All right. Well, well, thanks, thanks so much, everyone, for joining us. I'm Terence Flynn, the U.S. Biopharma analyst here at Morgan Stanley, and we're very pleased to have Arcus with us this afternoon. We have Terry Rosen, the company's CEO, and Jen Jarrett, the company's COO. Thank you both for being here. Before we get started, please see Morgan Stanley's Research Disclosure website at www.morganstanley.com/researchdisclosures. If you have any questions, please reach out to your Morgan Stanley sales representative. Well, again, thank you both for being here. I thought, you know, one, one place we'd start would be just, you know, high level.
Obviously, the Gilead collaboration has been very important for the company as we think about what it's allowed you to do in terms of kind of parallel process opportunities, strength of balance sheet, but then this collaboration was also expanded, you know, a couple months ago into immunology. So maybe just give us the latest perspective on kind of that collaboration and, you know, kind of what the forward looks like from here.
Great. So Gilead's been an awesome collaborator, from day one, and extremely enabling. So when you think about what we're doing as a company and trying to build a long-term independent company, we have a large discovery organization. We have a large development organization. We started from scratch, but now we have four registrational trials, as you said, a number of earlier stage programs, and then, you know, we've also moved into immunology. And so what it's enabled us to do is to continue to build out the late stage programs, execute on those, but not have to cannibalize any of the earlier stage research. So from their standpoint, from day one, we talked about being an R&D engine.
I think it enables that, but at the same time, it doesn't come at the cost of being able to compete when you think about, like, anti-TIGIT, for example, where we're having to go against Merck, primarily, Genentech, other companies that in that late stage that we can do the trials that we should do. The other part of that is it's not only capital. So when you look at Gilead Arcus, we're essentially co-localized. We're, you know, right across the San Mateo Bridge from each other. The human dynamics are great. They've actually got hundreds of people working on the programs. You name a function, not only R&D, but things like even as, you know, call it esoteric, like supply chain. We just work together on everything.
It's broadly enabling, and I would say, you know, expect to see more together.
Yep. What... Then where did immunology come from? I mean, again, some of you might think that's kind of out of left field, so where did the immunology angle-
Yeah, it's actually-
What generated that?
Yeah. So it's actually surprisingly somewhat right down the middle of the fairway as opposed to left field. But I think that is, like at high level, first glance, one might think that. But, a lot of what Arcus does, because it's an immuno-oncology, our biology is immunology. So we've probably got more immunology preclinical work going on, even though it's an oncology clinical, endpoint. And so that's, first off, scientifically what makes sense. When Flavius Martin joined, Gilead as the, you know, head of discovery, we had some past knowledge of each other. My co-founder, Juan Jaen, also knew him well. We got together even before he was officially on board. The dynamics were good.
Although the original way the collaboration was structured really focused on later stage programs, we felt it's always in our best interest to be aligned early on. We started talking about immunology together with Flavius early on, and Gilead, as you know, also had a substantial immunology development group. So that just very organically matured. We said: Why don't we do something together there? Again, towards that end of us being well capitalized to enable the R&D engine, it enabled Gilead to do that with us. And I think one of the advantages that we often talk about, the way that was structured, because we decided to pick those targets together, enables us to have alignment very early.
So the amount of investment that you have to go to, let's say, to get to Opt-In, that we feel like we're on a very good page, to begin with, with all the rest. So it's a very organic process that just has to do with the dynamics of the company that we're interacting all the time at a human level.
Okay, great. I guess just to start going through the pipeline here, obviously, you know, front and center is TIGIT, and again, a lot of data that's come out over the course of this year. You had your Phase 2 data and first- line lung at ASCO, and, you know, I think one of the debates that emerged was just control arm performance. But then since then, we've seen more real world data that started to come out. So maybe just walk us through kind of the key other data points that give you confidence in that control arm performance. And then we'll talk about some of the other competitor data that's come out more recently as well, but maybe just start on the control arm.
Yeah. So I think, you know, one of the stories that's probably just starting to emerge, as you were saying, was that, you know, KEYNOTE-024 and KEYNOTE-042 were probably not real-world studies. And so, actually, at ASCO Plenary, when our data was presented, Solange Peters, who's, you know, one of the SKY-01 PI, she's actually very close to us as well, actually walked through two recent real-world data sets that have been presented, I think, at ESMO IO, one of the big conferences, which showed that in the real world, pembro performs very differently than it did in KEYNOTE-024 and 042.
