Welcome, everyone, to the 44th Annual JPMorgan Healthcare Conference. My name is Anupam Rama. I am one of the senior biotech analysts here at JPMorgan. I'm joined by my squad, Rathi Pinhey, Priyanka Grover, and Joyce Soh. Our next presenting company is AnaptysBio, and presenting on behalf of the company, we have CEO Dan Faga. Dan?
Hello, everyone. Thank you for having me join today, Anupam. These are our forward-looking statements. This is going to be a transformational year for AnaptysBio. In September, we announced, September 2025, we announced the intention to separate into two businesses through the course of this year, and that is likely to happen in the second quarter at this point. The two businesses are generically referred to as Biopharma Co and Royalty Management Co at this time. The Biopharma Co will be anchored by three clinical assets. The operating business will be driven through ANB033. We are enrolling patients in a celiac trial in phase I-B, and we announced into this weekend that we are initiating a second trial in phase I-B in EoE. Rosnilimab is a pathogenic depleter of pathogenic T cells.
We had positive phase II-B results in our arthritis trial in 2025, and over the next six months, we'll be exploring how to move forward through phase III, including securing strategic or financial capital to run the phase III, and we have an end-of-phase III meeting with the FDA over the next quarter, and ANB101 is in ongoing phase I-A studies. The Royalty Management Company will have two core assets: the rights to royalties from JEMPERLI sold by GSK, and the rights to royalties from imsidolimab, which our partner Vanda recently filed the BLA in a disease called GPP that we expect approval later in this year.
The company today, coming into this year, has $310 million of cash, which should suffice moving forward in the biopharma business through the events of the trials I just outlined, and then as well as leaving behind sufficient capital in the Royalty Management business to operate over the next couple of years until we pay down an outstanding obligation to Sagard, and that company would become cash flow positive. I'll spend a few minutes talking through the Royalty business first, and then we'll transition into the biopharma operations. The value proposition for the Royalty Management Company would be to protect and return the value of the JEMPERLI and imsidolimab royalties to shareholders. We intend to run a capital-efficient business with the minimal operating structure. This company would remain as the parent company that is Anaptys today pre the separation.
Starting with JEMPERLI on the left-hand side of the page, the sales for this drug inflected in 2025. In the third quarter alone, there was $300 million, over $300 million of revenue, principally driven by the U.S. launch in frontline endometrial cancer for this PD-1 antagonist. They have consistently, at GSK, over the last four quarters, shown high teen% growth. They received approval in Europe in frontline endometrial in the beginning of last year, and through the course of this year, we expect to see uptake in OUS sales given reimbursement. There's a number of catalysts as well that I'll run through on the next slide, but the royalties that we received from GSK are significant. It initiates at an 8% royalty tier every year up to $1 billion of revenue.
It advances through a 12% tier, a 20% tier, and at $2.5 billion of annual revenue, we would receive 25% royalties from GSK. At the guidance that GSK has historically provided of GBP 2 billion, which is about $2.7 billion of peak sales for JEMPERLI on monotherapy indications alone, we'd receive $390 million of royalties at that peak sales value. The royalties have composition of matter in the U.S. through 2035 and in Europe in 2038 or 2036, and we have room for patent extensions from there. We do have non-recourse debt through Sagard that I referenced earlier. At the end of 2025, we anticipate that we'll have liabilities paid down of $250 million of $600 million, and we anticipate that the full non-recourse debt will be paid off by Q2 of 2027.
There is substantial ongoing investment by GSK to expand indications, particularly monotherapy indications that will roll out over the next one to three years. For imsidolimab, this is a drug that we also discovered and developed in-house at Anaptys over the last number of years. We out-licensed this drug to Vanda in the beginning of 2025, and through the course of this past year, they stood up the BLA filing. It was submitted in December and announced. We do anticipate additional filings in Europe and Japan later this year, but I'll leave the details there for Vanda to guide into. We have a 10% flat royalty. We have sales milestones as well as regulatory milestones from this collaboration, and we do expect approval in the U.S. this calendar year.
