Okay, great. Welcome everyone. I'm Yigal Nochomovitz, one of the biotech analysts here at Citi. It's my great pleasure to introduce John Houston and Ronald Peck from Arvinas. John Houston is the CEO. Welcome. Maybe as a starting off point, John, if you could outline Arvinas's broad strategy for those listeners that are less familiar with the story, and talk about what is the near-term mission for the company and as well, what is the longer-term mission for Arvinas. Thanks, Yigal, great having an opportunity to talk to everyone today. Yes, for those of you who don't know, Arvinas was founded in 2013 on the pioneering work of our founder, Craig Crews from Yale University, focused on protein degradation. At the time, people saw this as a very novel, innovative approach to coming up with a new therapeutic approach to the disease. Basically designing heterobifunctional molecules that hijack the cell's own ubiquitin proteasome system to push proteins that were causing disease into the degradation machinery and break them down. Very different from inhibition. If needed, we can go into details on that. Since then, Arvinas has had all series of firsts trying to prove the utility of the platform, all the way through the initial flurry of targets where we showed we could get degradation. As the company built up, leading to our IPO and becoming a public company just prior to getting our first compounds into the clinic. Those compounds are bavdegalutamide, which is an androgen receptor degrader, which is in patients for metastatic prostate cancer, and vepdegestrant, which is an estrogen receptor degrader in patients with metastatic breast cancer. A series of firsts that occurred since then, obviously the first to get into patients, the first data to show that PROTACs, which are the heterobifunctional molecules, actually showed good exposure, good safety, and most recently in both trials, showing the first significant signals of efficacy in both very late-stage patient populations. Very exciting in terms of the programs progressing, exciting for the patients in those trials, but in general for the industry, the small putative industry of protein degradation, also very exciting, showing that the protein degradation platform really does have utility as a potential new therapeutic approach. Arvinas' game plan obviously is to progress both those programs. As you may have seen recently, we did a significant deal with Pfizer on vepdegestrant, which will be co-development, co-commercialization on a global level. It will allow us to very comprehensively move that compound forward. It will allow us to build the company even more significantly, because our overall game plan is to become a fully integrated biotech company that can take the rest of our protein degrader pipeline all the way through the clinic onto the market. 471 is going to be the lead program for allowing us to do that, followed very closely by ARV-110 and the rest of the pipeline behind it. The company has been scaling in size over the last several years. We're now over 250 people strong in the Connecticut base. Although we access a significant number of CRO chemists as well. Really deploying quite a significant amount of resources towards protein degradation. We're primed in a very nice way right now to take advantage of the rest of our pipeline, move it forward aggressively and really position PROTACs and protein degradation as a truly new effective paradigm for treating a patient. Thank you. That was a great intro. As far as I understand it, while you are a protein degrader company, at least for four seven one, you don't really see the protein degraders as the competition, rather the competition commercially are the SERDs. Maybe you could talk about the competitive landscape in the SERDs space relative to what you're building with four seven one. Then just more generally, how is your chemistry platform and drug discovery platform differentiated when it comes to the other protein degrader companies? Yeah, a great question. As you know, Yigal, going back several years, we used to get asked this question a lot about the competition in the space. Initially, there wasn't much competition. There was us, maybe two or three other companies that were very early. Because of the data that's been generated by Arvinas and, to be fair, other companies now showing that protein degradation is a viable new modality, there's a lot of companies in the general protein degradation space, either generating heterobifunctional molecules or PROTACs, BiTACs, MONOTACs, GLUEs, LYTACs. It's just really exploded as a whole little mini-industry in the space of hijacking a cellular process. We've migrated our dialogue away from competing with other protein degrader companies, because it's a big space out there. There's lots of room for companies to do well. Really the maturation of an approach like this is not talking about which ligases are you using, which company's got the best degrader platform, but it's actually what's your pipeline like and how well is your pipeline progressing. We're certainly at that stage where when we look at the competition, we're definitely doing it from a pipeline perspective. With our prostate cancer drug, we're looking at the profile we need to have to be a leader in that space and looking at the competition. With ARV-471 in particular, because of the set of SERDs that are ahead of us, looking at that competition and seeing what would a best-in-class profile look like. Would ARV-471 reach that best-in-class profile with the recognition that we are a true degrader? A lot of the other SERDs have different levels of degradation when we see