Period of time. I think everyone who's dialed in, they know the housekeeping rule. Email me or we use the Zoom box to submit question, and I'll forward questions to Dan, I'll make sure to ask it. But be mindful, we have about, you know, 25 minutes for this session. So Dan, I think a great first question is, I think last year you guys announced sort of this idea of splitting the royalty pharma management and the ex-biopharma company, and that is expected to occur in early 2Q. Can't believe that 1Q is almost over. Maybe help us understand the strategy and sort of the timing around it, and what's sort of left to do. Yeah. So thanks for teeing that up. It's probably the number one priority on my plate right now, is to effect this, the separation of the royalty company and the biopharma. Just a quick clarification, just right out of the gate, 'cause I heard you say early Q2. I think what we're saying is, we're trying to get this done in Q2. That's what we're pushing for. It could be later, but things are on track, but I don't want to misguide the exact timing within Q2. This is definitely not happening April 1st. Okay. But things are moving. You know, big, big picture here, and I think, you know, you've seen it reflected in the share price. The royalties driven by Jemperli and Imsidolimab are substantial, and there's a big cost to capital arbitrage. And where we're focused on by separating out the biopharma businesses is truly allowing a public company that owns the royalties plus the NOLs to hold back and recognize the value of commercial entities with a very low cost of capital in a virtual or semi-virtual company with very low OpEx driven on an equity story for the next number of years of Jemperli growth, really driven by monotherapy sales and label expansion. Imsidolimab will be a second drug that we hope to be commercial this year. Our partner, Vanda, filed a BLA in December. So that's off and running, and, you know, I often go like this, where, you know, the drivers of the different companies in the biopharma company at some point come to a head, and that's why this is a priority. Biopharma company is consuming cash, royalty company is looking to protect and return cash to shareholders. So they're at very different points in how we're gonna think about running the two different businesses. We've announced I'll be running the biopharma company. Almost all employees will be dividended and moved into that new company. It's a taxable spin. It'll be a publicly traded entity right out of the gate, and we'll have three clinical stage assets in it. Rosnilimab, which we're trying to advance into phase III. We're looking at how to capitalize that between strategic or financial or a combination of the two. The base case is this will be in the biopharma business at this point. There's still a chance it could stay behind royalty, but we're not gonna likely get a deal, or I'm not gonna force a deal to be done ahead of the separation. And then where there's a lot of investor excitement is in ANB033 or CD122 antagonist, which we'll talk about. And then the third program is ANB101, which is a BDCA2 modulator in phase I-A. So, you know, a lot going on there. As it relates to the cash, we had $310 million of cash coming into the year, about $11 a share cash. We will put at least as much cash as we need in the biopharma company to get through the catalyst of celiac and EoE data, in through 2027. If we put all the cash in, we'd have cash well into 2028. So there's a decision point of how much, wearing the hats of both companies today, you could argue, leaving cash behind and returning that to shareholders, even through share repurchases, could create a lot of value for today's shareholders. So we have a decision to make there on the cash distribution, which will also come down to when does the spin of... when is the spin effective? Right now, every dollar we spend, more or less, is going to the biopharma business. That's super helpful. I mean, Jemperli continues to really hit record sales, right? I mean, it just reported in Q4, $343 million in the quarter. I mean, we're seeing a 13% quarter-over-quarter growth, but somehow Street is not really appreciating this really value-driving program. Why do you think that is? And two, maybe also remind us, what are some of the near-term catalysts related to Jemperli that could expand its co-commercial applicability, as that's gonna be an important aspect also. So Jemperli is the best-in-class PD-1 antagonist. There's head-to-head data versus Keytruda, in lung cancer. We're the only drug that has overall survival in frontline endometrial cancer. That's what's driving revenues today. GSK has done a great job in the monotherapy development with a thoughtful strategy here. A year, year and a half ago, we started talking about this a lot publicly. What's interesting with Jemperli at GSK, you know, going back that far, it was the 20th largest asset. Consensus curves at GSK analysts, the sell side there, they have this as the sixth or seventh biggest drug this year. Now, the irony of that is you can look into these models, and there's still negative growth