Morning, everybody. Thanks for joining us. We will get going here with the next fireside. Very excited to have First Tracks Biotherapeutics. From the company, we have Dan Faga, CEO. Dan, it has been a pretty interesting and busy year for you. Maybe walk us through kind of the First Tracks, ANAB journey, and then we can dig into what you guys are working on at First Tracks, but just a little background. Yeah. We announced in September of last year our 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 in our preclinical engine, into what is now called First Tracks. 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, ANB033, which is a CD122 antagonist that are ongoing, one in celiac disease and another in eosinophilic esophagitis, as well as our two other clinical stage programs. We have the PD-1 depleter rosnilimab, and our BDCA2 depleter, which we have just recently completed a phase I-A for. A lot happening in the company. We are well-funded. We raised some money in April. We have cash into the second quarter of 2028, and data coming soon in celiac disease. Excellent. It has been busy. Yeah. Maybe talk about ANB033 in terms of why you like CD122 as a target and kind of the overall utility of that in autoimmune diseases. Yeah. We are blocking a group of receptors, depending on the cell type, targeting CD122. There is two mechanisms embedded in blocking CD122. We are blocking IL-15 signaling as well as IL-2 signaling. It is not a bispecific, it is a straightforward antibody that does two different things. There has been really positive proof of concept data in multiple autoimmune disorders by only targeting IL-15, but then also blocking CD122. I think you could fast-forward here, the proof of concept is 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 in response to epithelial damage. ILC2s, again, another type of immune cell that is present in disease, is densely expressing CD122 and trimeric receptor. You are seeing specific cell types as well as CD8s and CD4s that are activated that express these receptors that show CD122. We think, and you have heard this in other places, we have the potential with a targeted agent here in what is called a pipeline and a product. There is dozens of diseases where we think this is important. We have 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 CD122, I think there is seven indications right now under development. There is a lot- Yeah. to potentially target here. Walk us through why you selected celiac as the primary indication. Does it play to that biology and that mechanism that you just talked about? Yeah, no, exactly. 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. There's so many of these patients who attempt to stick to a gluten-free diet, yet have mucosal injury. In many cases, severe mucosal injury when they think they're on a gluten-free diet or they're non-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. There's nothing approved, it's a huge market, and there was clinical proof of concept. Then you layer on top of that, I think we have the most potent of the CD122s that are out there today. We think with the dual mechanism relative to IL-15, 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. That was the reason to start there. Can you talk about in terms of this for celiac, my understanding is when these patients are challenged or at least they consume gluten, you see that IL-2 spike, and then maybe the IL-15 is implicated later. But can you just maybe talk through the disease process and ultimately, if we're looking for differentiation relative to IL-15, we just saw some recent data. So where do you think that'll occur? 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 signals in the epithelial cells, the IL-15 expression on the IL-15 receptor. You see a breakdown in the epithelial cells, which recruits an IEL. So there are dual pathways here in this autoimmune disease. We target both of those. So that's a little bit of how the mechanism works is what you're asking. Got you. Do you think just intervening there, it's kind of like stopping the process before it starts, so maybe IL-15's just a little bit later? Or I guess what I'm trying to understand is where could the differentiation be, or should we I think we had a dinner with argenx, and it was like, well, worst case is you're just like another IL-15, and there's so few but versus where could that differentiation come about? Yeah. I think in two different ways. One, already hit on a couple of times. We should have an effect on the CD4 side of the equation here. Yeah. The second is we might have a more potent effect, not only on CD4s, but also on the CD8s. Okay. Which the way IELs are presented are on CD8 panels. What we haven't seen presented, I think transparently yet, is the absolute impact on IELs relative to baseline. 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? We have a more potent impact on both of those pathways, in addition to the CD122 is playing a role on the CD4 side of the equation. Got you. No, helpful. Maybe let's talk about your trial that's ongoing. You have two cohorts. Provide a little bit of background on what you're actually doing with those two cohorts. We decided to, I think uniquely in the phase I-B, more or less enroll all comers. What I mean by that is patients who are presenting into the phase I-B 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 Vh:Cd ratio, villus height-to-crypt depth ratio. If it was greater than 2, you were initially enrolled in cohort 1, which is the gluten challenge study. That study is six weeks long. You're getting three doses, subcutaneous ANB033 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 2, initially, if you're less than 2.0, you would be moved into cohort 2, which you're not given the gluten challenge. You're treated 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 Vh:Cd on drug versus placebo. So two different cohorts, two different thematics of what we're assessing. Cohort 2 is exploratory. No one's done this before in a phase I-B setting to see if we can promote healing. Now, the interesting part is these patients who are presenting and are moving to cohort 2, they actually thought they were healthy. You are finding out that they are not, right? They were symptom low or asymptomatic with all that damage. We get this question often, what is the correlation between symptoms and Vh:Cd? That is like the opposite of that. There was none. There was an inverse correlation. We more recently have finished the enrolling of cohort 1. The data is coming out in Q4. We did change the protocol design to broaden it for cohort 2, so we are enrolling patients now less than 2.5 instead of only less than 2.0. Those patients that would have fallen in the 2.0- 2.5 range that were in screening, we will still capture them. Got you. For cohort 1, when you guys design these challenge trials, everyone's racing to do cross trial comparisons, as you can imagine. What would you highlight in terms of 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? Yeah. I think the most important thing is we're looking to see a statistical significant difference on Vh:Cd. 