Q2 2026 Arvinas Inc Earnings Call

August 4, 2026

Operator: Hello, welcome to Arvinas' Q2 2026 Earnings Conference 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 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.

Speaker #1: Hello. And welcome to ARVINA's second quarter, 2026 earnings conference call. At this time, all participants are on a listen-only mode. After the speaker's presentation, there will be a question-and-answer session.

Speaker #1: To ask a question during the session, you will need to press *11 on your telephone. You will then hear an automated message advising you that your hand is raised.

Speaker #1: To withdraw your question, please press Star 11 again. I would now like to hand the conference over to Jeff Boyle. Sir, you may begin.

Speaker #2: 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.

Jeff Boyle: Good morning, everyone, thank you for joining us. Earlier today, we issued a press release with our Q2 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.

Speaker #2: Joining us on the call today, we have Randy Teal, our President and Chief Executive Officer; Angela Cacace, our Chief Scientific Officer; and Andrew Saik, our Chief Financial Officer.

Speaker #2: 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.

Jeff Boyle: 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. I'll turn the call over to Randy Teel. Randy?

Speaker #2: 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.

Jeff Boyle: 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. I'll turn the call over to Randy Teel. Randy?

Speaker #2: Now I'll turn the call over to Randy Teal. Randy?

Speaker #3: 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.

Randy Teel: 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 G12V program, ARV-806, will only move forward in the hands of a partner.

Speaker #3: 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.

Speaker #3: We've reached three significant strategic milestones since the start of the year, beginning with the first-ever FDA approval of a PROTAC degrader, Depanil. Second, we completed an out-licensing of Depanil to Rigel Pharmaceuticals, who anticipate making Depanil available to patients in the very near future.

Speaker #3: And third, we made the strategic decision that our KRAS G12C 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.

Randy Teel: Third, we made the strategic decision that our KRAS G12V 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 H1 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, 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 differentiating profiles and compelling value propositions. I'll start with ARV-393, our BCL6 degrader.

Randy Teel: 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 H1 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, 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 differentiating profiles and compelling value propositions. I'll start with ARV-393, our BCL6 degrader.

Speaker #3: 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.

Speaker #3: We've fully shifted our focus to our phase one clinical programs, and we are confident about the opportunity ahead to create important therapies for patients.

Speaker #3: 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 propositions.

Speaker #3: 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.

Randy Teel: 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.

Speaker #3: 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.

Speaker #3: 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.

Speaker #3: 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.

Randy Teel: 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.

Speaker #3: 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.

Speaker #3: 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.

Speaker #3: When it comes to upcoming data for ARV-393, we are on track to share initial Phase 1 data by the end of the year.

Speaker #3: 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.

Randy Teel: 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.

Speaker #3: 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.

Speaker #3: 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 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 GLOFI.

Speaker #3: 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.

Randy Teel: 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 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.

Speaker #3: 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.

Randy Teel: 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 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.

Speaker #3: 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 ARV 027 has the potential to become the first therapy to target the primary driver of disease.

Speaker #3: SBMA is an excellent disease caused by the toxic buildup of the POLYQAR 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.

Randy Teel: 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.

Speaker #3: 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.

Randy Teel: 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 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.

Speaker #3: Guided by published preclinical evidence, we had established a target of achieving greater than 50% POLYQAR degradation in skeletal muscle, a level we believed would provide functional benefit.

Speaker #3: 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 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.

Randy Teel: 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 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.

Speaker #3: Today, I'm pleased to announce that in our ongoing phase one trial in healthy volunteers, we completed the single ascending dose cohorts and have now initiated the multiple dose portion of the trial.

Speaker #3: 027 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.

Randy Teel: 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 H1 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.

Speaker #3: 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.

Randy Teel: Taken together, these healthy volunteer data would provide proof of mechanism for ARV-027 and meaningfully de-risk the program. In H1 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.

Speaker #3: 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.

Speaker #3: 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.

Speaker #3: We believe this design will accelerate our development plan with the potential to move to a registrational study following the conclusion of the phase one trial.

Speaker #3: Finally, I'll move to ARV-102, our third program with upcoming clinical data, and discuss plans for upcoming disclosures. I'll also provide a brief update on our regulatory interactions as we plan the next trials for our LARC2 degrader.

Randy Teel: 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 PSP or 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 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.

Speaker #3: 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-shifting treatment for these patients.

Randy Teel: 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-shifting 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.

Speaker #3: 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.

Speaker #3: 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 oculomotor measures and CSF proteomics, at the MDS conference in October.

Speaker #3: 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.

Randy Teel: 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 US 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 H1 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.

Speaker #3: 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.

Speaker #3: 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.

Speaker #3: 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.

Speaker #3: 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.

Randy Teel: Stepping back, our accomplishments and decisive actions during H1 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?

Speaker #3: 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.

Speaker #3: 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.

Speaker #1: 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.

Angela Cacace: 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.

Speaker #1: 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.

Speaker #1: 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.

Speaker #1: I'll begin with ARV 6723, our oral HPK-1 degrader and our first immuno-oncology PROTAC. HPK-1 acts as a natural break on the immune system. It limits T-cell activation and suppresses anti-tumor immunity.

Angela Cacace: 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.

Speaker #1: What's particularly challenging is that HPK-1 biology extends beyond its kinase activity. HPK-1 also functions as a signaling scaffold. As a result, inhibitors of the kinase activity leave part of the biology intact.

Angela Cacace: 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.

Speaker #1: 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 anti-tumor activity.

Speaker #1: 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.

Angela Cacace: 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 have 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 I study in the coming weeks.

Speaker #1: We also demonstrated preclinically that the biology extends well beyond T-cell activation. HPK-1 degradation may remodel the tumor microenvironment through enhanced interferon signaling, and activation of the myeloid compartment.

Angela Cacace: 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 have 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 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-KRAS inhibitors. Our lead oral degrader showed potent activity across a broad spectrum of KRAS mutations.

Speaker #1: 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.

Speaker #1: We're excited to begin translating these findings into the clinic. We remain on track to initiate enrollment in our phase one study in the coming weeks.