We actually have a slide that's now on our corporate deck online, where we looked at other studies aside from some from the more contemporary studies related to KEYNOTE-024, 042, where you see the same trend, you know, whether it's how nivo performed in the study that supported the approval on dual mAbs. There was, like, multiple examples of when PD-1 is the control arm and not the experimental arm, it performed differently. So I think that's now very well accepted. I think the other thing that's very well accepted is that at the time, KEYNOTE-024 and 042 were conducted, it was, like, a very different time in the space. There was a lot less competition.
PD-L1 testing then took about three weeks, so you tended to lose all of the rapidly progressing patients, so you ended up with your healthier patients. Now, PD-L1 testing turnarounds are much faster. So for a whole bunch of reasons, we think that you would never be able to replicate the results that Merck then got with KEYNOTE-024 and KEYNOTE-042. So, you know, we feel very good about how Zim has performed. There's no one at Arcus or at Gilead has any doubt that Zim looks just like any other PD-1 antibody. I think the clinical world is very, very comfortable with Zim as a PD-1. And then also as a reminder, like, even if you don't believe all of that, you know, we're always combining Zim with something else, you know, Dom or whatever it is.
And so at the end of the day, if Dom plus Zim beats Pembro, you know, it won't matter. So, you know, we think it's just as good or better than Pembro. But like I said, because we're always using Pembro as a standard of care, so sorry, as a control arm, that's the standard of care. It doesn't really matter what Zim would do on its own.
Okay, and maybe to, to segue into the, the Roche SKY-01 interim OS data that came out, just, you know, reflect on that data in light of what, you know, you're just talking about, Jen, in terms of controlling our performance, but then also what this means in terms of confidence for the, the TIGIT hypothesis.
Yeah. So first of all, you know, I think our confidence in the TIGIT hypothesis has not changed. We have been consistently very confident based on our own data sets. The external world is probably now more confident, like the debate has shifted to, like, is TIGIT active? Is TIGIT gonna work? To, like, you know, do they hit, is it statistically significant or do they just miss? And so, you know, it kind of feels like at this point, the worst case outcome for SKY-01 is that, you know, they end up with a 0.8 hazard ratio, and they need to be at 0.79, or it's 0.79 versus 0.78. So it's a just miss, and we think either way, that's a win-win for us.
You know, either they hit, you know, the whole world is very confident in TIGIT's success, or they just miss and, you know, Roche loses what was probably gonna be its, its only real advantage, which was having a first mover advantage on the market. So, you know, we're excited with the, the Sky One data and the fact that, like, the external world is now even more confident. We actually just had a team that was at World Lung and meeting with a bunch of clinicians there. And, you know, I think a lot of clinicians, once they saw the Sky One data, are also more confident in TIGIT, and that's obviously what we care about, you know, even more than investors. So we feel really good about the setup and continue to be very confident in TIGIT.
I forgot, the other part of your question was,
No, I mean, the real world, I mean, the control-
Oh, in Atezo.
Yeah.
Yeah, so it's just another example-
Right
... of, you know, the control arm performed a little bit differently than when Atezo was the experimental arm in IMpower110. You know, the issue that they have is that they did not use what's considered the standard of care, which is Pembro. So even before this, like, when we were having ad boards 6 or 9 months ago, we were hearing then from clinicians that it was gonna be always hard to interpret their hazard ratio because they weren't using Pembro as a standard of care. They were using Atezo. There is a view that Atezo may be inferior to Pembro. So I think the fact that they did not use Pembro as the standard or comparator arm is gonna end up hurting them from a commercial perspective.
Okay, understood. And then maybe just remind us on your phase 3 lung program in terms of kind of status, enrollment, and timing of data.
Yeah. So, so we have 4 phase 3 studies. 3 of them are in lung. The first study, which is targeting the largest market opportunity within lung, largest one should be of all of our studies, is STAR-121, which is our, all-comer lung, TIGIT plus PD-1 plus chemo combo. So Roche has a similar study, SKY-06, Merck has a, a similar study as well. So we're super excited about that study. It is enrolling well. You know, I'd say that and then STAR-221, which is our first all-comer study in gastric. Those are our, our number one priorities, both us and Gilead, from an execution standpoint. The other 2 lung studies are PACIFIC-8, so that's our study in Stage III lung that AstraZeneca is operationalizing.