their data. Nonetheless, they've been ahead. Our whole game plan in terms of the competition is closing that gap, finding innovative ways of getting ahead of the SERDs, but more importantly, showing that ARV-471 actually has a best-in-class profile, so it will have a position in the market regardless. Now, clearly, Ron can go into more detail in terms of 471's positioning to the set of other SERDs, but that's really our perspective right now in terms of the competition. It's pipeline. In that last part of your question about chemistry, clearly, since the company was founded in 2013, the whole insight and competitive positioning we've had is because of the chemistry insights. There's no two ways about it. Our chemists do know how to make drug-like molecules. They understand all the nuances of PROTACs. They understood fairly rapidly how to make them orally bioavailable. They know how to make them brain penetrant. They know the features of the PROTAC that can be adapted to give you different features. The chemistry is a major part of the intellectual drive that we have in the company. How it's differentiated is through length of time in the role. There's no doubt about it. Our chemists have been solely focused on PROTAC design since 2013. We have the vast majority of chemists still in play that we had from 2013, and we've obviously built on that as well. It's years of experience. It's an understanding of the science around it and allied with a really superb biology team. Great. You touched on the theme of my next question with respect to getting into a little bit more detail on 471's profile, at least based on the phase I work that you've done. Obviously, you had several good tumor responses in the late-line breast patients where all 100% of patients had progressed on a CDK4/6 inhibitor. Given that, could you talk in a little bit more detail as to how competitive a profile you see for 471 relative to the SERDs? I'll hand over to Ron, our CMO, to talk about that in detail. Clearly the data we've generated so far in our last data release in December on 471 really encouraged us that 471 has the potential to have that best-in-class profile. From a clinical benefit perspective, from a safety perspective, even a degradation perspective, we're seeing it hit the mark early, but it is early. Maybe, Ron, you could go into a bit more detail about your views on the positioning of 471 in terms of the rest. Yeah, certainly. Thank you, Yigal, for inviting us also. The way that we are seeing this is, as John said, across a number of different parameters, we do believe that the profile really is on a path to best in class. We believe that the Pfizer partnership is a further validation to the promise and the potential of 471, even in this competitive environment. Just to walk through the key findings in more specifics. You mentioned that this is 100% post CDK4/6 inhibitor therapy population. That's critical because there's emerging data to point out that this is a population that has a particularly high level of therapeutic resistance to endocrine therapy. There is a publication that we've cited in the December disclosure that shows that nearly about 70% of patients have ER-independent resistance. It doesn't matter what modality is used against ER. It doesn't matter how perfect the drug is. These patients will progress and not respond. That's very different from the trials that have been reported for the competitor agents within this broader SERDs class. The other thing just to know is that there is also emerging clinical data that supports this very aggressive phenotype of the tumor after you progress on CDK4/6. There's a trial that was presented at ASCO called the VERONICA study. This is, to our knowledge, the largest prospective clinical trial of fulvestrant in this setting, post CDK4/6. Fulvestrant demonstrated a clinical benefit rate of 14% as a single agent. That's really the benchmark that we are looking at with regard to how to get a sense of what 471 is doing in this setting. As John mentioned, our clinical benefit rate in the phase I data back in December showed a clinical benefit rate of 41%. For those who are not familiar, clinical benefit rate is actually the preferred primary endpoint of phase II trials of endocrine therapies. That's the endpoint that all the other trials are looking at with the other agents in phase II. It's a summation of complete response, partial response, and durable stable disease being at least 6 months. We had a clinical benefit rate of 42% in this setting compared to the 15% that I mentioned earlier. Efficacy clearly looks good. We had a confirmed response. We had other patients who had tumor regression as well, that didn't meet confirmed response, but still showing tumor regression in many of the patients that were on trial at that time. Secondly, safety is particularly important in this setting. In ER-positive breast cancer, it's a setting where even in earlier settings of metastatic disease, you could be on therapy for years. Also you think about adjuvant therapy for ER-positive breast cancer. ER-positive breast cancer represents 80% of all breast cancers, adjuvant therapy for breast cancer is extremely common. There are a lot of patients there. It's still a high unmet medical need with patients recurring after that. Having a good safety profile is critical. That's another point of differentiation for 471 compared to a number of the other drugs that are in this class that have been hampered with GI toxicity, even things like visual disturbance, bradycardia. We think that the safety profile and the efficacy are really notable at this stage. As John mentioned, we