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

Good afternoon, everybody. Welcome back to the BofA Healthcare Conference here in Las Vegas. I am Tazeen Ahmad. I am one of the senior biotech analysts here at the bank. It's my pleasure to have our next presenting company, Arvinas. And sitting next to me are Sean and Randy. I will let you guys introduce yourselves, so your roles at the company. And then maybe, Sean, you can give us an overview of the company and some of the near-term highlights, and then we can go into some more specific Q&A if that works for you.

That would be terrific. I'm Sean Cassidy, the Chief Financial Officer. The company -- I actually had the pleasure to start with the organization when it was founded back in 2013. I'd like to thank Tazeen and Bank of America for having us here at this year's event.

Yes, and I'm Randy Teel. I lead corporate and business development for Aventus. I joined back in 2018, so just ahead of the IPO. So great to have us. Thank you very much, Tazeen.

And Randy is going to be our sit-in Chief Medical Officer and Chief Scientific Officer today.

Yes.

And he does a fantastic job at that. The company was founded in 2013 based on the work by Dr. Craig Crews, and we kind of are the leaders in targeted protein degradation. We've advanced multiple programs into the clinic: ARV-471, which is an estrogen receptor degrader; bavdegalutamide, which is an androgen receptor degrader for metastatic castration-resistant prostate cancer; and the ARV-766, which is another antigen receptor degrader also for prostate cancer. We have a packed series of events coming up in the second half of 2022 with multiple trial starts and data that we'll be talking to the investor community about. In terms of trial starts, the ones that are the most important to the organization, there are two pivotal trials with our ARV-471, which is in partnership with Pfizer as a monotherapy as well as in combination; as well as a pivotal trial start with bavdegalutamide in the 878/875 subgroup. We also have other clinical trial starts, not as important as the pivotal ones that we have, but also demonstrates the breadth of what we're pursuing, the 471 program with Pfizer. We have a combination trial with 6 agents, an umbrella -- excuse me, an umbrella trial with 6 agents that we'll be initiating later on this year. We have an everolimus combination study that we'll also be initiating later on this year. And we have a neoadjuvant study testing ARV-471 in earlier lines of therapy. With respect to 766, we expect to transition that program out of dose escalation and into Phase II. So very exciting year with respect to clinical trial starts. With respect to data releases, we will be releasing data on the VERITAC Phase II trial at the 200- and 500-milligram dose as well as dose escalation data on 766 later on this year. So an absolutely packed year. We're going to be very busy and expect a very fruitful year for our medicines in second half.

Okay. Now maybe just to back up all the way a little bit, I would say. What is a protein degrader? because we keep hearing that term, protein degradation, drugging the undruggable. What does that really mean? Because there are many companies now sprouting up behind you in development that also claim the title of focusing on protein degradation.

Well, sure. Let me just kind of talk a little bit about the mechanism. I'll use my hands. Dr. Crews will be happy when I do this. And hopefully, I do justice, quite honestly. So we use heterobifunctional small molecules where one end binds to a target protein of interest, for example the antigen receptor or the estrogen receptor; and the other end binds to an E3 ligase, and they're connected in the middle by a linker. And the whole idea here is you bring the target protein of interest in close proximity to an E3 ligase, cereblon and VHL, multiple others are out there in the marketplace. And four ubiquitins get deposited on the target protein. That complex falls apart. That target protein now sitting with four ubiquitins get shuttled off to a proteasome for degradation. And it's a very powerful platform. Look, compare that to a normal inhibition, where you actually have to have a binding event happen. Sometime that binding event falls apart, protein is still around and hasn't been degraded. Protein's still around causing disease. So it's a somewhat simple but fantastic invention that Dr. Crews really, quite frankly, pioneered. And there have been other companies that have followed in Arvinas' footsteps, and we're happy for those organizations, quite honestly. It really does show the power of this platform and the broad applicability of this platform. It really, in theory, can be applied to any intercellular target. And a good example of how broadly applicable this technology is, we actually have a joint venture with Bayer Crop Science, where we're actually pursuing this application in agricultural uses. So it really is something that's very broad. And quite frankly, I hope Dr. Crews gets the Noble Prize one day for his endeavors.

So would you describe as really a simple idea? So why has it taken this long to get to this point? So why did it take Arvinas moving into the clinic and really making protein degradation more mainstream for, I don't know, 60-some other companies now to be in the clinic suddenly?

