Arcus Biosciences at Leerink’s Global Healthcare Conference: Strategic Advancements

On Wednesday, 12 March 2025, Arcus Biosciences (NYSE: RCUS) participated in Leerink’s Global Healthcare Conference 2025. The company shared strategic insights into its clinical programs, highlighting both opportunities and challenges. A key development is Gilead’s decision not to co-develop Casdatafan, granting Arcus full ownership of this promising asset.

Key Takeaways

• Arcus retains full ownership of Casdatafan after Gilead opts out of co-development.
• The company is optimistic about its pipeline, particularly Casdatafan and Quemly.
• Arcus is well-capitalized with over $1 billion, supporting multiple program advancements.
• The HIF2 alpha inhibitor Casdatafan is expected to become standard care for RCC patients.
• Arcus differentiates its TIGIT program with an FC-silent approach.

Financial Results

• Arcus is well-capitalized, with over $1 billion in resources, enabling the advancement of its clinical programs and potential commercialization.

Operational Updates

• HIF2 Alpha Inhibitor (Casdatafan):

- Gilead’s decision not to co-develop Casdatafan allows Arcus full ownership.

- The first Phase III study with Casdatafan is about to commence.

- Collaboration with AstraZeneca continues, combining Casdatafan with Volrustomog. More details are expected midyear.

• Anti-TIGIT Program (Domvanalimab):

- The STAR-221 Phase III gastric study is fully enrolled with 1,047 patients.

• CD73 Inhibitor (Quemly):

- A Phase III study in pancreatic cancer has started enrollment and may complete by year-end.

Future Outlook

• Casdatafan:

- Data from the ARC-20 trial, involving Casdatafan and cabozantinib, is anticipated this year.

- A single-agent approval strategy for Casdatafan is being explored to potentially replace TKIs.

• TIGIT Antagonist Program:

- OS data from the EDGE gastric study will be released later this year.

• CD73 Inhibitor:

- A data readout from the Phase III pancreatic cancer study is expected next year.

Q&A Highlights

• Casdatafan Differentiation:

- The company addressed concerns about translating ORR differentiation into survival differences, emphasizing strategic development.

• Cabo Combination:

- Arcus aims to show better outcomes with Casdatafan and cabozantinib compared to individual components.

• TIGIT Concerns:

- Arcus highlighted the advantages of its FC-silent TIGIT approach over FC-enabled antibodies.

• CD73 Confidence:

- Confidence in Quemly’s potential in pancreatic cancer is based on promising data from the ARK8 study.

For more detailed insights, readers are encouraged to refer to the full transcript of the conference call.

Full transcript - Leerink’s Global Healthcare Conference 2025:

Dana Graybosch, Senior Analyst, Leerink Partners: My name is Dana Graybosch. I’m a senior analyst here at Leerink Partners. And I’m excited to welcome Terry and Jen from Arcus to have a thirty minute conversation, which is nearly impossible for the three of us. So we’ll see what we can do. You guys have multiple clinical assets in Phase three.

And so we’ll try to tick through a few of them, starting with Casdata Fan, your HIF2 alpha inhibitor. But maybe before we do that, I’ll just turn it over to Terry just to introduce yourself and just a couple of introductory words about ArQS. Arcus.

Terry Rosen, CEO and Founder, Arcus: Yes. Terry Rosen, CEO and founder of cofounder of Arcus. And I’ll be brief since, as Dana said, it’s hard for us to squeeze in thirty minutes and would like to maximize the questions. But we have two what we consider very near term value drivers, castataphan, our HIF2 inhibitor. We’ll talk a lot about that today, which is getting close to Phase III.

We have, an anti digit program that’s quite evolved. So we have three Phase III studies, two of which we’ll be reading out in the relative near term, one in the very near term, upper GI cancers, that should be re announced sometime in 2026. And then we have a full portfolio of programs, including our CD73 inhibitor, which has just started a Phase III study in pancreatic cancer. We hardly talk about it, but it’s actually a very exciting program. And Arcus is sort of a full company.

We have a very strong discovery group, so what we do is sustainable, and we’re well capitalized with over $1,000,000,000 So all of these programs that we’re talking about, they’re less theoretical in terms of what we’re doing with them, but actually we’re operationalizing all these programs and advancing them and pushing them towards commercialization.

