AnaptysBio. These are our forward-looking statements. Anaptys, our biopharma operations, we are focused on developing biologics or antibodies for autoimmune diseases. We have three clinical stage programs. The first is Rosnilimab, which is a selective and potent depleter of pathogenic T cells. We recently had a positive, robust phase 2b trial readout in arthritis earlier this year. I'll get into some of the details later, and we're currently assessing advancement into phase III trials for RA. Our second program, AMV033, is a CD122 antagonist. It blocks IL-15 and IL-2 signaling. We've recently initiated retreating patients in a phase 1b trial for celiac disease and are also assessing and will launch into a second indication in phase 1b in 2026. We also have AMV101, which is a pDC plasmacytoid dendritic cell depleter targeting BDCA2. That's currently in phase 1a in healthy volunteers. Stepping back from the biopharma operations, we're well capitalized with expected $300 million of cash coming out of this year, starting in January. We recently announced that we will be separating our business into two. If you own 1% of the company today, in the future, you own 1% of two different businesses. One is that biopharma business, the biopharma operations I just walked through the highlights on. The second is a royalty management business. This month, we actually hit 20 years in business at AnaptysBio. As part of being around for 20 years, you have some successful products over time. We have two collaborations that are going to be the founding drivers of royalties that will be part of this business. One is on a drug called Jemperli, which is a PD-1 antagonist currently sold by GSK. The second is a drug called imsidolimab, an IL-36 receptor antagonist. We did an outlicensing partnership with Vanda Pharmaceuticals, who will be advancing this drug through a BLA submitted this quarter in generalized pustular psoriasis, or GPP, which is a rare autoimmune disease of dermatology. First, I will dive into the royalty management business for a few minutes here. GSK's relationship and where and how they're selling Jemperli, they're doing very well right now. The drug launched a few years ago. Last year, they ran a trial in frontline endometrial cancer. They are the only PD-1 antagonist now approved with overall survival data in this disease. It was approved in the United States last August of 2024 and recently this year in January of 2025 by the EMA. Exiting this year, we anticipate Jemperli to be on a $1.4 billion-$1.5 billion run rate. We have substantial royalties from this business, ranging from 8% up to $1 billion, 12% up to $1.5 billion, 20% up to $2.5 billion, and 25% for every dollar sold over $2.5 billion. It is a very large royalty stream. The asset right now, I mentioned the run rate that they're on, they're growing in high double-digit or high teen double-digit growth quarter over quarter. We are in the early stage of the ramp still in endometrial cancer. They have just received reimbursement in recent months in Europe. We are in the early stages of the ramp in frontline endometrial. I think importantly here is that it is far from over in where and how GSK has been developing this drug. Last year, in a phase II study by Memorial Sloan Kettering, they showed a 100% complete response rate in rectal cancer, in DMMR rectal cancer. That trial and pivotal studies will read out in the second half of 2026. There are also trials ongoing in DMMR and MRP colon cancer. There is a trial going on, pivotal trial for head and neck cancer. GSK is also developing this drug in combinations with its ADC portfolio. A lot of advancements still come. The composition of matter IP is out through 2035 in the U.S., 2036 in Europe, and 2037 in Japan. There is room for patent extension from there. There is longevity here in terms of additional trials that are going to read out, some with partial proof of concept that is compelling. They are also developing areas that Keytruda is not. A number of the indications I mentioned, Merck is not developing in, and/or like in endometrial cancer, they do not have survival data. There is differentiation in the diseases as well as protection post-Keytruda loss of exclusivity in the future. On the imsidolimab side, as I mentioned, there is a partnership with Vanda. We have a 10% flat royalty. We anticipate approval of that program next year, assuming the BLA goes in this quarter, as has been advertised by Vanda. Let me put into more context how large Jemperli royalties may become. There is a green line on the top of this page. GSK's current guidance is far north of that green line, which represents $2 billion or $2.7 billion U.S. peak sales. I ran through the royalty tiers earlier. If they hit that green line, $2.7 billion, that converts to $390 million a year to AnaptysBio in the future. We do have a non-recourse debt obligation due to a group called SAGARD from a prior monetization. We anticipate paying that down by Q2 of 2027, which assumes 10% quarterly growth moving forward into that period of time on this royalty. As I mentioned earlier, the last three quarters were between 16%-19% quarterly growth. There is a lot more to come in the launches of endometrial cancer, plus those other readouts. We feel pretty good of having this pay down pretty soon in the next 18 months. Moving forward, the cash will accrue back to AnaptysBio. As I mentioned, we plan on separating this business out in 2026. It is possible that the separation will occur by the first half of 2026. Moving on to the biopharma operations, I introduced AMV033, which is a CD122 antagonist. This is a dual inhibitor of IL-15 and IL-2 signaling pathways. We designed AMV033 with an optimized epitope that squarely fits and blocks IL-15, IL-2 in the dimeric or trimeric receptors, depending on the