Good morning, everyone. Thanks for being here. My name is Yanan Zhu, and I'm one of the biotech analysts here at Wells Fargo. It is my great pleasure to be joined by the management team of Spyre Therapeutics. With me here are Cameron Turtle, CEO of the company, and Josh Friedman, SVP Clinical Development. Thank you for being here.
Thanks for having us.
Welcome.
Maybe to kick us off, could you start with a brief overview of the company before we jump into questions?
Sure. We're interested in what we hope to elevate the standard of care across a range of the large autoimmune markets. We started initially in inflammatory bowel disease, working on what we think are the three best biologic targets and engineering optimized versions of each of those antibodies. Then what we think is quite exciting is the possibility of combining these together in pairwise combinations, which we think has the potential to provide additive efficacy without safety downsides. We have the ability, we think, uniquely, to combine these in elegant co-formulations. We've expanded that strategy outside of IBD to explore the biology of TL1A and a range of other indications as well, in rheumatology initially, and then just recently, we also announced an expansion into dermatology and HS as well.
And really across all of these, the goal is let's see how well these molecules work individually and then ideally, in the long run, push the bar again by combining what we think are the best mechanisms in each of these indications. I'm sure we'll hit all of them individually.
Great. Thank you. You just reported IL-23 data, and by now we have all three single components data from the company. Can you review on IL-23, but perhaps also mention the other two, how these long-action product performed against their benchmarks? Then perhaps help us take a look at the combo study design and what to expect there.
Sure. So in IBD, we started with three classes of molecules, none of which our molecules are first in class. So we really do get to learn from the first generation set of molecules against each of these mechanisms. So the first one, alpha-4 beta-7, same target as Takeda's ENTYVIO, second TL1A, and third now IL-23. In the study that we're running, this platform SKYLINE study, we initially explored them as individual monotherapies to provide preliminary safety and efficacy. I think for two of the three, we largely expected, based on the dose exposure response and target engagement to the first generation molecules, that it was unlikely that we could do much better.
Meaning on both TL1A and IL-23, it looked like the first generation molecules likely saturate the target in the induction setting for sure, and that we thought that a long-acting version, we could probably do the same amount of efficacy with less drug. Basically, in a long-acting antibodies, we can give quite a bit less drug and get to full saturation. I think that's what we've seen with both our TL1A data set that we delivered a few months ago, and then the IL-23 data in the last week, that these perform like the in-class molecules in terms of safety and efficacy, and then we have the ability to dose them much less frequently in the maintenance setting, and then we can deliver a lot less drug in the induction setting.
Which is actually very helpful as you get into combination therapies in terms of the ability to get both antibodies into a single injection, having lower drug loads is key. On the third of them, the alpha-4 beta-7, that was one where we looked at the exposure response data for ENTYVIO, both in their phase III studies and in the real world, and we saw that they had a pretty steep exposure response relationship, meaning that we thought with higher target coverage, we might do better. Though all of these are relatively small 40 odd patient cohorts, I think our data for our alpha-4 beta-7 molecule does look like there might be greater efficacy to be had with higher dosing on that target.
Great. Yeah.
Then, so you asked again about the second part of this study now in terms of the combinations. We think this is both an innovative study in terms of its efficiency and a platform design to get all of these answers in one trial. Then it's also robust in terms of answering what's key for combination therapies, which is contribution of components. That's really the key goal of the study, and that's why in this second portion of the trial, we have a placebo group, we have all three of our monotherapies, and then we have all three of these pairwise combinations as well, and we expect to read that all out together next year, which will help us prioritize which of these combinations we think is the optimal one to advance to pivotal studies.
Got it. So part B had many simultaneous arms. I was wondering, did they all start enroll together, or is there a staggering of enrollment? Yeah, so.
Yeah, we finished, I think back in April, we announced that we had completed enrollment of the part A portion. Those were the monotherapy arms that we just described, and initiated enrollment in part B. Part B does include, as I described, all three monotherapies, actually two doses of the monos, and then high doses of the combination. Really we're testing do these monotherapies beat placebo as we would expect based on the class, and then how much do these combinations add together? The goal is to show monos beat placebo, combos beat the monos, and then we'll have the ability to prioritize which of these combos should advance, and in what order, I think, is the main question.
Okay, so they will come as one readout.
One giant readout, six different active agents in one readout. Yeah.
