Arvinas Q2 2026 Earnings Call Transcript

Arvinas (NASDAQ: ARVN ) reported second-quarter financial results on Tuesday. The transcript from the company's second-quarter earnings call has been provided below. APIs provide real-time access to earnings call transcripts and financial data. Visit to learn more.

Access the full call at Summary Arvinas Inc. reported significant progress, including the FDA approval of their PROTAC degrader Vepanu, an out-licensing agreement with Rigel Pharmaceuticals, and a strategic decision to seek a partner for their KRAS G12D program. The company is advancing its focus on its Phase 1 clinical programs, highlighting ARV393 for BCL6 degradation, ARV027 for targeting polyglutamine repeat androgen receptors, and ARV102 for LRRK2 degradation. 7 million in total revenue for the quarter, and maintains a cash runway into the second half of 2028.

Arvinas plans to present initial Phase 1 data for ARV393 by the end of 2026, and ARV027 and ARV102 are progressing through clinical trials with data expected in 2027. Management emphasized disciplined capital allocation and prioritizing programs with high unmet need and strong commercial potential, with a strategic focus on oncology and neurology. Full Transcript OPERATOR Hello and welcome to our Arvinas second quarter 2026 earnings conference call. At this time, all participants are in a 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-one-one on your telephone. You will then hear an automated message advising your hand is raised. To withdraw your question, please press star-one-one again.

I would now like to hand the conference over to Jeff Boyle. Sir, you may begin. Jeff Boyle, Investor Relations Good morning, everyone, and thank you for joining us. com.

Joining us on the call today we have Randy Thiel, our President and Chief Executive Officer, Angelica Casey, our Chief Scientific Officer, and Andrew Sayek, 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 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 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 Thiel. Randy Thiel, President and Chief Executive Officer Thanks, Jeff. And 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, Vepanu. Second, we completed an out-licensing of Vepanu to Rigel Pharmaceuticals, who anticipate making Vepanu available to patients in the very near future. And 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 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 fully shifted our focus to our Phase 1 clinical programs, and 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 differentiated profiles and compelling value propositions.

I'll start with ARV393, our BCL6 degrader. I'll explain why BCL6 is an attractive target, share where we are in the progress of the trial, and let you know what to expect in our data release later in 2026. BCL6 is an exciting therapeutic target with initial clinical validation. BCL6 is a previously undrugged transcription factor and a master regulator of multiple cellular processes during B cell development, including proliferation, survival, and apoptosis.

Altered BCL6 activity has been implicated as an oncogenic driver in several subtypes of non-Hodgkin lymphoma. We believe that ARV393 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 BCL6 program, no company had successfully demonstrated BCL6 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 Glofi combo portion of the trial has been strong since it began in the past few months, and 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 ARV393, we are on track to share initial Phase 1 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. But 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 ARV393, both as monotherapy and in combination with Glofi. 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 ARV027, our degrader targeting polyglutamine repeat 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 and 13,000 diagnosed patients in major markets. Genomic studies suggest that SBMA remains substantially underdiagnosed, and ARV027 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, ARV027 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 ARV027 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, ARV027 showed meaningful improvements in grip strength, endurance, and survival. Importantly, while we don't believe complete elimination of polyQ is required to achieve therapeutic benefit, our preclinical studies did demonstrate that ARV027 could achieve AR degradation far exceeding the levels required for functional improvement. Today I'm pleased to announce that in our ongoing Phase 1 trial in healthy volunteers, we completed the single-ascending-dose cohorts and have now initiated the multiple-dose portion of the trial. ARV027 is our first degrader aimed at a target in muscle.

With that in mind, our Phase 1 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 ARV027 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 1 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 1 trial. Finally, I'll move to ARV102, 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 AD/PD. 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 1 trial, including ocular motor measures and CSF proteomics, at the MDS conference in October. S. and globally. After successfully completing our Phase 1 trial in the Netherlands earlier this year, we submitted an IND to the FDA to support the initiation of the Phase 1B 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. Stepping back, our accomplishments and decisive actions during the first half of 2026 demonstrate our ability to embrace change, capitalize on new opportunities, and execute efficiently.

I'm proud of the entire team at Arvinas and how we've assertively concentrated our resources on the most promising opportunities for Arvinas. With disciplined capital allocation, we are prioritizing programs that address high unmet need and have strong commercial potential. Our pipeline is designed to maximize both clinical impact and long-term shareholder value. With that, I'll turn the call over to Angela.