rates assigned to Jemperli, quarter over quarter. That's how fast this is growing. It just hasn't been the biggest drug in the company, so I think it's a little bit of a sleeper over there if you're a GSK analyst looking at this. I think the folks who cover Anaptys have a very different view. So you know, why is Wall Street not. I just think it's, you know, it's a seventh-to-market, but best-in-class PD-1 antagonist, and GSK's balance on how they talk about it. If you go back to September, they were more or less pointed this as one of two drugs that's driving the wedge between consensus 2031 revenue guidance and consensus 2031 projections and their revenue guidance, which was a GBP 4 billion delta. So there's a lot of growth to come here. There's multiple indications that'll read out over the next two to three years in the monotherapy side. This year, it's rectal cancer, pivotal trial, dMMR rectal, is being guided to reading out this year. They have a priority voucher, which allows for one- to two-month approval timeline in the U.S. And then, again, another catalyst I think is a bit of a sleeper is phase II data in MSI-H colon is expected here. I almost guarantee you no analyst is valuing MSI-H colon in the projections right now. As a reminder, $2.7 billion peak sales is what GSK has been guiding to. You could trace back, they've pointed to endometrial and rectal cancer only as allowing them to get to the threshold. I think there's a lot more opportunity to be far north above that, and I'm more or less quoting the prior CEO from September in those, in the comments. Coming out of this year, they're at $1.45 billion run rate. You apply 10% quarter-over-quarter growth to that, you're getting close to $1.8 billion at the end of the year. So that's not anyone's guidance, it's just very simple math, and the drug is growing in the mid-teens, quarter-over-quarter. So I think it's a very realistic number. And, sell-side consensus, that's higher, what I just said, $1.8 billion, higher than consensus in 2027. So we see a lot of value here. It's one of the underpinning reasons we're separating the business out, and I think the royalty company on a standalone basis, you have a multibillion-dollar drug, and we have an 8%-25% royalty that kicks in under it as a foundational asset in the royalty business. Thank you, Dan. Would love to transition now, sort of understanding, you know, ANB033, right, which is a CD122 antagonist in celiac disease. Maybe just some housekeeping question, you know, like, help us understand, you know, I think last October you announced the study design, the rationale behind the target. But maybe first question for you is, how's enrollment progressing, when do you hope to report data, and how clear do you think, or I guess, what do you want to see, you know, to kind of warrant forward to moving forward in celiac disease? I think no doubt it's an untapped market opportunity, a large TAM, but helpful if you could just frame the timing and thoughts there. Well, this is a long question. I could spend the rest of the call answering this one. I mean, ANB033 is real. We're really excited about the potential here. I think it's a differentiated CD122 antagonist, potency driven by the affinity and the binding epitope relative to competitors in this space. And just as a reminder, we're the only one, at least as today, in the clinic with subcutaneous administration. All that said, there's a lot going on here just in the broader pathway of IL-15 signaling and blocking. CD122 antagonists block the signaling of both IL-15 and IL-2. So there's dual, dual mechanistic here, value, and where you see CD122 presented, at least on pathogenic immune cells, CD8 cells, particularly cells like IELs in celiac disease, which are generally made up of, CD8 phenotype, but also CD4 cells. So in celiac, it's relevant with TH1 cells, and we have shown data, showing a reduction of the proliferation, the cytokine activity of the TH1 cells that are the ones that are actually activated via, APC presentation of, the, the downstream product of the gluten, which is the antigen of the disease. So we're actually hitting on multiple paths of inflammation with the CD122 blocker relative to the IL-15s that are in the space. They're really only targeting part of the biology, of the CD8s and the IELs. So with all that said, when you, when you back out and talk about the celiac disease opportunity, there is proof of concept with two IL-15s and with another CD122 in the space. We have high confidence that we'll be able to do at least as good as, as the data that's already been observed in the public domain on patients that had been administered a gluten challenge. So I'll come back to that in a second. But the celiac market opportunity overall, we think there's well north of 2 million patients that have celiac in the United States alone. Over 1 million are diagnosed and confirmed on a gluten-free diet, and over 250,000 patients, you know, projected over the next few years, they're not controlled. They're, they're not controlled on a gluten-free diet. It takes trace amounts of gluten to initiate the autoimmune