Arvinas, Inc. (ARVN) Earnings Call Transcript & Summary

Great. Good morning, everybody. Thanks for joining us. I'm Terence Flynn, the U.S. biopharma analyst at Goldman Sachs. Today, at our virtual healthcare conference, we're very pleased to be hosting Arvinas. Today, from the company, we have Sean Cassidy, Chief Financial Officer; and Ron Peck, Chief Medical Officer. Thanks so much, both for taking time out of your busy day to join us. We really appreciate it.

Thank you.

Yes. Thanks, Terence, and we also want to thank you and Goldman Sachs for having Arvinas at the 42nd Annual Healthcare Conference. Hopefully, in person...

Looking forward to it -- yes, looking forward to in-person next year.

In-person next year.

Sure. Yes, for sure. Well, we've got -- I think we've got a lot to talk about. Obviously, the company has made a tremendous amount of progress here since its IPO. And I think maybe just to start, if you could just frame for those folks who aren't as familiar with the story here, the PROTAC platform and really, what's the opportunity set here as we think about the forward? And then we'll dive in more specifically to some of the lead pipeline assets.

Yes. Great. Thanks, Terence. So Arvinas was founded in 2013 based on the work by Professor Craig Crews of Yale University, who invented proteolysis targeting chimeras or PROTACs. I was actually fortunate to help put the company together with Professor Crews and our Series A investors back in 2013. Since that time, the growth of the company and the robustness of the technology has just been absolutely fantastic. Just look at over the past 9 months of some of the accomplishments that Arvinas has had, where we've moved 2 assets into Phase II testing; ARV-471, an ER degrader for ER-positive breast cancer; and ARV-110, an AR degrader for metastatic castration-resistant prostate cancer. And quite honestly, it feels like we are just getting started. Both programs demonstrated activity in heavily pretreated patient populations and the respective dose escalation trials, and ARV-471 appears to have a best-in-class profile. Beyond these 2 clinical assets, we have a deep pipeline of targets in oncology and neuroscience that are planned to deliver INDs in 2022 and 2023. And we also expect to be in the clinic with ARV-766, our second AR degrader, also for metastatic castration-resistant prostate cancer towards the end of this quarter. If we fast forward to the end of 2021, we expect to have 7 ongoing clinical trials, 4 with ARV-471, 2 with ARV-110 and 1 with ARV-766. With respect to ARV-471, we expect to have our 2 -- excuse me, our Phase II monotherapy VERITAC trial ongoing; a Phase I safety study with ARV-471 in palbociclib ongoing; a second Phase I safety study with ARV-471 and another agent ongoing; and a window of opportunity study also ongoing. That's just 471. With respect to ARV-110 and 766, we expect to have our ARDENT Phase II trial ongoing; a Phase I combination trial with ARV-110 and another agent ongoing; as well as having our ARV-766 dose escalation trial ongoing. We've come a long way since 2013. As I said before, this really is -- feels like this company is just getting started.

Great, great. Well, appreciate the framing of the conversation here. I guess 1 other question we get a lot is just how broad could this technology be applied? I mean we've talked in the past about maybe on the undruggable side as a huge range of targets there. So how do you guys think about that opportunity set? And then how do you narrow in on kind of the next set of opportunities here beyond the assets you mentioned, Sean, as you think about some of the other areas to go into?

Yes. Great question. The PROTAC platform is broadly applicable, quite honestly, to any therapeutic area. As I previously mentioned, we actually expect to have an IND for our tau program in 2022. So as you look at the company, we have very exciting oncology assets that are progressing, but we also have a neuroscience portfolio that we expect to deliver candidates in 2022, 2023 and beyond. In addition to that neuro -- the neuroscience targets that we're working on, some of our collaboration partners have expanded the utility of the platform outside of oncology and neuroscience. For example, our most recent partner, Bayer, is pursuing the platform in gynecological indications, cardiovascular indications, and we've even set up a joint venture with Bayer Crop Science, created a company called Oerth Bio, and it's pursuing the PROTAC platform in agricultural settings. I think you'll start to hear a little bit more from Oerth Bio at the end of this year, maybe early next year. We have a fantastic team down in North Carolina. And led with -- led by John Dombrosky, who has deep agricultural experience. So this platform, I'll maybe be cautious to saying this, it could be as big as antibodies, quite frankly.

