Conference Transcript - TRAX 2026-09-09

Dan Figa, CEO

All right.

Operator

All right. Good morning, everybody. Thanks for joining us. We'll get going here with the next Fireside. You're very excited to have First Tracks Biotherapeutics from the company. We have Dan Vega, CEO. And Dan, it's been a pretty, you know, interesting and busy year for you. So maybe walk us through, you know, kind of the First Tracks ANAB, you know, journey, and then we can kind of dig into what you guys are working on at First Tracks. But just a little background.

Dan Figa, CEO

Yeah, so we announced in September last year intention to create a new company spinning out the R&D operations and most importantly, I think the employees that go along with it for what is three development stage assets and our preclinical engine into what is now called First Tracks. The company was born April 20th of this year. We came out of the gate with a lot happening. A number of trials with our lead program, AMV033, which is a CD122 antagonist that are ongoing, one in celiac disease and another in EOE, as well as our two other clinical stage programs. We have the PD-1 depleter, Rosnilmab, and our BDCA2 depleter, which we've just recently completed a phase 1A for. So a lot happening in the company. We're well-funded. We raised some money in April. We have cash into the second quarter of 2028 and data coming soon in celiac disease. It has been busy.

Operator

Yeah, so maybe talk about, you know, 033 in terms of, you know, why you like CD122 as a target and kind of the overall kind of utility of that in autoimmune diseases.

Dan Figa, CEO

Yeah, so we are blocking a group of receptors, depending on the cell type, targeting CD122. There's two mechanisms embedded in blocking CD122. CD122. We're blocking IL15 signaling as well as IL2 signaling. So it's not a bispecific. It's a straightforward antibody that does two different things. And there's been really positive proof of concept data in multiple autoimmune disorders by only targeting IL15, but then also blocking CD122. So I think you can fast forward here. The proof of concept's already there, both in GI disorders and derm disorders. IL-15 is an important protagonist to certain types of prolific CD8 cells that are present in disease. IELs, intraepithelial lymphocytes, are important in celiac disease. They get recruited in a response to epithelial damage. ILC2s, again another type of immune cell that's present in disease is densely expressing CD122 and trimeric receptor. So you're seeing specific cell types as well as CD8s and CD4s that are activated that express these receptors that show CD122. So we think, and you've heard this in other places, we have the potential with a targeted agent here in what's called a pipeline and a product. And there's really there's dozens of diseases where we think this is important we've taken a first stab with celiac and EOE across the landscape of the less than handful of us that are in clinical development either targeting IL-15 or CD1-22 I think there's seven indications right now under development so there's a lot to potentially target here so maybe walk us through why you selected celiac as kind of the primary indication and I guess does it you know play to that kind of biology and that mechanism that you just talked about. Yeah, exactly. So I think the mechanism is spot on in this disease. There's nothing approved in celiac disease, no therapeutics approved. It's gluten-free diet or nothing. And there's so many of these patients who attempt to stick to a gluten-free diet yet have mucosal injury. And in many cases, severe mucosal injury when they think they're on a gluten-free diet or they're not responsive to their diet. The reason to start in celiac, and again, there's lots of choice, is there was proof of concept with some of these other agents that are out there. So there's nothing approved. It's a huge market, and there was clinical proof of concept. And then you layer on top of that, I think we have the most potent of the CD122s that are out there today. And we think with the dual mechanism, REL-DIAL-15s, is there an ability here not only to be first to market or in the same timeline, but also have a very different effect over time and be a leader in this disease. So that was the reason to start there.

Operator

I mean, can you talk about, you know, in terms of this for celiac, my understanding is, you know, when these patients are, you know, challenged, or at least they consume gluten, you see that IL-2 spike. And then, you know, maybe the IL-15 is implicated later. But can you just maybe talk through the disease process? And ultimately, like, if we're looking for differentiation relative to IL-15, right? We just saw some recent data. So, like, where do you think that'll occur?

Dan Figa, CEO

So when a patient with celiac disease is exposed to gluten, the down product that's broken down, gliadin, gets picked up and presented, and it activates CD4 cells. That happens very quickly. You just mentioned the IL-2 spike. That happens within an hour or two. It's measurable. That instigates the cascade that between the IL-2 and interferon gamma that it's expressed. it's signals in the epithelial cells IL-15 expression on the IL-15 receptor you see a breakdown the epithelial cells which recruits an IEL so there are dual pathways here in this autoimmune disease and we target both of those so that's a little bit of how the the mechanism works what you're asking.