immune cells of which CD122 is expressed. It is also designed with very high affinity. We think these are the two factors that will differentiate it moving forward in clinical trials and the data that it will produce. CD122 is expressed on a variety of subsets of autoimmune cells, subsets of CD8s, CD4s, as well as NK cells. Importantly, in select diseases that are principally driven by CD8 cells, there are different types of immune cells that are present in these diseases that you do not see in healthy individuals. IELs in celiac disease are heavily CD122 expressing and largely made up of CD8 T cells. In diseases like EOE, the cell type called ILC2s also densely expresses CD122. The IL-15 pathway is being assessed by a number of different players today. We're featuring a few that are in clinical development, Novartis and Teva, as well as a competitor of CD122 and Forte. There are a lot of diseases that we think are applicable for this target, both in GI and dermatology, as well as selected other diseases like type 1 diabetes. Novartis has already read out proof of concept in celiac disease and EoE, and have recently initiated a phase 2 trial in atopic dermatitis. Teva is in a celiac disease trial in phase 2. They previously had positive results in a phase 1B. They're also assessing a phase 1B in vitiligo. They'll be reading out next year both of those studies. Forte, similarly in celiac disease, has had proof of concept. They're in an additional celiac trial ongoing that'll read out next year, as well as in vitiligo and alopecia results next year. There is a lot of activity going on here, exploring a number of different diseases. As I mentioned, we're assessing our trial in celiac, which I'll get into more detail, as well as considering EoE and others for next year. We have run the phase 1A trial so far in healthy volunteers. It's ongoing, but substantially has completed. The results were unremarkable, which is what you're looking to see here. No SAEs, no AEs of note, no signs of viral infection. On the PD, we have a two- to three-week half-life. We have long-dated PD. The receptor occupancy is greater than 30 days. What we observed is the impact on cells like NKs and CD8s do have a long tail in terms of the decrease of those CD122 expressing cells over time that goes out well longer than a month, more like three months plus. I'll show you that data as well. We've modeled the IC greater than IC90 on the CD8 cells in the periphery, and we'll then show you the effects. That was important for how we're thinking about the hit on celiac disease on the CD8 IELs. Importantly, while we do impact CD4 cells, we have seen no negative impact in total Tregs over time in this study. The PD out of the phase 1A, in the top right, I'll direct you to the CD122 expressing NK cells. This is from one of the SAD doses. This is the peak impact. Greater than 90%, really closer to 100% reduction of the CD122 expressing NK cells. Importantly, not all NK cells express CD122 in humans. About two-thirds do. The one-third that result seems to be well north of the minimum NK cells you are looking in total lymphocytes, where you are still preserving immune competency. Again, we had no safety signals from our study. All the other drugs in these classes have also not had any issues, but have had similar impact on NK cells. The differentiation from our potency is hitting the CD8s as well as CD4 cells. Measuring the CD122 expressing CD8 cells in the periphery, see about a 70% impact, but a negligible impact of CD8s overall. We really are hitting the pathogenic CD8s in the healthy tissue. This is a diagram expressing the biology in celiac disease. You can see in the purple square, this is the IL-15 signaling impact, which comes from the epithelial cells and really induces the proliferation of IELs. By blocking IL-15 on the IELs, you will reduce this in the downstream side of celiac disease. The green box, the greater box, this encompasses the initiation of the autoimmune in celiac disease. Gluten's ingested even in trace amounts. What you see very quickly, gliadin is picked up by the ADCs, binds to CD4s, which induces a very rapid, within one hour, increase in IL-2 as well as interferon gamma. That's a trademark of celiac disease is that increase in IL-2 expression. CD122 antagonist with high affinity will block CD4 and reduce the IL-2. We're blocking upstream the initiation of this disease as well as downstream the proliferation of the IELs. We're showing some of the other products that have been used or attempted to use in development of celiac disease. As I mentioned earlier, the IL-15s, which are only going to impact the IELs directly, they're not going to have an impact on CD4s, have shown a positive read-through, particularly in the reduction of IELs, as you would expect given they directly are acting on them. Previous to that, though, there's been a lot of drugs that have been discovered and attempted to be developed here that are really targeting the gluten. What they're not doing is targeting the inflammation directly. They're really great at being successful in a gluten challenge study. When it comes to actually healing the villi in this disease, this is when we've seen these other types of drugs fail over time. In our view, it's important to hit both sides of the inflammation, as we know in autoimmune diseases. Targeting inflammation reduces the histology in all these diseases as well as symptoms for these patients, very different than targeting the antigen. We ran a mouse model study. On the left, you could see in sham, no impact on the villi. This is the histology of the gut. In the middle, we introduced gluten. You see destruction of the villi, that's the white space in between. On the right, when gluten is introduced with AMV033 surrogate, you see preservation of the villi. The