go-forward dose in combination with enzalutamide, we anticipate that the dose should be consistent in the two populations. We are almost complete with a dose escalation in combo with enzalutamide in frontline mCRPC, just to confirm that there are no issues there, but we do anticipate it should be very similar or the same. In terms of flat dose, right now we do not have plans for a flat dose. It would be possible in theory, but we are still using the microgram per kilogram dose.

Etzer Darout: Thank you.

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

Joseph Robert Stringer: Hi, thanks for taking our questions. Just a follow-up on the deal with Astellas for VR-5,500. What might this mean for the rest of the oncology pipeline? Is there an opportunity for some of these programs to be standalone for Vir Biotechnology, Inc., or do you see the long-term strategy here to seek partners or to partner these programs? Then a question for Dr. de Bono: just based on these updated data, what are the read-throughs in your outlook, and where do you see potential for VR-5,500 in earlier lines of mCRPC therapy? Thank you.

Marianne De Backer: Thank you, Joey. The Astellas deal again was a very strategic choice based on the fact that the unmet need in prostate cancer is incredibly high. The landscape is evolving very quickly. We thought that time to market is of utmost importance, so we really were looking for a global partner with scale and aligned incentives that would help us accelerate the program and also, as I mentioned earlier, really allow us to grow the pie, so to speak—how much more value could we bring to a broader subset of patients?

That is everything that the Astellas collaboration really delivers, while we can retain a significant portion of the value through the 50/50 profit split, the milestones, and ex-US 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 on the competitive landscape, the size of the commercial opportunity, and the indication, about the financial needs to bring these indications forward. We will be making very thoughtful choices on what to partner, how to partner, and what to keep for ourselves 100%.

Also, to remind you that we have seven preclinical masked T cell engagers, and for sure, on the preclinical programs, this is just too much for us to move forward on our own. We will certainly be looking for partners there. Because of the plug-and-play nature of the platform, it allows us to move actually pretty quickly in preclinical research. You will be seeing that we will be looking for partners in some of those areas. Your second question was related to read-throughs. Dr. de Bono is not available here during the Q&A, but Mark, do you want to take it? Sure.

Mark D. Eisner: Your question was about the potential in earlier lines of metastatic prostate cancer. Yes, we definitely believe there is potential there. We are planning first-line taxane-naive metastatic castration-resistant prostate cancer expansion cohorts, in addition to metastatic hormone-sensitive prostate cancer. We are really looking across the metastatic prostate cancer landscape to help these patients who really need better treatments.

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

Patrick Ralph Trucchio: Thanks. Good afternoon, and congrats on the data and the deal. Just a follow-up on the Astellas deal, with Vir Biotechnology, Inc. having an option in the US to co-promote, what would that look like? At what point in the development process would you be able to exercise that option?

Marianne De Backer: Thank you, Patrick. We have an option to co-promote alongside Astellas in the US, and up to a year before the start of our pivotal trials, we will be able to make that decision.

Patrick Ralph Trucchio: Great. If I could, just a follow-up question for Dr. de Bono. I am wondering, based on the data that you have seen so far, how confident are you that this treatment could potentially move into frontline? What would you need to see in order to give you that confidence?

Marianne De Backer: Thank you, Patrick. Unfortunately, Dr. de Bono is in transit, so he is not available for this Q&A. He will be at the ASCO GU this Thursday. But maybe, Mark, you want to—

Mark D. Eisner: Yes. I encourage everybody who can to attend his talk to understand his perspective there. We see potential across the metastatic prostate cancer landscape. We have generated, we think, compelling early data in the late-line mCRPC setting. We are currently enrolling patients in dose escalation in the frontline, taxane-naive mCRPC setting. We would anticipate, based on what we have 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 masked TCE approach should work, and we will be generating those data. As I mentioned before, we are also going to be looking at the metastatic hormone-sensitive prostate cancer setting as well.

That gives you an idea of where we are heading.

Patrick Ralph Trucchio: Terrific. Thanks so much.

Marianne De Backer: Thank you.

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

Sean McCutcheon: 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, whether that is saturating on the enzymatic activity or otherwise? Second question, how are you thinking about the partnership with Astellas and optionality for combining VR-5,500 with other ARPIs beyond enzalutamide? Thanks.

Marianne De Backer: Thank you, Sean. 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 the ARPIs, but that will be something that we will need to inform you about at a later time point.

Mark D. Eisner: Your first question was related to the dose. You are asking about dose response for CRS and efficacy and what is the limit of the dose on the high end. A couple of points there. Our goal has been to maximize and optimize the therapeutic window to get the best possible safety with the minimum possible adverse events and CRS. We have taken a careful look across the dataset on all the efficacy parameters and safety parameters, including PSA, RECIST, and PSMA PET, and all the safety events, CRS, etcetera.

We think we have gotten to a range—the 3,000 to 3,500 microgram per kilogram 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.

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

Alec Stranahan: Congrats on the really clean update here. Maybe first, just following up on an earlier question regarding durability, I would 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.

Second, in the six patients with the evaluable PSA but not RECIST, assuming these will feed into the overall PFS analysis, could you talk about why those were not 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.

Mark D. Eisner: Your first question has to do with durability and how PSA declines will track with PFS. In general, I would say that the deeper PSA declines, particularly PSA-90s and PSA-99, 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-99. In terms of radiographic PFS, you are correct we did not present those data at this update because, as you can see, the data, particularly for the high-dose cohorts, are still evolving, and the patients are still maturing over time. Those data really are not available yet.

In terms of exactly when we will present further data, we will have to give guidance on that at a subsequent time point. Could you clarify? I was not quite sure I got the second question. Was that why were some patients not RECIST evaluable?

Alec Stranahan: I think there were six patients that had a PSA—out of the 17, six were not evaluable for RECIST. Was it that you could not get the scans at baseline? Was that the driver there? What would you expect in terms of PFS for those patients?

Mark D. Eisner: Thanks for clarifying. In the 3,000 or above cohorts, we had 22 patients. We had 17 patients who were PSA evaluable. Two of those patients were just early at the time of the clinical cutoff, so we will get those subsequent PSA values; they were not part of the dataset. Three out of the five discontinued early, so they will not be PSA evaluable. That is very typical for prostate cancer trials in the late-line setting because these patients are quite sick with a very heavy disease burden. We have 11 patients who are RECIST evaluable. Among those we had five responses—four were confirmed, and one is still waiting for the next confirmatory scan between week nine and week eighteen.

That one is coming in time.

Alec Stranahan: That makes sense. Thanks, Mark. Congrats again.

Mark D. Eisner: Thank you.

Operator: This concludes the call. Thank you for participating.

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