Arvinas, Inc.

Good day and thank you for standing by. Welcome to the ARENA's first quarter 2026 earnings call. At this time, all participants are in listen-only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you will need to press star 11 on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star 11 again. Please provide that today's conference has been recorded. I would like to hand the conference over to your first speaker today, Jeff Boyle, head of investment relations. Please go ahead.

Good morning, everyone. Thank you for joining us. Earlier today, we issued a press release with our first quarter of 2026 financial results, which is available in the investor and media section of our website at arvenis.com. Joining us on the call today, we have Randy Keel, our president and CEO, Noah Berkowitz, our chief medical officer, Angelica Casey, our Chief Scientific Officer, and Andrew Sayek, our Chief Financial Officer. Before we begin, I'll remind you that today's discussion contains forward-looking statements that involve risks, uncertainties, and assumptions. These risks and uncertainties are outlined in today's press release and in the company's recent filings with the Securities and Exchange Commission, which I urge you to read. Our actual results may differ materially from what is discussed on today's call. A replay of the call as well as today's press release and an updated corporate deck will be available on the investor and media section of our website. And now I'll turn the call over to Randy Thiel. Randy?

Thanks, Jeff. And thank you all for joining us today. Since stepping into the role as CEO earlier this year, my appreciation for the strength of the Arvinas platform, the talent and execution capability of our team, and our deep and differentiated pipeline has only grown. As the first ProTac deGrader company, we believe we've built unmatched translational expertise in the protein deGrader space. I believe we're in a great position for a highly productive and value-generating 2026. Several months ago, after filing the new drug application for Vepdegastrant, we announced our intention to identify a third party with the capability to maximize its commercial opportunity. During this time, we remained confident that Vepdegastrin had the potential to become a meaningful treatment option for patients with metastatic breast cancer. Our optimism was validated by the recent FDA approval of Vepdeg, now known as Vepinu, and yesterday afternoon, we were pleased to announce that we and Pfizer have entered into a global licensing agreement with Rigel Pharmaceuticals for the commercialization, development, and manufacturing of Vepinu. I'll begin with the FDA's approval of Vepinu for the treatment of ESR1 mutant ER-positive HER2-negative advanced breast cancer. This is an important milestone for patients and physicians and demonstrates the potential of targeted protein degradation to treat disease. There have been minimal second-line treatment options for these patients, and as the lead investigator in our phase three trial said, the approval of Vepinu brings renewed hope to patients who need additional options. The approval of Vepinu was the first ever approval of a heterobifunctional protech degrader. In our industry, few biotechs are successful in bringing a molecule from discovery through approval. Fewer companies still make it onto the very short list of companies, big or small, that have ever been the first to bring a new therapeutic modality from inception to approval. We believe this achievement fully validates our innovative targeted degrader platform which Arvinas pioneered more than 10 years ago. It also strengthens our confidence in the breadth and versatility of our exciting phase one pipeline across oncology, neurodegenerative disorders, and neuromuscular diseases. I am deeply grateful to the team that has worked tirelessly on Vepinu with the unfaltering belief that it can bring renewed hope to patients who need new treatment options. We are committed to making sure Vepinu is available for patients as soon as possible. Rigel has a fully established oncology sales team and the infrastructure needed to ensure Vepinu is available soon. They are committed to unlocking the full value of Vepinu and we are confident that they are the right partner to bring this important treatment to the patients that need it. At the same time, this agreement allows our Venice to invest in the next wave of innovation across our pipeline while maintaining a strong and disciplined approach to capital allocation. Indeed, this was the rationale for seeking a new partner for Vepinu so that patients could receive Vepinu while Arvinas could dedicate itself to our next generation of degraders. I am fortunate to lead an organization advancing an industry-leading portfolio of degraders. Guided by patient genetics and by identifying the central drivers of disease, we deliberately select targets where protein degradation can deliver transformative impact. To date, We have dosed more than 2,000 patients and healthy volunteers using our ProTech technology. And our team has had remarkable success in advancing promising compounds from preclinical studies to clinical programs. As we look ahead, our ambition is clear. We are not simply advancing molecules to the clinic. We are relentlessly focused on creating differentiated therapies that raise the bar for patients on safety, tolerability, and efficacy. We're not looking for incremental improvements, but rather working toward fundamentally changing what's possible for patients and clinicians. And we are doing it from a position of strength. With a healthy balance sheet and a deeply committed team, we are well positioned to deliver long-term value for patients, their families, and our shareholders. We are in the promising position of having four phase one clinical programs ongoing with the capital needed to reach important inflection