Speaker #1: 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.

Angela Cacace: 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-KRAS 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 anti-tumor activity in combination with immune checkpoint blockade, highlighting the potential to favorably remodel the tumor microenvironment in a way that inhibitors do not.

Speaker #1: 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.

Angela Cacace: 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 anti-tumor 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. Andrew?

Speaker #1: Including difficult-to-treat mutations such as G12R and Q61. It also demonstrated activity against KRAS amplifications. A major mechanism of resistance. We also demonstrated superior anti-tumor activity in combination with immune checkpoint blockade.

Speaker #1: 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.

Angela Cacace: 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?

Speaker #1: 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.

Speaker #1: With that, I'll turn the call over to Andrew to review our quarterly financial results. Andrew?

Speaker #2: Thanks, Angela. And good morning, everyone. I'm pleased to provide financial highlights for the second quarter of 2026. As a reminder, detailed financial results for the second quarter are included in the press release we issued this morning.

Andrew Saik: Thanks, Angela, and good morning, everyone. I'm pleased to provide financial highlights for Q2 2026. As a reminder, detailed financial results for Q2 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 H2 2028. At the end of Q2, we had $567.9 million in 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.

Speaker #2: Reiterating the team's sentiment, we have much to look forward to later this year and are pleased with our strong financial position, which will allow us to continue advancing our pipeline into the second half of 2028.

Speaker #2: 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.

Speaker #2: 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 of EPANU and regulatory approval for the Rigel license agreement.

Andrew Saik: Q2 was a very busy period for us as during the quarter, we received FDA approval of the first ever PROTAC degrader vepdegestrant 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've recorded a liability of $52.7 million to cover our remaining obligations to complete ongoing development activities.

Speaker #2: 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.

Speaker #2: 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.

Speaker #2: We therefore moved all deferred revenue to the P&L, which resulted in a net revenue of $126.4 million. And we've recorded a liability of $52.7 million to cover our remaining obligations to complete ongoing development activities.

Speaker #2: Additionally, we recorded a $50 million milestone from Pfizer, triggered by the EPANU approval. Separately, we recorded $3.5 million in revenue under a Pfizer research collaboration agreement, where the research term has been completed.

Andrew Saik: 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 Q2. 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 Q2, compared to $25.3 million for the same period of 2025.

Speaker #2: 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.

Speaker #2: 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 EPANU and the entry into the Rigel license agreement.

Speaker #2: 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.

Andrew Saik: 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 Q2 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 Q2. Non-GAAP R&D was down $8.1 million compared to the same period last year, representing a reduction of 14%.

Speaker #2: 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.

Speaker #2: 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.

Speaker #2: 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%.

Speaker #2: 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.

Andrew Saik: 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. 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 run-out costs. 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 H2 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. Randy?

Speaker #2: 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 EPANU runout costs, so our future obligations under the collaboration agreement will be booked against the accrual and will not impact our P&L.

Speaker #2: 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.

Speaker #2: With that, I'll turn the call over to Randy for closing remarks. Randy?

Speaker #3: 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.

Randy Teel: Thanks, Andrew. We've entered H2 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.

Speaker #3: 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.

Speaker #1: Thanks, Randy. Operator, can you please open the queue?

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

Speaker #4: Thank you. Ladies and gentlemen, as a reminder to ask the question, please press start 11 on your cell phone. Then wait for your name to be announced.

Operator: Thank you. Ladies and gentlemen, as a reminder to ask a question, please press star one one on your telephone, then wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by while we compile the Q&A roster. Our first question comes from the line of Nick LaRusso with TD Cowen. Your line is open.

Speaker #4: To withdraw your question, please press *star one one* again. Please stand by while we compile the Q&A roster. Our first question comes from the line of Nick LaRusso with TD Cowen.

Speaker #4: Your line is open.

Nick LaRusso: Great. Thanks very much for taking our question. 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 glofitamab combo? Could this catalyze a potentially pivotal trial in an earlier line setting it with bispecifics? Any insight there would be great. Thanks.

Nick Lorusso: Great. Thanks very much for taking our question. 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 glofitamab combo? Could this catalyze a potentially pivotal trial in an earlier line setting it with bispecifics? Any insight there would be great. Thanks.

Speaker #5: Great. Thanks very much for taking our question. So on 393, can you discuss a little bit more about what you're thinking about the development path, especially considering the data coming mid-next year with the GLOFIC combo?

Speaker #5: Could this catalyze a potentially pivotal trial in an earlier-line setting with Pfizer specifics? Any insight there would be great. Thanks.

Speaker #2: Yeah, thanks for the question, Nick. The short answer is yes. The long answer is, the NHL space has a lot of opportunities to pursue, right?

Randy Teel: Yeah. Thanks for the question, Nick. The short answer is yes. The long answer is the NHL space has a lot of opportunities to pursue, right? As we've talked about over the years, we think that while there's a lot of therapies across the lines of therapy, across the different diseases now, there's plenty of chemo, there's plenty of CAR T, there's plenty of bispecifics. What there's not a lot of is orally bioavailable, tolerable small molecules. 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, a bit early to talk about exactly where we plan to go, but definitely can talk about the options, right? I think as early options, looking at later line monotherapy makes sense. Think about fourth line LBCL, maybe third line LBCL.

Speaker #2: And so, as we've talked about over the years, we think that while there's a lot of therapies across the lines of therapy, across the different diseases now—there's plenty of chemo, there's plenty of CAR-T, there's plenty of bispecifics—

Speaker #2: What there's not a lot of is orally bioavailable, tolerable, small molecules. And so we think that a BCL-6 degrader could slot into multiple areas within the disease landscape.

Speaker #2: So at this point, as we're in the phase one dose escalation, it's a bit early to talk about exactly where we'd plan to go, but we can definitely talk about the options, right?

Speaker #2: So I think as early options, looking at later line monotherapy makes sense. Think about fourth line LDCL, maybe third line LDCL. Think about later line AITL, a T-cell disease, that we've been enrolling patients with already in our phase one trial.