Dana Graybosch, Senior Analyst, Leerink Partners: Awesome. Maybe let’s start with your HIF2 alpha inhibitor, castataphan, because we’re in the thick of early data, which is an exciting time. Recently, Gilead decided not to opt in to co develop Kastatifan. And can you just tell us why you’re excited about keeping full ownership even though they decided not to opt in?

Terry Rosen, CEO and Founder, Arcus: Yeah, it’s truly a transformational event for Arcus. So there’s a number of reasons, to be very excited about having all of the rights to cast data fan. But probably the first is the simplest. It’s the most valuable asset we have. And the reason it’s the most valuable isn’t just the market, but it’s because of the probability of technical success.

So between, an approved drug that hits this target, belzutafan, and our early data, which shows a clear differentiation from belzutafan, it’s about as close to 100% probability of technical success that you could have at this stage. The second thing is it’s going to be a two horse race. So this is a very difficult, target to get a good small molecule. So it’s going to be us and Merck. It’s a very large market, and it’s a market that’s going to expand because it’s going to be driven by duration of therapy and this is a it’s a great mechanism.

And so the final piece is having this 100% and it’s actually two pieces. On one hand, it’s going to enable us to be much more efficient in its development. We’re about to start our first Phase III study with this, but we have a very broad plan. And the second component of that, it gives us a lot more strategic optionality where we own this 100% versus sharing fiftyfifty with Gilead, which has been one of the things about all of our programs. We like to say we’d rather have 50% of a lot than 100% of zero, but this one we feel is 100% of a lot.

Jen, Arcus: And one thing that I would just add to that is we did the clinical collaboration with AstraZeneca. And so to the extent anybody had concerns when the opt in didn’t happen, did Gilead see anything? AstraZeneca has seen all of our data. They’re extremely excited about our clinical collaboration combining Cas with Voluru. They’re putting a lot of resources against that program for competitive reasons.

We haven’t said a lot about what we’re doing, but I think about midyear, we’ll be able to say a lot more. And there’ll be just a lot more information out there about exactly what we’re doing and what exactly AstraZeneca is bringing to the collaboration.

Dana Graybosch, Senior Analyst, Leerink Partners: I think the biggest criticism is that on differentiation, you said it’s clearly differentiated. And I happen to agree, but that will this differentiation translate from ORR into a survival difference? Or may that be sort of modest and indirect comparison? Can you win? Because Merck is already on the market, so there’s several years ahead, you know, based on this indirect survival comparison.

Terry Rosen, CEO and Founder, Arcus: Sure. So, let me address two components. First, just the differentiation and then the when will we win, not if we will win, component of your question. So on the differentiation, I think a lot of times, and it’s probably more investor than investigator driven. There’s always, no matter what you have, there’s more, I’ll call it sometimes a narrative versus reality.

So the data, I think are unequivocal. If you look and compare every endpoint that you can look at, ORR, we’re about 50% better than what you see with belzutefan. And that’s in three different cohorts, and with a more advanced patient population. The rate of primary progression, which is a big liability of belzutifan, it’s about thirty four percent. So thirty four percent of the patients, in that Leitzparko five setting, thirty four, almost a third worse than ever alignments.

The control, don’t make it, to pass the first scan. So that’s one of the biggest Achilles heels that investigators pointed out before we even had our data. We’re about half that, and we’ve demonstrated that in three separate cohorts. So we’re somewhere, in the high teens, fifteen percent to less than twenty percent. And all those patients that make it past their first stand then contribute to median PFS.

And we should think of it the other way around. It’s not only that they’re contributing to meaningful PFS, but they’re benefiting from the drug. So whether they’re stable disease patients or, responders. So we’re likely to end up with a PFS that’s more than double that of belzutifan. So I think unequivocally, we’re doing better than belzutifan.

I think that’s also demonstrated by certain pharmacokinetic data. Maybe we’ll talk about that or pharmacodynamic data. Maybe we’ll talk about that. But the point about beating them also comes down to not only, the molecule, but the combinations and the settings. So really Merck is ahead.

They’re approved in late line and it’s a great proof of concept, but they’re not in earlier lines. We’re going into earlier lines, and we have a very differentiated development strategy. And so we can talk about that, maybe as we go along. But I think, that’s the place where we’ll also win is that we have a development strategy that leverages the advantages of our molecule.

Dana Graybosch, Senior Analyst, Leerink Partners: Is that double PFS spitballing or you guys model it? And so that’s, that’s simulated. You could hit that.