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 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 the gluten's administered, the baseline criteria of these patients beyond the gluten itself. Are you starting at 2.0? Are you starting at 2.5? Do you have a ceiling? 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 Vh:Cd is clinically significant. That also is dependent on did you start at 1.5 or did you start at 3.5, right? There's not really a set number that I think is accepted right now. The reason I'm going into this is Teva just presented data. They saw a 0.4 delta clinically significant. Yeah. They said that. We agree. They also saw a negative 0.4 on drug, right? It wasn't completely preventative. They had an 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. We are cautioning everyone not to do that. We are looking for a statistic difference on Vh:Cd, and ideally, that would be bigger than 0.25. Got you. Approximately. Yeah. For you guys, it is more about we just want to see activity, short trial. I mean, this is still. Yeah, proof of mechanism, phase I-B. Yeah. We want to show the drug works. Yeah. Understood. Now, I think you can see differentiation, but no one's showing that. 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 is going on there. We are not going to be presenting translational data at the top line readout, but I think there will be inklings to differentiation over time. Of these trials, but at the top line, I don't think that should be the focus right now. What will we get at the top line? Change in Vh:Cd and change in IELs. Got it. Okay. Similar what 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- Yeah. in a presentation from a company of our size. We will give some perspective on symptoms. 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. It's not clear across all of these studies what's going to happen over those 14 days, and maybe there's 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. I think there's a caution on, we're not trying to promote stat sig on anything there, nor has anyone showed that. Yeah. But trend towards some benefit would be nice to see. Yeah. So maybe in terms of cohort 2, again, as you discussed, you're looking more at mucosal healing. But 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 trends and ultimately, what would you think would be strong enough signals to get you confident? Yeah. So when you step back, these mechanisms are targeting the inflammation being presented in these diseases. So similar to other IBD disorders like UC 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 in a much longer horizon. So to 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 in UC and Crohn's. We're looking to clear out inflammation, or in the case of our cohort 2, depending on where patients are presenting. Again, they didn't even realize they were damaged, because we're looking to see numerical distinction on Vh:Cd 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 variance here, but we should see Vh:Cd 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. Got you. Which shouldn't be the expectation what we would present at a top-line report. Understood. I think, collectively, you'll have this data. We'll probably get some high-level data from argenx, and then we have the Teva data. How does this all start to inform a more traditional phase II trial? Ultimately, do you find that the all comers 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? Well, I think across all of our drugs, you have the first class that's truly treating inflammation in this disease. When you look at what's been done before, a lot of the drugs that have moved forward from gluten challenges to phase IIs, and what we've been seeing in phase IIs 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. It is called SIE, you are simulating inadvertent gluten exposure, giving 0.1 g or 0.2 g every few days to simulate what would happen in the real world. You are really looking to instigate healing. 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 are all generating data. We will all go speak with the agency. But when the draft guidance was put in place back in 2022, then these discussions to get to a draft guidance started years earlier, Yeah. none of the treatments that were being developed then were actually targeting inflammation. They were all trying to block some form of the gluten being presented. It is a very different environment we are in today than we were in five, six, seven years ago when that draft guidance was created. I think we are all going to be generating a lot of data and having discussions with the agency on what is the right path or paths forward. I do not 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. You can start at 1.5, or if you start at 3, you are looking to improve from there. I think we want to keep this as wide as possible, and if that is 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 U.S. alone, a quarter million patients are non-responsive on a gluten-free diet that have a confirmed biopsy diagnosis, not just from assessing antibodies over time. Yeah. 