cycle here and the inflammatory damage as a result. There's a huge market opportunity. A lot of folks are calling it the third IBD market. I think that's actually pretty fair. But what's unique here is there's no therapeutics approved yet today. This is a wide-open space, and finally, for this disease and the patients with disease, we have drugs like ours that are actually treating the inflammation directly, as opposed to targeting the gluten or other outside pathway drivers. So I think we're pretty excited about the approach we're taking. The design is unique. We're doing a gluten challenge, and I'll describe it first. It's 30 patients, 1-to-1 randomization. We're dosing at week 0, week 2, week 4, subcutaneously. Then you administer gluten to both of those groups, the placebo and the drug group. Gluten for 14 days daily, and then now you're at week 6, and you do a biopsy. What you're looking for there is the patients on placebo, you would expect them to now have damage. So you measure that by looking at the villi in the gut via the VHCD, villous height-to-crypt depth ratio. The patients that are in the study have minimal damage coming in. The ones on placebo, you should expect to get worse. The ones on drug, you should expect to be less worse. And so we're looking for a statistically significant difference versus placebo on VHCD, which is the histological outcome. We'll look at IELs, and then the second, outside the histology, is a PRO, which is a validated PRO, called the Celiac Disease Symptom Diary, CD-SD. Though between that and VHCD, those are the two endpoints in the draft FDA guidance that would be approvable at some point. So we'll look at that, and we'll look for stat sig difference versus placebo. The second cohort in celiac disease are patients who can't qualify for the gluten challenge, i.e., they had too much damage to the villi. This is defined by VHCD ratio of less than two. They'll be treated one to one versus placebo, week zero, week two, and week four, and then we're going to wait eight weeks, and we'll do a biopsy at week 12. And what we're going to look for here is: are patients doing better? Are they healing? Is the villi, the VHCD ratio improving on drug, whereas placebo improving less or if not, or not at all? Unlike the gluten challenge cohort, where this has been done many times, and it's, it's powered for a stat sig, we're powered in the second cohort, but we're looking for is a trend, a trend to improvement on healing on VHCD. What we don't know, because it hasn't been done before, is, is 12 weeks enough to see a wide enough delta? We have modeled this in gut tissue, to be above the IC90 after that third dose through week 12. So we're actually going to get a pretty good look, not just on the PD in general, but also the dosing profile. The whole idea here is this population is much more relevant for what we think the phase II-B, phase III population would be, and really the regulatory path in the commercially relevant populations. We're going to get a lot of information to help us run, I think, a more de-risked phase II-B trial, whereas the gluten challenge is like the pay to play. Is the drug effective at preventing worsening of disease? It's a long answer, but I want to give you the full picture. Yeah, no, that's super helpful, and the data is on track for Q4 of this year. Yeah. So we started enrolling in Q4 of last year. Yeah. We should be able to read out this trial in Q4 this year. That's the target. In terms of just visualizing the readout, it's more of a function of seeing the alignment across these endpoints rather than, is the numerical difference in some of these villi scoring systems that's considered clinically meaningful, that we should be aware of? Well, see, this is what's interesting. There's no threshold. Exactly, yeah. I think that's why we're getting this question, what's clinically relevant? What's clinically relevant? is improvement. Alignment. Yeah. That's what's relevant, and you need to get a first drug out there. Yeah. There's no reason to set a higher bar than that right now until there's someone that sets it. Hopefully, we'll be the one setting that bar. A healthy individual has north of 3.5, closer to 4 on VHCD. Patients in the 2-3 range, generally speaking, have symptoms. I see. If you're less than two, there's very significant damage, and then there's really the long-term consequences of the villi reduction. The villi is where all the, nutrition is absorbed, the nutrition absorbed through the diet. So you know, there's not a hard and fast, "What's the VHCD?" You need to be improved. For people actually saying these drugs, they need to feel better. It's very similar in concept to EoE, which we'll talk about, in a minute as well. You want the villi to be improved, you want patients to feel better, and that's why the histology and the PRO are the two primary endpoints the FDA has guided to here that you need to hit on both. Then given that, Dan, we're gonna see the celiac disease data ahead because the EoE data is more, it's kicked off in 1Q. Is there any translation from the celiac cohort to the EoE? So if you could