Terry Rosen, CEO and Founder, Arcus: No. So as we sit right now, we have one cohort that had a median PFS of 9.7 versus belzutifan’s five point six months. We have another cohort that isn’t quite as mature where we’ve, actually taken and combined those two cohorts together to get to sixty patients. If you look at the PFS now, it would come in over thirteen months. And if you look at our one hundred milligram cohort where we’ve had more early responders, you look at the spider plots, it’s clear that it’s going to end up in double digit PFS.

So my guess is that the number actually comes up more than, 2x that of belzutifan by the time it’s done. Go ahead. Yes.

Jen, Arcus: And Justin, I know you’re going to get to Keymaker, UO3B, but that was another very recent belzutifan data set. It was a Phase one, two study. So to the extent people have any concerns about us comparing our data to LightSpark O5, which is a Phase three study. But in that Phase one, two study, as you know, balsutifan showed almost exactly the same numbers, if not maybe a little bit worse than what they showed in LightSpark O5. Five.

So that was a 19% ORR and a PFS of five point four months. So even more contemporary data set, very similar patient population to what we’re enrolling in our 20, and again, numbers that are well below what we’ve been showing in our

Terry Rosen, CEO and Founder, Arcus: The interesting thing actually, speaking of, the patient population is that if you look at the demographics in all three of the cohorts that I was discussing when I was synthesizing those numbers, we have about twenty five percent of our patients, that wouldn’t have even been eligible for LightSpark O5 in a more advanced patient population.

Dana Graybosch, Senior Analyst, Leerink Partners: Got it. Maybe the most important question for anybody following you closely is we’re going to have the first outcomes this year from your CASP plus cabozantinib combination from ARC20, from proof of concept, because that’s the first combination that you’re taking into Phase three. So you’ve said that you’ve submitted for an upcoming conference. I wonder if you could talk about given the size and the maturity of the data, what bar in outcomes do you think support your differentiation thesis?

Terry Rosen, CEO and Founder, Arcus: Sure. So I think the best way to think about it at this point, if you look at Cabo data, there’s a number of studies. So in and they’re all somewhat different. And the reason they’re somewhat different tends to be, the patient demographics. But interestingly enough, there is a Cabo Bells, dataset out there where you see an ORR of just over 30% and, medium PFS, I think, of on the order of thirteen months or so.

When you look at our data, I think the way you really want to think about it is our data are going to look better than Cabo alone and they’re going to look better than CAS alone. Keep in mind that, this is a very early data set. So this study was done primarily to support the safety of the combination. But we will have enough efficacy data that I think you’re going to be able to see quite clearly that it’s looking better than either of those individual components.

Dana Graybosch, Senior Analyst, Leerink Partners: Why isn’t the bar Merck’s initial combo of BEL plus lamvatinib?

Jen, Arcus: Yes. Just those are two different agents, the fact that they’re combining with lamvatinib. And what they did see was a bit of a higher ORR, but they also saw a lower PFS, which is pretty consistent with what we’ve seen in LENVA in different studies. You know, LINVA is a more toxic agent than cabo. And so, you know, we believe that, you know, you can probably juice up the ORR by giving the higher doses of LENVA.

It’s available in like six or seven different dosages, but then it comes back to bite you a little bit on PFS. So if you look at Bell’s LENVA versus Bell’s Cabo, there’s about a two point five month difference in PFS that we’re seeing in those different combinations. So Bells Cabo had a PFS of about thirteen point five percent and then Bells LENVA in that Keymaker study was, I think, a little under eleven point five

Terry Rosen, CEO and Founder, Arcus: percent. No. One thing I think is a good place to frame what we were talking about earlier in terms of the development strategy. So I think it’s interesting because we kind of get questions on both end of this. And I think if you put it together, it comes together well.

So LENVA, clearly, if you talk to the investigator community, it’s probably the most disfavored PKI out there. And in fact, Merck chose because they own the rights to Lenva. It’s a self inflicted decision. They, ran their initial Phase III study that’s ongoing. It’s LENVA, BELLS versus CABO.

And in that investigator community, CABO is just dramatically preferred over LENVA for the reasons that Jen was talking about. It’s, not as well understood best way to dose it. It’s more toxic. There’s more, patients having to discontinue, etcetera, etcetera. But then we often get asked the question, well, but Merck is, talking about doing studies with Zanza.