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 U.S. alone. The market size is big, and then 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 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. There's going to be potentially multiple paths forward from here today and where this all presents itself over the next one to two years. I guess, how do you think the biology on the mucosal healing, how long do you think that will end up taking? 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. I think consistent with the other IBD disorders, it's likely going to take into that type of horizon anyway to see the full benefit. But between seeing a full efficacy response plus the need for safety data, you're going to start seeing up to one-year trials- Got you. being played out here. We talk a lot about celiac, but this is potential pipeline and a product, and obviously, as you said, we have a variety of different indications being explored with CD122. You guys have chosen EoE as the next one. Yeah. Maybe talk why that specific indication, and is that biology as strong as you feel with celiac? Yeah. 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 are only targeting IL-15. That said, stepping back here, similarly to celiac disease, two pathways driving the overall inflammatory response in EoE patients. The only drug that has worked so far that we have seen data, acknowledging TSLP with AZ just announced some positive outcome, we have to see what that data looks like. DUPIXENT has had positive impact on preventing eosinophil influx, as well as symptomatic benefit. The way DUPIXENT 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 seen in an EoE patient. We know we do that with our drug based on animal models and preclinical data, and what we observed in the phase I-A trial results. Calypso Biotech was a company that was developing IL-15. This is where Novartis got their IL-15 program via an acquisition a couple of years ago. They ran a small study, again, only targeting IL-15. They showed a prevention of eosinophil influx and a numerical trend of symptomatic benefit in a small study. That is only targeting the CD8 side of the autoimmune pathway, which is relevant in EoE as well. We are doing both. We think we can do what DUPIXENT is doing, and we know we are already doing what the Calypso Biotech data was showing, two different pathways that could prevent eosinophil influx. Two different pathways that are having an impact on symptoms. We decided to go run a phase I-B trial in EoE, where there is only one approved therapy today. About 40% of patients are non-responsive or have minimal response on DUPIXENT, and DUPIXENT did about $2 billion- $3 billion in revenue last year in this disease alone. This is, again, a huge market opportunity. I think we are potentially the first therapy that could hit both sides of the biology here in this disease. Right now, at least as of today, we are the only company across the CD122s and the IL-15s targeting this disease. Our phase I-B trial is 50 patients. We are powered to see a delta on eosinophil relative to placebo, as well as powered on the DSQ, which is the- Yep. PRO in this disease. We are powered to see a significance relative to placebo there as well. How are you thinking about the dose? Because it is 50 patients, it is probably what, a single dose? Yeah. It is single dose. Yeah. It is every other week dosing. Through week 12, single dosing size- Yeah relative to placebo. Got you. And j ust a reminder, DUPIXENT is weekly. Yep. How do you feel about understanding the dose and obviously just the overall kind of, I guess, PD effects that you will ultimately see at that dose? Yeah, we have been answering this a lot in the celiac trial as well. I think what we are hitting, in celiac, it is gut tissue. Esophageal tissue is similar, I think, in terms of penetration. You need to make sure you are 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 is opportunity to give less drug. We had a huge range based on tox coverage. As well as what we saw in the phase I-A, to know we could push here a little bit. I will lean back into the celiac trial, right? We are only dosing for a month, and then we are eight weeks off drug. In these phase I-B studies, you do not want to miss on efficacy. That is the goal out of the gate. Got you. What is the path here for EoE post this data? That will be next year. Yep. Moving into a more robust phase II-B, it doesn't seem like you might need to do any dose work, so could you go into a registrational? It's possible. Okay. 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. 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. If you look at the totality where this is moving, we're moving forward in celiac, we're moving forward in EoE. You're starting to generate a broad- Yeah. safety database within the GI division altogether within these two trials. Clearly, there's other diseases we can go into as well. On the derm side, I am sure you want to get to that. Yeah, we will. Look, next year, I think the expectations here are we have cohort one data in celiac in Q4, cohort 2 in Q1 of next year, and the back half of next year EoE data. We are also going to initiate two additional indications in the first half of 2027. It will be a year from now, ideally here in four indications, assuming success in celiac and EoE. We are going to be looking for the fastest paths to approval that we can take across the continuum of all these diseases. Got it. Just to revisit, for the DSQ, how variable could that be in that trial? I guess, small number of patients, so could be one or two patients could skew it. How do you feel about the variability? I think we're hitting the limits of how big a phase I-B can be with 50 patients, but that was intentional to solve around some of that variability. I mean, there's benchmarks out there from DB. I forgot the name of. There's the steroid as well. There's a couple steroids that are approved 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. If the drug's going to move forward, we know we have to see a difference on symptoms. Got it. I guess, 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 best in class, or are there other opportunities that you would look outside to more white space, kind of like an eosinophilic esophagitis where you're the sole company at the moment? Yeah. We've had a page that's existed since October of last year where it says a number of different indications you could be in GI and derm, and then other therapeutic areas. We're likely going to move into a couple of those that we've been talking about. It's great to see competitors in derm inflam. We've recently had both Forte, which was recently acquired by argenx, as well as Teva show different types of trials, but positive leaning data in vitiligo. Argenx will have data in alopecia upcoming. Novartis with their IL-15 are running trials in atopic dermatitis, vitiligo, and recently, cutaneous lichen planus. 