Randy Teel: Think about later line AITL, T-cell disease, that we've even 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. There's a lot of different places that we could go, and I think that the common thread is if we 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 glofitamab. 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.

Speaker #2: As we move forward with combinations, that could open up further access to the third line LDCL space, second line LDCL, and perhaps moving ahead in T-cell disease as well.

Speaker #2: So there are a lot of different places that we could go, and I think that the common thread is to get to any of them.

Speaker #2: We've got to get through the monotherapy dose escalation, show some efficacy, and see some signals there. We've also got to show we're combinable with other therapies.

Speaker #2: Most immediately, a bispecific like GLOFI. And 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.

Speaker #5: Great. Thanks very much.

Nick LaRusso: Great. Thanks very much.

Nick Lorusso: Great. Thanks very much.

Speaker #4: Please stand by for our next question. Our next question comes from the line of Derek Archella with Wells Fargo. Your line is open.

Operator: Please stand by for our next question. Our next question comes from the line of Derek Archila with Wells Fargo. Your line is open.

Speaker #6: Good morning. This is Jacob Monfort, Derek. Thanks for taking our question. I was just wondering if you could comment on the path forward for ARV102 and PSP and what does the timeline and registrational path look like for it in light of some of your more recent regulatory interactions?

[Analyst] (Wells Fargo): Morning, this is Jacob on for Derek. Thanks for taking our question. I was just wondering if you could comment on the path forward for ARV-102 and PSP, and what does the timeline and registrational path look like for it in light of some of your more recent regulatory interactions?

Jacob Goell: Morning, this is Jacob on for Derek. Thanks for taking our question. I was just wondering if you could comment on the path forward for ARV-102 and PSP, and what does the timeline and registrational path look like for it in light of some of your more recent regulatory interactions?

Speaker #2: Yeah, thanks for the question, Jake. So just to rehash a little bit where we are, right? So we began the year with a couple of phase one trials, one in healthy volunteers, one in patients with PD.

Randy Teel: Thanks for the question, Jake. Just to rehash a little bit where we are, right? We began the year with a couple of phase I trials, one in healthy volunteers, one in patients with PD. What we planned to do over the course of the year was to start two other trials, a phase I-B in the US and a registrational-oriented study globally. What we had 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 US. 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'll take into 2027 to start those studies.

Speaker #2: And what we plan to do over the course of the year was to start two other trials, a phase one B in the US and a registrational-oriented study globally.

Speaker #2: So what we had announced a couple of months ago is that after submitting the IND to the FDA, they asked us to wait before starting that study.

Speaker #2: So that's technically a clinical hold before starting the studies in the U.S. And then 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'll take into 2027 to start those studies.

Speaker #2: So overall, the registrational path in PSP—we would think about the two-part study there: the phase 1b and a registrational study. That continues to be where we aim.

Randy Teel: Overall, the registrational path in PSP, we would think about the two-part study there, the phase I-B 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. 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. Definitely worth saying, though, that 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.

Speaker #2: 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.

Speaker #2: 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.

Speaker #2: Definitely worth saying, though, that 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 already now, we'll be taking that to finalize the path that we will then set out on as we've said in 2027.

Speaker #1: Great. Thank you.

[Analyst] (Wells Fargo): Great. Thank you.

Jacob Goell: Great. Thank you.

Speaker #4: Thank you. Our next question comes from the line of Lai Wattsek with Cantor Fitzgerald. Your line is open.

Operator: Thank you. Our next question comes from the line of Li Watsek with Cantor Fitzgerald. Your line is open.

Li Watsek: Hey, good morning. Thanks for taking our question. Maybe a follow-up on ARV-393. What would 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 glofitamab, 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 early trends on combinability?

Speaker #7: Good morning. Thanks for taking our question. Maybe a follow-up on ARV-393. What would be a good outcome from the Phase 1 monotherapy cohorts that you're going to present later this year?

Speaker #7: It sounds like these are going to be at subtherapeutic levels. And as we think about a combination with GLOFI, would you be able to share where you are with the dose levels right now?

Speaker #7: Did you start at the subtherapeutic levels as well? And early trends on combinability?

Speaker #2: Yeah, thankfully. The short answer on that second one is yes. And just as a rehash, we've talked about this in other venues. We were the first company to start working on BCL-6, at least to bring it into the clinic to our knowledge.

Randy Teel: Yeah, thanks Li. The short answer on that second one is yes. Just as a rehash, we've talked about this in other venues. 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 the monotherapy. As we talked about with some operational questions, that enrollment has been certainly slower than we would've liked. On the flip side, as we've gotten close now to the predicted efficacious exposures, we've seen a clear uptick in enrollment. In the combination study, which started a couple months ago, that enrollment there has been quite strong ever since the start.

Speaker #2: And based on that and some other factors, we got a some feedback to start with a very low starting dose for BCL-6 as a monotherapy.

Speaker #2: And as we talked about, with some operational questions, enrollment has been certainly 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.

Speaker #2: And in the combination study, which started a couple of months ago, that 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 be still very much in the below the efficacious range for most of the patients.

Randy Teel: When it comes to the data that we will have at the end of the year, you are right to highlight we will be still very much below the efficacious range for most of the patients. In the doses that we're at now, we're starting to get to the exposure that we would expect the efficacy, 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've anticipated based on the overall population. We think it'll make sense to focus on that population and exposure that's coming up. Also, as we talked about heading into next year, focusing on LBCL patients as both monotherapy and combo. The data at the end of this year will certainly be focused on mono. We do not anticipate sharing combo data.

Speaker #2: In the doses that we're at now, we're starting to get to the exposure that we would expect the efficacious. So we'll start to see some of that.

Speaker #2: 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.

Speaker #2: So we think it'll make sense to focus on that population and exposure that's coming up. And then also, as we talked about, heading into next year, focusing on LDCL patients as both monotherapy and combo.

Randy Teel: Also, as we talked about heading into next year, focusing on LBCL patients as both monotherapy and combo. The data at the end of this year will certainly be focused on mono. We do not anticipate sharing combo data. We didn't start quite as low for the combo as we did for the mono, it certainly did start at levels that in monotherapy were not predicted to be efficacious in patients with T-cell lymphomas.