Now the two things tell you something, and people shouldn’t have cognitive dissonance about this. The fact that they’re starting something with Zanza sort of negates the thing, oh, you’re so far behind Merck. If they’re gonna be doing something starting our KABO combination, you know, in the first half of this year. We’re on full speed ahead to do that. There’s strong, you know, tailwinds.

The investigators love it, etcetera. And Zanza is clearly, again, a molecule that has been very little is known about it in the RCC context. So clearly, Merck, if they’re moving away from Zanza, sees the same thing that everybody else sees. If they’re going to another TKI, it’s telling you that Zanza is not the preferred combination.

Dana Graybosch, Senior Analyst, Leerink Partners: You mean, Lenda.

Terry Rosen, CEO and Founder, Arcus: Lenda is not the preferred combination.

Dana Graybosch, Senior Analyst, Leerink Partners: Let’s talk more about development strategy. Let’s first, we’ve been talking about the TKI, but there’s a couple other elements of your development strategy. There is where you’re going to do single agent and then there’s your frontline combination and partnership with AstraZeneca. So let’s talk about that one first because you’re going to do a proof of concept study combining with their CTLA-four bispecific for Rustamog. And we have some experience of trying to combine with IPI CTLA-four in the front line, COSMIC three thirteen, which was CaboNivo IPI versus Nivo IPI was pretty disappointing.

It had a PFS benefit, but nothing on OS. So why is this strategy to go with forrestimorgancast going to be different?

Jen, Arcus: Yeah. I mean, you actually got to exactly why AstraZeneca was interested in that combination. So, you know, in the COSMIC study, in the overall survival data was just presented at ASCO G. I know you saw that. But, you know, it was interesting to discuss in presentation what they really honed in on was the toxicity of those two mechanisms in combination.

And that’s what they were getting to as to why they did not hit on overall survival. AstraZeneca actually did think about it and actually did combine Volru with the TKI and also saw a lot of toxicity. So that’s exactly why they were very interested in combining with the HIF2 alpha inhibitor and specifically CAST because CAST has had that lower incidence of primary progressive disease. So PD-one CTLA-four is, if it works, it works very, very well and it can be a cure for patients. But for some reason, twenty five percent of patients do not respond to ipinivo and just progress right through therapy.

And so one of the really appealing things about CAST or AstraZeneca was we do have this very low incidence of primary progressive disease relative to belzutifan. So it made it, we think, the ideal HIT-two alpha inhibitor to be combining with. But as I said, PD-one CTLA4 plus the TKI is just too toxic, especially in that first line setting. But that’s exactly why PDUN CTLA4 plus HIT2 alpha inhibitors should make a lot of sense because the toxicity profile is so much more benign for HIT2 alpha versus TKI.

Terry Rosen, CEO and Founder, Arcus: No, Dana, I think the thing that this also illustrates is what probably will end up being a big shift in, for those who aren’t overly familiar with the clear cell RCC space, the thing about HIF2 alpha inhibition is it’s an extraordinarily safe mechanism for an anticancer agent. So the only AEs really are on mechanism in their Anemia, which is very well managed and as well as occasionally hypoxia, which is also, well managed. And so what you’re going to see a shift, we think every single patient that gets clear cell RCC in the life cycle of their treatment is going to get a HIF2 alpha inhibitor. But this is the part where the Merck molecule demonstrated great proof of concept in late line and is doing quite well there. But we think that what’s going to happen is HIF2 alpha inhibition is going to move up in the lines of in the line of treatment.

And what you’re going to see is that, physicians would like to hold off as long as possible before they have to give the TKI for just what Jen was saying because of the toxicity. And the HIF2 alpha inhibition really looks good for moving into the earlier line of therapy. And what I’ll contrast, belzutafan and casadaptafan is that in going into that early line of therapy, that limitation of that high rate of primary progression is something that physicians hate to be giving early line patients. So they really don’t wanna do that. Have a third of the patients that don’t even make it to a scan.

And so that’s where we see another advantage as you move this into earlier lines of therapy. And the point that I would also make, I think is really critical, is we spend a lot of time and I think it’s going to start to shift as the year goes along and we put out more and more data that it’s not only that, castatofan looks better than belzutafan, castatofan looks better than TKI monotherapy. So the idea of moving castatofan earlier in the treatment paradigm is well supported by its profile to date.