Operator

Gotcha so do you think just intervening there it's kind of like stopping the process before it starts so maybe you know IL-15 just a little bit later or I guess like what I'm trying to understand is like where could the differentiation be or should we at least I think there was a we had a dinner with Argenix and it was like well worst case is like you're just like another IL-15 and there's so few but versus where you know where could that differentiation come come out and come about yes I think in two different ways so one already hit on a couple of times we should have an effect on the CD4 side of the equation here but the second is we might have a more potent effect not only on CD4s but also on the CD8s which the way IELs are presented are on CD8 panels and what we haven't

Dan Figa, CEO

seen presented I think transparently yet is the absolute impact on IELs relative to baseline so for the data sets that exist today is there a further ability to reduce the IELs beyond the change from baseline in a gluten challenge setting so we could have a more potent impact on both those pathways in addition to the CD2122 is playing a role on the CD4 side of the equation.

Operator

Gotcha. Now helpful. So maybe let's talk about your your trial that's ongoing so you have two cohorts provide a little bit of background on you know what you're actually doing with those two cohorts.

Dan Figa, CEO

So we decided to think uniquely in the phase 1b enroll more or less enroll all comers and what I mean by that is patients who are presenting into the phase 1b trial overall, they are on a gluten-free diet, they are asymptomatic or have low symptoms, they screen, they get a biopsy, and based on that biopsy results you get a VHCD ratio, velocity to crypt depth ratio. If it was greater than 2, you were initially enrolled in cohort one, which is the gluten challenge study. That study is six weeks long. You're getting three doses of subcutaneous AMB0 through 3 or placebo over the first month, and then you're doing a 14-day gluten challenge, and you get a biopsy, and we're looking to prevent damage relative to the patients that were on placebo. In cohort two, initially, if you're less than 2.0, you would be moved into cohort two, which you're not given the gluten challenge. you're treated with drug or placebo again at week zero, week two, week four subcutaneous, and then we wait eight weeks and measure at week 12 to see if there was an improvement on VHCD on drug versus placebo. So two different cohorts, two different thematics of what we're assessing. Cohort two is exploratory. No one's done this before in a phase 1b setting to see if we can promote healing. Now the interesting part is these patients who are presenting and are moving into cohort two they actually thought they were healthy and you're finding out that they're not right so they were symptom low or asymptomatic with all that damage and so we get this question often what's the correlation between symptoms and VHD and that's like the opposite of that there was none there was an inverse correlation we more recently have finished the enrolling of cohort one the data is coming out in Q4 we did change the protocol design to broaden it for cohort two so we're rolling patients now less than 2.5 instead of only less than 2.0 so those patients that would have fallen the 2.0 2.5 range that were in screening will still capture them

Operator

josh so for cohort one should you know when you guys design these challenge trials i mean you know everyone's racing to do cross trial comparisons as you can imagine so what would you kind of highlight in terms of like how you've structured yours relative to some of the competitors and some of the past ones, and how should we take into account those differences?

Dan Figa, CEO

I think the most important thing is we're looking to see a statistical significant difference on VHCD, the change of that in placebo versus drug, and are you preventing the destruction of the villi relative to what we expect to see on placebo in on gluten when administered gluten it's hard to do cross trial comparisons when the amount of time you're in a gluten challenge the dose of the gluten challenge the way that the gluten is administered the baseline criteria of these patients beyond the gluten itself are you starting at 2.0 you start at 2.5 do you have a ceiling and then what's the distribution there there's a lot of perspective out there I think across KOLs I don't think there's a specific consensus but seems like 0.25 Delta on VHCD is clinically significant but that also the is dependent on did you start at 1.5 or you start at 3.5 all right so there's not really a set number that I think is accepted right now and the reason I'm going into this is Teva just presented data they show up they saw 0.4 Delta clinically significant they said that we agree but they also saw a negative 0.4 on drug right so it wasn't completely preventative but they had a eight-week gluten challenge we have a 14-day gluten challenge it's going to be very hard to just look at that one number that change and look across any of these trials and we're cautioning everyone not to do that. We are looking for a statistic difference on VHCD and ideally that would be bigger than 0.25 approximately.

Operator

Yeah so for you guys it's more about we just want to see activity, short trial, I mean it's still the mechanism phase 1b. Yeah, the drug works. Yeah, yeah, understood.