Speaker #2: The data at the end of this year will certainly be focused on mono. We do not anticipate sharing combo data. We didn't start quite as low for the combo as we did for the mono, but it certainly is starting—it certainly did start—at levels that, in monotherapy, were not predicted to be efficacious in patients with B-cell lymphomas.

Randy Teel: We didn't start quite as low for the combo as we did for the mono, it certainly did start at levels that in monotherapy were not predicted to be efficacious in patients with T-cell lymphomas.

Speaker #4: Thank you. Our next question comes from the line of Edward Tenhoff with Piper Sandler. Your line is open.

Operator: Thank you. Our next question comes from the line of Edward Tenthoff with Piper Sandler. Your line is open.

Edward Tenthoff: Great. Thank you very much, looking forward to more data this year, congrats on all the progress. I'll ask about SBMA and ARV-027. Really interesting mechanism here. Just to confirm, the IND cleared there, what are we waiting for to Oh, I'm sorry. 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? Thanks.

Speaker #5: Great, thank you very much. I'm looking forward to more data this year and congratulations on all the progress. So I'll ask about SDMA and 227.

Speaker #5: Really interesting mechanism here. Just to confirm, the IND cleared there, and what are we waiting for to—well, I'm sorry—where are you in multiple ascending dosing?

Speaker #5: And can you kind of characterize—you mentioned exposure and degradation. What are the clinical endpoints that we would ultimately be modeling or expecting in SDMA things?

Speaker #2: Thanks, Ted. Maybe I'll pass to Angela in a moment on some of the path forward questions. To reiterate where we are, on that question, right, so we have been dosing healthy volunteers with O27.

Randy Teel: Thanks, Ed. Maybe I'll pass to Angela in a moment on some of the path forward questions. To reiterate where we are on that question, right. 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 at the beginning, or in the H1 rather, of next year. We do anticipate including some patients with SBMA in the latter stages of that phase I study. Just to reiterate for everyone, this program, well, SBMA is certainly a rare disease. We're talking 10,000, 13,000 patients in major markets or so. 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.

Speaker #2: 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, and we're expecting to share some data at the beginning, or in the first half, rather, of next year.

Speaker #2: We do anticipate including some patients with SBMA in the latter stages of that Phase 1 study. And just to reiterate for everyone, this program—well, SBMA is certainly a rare disease.

Speaker #2: We're talking 10, 13,000 patients in major markets or so. The great thing about this target is that we are hitting the actual driver of disease.

Speaker #2: So polyglutamine AR is what drives disease. That's what we're degrading. We're not degrading an upstream transcription factor or some other factor. We're degrading the actual cause of the disease.

Randy Teel: We're not degrading an upstream transcription factor or some other 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'd like you to speak a bit more about plans there and endpoints and so on.

Speaker #2: When it comes to the next phases, we've talked about being able to move into registrational-intended studies even after Phase I, but Angela, I invite you to speak a bit more about plans there, and endpoints, and so on.

Speaker #7: Sure. As we move forward, the goal is to really demonstrate that we can target 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.

Angela Cacace: Sure. As we move forward, the goal is to really demonstrate that we can target 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. 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.

Speaker #7: 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.

Speaker #7: And there we'll be looking at meaningful scales like the SBMA functional rating scale and those endpoints as well.

Speaker #5: Great. That's helpful, Angela. Thank you.

Edward Tenthoff: Great. That's helpful, Angela. Thank you.

Speaker #4: Thank you. Our next question comes from the line of Jonathan Miller with Evercore ISI. Your line is open.

Operator: Thank you. Our next question comes from the line of Jonathan Miller with Evercore ISI. Your line is open.

Speaker #6: Thanks for taking the question and congrats on the progress this quarter, guys. I'd like to follow up first on the PolyQAR. There'll be a couple of patients you said next year.

Jonathan Miller: Thanks for taking the question and congrats on the progress this quarter, guys. I'd like to follow up first on the polyQ AR. There'll be a couple of patients you said next year. Am I right to assume that we shouldn't expect to see good translation of degradation rates from healthy volunteers to patients that have different levels of protein at baseline? If that's the case, 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 the other data sets where we'll get early data from, I'm thinking of HPK1, where you're going to dose in healthy volunteers to start. Are there particular endpoints that we should be paying attention to when we eventually see that data that you think will translate well?

Speaker #6: Am I right to assume that we shouldn't expect to see good translation of degradation rates from healthy volunteers to patients that have different levels of protein at baseline?

Speaker #6: And if that's the case, 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?

Speaker #6: And then similarly, on the other data sets where we'll get early data from I'm thinking of HPK1 where you're going to dose in healthy volunteers to start.

Speaker #6: Are there particular endpoints that we should be paying attention to when we eventually see that data that you think will translate well?

Speaker #2: All right. Thanks for the questions. That's good. So on O27, the short answer on translating the degradation of O27 in polyglutamine AR, which the patients with SBMA have, versus wild type AR, which healthy volunteers will have, is that it's the same.

Randy Teel: All right. Thanks for the questions. That's good. On ARV-027, the short answer on translating the degradation of ARV-027 in polyglutamine AR, which the patients with SBMA have, versus wild type AR, which healthy volunteers will have, is that it's the same. We effectively degrade wild type AR and polyQ AR the same. That will be really helpful to see, as I mentioned, as we share the healthy volunteer data in H1 of next year. Just to reiterate, there's a couple pieces there that we have not done before, and we are looking forward to see if we can do. One is getting an orally available PROTAC into muscle. That alone, we haven't been looking for before. Second of all, getting degradation there.

Speaker #2: We effectively degrade wild type AR and PolyQAR the same. So that'll be really helpful to see as I mentioned that as we share the healthy volunteer data in the first half of next year, just to reiterate, there's a couple of pieces there that we have not done before and we're looking forward to see if we can do.

Speaker #2: One is getting an orally available PROTAC into muscle. So that alone, we haven't been looking for before. And second of all, getting degradation there.

Speaker #2: And 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 PolyQAR in patients.