So there we're combining TIGIT, our TIGIT antibody, Dom, with Zim, versus Zim. And then the last lung study, her lung study is ARC-10, so that's the equivalent to SKY-01, so that is in the PD-L1 high patient population.
Yeah.
The study that, you know, actually I think could read out first is STAR-221 in gastric, so actually outside lung. So we'll say right now, that and STAR-121 are neck and neck. Those are all-comer studies, so you know, easier to enroll. STAR-121 has a little bit more competition, obviously, because it's in lung versus gastric. But like I said, both the studies are getting a lot of interest and are enrolling well.
Okay.
You know, the one thing I would add to that in the context of anti-TIGIT is Jen was talking about STAR-221. Our next data set in the TIGIT field is going to be, you know, probably later this year, at the latest, very early next year, and that's in exactly the same patient population as STAR-221. So it's a study called EDGE Gastric or ARC-21. It was really designed... That study is enrolled, the phase 3 study is already enrolling very well, but this platform study included the arm that I'm about to talk about, and the idea there was, in certain regions of the world, they wanna see exact combination, exact setting is what you're gonna do in your phase 3.
So this study was designed to do that, and so we're gonna have 40 patients in this exact setting. It we'll break them out by PD-L1 status. You'll see ORR, and you'll see six-month PFS. I think what's also important is that, not only will it give a feel for the depth particular setting, but if you just think about our doublet, there's actually a very contemporary study that BeiGene just presented in the same patient population with their anti-PD-1, their anti-TIGIT. And what you've got there is a very good surrogate for the field, like whether you think about Merck with their anti-PD-1 and anti-TIGIT.
The combination of an anti-PD-1 with an anti-TIGIT Fc-Enabled, and data sets to date have consistently shown that when people report on it, Fc-Enabled anti-tigit deplete Tregs in the periphery, and you see immune-associated AEs. That BeiGene data set, you'll be able to look at the safety data from that set, and you'll have a very contemporary data set, with the only primary difference being, in our case, we have the Fc-Silent Anti-TIGIT. You'll be able to look at the efficacy as much as whatever you feel like you like to do when you look cross-trial comparison, but you'll also see data in the context of the AEs associated with that.
I think it's gonna really reflect not only on that setting, but when you start to think about the competition, and we view our primary competition in the broader field is Merck. When you start to think about Vibo Keytruda versus Dom Zim, and the big difference being the Fc-silent and anti-TIGIT, I think you'll start to see perhaps a foreshadowing of what those differences might be and which might really be the better doublet. Yeah.
Okay, great. Maybe just to go back to this, I want to ask one question on the stats. Are you planning to make any changes to your lung program based on what you saw, or you were already kind of planning for that base?
Yeah. I mean, I don't think we were super surprised by what we saw. You know, we've had our own data set with ARC-7, and, you know, so that certainly informed how we think about stats. So we're always pressure testing our statistical analysis plans and, you know, making sure that we continue to feel good about our stats, as is Gilead. But I think right now, you know, feel very good about our study designs and our statistical analysis plans.
Okay, great. And the other question, again, it relates probably to both indications, is just this question of competing commercially with not just Roche and Merck, but also this issue of co-formulation. And so would love your perspective on that, because that's another question we get pretty frequently is like: All right, it seems like co-formulation is gonna be a lot easier for, you know, centers, physicians, et cetera. Again, you know, I asked Gilead the same question earlier today, but would, you know, welcome your
I'm not sure I do seven. Yeah, it should have been interesting because I think we're all aligned on, you know, but for-
This one is like a lob this time.
We have a lot of discussions about this with them, actually. But, you know, actually, probably two years ago, we did some market research because we were trying to figure out what we wanted to do, if we wanted to do co-form, if we wanted to do just co-admin. And that research showed that clinicians actually prefer having individual agents versus a co-formulation. So they like the idea if you are seeing some AE, you don't necessarily have to withhold two drugs. You could potentially just withhold one of the drugs. Interestingly, also, like, payers particularly don't like co-forms. I mean, they, they're smart, you know, obviously, and they see co-forms for what they are and, you know, the way to get around, patent expiry. So for both those reasons, we decided to go down the path of co-admin.