Oh, we had two very successful programs on our new platform. I'd say Arvinas was very successful at that. So we're very proud of that. But, I mean, some of the challenges around these compounds are, quite honestly, that they're high molecular weight, right? So what Arvinas' core competencies are is really taking these compounds that are well outside of the Lipinski Rule of Five and making them into drugs. What you'll see is a lot of folks can make degraders and do it in a petri dish. And that happens all the time. It happens in academics. But where Arvinas' true capabilities are is turning that into a drug with pharmaceutical properties. And some of the key scientific breakthroughs that we had going all the way back to 2016 really was making these compounds not just getting into cells but also orally bioavailable. And those fruits have paid off with our -- all three of our programs right now being orally delivered therapeutics.

Yes. So for 471, this is partnered with Pfizer in a breast cancer indication. I'm sure you've talked about this many times, but why did it make sense to want to partner the program at this juncture? And why was Pfizer the best partner for you?

A great question. So it's a question I'm sure every biotech goes through, when is the right time to partner. And for us, it really comes down to two simple things. Can a partner help you develop it faster? And can a partner help you develop it more broadly? And we think we have, quite honestly, one of the best partners to be able to do that. I kind of mentioned a little bit all of the clinical trial starts that we're going to be embarking on later on this year, of which two are pivotal trials. That's a great example of the acceleration that the Pfizer partnership has allowed us to execute on. And then the broadness. As you looked at all the other clinical trial starts, particularly like the umbrella study, the neoadjuvant study and the combination with everolimus, it shows the broadness in which Pfizer and Arvinas intend to develop the program. Now could we have done all that on our own? I would say that is a very heavy lift for a biotech company to be able to initiate two pivotal global Phase III trials in the time frame that we're executing on those.

What data did Pfizer have access to when you were negotiating terms with them?

They had all the data that we disclosed back in December 2020 as well as updated data, as you'd expect with any very thorough diligence process that you would expect to come from a Pfizer.

And was it a competitive process?

It was a competitive process, highly competitive process.

Okay. So you've talked about some data readouts. Let's focus on the breast cancer readouts. You've got a Phase II that's coming out, you said, in a year?

Second half.

Second half of the year?

Yes, second half of the year.

What data should we expect to see at that top line readout? And what would you consider to be positive data?

I'll that turn that over to our stand-ins. Anyhow, he has -- does a fantastic...

Go for it, Randy.

Yes. So think about the ongoing trials, the VERITAC, which is the Phase II, as well as the combination Phase Ib as informing our pivotal trial. So we've already said we'll be starting two pivotal trials by the end of the year.

Right.

The VERITAC study is at 200 and 500, really helping us choose a dose. So we have a lot of backfilling in that trial as well, in the escalation, and going into the expansion. So that's the main readout. Beyond what we already showed in -- last December and the December before in terms of the CBR in very heavily pretreated patients, all of whom are post CDK4/6, the main thing, we're picking the dose. From the Phase Ib combo, that's also about dose finding, making sure we don't see any unexpected DDI with a CDK4/6 inhibitor. So certainly, the pathway towards registration will be both, as we've said, in monotherapy and in combination. But that's also really not an efficacy study.

Okay.

They're all those patients who are post CDK4/6. So they're getting CDK4/6 again plus 471.

So how many doses total will you have studied?

Well, we started at 30, and I think we went as high as about 700 with backfilling in between there for lower doses that -- once they've cleared. So it's a pretty broad range of doses.

And then if you kind of think about what the practical way of moving forward would be, you have all this data on all these different doses, how many doses do you think you'll ultimately need?

Probably just one.

Just one.

Yes.

Yes. so -- and I think it's worth mentioning the Project Optimus from the FDA, right, which has really changed our thinking a bit at least for the industry.

Yes.

I think they've been starting to put some muscle there. But we had already started in early 2021 with the 200-milligram dose. As soon as we saw good PK, good efficacy, we moved forward with that, and then started the 500-milligram dose shortly thereafter to make sure we had a good range, PK coverage of what we were seeing. But ultimately, we would expect to move on dose for the pivotal studies.

How do you know -- you don't need to go higher than 700? Or can you go higher than 700?

I think we could have. We didn't hit an MTD.

Yes.

But at some point -- and if you look at the data from the Phase I, there wasn't much safety difference at all. It was -- safety was excellent at all doses. So it wasn't that it was safe for 200 versus 500. So it's really -- the decision on dose will be based on the totality of PK exposure, the degradation that we're seeing, efficacy that we're seeing, all that.

