ARVINAS, INC. (ARVN) Q2 2026 Earnings Call Transcript

Hello, and welcome to Arvinas Second Quarter 2026 Earnings Conference Call. The operator provided instructions. I would now like to hand the conference over to Jeff Boyle. Sir, you may begin.

Good morning, everyone, and 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 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 Teel. Randy?

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, VEPPANU. Second, we completed an out-licensing of VEPPANU to Rigel Pharmaceuticals, who anticipate making VEPPANU 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 I 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 ARV-393, 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 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 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 combination 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 angioimmunoblastic T-cell lymphoma (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. 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 diffuse large B-cell lymphoma (DLBCL) treated with ARV-393, 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 ARV-027, 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 10,000 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 derisk 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. Finally, 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 progressive supranuclear palsy (PSP) or Parkinson's disease (PD), and we believe 102 has the potential to become a paradigm-shifting 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 I trial, including ocular motor 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 Ib 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 toxicology 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.

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 ARV-6723, 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 antitumor 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 ARV-6723 has produced a differentiated preclinical profile compared with inhibitors. Across multiple tumor models, including tumors with both high and low immunogenicity, ARV-6723 produced robust antitumor 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, ARV-6723 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, it 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 I 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 KRAS 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 KRAS amplification, a major mechanism of resistance. We also demonstrated superior antitumor activity in combination with immune checkpoint blockade, 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.

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's 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. At the end of the second quarter, we had $567.9 million in cash, cash equivalents and marketable securities on the balance sheet compared with $685.4 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 is a very busy period for us as during the quarter, we received FDA approval of the first ever PROTAC degrader VEPPANU and regulatory approval for the Rigel license agreement. These events had a significant impact to our financial statements, which I will summarize now. First, as a result of the license agreement with Rigel, we recorded license revenue of $62.5 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. We, therefore, moved all deferred revenue to the P&L, which resulted in a net revenue of $126.4 million, and we recorded a liability of $52.7 million to cover our remaining obligation to complete ongoing development activities. Additionally, we recorded a $50 million milestone from Pfizer triggered by the VEPPANU approval. Separately, we recorded $3.5 million in revenue under a Pfizer research collaboration agreement where the research term has been completed. Total revenue for the quarter was $249.7 million. Turning to expenses. During the quarter, we introduced a new cost of license revenue line, which represents royalties and other amounts payable to third parties that are directly attributable to revenue under our licensing agreements. Cost of license revenue was $9 million in the second quarter. The $9 million is comprised of payments to Yale under the amended Yale agreement and were triggered by the FDA's approval of VEPPANU and the entry into the Rigel license agreement. General and administrative expenses were $24 million for the second quarter compared to $25.3 million for the same period of 2025. The decrease of $1.3 million was primarily due to decreases in personnel and infrastructure-related costs of $3.9 million and costs related to developing our commercial operations of $1.4 million, partially offset by an increase in professional fees of $4.2 million, primarily due to the Rigel license agreement. Research and development expenses were $52.6 million in the second quarter compared to $68.6 million for the same period of 2025. The decrease of $16 million was primarily driven by a decrease in compensation and related personnel expenses of $11 million, which are not allocated by program and a decrease in program-specific expenses of $0.6 million and non-program-specific expenses of $2.6 million. Our cost reduction programs initiated last year were completed during the second quarter. Non-GAAP R&D was down $8.1 million compared to the same period last year, representing a reduction of 14%. Non-GAAP G&A increased by $0.3 million or 2% compared to the prior year. During the quarter, we recognized all remaining deferred revenue from the Pfizer collaboration agreement. So going forward, there will be no revenue recognition related to the original Pfizer collaboration. Additionally, we booked a liability of $52.7 million to cover estimated remaining liabilities related to the VEPPANU runout costs. So our future obligations under the collaboration agreement will be booked against the accrual and will not impact our P&L. We continue to maintain our cash runway guidance into the second half of 2028. And in doing so, we will be able to fund operations through key data milestones over the coming months and continue to support our highly differentiated pipeline programs that have the potential to meaningfully improve patients' lives. With that, I'll turn the call over to Randy for closing remarks.

Thanks, Andrew. We've entered the second half of 2026 with multiple opportunities to advance our mission of developing pioneering transformational therapies for patients. We have important catalysts in the coming months and a healthy balance sheet to reach critical milestones. I'll simply close by thanking the patients, investigators and the entire Arvinas team for their continued support and commitment to helping us achieve our mission.