Angela Thank you, Randy. The Arvinas approach to breakthrough medicines begins with choosing the right biology. The most important decision is selecting targets where targeted protein degradation can fundamentally change the course of disease. We started with two highly validated targets, androgen and estrogen receptor, to establish the clinical power of our degrader platform.

Today we're applying those same principles to build the next generation of differentiated, disease-modifying medicines across oncology and neurology. Randy highlighted the progress of our clinical portfolio. I'd like to spend a few minutes on two oncology research programs that illustrate where we believe protein degradation can deliver unique advantages. I'll begin with ARV6723, our oral HPK1 degrader and our first immuno-oncology PROTAC.

HPK1 acts as a natural brake on the immune system. It limits T cell activation and suppresses anti-tumor immunity. What's particularly challenging is that HPK1 biology extends beyond its kinase activity. HPK1 also functions as a signaling scaffold.

As a result, inhibitors of the kinase activity leave part of the biology intact. Instead, degradation eliminates both kinase and scaffolding functions. We believe that's why ARV6723 has produced a differentiated preclinical profile compared with inhibitors across multiple tumor models, including tumors with both high and low immunogenicity. ARV6722 produced robust anti-tumor activity.

In these studies, degradation consistently outperformed both an HPK1 inhibitor and anti-PD-1 therapy alone. Perhaps most exciting is what we've observed in checkpoint-resistant tumors. In seven preclinical models, ARV6723 demonstrated meaningful single-agent activity where neither an HPK1 inhibitor nor anti-PD-1 therapy showed benefit. We also demonstrated preclinically that the biology extends well beyond T cell activation.

HPK1 degradation may remodel the tumor microenvironment through enhanced interferon signaling and activation of the myeloid compartment. We believe this broader immune remodeling may be due to elimination of the scaffolding activity that contributes to the differentiated profile we've observed and, if it translates clinically, could support broader combination opportunities and activity in tumors that have historically responded poorly to immunotherapy. We're excited to begin translating these findings into the clinic. We remain on track to initiate enrollment in our Phase 1 study in the coming weeks.

We look forward to sharing updates as the program advances. Finally, I'd like to highlight our first-in-class oral pan KRAS degrader program. We recently presented preclinical data demonstrating the potential to overcome key limitations of current pan RAS inhibitors. Our lead oral degrader showed potent activity across a broad spectrum of CRAF mutations.

Importantly, our lead oral pan KRAS degrader targets KRAS mutations found in more than 90% of patients with KRAS-altered cancers, including difficult-to-treat mutations such as G12R and Q61. It also demonstrated activity against cross amplification, a major mechanism of resistance. We also demonstrated superior anti-tumor activity in combination with immune checkpoint blockades, highlighting the potential to favorably remodel the tumor microenvironment in a way that inhibitors do not. Together, these findings support the potential for broad activity across KRAS-driven cancers, a differentiated therapeutic index, and extensive combination opportunities.

We will present these exciting combination data at an upcoming scientific conference. The team continues to make outstanding progress and we look forward to sharing additional updates in the coming months. With that, I'll turn the call over to Andrew to review our quarterly financial results. Andrew Sayek (Chief Financial Officer) Thanks, Angela, and good morning, everyone.

I'm pleased to provide financial highlights for the second quarter 2026. As a reminder, detailed financial results for the second quarter are included in the press release we issued this morning. Reiterating the team sentiment, we have much to look forward to later this year and are pleased with our strong financial position that will allow us to continue to advance our pipeline into the second half of 2028. 4 million at the end of 2025.

With our healthy balance sheet and focus on our early pipeline, we are well positioned to continue developing our promising oncology and neurology programs. Q2 was a very busy period for us as during the quarter we received FDA approval of the first ever PROTAC degrader Vepanu and regulatory approval for the Rigel license agreement. These events had a significant impact to our financial statements, which I will summarize now. 5 million, of which $35 million was received within the quarter.

We have also concluded that the method by which we were recognizing revenue under the original Pfizer agreement is no longer applicable under ASC 606 as a result of the Rigel agreement. 7 million to cover our remaining obligations to complete ongoing development activities. Additionally, we recorded a $50 million milestone from Pfizer triggered by the VEPIDU approval.