So what we're gonna be doing is two vials. They will come in the same package, so it'll probably be marketed under one brand name, and then the actual solutions will be mixed into one bag. So you get all the same advantages, the convenience advantages that you would get from the co-form. And what really matters at the end of the day is how long the patient is in the infusion chair. So our goal is to, you know, meet whatever Merck is doing from that perspective. But we have decided to go the co-admin, co-packaging path. We'll continue to keep an eye on co-form, and if all of a sudden we feel like co-form is the way to go, you know, we'll certainly pivot a bit, but right now we feel very strongly that co-admin is the right way for us.
Okay.
Now, I'll make one comment that gets to... You know, we talk about the safety advantage, but the safety advantage can actually translate to efficacy advantages if you're forced to either take patients off or back down in the dose that you're using of your anti-TIGIT because of Treg depletion. So remember that, that, that Treg depletion is an on-target activity, so Fc-Enabled anti-TIGIT, if they're depleting Tregs, that's through direct interaction with TIGIT. So if you back down to avoid that, then you're also risking, whether it's in certain patient populations, certain individual patients. Obviously, you're reducing target engagement, and you could imagine manifestations and so far as efficacy as well.
Okay. Maybe just one more on the lung cancer side before we go back to gastric. Is it... You know, obviously there are multiple mechanisms going forward now in frontline, so you've got, you know, TIGIT, as we just talked about. You have Trop-2, B6A is another one, and so, you know, kind of our view is that there's gonna be a fragmented market more as opposed to now it's just Keytruda's, you know, 80%-90% of the market. And so you think about like evolution of the frontline lung market, what's kind of the take on how that plays out here?
Yeah, we actually think we have the easiest path because we are building upon the standard of care, which is actually much easier to do than trying to displace part of the standard of care. And so that's, you know, I think the primary difference between the Trop-2s and what we're doing. I mean, I think Trop-2, at the end of the day, is going to try to displace chemo. I mean, ADCs obviously, you know, I think still toying around with Trop-2 plus chemo plus PD-1, but that I think looks too toxic. So I think at the end of the day, you know, like Gilead, they're gonna be combining Trop-2 with just PD-1, and they're trying to displace chemo, which I think is a high bar. I mean, I think the Trop-2s are a really, really exciting class, including in lung.
But I think so far, we probably haven't quite seen data that shows that it's better or less toxic than chemo. I do think very strongly that it's gonna have a very significant place in second line. I think that's how you might see the lung cancer market really evolve is, you know, in the past, you kind of had, you know, chemo, and then chemo plus PD-1, and then you had docetaxel second line, and that was it, you know, if you were a patient that didn't have a mutation. So I think what is gonna change is, you know, now you start to have the KRAS inhibitors, so, you know, I think that'll become more and more established for KRAS patients in second line. I think you'll start to see the Trop-2s, other ADCs, used in the second line.
So I think what you'll start to just see is, like, more evolution about sequential therapy in lung, which is something we just really haven't had in the past.
Yeah. Okay. Okay, great. So maybe just going back to the gastric data and this, the EDGE study you're gonna have. So have you talked about a venue yet where we're gonna see that data?
For EDGE-Lung, we have not, but I think-
For EDGE Gastric.
EDGE Gastric, right. We, we haven't said exactly when we're gonna present that data, so our goal is to present the data either by the end of this year or very early next year at the latest.
Okay.
You know, we have a plan in mind, but we haven't disclosed exactly what that plan is yet.
Because we haven't. We basically know what we wanna do, but until we have an accepted abstract, we-
Okay. Got it. Understood. Since you mentioned 40 patients, stratified by PD-1 status, we'll get ORR 6-month PFS. What... Just remind us the relevant benchmark here for Opdivo chemo as we think about, you know, what you guys are trying to look and compare against.
Yeah. So I mean, there's actually, like, 3 studies out there that are all pretty much in line with one another. So the study that you're referencing for Opdivo plus chemo is CheckMate 649. There's also a KEYNOTE study, KEYNOTE-859, and then actually a BeiGene study with RATIONALE 305. And if you look at all of those studies, the highest ORR that you see is 60%, 60%, in the CPS high patients. And then it sort of goes down to 50% for patients that are CPS low. BeiGene was a little bit lower for some reason. So they were, I think, at the high, sorry, low 50s%, in the CPS high patients. And then the PFS ranges, you know, kind of anywhere from 7-8 months. So 8 months is the very highest.
