All right, everyone, we'll get started with our next fireside discussion. My name is Derek Archila. I'm one of the senior biotech analysts here at Wells. Very excited to have with us AnaptysBio, and from the company, we have Dan Vega, the Chief Executive Officer. So Dan, thanks so much for joining us.
Thank you, Derek. Good to see you.
Awesome. Maybe just at a high level, just start us off in terms of, you know, what you guys are all about, what you're working on, and then we can dig into the specifics here.
Yeah. So, exciting times for Anaptys. We have two lead therapeutic antibodies in development right now, mid-stage development. One targets the co-inhibitory receptor BTLA, second targets the co-inhibitory receptor PD-1 on immune cells. Two things, you know, one is best-in-class potency. Both these drugs have the potential to drive broad immunological outcomes. Second is we have phase II-B readouts upcoming, both of them within the first six months or the next six months. We have two other programs, two other antibodies that will be in clinical development headed into 2025. We have approximately $500 million of cash out of Q2 pro forma for the recent capital raise that we had done. So a lot going on in the company. Gonna be exciting next, one to two years.
Yeah, maybe just, you know, at a high level, too also, just in terms of the role of, you know, checkpoint agonists in autoimmune, just, you know, a little background about, you know, kind of the rationale there and ultimately, you know, why PD-1 and BTLA as the targets that you're going after.
Yeah. So we're focused in autoimmune diseases, but the next level down from that is there are diseases where the patient population is made up of a heterogeneous subset or disease, where you're seeing systemic impact. So there's disease initiating or proliferating in the periphery, in the blood, as well as in the inflamed tissue. And the idea with the checkpoint agonists, when you level that up as well, is we are taking a top-down approach, interacting directly with the cells, the activated immune cells in these diseases that are driving disease. And that's measurable. You can measure BTLA, you can measure PD-1 activity within tissue, within these diseases.
And so, the idea here is that there's modestly low efficacy bars in these diseases because the types of antibodies or small molecules that are targeting them are very specific, too specific than the breadth that we think is needed. And so the agonists, we're hitting multiple types of effector T cells. In the case of PD-1, it's highly specific to T cells that are activated. For BTLA, we also see expression in disease on dendritic cells and B cells, so that opens up a pretty big opportunity of where we can focus.
Got it. So maybe we'll start with rosnilimab and the PD-1. So I guess, you know, maybe you can share a little bit more about some of the preclinical data you guys have generated, and also, you know, there's a competing program that's generated some early data. So what has that really kind of informed for your program?
Yeah. So I actually almost just led into this.
Okay.
So in rheumatoid arthritis and ulcerative colitis, it's the two trials that we have ongoing in phase II for rosnilimab, a PD-1 agonist. There's almost a precedent to some degree here, where, like I mentioned, you could measure PD-1 expression in this disease. In a healthy individual, 15% of T cells are activated that would therefore present PD-1, and single digits would be PD-1 high activated T cells, so a high density expression of PD-1 on these in the activated state. Less than 15% in healthy. If you have moderate to severe RA, approximately 80% of the T cells in the synovium are PD-1 activated, half of those are PD-1 high activated. There's a lot of substrate there to interact with, with an on-point specific mechanism like a PD-1 agonist. We see that in RA.
In ulcerative colitis, approximately 40% of the T cells in the lamina propria, which is the tissue that's inflamed in the colon, that drives UC. So that's a starting point. What we've shown, preclinically, in vitro models is a decrease of the cytokines that have been known to be expressed in these diseases. In ulcerative colitis, there's literature of animal models that correlate reduction of PD-1 high T cells to remission, clinical remission in disease. We see an imbalance of PD-1 and PD-L1, the natural ligand in these diseases. So there's lots of different ways to come at measurement.
You mentioned, Eli Lilly's phase II program that's also in RA with their, their PD-1 program. They did show best-in-disease efficacy almost a couple of years ago now in their phase II-a study, that was presented at ACR. They're setting a new bar that looks not just best biologic, but, the data they showed was even better than the JAKs in a second line setting. So exciting proof of concept in that disease with a less potent program relative to ours.
Got it. Yeah, maybe we can talk about some of the differentiating features of rosnilimab versus peresolimab, and then also Gilead's, you know, PD-1 in terms of just, you know, how you thought through, you know, the actual antibody, you know, construction.