Right. The study is being conducted in 260 sites, and in a dozen countries, right? Is that fairly a standard practice? If not, does that introduce any potential placebo response rate variation and things like that?
Yeah. I think what we like about the SKYLINE size is that it is frankly closer to a phase III than most phase IIs are. There's approximately 500 good sites in the world for IBD trials. As you pointed out, we're going to be using almost 300 of them. This is as global a study or very close to a complete global study in IBD, and I think what we think is great about that is the ability to translate results from this trial to the subsequent study. There's not going to be this. Sometimes you see a relatively large shift from small proof of concept phase II studies to larger phase IIIs. I don't expect as much of a jump here.
We're largely using a large global footprint, and I think that will deliver results that will be very helpful to inform what we take forward into phase III.
Got it. Can you help us understand the cadence of data next year? There are a few things, the induction of the big study, the induction portion, and also part A may have maintenance data, right? How should we expect the timing of these data?
Yeah. In part B, as I mentioned, it'll be one readout, right? So it'll be all the arms against placebo in one large readout, so we can compare between them. We said our guidance is still 2027, so we feel good about that. Enrollment has been on track or ahead of schedule from our expectations, so we feel comfortable with our guidance of reading out next year. I suspect, towards the end of this year, early next, we can narrow that window in terms of when exactly in 2027 we'll have the big part B induction readout. So we'll update that as we get a little bit closer to last patient in. And then in terms of the part A maintenance data sets, I think, in general, for all of the studies we're running, it's about nine months after the induction data, we'll have the maintenance data.
In this case, I think we may decide, as we have three different agents, we can either read them out individually, as we have for the part A data sets so far, or it's always possible that we can present these at a medical meeting where we present all of them together in one larger data release. We haven't committed to one of those yet.
Great. Yeah. Looking forward to those readouts. Maybe touch on the selection criteria for advancing into phase III, from the big part B's induction portion.
Sure. Across the board, what we're looking for is products that can return the cost of the phase III, if not far exceed that in terms of the return on investment for the phase III. That's the overall capital allocation goal. When we look at the IBD commercial market, it's a remarkably concentrated market, and it has been for over a decade, where functionally the top three drugs in the space take 70% of the market. That is, it used to be HUMIRA, REMICADE, STELARA. Today, it's ENTYVIO, TREMFYA, SKYRIZI, and basically these new products that take the lion's share of the market, they basically beat yesterday's standard of care by a clinically meaningful amount, about 10 percentage points on clinical remission.
Basically, that's about what we've seen in terms of those head-to-head victories that have led to those products being these huge drivers of revenue in this space. We think it's credible, if not probable, that our combinations can beat the current today's standard of care, those drugs, by 10 or more points on clinical remission, and we think they can similarly take large portions of this market overall, certainly more than enough to return the costs of running these phase III studies. I think our main goal here is picking in what order would we advance the combinations to phase III, which one goes first, maybe which one goes second, maybe which one goes third. This is how we will think about it and get one large phase III infrastructure going to get all of these drugs moving and hopefully towards market.
In terms of how we will pick, I think it is efficacy first. We have good evidence for why all of these mechanisms should be additive with each other. They are orthogonal mechanisms of addressing this disease. We have animal studies and human genetics that support that these have additive benefits for these patients. It is a head-to-head clinical study, and that is really the gold standard in terms of comparing between these mechanisms, and we will stack ranking the efficacy, we think is the most likely way that we will be picking between these. I think we are optimistic that combining three, what we think are individually safe molecules and classes together, will be well-tolerated, and all of them we can deliver on a convenient, long-acting co-formulation. Really the main parameter that we think will vary will be the efficacy between these combinations.
What if there are two combinations that look equally good? What is the strategy there?
Yeah, I think it is maybe my base case, actually, that all of these provide additive efficacy between the mechanisms, and they could be closer than they are different in terms of the level of efficacy between them. That would be a home run scenario, because I think that would give us what I think would look like the three best products in the space, and we would have lots of choices in terms of what to do from there. A few months ago, I probably would have erred towards alpha-4 beta-7 and IL-23, mostly from their safety perspective. These molecules have been tested in tens of thousands of patients in the real-world setting. They are probably the first and second safest classes in IBD overall, and so the combination of them I would feel very good about.