Thanks, Randy. Operator, can you please open the queue?

The operator opened the question queue and introduced the first question.

So on 393, can you discuss a little bit more what you're thinking about the development path, especially considering the data coming mid next year with the glofi combo. Could this catalyze potentially a pivotal trial in an earlier line setting with bispecifics? Any insight there would be great.

The short answer is yes. The long answer is the non-Hodgkin lymphoma (NHL) space has a lot of opportunities to pursue, and as we've talked about over the years, we think that while there's a lot of therapies across the lines of therapy and across the different diseases now — there's plenty of chemo, there's plenty of CAR-T, there's plenty of bispecifics — what there is not a lot of is orally bioavailable, tolerable small molecules. So we think that a BCL6 degrader could slot into multiple areas within the disease landscape. At this point, as we're in the Phase I dose escalation, it's a bit early to talk about exactly where we plan to go, but definitely we can talk about the options. So I think as early options, looking at later-line monotherapy makes sense: think about fourth-line LBCL, maybe third-line LBCL, think about later-line AITL T-cell disease that we've been enrolling patients with already in our Phase I trial. As we move forward with combinations, that could open up further access to the third-line LBCL space, second-line LBCL and perhaps moving ahead in T-cell disease as well. So there's a lot of different places that we could go. The common thread is that to get to any of them, we've got to get through the monotherapy dose escalation, show some efficacy, show some signals there. We've got to show we're combinable with other therapies, most immediately a bispecific like glofi. Once we've done that, I think it becomes a lot easier to talk about where we'll go next, especially as the landscape continues to evolve around us.

The operator introduced the next question.

This is Jacob on for Derek. I was just wondering if you could comment on the path forward for ARV-102 in PSP. And what does the timeline and registration path look like for it in light of some of your more recent regulatory interactions?

Yes. So just to rehash a little bit where we are: we began the year with a couple of Phase I trials, one in healthy volunteers and one in patients with PD. What we planned to do over the course of the year was to start two other trials, a Phase Ib in the U.S. and a registrational-oriented study globally. What we announced a couple of months ago is that after submitting the IND to the FDA, they asked us to wait before starting that study, so that's technically a clinical hold before starting the studies in the U.S. This morning, we announced that with a number of ongoing regulatory interactions that we're currently pursuing and going back and forth on, we think it will take into 2027 to start those studies. Overall, the registrational path in PSP we would think about a two-part study there, the Phase Ib and a registrational study; that continues to be where we aim. A registrational path for PSP where we haven't even dosed patients yet would more likely be a longer-period study. The studies we've done so far are only 28 days, so dosing more like six months or a year in patients with PSP would be what we'd be aiming to start with a registrational study. As we go back and forth with the different regulatory authorities — which actually is quite beneficial to be getting feedback from the three major agencies all right now — we'll be taking that to finalize the path that we will then set out on, as we've said in 2027.

The operator introduced the next question.

Maybe a follow-up on ARV-393. What will be a good outcome from the Phase I monotherapy cohorts that you're going to present later this year? It sounds like these are going to be at the subtherapeutic levels. As we think about combination with glofi, would you be able to share where you are with the dose levels right now? Did you start at the subtherapeutic levels as well and any early trends on combinability?

Yes. The short answer on that second one is yes. As a recap, we were the first company to start working on BCL6, at least to bring it into the clinic to our knowledge. Based on that and some other factors, we got some feedback to start with a very low starting dose for BCL6 as monotherapy. As we've talked about, enrollment has been slower than we would have liked. On the flip side, as we've gotten closer now to the predicted efficacious exposures, we've seen a clear uptick in enrollment. In the combination study, which started a couple of months ago, enrollment there has been quite strong ever since the start. So when it comes to the data that we will have at the end of the year, you were right to highlight we will still be very much below the efficacious range for most of the patients. At the doses that we're at now, we're starting to get to the exposure that we would expect to be efficacious, so we'll start to see some of that. We also mentioned that we have been enrolling a greater proportion of patients with T-cell lymphomas than we would have anticipated based on the overall population. So we think it will make sense to focus on that population in the disclosure that's coming up. As we head into next year, we'll focus on LBCL patients as both monotherapy and combo. The data at the end of this year will certainly be focused on monotherapy. We do not anticipate sharing combo data now. We didn't start quite as low for the combo as we did for the mono, but it certainly did start at levels that in monotherapy were not predicted to be efficacious in patients with B-cell lymphomas.