Yeah. So Anaptys, we're on year nineteen as a company. We've been developing antibodies for quite some time. We have a PD-1 antagonist that GSK sells now, called Jemperli. It's the best-in-class PD-1 agonist or antagonist. We've been doing this for a long time. We're not on generation one PD agonism today.
We have multiple iterations of programs through the life cycle of this company. We say often that we have a more potent antibody than Eli Lilly. There's a framework that we're on record for what drives that potency difference. Some of that has to do with where you bind on the actual, the PD-1 receptor, the binding epitope. Some of that has to do with how you engage with the Fc presentation on the other end. So there's a framework there. We're clearly differentiated in what that looks like with Lilly and Gilead. The outcome of this, to give some data around it, Lilly presented translational data from their arthritis study, showing a 60% depletion or reduction in PD-1 high T cells in the periphery and RA.
We've shown in multiple trials, 90% reductions of those PD-1 high T cells, so that's a direct outcome of a more potent molecule. We've made their drug, we've made Gilead's drug, and we see a consistency of that delta in our hands in vitro. So there's reason to believe here that potency, we know, drives broader immunological outcomes, and we think that'll translate into clinical differentiation.
Got it. And maybe can you just talk about, maybe as a class, but also for rosnilimab itself, what's the safety profile look like thus far? And I guess, you know, relative to other RA treatments and maybe even UC treatments, I mean, where, where do you think this will play?
The data in the agonist class, whether it's BTLA, PD-1, whether it's Gilead, Lilly, J&J, ourselves, to date, there's a benign AE profile. We often reference Amgen's OX40 depleter, so that's again, interacting directly with T cells. OX40 is heavily expressed on T regs. 50%-75% T regs express OX40. Amgen's molecule is depleting those. Amgen saw, at least in their phase II-A or phase II studies, flu-like symptoms that were moderate to severe. We haven't seen anything like that. We're much more specific in where we're depleting. PD-1 is expressed maybe in less than 5% of T regs, is what the literature suggests. So differentiation there. On the flip side, our preclinical data, our phase I data for both our drugs, no suggestion of a cytotoxicity, nothing required from the FDA.
To date, things look clean. Our studies in RA and AD are really far through for PD-1 and BTLA, and nothing on a kinda aggregate blinded surveillance is presenting as severe at this point in time.
Got it. And so maybe just in terms of the phase II trial design, you know, for rosnilimab and RA, I guess, can you just give us some color on, you know, how that compares to other trials, in particular, obviously, the Lilly trial? You know, are we talking about very similar patient populations, endpoints, timelines, all that sort of stuff?
Yeah. Our phase II-B trial, it's designed to enroll 420 patients, three active arms versus placebo. The active arms will be either every other week or monthly dosing. In terms of inclusion, exclusion criteria, these are moderate to severe patients. There's nothing unique there. For design, driven by the FDA, it's standard 12-week, three-month endpoint. The rheumatology division of the FDA requires that. Our study, if you've hit low disease activity, defined by the CDAI scale of less than or equal to 10 at week 12... I'm sorry, at week 14, after the primary endpoint, you will be able to stay on drug through month 6 and continue receiving drug, and what we'll be looking for is stability of response.
If you have not responded at that point in time on drug or all placebo, patients have to exit the study. This is required, again, by the Rheumatology Division to run the trial this way. What we won't be able to see is would we have gotten incremental responses after month three if you had not hit that low disease activity. However, Lilly's trial, given they've already run a phase II-A, they have a placebo crossover at three months, so it's a 500-patient trial. Again, there's multiple active arms versus placebo, so from month three to month six, what we're going to be looking for there is not just stability of outcomes, which they did show in phase II-A, but also incremental response potential.
Their trial goes on beyond that, from month six to month 12 or week 60, so I guess month 14. They're doing monthly or every three-month dosing. So they're going to have a longer-term tail. We will be looking at that. We have a more potent response at 12 weeks. We'll look to leverage class effect of how stability, incremental response, and potentially, off-drug periods and stability longer term, would translate into phase III design.
So what do you think the bogey is on efficacy for this class? Like, again, just... or just for a new mechanism in RA.