Dan Figa, CEO

Now I think you can see differentiation but no one's showing that. So in the translational data like we were saying earlier, what's the real impact on IELs, what are the impact on CD4 cells. In trials to date you haven't seen anyone present on CD4 activated T cells and what's going on there. We're not going to be presenting translational data at the top-line readout. I think there will be inklings to differentiation over time from these trials, but at the top line I don't think that should be the focus right now.

Operator

So what will we get at the top line? change in VHCD, and change in IELs.

Dan Figa, CEO

Similar with Teva just presented, I think that's the bare minimum. We will commit to providing more on safety and tolerability and more information on baseline characteristics. I think that would be standard in a presentation from a company of our size. We will give some perspective on symptoms, but the interesting thing on symptoms, and I'll acknowledge there's draft FDA guidance that you need to show differentiation on histology and symptoms but in these short gluten challenge studies these patients are presenting asymptomatic or low symptoms and so it's not it's not clear across all these studies what's going to happen over those 14 days and maybe their symptoms out of the gate but over 14 days they subside or they're not as severe there's a lot to really sift through when it comes to symptoms so I think there's a caution on we're not trying to promote stat sig on anything there nor has anyone showed that but a trend towards some benefit would be nice to see yeah

Operator

yeah so maybe in terms of cohort two so again as you kind of discuss you're looking more kind of mucosal healing but you know i guess the challenge here is that we don't really know how long that takes so this is still also a fairly short trial but i guess what's your hope again is more to see kind of trends and ultimately what would you think would be strong enough signals to get you get you confident yeah so when you when you step back right these mechanisms are targeting the inflammation being presented in these diseases.

Dan Figa, CEO

So similar to other IBD disorders like you see and Crohn's disease, you see remissions in those diseases over six months to a year. That's what you're really tracking against. I think there should be similar expectations here is that you're getting towards a max benefit, you know, much longer horizon. So kind of to your the point of what you're saying. We're looking to see a trend towards improvement at three months. I think also similar to what you see and you see in Crohn's. We're looking to clear out inflammation or in the case of our cohort two, depending on where patients are presenting, again they didn't even realize they were damaged, because we're looking to see numerical distinction of VHCD between placebo and drug over that 12 week period. What should be expected within some realm of variability is some improvement even just on placebo over time. You're in a study, you're probably going to follow that gluten-free diet better than you would in real life. So there's going to be variants here, but we should see VHCD numerically better over that 12-week period on drug. I think then the more interesting information will be what's happening underneath and the signals towards healing translationally, which shouldn't be the expectation we would present at a top-line report.

Operator

Understood. So I think, you know, collectively you'll have this data, you know, we'll probably get some high-level data from Argenix, and then we have the Teva data. You know, how does this all start to inform, you know, kind of a more traditional phase two trial? And ultimately, do you find that the all-comers kind of approach will be the best in celiac, or do you think we'll start narrowing this down once we start seeing a lot of these data sets?

Dan Figa, CEO

Yeah, well, I think across all of our drugs, you have the first class that's truly treating inflammation in this disease. So when you look at what's been done before, a lot of the drugs that have moved forward from gluten challenges to phase twos, and what we've been seeing in phase twos are patients who have more damage. You're not giving large amounts of gluten, but you are giving smaller amounts of gluten, trace amounts that you would see in the real world. So it's called SEED, you're simulating inadvertent gluten exposure, even 0.1 or 0.2 grams every few days to simulate what would happen in the real world, you're really looking to instigate Now, that might not be the only path to regulatory approval. There could be a path towards prevention of worsening in exposure of gluten as well. I think this across all of us needs to be explored further. We're all generating data. we will all go speak with the agency but when the draft guidance was put in place back in 2022 and then these discussions to get to a draft guidance started years earlier none of the treatments that were being developed then were actually targeting inflammation they're all trying to block some form of the gluten being presented so it's very different environment we're in today than we were in five six seven years ago when that draft guidance was created so think we're all going to be generating a lot of data and having discussions with the agency what's the right path or paths forward so I don't think it makes sense today to sit here and lock in narrowing what the populations might be we want to take patients who have some presentation of damage to villi and be able to treat them and make them better over time and you can start at 1.5 if you start at 3 you're looking to improve from there so that we want to keep this as wide as possible if that's one trial or two trials for different presentations that's okay versus just narrowing us into what this could look like we have market sizing data that's out there in the United States alone a quarter million patients are non-responsive on a gluten-free diet that had a confirmed biopsy diagnosis not just from you know assessing antibodies over time that patient population alone has damage at presentation regardless of symptoms severe symptoms, asymptomatic, they have damage. And if you have anywhere near IBD pricing, which is based on our initial payer research, we should be seeking here. If you just treat that population, that's a $5 billion market in the United States alone. So the market size is big. And I think there's lots of people describing ways to make that bigger, either confirming celiacs out there because there actually is a therapy. That's one way to make the market bigger. The other way to to make the market bigger would be taking patients who are controlled on that gluten-free diet and let them have exposure to gluten. I think that's a horizon to some degree, but we'll see how this all goes. I mean, there's going to be potentially multiple paths forward from here today and where this all presents itself for the next one or two years.

