Arvinas Inc ARV-471 Program Update Call Transcript

The following is excerpted from the question-and-answer section of the transcript.

Question: Eliana Merle - UBS Investment Bank - Analyst : Just in terms of safety, could you elaborate a bit on the QTc elongations seen in one patient as well as sort of the liver elevation seen in one patient that were Grade 3? And then just in terms of the planning for the Phase 3, could you talk a little bit about how you're looking at the AMEERA-3 data as well as the data from Radius? And any implications in terms of your trial planning?

Question: Joon Lee - Truist Securities, Inc. - Analyst : Congrats on the very impressive data. In the swimmer plot data, there are 5 patients with stable disease past six months who are no longer on 471. What's their disposition? And I have a follow-up.

Question: Joon Lee - Truist Securities, Inc. - Analyst : Got it. And the other question is post CDK4/6 is expected to drive high rates of your ER-independent resistance mechanism. Yet a lot of people -- is 100% of patients were on CDK4/6, yet you have high rates of response. So what's the mechanism by which ER is having an impact in these presumably resistant patients?

Question: Ted Tenthoff - Piper Sandler & Co. - Analyst : Great. My congrats on the data today. It's really cool to see how far the technology is coming, and I really love the broad development plans. I wanted to focus in on the Phase 3 trials and get a sense. It seems like this is going to be building on this experience in later-stage women. Can you give us any idea of patient population, maybe even size of a potential Phase 3 trial? I appreciate you guys answering the question. REFINITIV STREETEVENTS | www.refinitiv.com | Contact Us consent of Refinitiv. 'Refinitiv' and the Refinitiv logo are registered trademarks of Refinitiv and its affiliated companies.

Question: Michael Schmidt - Guggenheim Securities, LLC - Analyst : Congrats on the data as well. Just wondering if you could provide some additional comments around the dose response? And you're to select 2

Question: Matthew Luchini - BMO Capital Markets Equity Research - Analyst : Thank you so much for taking the questions and for providing a nice update this morning. I guess, first for me, as it relates to the combo -- the Phase 1b combo study you're going to be starting next year. I was just curious if you have any sense as to, I guess, first, when we might expect some initial results from that study. But I guess more generally, you've talked about maybe looking at CDK2, CDK2/4/6, if there's any of these mechanisms that you think might be particularly synergistic with 471? And then on the data presented today, I was just hoping you might be able to provide or remind us with some additional color as it relates to both the two patients who have had, I think it's now north of 18 months of treatment, as well as the patient that achieved a partial response with the -- despite having liver metastases since that certainly is an interesting result given the patient population.

Question: Zegbeh Jallah - ROTH Capital Partners, LLC - Analyst : Great results. As highlighted, we've seen encouraging efficacy observed in a heavily pretreated patient population. So if I can have you speculate just a little bit. So based on what you're seeing here, can you comment on what you think the resistance mechanisms could be? And what your thoughts are regarding the level of efficacy and the durability we could see in early adjuvant setting relative to fulvestrant, for example, particularly given the reported efficacy in ESR1 mutant patients? And I have a quick follow-up.

Question: Zegbeh Jallah - ROTH Capital Partners, LLC - Analyst : And then just a quick follow-up. I know this is a difficult one. I think you've all been trying to answer this question on the call, but just curious on your thoughts regarding whether the efficacy seen in supposedly non-ER-driven tumors could be something unique about how 471 binds the receptor? Or could it be something unique to the iterative effect of degraders and their ability to kind of be effective under low substrate conditions? So maybe more broadly beyond that, you could talk about how this data perhaps, even coupled with data from ARV-110, influences your conviction and the rest of your pipeline efforts, which is expected to probably become more of a focus during 2022. REFINITIV STREETEVENTS | www.refinitiv.com | Contact Us consent of Refinitiv. 'Refinitiv' and the Refinitiv logo are registered trademarks of Refinitiv and its affiliated companies.

Question: Brad Canino - Stifel, Nicolaus & Company, Incorporated - Analyst : I appreciate the data update this morning. Just so we have the specific details, can you tell us what number of the -- I think it was 47 CBR-evaluable patients had a documented ESR1 mutation. And then what was the CBR in both patients with mutated and wild-type ESR?

Question: Brad Canino - Stifel, Nicolaus & Company, Incorporated - Analyst : Okay. And then on your Phase 2, you mentioned it was fully enrolled. Can you tell us the end, the sample size there that we will be getting?

Question: Mark Breidenbach - Oppenheimer & Co. Inc. - Analyst : Thanks for taking the question and very glad to just see the CBR rate holding up in the larger data set. Just a very simple question from me. Since you mentioned VERITAC's completed enrollment, I'm just wondering if you can give us any granularity on when in 2022 we can expect to see initial data from VERITAC as well as the Phase 1b evaluating 471 in combination with IBRANCE?

Question: Maneka Mirchandaney - Evercore ISI Institutional Equities - Analyst : I actually just had a couple of quick clarifications. The first one is aside from the Grade 3 QTc event that you guys flagged, just wanted to double check that there weren't any Grade 1 or 2 QTc prolongation or bradycardia type event? REFINITIV STREETEVENTS | www.refinitiv.com | Contact Us consent of Refinitiv. 'Refinitiv' and the Refinitiv logo are registered trademarks of Refinitiv and its affiliated companies.

Question: Yigal Nochomovitz - Citigroup Inc. - Analyst : I had two efficacy-related questions. The first one is are we going to see PFS data at some point? Or is CBR really the critical metric? And if we do get PFS data, what do you think you need to show there? And then secondly, with regard to ER degradation correlating with clinical benefit, I appreciate that the numbers are too small with the current data to draw any conclusions on correlation of degradation with clinical response. But I'm just wondering, once you do have more data, would it be your expectation that you'd start to see the magnitude of ER degradation start to correlate with clinical benefit?

Question: Tyler Van Buren - Cowen and Company, LLC - Analyst : I guess the first one is what do you view to be the most significant safety and tolerability benefit relative to Sanofi's amcenestrant as we think about you both eventually competing in the market? And then just secondarily related to the Emerald data, can you just discuss why you think the PFS and CBR rates were higher in mutant patients versus wild type?

Question: Christopher Liu - SVB Leerink LLC - Analyst : I just had two. With the first one, I was just thinking about your go-forward doses with 200 and 500 milligrams. When I look at the CBRs here for 200 and 500 milligrams, it looks like -- albeit in small patient numbers, but it looks like 500 milligrams has a meaningfully higher CBR rate. So just wondering if you thought that could mean something, if that kind of leans you towards going towards the 500 milligrams?

Question: Christopher Liu - SVB Leerink LLC - Analyst : Got it. And for my second question, I was just hoping to get additional color on the Grade 3 AEs that you saw in the 500-milligram cohort as well as the 180/200-milligram cohort?

Question: Christopher Liu - SVB Leerink LLC - Analyst : Okay. So is there anything you could tell us specifically on what the Grade 3 AE was in the 200-milligram cohort and then the two in the 500-milligram cohort?