have data from paired biopsies that shows that the drug is doing what it's supposed to be doing, which is degrading ER. We saw this in all patients, that there was degradation in ER, with some patients having degradation up to 90%, an average of degradation of just over 60%, which is more than has been reported for fulvestrant in human tumors. Were you able to do an analysis of the correlation of the degree of degradation in the clinical response? The data are not sufficient to be able to analyze that. The number of patients is too small to do that. Also with this nearly 70% ER-independent resistance, you end up taking patients off the table just for that, so it becomes really impossible to look for that right now. Okay. Just remind us, when are we going to get the next update from this phase I? Is that happening soon or no? Yes. For 471, end of phase I data will be at the San Antonio meeting later this year. Okay. Are you able to give us a rough sense as to how many patients and the duration of therapy for that update? We have not provided specific guidance. What we can say is that at the time of the December disclosure, we were still dose escalating. We had not reached any dose-limiting toxicities or anything. There was really quite minor safety findings, grade one and grade two adverse events. We were dosing at that time at around 500 milligrams, just starting at 500 milligrams. Dose escalation has proceeded. We'll have more data in terms of patients. We'll also have more data on paired biopsies at that time, and also, of course, more safety. Okay, great. I'm really interested in your combo strategy. You're doing a study, which I believe you recently started, for 471 plus palbociclib in first-line metastatic breast, and this is again in the post-CDK4/6 setting. I'm curious, I understand that the goal of the study is mainly for safety and dose finding, not for efficacy. I'd be interested to know a little bit more as to why efficacy isn't the focus for this first combo study, and when would you be embarking upon such a combo trial where efficacy is the focus for, say, combining with palbo? Yeah, certainly. As you would expect, it's very difficult to understand the contribution of two drugs when you know that the established drug, in this case palbociclib, is active on its own or in combination with other endocrine therapies. We also know from the monotherapy experience, we have direct evidence of what this drug can do for patients. For us, in order to be as efficient as possible in development, the focus became safety and to confirm the recommended dose for the combination for phase III studies. The focus was on safety. In order to ensure that we can enroll as quickly as possible, we did not restrict prior CDK4/6 therapy. We allow prior CDK4/6 therapy. In that way, it also becomes very difficult to learn anything from an efficacy perspective. We believe that the monotherapy experience, including the VERITAC expansion, is really going to be the most important thing for understanding the potential. We think we're already in a good place with understanding the profile of the drug by itself. Okay, good. Is there any guidance you can give in terms of how much of an efficacy boost you might expect with 471 on a background of a CDK4/6 inhibitor, or is that just time will tell? Certainly, with our partners, as we start to think about registrational programs in more detail, certainly we have a very keen eye on determining what is something that's clinically meaningful, something that we believe is achievable with 471, and certainly our goal here is to show superiority. We have not disclosed any of the details in terms of what that might look like. How far away are you from potentially doing a randomized study? With the announcement of the partnership in July, we had with Pfizer stated, and it's also stated in our press release, that we have the plan to initiate a multi-indication phase III program beginning in 2022. You're also starting in the second half of this year, I understand it, a phase I-B for 471 plus everolimus in the third-line metastatic ER-positive breast cancer setting. Could you talk a little bit about why you chose everolimus to do this study, as well as what other targeted therapies might you consider for future combo work? Yeah, certainly. The way that we went about this is to start off with the basic, with what we already know about the profile, our confidence in this as a potential best-in-class. It was the imperative that we want to develop this as the drug of choice for patients with ER-positive breast cancer. That means thinking about this with the current paradigm, which is both monotherapy, endocrine therapy is used in the monotherapy setting. It's also used in combination with targeted therapy. If you go back nearly 10 years ago to the approval of everolimus in combination with the aromatase inhibitor exemestane, you will see from the study known as BOLERO-2, that was the basis for approval that everolimus had had a pretty substantial improvement in progression-free survival when added to endocrine therapy, namely exemestane, to the tune of about a 65%, roughly, improvement in progression-free survival or a hazard ratio of about 0.35. That is pretty substantial. Our sense is that while it may not be the preferred way to give endocrine therapy, it is certainly a choice that is being used, and it seems to be also preferential for the patients with more aggressive disease, where chemotherapy might be an alternative choice for those. The idea is that if we can find out how to administer this drug when it's in maybe the more difficult patients where you need a boost