Randy Teel: 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. I think the translatability there will be quite good. I can move on to the HPK1 question, but Angela, anything to add on the polyQ question?

Speaker #2: So I think the translatability there will be quite good. I can move on to the HPK1 question. But Angela, anything to add on the PolyQ question?

Angela Cacace: Just to add, John, that we did look at iPSC-derived skeletal muscle from both healthy volunteers and SBMA patients, and the pharmacology was exactly intact, which is exactly what Randy was saying we would translate. That's our goal and that's our reason to believe.

Speaker #7: Just to add, John, that we did look at IPSC-derived skeletal muscle from both healthy volunteers and SBMA patients. And the pharmacology was exactly intact.

Speaker #7: Which is exactly what Randy was saying we would translate. And so that's our goal. And that's our reason to believe.

Speaker #2: And on the HPK1 program, 6723, so again, as we said this morning, that's going to start dosing patients here in the quite near future.

Randy Teel: On the HPK1 program ARV-6723, again, as we said this morning, that's going to start dosing patients here in the quite near future. The thinking there, look, this is our first IO therapy. The first couple of trials will look very similar to other oncology trials, right? These will be in patients, not healthy volunteers, just to clarify that. It's an escalation design. We will be looking at monotherapy. The phase I also includes combination setting as well. We think it's really important there to show some initial science efficacy and, of course, safety, tolerability, and combinability as well. The HPK1 program is interesting, right? As a first IO therapy, it's got quite a large opportunity. We've certainly got to show, as we are very aware, something that the HPK1 inhibitors have not shown, which is good response rates and so on in patients.

Speaker #2: The thinking there—look, this is our first IO therapy. So, the first couple of trials will look very similar to other oncology trials, right?

Speaker #2: These will be in these will be in patients, not healthy volunteers, just to clarify that. It's an escalation design. We'll be looking at monotherapy.

Speaker #2: The phase one also includes combination setting as well. And we think it's really important there to show some initial scientific efficacy and, of course, safety tolerability and combinability as well.

Speaker #2: The HPK1 program's interesting, right? So as a first IO therapy, it's got quite a large opportunity. We've certainly got to show, as we're very aware, something that the HPK1 inhibitors have not shown, which is good response rates and so on in patients.

Speaker #2: But we are really confident that we'll be able to do that based on the preclinical data that we have, which really goes a long way to show, including some recent preclinical data this year, that we can have differential effects in getting responses, get inhibition, and affect the tumor microenvironment in ways that HPK1 inhibitors have been unable to do, TD1 therapies have been unable to do.

Randy Teel: We are really confident that we'll be able to do that based on the pre-clinical data we have, which really goes a long way to show, including some recent pre-clinical data this year, that we can have differential effects in getting responses, get inhibition, and affect the tumor microenvironment in ways that HPK1 inhibitors have been unable to do, PD1 therapies have been unable to do. For that reason, we have some good confidence moving into phase I, but look forward to sharing those data.

Speaker #2: And so for that reason, we have some good confidence moving into the phase one, but look forward to sharing those data.

Speaker #6: Great. Thanks so much.

Jonathan Miller: Great. Thanks so much.

Speaker #4: Thank you. Our next question comes from the line of Yigal Nochimovitz with Citigroup. Your line is open.

Operator: Thank you. Our next question comes from the line of Yigal Nochomovitz with Citigroup. Your line is open.

Speaker #8: Hi, great. Thank you very much for taking the questions. I had two: one on BCL6. I think you mentioned, Randy, that the enrollment was a bit slow at the subtherapeutic doses, but you also mentioned that you saw some effective responses at the lower doses.

Yigal Nochomovitz: Hi. Great. Thank you very much for taking the question. I had two, one on BCL6. I think you mentioned, Randy, that the enrollment was a bit slow at the subtherapeutic doses, you also mentioned that you saw some effective responses at the lower doses. I was just trying to square those two things. I guess I would have thought that if you saw responses below therapeutic doses, that would catalyze the enrollment curve. Secondly, on LRRK, could you just comment on the, obviously since the last earnings, Biogen and Denali had the phase II-B for their inhibitor, which as you know, didn't work. I'd just love to get your thoughts on that and why a degrader may be a more promising approach. Thank you.

Speaker #8: So I was just trying to square those two things. I guess I would have thought that if you saw responses below therapeutic doses, that would catalyze the enrollment curve.

Speaker #8: And then secondly, on LLRK, could you just comment on the obviously, since the last earnings, Biogen and Denali had the phase two B for their inhibitor, which, as you know, didn't work, but I'd just love to get your thoughts on that and why the degrader may be more promising approach.

Speaker #8: Thank you.

Speaker #2: Thanks for the question, Yigal. Yeah. So on BCL6, what you said is correct, and you did point out a bit of a contradiction, which we're certainly aware of.

Randy Teel: Thanks for the question, Yigal. On BCL6, what you said is correct, and you did point out a bit of a contradiction, which we're certainly aware of. We started pretty far below the predicted efficacious range. The other feedback that we got was around the design and the escalation of it. Not only did we start low, we've also escalated pretty slowly. Seeing the responses that we have has certainly helped. I think, especially in where we're doing the trial in the US, especially in LBCL patients, there are quite a number of other options that patients can take before they get onto a clinical trial. I think there's quite some natural hesitance by physicians to put patients on a dose that they might not expect to be efficacious when there are other options out there.

Speaker #2: So yeah, we started pretty far below the predicted efficacy range. And the other feedback that we got was around the design and the escalation of it.

Speaker #2: So not only do we start low, we sorry, not only do we start low, we've also escalated pretty slowly. Seeing the responses that we have has certainly helped, but I think especially in where we're doing the trial in the US, especially in LBCL patients, there are quite a number of other options that patients can take before they get onto a clinical trial.

Speaker #2: And I think there's quite some natural hesitance by physicians to put patients on a dose that they might not expect to be efficacious when there are other options out there.

Speaker #2: So do recognize that it has certainly picked up as we've gotten closer. The responses have helped. And it's another reason that we're excited to get some of these data out by the end of the year.