Okay.

And yes, we're seeing really good clinical benefit rates in the other two doses that we brought forward into Phase II.

So you kind of already have decided, I'm guessing, what your Phase III should look like. You're kind of waiting for that validation to come in, in the middle of year -- or the second half of the year. But how quick of a turnaround will you need from the time that you see that Phase Ib and Phase II data to start your Phase III? Or do you not need to actually see that to start?

Yes. Not very long. To your assumption, yes, we have a pretty good idea, broad structure, what they'll look like.

Yes.

All we've said publicly is in combo and in monotherapy metastatic breast cancer. But beyond that, we really haven't said. But it's -- there's -- there are other ER-targeting therapies in the space that have trials that will look similar to what we have. We've certainly been looking and watching the space as to what's been working better than other things, and we'll certainly learn from that as we move ahead with our pivotal trials. But you're totally right that the broad structure of those trials are pretty well established.

Okay. So how far along are you in the setup of the Phase III? Have you chosen your sites, your principal investigators?

Yes. So all of this is in combination or in conjunction with our colleagues at Pfizer. But they are quite far along.

Okay.

Yes.

And how involved are you -- is Arvinas in those efforts to design the study and do some of the legwork and prepping?

Very tightly linked at all fronts. On the medical side, on the clinical side, commercial side, we've been working -- it's been a great partnership, honestly. And I think the key is that, as Sean said, they share the vision, right? The vision here is that 471 is the backbone of care from early lines to late. That may mean combinations with Pfizer products. That may mean combinations with non-Pfizer products. It really is about maximizing the opportunity for 471 across the spectrum.

We couldn't asked for a better partner on that front really. This really -- everything that we do is joint, right? Every decision we make is with the team Pfizer folks and the team Arvinas folks. And even as you look at the agreement, the escalation process ends up you're going into status quo. So it almost forces you into an agreement with either party with no one party having the upper hand on the other. It really is truly a fantastic collaboration.

Okay. So once you start the study or once you and Pfizer start the study in breast, how long do you think it'll take to enroll?

It's hard to say. I mean I think as we get rolling in those studies, as we announce those and talk about the designs, it's probably an easier time then to talk about enrollment time, approval time, all those things. For now, we'll focus on getting them kicked off and then provide that.

And like rough estimate, how long would the patients be observed in the study?

Well, at least in the studies to date, right, patients typically stay on until they progress.

Yes.

So some of the durations have been quite long. But to date, patients are followed throughout. They'll be watched as long as they're enrolled for sure.

Okay. So because it's still in its nascent stage as a category approaching degraders, I think people have been trying to look for validation from maybe related mechanisms for studies that other companies have brought, mainly SERDs. So can you talk to us about why people want to kind of tag protein degraders to SERDs? And with the recent, let's say, the AMEERA study readout from Sanofi not being positive, what does that really mean for protein degraders for you in particular if anything?

Yes, we've been really consistent in thinking that whatever happened with the SERDs, we have a different mechanism. We're not a SERD, right, so we're -- as Sean went through, we directly bind the ER and link it to the degradation mechanism. So we had always thought that if the SERD trials were positive, good for patients, fine for us. We think we'll be better. And if they're negative, not so great for patients but still just fine for us because we think that a better mechanism of degradation will lead to activity where they're not seeing it. So what's happened in the past few months with Radius being successful and Sanofi and Roche being unsuccessful in their trials, it doesn't change that at all. But of course, like I said before, we're certainly looking at the same information that everybody else is. And we'll look at the data as it comes out, which hasn't come out from those trials yet for most of the -- or for two of those at least, and we'll certainly learn from that. That's one advantage to starting the pivotal trials after we get to see that data. But it doesn't change our path at all really. We still think that having a better degrader will lead to better outcomes. That was true preclinically. It's been true clinically so far in our comparisons we've done of other Phase I studies. It was true of fulvestrant when they doubled their dose years ago from 400 to 500, better degradation led to better outcomes. So we still very much think that's the case.

Yes, the Sanofi and Roche failures for -- to me was one of the biggest positives we had, right? So two folks that were ahead of us kind of out of the picture with respect to pursuing it in the second line. So I think that's a fantastic result. And also, if you -- as you look at those trials, you see that they were, quite frankly, somewhat smaller in design when you compare to the Radius trial, which also had a -- what I would say is a nice outcome, but we think it's somewhat of a -- more of an inferior compound. So we get all the learnings from those successes and mistakes that potentially could have been made, and we can apply that to our own program. And it's not like the Sanofis or Roches of the world are abandoning the program. They're continuing to make significant investments in those programs, no different than we and Pfizer will. So we think we're actually in one of the better seats that you could possibly want to be in with respect to what happened to Sanofi and Roche.