Great. Great. I guess as you think about that, the partnership opportunity, you guys have done deals with Pfizer, Roche, Bayer, as you mentioned. As you think about the forward, are there other opportunities you're thinking about carving out? Or you feel like that's kind of a good place to start and you're more focused on kind of internal execution here instead of leveraging the platform via other partnerships?

Yes. Those partnerships were fantastic for the company when we were a bit less mature. I guess, is the best way to really characterize that. So do I see the organization pursuing, call it, target-based deals is the way I'll refer to those? I don't. And there's really quite honestly no need for us to do that. So we really are focused on execution around our wholly owned assets at this time. That being said, you can fast forward not too far from now, and we will have what we hope is registrational trials ongoing for our 471 asset as well as our 110 asset. And there may be a very good opportunity at that time, where we'd bring in a partner to help with some of the global development that may be required around both of those assets. But as of now, from an external perspective, you should consider those wholly owned assets over the near term.

Okay. Okay. Great. Maybe 1 for Ron. Just in terms of the differentiation of PROTACs versus maybe some of the other approaches, we've heard about molecular glues. But maybe just remind us, what are the areas of differentiation? What are the advantages that a PROTAC platform has maybe over some of these other approaches?

Well, I mean, what's exciting to us and -- around the PROTAC platform is that these are designed -- that they can be designed against any particular targets, as Sean said, any therapeutic area. It's just a matter of having the warhead and putting the construct together for the hetero bifunctional molecule. It's also exquisitely specific. And that's one of the beauties about this platform. Then the last thing I would say is this catalytic mechanism of action. So something that an inhibitor doesn't have. For inhibitors, it's a one-to-one relationship between the drug and the functional pocket. With a PROTAC, 1 PROTAC, in our hands, can degrade up to 200 targeted molecules. So that translates into a very potent molecule. And that's already being demonstrated in our clinical programs. So we just think that this is just a very attractive way of developing drugs against both the targets that we think that PROTAC could succeed even greater than an inhibitor, either at the same time or after an inhibitor has kind of run its course, but also the upwards of 80% of disease-causing targets that are undruggable. So we're very excited by our platform.

Great. Great. Maybe we'll dig into some of the pipeline assets now. Again, 471 is your estrogen receptor PROTAC degrader. You guys have guided to completing this Phase I HR-positive breast cancer dose escalation study first half of this year, and then presenting data in the second half of the year. So maybe just walk us through how much incremental data we're going to see here? Is 360 mg the top dose? And then what's a potential presentation venue for these data?

Certainly. So when we presented the data back in December, as you mentioned, 360 was the top dose that we had safety data for. And at that time, we had no dose-limiting toxicities or anything, frankly, that came close. We had no treatment-related grade 3 or 4 toxicities. We had mostly grade 1 adverse events. So nothing that came close to dose-limiting toxicity. Number two is that 471 was extremely well-behaved from a pharmacokinetic perspective. Even as an oral therapy, with this class of drugs that are larger than average small molecules, we were getting very clean pharmacokinetics. We were having dose proportional increases in exposure. So in essence, nothing that was limiting us for going further in dose escalation. I think we did mention that we were dosing at -- patients at 500 back in December. Of course, we didn't have data for that. And we had previously said that we would continue to dose up to maximum tolerated dose. And maybe that for 471 and for this target, we may never show that. But the point is that we were -- we still had very much an ongoing Phase I at that time. So -- again, as we mentioned and as you described, we said that we would anticipate that we would complete the trial, we would have data presented at the end of the year. So what we have said is that it would likely, unlike the December disclosure, it would likely be in a congress. One could probably imagine what those could be. So for 471, it could be things like San Antonio, the triple meeting is in the fall as well and then ESMO, of course. So we're just following based on where we are in the trial and what makes the most sense.

Okay. Okay. Great. And -- so can you confirm if the trial is done yet or it's still ongoing? Because I know we're not technically at the middle part of the year yet.

Yes, we can't comment on that.

Okay. Okay. Got it. Okay. And then I guess the other one is just the biopsy data. Will you also have additional biopsy data to share? And when we see the updated data, I think we initially had 5 paired biopsies back at the end of last year. So have you been collecting more biopsy data?