put some color around that, and then also kind of frame the mechanistic rationale to work in EoE. One of the reasons to look at EoE, I mean, beyond the fact it's a huge commercial market, and the biology and the pathways and the preclinical data, which I'll, you know, hopefully I can address here, are compelling for us, is we're actually looking at slightly different biologies in the diseases. Now, there's a CD8 component to EoE. There's a company called that used to exist, Calypso, which Novartis acquired. It's one of the IL-15s. They ran a small trial in EoE, where they showed that the IL-15 blocker, so this is one of the cytokine ligands, they showed a reduction in eosinophils in that trial. Now, CD122 is not on the eosinophils, it's not primed by IL-15 in any way, or it's not needed for survival, so you're upstream, and you're still showing a reduction in eosinophils. That's a really positive sign that you could target the CD8 biology and reduce the recruitment of the eosinophils. So we know there's activity there. What's important for us here is we are also on the CD4 TH2 cells with CD122, as well as ILC2s. There's one approved biologic in EoE. It's weekly dosed dupilumab, which targets TH2 and ILC2s. We do that, and we have really compelling clinical data from an animal model, an Aspergillus eosinophilic model, where we're showing the prevention of increases in ILC2s, increases in TH2, increases in CD8 cells, in that disease. We're flooring the eosinophils relative to any of these other drug classes. We're reducing chemokines like eotaxin, which actually recruits the eosinophils. So we're seeing all the right biomarker activity and direct immune cell activity. We're impacting the pathways that dupilumab works in, but we're also enhancing it, and again, via the proof of concept, Calypso data, the CD8 side. As a reminder, 30%+ of patients don't respond to dupilumab who have EoE. Those patients, generally speaking, have an increase in IL-15. So we arguably could have a drug here that hits the entire population, not just the dupilumab population. But even if we only impacted the patients with dupilumab, that's a great secondary market for us. There's a $5-$6 billion market. Dupilumab is doing about $2 billion a year in EoE alone. So huge market opportunity, and we're a leader in this space as it relates to our drug. We do believe that CD122 antagonists, we really can show differentiation here in this disease relative to any other IL-15s, if they ever go pursue. Thanks, Dan- So between celiac and EoE if we're successful in one or the other or both, there's a host of other diseases p articularly, again, what we're going to learn translationally, we could expand into. What with the study expected to start this quarter, maybe, you know, can you maybe frame what sort of the rate-limiting steps to get it up and running? And then, walk us through that rational design for that POC study, and same idea, what signals do you need to see out of that one B? There's nothing rate limiting other than the standard operational components of initiating different countries and getting the sites up and running at this point. We're on track for what we committed to. We'll have sites initiated imminently, and should be enrolling before the end of this quarter. Guidance here, we have to be more specific than it's just given when we're starting, the data won't be until 2027. We will come back around post the initiation and lay out the trial protocol in more details. But just at a high level, there are two things that matter in this design for the phase I-B. You know, again, very similar to celiac, there's two primary endpoints you need to hit. One is the reduction in eosinophils, and the second is a PRO called the DSQ, which is what we'll be using here, and that's what dupilumab used for their approval. We're powered for both of those endpoints in the phase I-B, where a lot of drugs have failed in this disease, where they target the eos directly, or they target other mechanisms that might reduce eos directly or indirectly, but they don't actually have an impact on the symptoms. And that's because they're actually treating the upstream inflammation, which is what dupilumab is doing. Dupilumab doesn't target eos. They're hitting TH2 and ILC2s, and you're seeing a symptomatic benefit. So it's important for us not to just show that those eos are reduced by targeting upstream, but to be powered to show the symptomatic outcomes. We think this will very meaningfully de-risk phase II-B, where other companies have failed, where they just show eos reductions early, and then they don't ever show the clinical benefits later. So we're trying to do all that in one phase I-B study, so we think it will be very significantly de-risking here. Thanks, Dan. I know we have, like, a minute or two left, but I want to also talk about rosnilimab, right? I think you guys have said you're going to give an update at some time this first half in regards to phase III advancement. So maybe help us understand how you're thinking about opportunity and potential, and when you could provide more color around how you're thinking