Randy Teel: Do recognize that it has certainly picked up as we've gotten closer. The responses have helped. It's another reason that we're excited to get some of these data out by the end of the year, and especially with respect to T-cell patients, where we think we'll be the first to share data for BCL6 degrader, looking at that patient population. When it comes to the LRRK2 program and LUMA, I think that, and Angela, invite you to chime in here as well. We've gotten asked about that over the past couple of months, the questions have largely followed the same path, which is, look, LUMA trials didn't work. We didn't expect it to work. Is there anything to learn?

Randy Teel: The responses have helped. It's another reason that we're excited to get some of these data out by the end of the year, and especially with respect to T-cell patients, where we think we'll be the first to share data for BCL6 degrader, looking at that patient population. When it comes to the LRRK2 program and LUMA, I think that, and Angela, invite you to chime in here as well. We've gotten asked about that over the past couple of months, the questions have largely followed the same path, which is, look, LUMA trials didn't work. We didn't expect it to work. Is there anything to learn? I think that for us, what we've been really focused on since the beginning of this program really, was the fact that we don't think that inhibiting the kinase function of LRRK2 is enough.

Speaker #2: And especially with respect to T-cell patients where we think we'll be the first to share data for BCL6 degrader, looking at that patient population.

Speaker #2: When it comes to the LARC2 program and LUMA, I think that, and Angela, I invite you to chime in here as well, as we've gotten asked about that over the past couple of months, the questions have largely followed the same path, which is, look, the LUMA trial didn't work.

Speaker #2: We didn't expect it to work. Is there anything to learn? And I think that for us, what we've been really focused on since the beginning of this program, really, was the fact that we don't think that inhibiting the kinase function of LARC2 is enough.

Randy Teel: I think that for us, what we've been really focused on since the beginning of this program really, was the fact that we don't think that inhibiting the kinase function of LRRK2 is enough. We think there are other aspects of LRRK2, there's GTPase function, there's scaffolding function, that we know drive activity, inflammation, and the lysosomal capabilities by itself, and we think that those are critical. We weren't terribly surprised to see that a program that by their reporting gets something like 30% kinase inhibition, we weren't surprised to see it fail. It doesn't deter us in what we're doing. A LRRK2 degrader, we think can hit all three different factors and features of LRRK2. We think that matters.

Speaker #2: We think there are other aspects of LARC2. There's GTPase function. There's scaffolding function. That we know drive activity information endolysosomal capabilities by itself. And we think that those are critical.

Randy Teel: We think there are other aspects of LRRK2, there's GTPase function, there's scaffolding function, that we know drive activity, inflammation, and the lysosomal capabilities by itself, and we think that those are critical. We weren't terribly surprised to see that a program that by their reporting gets something like 30% kinase inhibition, we weren't surprised to see it fail. It doesn't deter us in what we're doing. A LRRK2 degrader, we think can hit all three different factors and features of LRRK2. We think that matters. We think that degrading it will even clearly affect the kinase function even more, it doesn't deter from where we're going, which as we've talked about is first in PSP, where there's really substantial unmet need in a very rapidly progressing neurodegenerative disorder versus PD anyway, and then ultimately PD as well.

Speaker #2: So we didn't—we weren't terribly surprised to see that a program that, by their reporting, gets something like 30% kinase inhibition—we weren't surprised to see it fail.

Speaker #2: It doesn't deter us in what we're doing. A LARC2 degrader, we think, can hit all three different factors and features of LARC2. We think that matters.

Speaker #2: We think that degrading it will even clearly affect the kinase function even more. And it doesn't deter from where we're going, which, as we've talked about, is first in PSP, where there's really substantial unmet need and a very rapidly progressing neurodegenerative disorder versus PD anyway.

Randy Teel: We think that degrading it will even clearly affect the kinase function even more, it doesn't deter from where we're going, which as we've talked about is first in PSP, where there's really substantial unmet need in a very rapidly progressing neurodegenerative disorder versus PD anyway, and then ultimately PD as well.

Speaker #2: And then ultimately PD as well.

Yigal Nochomovitz: Okay. Very helpful. Thanks.

Speaker #7: Yeah. And just to add, just briefly to add, Yigal, biologically, we understand why the inhibitors aren't ineffective, right? We saw greater than 50-fold enhanced target engagement and phosphorab pathway engagement in the brain.

Angela Cacace: I'll just add.

Randy Teel: Yeah. Please, Angela.

Angela Cacace: Just briefly to add, Yigal. Biologically, we understand why the inhibitors are ineffective, right? We saw greater than 50-fold enhanced target engagement and phospho-Rab pathway engagement in the brain. Then we'll be talking about some exciting synaptic markers at MDS that'll, in our minds, really prove that the degrader is different in Parkinson's disease patients with looking at eye tracking as well as CSF synaptic markers that are unprecedented changes in markers that are prognostic of progression in Parkinson's disease.

Speaker #7: And then we'll be talking about some exciting synaptic markers at MDS that'll in our minds, really prove that the degrader is different in Parkinson's disease patients with looking at eye tracking as well as CSF synaptic markers that are unprecedented.

Speaker #7: Changes in markers that are prognostic of progression. In Parkinson's disease.

Yigal Nochomovitz: Got it. Thank you very much.

Speaker #6: Got it. Thank you very much.

Speaker #4: Thank you. Our next question comes from the line of Edsa DeRaut with Barclays. Your line is open.

Operator: Thank you. Our next question comes from the line of Etzer Darout with Barclays. Your line is open.

Etzer Darout: Great. Thanks. Just a couple, one on pipeline and maybe one for Andrew. First on the pipeline, you would expect to enroll tumor types in the HPK1, the greater program, similar to what we've seen from in the HPK1 inhibitors like gastric lung. Anything there would be helpful. Is PD1 the most likely initial combination partner initially? For Andrew, maybe if you could help us out on how we should think about maybe the modeling of the cost of licensing moving forward, and anything there would be helpful as well. Thank you.

Speaker #5: Great. Thanks for just a couple, one on pipeline and maybe one for Andrew. First on the pipeline, if you would expect to enroll HPK1 degrader program similar to what we've seen from in the HPK1 inhibitors like gastric, lung, anything there would be helpful.

