Good afternoon, and welcome to the Jefferies Global Healthcare Conference in New York. My name is Lucas Christensen with Jefferies Investment Banking, and it is my great pleasure to introduce Dan Faga, CEO of First Tracks Biotherapeutics. Thank you. Good afternoon, everyone. Thanks to Jefferies for having us here today. Again, my name is Dan Faga, I'm the CEO of First Tracks Bio. These are our forward-looking statements. Our company is young in terms of how long we've been around as a corporation, but there's a deep legacy for almost two decades of where our science has originated. We'd sprung out of a company called AnaptysBio about a month and a half ago, funded with $100 million of cash from Anaptys, as well as some additional capital that raised at the time. We are developing antibodies to treat autoimmune diseases. We're looking at novel targets. Our lead program in clinical development is ANB033. It is a CD122 antagonist. We also have two other programs in development, a PD-1 depleter called rosnilimab, where we have had successful phase II-B data in arthritis, as well as ANB101, a BDCA2 modulator. All three programs are in various stages. ANB033, we have two ongoing phase I-B trials, one in celiac disease and one in eosinophilic esophagitis. The celiac trial will read out data in Q4, and the EoE trial by middle of 2027, and we'll talk a lot more about that in subsequent slides. As it relates to rosnilimab, the PD-1 depleter, we are undergoing a strategic alternative review. Again, we had positive data last year in a 424-patient arthritis trial. We will not be moving that program forward ourselves into phase III in arthritis. That has to do with the commercial implications of the disease and the size. We do believe that there is a market for this drug in second, third-line plus arthritis, as well as potentially other indications in dermatology. The BDCA2 modulator ANB101, we are completing a phase I-A trial in healthy volunteers. We've seen robust depletion of the target cell plasmacytoid dendritic cells, as well as long profile PD, complemented by a long half-life. We will look to present that data at medical conference at some point over the next 6-12 months. We are watching competitive data there as Biogen has two phase III trials reading out in SLE later this year and one in CLE in Q1 2027. Based on the competitive results and our own profile, we will then make decisions on how to further advance proof of concept studies in patients with this drug. As I mentioned earlier, we have $180 million of cash at inception, that is a two-year runway that will drive through the principal focus ANB033, the two phase I-B trials, as well as the initiation of a third and fourth indication of phase II for ANB033 that we anticipate in 2027. I'll focus the remainder of this discussion on ANB033, our lead program. CD122 is part of either a dimeric or trimeric receptor that is found on activated T cells. CD122, the component there, drives the signaling of IL-15 and IL-2 on those T cells, which would express an activated state, this dimeric or trimeric receptor. ANB033 antagonizes CD122. We've designed this program to have a very specific epitope and is very high affinity, driving a potent outcome of the signal blocking. The result of blocking IL-2 and IL-15 would be the reduction of the proliferation of CD4s or CD8s, as well as reduction of the resultant secretion of various cytokines and chemokines. In diseases such as celiac disease and EoE, and I'll get more into the biology in future slides, there are specific cell types that express CD122 that are of the T cell phenotypes, cells like IELs, intraepithelial lymphocytes, that densely express the dimeric receptor, including CD122, and other cells such as ILC2s that express the trimeric receptor, including CD122. Stepping back, there is a number of different disease areas within dermatology, GI, and others that we think are applicable for a target of CD122. As I mentioned earlier, one of the mechanisms, IL-15 blocking, is in the IL-15 pathway. There are a couple of competitors that across the space that's what's going on right now, including ourselves. We are in five different autoimmune diseases. There is I think interesting data that will be presented over the next 3 - 12 months across diseases like vitiligo and atopic dermatitis that we are not yet exploring with our drug ourselves. As well as proof of concept in the biology of celiac disease, which is our near-term readout coming out later this year. We have run and completed a successful phase I-A trial with ANB033. The results, I guess no surprise at this point, as we moved forward, we showed a very safe, tolerable profile. The PK/PD was long-lasting. We observed with both IV and subcutaneous dosing up to three-week half-life, long-term PD effect, receptor occupancy north of 30 days. That's all off of single dosing. At all doses, we did not see an impact on peripheral total Tregs. I think more interesting are the PD results of the cell types of interest. Again, in healthy volunteers in the periphery, if you look in the top right corner of this slide, in blue, you're looking at a middle dose with IV administration, single dose, and in green, you're looking at the initial starting dose subcutaneous administration. The top right quadrant is looking at CD122 expressing NK cells. NK cells express the dimeric receptor. These cells are highly sensitive to IL-15 for survival. By blocking or antagonizing CD122 with a potent antagonist, you're seeing a complete reduction of CD122 expressing NK cells in the periphery, 97%, 98% off of a single dose. If you look in the bottom right, when you look at total NK cell impact, what we're showing here is really the variability across patients that not all NK cells in healthy individuals or likely in disease as well express CD122. While we're potent on what our target is, you do sustain immune competency by not engaging with or impacting total NK cell counts to full depletion. On the top left, we are showing the impact on CD122 expressing CD8 cells or TEMRA cells. Again, off of a single dose, same setup here. You're seeing three-quarter plus reduction of those CD122 expressing cells, but no significant impact in CD8 