Spyre Therapeutics, Inc. (SYRE) September 2026 Conference Transcript

Good morning, everyone. Thanks for being here. My name is Yanen 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 Spire 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. You're welcome.

Maybe to kick us off, could you start with a brief overview of the company before we jump into question sure so we're interested in what we hope to elevate the standard of care across a range of the large autoimmune markets we started initially an inflammatory bowel disease working on what we think are the three best biologic targets and engineering optimized versions of each of those antibodies and 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 and we of 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 in 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. So you just reported our 23 data, and by now we have all three single components data from the company. Can you review on our 23, but perhaps also mention the other two, how these long action product performed against their benchmarks and then perhaps help us take a look at the combo study design and what to expect there.

So in IBD, we started with three classes of molecules, none of which are 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 and Tibio. second TL1A, and third now IL-23. And 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, long-acting antibodies, we can give quite a bit less drug and get to full saturation. And 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 Intibio both in their phase three 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. And 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.

And then, so you asked again about the, you know, the second part of this study now in terms of the combinations. So, you know, we think this is both an innovative study in terms of its efficiency and the platform designed to get all of these answers, you know, in one trial. And 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, got it. So Part B had many simultaneous arms. I was wondering, did they all start to enroll together, or is there a staggering of enrollment?

Yeah, so 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. And so Part B does include, as I described, all three monotherapies, actually two doses of the monos, and then high doses of the combination. So really we're testing do these mono therapies beat placebo as we would expect based on the class and then how much do these combinations add together. So 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. So they will come as one readout? One giant readout, six different active agents in one readout.

Right, right. the study is being conducted in 260 sites so and in a dozen countries right is that fairly 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 three than than most phase twos are.

I mean, there's approximately 500 good sites in the world for IBD trials. As you pointed out, we're gonna be using almost 300 of them. So 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 two studies to larger phase threes. 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, you know, be very helpful to inform what we take forward into phase three.

Got it, 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? So yeah, how should we expect the timing of these data?

Yeah, so in part B, as I mentioned, it'll be one readout, right? So it'll be all the arms against placebo and 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 expectation, so we feel comfortable with our guidance of reading out next year. I suspect towards the end of this year, early next, so we can narrow that window in terms of when exactly in 27 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 you know, 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. So we haven't committed to one of those yet.

Great, great. Yeah, looking forward to those readouts. Maybe touch on the selection criteria for advancing into phase three from the big part B's induction portion.

So, you know, across the board, what we're looking for is, you know, products that, you know, can return the cost of the phase three, if not far exceed that in terms of the return on investment for the phase three. That's the overall capital allocation goal. And when we look at the IBD commercial markets, 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. And that is, it used to be Humira, Remicade, Stellara. Today, it's Intivio, Tromphaea, Skyrisi. And basically, you know, 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, you know, that's about what we've seen in terms of those head-to-head victories that have led to those products being these, you know, huge drivers of revenue in this space. You know, 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, you know, similarly take, you know, large portions of this market overall, certainly more than enough to return the costs of running these phase three studies. So, you know, I think our main goal here is picking in what order would we advance the combinations to phase three, which one goes first, maybe which one goes second, maybe which one goes third. You know, this is kind of how we will think about it and get one large phase three 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. There are orthogonal mechanisms of addressing this disease. We have animal studies and human genetics that support that these have additive benefits for these patients, but it's a head-to-head clinical study, and that's really the gold standard in terms of comparing between these mechanisms, and we'll stack ranking the efficacy we think is the most likely way that we'll be picking between these. I think we're 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. So 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's the strategy there?

I think it's 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'd have lots of choices in terms of what to do from there. A few months ago, I probably would have erred towards alpha four beta seven 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're 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've seen from Merck that they said that their phase three saw no safety signals, so that's the largest data so far for TL1A in terms of patient exposures. And then in our rheumatology study as well, which is our first, you know, 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, you know, it will be hard to tell which of our children are the cutest.

Got it, got it. Then 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. You know, going into this, we know each of these individual mechanisms work in both. You know, so as a proof of concept for the monotherapies, you know, we largely know both all of these mechanisms are going to be effective in both. And 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. And that really comes from looking at other data sets. So J&J has read out the two DUET trials, one in ulcerative colitis and one in Crohn's. And 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. And then maybe just as helpful, if not more helpful, is AbbVie. They're testing a 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 you know that combinations will add up similarly in Crohn's as they do in in ulcerative colitis and I think we would feel comfortable taking the winner or winners from this trial forward in both in parallel got it that's great great great color thanks for that so 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 so maybe a question