Operator

How do you think the biology on the mucosal healing, like how long do you think that will end up taking?

Dan Figa, CEO

I think another way to answer that is we're highly likely going to have to conduct studies that are six months on drug out to a year on drug or not and then looking at safety and impact so I think consistent with the other IBD disorders it's likely going to take into that type of horizon anyway to see this will benefit but between seeing a full efficacy response plus the need for safety data you're gonna start seeing you know up to one-year trials played out here.

Operator

So we talked a lot about celiac but this is you know potential pipeline in a product and obviously as you said you know we have a variety of different indications being explored with CD122 so you guys have chosen EOE as the next one maybe talk why that specific indication and you know is that biology as strong as you feel with celiac?

Dan Figa, CEO

Yeah so I think this is going to be a great example where blocking CD122 you might be able to see differentiation a lot faster than what could happen if you're only targeting IL-15. So that said, stepping back here, similarly to celiac disease, two pathways driving the overall inflammatory response in EOE patients. The only drug that's worked so far that we've seen data, acknowledging T-slips with AZ just announced some positive outcome, we have to see what data looks like. DUPI has had positive impact on preventing EOS influx as well as symptomatic benefit. The way DUPI works is it targets TH2 CD4s as well as ILC2s. We mentioned this a little bit earlier here. We hit both of those pathways on that side of the overall inflammatory response scene in an EUA patient. We know we do that with our drug based on animal models and preclinical data and what we have observed in the phase 1a trial results Calypso was a company that was developing IL-15 this is where Novartis got their IL-15 program via an acquisition a couple years ago they ran a small study again only targeting IL-15 they showed a prevention of EOS influx and a numerical trend symptomatic benefit in a small study that's only targeting the CD8 side of the Ottoman pathway, which is relevant in EOE as well. We are doing both. So we think we can do what DUPI is doing, and we know we're already doing what the CLIPSO data was showing, two different pathways that could prevent EOS influx and two different pathways that are having an impact on symptoms. So we decided to go run a phase 1B trial in EOE where there's only one approved therapy today. About 40% of patients are non-responsive or have minimal response on DUPI and DUPI did about $2 billion to $3 billion in revenue last year in this disease alone. So this is, again, a huge market opportunity. I think we're potentially the first therapy that could hit both sides of the biology here in this disease. And right now, at least as of today, we're the only company across the CD122s and now 15s targeting this disease. So our Phase I-B trial is 50 patients. we're powered to see a delta on EOS relative to placebo as well as powered on the DSQ which is the PRO in this disease we're powered to see a significance relative to placebo there as well.

Operator

How are you thinking about the dose because it's a 50 patients it's probably what a single dose?

Dan Figa, CEO

Yeah so it's single dose what it's every other week dosing through week 12 single single dosing size yeah relative to placebo. Gotcha. And as a reminder DUPI is weekly.

Operator

Yep. How do you feel about understanding like the dose and obviously just the overall kind of yeah I guess PD effects that you'll ultimately see at that dose?