So with that told you, I think, like, anything above 60% ORR would certainly seem like you're adding something. And then I think once you get beyond sort of 7.5 months PFS, you know, that's when it seems like you're adding something to PFS.
Yeah. Okay. Got it. Okay, great. And then maybe just remind us that how to think about the commercial opportunity there. I mean, again, that is one of the, you know, kind of more below the radar cancers where, again-
Yeah, for sure, and it's a huge cancer. I mean, that is something people get a little bit confused by. There's another histology for esophageal cancer, esophageal squamous cell carcinoma, so that's what Roche is pursuing with their SKY, I forget the number now. I think SKY-08.
Okay.
That study is much more prevalent in China and much less prevalent in the US and Western Europe. So the histology that we're looking at, which is the adenocarcinoma histology, is much more prevalent in the US and Western Europe. So there's about 25,000 patients in the US alone. There's 100,000 if you look at,
Mm-hmm
... the US plus other G7 countries. I think just the other day, I figured out what the G7 countries are, but, if anyone wants to know, they can ask us afterwards. But anyway, if you look just at those countries, that translates into a market opportunity worth $3 billion, and then obviously you tack on other countries and it grows from there. So it is a big opportunity. So we like to say, you know what? There's obviously people that wanna believe your market is just gonna take the whole market in lung, which we don't think that's gonna be the case. But let's say you wanna believe that, you know, we're well ahead of anybody in gastric, so we're the only company with a TIGIT antibody that's running a phase 3 study today in gastric. There's also just very little competition from other mechanisms.
The only thing that's really out there that we're obviously keeping an eye on is the Claudin 18.2. That's only like, you know, a small subset of gastric cancer. So it's a huge market opportunity, and it's a market that we could really own for a few years.
Okay, great. Maybe I just wanna move on HIF-2 alpha here. Again, I think, you know, TIGIT, and all the IO work has taken up a lot of the, the focus from investors, but HIF-2 alpha, you know, we've been talking about this for a year now, and you've been excited about it, and I saw some, you know, phase three data from Merck in, in RCC setting. So maybe just remind us kind of the strategy, differentiation, and then kind of next milestone here as we think about this, this asset.
Sure. So this is one, and fortunately, as this SKY-01 overhang disappears, we're getting tons of interest now from investors because this is AB521, which is our HIF-2 inhibitor, is the drug waiting to happen. And so, the differentiator is very simple. The belzutifan is given clinically at a dose of 120 milligrams. The reason at a 120-milligram dose has nothing to do with an MTD, it has nothing to do with modeling. It's simply that it has absorption-limited pharmacokinetics. So if you go above 120 milligrams, you simply don't get a substantially greater drug levels. HIF-2 is a very challenging target to get a small molecule. It's a transcription factor. That's why you don't see a million programs, despite the fact that you have an approved drug.
So you've got a validated mechanism and approved drug, and what we've shown first in healthy volunteers, and now our next data set, which is imminent, imminent will be from our dose escalation study in patients. And what you can expect to see is similar to what we showed in those healthy volunteers, that basically we achieved 3- to 4-fold, so it's not just incremental, 3- to 4-fold, the exposure that Merck gets with our 120 milligram dose. At the go-forward dose that we selected, which is 100 milligrams, there's a very good pharmacodynamic marker that has nothing to do with the anticancer activity, but it's easy to measure. That's if you inhibit HIF-2 in the healthy kidney, you see reductions in EPO levels.
So you'll be able to see pharmacodynamically that we hit and reduce that, same as belzutifan. What they do at their clinically used dose, we can demonstrate at a dose that's roughly 3- to 4-fold lower than that, will similarly show a very similar safety profile. And the next data set that we share will be from that dose escalation study. And while the numbers are small, there are a good number percentage wise of RCC patients, and I think you'll be able to pick out the RCC patients, which starts to bode well for the efficacy piece as well. And so far as what else is happening, we started a dose expansion study in clear cell RCC patients. That's enrolling incredibly well. A start of a combination study with a TKI is imminent.
We haven't shared exactly that partner, but we feel it's gonna offer an advantage of the doublet with a better TKI than the lenvatinib. And our aim there is to be in the phase 3 study by the end of next year.