I would say TL1A has caught up in the last few months in terms of the safety. We have seen from Merck that they said that their phase III saw no safety signals. So that is the largest data so far for TL1A in terms of patient exposures. Then in our rheumatology study as well, which is our first placebo-controlled study using a TL1A, we also saw that this class was well-tolerated, as good or better than placebo in that study as well. So TL1A, I would say, has caught up a bit, and it will be hard to tell which of our children are the cutest.
Got it. How do you translate that data into Crohn's, and what's the strategy there?
Yeah. We're obviously very interested in Crohn's disease as well. Going into this, we know each of these individual mechanisms work in both. As a proof of concept for the monotherapies, we largely know all of these mechanisms are going to be effective in both. Again, over the last few months, I think we've gotten more conviction, actually, that the combos that work in ulcerative colitis are likely to work as well in Crohn's disease as well. That really comes from looking at other data sets. J&J has read out the two DUET trials, one in ulcerative colitis and one in Crohn's. I think those results were more similar than they were different in terms of you saw additivity in both of these, and I think that makes sense mechanistically as well. Then maybe just as helpful, if not more helpful, is AbbVie.
They're testing an alpha-4, IL-23 combo. Granted, it's an open label study in Crohn's disease, but they also saw on an objective endpoint endoscopic remission that the combination, they said, roughly doubled the endoscopic remission on the combination than the two monotherapies. I think that gives us good confidence that combinations will add up similarly in Crohn's as they do in ulcerative colitis. I think we would feel comfortable taking the winner or winners from this trial forward in both in parallel.
Got it. Got it. That's great color. Thanks for that. You touched on how the J&J and AbbVie's data on their combo kind of give you confidence about the combo approach that you are approaching. Maybe a question about the co-formulation you're pursuing. There are activities in the field to go after bispecific antibodies for a similar goal, but a different approach. Can you comment on that?
Yeah. At the highest level, Vega came out almost four years ago now, and that was a little bit of the starting gun for combinations, certainly in IBD, and I think in I and I more broadly. It was a little bit right place, right time for us in terms of we were working on long-acting versions of the best biologics in IBD, and this combination study comes out showing that adding them together is going to deliver much better results or at least suggests that it might. So what that gave us the opportunity to do was pick antibodies that could be developed as co-formulations, at the highest level of target product profile.
At the time, we certainly thought about, "Hey, should we make these as bispecifics instead?" We really debated the pros and cons of really probability of success of getting this optimal product profile in terms of additive efficacy, no safety downsides, long-acting, convenient, single injections. Overall, we think the approach that we're taking was the highest probability way of getting to that product. On alpha 4, beta 7, we think that is a very tricky target to make a multispecific for, given that it's on the surface of immune cells that are in the periphery, whereas the other two are cytokines that are predominantly soluble in the target tissue. So a multispecific is not going to engage both of those at the same time. If it did, you might actually be worried about it.
You'd basically be bringing an inflammatory cytokine to an immune cell expressing the alpha 4, beta 7 integrin. Then, so for the other combination, the TL1A, IL-23, that's a more possible bispecific target. Granted, TL1A is still membrane-bound sometimes as well, so you can still have the same issue that I just described. But there, we looked at the probability of success for a bispecific versus a co-formulation of antibodies, and we think it's substantially in favor of the co-formulation in terms of we've seen there are many TNF bispecifics that have been made.
We've seen a couple TL1A bispecifics report clinical data so far, and I think it's broadly true that they carry more risks for increased immunogenicity, a reduction in avidity, declines in half-life relative to these long-acting monotherapies, and we think that the way that we're developing these molecules in this platform study kind of negates any timeline advantage that a multispecific could have too. So we think this is the highest probability way of delivering the best combination products, and I also think we're relatively ahead of anything else that might catch up.
Got it. Very helpful. Let's talk about rheumatic disease. That is another focus for the company. You have reported the RA study. At a high level, both doses demonstrate activity on at least one clinical endpoint. Safety was good, but you concluded the magnitude doesn't justify pursuing monotherapy strategy. Could you elaborate on that and how do the RA data influence your expectation for the upcoming PsA and axSpA readouts in Q4?
Yeah. No, I think this year is the year of where does TL1A work. We are running these three proof of concept studies from other sponsors that own TL1A. We will see four others as well. There are seven indications where we should see proof of concept data for TL1A this year. Like most autoimmune targets and markets, it works differently in different indications in terms of how effective this is. I think there are levels of evidence in each of the seven indications where it is being explored.