in efficacy, adding on top of a backbone of 471, that would be one approach. It's not the only combination that we're interested in, even before the partnership with Pfizer. There is a list of combination partners that we have been thinking about, and we've already begun to align with Pfizer on some of the basic ones. I won't go into those in detail. If you look at the targets that certainly exist today, and you think about that have already been validated in breast cancer, ER-positive breast cancer, and you think about combinations that may be of interest in the future based on some emerging science and emerging therapies, then you pretty much come up with a list of therapies. We have the interest with Pfizer to pursue multiple other combinations by way of other trials. Okay, thanks. Then moving to discussion of the adjuvant landscape. You had a so-called window of opportunity trial for 471 that originally was telegraphed as an adjuvant breast cancer study, but apparently it evolved into a neoadjuvant trial that's supposed to start in the second half of this year. Just curious as to what was more compelling about neoadjuvant versus adjuvant that resulted in the change in the design of this study. Are you going to enroll a combo cohort with palbo as well in this neoadjuvant trial? Yeah, it's worth me just making certain clarifications and I guess level set on what these terms mean. We had in the past referred to a window of opportunity study. Those are very commonly done in ER-positive breast cancer. They're very short duration treatment studies and are done with treatment preoperatively. It's generally typically two to three weeks or four weeks of therapy, really in the window between the time that a patient has consented for this trial, a patient with early-stage breast cancer, and the time that they have their definitive surgery already scheduled. Hence the terminology window. The idea is that you can learn about biology and the impact of the drug on, for our case, ER degradation, other biomarker endpoints. We ended up moving towards a neoadjuvant design. The difference there is really just duration of treatment. Whereas window study is short duration, get to the post-biopsy and let the patient go on for surgery. This is more with the intent of longer duration treatment. We get additional data as a result of the longer duration treatment. You get clinical endpoints, you get more informative safety in the early breast cancer setting. Really, this is more of a springboard for getting early on into pivotal adjuvant studies. The neoadjuvant is really just a model for evaluating the drug in the early breast cancer setting. This is really more a decision because we thought this was going to be a better way to accelerate a start of a pivotal adjuvant program. Just so I understand correctly, in this neoadjuvant trial, once they've had their surgery, do they continue on the therapy or no? We haven't disclosed the details of the design. The main thing is that these studies typically are more about getting the data earlier in terms of biomarkers, still in this case, but also some additional clinical endpoints, which really help be able to create momentum and interest among the investigators that we're doing adjuvant study. Okay, you also mentioned the VERITAC trial, which is the phase II dose expansion in second-line metastatic ER positive. Could you talk a bit about, I don't know, to the extent that you're able to comment, what is the late-stage development strategy going to look like for 471, both as a monotherapy or as in combo with approved agents? You're doing preparatory work across the spectrum from, as you say, from neoadjuvant all the way through first, second, third line metastatic. One thing I'll start off saying is that the partnership with Pfizer allows us to go much deeper into this space. That's one of the reasons. The other one is allow us to accelerate, hence our excitement about having the partnership. We have not yet disclosed details about the registrational program. I already mentioned that there is the plan to initiate a phase III program in the metastatic setting across different lines, in 2022, which is just next year. I would say that essentially the goal here again, is to have the data support indications that allow patients to have this as a drug of choice across lines of therapy. Certainly, we're doing the palbociclib combination. Palbociclib is certainly standard of care in combination with aromatase inhibitors, in combination with fulvestrant for patients who've already gone through aromatase inhibitor therapy. For later line settings the program will meet the needs of registering the drug in settings where it's going to be most useful. We're again, looking at ways over the longer term to make this a drug of choice for all settings. Okay. Maybe, John, I can ask you this one. Just in terms of the Pfizer partnership, could you talk a bit, at least, to the extent that you can, how much does having Pfizer on board accelerate the overall strategy and the overall plan for 471 in terms of getting to filing an NDA? I won't go into the specific details other than the fact that it is much more comprehensive in terms of the game plan, and it does accelerate 471. It really ticked the box quite significantly for us in terms of seeking a strategic partner that would enable 471 to get to more patients and hopefully get to the market in a quicker fashion. We are excited by the fact that the game plan that's been laid out and the joint plan of development between Pfizer and Arvinas will achieve that. Yes, it'll be more comprehensive, and it'll be accelerated. Just let me squeeze