The operator introduced the next question.

Looking forward to more data this year, and congrats on all the progress. So I'll ask about SBMA and 027, really interesting mechanism here. Just to confirm the IND cleared there and where are you in multiple ascending dosing? And can you characterize — you mentioned exposure and degradation — what are the clinical endpoints that we would ultimately be modeling or expecting in SBMA?

Maybe I'll pass to Angela in a moment on some of the path-forward questions. To reiterate where we are: we have been dosing healthy volunteers with 027. We've now completed the single ascending dose portion of the study and have just begun the multiple dose portion of the study. That will continue. We're expecting to share some data in the first half of next year. We do anticipate including some patients with SBMA in the latter stages of that Phase I study. To reiterate, SBMA is a rare disease; we're talking 10,000 to 13,000 patients in major markets. The great thing about this target is that we are hitting the actual driver of disease. Polyglutamine AR is what drives disease; that's what we're degrading. We're not degrading an upstream transcription factor or another factor, we're degrading the actual cause of disease. When it comes to the next phases, we've talked about being able to move into registrational-intended studies even after Phase I. Angela, I invite you to speak a bit more about plans there and endpoints.

Sure. As we move forward, the goal is to really demonstrate that we can target a 50% reduction of the polyglutamine repeat androgen receptor. In our preclinical studies and in other preclinical studies, 50% reduction is the target that we aim to achieve in muscle. So that's our goal from a biomarker perspective, and we'll also look at some other endpoints as well. Those will be the early endpoints. We will not be able to demonstrate functional change until we go into those registrational studies that Randy mentioned. There, we'll be looking at meaningful scales like the SBMA functional rating scale and those endpoints as well.

The operator introduced the next question.

Congrats on the progress this quarter. I'd like to follow up first on the polyQ-AR. Regarding healthy volunteers versus patients who have different levels of protein at baseline, should we expect good translation of degradation rates? If not, are there particular measures from healthy volunteers that you think will translate well to eventual degradation efficiency in patients and thereby efficacy and functional endpoints? Similarly, on other early data sets, like HPK1 where you'll dose patients to start, are there particular endpoints we should be paying attention to that you think will translate well?

On 027, the short answer on translating degradation of polyglutamine AR versus wild-type AR is that it's the same; we effectively degrade wild-type AR and polyQ-AR similarly. That will be really helpful to see. As I mentioned, when we share the healthy volunteer data in the first half of next year, there are a couple of pieces we have not done before: getting an orally available PROTAC in muscle and demonstrating degradation there. We think that if we can see degradation of the wild-type AR in healthy volunteers, that will bode very well for our ability to degrade the disease-causing polyQ-AR in patients. So I think the translatability there will be quite good. Angela, anything to add?

Just to add, Jonathan, we did look at iPSC-derived skeletal muscle from both healthy volunteers and SBMA patients and the pharmacology was exactly intact, which supports the translatability Randy described. Regarding HPK1 program ARV-6723: that program will start dosing patients in the near future. This is our first immuno-oncology degrader, so the first trials will enroll patients, not healthy volunteers. It's an escalation design, and we'll be looking at monotherapy and combination cohorts. It's important there to show initial signs of efficacy, safety, tolerability and combinability. We have preclinical data showing differential effects compared with HPK1 inhibitors, including effects on the tumor microenvironment, which gives us confidence as we enter Phase I.

The operator introduced the next question.

I had two questions. One on BCL6: you mentioned enrollment was a bit slow at the subtherapeutic doses, but you also mentioned that you saw some effective responses at the lower doses. I would have thought that if you saw responses below therapeutic doses that would catalyze enrollment. Can you reconcile that? Second, on LRRK2, could you comment on the recent Phase IIb inhibitors that didn't work and why a degrader may be a more promising approach?

On BCL6, you did point out a bit of a contradiction, and that's fair. We started pretty far below the predicted efficacious range and escalated relatively slowly. Seeing responses has certainly helped, but especially in the U.S. and particularly for LBCL patients, there are a number of other options physicians can pursue before enrolling a patient in a clinical trial. There's natural hesitance by physicians to put patients on a dose they might not expect to be efficacious when there are other options. That said, enrollment has picked up as we've gotten closer to predicted efficacious exposures, and the responses we've seen have helped. We're excited to get some of these data out by the end of the year, especially with respect to T-cell patients where we believe we'll be the first to share data for a BCL6 degrader. Regarding LRRK2, the questions mostly follow a similar theme: an inhibitor trial didn't work, so what does that mean for degraders? We did not expect those inhibitor results to necessarily predict the degrader outcome. We think inhibiting the kinase function of LRRK2 is not sufficient. There are other aspects — GTPase function and scaffolding function — that drive activity, inflammation and lysosomal dysfunction. A degrader can remove the entire protein, addressing those additional functions. We don't think the inhibitor data deter our approach. We remain focused on PSP first, where there's substantial unmet need, and ultimately PD as well.