Dana Graybosch, Senior Analyst, Leerink Partners: Can you talk about your strategy to have Cas approved as a single agent and how that’s different?

Jen, Arcus: Yes. So we haven’t said anything about a registrational strategy for CAS mono, but, yes, we have some different ideas. We also just added some new arms to Arc20 that’s looking at CAS mono. So there’s one arm that’s evaluating CAS mono. Sorry, Cas plus PD-one, so not Cas mono, but Cas plus PD-one first line all comers.

But then there’s a Cas mono arm that’s evaluating favorable risk patients. So that’s about a third of the first line patient population. And then there’s another Cas mono arm that’s looking at patients that have had one prior line of therapy. So to Terry’s point, that is the arm that’s really looking at can we displace TKIs because we’re evaluating specifically in the setting where you’d expect to be using a TKI mono therapy. So we’ll look at that data and continue to think about, like, what kind of CAST monotherapy strategy might make sense.

In a minimum, we think these cohorts, if we’re going to continue to expand upon them, could support an NCCN guideline inclusion. We’re already hearing anecdotes about belzutafan moving up interestingly, which speaks a little bit to Terry’s point. So if you talk to MD Anderson, kind of very consistent with what Terry was saying, they start basically every patient does get PYCDLA-four on a TKI. And instead of going to another TKI after, they really want to give patients a TKI break. And so they are using belzutafan in second line, even though I think most places are probably preserving belzutafan for third line.

So that’s the type of setting that we would love to be able to evaluate CAS mono in. And that’s exactly what we’re looking at in our 20 with that new cohort.

Dana Graybosch, Senior Analyst, Leerink Partners: Did you ever consider adding CAS Arm to PEAK1?

Jen, Arcus: It’s funny that someone else brought that up, and we have thought about it a little bit. Yes, I think it’s probably too late at this point. And really the primary objective of PEAK1 is to get it enrolled as quickly as possible. So if you have another army, it’s just more patience and more time. We think right now we have a really well designed study that’s teed up to enroll very, very quickly.

So we just want to get it going and get it enrolled. But we are thinking a lot about what a peak mono I’m sorry, what a CAS mono strategy might look like.

Dana Graybosch, Senior Analyst, Leerink Partners: So I want to spend a few minutes on your other programs in Phase three. So you have Dom Van Alim, Dom, say Dom, your TIGIT antagonist. And so I guess the pressing question here is why should any investor believe in Tigit after Merck and Roche’s failures? I know there’s an FC difference, but a lot of investors are, look, the simplest explanation is TIGIT just doesn’t work that well.

Terry Rosen, CEO and Founder, Arcus: Yes. I think the that investor thesis and, you know, not trying to kidnap anybody into believing something they don’t want to believe, but if you’re a data driven person, what you have to recognize is that FC difference in this particular case is not some subtle difference. There’s, you know, in one case, you get dramatic, and it is, it’s probably above 80% depletion of peripheral Tregs with, an FC enabled anti digit like Merckhead, with Vivo, Velrole Vivo. And what that leads to is immune AEs. If you deplete 80% of your Tregs, you’re going to see immune AEs.

And in Merck’s case, they were being cute. They did a co formulation to extend the life of Keytruda and they put it in the same bag. And so patients have to come off of both drugs. So they end up seeing a lot of immune AEs in the study arm, and that leads to withdrawals and discontinuations and loss of efficacy. On the other hand and by the way, just yesterday, if you want to look at proof of concept between us and AstraZeneca, so AstraZeneca has a bispecific anti TIGIT, anti PD-one where the anti TIGIT is also FC silent.

The the these FC silent anti TIGITs are extraordinarily clean. Everything that’s going on is going on in the tumor. They just started their eighth registrational study yesterday and that they started one in high PD L1, non small cell lung. And essentially what we were doing in ARC, ten, which we, you know, we kind of gave them the proof of concept data, there. But you have between us and AstraZeneca, we’ve run five studies.

They’ve all been positive. You know, our ARC ten data is a randomized data set. It’s in high PD L1 non small cell lung. It has a hazard ratio of zero point six four for OS. That’s with two years of follow-up with anti PD one having an OS of over two years.

Our upper GI gastric study, we showed a median PFS in the phase two correlate that’s called EDGE gastric of over twelve months where standard of care, EVO chemo or also KEYTRUDA chemo or TSLA chemo show about seven months. We’ll be sharing OS from, that same study, later this year. We have publicly said that at eighteen months of follow-up, over fifty percent of the patients were still on study. So keep in mind, the standard of care there has an OS of about twelve to thirteen months. Our PFS was in that range.