about development and the capital needs for that program. At a high level, we have a drug that works very well in RA, as a result of the phase II-B trial readout last year, with data that gets better over time and is stable off drug way out, you know, up into nine months, at least in that 424-patient study. Really impressed with the data, so is the medical community, and the drug needs to advance. That's the mission here. I outlined a little bit earlier, there's different ways of how to do it. We're not going to use balance sheet cash. I think what the reality here is you kind of have to put your hand up and say that, "You know, we're not going to be commercializing this ourselves in the biopharma business." Once you're clear-eyed about that, it opens up a lot more opportunity for how you can advance this, thinking about an ROE for us, but working with the right groups out there to execute on a phase III program. By the end of this quarter, we'll have met with the FDA and end -of- phase II meeting. It's gonna define better for us the size of the overall program needed for approval, the size of the safety database, and some definition around the different trials that we are part of the program. That's a gate, because that's going to then be highly correlated to the cost to run the program, to move it forward. With the timing of the spin in Q2, things start to become on top of each other, which is why I'm saying base case is rosnilimab would just go into the biopharma company, and we look to put the right relationship in place, thereafter. We will give an update on where we are in that process, later on this first half. Perfect. And then maybe one last question. 101, which is a BDCA2 modulator, it's in development in phase I. Maybe help us understand how you're thinking about this asset. What's the evidence to support, you know, sort of moving this forward and indication selections? Yeah. BDCA2 is a cell surface protein that's found preferentially on a cell type called plasmacytoid dendritic cells. And these are really only exist in disease, very little in healthy individuals. So with that background, there is a company called Biogen, who has three phase III trials ongoing with a first-generation BDCA2 in SLE, which will read out by the end of this year, their guidance, and one in CLE, which will read out, it sounds like in early 2027, and they actually recently updated last week. Sounds like some phase II CLE data might be presented in an upcoming conference. So we're tracking that pretty close. We're excited about the drug we have. The preclinical data that we've generated internally, and then what we've seen initially in the phase I-A so far is validating this. We have a more potent drug, observed in extended half-life, and then the PD effect, where we have a stronger depletion profile of the pDCs. So when you add that all up, I think we have a very differentiated drug. If we see positive results from Biogen, I think there's going to be a pretty clear path on how you can move the drug forward in those diseases. If we don't see positive results from Biogen, I think we're gonna have to put a little more thought into where else we'd want to develop, if at all. There are choices here. We're keeping those in our pocket. We've done a lot of work on where else we could develop the drug, but I think the decisions on when and how to advance will come post the Biogen data. We have a differentiated drug, but as it relates to a return on our capital right now with ANB033, we're into disease we're excited about. There's many other diseases we want to be ready to go on in 2027, based on how other readouts happen in the space and the success of our own drugs and based on that translational data. So we have our priorities, I think, in the right order. But a number of catalysts this year. I think, look, in summary, advancing rosnilimab getting celiac data, enrolling the EoE trial, seeing the Biogen data, BDCA2. On one hand, the separation in general, quarterly growth for Jemperli, two other readouts I mentioned, rectal and colon cancer this year, and then we have litigation with GSK that, you know, look, at the end of the day, while I think they've done a great job in monotherapy development, there are real contractual issues what they're trying to do In combinations, where we think they're in material breach, in a number of different ways. There's a possibility that the drug reverts back to us in the royalty business, post the trial, which is set in July. So coming up pretty quick. So look, we're excited about various opportunities, and, you know, litigation is never fun to go through, but, you know, at the end of the day, we have to defend the contract there, and that's another catalyst, I think, for the stock over the next five months. Lots going on, Dan. I know you're extremely busy, and this was super helpful to kind of frame sort of how important 2026 is for the company, between the catalyst and the split of the two. So thank you so much for being part of the Immunology Day, and talk very soon. Thank you. Appreciate this opportunity. See you soon. Thank you. you. See you soon.