Speaker #5: And is PD-1 the most likely initial combination partner initially? And then for Andrew, maybe if you could help us out on how we should think about maybe the modeling of the cost of licensing moving forward and anything there would be helpful as well.

Speaker #5: Thank you.

Speaker #2: All right. Thanks, Edsa. Yeah. So on the maybe I'll answer the easiest ones first. PD-1, yes. That is the likely combination partner first. Haven't said specifically which one, but we will certainly get into that as the months go by.

Randy Teel: All right. Thanks, Etsa. Maybe I'll answer the easiest ones first. PD1, yes. That is the likely combination partner first. Haven't said specifically which one, but we will certainly get into that as the months go by. Tumor types, not far off either. Things like lung is the right place to be thinking about. That trial will enroll patients that have had prior immunotherapy. Think of it as a traditional sort of escalation trial that we'll get into data. Haven't talked about when, but as that gets going, gets easier to talk about data coming out. Andrew, questions on modeling.

Speaker #2: Tumor types, not far off either—things like lung—is the right place to be thinking about. That trial will enroll patients that have had prior immunotherapy.

Speaker #2: And think of it as a traditional sort of escalation trial that we'll get into data. Haven't talked about when, but as that gets going, gets easier to talk about data coming.

Speaker #2: Andrew, questions on modeling?

Speaker #6: Yeah, sure. So, yeah, a lot of changes to the accounting. At a high level—and I'm happy to take a follow-up if this doesn't clear up your question.

Andrew Saik: Yeah, sure. A lot of changes to the accounting. At a high level, and I am happy to take a follow-up if this doesn't clear up your question. At a high level, we have been deferring revenue from the original Pfizer collaboration agreement over the life of the collaboration. Due to the Rigel license agreement, we deemed that our contributions to that collaboration are complete, and therefore we took all of the residual collaboration revenue through the P&L. Going forward, you will see no additional revenue recognition. We do have tail liabilities on the closeout costs of the VEPPANU development plan. We booked a liability on the balance sheet for that. When the Q comes out, you are going to see a current portion of that of $28.4 million, a long-term portion of $24.3 million for a total of $52.7 million.

Speaker #6: At a high level, we've been deferring revenue from the original Pfizer collaboration agreement over the life of the collaboration. Due to the rise, we'll out-license.

Speaker #6: We deemed that our contributions to that collaboration are complete, and therefore, we took all of the residual collaboration revenue through the P&L. So, going forward, you'll see no additional revenue recognition.

Speaker #6: We do have tail liabilities on the closeout costs of the VEPNU development plan. We booked a liability on the balance sheet for that. When the queue comes out, you're going to see a current portion of that of 28.4 million a long-term portion of 24.3 for a total of 52.7.

Speaker #6: So additional payments that we make for that collaboration cost will go against that liability. So essentially, our P&L going forward is somewhat cleansed from the previous VEPNU collaboration agreement.

Andrew Saik: Additional payments that we make for that collaboration cost will go against that liability. Essentially our P&L going forward is somewhat cleansed from the previous VEPPANU collaboration agreement. We will be booking milestones and royalties going forward, but those will be sort of traditional in that they will be real royalties that we will receive from Rigel on a go-forward basis. We additionally added that cost of sales line. That was really just to segregate Yale payments from our normal G&A. You will see that cost of sales line. For the time being, that is going to be 100% payments to Yale. We have a small royalty that we pay to Yale on any royalties in, and they get a small portion also of milestones going forward. You will see those picked up on that collaboration cost of revenue line. Please let me know if that answered your question.

Speaker #6: We will be booking milestones and royalties going forward, but those will be sort of traditional in that they'll be real royalties that we'll receive from Rigel on a go-forward basis.

Speaker #6: We then additionally, we added that cost of sales line that was really just a segregate Yale payments from our normal G&A. So you'll see that cost of sales line.

Andrew Saik: You will see that cost of sales line. For the time being, that is going to be 100% payments to Yale. We have a small royalty that we pay to Yale on any royalties in, and they get a small portion also of milestones going forward. You will see those picked up on that collaboration cost of revenue line. Please let me know if that answered your question. I know that is a lot.

Speaker #6: For the time being, that's going to be 100% payments to Yale. We have a small royalty that we pay to Yale on any royalties in, and they get a small portion also of milestones going forward.

Speaker #6: So you'll see those picked up on that collaboration cost of revenue line. Please let me know if that answered your question. I know that's a lot.

Andrew Saik: I know that is a lot.

Speaker #5: Yeah, no, great. Thank you. Thank you for that color.

Etzer Darout: Yeah. No, great. Thank you. Thank you for that color.

Speaker #6: Sure.

Andrew Saik: Sure.

Speaker #4: Thank you. Our next question comes from the line of Paul Choi with Goldman Sachs. Your line is open.

Operator: Thank you. Our next question comes from the line of Paul Choi with Goldman Sachs. Your line is open.

Paul Choi: Hi. Thanks. Good morning, and thank you for taking the questions. My first question is on LRRK2, and you indicated you will present additional biomarker data in October. Can you maybe frame for us what the sort of cadence over 2027 will be in terms of additional updates for that program and any additional clinical measures or potential advancements to the next stage? My second question on BCL6 is, after you present the glofitamab combination data in mid-2027, as you think about clinical development, can you maybe outline for us how you are thinking about potential comparator arms versus a monotherapy trial and just how you think about that down the road? Thank you.

Speaker #5: Hi. Thanks. Good morning, and thank you for taking the questions. My first question is on LAR-2—and you indicated you'll present additional biomarker data in October.

Speaker #5: Can you maybe frame for us what the sort of cadence over 2027 will be in terms of additional updates for that program, and any additional clinical measures or potential advancements to the next stage?

Speaker #5: And then my second question on BCL6 is after you present the GOFI combination data in mid-2027, as you think about clinical development, can you maybe outline for us how you're thinking about potential comparator arms versus a monotherapy trial and just how you think about that down the road?

Speaker #5: Thank you.