points for each of the programs that will inform our investment priorities and ongoing development strategies. Now, I'll turn the call over to Noah and the team. Noah? Thanks, Randy. Good morning, everyone, and thank you for joining us today. We have an exciting year ahead at Arvinas, beginning with the recently presented Phase 1 data for our lead program, ARV102 at ADPD. These results represent a key milestone and provide strong validation of our approach in neurodegenerative diseases. ARV102 is an orally administered protact designed to cross the blood-brain barrier and potently and selectively degrade LRRK2, a multi-domain protein that regulates neuroinflammation, lysosomal, and synaptic function. Elevated LRRK2 levels are implicated in disorders, including progressive supranuclear palsy, or PSP, and Parkinson's disease. By degrading the full LRRK2 protein complex, including its scaffolding, GTPase, and kinase functions, ARB102 addresses multiple disease-relevant pathways in contrast to kinase inhibitors, which target only a single function. We have shown that ARB102 penetrates the CNS, produces dose-dependent reductions of LRRK2 in cerebrospinal fluid, and modulates downstream disease-associated proteins. At ADPD, phase one data in patients with Parkinson's disease demonstrated approximately 50% or greater reductions in CSF LRRK2 by day 14 across dose levels sustained through day 28, consistent with our goal of normalizing the approximately twofold LRRK2 elevation observed in Parkinson's disease. Importantly, LRRK2 degradation led to dose-dependent reductions in biomarkers of neuroinflammation and lysosomal stress, including CD68 and GPNMB. To our knowledge, this degree of biomarker modulation has not been observed with LRRK2 inhibitors. ARV102 was also generally well tolerated with no serious adverse events through 28 days of dosing. These findings support advancement into PSP, our immediate clinical focus. PSP is a rapidly progressive tauopathy driven by 4R tau accumulation with the typical survival of five to seven years and no disease-modifying therapies. In patients with PSP, elevated LRRK2 expression is associated with accelerated and clinically meaningful progression within one year. Preclinically, we have shown that ARV102 impacts neuroinflammation, enhances endolysosomal function, and most importantly, reduces tau pathology in multiple relevant disease models, aligning with our clinical observations of improved endolysosomal function and reduced neuroinflammation. Together, These data reinforce our view that LRRK2 degradation offers a differentiated disease-modifying approach to the treatment of PSP, a devastating fatal disease without available therapy, which affects 25,000 patients in the US. I also want to provide an update on the timeline for initiating our Phase 1B clinical trial with ARB102 in patients with progressive supernuclear palsy. We submitted an IND earlier this year with the intention of initiating the trial in the US during the first half of the year. Following the 30-day review period, the FDA requested final data from our chronic tox studies in non-human primates prior to authorizing the initiation of the phase 1B in the US in patients with PSP. Given this requirement, while no patients in the US have been treated, The planned trial is on clinical hold and will not begin until we provide these data, which we expect will be available in mid-2026. We anticipate the U.S. trial will begin by the end of 2026. We do not anticipate this will impact our plans for trials in the EU, so there's no change in our guidance on the start of the phase two study, which we are planning as a global study. Turning now to oncology, I'll begin with ARV806, our KRAS G12D degrader. KRAS G12D is a well-characterized oncogenic driver associated with poor outcomes and resistance to standard therapies across multiple tumor types, including pancreatic, colorectal, and non-small cell lung cancers. ARV806 is designed to potently and selectively eliminate both on and off forms of KRAS G12D, a key differentiator for a challenging target in solid tumors. Our confidence in ARV806 is supported by compelling preclinical results, which demonstrated approximately 25 to 40-fold greater potency than clinical stage KRAS G12D inhibitors and degraders. These data also showed durable degradation greater than 90% for seven days after a single dose, with efficacy responses across pancreatic, colorectal, and lung cancer models. As we shared on our prior call, we completed enrollment of the dose escalation for once weekly administration in our ongoing phase 1 trial well ahead of schedule. We view this rapid enrollment as a strong indicator of investigator enthusiasm and unmet medical need in KRES-driven cancers. We believe the initial data we show later this year will be the first step in showcasing ARV806's potential as a differentiated and clinically meaningful treatment option for patients with KRAS-driven cancers. Finally, turning to ARV393, our PROTECT BCL6 degrader, we continue progressing through the Phase I monotherapy dose escalation trial for patients with both B-cell and T-cell lymphomas who have received multiple prior therapies. We are particularly encouraged by early responses observed across both populations, including responses at exposure levels below what we predicted to be efficacious. We have also observed robust BCL6 degradation, a notable finding given that BCL6 is rapidly resynthesized. We look forward to sharing additional clinical data from our ongoing phase one monotherapy trial in patients with relapsed or refractory non-Hodgkin's lymphoma later this year. In parallel to enrolling the monotherapy cohort, we've initiated a combination trial with Glofidamab in patients with diffuse large B-cell lymphoma, an important next step as we look to expand the potential opportunity with ARV393. With that, I'll now turn the call over to Angela. Angela?