Dan Figa, CEO

Yeah and we've been answering this a lot in the Celiac trial as well. I think what we're you're hitting in Celiac it's gut tissue it's esophageal tissue is similar I think in terms of penetration you need You need to make sure you're getting enough drug to get into that tissue, which is different than I think a lower bar getting into the skin, the epithelial layers. So we are ensuring by giving every other week dosing that we are above the IC90 in that tissue through the course of this 12-week study. There's opportunity to give less drug. We had a huge range based on tox coverage as well as what we saw in the Phase 1a to know we could push here a little bit but I'll lean back into the celiac trial right we're only dosing for a month and then we're eight weeks off drug in these phase 1b studies you don't want to miss on efficacy and that's the goal out of the game gotcha so what's the path here for you know you know we post this data so that'll be next year yeah then moving into like a more robust phase 2b I mean it doesn't seem like you might need to do any dose work so like could you go into a registration or it's possible I mean I don't want to commit to it sitting here today but I think that would be a nice upside here that there's a one-and-done trial beyond this and the registration path is much clearer in EOE so it's really about running a big enough trial or trials to have enough safety data more so than powering for efficacy in some of these diseases but if you look at the totality where this is moving moving forward in celiac moving forward in EOE you're starting to generate a broad safety database within the GI division all together within these two trials and clearly there's other diseases we can go into as well on the Dermen side I'm sure you want to get to that you know look next year I think the expectations here are we have cohort one day in celiac in Q4 cohort due to in Q1 of next year and the back half of next year EOE data we're also going to initiate two additional indications in the first half of 2027 so it'll be a year from now a deal here in four indications assuming success in CELAC and EOE and you know we're gonna be looking for the fastest paths to approval though that we can take across the continuum of all these diseases and then just so for the DSQ like you know how variable could that be in that trial and I guess you know small number of patients so it could kind of be you know one or two patients could skew it but like how do you kind of feel about the variability I think we're hitting the limits of how big a phase 1b can be with 50 patients, but that was intentional to solve around some of that variability. There's benchmarks out there from Dupi, like on the name of, there's the steroid as well, there's a couple steroids that are proven in this disease. There's enough data out there to assess what we're powering against relative to comps to hit STAT-SIG and that's the expectation.

Operator

If the drug is going to move forward, we know we have to see a difference on symptoms got it so I guess you know when you think about indication expansion and as you listed a bunch of them from your competitors or contemporaries there do you want to go there and prove you know best in class or are there other opportunities that you would look outside to kind of you know more white space kind of like an EOE where you're kind of the sole sole company at the moment yeah and we we've had a page that's existed since October of last year where it says a number of different occasions you could be in in GI and derm and then other therapeutic areas you know we're likely going to move into you know a couple of those that we've been talking about it's great to

Dan Figa, CEO

see competitors in Derm Inflam right we've recently had both Forte which was recently acquired by Argenix as well as Teva show different types of trials but positive leaning data in vitiligo Argenix will have data in alopecia upcoming Novartis with their IL-15 are running trials in atopic dermatitis, vitiligo, and recently cutaneous lichen planus, right? So those are all derm disorders. It's clearly an area that we can and probably should be looking at. We have locked in the two indications that we will be expanding into. So we're on track. We committed in our most recently quarterly update. We narrowed the guidance into first half of next year. We know exactly what we want to do. Getting the cohort one data from celiac is important to really lock in the final dose selection for what we want to do on the derm side or the other therapeutic area indications you want to look into. So look, I think we're going to hold the exact indications in our pocket until we initiate. It's highly competitive field, but we're out there with a dozen to 20 indications of the subset of what we could be looking into.

Operator

So what are you contemplating for those two additional indications uh in terms of generating proof of concept is that something that will be kind of what you're running kind of these phase 1b smaller trials or they'll be there'll be phase two trials okay more traditional phase two trials yes at this point yeah the phase 1b stages are over yeah now we're going to the bigger trials bigger trials you got it okay i mean anything else as you think about just the overall landscape for cd122 or or aisle 15 i mean space is hot as you mentioned you know argenics doing the deal for forte um you know certainly brought more attention to the field, but also potentially 122 in general just because maybe they favored it because they think it's a stronger mechanism versus IL-15, but I guess what do you kind of view what's going on in the overall competitive landscape and are you guys the only two CD-122s out there between you and Forti? That might be true for this present moment. But rapidly evolving.