Speaker #2: All right. Thanks, Paul. Yeah. So on LARC2, I'll reiterate what I said before on where we are with 102, which is really focused on the regulatory approach, right?

Randy Teel: All right. Thanks, Paul. Yeah. On LRRK2, I will reiterate what I said before on where we are with 102, which is really focused on the regulatory approach, right? What we are focused on right now is incorporating feedback and developing that plan for how we move forward with the trials that we have talked about before while incorporating that feedback. When it comes to the cadence of trials, really the cadence will be, we would like to start them. That is the cadence. When it comes to providing a bit more clarity on where we are going, as we begin those trials, as they get close or even before, we will certainly talk about how those are shaping up. The cadence following the biomarker data that we plan to show at MDS will really be dictated on those trial starts.

Speaker #2: So what we're focused on right now is incorporating feedback in developing that plan for how we move forward with the trials that we've talked about before.

Speaker #2: While incorporating that feedback. So when it comes to the cadence of trials, really the cadence will be, we'd like to start them. That's the cadence.

Speaker #2: When it comes to providing a bit more clarity on where we're going, as we begin those trials, as we get close, or even before, we'll certainly talk about how those are shaping up.

Speaker #2: But the cadence following the biomarker data that we plan to show at MDS will really be dictated on those trial starts. When it comes to for BCL6, look, as we move as I said, all roads lead through the monotherapy and the combination right now with GLOFI, and we'll talk a bit more about where we go after that.

Randy Teel: When it comes to BCL6, look, as I said, all roads lead through the monotherapy and the combination right now with glofitamab, and we will talk a bit more about where we go after that. There is a lot of options, right? The bispecifics, there is more than one. Those are potential combinations. There is chemo, there is other things as well. I think that we will really have to watch the landscape evolve to see a bit of where the puck is going, to see where it makes most sense for us to combine. I will reiterate what I said around the opportunity to move earlier and faster with monotherapy approaches the ability to follow up with combination approaches that have the opportunity to reach bigger patient populations in earlier lines of therapy. Beyond that, a bit hard to specify what the details will be.

Speaker #2: There's a lot of options, right? The bispecifics, there's more than one. Those are potential combinations. There's chemo. There's other things as well. I think that we will really have to watch the landscape evolve to see a bit of where the puck is going, to see where it makes the most sense for us to combine.

Speaker #2: I'll reiterate what I said around the opportunity to move earlier and faster with monotherapy approaches. And then the ability to follow up with combination approaches that have the opportunity to reach bigger patient populations in earlier lines of therapy.

Speaker #2: So beyond that, it's a bit hard to specify what the details will be, but as we've started talking about this program, as we've shared the progress that we've made, certainly lots of companies are interested in the space, including strategics that clearly are following a traditional path in the NHL space, which is to identify ways to build out the treatment combinations that we're able to get to patients to extend responses and get responses to more patients.

Randy Teel: As we've started talking about this program, as we've shared the progress that we've made, certainly lots of companies that are interested in the space, including strategics that clearly are following a traditional path in the NHL space. Which is to identify ways to build out the treatment combinations that we're able to get to patients to extend responses and get responses in more patients.

Speaker #5: Great. Thank you.

Paul Choi: Great. Thank you.

Speaker #4: Thank you. As a reminder, ladies and gentlemen, please press *101 to ask a question. Our next question comes from the line of Jeet Mukherjee with US Bancorp BTIG.

Operator: Thank you. As a reminder, ladies and gentlemen, that's star one one to ask the question. Our next question comes from the line of Jeet Mukherjee with US Bancorp BTIG. Your line is open.

Speaker #4: Your line is open.

[Analyst] (BTIG): Hi, it's Blake on for Jeet. Quick question on ARV-102. Do you feel there's an intended PSP population that you're targeting, or is it going to be an all-comers trial? Thinking more on the lines of Richardson syndrome patients or specific LRRK2 variants. Thanks for taking our question.

Blake Gitler: Hi, it's Blake on for Jeet. Quick question on ARV-102. Do you feel there's an intended PSP population that you're targeting, or is it going to be an all-comers trial? Thinking more on the lines of Richardson syndrome patients or specific LRRK2 variants. Thanks for taking our question.

Speaker #7: Hi. It's Blake on for Jeet. Quick question on R of 102. Do you still have an intended PSP population that you're targeting, or is it going to be an all-commerce trial?

Speaker #7: Are you thinking more along the lines of Richardson syndrome patients or specific LARC2 variants? Thanks for taking our question.

Speaker #2: Great question. And maybe I'll have Angela get some more color here. The shortest answer is you're thinking about it right, right? Which is that we could look at all the PSP, Richardson is the largest subtype.

Randy Teel: Great question, maybe I'll have Angela give some more color here. The shortest answer is you're thinking about it right, which is that we could look at all of PSP. Richardson's is the largest subtype. When it comes to narrowing more than that, I think it's less likely, but maybe Angela, a bit more detail on how we think about the population there.

Speaker #2: When it comes to narrowing more than that, I think it's less likely, but maybe Angela a bit more detail on how we think about the populations there.

Speaker #7: Right. I think that we would not restrict further. Richardson syndrome is really a very uniformly progressing population, which is why we like it. And we like the focus there.

Angela Cacace: Right. I think that we would not restrict further. Richardson syndrome is really a very uniform progressing population, which is why we like it. We like the focus there, but this does not restrict us from expanding to all of PSP. I hope that helps.

Speaker #7: But this does not restrict us from expanding to all PSP. I hope that helps.

Speaker #4: Thank you. Ladies and gentlemen, I'm Sean. No further questions in the queue. I would now like to turn the call back over to Randy for closing remarks.

Operator: Thank you. Ladies and gentlemen, I'm showing no further questions in the queue. I would now like to turn the call back over to Randy for closing remarks.

Speaker #2: Thanks, operator. Thanks, everybody, for joining this morning. Look forward to providing further updates as we move forward. And thanks again.

Randy Teel: Thanks, operator. Thanks, everybody, for joining this morning. Look forward to providing further updates as we move forward, and thanks again.

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

Q2 2026 Arvinas Inc Earnings Call

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