We're talking about a second-line, third-line market, right? Like, TNF are generic. We're seeing the erosion in that market. However, in the second-line plus setting, 500,000 patients exist there today. That's a $10 billion U.S. market on its own, post TNF. So that's the market we're looking to play in, the second and third line. There is increasing share with Rinvoq, one of the JAKs, which does have all the AE baggage that JAKs are associated with, and we should be able to look to seek label that sits in front of the JAKs relative to the other biologics. ACR20 is the regulatory endpoint. What's going to matter commercially here are deeper responses, and that's consistent with what I was saying earlier in all the diseases that we're looking at. So deeper responses, ACR50, ACR70, some benchmarks.
Doesn't matter what class of biologic we've seen, IL-6, rituximab, you're seeing 20% ACR 50s plus or minus across those classes. The JAKs are into the low-mid 30s%. So if you have a biologic that's approaching JAK-like efficacy, but without the AEs associated with the JAKs, that is a second line player, second, third line player, where we could see significant share as a class. Eli Lilly, at 14 weeks in phase II-A, had 57% ACR50. So I was mentioning earlier-
Yeah.
You do not need to be anywhere near that. We all have much more robust studies in the phase II-B's, so if we're anywhere near the JAKs as a class, that's something that'll, that'll play. And ironically, here, that's a payer definition. If you go talk to a rheumatologist, all they want is another class. They just need something that looks like another biologic, so the demand is going to be there on the doctor side, the reimbursement will be there if you get a biologic that looks like a JAK.
Got it, and then maybe on the UC side, so it seems like, you know, here you might be more ahead of the pack in terms of the timing, but, again, just in terms of that trial and the design, you know, what patient population are you really focused on there? And I guess, how does it compare to some of the more recent trials that we've seen?
Yeah. We've started a trial in colitis, coming into this year. Our guidance is Q1 2026 readout, 130 patients, two active arms versus placebo. We'll be looking at every other week and monthly dosing in that trial. Our endpoint to what we're all looking at is clinical remission. I think similar you see with the JAKs, you know, into the 30% range for the all-comer population, and then specifically with severe patients, clinical remission, the TL1As, other classes are somewhere in the mid-high 20s on an absolute basis. There's a lot of talk about placebo rates here, no different than in AD.
One of the major things that's going to matter for any trial moving forward is ensuring that via an endoscopy, that you have real moderate or severe patients in this trial, that you don't have these marginal patients squeaking in into trials. Having local reads as well as matching up with central reads as inclusion criteria in your screening is critical in running trials. There's differences historically on doing this robustly over time, that's correlated to placebo outcomes. We're not guiding to where we're going to be yet. I think we're going to reserve that for post our RA data coming up. But, generally speaking, these other drugs are in the high twenties, into the thirties. There's a lot of uptake on things that are not yet approved in that range. That's expected. So something there or better, but we'll get more specific as we end of 2025.
Got it. So, and you're in UC right now, but would you look to do Crohn's as well? Does it make sense, you know, biologically also to pursue that?
I think there's a natural progression-
Yeah
... to folks looking at Crohn's disease after UC. Not every drug that works in UC works in Crohn's. Ulcerative colitis is a focused inflammation in the colon, in the lamina propria I mentioned earlier. Crohn's is more ubiquitous, even outside of the colon and through the digestive tract. I mentioned earlier that systemic implications matter in how we're thinking about these diseases. Activated T-cells in the periphery, in UC, are twofold increase than what you'd see in a healthy individual. So we are looking for correlations and having impact in the blood. One of the interesting things, alpha-4 beta-7s, the way they work is prevent trafficking from the blood of T-cells into the colon. We should be depleting those, which by definition are the PD-1 high T-cells.
They're TPH cells, a specific subclass. So we know they're there. We know they're there twice as often in what is normally pretty small. We should be depleting them, no different than alpha-4 beta-7 would bind to and prevent the trafficking in. That's just one of the mechanisms of action of our drug in UC. The other is directly impacting the T cells that are activated in the gut, which is where things like TL1As would be at working.
Got it.
There's different ways in which we think that we're going to be driving and potentially improving outcomes in this disease. There's proof of concept points that are doing one or the other, but not both.
Got it. Yeah, maybe shift gears to the BTLA program. So obviously, big readout for you, internally in the fourth quarter. Yeah, maybe just tee that up in terms of, like, the trial design there, and also just kind of your view in the potential efficacy in, you know, kind of Dupixent experienced patients and, and why that's important.