Dan Figa, CEO

There's at least two IL-15s coming out of China that are in clinical development right now beyond what Teva and Novartis are doing. I feel really confident across the landscape as exists in clinical development today that we have the most potent molecule of this landscape relative to the Forte Argenix drug. Can you talk through that a little bit more? Why do you believe that? Yeah, so we have a differentiated affinity for starters and we've spoken and I think educated Wall Street a lot on the importance of targeting the trimeric receptor that impacts CD4 cells. We've done a lot of in vitro work. We've done cross-comparative pharmacology work. There's been IP in this space for quite some time, and there have been failures in this space as well, historic or kind of earliest generation IL-15s and CD122s that couldn't, that didn't have the potency to have a real effect on, I'd say the lower hanging fruit of just CD122 expressing NK cells in the plasma. And so those have all passed. We've solved for what will create a more potent outcome in terms of the exposure. We've shown that pre-clinically. We've shown in our phase 1a readout. Just a single dose, the lowest subcutaneous dose we tested, had a 98% reduction of CD122 expressing NK cells within the first couple of weeks. You can't do better than that. But we were also the only company that showed in our healthy volunteer study the impact on CD8 cells from a single dose right so this is a very potent molecule the PD effect is long the reason you're able to run a phase 1b trial with eight weeks off drug exposure is because we see a PD effect both in the animal work as well as in the phase 1a so the potential here to have longer dosing over time particularly in the maintenance phase is already there you're not going to YT a CD122 program and get a differentiated outcome we're already doing it with the first generation molecules so it's hard to sit here and say at least with just targeting a dual mechanism like CD122 which already has an advantage of all 15 there's anything in the near term horizon that's going to come out there and look more differentiated than what we have but I think we have enough data sets that we've produced that showed differentiation potential on the cell types that we're targeting. We have to prove this in the clinic, but I feel really confident on the profile of what we have that exists relative to the competitive landscape right now. And again, I think it's important differentiation. Argenics will eventually be able to figure out a subcutaneous dose, but they still have to go do that. We're already there. I think that gives us a time advantage as well and it is a bit of a race. And as a small cap biotech company who will be in four indications next year, and we have bigger ambitions beyond that, I think we're moving pretty quickly. On paper, we're all in the same timelines, I think, today in Celiac. We'll see how that continues to play out. Clearly, there's companies in vitiligo right now that are ahead of us, but in EOE, we're ahead. So I think we're in a good competitive standing with the best drug. Got it.

Operator

And maybe just with the last couple of minutes, you know, talking about the aspirations beyond 122, you know, you brought up 101, you know, BDCA2, so we've got some data, you know, or I think we're going to get some data, or we have some data, remind me there.

Dan Figa, CEO

Both of those things are true.

Operator

Yeah, both things are true, and then, you know, we also will have some additional data from Biogen's program, you know, with the same target, so, you know, just think about, you know, or tell us how you think about the opportunity for this program, and ultimately, you know, what direction you would want to take it Yes, again, this is a target that's been known for some time.

Dan Figa, CEO

We actually in-licensed this drug a couple of years ago with the hypothesis that there was compelling proof of concept with Biogen's BDCA2 program, which is a non-depleting antagonist targeting plasmacytoid dendritic cells. Biogen's running three pivotal trials right now, two in SLE that read out in the fourth quarter and one in CLE that reads out in Q1 of 2027 and we do expect there to be some phase 2 CLE data coming up with 52 week data at a near-term conference so there's gonna be a lot of information put into the into the literature near coming and that will inform where we're moving forward with our program which was licensed on the hypothesis that we have a differentiated PD effect what we we're able to reproduce pre-clinically relative to what we've bought and then what we've shown in phase 1a we're speaking to we haven't presented the data is a long-form PD effect a differentiated half-life and a much stronger depletion profile of PDC is relative to the biogen agent we will eventually present the phase 1a data but the phase 1a is is complete and we're wait and see the biogen results to discuss publicly the path forward. Understood.

Operator

I mean we obviously have a couple options with SLE and CLE there's other indications that we think are interesting here. Would you look at other type 1 interferon related diseases and I feel like that's kind of an area where some other biotechs are going with other mechanisms but you know this is a pretty you know straightforward biology.

Dan Figa, CEO

Right so we haven't committed publicly where we want to go the biogen results will impact some of that decision making you don't need to hit an SLE to hit in CLE and again there's other other diseases if if their drugs a complete flop everywhere it probably won't be the right relative source of or use of capital relative to the breadth of what we do with a and b 033 but if the data looks good we have a differentiated drug i think we've seen there's a real market for drugs that have the type of profile differentiation I just described, and the fact that we're done with the Phase 1a, we are ready to move forward into other additional indications relatively quickly based on where those other results are. So I think, you know, for us, it's more of a return on equity for the story overall and where we could best create value. There's a lot happening with CD122, and so everything has to be looked at on a relative basis at the expense of that. So it's just prudent for us to wait and see what happens with Biogen before we pick a All right, well, maybe we'll leave it there. Dan, thank you so much.

Operator

Thank you for seeing you.