Yes. Yes. We have been. Our best opportunity for getting biopsy tissue in the Phase I is in the backfill patients, meaning that those who are beyond a 3 or 6 patient cohort. We have a mandate to include that. So -- and also, as we've gotten into higher doses, we have been putting some additional patients on kind of utilizing that backfill mechanism. So we will have more biopsy data, likely at higher doses because of the progress of the dose escalation. I mean the good thing for us and why we're very excited by the molecule is that we were seeing degradation in all patients just in the first 3 dose levels, up to 120, even as we said we were dosing patients at 500 and showing numerically better degradation than fulvestrant even at that stage. So we will have more biopsy data.

Okay. Okay. Great. And another question we get is trying to establish a correlation between level of degradation and then kind of traditional efficacy measures. So is that something that you think will be able to determine based on -- I know this is the same question for kind of the 110 program. Is that something where you think via a Phase I study, you'd be able to have enough information to kind of make a determination there of any correlation? Or do you think that, that could be challenging for any number of reasons?

Yes. It's the latter. Probably the biggest challenge here is that we're in a setting and just to, I guess, remind the audience, for our trial versus all the number of ER-directed treatments, the SERDs that are out there in development, ours is the only one that required a treatment with a CDK4/6 inhibitor. So 100% CDK pretreated, that's different from the other trials. What we know about that also is that from a molecular profiling literature is that nearly 70% of patients have ER-independent disease, which means that even if you have the perfect degrader or targeted therapy for ER, 100% effect of engaging the target, you'd only have benefit in upwards of 30%, 35% of patients. So that means that it's a major confounder for starting to do that, and that's putting aside small numbers. So the -- I guess the challenge is that, that won't be there. However, the literature with fulvestrant really does paint a picture of how ER degradation and the magnitude on that effect does seem to correlate with efficacy. So I'll just tell you real quickly about that. So fulvestrant -- for those who are not familiar, fulvestrant which is the last endocrine therapy that was approved, it was approved in 2002, it degrades ER. It's a sort of a blunt degrader, means it's indirect of the ubiquitin-proteasome system. It degrades between 40% and 50% ER when you look across patients. What was shown over time is that when you increase the dose from the original approved 250 to 500, and there actually have been randomized studies that have looked at ER degradation between those 2 doses, you see a very important increase in degradation. So at the lower dose, it's maybe more about 17%. At the higher dose, between 40% and 50%. And then subsequently, there have been randomized trials looking at -- powered for progression-free survival that have shown that 500 was better than 250 in efficacy. So if you put it all together, that higher degradation translates into better outcomes. And as I mentioned, our initial data up to 120 showed a degradation that numerically was greater than the degradation of the top dose.

Okay. That's extremely helpful. I guess that the other one is just as we think about durability of response here, again, what's the relevant benchmark we should look to as we think about looking to your updated data here versus any relevant analogs?

Yes, sure. That's a really good question, and it's a bit of a trick question because if you look at ER-positive breast cancer and advanced disease, and you can -- we've talked about fulvestrant. If you look at fulvestrant and the indication for which it was approved and you look at even at the top dose of 500 milligrams, you'll see ER -- you'll see objective responses that can be as low as single digits. It's sort of a nature of the disease. And that's even with fulvestrant being, by most accounts, the most effective endocrine therapy in the marketplace today. You add to that this post CDK phenomenon that -- where you suddenly have nearly 70% of patients who are ER resistant, so you can expect response rates that are very, very low. So as a result, the endpoint of choice in ER-positive breast cancer in advanced settings and all the SERD trials and our Phase II study are designed this way is a primary endpoint around what's called clinical benefit response. So what that is a summation of objective response -- confirmed objective response, PR/CR, plus which patients have stable disease of at least 6 months duration or more specifically 24 weeks duration. So in our Phase I data that we presented back in December, we did present the CBR rate, and we had about a 42% response across doses. And I think the last thing I'll say here is that it turns out that data presented at this past ASCO just last week with the VERONICA study. So the VERONICA study is the best data to benchmark for post CDK. This is a trial that was fulvestrant plus or minus the BCL2 drug, venetoclax. It was a total of 100 patients, all of which have gotten prior CDK, which is unusual for a child that size. And the CBR rate for fulvestrant in this setting was between 11% and 14%. So that's sort of the benchmark that we are now using when we look at our data in this post CDK setting.

Okay. Okay, great. That's helpful. I guess the other question I had on this is just, is there an accelerated approval path here in this setting? Because, again, I think maybe Sanofi is doing their AMEERA study. It's kind of a Phase II single-arm study. Do you see that as a viable registration path? Or do you think it's more likely you guys are going to need kind of a fuller Phase III program when you think about potential path to market?

