Arvinas, Inc 2026 Q2 Earnings Call

Thank you for joining us. Earlier today, we issued a press release with our second quarter 2026 financial results, which is available in the investor and media section of our website at arvinas.com. Joining us on the call today, we have Randy Teel, our President and Chief Executive Officer, Angela Cacace, our Chief Scientific Officer, and Andrew Saik, our Chief Financial Officer. Before we begin, I'll remind you that today's discussions contain 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 filing 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 this 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. Now I'll turn the call over to Randy Teel.

Randy? Thanks, Jeff. Good morning, everyone.

As a company, we've made significant progress over the past several months. Our focus has been on positioning Arvinas for our next phase of growth, guided by a clear strategic vision. Central to that vision is a relentless focus on advancing transformational improvements for patients. Through continued innovation and disciplined execution, we are focused on unlocking the full potential of our pipeline for patients and shareholders. We've reached three significant strategic milestones since the start of the year, beginning with the first-ever FDA approval of a PROTAC degrader, VEPPANU. Second, we completed an out-licensing of VEPPANU to Rigel Pharmaceuticals, who anticipate making VEPPANU available to patients in the very near future. Third, we made the strategic decision that our KRAS G12D program, ARV-806, will only move forward in the hands of a partner.

While we believe ARV-806 has the potential to become a meaningful treatment option for patients, it will require investment that is inconsistent with our current capital allocation strategy. Taken together, our progress and decisions in the first half of 2026 have positioned Arvinas to fully capitalize on the promise of our platform in oncology and neurology. We've fully shifted our focus to our phase I clinical programs. We are confident about the opportunity ahead to create important therapies for patients. With that, I'll spend a few moments diving into our three assets with significant clinical data catalysts in the next 12 months. I'll review their differentiating profiles and compelling value propositions. I'll start with ARV-393, our BCL-6 degrader.

I'll explain why BCL-6 is an attractive target, share where we are in the progress of the trial. Let you know what to expect in our data release later in 2026. BCL-6 is an exciting therapeutic target with initial clinical validation. BCL-6 is a previously undrugged transcription factor, a master regulator of multiple cellular processes during B-cell development, including proliferation, survival, and apoptosis. Altered BCL-6 activity has been implicated as an oncogenic driver in several subtypes of non-Hodgkin lymphoma. We believe that ARV-393 has the potential to become a foundational treatment option and pave the way as the first all-oral chemotherapy-free approach for patients with B or T-cell lymphomas. When we initiated our BCL-6 program, no company had successfully demonstrated BCL-6 degradation or advanced a degrader to the clinic.

Based on feedback from the FDA, our trial began with doses well below our predicted efficacious exposure levels, leading to challenges with enrollment and extended enrollment timelines. However, we've seen a clear acceleration in the enrollment of the trial as we've dosed closer to the expected efficacious range. At the same time, enrollment in the glofitamab combo portion of the trial has been strong since it began in the past few months. As we reported late last year, even at the doses we would not have expected to be efficacious, we've seen early responses in difficult-to-treat T-cell lymphomas like AITL, as well as in patients with B-cell lymphomas. When it comes to upcoming data for ARV-393, we are on track to share initial phase I data by the end of the year.

Our safety profile has supported continued dose escalation, though the majority of the data in 2026 will be from the early cohorts dosed below the expected efficacious range. These early cohorts, when compared with the overall lymphoma population, include a higher-than-predicted proportion of patients with T-cell lymphomas, likely reflecting the limited treatment options for these patients. As I mentioned, as we've approached the predicted efficacious range, enrollment of patients, including those with B-cell lymphomas, has increased. In 2027, we will plan a subsequent disclosure that will include more mature monotherapy data, including patients with DLBCL treated with ARV-393, both as monotherapy and in combination with glofitamab. We are optimistic about the potential of this program to benefit patients who have historically experienced poor clinical outcomes, especially given the positive feedback we've received from investigators over the past few months.

I'll turn now to ARV-027, our degrader targeting polyglutamine-expanded androgen receptor, or polyQ-AR. What's immediately interesting about this program is that the polyQ-AR protein is well understood to be the driver of pathology for patients with Spinal and Bulbar Muscular Atrophy, or SBMA, also known as Kennedy's disease. SBMA is a rare neuromuscular disorder with between 10,000 and 13,000 diagnosed patients in major markets. Genomic studies suggest that SBMA remains substantially underdiagnosed, and ARV-027 has the potential to become the first therapy to target the primary driver of disease. SBMA is an X-linked disease caused by the toxic buildup of the polyQ-AR protein in skeletal muscle. This accumulation disrupts normal muscle function, drives muscular atrophy, and over time, leaves patients with long-term physical disabilities, and often unable to accomplish daily activities.

As an oral therapy, ARV-027 could be uniquely suited as a convenient treatment option to degrade the protein known to cause the disease. In February, we presented preclinical data supporting the potential of ARV-027 in SBMA. Guided by published preclinical evidence, we had established a target of achieving greater than 50% polyQ-AR degradation in skeletal muscle, a level we believed would provide functional benefit. In an aggressive mouse model of SBMA, 027 showed meaningful improvements in grip strength, endurance, and survival. Importantly, while we don't believe complete elimination of polyQ-AR is required to achieve therapeutic benefit, our preclinical studies did demonstrate that 027 could achieve AR degradation far exceeding the levels required for functional improvement. Today, I'm pleased to announce that in our ongoing phase I trial in healthy volunteers, we completed the single ascending dose cohorts and have now initiated the multiple dose portion of the trial.

027 is our first degrader aimed at a target in muscle. With that in mind, our phase I trial must demonstrate two measures that we've never demonstrated before in human muscle tissue. The first step is achieving adequate exposure, and the second is to demonstrate AR degradation in muscle. Taken together, these healthy volunteer data would provide proof of mechanism for ARV-027 and meaningfully de-risk the program. In the first half of next year, we intend to show data for both of these measures, as well as initial safety data from the trial. Following the dosing in healthy volunteers, our plan is next to dose patients with SBMA. The phase I trial design already includes a multiple dose cohort in patients with SBMA. We believe this design will accelerate our development plan with the potential to move to a registrational study following the conclusion of the phase I trial.

I'll move to ARV-102, our third program with upcoming clinical data, and discuss plans for upcoming disclosures and provide a brief update on our regulatory interactions as we plan the next trials for our LRRK2 degrader. As a reminder, there are no approved disease-modifying treatment options available for patients with either PSP or PD, and we believe 102 has the potential to become a paradigm shift in treatment for these patients. This is supported by biomarker data that we presented in March at ADPD. These data were the first to show modulation of key biomarkers implicated in both PSP and PD, an outcome that has not been demonstrated by LRRK2 inhibitors. This reinforces the potential for 102 to provide a unique approach in neurodegenerative diseases. We will share additional biomarker data from the phase I trial, including oculomotor measures and CSF proteomics at the MDS conference in October.

When it comes to our regulatory interactions for 102, as you'll recall, we are currently working to initiate clinical trials for 102 in patients with PSP, both in the U.S. and globally. After successfully completing our phase I trial in the Netherlands earlier this year, we submitted an IND to the FDA to support the initiation of the phase I-B trial in the first half of the year. As previously communicated, prior to authorizing initiation of the trial, the FDA requested additional information as well as final data from our chronic tox studies, which we've now completed. During the quarter, we've also had productive engagement with both European and Japanese health authorities. Interactions with the agencies are ongoing, and we look forward to updating you on our timing for initiating our next clinical trials, which we now expect to begin in 2027.