Yeah. Dupi was game-changing at the time in this disease. Th2 pathway impacting IL-13, IL-4 secretion of cytokines or blocking of those cytokines. What you're seeing with Dupi and everything else that's Th2 only pathway driven are 50% plus or minus responses on EASI-75. That's okay for some patients. Patients stay on these drugs because there's no better alternative to move to. The reason for this is, again, it's a heterogeneous disease. Th1, Th17, Th22 effector T cells, drive cytokine activity that perpetuate the inflammatory state that's causing the inflammation of the skin. What the OX40 ligand class did with, I think, moderate efficacy that looks like Dupi over time was show...
So it's an important proof of concept for us, was to show that hitting a broader pathways, not as hard as the IL-thirteens hit in Th2, so less than that, but broader, you get to the similar efficacy. BTLA, the mechanism of action here, does all that and more. The OX40, OX40 ligands, it's not clear that they're impacting the Th1 pathway. BTLA is on Th1 cells. We show a significant reduction in interferon gamma. We think that's gonna drive disease. BTLA is also on dendritic cells, like I was saying earlier, which is one of the differentiating properties versus PD-1. Conventional dendritic cells are a tenfold increase in inflamed skin.
We're modulating those dendritic cells directly, reducing antigen presentation and costimulatory receptor presentation by more than 50%, so things like OX40 ligand, CD40, CD80 are being reduced. So the reason I'm taking you through this is, this disease, and to get materially different step-ups in efficacy, are gonna happen from hitting it in a broader way than just Th2. People talk a lot about combinations. We should be seeing a broad outcome just from one drug with this mechanism of action. So thank you for bearing with me on this. That's the background for why we designed our phase II proof of concept trial with a 15% of the patients have Dupi experience coming to the trial, so it's almost like a phase Ia within the broader phase II-B trial.
We're looking for a signal in Dupi-experienced patients that looks like what OX40 ligands did, 40% EASI-75, or what Dupi did, 50% EASI-75, in the frontline setting. We're looking to see that type of signal in a second-line setting and have the frontline patients that we're treating, which is up to 200, in the overall study, we over-enrolled the study, a consistency in the front line. That profile opens up what's going to emerge as a greater than $10 billion market in the U.S. in the second-line setting. It's a huge market opportunity. Our competition are things like the OX40 ligand, and there's reason to believe that we're gonna have a deeper and broader response profile than those drugs.
Secondly, it's an upside, but it's a realistic potential to have this upside, is to have something in the order of 60% or higher on EASI-75. It's gonna require something like that to have any material frontline share in a kind of saturated IL-13 market by the time we'd be out there. Dupi will be on the market for greater than a decade. So we're looking for something north of EASI-75 to 60%, and then the second component there is a durable profile. We do think that this approach can modify disease. Our trial is designed where it's a 12-week dosing, week 14 primary endpoint, so we'll take a read there, and then we're gonna be observing patients for a 6-month off-drug period. We're gonna be looking for a consistency of patients in response for 6 months. Just...
Just to put some perspective on this, if you're on Dupi and you come off drug, half those patients will be back to baseline between month three and month six. Half. If you come off of a JAK, three months in, almost all patients are back to baseline. There's a lot of literature on this. The OX40 ligand class, 80% of patients were consistent in disease out six months off drug. So that's game-changing in terms of disease modification, but with modest efficacy. So if we can have better efficacy and that type of profile, those are all upsides to a, kind of a second-line story that I think is a big opportunity on its own.
Got it. You know, one of the questions we get asked often is around, you know, Lilly's former BTLA program that was, you know, essentially killed. I believe it was mostly for the efficacy component versus safety, but can you just walk us through why that, you know, doesn't hurt the case for BTLA?
Yep. So Eli Lilly had a BTLA program. I hesitate calling it a BTLA agonist. They chose SLE as a indication to move into as proof of concept. That's rational. Mentioned earlier, BTLA is on B cells. SLE is known to be a B cell-driven disease. So we agree that that's interesting, but it's a challenging disease. There's a lot more happening than just B cell activity that drives disease there. We custom picked AD as a proof of concept, given what I walked through earlier. So we think they chose a challenging disease. That's probably not why the drug didn't work, though. The drug didn't work 'cause it's not a good drug. I mentioned earlier, binding epitope matters on the receptors that we're targeting.