Yes. I can -- I'll touch on how we're looking at it, which -- so ER-positive breast cancer has been a setting where there hasn't been a precedent. And again, the usual endpoint for accelerated approval is a response rate and there's lots of literature out there even from the FDA about what the range of response rate is. As we mentioned, response rates in this setting are expected to be no better than single digits. So that becomes a challenge. But on the flip side, we just go back to the post CDK setting and what I just mentioned about VERONICA being the best benchmark for this setting. What that means is that you can do a randomized study. And because, unfortunately, these poor patients do so poorly, that means that the outcomes come very quickly. If you think about a progression-free survival, the median progression-free survival here was about 2 months. That means that your follow-up is very short and your trials can be very small. So in essence, you can do a randomized trial that can be completed, probably not much longer than a single-arm approval in a lot of other diseases. So that does -- so we still think that there's a -- could be a fast track to market in this particular setting. You mentioned Sanofi. I think the trial that we asked -- we get asked a lot about is AMEERA-3, which I think is due to report out later. The question that we're often asked is what -- how are we looking at this? And the truth of the matter is we're not really thinking about how this informs us because it's a different -- a whole different class of drugs. This is -- these are SERDs. We have a PROTAC. When we look at our data post CDK and we compare against the competitors, we have -- we think we have a very good reason to believe that we could be a best-in-class ER drug. So we're not, in any way, thinking that this is going to inform us. If it's a positive study, then we think that 471 could deliver even a better profile for patients.

Okay. Okay. Great. Maybe 1 follow-up on that is just have you guys looked at in vitro assays comparing your degradation versus the SERDs? Have you been able to do that? And do you see enhanced degradation?

Yes. So we have. I mean, of course, we've done a lot of our research with fulvestrant. So that's the original SERD. But we have -- when products have been -- when structures have been disclosed, we have a cracker jack large chemistry group. So we'll synthesize and test our compounds. And so fortunately, we've been able to continue to convince ourselves that we're going to have the best degrader out there.

Okay. Okay. Great. I know the other study that I think Sean had mentioned was the Ibrance or palbo combo trial here. You're going to have some data in the second half of this year. Maybe just remind us, what's the key objective of that study? How large is this trial going to be? And then if, again, assuming you meet your objectives, what would be the next step for that part of the development program?

Yes, certainly. And thank you for giving me the opportunity to talk about it because it gives me the -- it gives me an ability to explain that this is actually a small study. It's -- our goal here is very simply to establish the safety for the combination, determine the recommended dose for the combination. We're collecting pharmacokinetics, intensive PK in all patients to ensure that there's no interactions and if there are, then we can adapt the doses accordingly. It is not designed for efficacy. In fact, in order for us to move this along, and this is obviously something we spend a lot of time thinking about is how can we continue to close the gap and keep pace. Our -- we wanted to make this more of a safety study to declare dose and to make sure enrollment was quick. We actually are allowing prior CDK. So that makes it even less useful as an efficacy trial. So it's all about safety, all about dose, and that's really where the matter ends. And to the point of what do we do after this, we're really using the monotherapy trial to drive the path forward. And even for the data that we had in December, the fortunate thing is that we had essentially Phase II data in our Phase I trial to say that our next question is really what's the right dose. We started a Phase II. We have the desire to pick a second higher dose so that we have the best information to choose the right dose for Phase III. And all we're looking for is a profile that is -- we just want to consolidate the profile that we have and really have the right dose to take forward into Phase III. We do not need efficacy data from the palbo study. It's more about getting dose and just moving forward as quickly as we can.

Okay. And sorry, the second dose would be a part of the palbo study, like you have your kind of starting dose and then you'd have the ability to go to a second higher dose if...

We can go -- yes, well, it's actually both. It's -- the monotherapy trial will also take -- the goal here is to take a second higher dose so that we have essentially bookmarks of doses that we have good confidence in but gives us a range of exposure so that we have the right data to pick the right dose going forward because we really are very well aware that we have an opportunity to have the best-in-class drug, and part of that is also being as confident as we can be on the dose that we take into Phase III.

Yes. Okay. And that -- that's the 200 mg dose, right, that I think you guys moved into the dose expansion, and that's also being used in the palbo study?

Yes.