We thought the rheumatic diseases had a strong set of evidence, and I would say our data actually somewhat support that. It is clearly an active molecule there. But the magnitude of benefit in a highly competitive market like RA has to be excellent. It cannot be lower efficacy than the existing products, even though we thought we should have a safety and convenience advantage.
We thought the data that we saw on RA didn't quite meet that efficacy bar, but it is one of the few products in RA that beats placebo on multiple endpoints and doesn't have safety downsides. We think that lends it towards being actually a pretty good combination component. In terms of the read-through to PsA and axSpA, it is incomplete. I think there is some correlation between these indications, obviously, as there is with IBD, actually, but they are not always the same. I think there are specific mechanisms like the IL-17 and IL-23 class that frankly don't show that much activity in RA, and then those are the leading classes in PsA and axSpA. I think there is some overlap between the TL1A biology and those, of course, and so we think it is still very possible that it could work as a monotherapy in those indications.
I think maybe even more likely that it could be a great combination partner as well.
Got it. PsA and axSpA are frequently comorbidities with IBD. Does that have any implication on the probability of TL1A working in those diseases?
Yeah, I can speak to that. I do think that it is suggestive. I think of the three, the strongest epidemiologic association is with axSpA and IBD, and so the proof of concept for TL1A and IBD points in that direction for axSpA. The genetic evidence is probably strongest for axSpA as well for linkage and association with the TL1A pathway. On the other hand, we have preclinical data supporting efficacy in psoriasis models. Ultimately, it will come down to the readouts we get later this year, but I think there is reason to believe for efficacy in axSpA and PsA.
Great to hear. Thanks, Josh. Wondering about for the 4Q readout, what would be the bar? I think you mentioned for monotherapy, it needs to be better than the standard of care, right? Could you speak to the bar in your head for those two readouts?
Yeah. I think we try to be as transparent about our bar publicly as we are internally. At the back of our corporate deck, as we did for RA, we show what we think the bar should be in PsA and axSpA as well. We think you need an indication leading product to move forward, and we think that could mean best in indication convenience, best in indication safety, and similar efficacy to the existing commercial drugs. We think that would be a winning profile to advance. In PsA, it is frankly not that different from RAs. It is about 30, 20, 10 on the ACR, and then on PASI 75 in terms of the skin benefit. There we see a bit more of a divergence between the TNFs and the JAKs are maybe not quite as effective on PASI as the IL-17s and the 23s.
That will be interesting in terms of where we land in that group or where TL1A lands relative to those different classes. That is what I would say is the monotherapy bar to advance it forward. It has to be as good on efficacy and then similar or better on convenience and safety. Then, I think if it to advance as a combination, we have the long-acting 17, the long-acting 23. I think there is a very reasonable world that those would be the right things to combine with TL1A if we saw even a benefit like we saw in RA. I think that could support advancing those combinations in PsA and/or axSpA.
Got it. Very helpful. Maybe then let us pivot to hidradenitis suppurativa. A lot of activities. One additional opportunity just presented itself after Merck reported their positive top line for their phase IIB study. Let me ask, when the full result is available, what efficacy durability or subgroup findings we will be watching most closely to help inform your strategy?
Sure. When we initially picked indications for TL1A, HS was certainly on the list and one that we thought was interesting, though there was not a ton published on TL1A and HS. Over the last year or so, we have seen more and more publications, presentations by Merck and others, and then we replicated some of those data that to us gave us increased probability that TL1A would work as a monotherapy in HS. Some of the same analysis suggested to us that TL1A and IL-17 do not overlap, or they do not overlap completely. There is plenty of orthogonal biology that they are each addressing in HS. We looked at that paradigm and knew, of course, Merck will have their data this year and said, "Okay, do we need to do a monotherapy proof of concept for our TL1A?
We think we have reasonable confidence that Merck is going to show data, and we think it is going to be positive." What we thought, like we are doing in IBD, combining the best mechanisms in the space, we think is reasonably likely to provide enough additive benefit on efficacy that it can make the monotherapies not as relevant in terms of if you can beat them on efficacy with no downside on safety and we would have these convenient co-formulations, we think that could be the winning product. That really was the justification for launching the SKYLIGHT study. We got, frankly, a little lucky in terms of the announcement of the positive TL1A monotherapy in HS right before we announced our study.