They were distal on that epitope, and they actually had blocking properties of each of them, which is a natural ligand that drives the co-inhibitory path. And at least in our hands, we're seeing signs of antagonism. So what you mentioned earlier is they publicly said they didn't kill the drug for safety. That's a good sign. They killed it for efficacy. We were talking about this 18-24 months ago. We didn't think their drug was gonna work. We've done a lot of head-to-head work in our hands. There's a very different signature on cytokine reduction, proliferation impact, where there's distinct differences between these two drugs. We did a head-to-head study in a GVHD model, where the Lilly drug almost looks like isotype. We see a long-term survival of mice in that study.
Gilead MiroBio has a BTLA program that's also in phase I-B for SLE and RA, and they actually recently, a couple of months ago, they expanded the RA portion of their study from 30 patients to 80, so that's probably a good signal. The differences between our drug and the Gilead drug is kind of a second thing that was different with the Lilly drug. They have a much more targeted or specific Fc receptor. We designed ours to maximize Fc receptor engagement, which we think is gonna drive maximal efficacy or potency of outcomes. The Gilead drug and the Lilly drug, so kind of a second issue for the Lilly drug, was much more focused Fc binding. We think that had to do with concerns about safety, going back five, six, seven years in the earlier days. We haven't seen those issues play-...
but what we do see is less potency of efficacy. So we think the Gilead Miro drug sits somewhere in the middle. Hopefully, there is some sign of efficacy from them. But at the end of the day, you know, we're gonna have our data within three months, and I think that'll speak for itself.
Yep, understood. And then just in terms of, like, if the trial is successful, you know, moving forward to, you know, I guess, pivotal and registrational trials for BTLA, I guess, what's that look like to you? And ultimately, I guess, the timeframe in terms of, like, when you can get those going?
Yeah. What's great about the AD market today is it's a huge growth market. You don't need contracting to break into the front or second line. You could go out there with one drug in the U.S. and commercialize this on your own today. So we believe that a phase III program, there's gonna be two studies that look the same or identical. They're larger studies, generally speaking, in a naive setting, we're gonna have some choice. There'll probably be something with topical corticosteroids sitting on top of it, and then we'll have some choice. What you're seeing with the OX40 ligand phase III program from Sanofi is that design, plus a fourth trial, that's specifically in the second line setting to be experienced.
It looks somewhat like that phase II-A component of our trial. They're now running on their own. And that's for switch relative to Dupi, which they also sell. So it looks like it'll be something like that. We'll have data in December at the primary endpoint. Through the course of next year, we'll have that six-month follow-up. We'll have translational data. A subset of patients opted in for biopsies. So we'll start to see what's going on there across the different pathways, what's winding out. So there will be subsequent catalysts from us on future data, and you could look to phase III start in 2026, and we'll get more specific post the data.
Got it.
That's something that we do intend on running ourselves.
Okay.
The other thing that we are working on right now. We raised some money last month. We are investing into the drug supply that will be needed for phase III for both of our drugs. We are investing into more drug supply to have phase II expansion indications. So the thing that's happening in the background is where do we go next once you prove concept in AD? And so, the plan here is to start additional trials over time as well.
What makes the most sense for BTLA? I mean, obviously, you talked about lupus. You-- it seems like you feel like that might be okay, but what, what else, you know-
There's also other choices I think that might be clear B-cell-
Yeah
... driven targets. We are gonna wanna, ultimately explore B-cell biology. We have internal data that we haven't published yet, but we do directly modulate B-cells, that should benefit in autoimmune disease, with the BTLA program. If you work in one skin disorder, there's other areas that you may wanna go to there, but between dermatology, rheumatology, and GI there's work that we have ongoing, and it's gonna be somewhat guided on the translational data, too.
Right. Understood. Maybe with the last five minutes, just... I mean, you have a bunch of other, you know, interesting candidates as well, and you did forget, you remember you guys created Nipocalimab, by the way. I always like to remember because of FcRn, but-
It is amazing.
Yeah, it's amazing. So again, the antibody development is extraordinary and very good out of AnaptysBio, but you have a couple other, you know, programs that are early stage. Maybe just talk about those targets, and again, maybe not the focus right now because we're not gonna see probably data for a while, but, like, I guess, just give us the timelines there.
Yep. So the first program where we cleared the IND recently, we're about to initiate phase I in healthy volunteers, is the CD122 antagonist. This was discovered in-house at Anaptys. We haven't disclosed the 1B indication. We will do that next year. But the, what CD122 is, it's a dimeric receptor, beta subunit, blocking IL-15 and IL-2. This receptor is dominantly found on CD8 cytotoxic T-cells, and then in NK cells, and to some degree, resident memory T-cells.