Okay. Okay. Got it. Understood. Maybe just the last one here is the -- I guess, maybe it's a 2-part one, just on palbo, that study, is that also a kind of medical conference type presentation? Or is that, because it's kind of a smaller study, it sounds like we won't -- there won't be much efficacy data. Is that more of just a kind of press release type disclosure?

We haven't -- for that, unlike the VERITAC study and the Phase I for the palbo, we haven't determined yet which mechanism we will apply.

Okay. Okay. And on the Phase II dose expansion at the 200 mg dose, again, I know we're obviously coming out of COVID, it seems like most centers are back up and running enrolling patients. So I would assume you guys haven't run into any kind of enrollment issues or hurdles there as we reopen here in the states?

Yes. We haven't disclosed any concerns in terms of enrollment.

Okay. Okay, great. Maybe now we can move on to ARV-110, which is your AR degrader program. Here, again, similar to 471, you've guided to wrapping up the Phase I dose escalation trial, presenting the data second half of this year. Again, I think as of the last update, end of last year in November, you had 37 patients, top dose was 420 mg. Maybe just, again, any update in terms of how many incremental patients we might see when we get the next set of data? And again, similar question as I asked before, just what are the likely venues or data disclosure plans for this data set?

Yes. So I maybe start -- work backwards. So the venue, we have said a scientific congress and I think it's the same kind of group of 3 that I mentioned for 471, just in terms of timing, triple meeting. Not San Antonio, that's pretty clear, but the triple meeting as well. So these are things that are currently in our thinking. And then I can't really specify exactly numbers and things have been. Of course, it's ongoing. But I would say that this is maybe to help. This is a 3 plus 3 dose escalation study. We did have backfilling of patients and -- so it's just more rounding out the Phase I experience.

Okay. And is that similar to what you're doing with 471, the backfill patients? Are you requiring a biopsy? I know here, it's maybe a little bit more challenging to get a biopsy, or is that the protocol?

Yes, that's exactly right. I mean it's just a population where it's hard to find biopsiable disease outside the bone. Oftentimes, patients will only have bone disease. I mean that's been the challenge for us. I mean, especially, a year ago when we presented ASCO, we had 1 biopsy there. But we are trying to get biopsies whenever possible. But honestly, the expectations have to be low. The good news is that PSA is a surrogate that we can use to understand what this drug is doing.

Okay. Okay. Great. And here, I know you've also moved into a Phase II dose expansion study. I think you're targeting about 100 patients. This trial started back in October. Maybe, again, just remind us that the kind of key components of this design, but then also the patient population that you're targeting here versus the Phase I study, how is it similar? How is it different? Any nuances that we should appreciate?

Yes, certainly. So there's -- I'll kind of break it down in 2 ways. The first one is that most patients will be, let's say, similarly advanced pretreated. This is where in castrate-resistant disease, they may have gotten chemotherapy, they may have also gotten chemotherapy, both in the castrate sensitive where docetaxel was now well established, and then also in castrate resistant where you have drugs like cabazitaxel. They will also have gotten their share of AR-directed therapy, not just chemical castration, but also all the AR-directed second line drugs -- or second-generation drugs; enzalutamide, abiraterone, the 2 new AR inhibitors. So it's a pretty good, let's say, experienced population in terms of extensiveness of prior therapy. And -- so that's -- and then we also have introduced, for the first time, a more lightly pretreated group. So we have sort of carved out cohort of patients who've had no more than 1 prior regimen in the castrate resistant. They could have only gotten 1 second-generation drug, either enzalutamide or abiraterone, and they had to have been chemotherapy resistant. And this gives us a chance to begin to get into a population that would be -- potentially have less AR-independent resistance, which is a big factor for the population that we studied since they were so heavily pretreated with median of 5 prior lines of therapy. So that's a breakdown by -- of treatment. And then within the first population that I mentioned, which is this traditional unmet need population, we have followed the queue from our initial data to say that there seems to be a population that seems to be particularly responsive. And that's this group of patients who have the more common AR mutations, 878 and 875. It appears that this is a population that responds particularly well despite the fact that they're in such a beat up group, where there's a lot of AR-independent resistance. So we have a population that is zeroing in on that group. So we can get more experience because we think that this group could be a springboard for accelerated approval, much like Rubraca had been approved on a year ago, certainly not in BRCA1 and 2, but in this particular subgroup of patients. And then we're -- and then also, we're looking at all other AR subgroups here because we know that as we get into earlier settings, this is where -- we know that this drug is going to be more active against the wild type patients, the other mutations with 1 exception, which is the L702H mutation that we know we don't degrade, which is prevalent in about 10% of patients.