Well, why did it make sense to look at metastatic breast cancer first?

You mean versus...

Just as an indication. Just as an indication.

Oh, as an -- well, so back when the company was founded, we hit AR and ER first. Really the thinking then was there weren't dozens of protein degradation companies. We're the only one.

Right.

So we, not knowing if we'd be able to make the technology work, chose targets that were extremely well validated. We knew what would happen if we get ER or AR, which is why we went after those first.

Yes.

We've obviously broadened out dramatically since then and have multiple undruggable and other targets in the pipeline, but that was the rationale behind AR and ER as the initial targets. So well validated that we would have a good sense of if we're able to degrade it, which was definitely not a given at the time, that we would know what to expect.

Yes. So as far as like the actual patient population, what do you think about like a relatively high percent of patients who have ER-independent disease in the second line and after? And how does that come into your calculation?

Yes. It's -- I think it puts our results from the Phase I that we've shown in pretty good relief, right? So post CDK4/6, something like 66% or 70% of patients will have ER-independent mechanisms. So that's why our 40% CBR is pretty dramatic if you assume that only 1/3 or so of patients even are driven solely by ER. So -- and in that comparison that we always did with the other Phase I trials, we had 100% pretreatment with CDK4/6, 80% prior fulvestrant, 80% prior chemo and, despite that, still had a better clinical benefit rate than any kind of programs. So I think that certainly makes things more complicated because you don't know which patients are ER driven, but it also reinforces that we think we can be successful in the late lines based on the data we've already shown. And absolutely, we think that we can move forward in combination in the first line and even in the adjuvant space and be successful there, too, because the percent of patients that are still driven by ER should be even higher in those settings. And that's why, as Sean said, even the competitors that have fallen by the wayside in the late lines are still very much gunning for first-line and adjuvant space, because the rationale is very clear that an ER-targeted therapy should work better there.

Okay. You are pursuing several combination studies. How are you thinking about what makes the best combination? Do you have an idea as you sit here today of what combination is going to be most successful?

Yes. It depends on the line, right? So in later lines, we've talked about an adjuvant -- sorry...

Everolimus.

Started an everolimus combination. There could be others as well. In first line, the status quo is very much a CDK4/6 inhibitor. But we also, as Sean said, will be starting an umbrella trial with Pfizer later in the year, trialing multiple different modalities that can go alongside 471, which could include other CDK4/6 inhibitors, could include other programs that are in Pfizer's pipeline but earlier, they've talked about that explicitly, but could also very much include non-Pfizer programs. And that's very much in line with their vision as well.

And when is that umbrella study like this year supposed to start heading into more...

Within the second half. Second half, yes.

Okay.

Second half, yes.

And how many patients do you think that study could enroll?

Well, so there could be a number of different combinations, so it's hard to say exactly how many.

Yes. And does that make it complicated to understand what's happening if you have all sorts of combinations in the same study?

I don't think so only because the intention of that wouldn't be to compare them sort of head-to-head. It's -- i would think of it as sort of pilot studies and you could look for a signal. Signal finding.

Would the plans be to take various interim looks at the study at certain points in time?

Yes.

Yes, absolutely.

I mean it would be signal finding really to inform other trials that we would do with -- bigger trials that we do in combination.

Okay. Now how do you define the market opportunity? Because you're still trying to figure out what the best addressable patient populations are. But let's just focus on the portion of 471 that's partnered with Pfizer. Like how big is that opportunity?

Well, quite large. I mean, it's -- so if you -- if we can be active in second line plus -- and first line and adjuvant, that is a lot of patients. And as they move earlier, the durations get longer and longer. Patients in the adjuvant setting can be on therapy for 5 years, right? So it's a pretty broad opportunity across the spectrum.

And is that, I mean, north of $2 billion? Is that...

We haven't talked about dollars. But anyhow, in terms of patients that -- I mean, think about fulvestrant's a $1 billion drug, right, that has a lot of drug action limitations. So a better fulvestrant that you could use in adjuvant, which they've been unable to do because of the dosing of fulvestrant. Yes, it's a much bigger opportunity than that.