in one more on 471, then we'll switch over to 110. I'm curious, what is your understanding or what is your view as to the reason why 471 has been so clean on the safety so far? Good question. We get this a lot. Folks started to develop expectations that we would have some of the similar types of safety signals, which we haven't. Really, it's not 100% clear what is clear to us, and we had this feeling even before we saw our data back in December, was that it's not clear that these things are ER on target effects. Things like bradycardia has not been seen with drugs like fulvestrant, certainly, and some of the other older drugs. Visual disturbance seems to be limited to one or two of these other drugs. GI toxicities has been more of a pattern for the broad SERDs class. We speculated about certain chemistry explanations for that that are not shared by 471. The main takeaway is that it tells us that a lot of these things that we've seen with the broader SERDs class are not ER dependent. Okay, let's switch to 110 before we run out of time. For 110, could you talk about what you believe are the attributes that make this molecule a best-in-class AR degrader in your view? The difference just to highlight is that while in breast cancer, we're in competition with this broad class of SERDs, even as the only PROTAC, for prostate cancer, we have a different competitive set. We are aware that BMS is developing a degrader. They started after us. Otherwise, it's other non-AR directed therapies that are really more things that we're tracking right now. What I would say about 110 is, number one, we're going against the age-old target, but with a whole different mechanism of action. AR has been a validated target since, it was the 1940s. The idea of going with a time-tested target is critical and gives us faith even before we had our data. Number two is that 110 as an oral PROTAC offers other advantages for this older population who has had to go through IV therapies, chemotherapy. Having an oral therapy is still going to be quite a differentiator, especially when you look at the other therapies that are in this space. The other thing is that when you look at other regimens that are being tested, such as multi-kinase inhibitors either alone or in combination with anti-PD-1 or anti-PD-L1 therapies or other types of biologic treatments, those will introduce toxicities that could be really a challenge for patients who have already gone through things like chemotherapy and really would like something that's a little bit easier on them. I do think that there is those aspects between convenience and safety, and then we talked about AR, and then we have the data right now that tells us that we have a proof of concept, even in a very late line setting. Just as a reminder, in the disclosure that we had in December, these patients were really, unfortunately, quite beat up. They had very few, if any, alternative treatment options at the time. 80% of patients had gotten prior chemo. Median number of lines of therapy was 5. Actually, 80% of patients got both enzalutamide and abiraterone. It's a pretty far advanced setting, and frankly, a setting where there's a lot of AR-independent mechanisms of resistance. Despite that, this drug showed clear activity. Okay, great. I just want to pivot for a second. We have a question coming in from one of the listeners. They're asking about the drug-drug interaction that was reported last year with rosuvastatin. Could you remind us what we learned about that interaction since it was reported? Does it in any way limit the market reach of 110 given the broad use of statins? Was it specific to rosuvastatin? Does it have any implications for the overall PROTAC platform? Yeah, I'll start with the last one. This is not a PROTAC-wide observation. We see very different things between 471 and 110. That's an easy question. With regard to what we've learned, well, very simply, it was something that we came up with quite early. We saw it in two out of two patients who were on rosuvastatin. Rosuvastatin is particularly unique in its impact on drug-drug interactions through the BCRP transport pump, and other statins are not as, let's say, dependent on just BCRP. Essentially what we've done is we've excluded drugs like rosuvastatin from being used concurrently with 110. That has not in any way impacted enrollment. Number two is that we have not seen the same types of adverse events that we saw early in the program before we discovered that interaction. That shows that really made a difference by making that change in the protocol. The last point I would make is that we have a very robust clinical pharmacology plan to investigate drug-drug interactions, to really get a better handle on, is this really going to be limited to drugs like rosuvastatin? Are there other drugs that may be impacted? Certainly, when you think about rosuvastatin, again, it could be that this is something that could be unique. We'll find out with more data. In an advanced prostate cancer population, this has not been a hindrance at all in the program since there are other choices for patients. A lot of these patients, they're more aware of the seriousness of their prostate cancer. Okay, good. Obviously you have a relatively important readout coming up soon, as far as I understand, the interim readout from the ARDEN phase II trial in the second half of this year. Help frame expectations for just how much data we're going to receive at this update, and then to the extent that you can comment, what you believe you need to achieve on a PSA 50 response to justify continuing to develop this drug. Maybe just before Ron does