Yes. Okay. And maybe a couple of follow-ups is just on the 878/875 subset. I think you guys have said before that, that's about 4% to 10% of the patient population, but I think you're enriching this trial for that group of patients. So is this going to be like it's half the trial? Or is it 75%? Like how highly are you going to enrich this study?

And so what -- yes, I guess I'll start off by just clarifying. So if you look through the literature, you may see around 10%. What is apparent in our experience, even from the disclosure back in December, is that it seems to run around 20%. Our assumption here is, like with many things in oncology, as you get into later lines, these biological subsets can be enriched. So -- and that's actually in the same range, frankly, as BRCA1 and 2, in the case of the PARP inhibitors. So that's point #1. And we haven't really broken down publicly about how much of the population is present. But what I can say is very much like we do want to get more information to consolidate the signal here, we're also very much interested in understanding about the wild types, the amplifies, the other mutations. And at the same time, there's a lot of controversy, let's say, about ARV-7. We know that we don't degrade that splice variant, which is prevalent in maybe about 30%. But what we knew even back in December is that some patients with ARV-7 have PSA reductions. So we're still also trying to understand, is this really a driver or a passenger here for us? It may be that the ARV-7s may respond as well. So we have a lot of -- we want to use this trial to really kind of bear out all these questions. So I guess what I would say is I wouldn't expect that it's going to be majority of the 100 patients. We want to get information from all these groups.

Okay. Okay. Great. And then I guess the last question just on this topic is the -- as we think about -- you mentioned Rubraca, the TRITON2 study is kind of a path, there's an accelerated path to market here. Would you be able to take this trial and further expand it to get up to the required number of safety exposure data that you'd have to have in that -- the subset -- the mutational subset population? Or do you think this data set you're going to have is going to be sufficient to kind of meet an accelerated approval threshold from the safety side?

From the safety -- I mean -- yes, I mean, all these data will be part of the safety data set, which is great. And -- yes, and it gets -- I think your question also gets into where do we go from here? It's almost like a tactical decision of whether we use this trial to sort of expand out into a TRITON2 like study or if we do a separate study. It's really more just an operational exercise of that. The good thing is that we are hunting in a population that we can do this. All these data will support the safety. And once we have the data that we need to go forward and move forward with the actual registrational trial, then we're going to be as quick as we can.

Okay. Okay. Great. Maybe Sean, back to you just to close it out here. Just as you think about kind of the expenses of the company, obviously, ramping here, you talked about the building number of clinical trials. We were talking earlier about the number of personnel you guys have been hiring lately. And so where do you see that burn going over the near term? And how do you think about financing needs on the forward?

Yes. The company is very well capitalized. As you know, we did a very successful financing back in December. If you look at where the cash balance is, at the end of the first quarter, $651 million. And if you want to look at some of the historical burn numbers, directionally, last year, we were just north of $100 million; I think it was $105 million. That's going to increase. There's no doubt that's going to increase. And our public statements are we have capital into 2024, which is a pretty long time. I think really where your question is, as these assets potentially go to a point where they're going to be in, what could be large Phase III trials, is that a situation or is that a point in time in which we would look to garner a partner to help us with some of that? Or quite frankly, if we would build those capabilities and raise money on the public markets? It could go either way, quite honestly. But as you look at it, there is and there always has been a lot of interest around both of these programs from pharma companies. ARV-471 in particular, and also that's the one that leads -- lends itself to more of a partnership scenario. But in terms of the audience, I think you really need to look at both of those assets as wholly owned assets on Arvinas' pipeline over the near term. And it's hard to really comment on how long is that near term, but you'll know it when you see it, right? When -- if you're looking at multiple global Phase III trials, that's the time that we would potentially look to get some help in. But anything that we would do, we would always retain significant commercial rights around these programs. We fully intend to be an integrated biotech company. And that is our goal, and we intend to hit that goal.

Okay. Well, great. Well, thank you both so much for the time today and the very productive discussion, appreciate it. And best of luck for the remainder of the year and stay safe.

Thank you. [indiscernible]

Take care.

Bye-bye.

Bye.