In that study, the Phase III correlate, which is called STAR-two 21, was fully enrolled as of June of last year with ten forty seven patients. And you can do the math. The standard of care, it’s twelve months, so we’ll be out at eighteen months since the last patient in by the end of this year. So there’s a ton of data in the anti TIGIT field. And what you should be thinking, if you want to get convinced, you want to get convinced in time, is that in this particular field, FC enabled versus FC silent, you should almost think of them as a different mechanism.

In one case, you’ve got a blocking antibody where the biology totally supports the role of anti TIGIT as a checkpoint enhancing the activity of anti PD-one. And in the case of the FC enabled anti TIGIT, you have something that’s going around and basically chewing up cells that have TIGIT on them, and that’s a dramatically different mechanism that leads to dramatically different outcomes.

Dana Graybosch, Senior Analyst, Leerink Partners: In the last three minutes, let’s talk about CD73 and adenosine, perhaps. Just a quick question. You said you started to enroll your Phase III in pancreatic with Quembley, your CD73. I know that those could enroll and read out pretty rapidly. So sort of what’s the timing on that?

And then also just that’s another one that you sort of wholly own, although Gilead used to be partnered and then you’re taking that Phase three out yourself. So I just wonder if you could help us with why you’re so confident there.

Terry Rosen, CEO and Founder, Arcus: Yes. So our confidence stems from the study we ran called ARK8, where we saw an OS of on the order sixteen months, pretty unprecedented in pancreatic cancer. We also had a synthetic control arm that was well matched, that showed that advantage not only in it showed in basically every demographic we looked at in subpopulation. So it’s a great data set, well matched synthetic control. And to your point, while we haven’t given any guidance yet, you are absolutely right in terms of the enrollment.

It’s even though it’s only been running for a month, we feel like this is one that could probably even be fully enrolled by the end of this year. It’s obviously a big extrapolation. I wouldn’t give that as guidance. But given how fast it’s already enrolling and we hit the ground running, investigator enthusiasm is enormous. There’s been an IST, that’s sort of looking at even earlier line that has very positive data.

The surgeon’s been very positive. So it’s looking extraordinarily promising. I don’t know. Would you add anything to that, Jen?

Jen, Arcus: Yes. No. Just yes, the study will enroll very, very quickly. I know RevMed was making comments yesterday or two days ago about their study and how quickly it’s going to roll. I think ours, based on what we’re seeing so far, will be very, very similar and, you know, we’ll probably roll well ahead of schedule.

And so, you know, that is data that will probably now come into next year. Just to your point, unfortunately, OS is not long in that patient population. So given how fast we expect the study to now enroll and just the fact that OS is not particularly long, that would be a readout that would happen next year. And to Terry’s point, and I think you were the one that probably first saw the presentation ACR IO, but we are doing a very interesting IST was at Wayne Berg at UCLA, where he is looking at Quemly, plus ZEM, plus chemo in the neoadjuvant setting. The data has not been publicly presented.

But when he compared that data to what he has seen historically in that patient population, it was very, very interesting. He’s now going to expand that study out of control arm. You saw some of the biomarker data that was generated from that study. So we just think of that as more evidence that, you know, Quemly is definitely doing something pretty profound in this disease.

Terry Rosen, CEO and Founder, Arcus: I’ll say in our remaining minus fourteen seconds that, the one other piece that enhances confidence is we do have biomarker data from ARCH8, which was the progenitor study, to the registrational study. And in fact, what’s nice about the biomarker data is you have a couple of markers that are actually negative prognostics and those were the patient that did better in the study. So the patients that would have been expected to perform more poorly actually did better on treatment. And both of those markers that we are talking about are correlative with enhanced adenosine activity.

Dana Graybosch, Senior Analyst, Leerink Partners: So it’s on target. Correct. And negative prognostic and you flip it?

Terry Rosen, CEO and Founder, Arcus: Right.

Jen, Arcus: Which is

Terry Rosen, CEO and Founder, Arcus: Yes. That’s pretty positive when you have those sorts of data.

Dana Graybosch, Senior Analyst, Leerink Partners: Awesome. Thank you. We got

Terry Rosen, CEO and Founder, Arcus: Thank you. I appreciate it.

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