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'll be expanding into. We are 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 1 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. 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. What are you contemplating for those two additional indications, in terms of generating proof of concept? Is that something that will be what you are running these phase I-B, smaller trials, or could you do more They will be phase II trials. Okay. More traditional- Yeah. phase II trials. Yes. At this point. Yeah, the phase I-B stages are over. Yeah. Yeah. Now we're going to the bigger trials. The bigger trials, yeah. Got it. Okay. I mean, anything else as you think about just the overall landscape for CD122 or IL-15? I mean, space is hot, as you mentioned, argenx doing the deal for Forte certainly brought more attention to the field, but also potentially CD122 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 view what's going on the overall competitive landscape and are you guys the only two CD122s out there between you and Forte? That might be true for this present moment. Yeah. I can assure you we'll be. But rapidly evolving. Yeah. I could. Look, 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 it exists in clinical development today that we have the most potent molecule of this landscape relative to the Forte argenx drug. We're- Can you talk through that a little bit more? Yeah. Why you believe that? Yeah. 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 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. Those have all passed. I think 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 I-A 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're also the only company that showed, in our healthy volunteer study, the impact on CD8 cells from a single dose. This is a very potent molecule. The PD effect is long. The reason you're able to run a phase I-B 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 I-A. 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, right? We're already doing it with the first generation molecules. Yeah. It's hard to sit here and say, at least with just targeting a dual mechanism like CD122, which already has an advantage over IL-15, that there's anything in the nearer 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 have produced that show differentiation potential on the cell types that we're targeting. We have to prove this in the clinic. Sure. I feel really confident on the profile of what we have that exists relative to the competitive landscape right now. Again, I think it's important differentiation. Argenx will eventually be able to figure out a subcutaneous dose. Sure. Right? They still have to go do that. We're already there, and I think that gives us a time advantage as well, and it is a bit of a race. 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 on 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. I think we're in a good competitive standing with the best drug. Got it. Maybe just with the last couple of minutes, talking about the aspirations beyond CD122, you brought up ANB101, your BDCA2. So we've got some data, or I think we're going to get some data, or we have some data. Remind me there. Both of those things are true. Both things are true. We also will have some additional data from Biogen's program with the same target. Just think about, or tell us how you think about the opportunity for this program and ultimately, what direction you would want to take it. This is a target that's been known for some time, and 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. We do expect there to be some phase II CLE data coming up with 52-week data at a near-term conference. I think there's going to be a lot of information put into the literature 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 were able to reproduce pre-clinically relative to what we've bought and then what we've shown in phase I-A, 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 PDCs relative to the Biogen agent. We will eventually present the phase I-A data, but the phase I-A is complete, and we're now going to wait and see the Biogen results to discuss publicly the path forward. Understood. We obviously have a couple options with SLE and CLE. There is other indications that we think are interesting here. Well, that is what I was going to ask. Would you look at other type I interferon-related diseases? I feel like that is kind of an area where some other biotechs are going with other mechanisms, but this is a pretty straightforward biology. Right. We have not committed publicly where we want to go. The Biogen results will impact some of that decision making. You do not need to hit in SLE to hit in CLE. Again, there is other diseases. If their drug is a complete flop everywhere, it probably will not be the right relative source of, or use of capital relative to the breadth of what we do with ANB033. Right. If the data looks good, we have a differentiated drug. I think we have seen there is a real market for drugs that have the type of profile differentiation I just described, and the fact that we are done with the phase I-A, we are ready to move forward into other additional indications relatively quickly based on where those other results are. I think for us it is more of a return on equity for the story overall and where it could best create value. There is a lot happening with CD122- Everything has to be looked at on a relative basis at the expense of that. It is prudent for us to wait and see what happens with Biogen before we pick a path. Got you. All right. Well, maybe we will leave it there. Dan, thank you so much. Excellent. Thank you for your time. Good to see you. Yeah.