I think that gives us the opportunity to not just match either the existing standard of care with the IL-17AF or whatever we see for TL1A monotherapy. If these are the top mechanisms in the space or near the top, we think it's quite likely that that combination is going to outperform those meaningfully and that would be the winning product. In terms of what we need to see from Merck to inform that strategy, I frankly think the top line thumbs up is enough in terms of it can't be that much worse than bimekizumab in terms of efficacy to have hit stat sig in that result. Of course, that's the current best in indication mechanism, and so we think the combination of the two is quite likely to be good.
I think we will be keenly interested in the data that you suggested around what subgroups does it work best on? Are there endpoints where it works differently than bimekizumab? That could help us inform some decisions. But we've already made a lot of those choices. We can adjust a bit who we enroll in the trial. But we've made some choices around primary endpoint for our combination, which we think are rational. For example, looking at HiSCR 75 as the primary endpoint. Really, we think learning from IBD, the combos tend to outperform more on the deeper endpoints than the shallower ones, and we think that's an opportunity to really demonstrate a product that's delivering a much greater level of efficacy in a patient population that clearly needs it.
Got it. So you have a combo strategy, as you said, and this involves your proprietary IL-17AF antibody. Can you talk a little more about that antibody, which is relatively new to our understanding? Obviously your strategy is to use the bimekizumab as a surrogate initially. So, talk about that strategy and what that could achieve.
Yeah, absolutely. I think one of the themes we've touched on is being efficient in our development. So we recognized, A, that IL-17AF is probably the best MOA for HS, and we wanted to go directly to testing the concept that the combination of the two would be effective. So we triggered developing our own anti-IL-17AF, very much modeled on bimekizumab, but with half-life extension, and at the same time triggered SKYLIGHT to test the concept that the combination would work well together and be safe and effective. So the way that is intended to work is that if we have a positive readout from SKYLIGHT, we will in the meantime have been developing our own anti-IL-17, which happens to be called SPY007.
And that preclinical development and then phase I development will not be on critical path, such that when we have a SKYLIGHT result, we will be able to go directly into later stage development with our own combination of anti-IL-17 and TL1A.
Got it. Is your IL-17AF targeting a similar or different epitope as bimekizumab? In terms of efficacy, safety, do you think it's going to be similar, or could there be room for improvement?
Yeah, I think design here, we think that's a great antibody in terms of its efficacy, its indication leading across a number of different indications. We do not think we should be testing new biology in terms of hitting the target in a different way. Yes, we are going to aim for the same epitope, similar or better potency, obviously much longer half-life. Then key, again, expecting this as predominantly a combination agent. I am not sure we are that interested in it as a monotherapy. It's incredibly important that we are able to co-formulate it with especially our TL1A antibodies. I think folks do not appreciate that that's not trivial. That to get antibodies that are the very stable, low viscosity co-formulations in the same pH and excipients between multiple antibodies, that's not trivial.
It's much easier to do it if you are doing it when you pick the antibody in terms of it's part of our screening funnel that we can get to these excellent combination products. I think that's the other key parameter that we will look for.
Got it. The trial design does not include a TL1A only arm, right? How should we think about incremental contribution of SPY072 in the study when we see the result?
Yeah. I think our interest here is running the killer experiment, basically. What is the unanswered question that we need to know in this space? We know how bimekizumab works alone. Plenty of studies demonstrating that efficacy over placebo. From the Merck data, we expect we are going to understand how well TL1A works alone, based on their delta versus placebo on all the different endpoints. The last key question for functional and contribution of components is how much better is the combination than the components? I think, to get that, we need a demonstration of the combination efficacy. Then in terms of the comparator here, we know we think the most attractive comparator to offer to patients is bimekizumab in terms of the existing standard of care.
We thought that was the most logical approach to look for, can we beat the existing standard of care by a meaningful amount with this combination? We think that is the most efficient way to run this study.
Got it. Would you be looking to initiate phase I, phase I-B for SPY072 as well? If so, can you talk about the design and approach?
Yeah. Our concept is very much focused on the combination. With a positive result from SKYLIGHT 1, we would initiate SKYLIGHT 2. We haven't shared any real specific details about that, but one could imagine that we would design it as a seamless phase II-B/III, again, in the name of efficiency, maybe with an initial stage in which we test each of the monotherapies, with the intent that that could contribute towards demonstration of contribution of components. Perhaps with dose ranging, such that an initial component of the study, we could select the doses of the monotherapies to put into the combination, and then in the phase III component test the combination itself against either a placebo or an active comparator.