about you know the co-formulation you are a pro you you're pursuing there are activities in the field to go after by specific antibodies you know for a similar goal but a different approach can you comment on that yeah me you know at the highest level you know 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 INI more broadly and it was a little bit right place right time for us in terms of we were you know working on long-acting versions of the best biologics and IBD, and this combination study comes out showing that we can, adding them together is going to deliver much better results, or at least suggest that it might. And so what that gave us the opportunity to do was pick antibodies that could be developed as co-formulations, you know, at the highest level of target product profile. You know, and at the time, we certainly thought about, hey, should we make these as bispecifics instead? And we really debated the pros and cons of, you know, really probability of success of of getting this optimal product profile in terms of additive efficacy, no safety downsides, long-acting convenience, single injections. And overall, we think the approach that we're taking was the highest probability way of getting to that product. You know, 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. And so a multispecific is not going to engage both of those at the same time. And 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. And then so for the other combination, the TL1A out of 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 you know substantially in favor of the co-formulation in terms of we've seen you know 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 they carry more risks for increased immunogenicity a reduction in avidity declines in half-life relative to these long-acting monotherapies and and we think that you know the way that we're developing these molecules in this platform study kind of negates any timeline advantage that a multi-specific could have to so we think this is the highest probability way of delivering the best combination products and I also

think we're you know relatively ahead of anything else that might catch up God God very very helpful let's talk about rheumatic disease that's another focus for the company. So you have reported the RA study. At a high level, both those demonstrated 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 XBAR readouts in 4Q?

Yeah, I think this year is the year of where does TL1A work. We're running these three proof of concept studies from other sponsors that own TL1A, we'll see four others as well. There's seven indications where we should see proof of concept data for TL1A this year. And like most autoimmune targets and markets, it works differently in different indications in terms of how effective this is. I think there's levels of evidence in each of the seven indications where it's being explored. We thought the rheumatic diseases had a strong set of evidence, and I would say our data actually somewhat support that. It's clearly an active molecule there. But the magnitude of benefit in a highly competitive market like RA has to be excellent. It can't be lower efficacy than the existing products, even though we thought we should have a safety and convenience advantage without the data that we saw in RA didn't quite meet that efficacy bar but it's one of the few products in in RA that you know beats placebo on multiple endpoints and doesn't have you know safety downsize and we think that lends it towards being actually a pretty good combination component in terms of the read through to PSA and Axpa it's incomplete I mean I think there is there's some correlation between these indications obviously as there is with with IBD actually but they're they're not always the same I think you know there's 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 AXPA I think there's some overlap between the TL1A biology and those of course and so you know we think it's still very possible that it could work as a monotherapy in those indications and I think maybe even more likely that that is you know could be a great combination partner as well got it got it.

PSA and X-SPA are frequently comorbidities with IBD. Does that have any implication on whether TL1A could, the probability of TL1A working in those diseases?

Yeah, I can speak to that. I mean, I do think that it's suggestive. I think of the three, the strongest epidemiologic associations with X-SPA and IBD, and so the proof of concept for TL1A and IBD points in that direction for AXPA. The genetic evidence is probably strongest for AXPA as well for linkage and association with the TL1A pathway. On the other hand, we have preclinical data supporting efficacy in psoriasis models. And so ultimately, it will come down to the readouts we get later this year, but I think there is reason to believe for efficacy in AXPA and PSA.

Great to hear. Thanks, Josh.

So wondering about for the 4Q readout, what would be the bar I think you mentioned it for monotherapy it needs to be better than standard care right could you speak to the bar in your head for those two readouts yeah I mean we I think we try to be as transparent about our bar publicly as we are internally so you know that the back of our corporate deck as we did for RA we show what we think the bar should be in PSA and Axpa as well when you know we think you need an indication leading product to move forward and we think that could mean you know best in indication convenience best in indication safety and similar efficacy to the existing commercial drugs we think that that would be a winning profile to advance so in PSA it's frankly not that different from RAs you know it's about 30-20-10 on the ACRs and then on PASI 75 in terms of the skin benefit there we see a bit more of a divergence between you know the TNFs and the Jacks or maybe not quite as effective on PASI as the IL-17s and the 23s and so you know that they'll be interesting in in terms of where we land in that group or where does TL1A land relative to those different classes. And that's 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. And then I think if it do advance as a combination, we have the long acting 17, the long acting 23, I think there's a very reasonable world that those would be the right things to combine with TL1A if we saw kind of even a benefit like we saw in RA, I think that could support advancing those combinations in PSA and or AXPATH.

Got it, got it, very helpful. So maybe then let's pivot to heterotinitis superTIVA. A lot of activities, so, one additional opportunity just presented itself after Merck reported their positive top line for their phase to be study I think for result you know let me ask you know when the full result is available what efficacy durability or subgroup findings will be watching most closely to help inform your strategy sure so you know we when we initially picked indications for TL1 a HS was certainly on the list

and one that we thought was was interesting though there's not a ton unpublished when, you know, on TL1A and HS. And over the last year or so, we've seen, you know, more and more publications, presentations by Merck and others, and then we replicated some of those data that to us, you know, gave us increased probability that TL1A would work as a monotherapy in HS. And some of the same analysis suggested to us that, you know, TL1A and IL-17 do not overlap, or, you know, they don't overlap completely. There's plenty of orthogonal biology that they're each addressing in HS. And so 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, or we think we have reasonable confidence that Merck's going to show data and we think it's going to be positive. And so what we thought, like we're doing an 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 beat them on efficacy with no downside on safety and we'd have these convenient co-formulations, we think that could be the winning product. So 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. But I think that gives us the opportunity to not just match either the existing standard of care with the IL-17AF or kind of whatever we see for TL1A monotherapy but you know 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 help perform those meaningfully and that that would be the winning product in terms of what we need to see from Merck to inform that strategy you know I frankly think the top line thumbs up is a is enough in terms of you know this it can't be that much worse than than bimikizumab in terms of efficacy to have hit stat sig and that that result and of course that's the current best in best in indication mechanism and so we think the combination of the two is is quite likely to be good um you know i think we will be keenly interested in the you know the data that you suggested around you know where what subgroups does it work best on are there endpoints where it works differently than bimikizumab and you know that could help us you know inform some decisions but we've already made a lot of those choices you know we can adjust a bit who we enroll in the trial but we've made some choices around you know primary endpoint for our combination which we think are rational for example looking at high score 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 you know delivering a much greater level of efficacy in a patient population that clearly needs it.