Okay. We've, in the past, talked about prostate, but there are other things that are going on at the company that I think are probably worth spending a few minutes on. Does -- the one that really strikes me is the focus on potentially moving into CNS indications. So it's still pretty differentiated. There might be another company or two trying also to move into CNS now. But why does CNS make sense? And when could we start to see movement in that space from you?

Yes. I mean I think the reason it makes sense is that the current options haven't been very good. I mean our general thought is that most targets in neuroscience haven't been very well targeted, haven't been well drugged, which makes sense, right? So a PROTAC could ultimately -- we think, could be dosed orally, cross the blood-brain barrier, get it not just into the CNS but into cells of the brain and degrade disease-causing proteins in cells, which is something that nothing else could do. Antibodies don't get into the brain very well. They're certainly not getting into the cells in the brain, right? ASOs, dosing intrathecally is certainly not as advantageous as dosing orally. So for those reasons, the opportunity is pretty big, in addition to the fact that obviously, most neuroscience -- most neurology diseases just don't have good targets, good drugs against them. And when will you start seeing something? We've said that by the end of 2023, we'll have 3 -- or, sorry, 4 additional INDs, and at least one of those will be in neuroscience. So...

I mean neuroscience is so broad. I mean would you consider Alzheimer's -- something that's complicated as Alzheimer's, ALS, Parkinson's?

So the disclosed targets in neuro are taus, nuclear in Huntington.

Yes.

And so taus certainly could be relevant in Alzheimer's. There are multiple other therapeutic areas or indications that could also be relevant for tau. Things like PSP may be more purely or solely driven by tau than an Alzheimer's is.

Yes.

But certainly, we'd be interested in that. A similar story you could tell for synuclein, and Parkinson's comes to mind. But there are other more targeted diseases that you could think about there.

And what would the advantage of your approach again using a PROTAC platform be versus other companies who are already trying to do Huntington's and Parkinson's and Alzheimer's, focusing in on tau and synuclein and Huntington's in a big way?

Well, the -- I mean, the ability to get into a cell and degrade would be one. The ability to differentiate between a mutant and a wild type -- PROTAC is highly specific. So they'd be able to differentiate between a mutant and a wild type or different isoforms could all be ways that it'd be advantageous versus competition.

And how complicated would that be in the early stages to really know if that's working? Because you have to, number one, demonstrate that there is protein degradation happening. And secondly, you might have to pick some biomarkers, and, frankly, the biomarkers in any of those indications are still kind of not validated, let's say. So you're kind of going to have two balls up in the air in the early stages. And how does -- how do you approach that? Would you want to do that with a partner? Or do you feel confident you can do that by yourself?

Yes, that's fair, right? All biomarkers-related studies will have to be -- come along at the same time. There will have to be advances there, there's no question. The trials for things like Alzheimer's and Parkinson's would be obviously enormous. When we think about partners in -- from a broad sense at Arvinas, we're generally looking -- as Sean said, looking at partners that could help us accelerate or broaden what we're doing. In general, we think we're very well resourced capability-wise to get things into the clinic. Certainly, if we are looking at Phase II, Phase III Alzheimer's-, Parkinson's-type studies, I think it's a safe bet we'll want to be -- we want to do that with a partner. But we've built a lot of capability in neuroscience over the past few years that we've been -- that I've been here since 2018, and we feel very good about getting things into the clinic, making sure we really know the value that we have before we think about partnering. But certainly, there's an opportunity there.

And would that be a near-term consideration, to partner?

Well, we've got -- I mean, in neuroscience specifically, the most we've said is what I just did around IMiD before the end of 2023. So we probably want to be in the clinic before we think about, yes, partnering. We have the capability to bring those -- bring that into the clinic. So at that point in time, we'd look through the two criteria that we evaluated with Pfizer, the 471 program. Can someone help us go faster and more broadly? And I think that answer will be yes when we get there, but that's the check boxes we'll start to look at.

Okay. You've talked about other early-stage programs, KRAS, BCL6, I think AR-V7. How should we be thinking about those? Because those are further behind. We talk about your more advanced programs now, but should we expect those to have updates over the next 12 months?

Yes. And from a portfolio perspective, we're trying to create a pipeline in this area, right, some targets like AR and ER that are more validated, some undruggables in there like the KRASes in the mix and so on. You should look to see data as we're getting close to the clinic. We haven't seen much reason to provide a lot of specificity around the preclinical programs. We just had a good BCL6 update at ASH showing great degradation program there. So you'll see more as we get closer to the clinic but just haven't felt too compelled to share a lot prior getting to the clinic.