To add briefly, biologically we understand why inhibitors may be ineffective in some contexts. We observed much greater target engagement and phosphoRab pathway engagement in preclinical models with degradation. We'll be discussing synaptic markers and ocular motor measures at MDS that we believe will demonstrate that the degrader has distinct and meaningful effects in patients, including changes in CSF synaptic markers that are prognostic of progression in Parkinson's disease.

The operator introduced the next question.

Just a couple, one on pipeline and maybe one for Andrew. First, on the pipeline, would you expect to enroll tumor types in the HPK1 degrader program similar to what we've seen from HPK1 inhibitors, like gastric and lung? Is PD-1 the most likely initial combination partner? And then for Andrew, how should we think about modeling the cost of licensing moving forward?

On the HPK1 program, PD-1 is the most likely initial combination partner. Tumor types similar to what we've seen with HPK1 inhibitors, including lung, are reasonable to consider. The trial will enroll patients who have had prior immunotherapy and follows a traditional escalation design with monotherapy and combination cohorts. Regarding modeling, I'll let Andrew add color.

Yes, there have been many changes to the accounting and I'm happy to follow up if helpful. At a high level, we've been deferring revenue from the original Pfizer collaboration over the life of that collaboration. Due to the Rigel out-license, we deemed our contributions to that collaboration complete and therefore took all residual collaboration revenue through the P&L. Going forward, you'll see no additional revenue recognition from the original Pfizer collaboration. We do have tail liabilities for closeout costs of VEPPANU; we booked a liability of $52.7 million split between a current portion of $28.4 million and a long-term portion of $24.3 million. Additional payments we make for collaboration costs will be charged against that liability. So our P&L going forward is somewhat cleansed from the prior VEPPANU collaboration. We will book milestones and royalties from Rigel going forward, which will be recorded in the usual way. We also added a cost of license revenue line to segregate Yale payments from our normal G&A — for the time being that will represent payments to Yale triggered by VEPPANU approval and the Rigel license agreement, and you'll see a small royalty and a portion of milestones payable to Yale reflected there. Please let me know if you'd like more detail.

The operator introduced the next question.

My first question is on LRRK2: you indicated you'll present additional biomarker data in October. Can you frame the cadence over 2027 in terms of additional updates for that program and any potential advancements to the next stage? Second, on BCL6, after you present the glofi combination data in mid-2027, how are you thinking about potential comparator arms versus the monotherapy trial and how you think about that down the road?

On LRRK2, the immediate next public disclosure will be the biomarker data we plan to show at MDS in October. The cadence in 2027 will be driven by trial starts and regulatory interactions — as we begin those next trials and finalize design based on agency feedback, we'll provide clarity on timing and planned updates. For BCL6, all roads lead through monotherapy and the glofi combination now. There are many options after that — combinations with various bispecifics, chemotherapies and other modalities. We'll watch the evolving landscape to identify where the best opportunities exist. As we show more data, it will become clearer how and where to position comparator arms and development paths, especially to move earlier in lines of therapy if supported by safety and efficacy signals.

The operator introduced the next question.

A quick question on ARV-102. Do you still have an intended PSP population that you're targeting? Or will it be an all-comers trial — thinking more along the lines of Richardson syndrome patients or specific LRRK2 variants?

You're thinking about it right. Richardson syndrome is the largest PSP subtype and it's a uniform progressing population, which is why it's attractive for a registrational approach. We would not likely further restrict beyond that at this stage.

Right. We would not restrict further; Richardson syndrome is a very uniform progressing population, which is why we like it, but this does not restrict us from expanding to all PSP.

There were no further questions in the queue. The operator turned the call back to management for closing remarks.

Thanks, operator, and thanks, everybody, for joining this morning. We look forward to providing further updates as we move forward, and thanks again.

This concludes today's conference call. Thank you for your participation. You may now disconnect.