Got it. Apparently, you have been working on HS opportunity, and you acted really fast into the update from the field. Was wondering, are there other indications, not like you don't have enough to work already on your plate. Are there other interesting opportunity for your pipeline? Also, Merck announced TL1A didn't work in SSc-ILD. What can we take away from that?
Yeah, I think our plans for what will come next does hinge on the readouts over the next few months. I think, as I mentioned, there's seven TL1A readouts this year. We're done four of them, or we have four left, actually. We have PsA, axSpA, atopic dermatitis, and MASH left between us and Roche. I think all of those will help us inform, does TL1A make sense as a monotherapy in any of these markets, or would it make sense-- Is it active enough and well-tolerated enough? That's really the formula for a good combination component. Does it demonstrate benefit? Is it orthogonal to the other mechanisms, and is it well-tolerated? I think that makes it a great combination component. So we've seen SSc-ILD, RA, and HS so far.
We'll see four more before the end of the year, and I think we'll do our best to be ready to capitalize on any opportunities where it looks like we could have an indication-leading product.
Right. The lack of efficacy in SSc-ILD, does that change the thinking around TL1A and fibrosis, for example?
Yeah, that was the intent of the trial, was to test a very fibrotic indication. I think, the challenge with fibrotic indications is fibrosis both takes a while to develop and it takes a long time to reverse as well. So I think, these are difficult trials. We haven't seen the details of did it totally fail or does it show some activity and just not a lot? I think, we'll be interested in seeing those data when they come out. I think, fibrosis is a very tricky thing to measure clinically, and so it wasn't all that surprising to us that it's hard to show a significant benefit in that type of trial.
Got it. I have a couple capital allocation questions, prioritization of the portfolio questions, if we may. For the balance sheet, how many parallel big phase III efforts does it support? Would you consider partnering rheumatology or HS to support IBD, for example?
Yeah. We start from a very strong position in terms of balance sheet. As the last quarter, we had about $1.1 billion on the balance sheet, which is far more than enough to fund all the phase II activities that we're doing, plus multiple years of runway beyond these readouts. So, we're coming from a very strong place. I would say that we actually have, or we're both funding phase III activities now in terms of manufacturing these drugs and all the different ways that we might need them for phase III. So, that work's already ongoing, and I would say we've even pre-funded some of the phase III costs. In terms of which phase IIIs we're going to be executing, we don't know yet, right?
We're kind of in the middle of this pivotal period of how good are each of our monotherapies and combos in each of these markets, and we'll need to prioritize which ones of these we're going to advance and how many we're going to advance in parallel. I typically think about this in a, each of these programs has to be justifiable on its own. That's why when we turn over a phase II data set, we need to look at it and say, "Does this justify advancing to phase III?" We know what the cost of all these trials is, and we need to see, can these products be winners in these long-term markets. I think there's plenty of ways for us to look at financing these as well. I think we're coming from a great spot.
I think equity could continue to be part of the story to fund the late-stage development. I think as you get into those later stages of development, there's even more opportunities as well for either strategic royalty financing or strategics are quite interested, obviously, in all of these markets. I think as we start to turn over phase II data sets that look like indication-leading products, I'd be surprised if we don't have multiple options on the table in terms of how to advance them.
Great. Thanks for that thoughtful answer. We only have 1 minute left. I was hoping maybe help us understand the catalyst ahead of us. There's a lot going on. Thank you.
Yeah. I think, as we mentioned, we have six readouts this year, monotherapies basically to see how, prove that our monotherapies in IBD work the way we thought they did, which I think we're largely through. Now between us and others, we're going to see how good is TL1A in all these different markets. Next year it turns to, we could have four combination readouts next year, three in IBD and one in HS, all of which I think have the potential to deliver something that is just a different level of product than has been seen in these spaces to date, and I think would be some of the most attractive products in those areas. We're really putting the pieces in place this year to deliver those next year.
Hopefully we'll see that TL1A works in other indications as well and get to expand beyond just the IBD and HS combinations.
Great. Exciting times. I think with that, we'll end the session here. Thank you, Cameron, and thank you, Josh, for all the insights and for your time.
Thank you.