I mean hypothetically, what indications would make most sense for these?

Well, there's a range, right? So, I mean, our first I-O target is APK1 (sic) [ HPK1 ] that's in there for KRAS, some of the same sorts of indications that others are going after. But more specifically, we're looking at G12D and G12V for KRAS, G12C being fairly well drugged these days. BCL6 could be, well, multiple indications in lung and other things. So there's quite a range.

Okay. And maybe in the few minutes that we have, let's just do a quick recap of the prostate cancer update that you have provided a few months back. For people in the audience that aren't familiar, can you just give us a quick, 1-minute review of what you presented?

Yes, absolutely. So we shared at ASCO GU an update on the completed Phase I data as well as an interim look at our Phase II data for bavdegalutamide. And rewinding back almost 1.5 years, we had shown really an interesting signal in a subgroup with a specific point mutation, 878 and 875 in late-stage prostate cancer. And based on that, we had designed a Phase II study to look specifically at that subgroup as well as a broader subgroup. And in the data we showed in February, we had a 46% PSA50 rate in that defined population and 75% without the presence of other mutations. And what we had said going into that update was that if we had at least a 25%-or-so PSA50, we would feel great about going to the FDA and talking about an accelerated approval pathway for bavdegalutamide, something like rucaparib did a couple of years ago in prostate cancer. So that's the present that we're looking at. So the plan now is to start a pivotal study, a single-arm, Phase II, accelerated approval-type study, with bavdegalutamide by the end of the year. That's a narrower population but very well defined. Companies like Foundation already make assays and tests that will help identify those patients. So we feel like it's a very-high-odds opportunity that can then be broadened. So ARV-110 or bavdegalutamide, we expect to have activity outside that subpopulation, too, could use -- look in combination for other late-stage prostate cancer patients, maybe even move to early lines pre NHA. But for now, it's a very clear opportunity in late-line, genetically defined population.

Were you expecting it to be so narrowly defined when you embarked on that study?

There's no reason to think that bavdegalutamide degrades 878 and 875 any better than anything else.

Right.

So the answer is really no, and we still don't think it is. We think of those markers as -- of those mutations as really just marking AR-driven disease. So as you move earlier in lines of care, you'd expect to see more AR-driven disease. So we still see it as a broader opportunity, but the first, most obvious opportunity staring us in the face with a very high response rate is that narrower population. So we'll hit that, but we're also very much planning for broader populations beyond that.

And what kind of planning are you doing for the broader population?

We already have an abiraterone combo study ongoing. It's been ongoing for a while. It could be relevant in the later lines to patients that may not still be driven that way. And then beyond that, looking at the pre-NHA space, that's something we just haven't shared as much on, but that could be relevant monotherapy combo. But the other interesting piece of data that we shared in February was that post NHA, the patients all looked pretty similar from a genetic AR and non-AR mutations perspective, which is good news because it means that every patient post an NHA enza abi and so on could be relevant for raising these markers. And the general -- what's happening in the patients now is they're getting NHA therapies earlier and earlier. So a lot of patients in the castrate-sensitive space are already getting enza or darolutamide or something else, which might make them develop these mutations that bavdegalutamide can have. So that's all good news from our perspective.

Okay. And any guidance on when we can get color on how these studies are running?

Probably, as we get moving into the pivotal studies with bavdegalutamide, at that point, probably a good point for us to share more detail on where else we'll go beyond that space.

Okay. Maybe last question is your current cash balance. And we talked about a lot of programs in the last half hour. Are all of those going to be supported by the cash balance that you have now?

Yes. So we have $1.43 billion of cash based on our first quarter numbers. Our financial guidance is multiple years beyond 2024, and that's on the assumption that we are going as quickly as we possibly can. I mean a couple of key things with respect to the Pfizer deal, right? They're covering half the cost of the program, right? That's important. And they'll also be taking half the profits. We'll be taking the other half of the profits. So we are very fortunate to be in the cash position that we are based on the current market environment. I know that's -- for other companies that are out there, I feel for them. I've been in those situations. But we feel very good about our capital position.

Okay. Great. With that, thank you for presenting today at our conference. And thanks, everybody, for attending. We look forward to the updates from your programs in the second half of the year.

Yes. It'll be an exciting second half of the year. There's no doubt.

Thank you very much for having us.

Yes. Thank you.

Thank you.