cells overall. Again, exactly what we'd want to be seeing here from this study off of one dose. To give an example of the PD effect, again, the same doses that we saw in the last slide. In green here, you can see that full reduction out over a month in the NK cell impact, and then you see a sustained duration over time that goes out multiple months off that initial dose. From a safety perspective, we are referencing Teva's data sets in the right-hand side of this page. They have an IL-15. They have a long-lasting IL-15, and you see data that exists from a longer duration phase I-A trial that goes out well over a year and no safety signals. I'll switch over to now our initial phase I-B indication in celiac disease. From a commercial sense, there are over 2 million patients in the U.S. alone that are projected to have celiac disease today. Over 1 million of them are confirmed diagnosed, confirmed via biopsy, where you could see the inflammatory damage. From there, about a quarter million patients have mucosal injury while conforming to a gluten-free diet. That's ultimately, in our opinion, the target patient population of interest. The idea here is that we are looking to treat these patients who are on gluten-free diets, have mucosal injury, clear out the inflammation, and see a return to a sustained mucosal environment, and I'll get into some of those endpoints in a little bit. We think this is approximately a $5 billion market in the U.S. alone. Preliminary discussions with payers suggest that pricing here would look like other IBD diseases like ulcerative colitis or Crohn's disease. I think it's important to note, and this really speaks to where this market can go over time and grow, there are no approved therapies today on the market for celiac disease. Right now, if you cannot sustain a healthy environment within your gut on a gluten-free diet, there's no treatment for these patients right now. There's a huge white space opportunity for us moving forward if we're successful here post the phase I-B trial that we're currently enrolling. A little bit of the biology of the disease. What you see here are two boxes on the page, one in gold, which is really targeting the IL-2 signal blocking, and then in green, targeting the IL-15 blocking signaling component of our mechanism. What happens when a patient ingests gluten is that's processed to gliadin. It's picked up as an antigen for those who have this disease by the APCs. It's expressed, and that activates CD4 T cells. You see within an hour a spike of IL-2 as well as an increase in interferon gamma. The interferon gamma then downstream activates secretion of IL-15 for epithelial cells, which signals and pulls through intraepithelial lymphocytes. Those IELs then secrete chemokines such as granzyme B, which result in acute symptoms, such as nausea, diarrhea, bloating, pain. That continues on in a cycle. This happens from trace amounts of gluten. Again, if you're on a gluten-free diet, you can still be exposed, and patients are, in these trials that initiate this autoimmune mechanism for these patients. CD122 antagonists, and specifically ANB033, target both pathways. By blocking IL-15 signaling on the IELs in the top right corner, and again, this is where we've seen proof of concept of other IL-15 blockers, we should shut down and eliminate those IELs through starvation. That's reminiscent of what I showed in the phase I-A trial, where we reduced the CD8-expressing TEMRA T cells. In the gold box, we're looking to suppress the activation cycle of the CD4s in response to the gluten itself, decrease the interferon gamma and stop the initiation of the IL-15 secretion. By having a mechanism that targets both pathways, we could shut down at source where gluten is presented, as well as what's driving symptomatic impact and epithelial damage. We think we have a strong focus here on both pathways with our specific approach, then over the IL-15s over time, where I don't think they can show the same response of what we're highlighting here in the gold box. We're in, pre-clinically, a mouse experiment in celiac disease animal mouse model. On the left-hand side of the page is sham. You're seeing the colon of the mouse. There's no impact. You have a healthy villi system. In the middle, with isotype on top of gluten, which was then introduced, you see the deterioration. That's the white space in the middle. On the right, not the case with gluten plus ANB033. It's protective. Looks more like the sham. What you're seeing there in terms of deterioration in the middle are the villi. The way you measure this in clinical trials, and what we've done in this mouse experiment, is on the ratio of villus height to crypt depth. Represented on the right-hand side of this page, again, sham on the left, control on gluten in the middle, and drug plus gluten on the right. You're seeing a deterioration in the middle of the Vh:Cd ratio as the villi have reduced. You're seeing a sustained Vh:Cd ratio on the right-hand side of that graphic compared to the sham. Interesting proof of biology from our own mouse experiment. Here, you're looking at the effect of the different cell types on PBMCs with patient-derived blood for those who have celiac disease. We are represented in the line in blue. We have a very potent antagonist, as I mentioned, seen in terms of the lack of proliferation, both on CD8s and CD4 T cells. We're comparing this to other programs in the space, whether that's Teva's IL-15 in orange or Forte's CD122 in red. You're seeing a differentiation in potency on the impact on the Th cells, T cells, and as well as the downstream cytokine or chemokine activity. I mean, you can see in the bottom right the interferon gamma, same trend. We have a more potent asset. The trial design, what's ongoing right now in phase I-B, we uniquely have two different cohorts of patients. I think the consistency here across various trials is in cohort 1, we're looking at a gluten challenge. These trials do look different across companies, but the idea here is that you're taking patients who are well-controlled on a gluten-free diet, you're giving them gluten, and you're looking to see patients who were on placebo deteriorate, both on Vh:Cd as