that, yeah, the game plan is still end of phase I data by the end of the year. The whole game plan there was to make sure that we've completed phase I, because this will be the fourth time we've gotten an update on 110. That'd be the end of phase I. The idea was to have interim readouts of ARDEN. Of course, that's going to be the data set we have there is totally dependent on what stage of the trial's at. Ron can maybe talk to aspects of how the trial is designed and expectations over a period of time. Yes. Maybe I'll just focus my comments on phase I for now then, and then I'll tackle the other question you asked about expectations. The phase I, where we left it in the December disclosure, is that we are still doing some additional dose escalation in phase I. T hat the highest dose that we had reported back in December was 700 mg. We had started the phase II study at 420 mg administered daily, that being the ARDEN phase II expansion. To think about a follow-up on the phase I, which would essentially be the completion of the dose escalation, it would be looking at additional patients, looking at higher dose levels, and more information around safety at these alternative doses that were investigated in phase I. Your second question was around. The bar. I mean the bar for success, what you think there? What I might do is to just refer back to the ARDEN because the phase II expansion was really designed with the early efficacy data in mind. When we had our first disclosure, which was a year ago, ASCO, number one, we saw early responses, PSA 50, we saw a RECIST confirmed response. The most notable activity was in patients that had certain mutations in the AR receptor. What we wanted to do in phase II was to ensure that we were really stratifying based on AR biology. We included a cohort of patients with the same mutations, both of which were present in the most profound responders. In December, we had presented some data, not from the ARDEN, but from phase I, with more data in that particular subset, patients with the H875Y and T878A AR mutations. We saw that even with now up to five patients back in December, that there did continue to be a pattern where those patients, again, in this very late line setting, where there's a lot of AR-independent resistance, that they still seem to do, let's say, a bit better than the broader population. Better enough that we felt, and still feel, that this is a population that could be a basis potentially for accelerated approval once we get additional data in that setting and move forward with a pivotal study that would be in the future. In that population, so again, this is let's say a precision medicine population based on AR mutations. What we would think would be a basis for accelerated approval could be a RECIST response rate. About 25% would probably be the floor we think for what could support accelerated approval. That's based on a review of some of the publications that the FDA has come out with, others have come out with, looking at response rate as a basis for approval across multiple tumors. You see a range in 20%, and that 25% is somewhere in the middle of that range. We feel, especially given what I talked about earlier, the unmet medical need, the older population, and the value that this could be for patients, that could be let's say a low bar for thinking about this type of approach. If I understand correctly, you're referring to the T878A/H875Y group. Is that correct? Yes. Okay. Just wondering, is it understood biologically why it appears that those patients, mechanistically, it's easier to degrade their mutant AR? I would correct you is that this we don't believe is a consequence of the drug in that we have robust preclinical data looking at the ability of 110 to degrade AR in vitro systems, in vivo systems, and also looking at wild-type versus other mutation forms. This is not in our opinion or in our strong belief, this is not because of 110 degrading 878, H875Y any differently. It degrades in these laboratory settings consistently across, with one exception being this mutation L702H, which we know 110 doesn't degrade and is also in a low frequency in castrate-resistant prostate cancer. On the other hand, we do think that this is likely an indicator of which tumors, which patients have tumors that are still addicted to the AR pathway, that this is some marker of responsiveness to AR therapy. Here, these are patients who've already progressed through second-generation drugs inhibitors, abiraterone and enzalutamide. These patients may still be addicted to the AR pathway such that a degrader can do the job. Okay, thanks for the clarification. John, just one final question before we wrap up here. Just at the level of corporate strategy, are you currently envisioning entering into a partnership with 110, similar in scope to what you've achieved with Pfizer for 471? At the moment, we're going to progress 110 ourselves. We have the ability to do that. There's a very clear path there. Ron indicated even maybe a fast-track method for moving forward. Obviously, we remain open to the idea of a strategic partner helping us at the point where we either could go faster or more comprehensively. We'll always remain open to that. Right now, our plan is fairly aggressive, and we can do that with the investments we have to take this compound forward ourselves. You'll never get me saying we're not open to good partners and acceleration of our programs. Makes sense. Well, thank you both very much for the insights, and we look forward to further conversations. Great. Thanks, Yigal. It was fun. Thank you very much. Good talking with you. Bye. Thank you.