endpoints in these studies, the histological endpoint is VH:CD, villus height to crypt depth ratio. I just showed you the destruction of the villi with gluten and on placebo. You could see that here now in the middle isotype. You see reduction in that ratio based on that measurement. On the right, you can see that we're preserving function in this gluten challenge mouse study. Similarly, data is not shown, but we do have in the public domain. We've prevented an increase in IELs on our drug as well. These are the two surrogate markers that you're going to be looking for in the clinical trials. As I mentioned, we did start our phase 1B trial. It is a 60-patient trial, one-to-one randomization, drug versus placebo. We have two different cohorts. The first is a classic gluten challenge. You're giving subcutaneous AMV033 at baseline, week two and week four. From there, you introduce 6 grams of gluten daily for 14 days. You have the biopsy right out of the gate. Then you're assessing a second biopsy at week six post the gluten challenge. What you're looking for there are a few different things. On placebo, as we just showed you in the mouse model, you should see reduction in the villi or a decrease in the VH:CD. On drug, you should see a preservation of that on a relative basis. We're also going to be inducing symptoms. You're taking well-controlled patients. You're giving them gluten. You should see the symptomatic response on placebo that hopefully would not be present on drug. We're powered greater than 80% to see changes in both of those endpoints. Interestingly, and this is novel, is the second cohort. For patients who do not qualify for the gluten challenge, i.e., their VH:CD ratio is less than 2, they would move into the second cohort, where you will receive a dose similar to the first of AMV033 or placebo at baseline, week two and week four. For these patients, we will not be introducing gluten. It would be unethical. We are going to assess healing over time. Their villi have already been destructed. We're going to do a biopsy at week 12. The modeling, what we've seen in Sinus, in the Toxwork, and in the phase 1A suggests that there will be long PD here covered above the IC90. After four weeks of treatment or placebo, we'll measure was there healing at week 12 for the patients who had less than 2 on the VH:CD. We'll also be assessing the symptomatic scores as well. We anticipate having results from this trial in Q4 of 2026 next year. Celiac disease has zero approved therapeutics today. For patients who are not well-controlled on gluten-free diet, there is no other treatment for them. We estimate over 2 million patients in the U.S. have celiac disease, with over a million that are presently diagnosed via biopsy. We estimate 250,000 patients into the 2030s will be eligible for a biologic. These patients are non-responsive on a gluten-free diet and express symptoms. That is ultimately the target patient population. That second cohort I just walked you through is a good proxy for this future commercial population that we'd be assessing in phase 2 or phase 3. We've done initial market research. There are a number of big pharma companies looking at this disease. We do think that a therapeutic or antibody therapeutic in this disease would be able to command IBD-like pricing. I mentioned earlier that we're also assessing AMV033 in EoE. There are two different inflammatory pathways in EoE. Dupilumab is the only approved therapy for this disease. It's a weekly subcutaneous administration. Dupilumab targets CD4s and ILC2s. I mentioned earlier that CD122 is densely expressed in ILC2s. What happens in this disease is these ILC2s express large amounts of IL-5 and IL-13. By binding these ILC2s, we have shown preclinically in vitro reduction of the ILC2s and reduction of those cytokines. We should be able to impact this disease in the same way as why Dupilumab works. Importantly, 25%-30% of patients who take Dupixent with EoE do not respond to Dupixent. We believe it is because of the second inflammatory pathway, which is sensitivity to CD8s and NK cells. I have just shown you a lot of data and how CD122 is a central receptor there that blocks IL-15, which is a these cells are very sensitive to IL-15. We should be able to reduce granzyme B and interferon gamma expression, which is driving the symptoms in this disease. We've also shown in vitro this effect. There have been a number of drugs also here that have not worked. One of the hallmarks of treating EoE is reducing EOs or eosinophils. They get recruited in this disease. A lot of the drugs that have failed have directly targeted EOs. You see a reduction in the EOs, but you don't see impact on symptoms because they're not actually treating the inflammation. Very similar to the idea in celiac disease that I just walked you through. Interestingly, there has been one of the IL-15s with Novartis right now, where they have shown a reduction in the EOs, and they've shown a reduction in symptoms. There is proof of concept around this disease just targeting the pathway in the purple box. Again, in CD122, we think we could do both. The mechanisms that have failed have directly targeted EOs or downstream from the actual inflammation of the disease. We did run an Aspergillus model in mice. What you could see here is in black, in isotype control, you could see an increase of the EOs, but you're seeing a controlled impact of the EOs over time in blue, both in the esophagus and in the lung. Importantly, it's proof of concept that by not targeting the EOs, you could still reduce them because you're upstream of that pathway. There's a large market here. Dupilumab is selling $2 billion. It's been on the market for three or so years in this disease. Rapid uptake and a growing market. Now that there's a therapy, more people are being