So the data imminent, I think, you used to talk about maybe this year, more likely next year. So it seems like that's pulled forward a little bit. Is that fair?
That's probably pulled forward potentially a little bit. Like, we're still thinking through exactly when we would present, the data, but yeah, it could be pulled forward a little bit.
Okay. Okay, got it. And the phase three program, maybe just again, what's limiting to starting that? Because you said by end of next year.
Yeah, just time really. You know, just phase 3s take about a 12-month process from beginning to end. So, some of it's time, and some of it is, you know, you need to generate, like, a sufficient amount of safety and efficacy data to support your filings in different countries, so just supporting that data. But, you know, we're, we're being as aggressive as we can, and, you know, we're excited to, you know, continue on this path to get a phase 3 study going by the end of next year.
Remind us, this, Gilead has an option on all these programs, and so-
Yes.
Maybe just remind us, like what, what's the minimum data you have to deliver to them? How does all that stuff work?
Yeah, so for every molecule, it's a little bit different. You know, the idea is that it's supposed to be whatever would be considered clinical proof of concept for that molecule. We actually just went through the process to align with them on what the opt-in trigger would be. So we do know when it's gonna be. It's not tomorrow, but, you know, I'd say it's not, you know, a few years out either. You know, I think it's a very reasonable period of time from now. And we're staying in very close contact with them about the program. So I mean, they still see all the data. You know, anything we would do clinical collaboration-wise, you know, they know about it. They, you know, can have some influence just if they wanna provide advice on study designs or whatever else. So we'll see.
We know they like the mechanism, and, you know, we hope they're there, but, you know, if they decide not to opt-in for some reason, it's also an asset that we'd love to own on our own, or we find another partner or whatever else, so.
So sorry, the opt-in is not standard for every program. You have, you have, like, some discussion about it?
Yeah, it just depends on, you know, a little bit on, like, what you would consider to be clinical proof of concept for that molecule. And so, you know, obviously, like HIF-2 alpha, it's just a little bit different than like, you know, a classic IO molecule. So, you know, I'd say because of that, also, you know, the opt-in triggers relatively soon. So we'll see.
Okay, all right. Sounds promising. Okay, and then the phase 3, so would the phase 3 program differ if Gilead opt in versus if you did it alone, or you think it's pretty boilerplate?
No. Yeah, no.
Pretty standard.
I think it's pretty standard, and yep.
Okay. Would you have to do, like, how would you handle the control arm given, you know, if Merck's already approved, like, how would that work?
It wouldn't be approved by the time we started the phase three.
Okay.
And it's in-
Okay.
Certainly, approved in a lot of countries.
'Cause you only do RC.
Yeah, exactly.
Okay.
Yeah. I think we feel pretty good about, like, what our strategy would be.
Yeah.
We haven't said a whole lot about it, obviously, but-
Yeah.
I think we have a good strategy in place.
Okay, got it. The other... Oh, we only have 20 seconds left. I was just gonna say quemliclustat-
Yeah.
Oh, 20 seconds?
Yeah. Well, quemliclustat is very exciting. So, it's our CD73 inhibitor. We're looking in front line pancreatic cancer. This is a study that's been ongoing for some time. The last patient in, keep in mind, was like end of 2021. We're gonna share very shortly OS data. So we think we have the opportunity to be the first meaningful change potentially in pancreatic cancer therapy in the better part of a decade. Since we only have 20 seconds, we'll just say the gemcitabine data are out there. There's a number of studies. You can tend to think of OS for gemcitabine in the probably 8-10-month range. You can think of FOLFIRINOX, slightly better than that. It tends to be a healthier patient population because it's a more toxic regimen.
We'll have a 120-patient population, 90 of which were randomized to determine whether anti-PD-1 brought any benefits. Anti-PD-1 does not bring any benefits, and what we'll be sharing is the OS data, and we think they're exciting. They look meaningfully different no matter how you cut these historical data and compare gemcitabine, whether you look at patients with liver mets, without liver mets, with pretreatment, without pretreatment, you combine them all together. We look favorable compared to historical gemcitabine on all those fronts, and we think it'll be a very exciting data set, both for that for pancreatic cancer and for the molecule itself and the role it might have in other settings where you're using immunogenic chemotherapy.
Great. Well, thank you so much, Terry, Jen. Really appreciate the time.
Thank you.
Thanks.
Appreciate it. Great.