Got it, got it. So your you have a combo strategy as you said and this involves your proprietary L17A F antibody.

Can you talk a little more about that antibody which is relatively new to our understanding and obviously your strategy is to use the bamechizumab as a surrogate initially so you know talk about that that strategy and what that could achieve yeah absolutely I mean I think that one of the themes we've touched on is being efficient in our development and so we recognized a that IL-17 AF 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 and so we triggered developing our own anti-IL-17 AF very much modeled on bimikizumab but with half-life extension and at the same time triggered Skylight to test the concept of the combination would work well together and be safe and effective and 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 SPY-007, or we call it 007. And that preclinical development and then phase one development will not be on critical path, such that when we have a skylight result, we'll be able to go directly into later stage development with our own combination of anti-IL-17 and TL1A. Got it.

So is your IL-17 AF targeting a similar or different epitope as bamepizumab, and in terms of efficacy safety, do you think it's gonna 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, it's indication leading across a number of different indications. We don't think we should be testing new biology in terms of hitting the target in a different way. So yes, we're gonna aim for the same epitope, similar or better potency, obviously much longer half-life, And then key, you know, again, expecting this is predominantly a combination agent. I'm not sure we're that interested in it as a monotherapy. It's incredibly important that we're able to co-formulate it with especially our TL1A antibodies. As, you know, I think folks don't appreciate that that's not trivial, that to get antibodies that are, you know, very stable, low viscosity co-formulations in the same pH and excipients between multiple antibodies, that's not trivial. and it's you know it's much much easier to do it if you're 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 and I think that's you know the other key parameter that we'll look for.

Got it, got it. So the trial design does not include a TL1A only arm, right? How do we think about you know 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's the unanswered question that we need to know in this space? We know how bamakizumab works alone. Plenty of studies demonstrating that efficacy over placebo. From the Merck data, we expect we're gonna understand how well TL1A works alone, based on their delta versus placebo on all the different endpoints. And so the last key question for functionally and contribution of components is how much better is the combination than the components? And I think to get that, we need a demonstration of the combination efficacy. And then in terms of the comparator here, we think the most attractive comparator to offer to patients is bimekizumab in terms of the existing standard of care. And so 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's the most efficient way to run this study.

Got it, got it, got it. So would you be looking to initiate phase 1, phase 1B for SP1007 as well? And if so, can you talk about the design and approach?

Yeah, I mean, so our concept is very much focused on the combination. And so with the 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 VIII, 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 to test the combination itself against either a placebo or an active comparator got it got it got it apparently you have been working on HS opportunity and you acted really fast into into the update from the field was wondering is there

other indications not like you don't have enough to work already on your played. Are there other interesting opportunity for your pipeline? And Merck also announced TL1A didn't work in SSC IOD. 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 as well. I think, as I mentioned, there's seven TL1A readouts this year. We're four left actually, PSA, Axpaw, atopic dermatitis, and MASH left between us and Roche. And 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 SSE, ILD, RA, NHS 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, right. And 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 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, got it. I have a couple of capital allocation questions, prioritization of the portfolio questions, if we may. For the balance sheet, how many parallel phase three efforts does this support? Would you consider partnering rheumatology or HS to support IBD, for example?

Yeah, so we start from a very strong position in in terms of balance sheet, as the last quarter we had about 1.1 on the balance sheet, which is far more than enough to fund all the phase two 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 three activities now in terms of manufacturing these drugs and all the different ways that we might need them for phase three. So that work's already ongoing, and I would say we've even pre-funded some of the phase three costs. In terms of which phase threes we're going to be executing, we don't know yet. 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 That's why when we turn over a phase two data set, we need to look at it and say, does this justify advancing to phase three? 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. and I think as we start to turn over phase two 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, great, thanks for that thoughtful answer. Could you in, we only have one minute left, I was hoping maybe help us understand the catalyst ahead of us, there's a lot going on, thank you.

I mean I think, as you mentioned, we have six readouts this year, mono therapies basically to see how, you know, prove that our monotherapies and 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. You know, next year it turns to, you know, we could have four combination readouts next year, three in IBD and one in HS, all of which I think, you know, have the potential to deliver something that is, you know, 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 and really putting the pieces in place this year to deliver those next year. And then hopefully we'll see that TL1A works in other indications as well and get to expand beyond just the IBD and HS combinations.

Great, 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.