diagnosed with this disease. In the last few minutes here, I'll quickly spend some time on Rosnilimab. I mentioned earlier we ran a phase 2b in arthritis. It was robust, a large study, 424 patients. Read out initial data in February at 12 weeks. Importantly, we were recently at ACR. We were the number one late breaker that was presented in the plenary session a few weeks ago. The trial design, we had three different doses versus placebo. Again, over 12 weeks, placebo-controlled. Patients who were in low disease activity on the CDI scale, which is a very high bar, were able to stay on drug from month three to month six. We also observed patients after month six off drug for an additional 14 weeks. We had a best disease profile, particularly at six months. There were no safety observations on this drug. Very high tolerability, less than 2% of patients left the trial due to AE. After three months, only one patient left due to AE, which was moderate migraine. Max response rates have not been observed. Patients who were responding, we had many patients in the trial that were at ACR 50 at three months. 60% of the patients who did not hit LDA, 60% were still at ACR 20. All those patients who were in LDA were removed from the trial. We do believe that those patients were improving and could have hit deeper responses over time. The trial design is mandated by the FDA, would not let them stay on drugs. We think the response rates could even be better. Importantly, what we just showed at ACR is that off-a-drug responses were sustained. Patients hit deeper response over time from three months to six months. We saw a deepening in remission. Those patients were stable. I'll show you a little bit of the data. First, preclinically—I'm sorry, translationally, again, the target here is pathogenic T cells. This is in the synovium. You could see at both doses, what's lit up here are the PD-1 high expressing TPH cells. That's on the left at baseline. They're gone at week six. The drug's doing exactly what we want to do, is targeting that very specific type of T cell that's pathogenic upstream from the initiation of plasma blasts into B cells and autoantibody production. That's the mechanistic of what's going on here. On placebo, we saw an increase. On the lower dose trial, not shown here, it was inconclusive. There was no meaningful impact. This is some of the data on the CDI scale. There are a lot of lines here. The green are the patients who responded low disease activity by 12 weeks. The dark blue are the patients who then got there at week 14. Those are the patient set that continued on through six months. It was 70% of patients who were on Rosnilimab. This is bundled across all three doses. Interestingly, the light blue line that starts at a high end of the CDI scale, dramatic improvement through 14 weeks. Did not get to stay on drug because they did not hit low disease activity. That is not real world. That was a function of the trial design. Dramatic impacts right out of the gate in 12 weeks. What this slide is showing, half this trial was in bioexperienced patients. 40% of the trial was in bioexperienced patients. What we are showing here is a breakdown of that set by response rate across the different colors. These are the higher order responses: ACR 50, 70, CDI LDA, and CDI remission. Whether it's post-TNF, post-JAK, which was almost 30% of the trial, post-IL6, as well as if you were third-line therapy, not just second, we're seeing response rates here that are best in disease. Importantly, like I mentioned earlier, off-drug. After six months, we assess patients 14 weeks later. On the page, you're showing about 75%-80% of the responses. Again, all high-order response rates are sustained off-drug. We also looked at the patients who were no longer in low disease activity or remission, and they just missed. These patients weren't flaring. The median patient who missed wasn't flaring. We had great sustained activity. For a drug that was monthly administration for six months, off-drug, what this is showcasing here is potentially have an induction regimen that's monthly and then a maintenance regimen afterwards that could be Q8 weeks or Q12 weeks moving forward, subcutaneous dosing. This is the safety chart. Again, there's nothing here of note. Well-balanced versus placebo. You're seeing that on the placebo-controlled portion on the left at 12 weeks. After that, there is no longer a placebo control. We're showing it as a rate in patient years relative to where placebo would be. There's nothing of note on the slide, whether that's no severe infections, no malignancies, no MACE, with the exception of one patient that had prior MACE. This is a huge market opportunity. There hasn't been a drug approved for arthritis, a new class, in about 15 years since Jakafi was approved in RA. There's very little innovation here. Over 500,000 patients cycle off one or two lines of TNF. Over 100,000 patients, this is just in the United States, flow through three, four, five lines of biologics and are in salvage therapy. Our target market is somewhere in between. There are hundreds of thousands of patients that are experienced with biologics, are looking for a similar type of therapy. Again, there's nothing in front of us in phase 3 of note moving forward. Right now, we're assessing strategic and financial collaborators' relationships to start, new initiate a phase II trial into 2027. In summary for the biopharma operations, with AMV033, we'll have data in celiac disease by the end of next year in Q4. We will start a second trial for AMV033. For Rosnilimab, positive data that was just presented at ACR, we're looking to move into phase 3 next year. And AMV101, I didn't have time for in today's presentation. But it's in phase 1A in healthy volunteers, and that'll read out next year. Thank you.