well as C symptoms, and those patients on drug to have a more protective effect on a relative basis. We are dosing subcutaneously at baseline, week two, and week four. You're giving gluten for 14 days, and at week six, you're doing a biopsy and measuring those endpoints. That's a 30-patient trial, one-to-one randomization. The second cohort of patients we think is ultimately going to be more interesting in terms of informing phase II-B design and the regulatory pathway. In this cohort, we're enrolling patients who have mucosal injury at baseline. Their Vh:Cd in this cohort, by definition, will be less than or equal to two, how we've initially set this trial up. These patients will be dosed one-to-one randomized with drug or placebo at baseline, week two, and week four. We'll wait eight weeks, and at week 12, we'll do a biopsy. What we're looking there is to see a numerical trend towards improvement at week 12 relative to the patients that are on placebo. These patients are controlled in a sense that they don't have severe symptoms at baseline. We're not explicitly looking for a material change on symptomatic scores given the baselines are already starting in a well-controlled spot. On Vh:Cd, we should see a numerical benefit. Whereas in that first cohort, we are looking for statistical significance, and we're powered for a change in Vh:Cd reduction. This trial is set to read out across both cohorts in the fourth quarter of this year. Moving on to EoE, or eosinophilic esophagitis. This is also a very large commercial market. 340,000 patients diagnosed with EoE in the United States alone. This is increasing at a pretty rapid pace, 8% CAGR, year-over-year, instigated a bit by having the first approved biologic, DUPIXENT, on the market now for a few years. Based on claims data, we estimate that DUPIXENT sold approximately $2 billion in the U.S. alone last year in this disease. It's administered on a weekly basis subcutaneous. That said, up to approximately 30% of patients don't respond to DUPIXENT, and another meaningful percent of patients aren't full responders, even if they have a directional benefit on that drug. There's a big opportunity here to bring a second drug to market into this disease. I'd say about half the patients or so respond to initial lines of therapy, PPIs or other steroid regimens, before they move on to the biologic and biologic-eligible population. We do have a phase I-B trial that was recently initiated. It is a 12-week study. We are dosing subcutaneously every other week for that period of time, and we are powered to see both reduction in eosinophils as well as the PRO DSQ. Both of those, at least in the DUPIXENT trials for approval, were the co-primary endpoint. We are powered to see a change in both of those in this trial, and it's a 50-patient trial, one-to-one randomization versus placebo. Here, similar to celiac disease, there's two paths of immunology driving autoimmune disease. We are defining these for simplicity as a dupi-sensitive path, i.e., targeting TH2 cells as well as ILC2s. This is where dupi hits. As I mentioned earlier, both of these cell types express the trimeric receptor, including CD122, and I'll show you some data from animal studies in a little bit that shows a direct on-target hit on these cell types in terms of the reduction of proliferation and resultant cytokine activity. On the right-hand side, patients who were not effectively treated with dupi are correlated with an increase in expression in IL-15, similar to celiac disease by blocking CD122 on the CD8 cells that are reacting to the IL-15, we should see a significant reduction. There is proof of concept in this disease with another IL-15 inhibitor in a very small study, for phase I-B, by just targeting IL-15 alone, they saw a reduction in eosinophils and a numerical trend and benefit on patients' symptoms. This is important because CD122 is not expressed on eosinophils. We know that by targeting IL-15 or CD122, we are upstream in this disease by impacting inflammation directly from these upstream pathways and minimally from the proof of concept of IL-15s. You're reducing the influx of the eosinophils downstream. We do believe there's good patient data that exists already out there as a proof of concept to what we're showing, and we already know DUPIXENT works, and they're acting only in the green on the left-hand side. Here's a little bit of data to support what I'm just saying. We did run an Aspergillus-induced eosinophilia mouse model. You're looking on this slide both at the eosinophils in the esophagus as well as the lung, and you're seeing in blue ANB033, which is more or less a full prevention of eosinophil recruitment relative to other mechanisms and then relative to black isotype control. You're also looking here, we were able to measure there was enough ILC2s to measure differences in the lung. Aspergillus, again, this is a lung-induced eosinophilia. You are able to see the ILC2 recruitment in lung. We completely floored that in terms of the prevention of ILC2 increase with ANB033. Lastly, from the same study, we're looking at the resultant chemokines and cytokine activity. IL-5, IL-13, these are cytokines that are responsible. They're secreted from the CD8s. They're responsible for pulling in the eosinophils into the inflammatory environment. You're seeing a similar reduction there as well with ANB033 versus other comparators. In summary, really excited about where we're going here with ANB033. Two ongoing trials in celiac and EoE, both on track to read out celiac later this year, EoE next summer. We are publicly committed to expanding two additional diseases. There's a lot of clinical activity ongoing in the space with other IL-15s and CD122s, again, across five different diseases with the four players. We do believe that this is a pipeline and a product-type asset. We're really excited about the future where we're going here, both in these GI diseases and where we're able to expand to. We do have two other clinical development stage programs in the portfolio into 2027. We do believe that there's increasingly path forward with both of those as well. We have four minutes left. If there's any questions, happy to take them. Thank you.