So there's a lot of choice in where we can develop these programs. There's earlier generation CD122s that are out there. We will eventually publish data that shows a potency difference relative to our competition. But a private company called Villaris, that Incyte acquired a year and a half ago, is being developed in vitiligo. Rational approach, particularly for Incyte's portfolio. That's not where we're gonna start, but it'll be interesting to see kind of a lower potency CD122 antagonist, how that plays out over time. In their Q2 earnings update, they did guide to data in 2025 from that trial and their phase I-B. So that, that'll be a read-through next year just as a class. There's a company called Forte, a smaller company. They just talked about moving their CD122 into celiac disease, which is rational.
The IL-15s are starting to generate interesting data in celiac. Calypso was acquired by Novartis off the celiac and EoE data sets, earlier this year. Teva and Amgen have IL-15s that are in mid-stage development for celiac disease and EoE. So there's some things to watch, I think, in the space that are mechanistic read-throughs into where we're going. We know exactly what we're gonna be doing in 1B, but we'll talk about it after we get through the agonist data sets coming up. We licensed in our first, program in the history of the company last year, a BDCA-2 modulator. It's a more potent, program than Biogen's, which has best in disease activity in SLE, to date, in a robust phase II trial.
I mean, there's very small data sets that look interesting in lupus, but for a robust, moderate, severe, biologic-eligible SLE trial, that data was interesting. I think Biogen's now, it's one of their top three or four programs in the company. They have two SLE trials that in phase III that read out next year, and subsequent to that, a phase III trial in CLE that'll read out. So we're tracking that. Our IND is going in in Q4 and into next year, we should be able to start the phase I. And you know, again, we're obviously going to have some competitive read-throughs into the SLE space.
It's not the only place that we're thinking about playing, but if there's positive, robust phase III data there, SLE is somewhere that we would go in at least one of the phase I-B's that we would do.
Just kind of your thoughts on, like, again, the BDCA-2 target versus, you know, again, just doing a full depletion of the pDCs. Obviously, I think, you know, I think it was like Horizon, now Amgen. You know, that data was a little bit more, you know, kind of maybe mixed, but like, why, why did that end up happening?
Yeah, so I sort of said this earlier. BDCA-2 is found preferentially in plasmacytoid dendritic cells. These dendritic cells are not really found in a healthy state. You see them amplify in s ome of these B-cell-driven diseases, and they express a thousand-fold increase in interferon. You mentioned Biogen's program that was the clear BDCA-2s. We think what's happening when you're binding BDCA-2 that's expressed on these pDCs, is it's getting internalized, and you're actually influencing the pDC into a more tolerogenic state. And it's potentially having subsequent interaction, not just by eliminating the interfering expression, but tolerizing the pDCs to further express cytokines that are suppressive to inflammation. So, i.e., another way of saying this, you don't want to deplete them. If you can modulate them.
Right. Got it.
We think ultimately that's the difference, is you never wanted to deplete these cells to begin with.
Got you. Okay. And then just, you know, maybe last question here, like, kind of overall, you know, kind of strategy for the company. So you kind of talked about, you know, running these kind of next stage of studies, you know, probably for BTLA and PD one. So I mean, is the goal to be, you know, fully commercial type of company, or would you look to partner at some stage, you know, for some larger, you know, trials? I guess, what's kind of the overall strategy?
Two and a half years ago, when I came into the company and we relaunched and had the broad vision, what you could do with agonists, there's no way that we can do all this on our own. It's impossible, right? If two programs are successful across all these biggest autoimmune diseases, we will need more capital in the company at some point to run phase IIIs. We have cash out in 2026. I talked a little bit earlier around AD being something that's viable, but if the AD program looks great, the RA program looks great, we have UC, we are ultimately going to need some self-help.
In the company to move things forward, not just in those areas, but also expanding in other phase IIs. It's helpful today as a company where our competition is Lilly, Gilead, J&J, and we're the only other SMID cap out there. I do think there could be opportunities to work with parties in these big markets if we have, meaningfully differentiated efficacy. We will work through that in 2025 and 2026. We have time to develop not just the top-line outcomes, but those subsequent further data reads, off-drug reads, and translational reads to help drive to what's the optimal way to move programs forward.
Got it. Cool. Well, we'll leave it there. Thanks, Dan.
Excellent. Thanks for your time.