This is a slide that just highlights a lot of detail, the ongoing catalysts and mainly the trials that GSK is ongoing right now in monotherapy development for JEMPERLI. Two highlights for this calendar year: the AZUR-1 trial in locally advanced rectal cancer for dMMR. There's phase II proof-of-concept data that already exists, 100% complete response rate in over 40 patients. The pivotal trial will read out this year. The company, GSK, did receive a national priority review voucher this past year that entitles them to a three-month review cycle upon submission of the sBLA. So we do anticipate that this year. The second trial that we do expect primary completion would be in phase II in MMRp colon cancer. So this is proof-of-concept study, and from beyond this, you would expect a phase III advancement.
The point of this page is, while there's a lot of growth right now in endometrial cancer, there's indications that are going to read out this year, in 2027 and in 2028, to further expand monotherapy development. To try to drive this home on just how large this royalty can be, this page is reflecting peak sales forecasts for JEMPERLI. The green line on the top of the page represents the GBP 2 billion, of which the prior CEO of GSK last quarter said will be far north of this GBP 2 billion threshold of $2.7 billion. There's a number of blue lines on this page that represent consensus forecasts from GSK analysts. The dotted blue line was where they were a year ago, peaking at less than $1.5 billion.
Through the course of last year, and given this inflection, I really think the attention now being focused on by the street for this asset, as of November of 2025, peak sales forecasts are $2.2 billion. Still shy of where GSK has been guiding over time, but we see that gap colliding through the course of the rest of this year with the current trends. $1.4 billion in 2026 is the current sell-side consensus. We anticipate year-end 2025 sales to already be on a run rate that reflects that number. So I think these forecasts are already dated, and there's a lot of upside from here in what we're seeing just in endometrial cancer and the ongoing launch.
JEMPERLI is competing against KEYTRUDA, but KEYTRUDA does not have overall survival data in endometrial cancer, and GSK has taken a strategy with the monotherapy development in some of these other diseases like rectal cancer where KEYTRUDA has not improved. So they've taken a smart strategy in a lot of women's cancers where they're going to be able to compete in spaces where they have differentiated data and/or places where KEYTRUDA is implied. The other lines on this page are reflecting the Sagard paydown. The orange line is a 10% quarter-over-quarter growth rate. That's conservative relative to what they've been doing recently, but if you just follow that orange line through, Sagard will be paid down by Q1 of 2027 or Q2 of 2027. So a lot of upside from here on how we view this individual royalty playing out.
So with that, I'll transition and spend the rest of this discussion on the biopharma business, and primarily focusing my remarks on ANB033, given the initiation of the celiac trial and the announcement into this weekend that we'll be pursuing a second indication in EoE. So ANB033 is a CD122 antagonist. It blocks the signaling of both IL-15 and IL-2. We believe that we have potency differentiation from the binding epitope that we target, as well as the affinity of this molecule that shows functional differentiation from other CD122s in the space. The cell types that we target that express CD122, certain subtypes of CD8 cells, CD4 T cells, and then very specifically pathogenic immune cells in diseases like celiac disease, IELs, express CD122 in EoE, ILC2s, very relevant immune cell in that disease, densely express CD122.
There's broad therapeutic potential for CD122 antagonists across both GI, dermatological indications, and other areas. There are a number of competitors, both with IL-15 cytokine blockers as well as another CD122 antagonist. There will be a lot of data, clinical data in the space just this year in diseases like vitiligo through some of the competition, in celiac disease from Teva and Forte, as well as our own data in celiac disease in Q4. Novartis and Teva both have IL-15 blockers. They're committed not only to what's on this page but also into additional indications. They've each said they're going to expand to two additional indications this year. So there's a lot happening in the space right now in the earlier days of generating proof-of-concept and also additional catalysts that will end up presenting themselves in 2027.
We've finished our phase I-A study in healthy volunteers, demonstrated a favorable safety and tolerability profile. The study was run in both IV and subcutaneous forms, two- to three-week half-life in both administrations, full receptor occupancy for north of 30 days off of one dose, and no other observations of note. Interestingly here, when we look in the periphery, we hit hard the target cells that we need to go then target in disease. On the top row, we're looking at the CD122 expressing CD8 and NK cells, both in IV and subcutaneous administration off of a single dose. The bottom row is focused on overall cell counts of the same cell types. You can see in the top right is we are fully eliminating all the NK cells that express CD122. Importantly, that is not all the NK cells in a healthy individual.
We do about a third of NK cells totally not express CD122, which is sufficient to sustain immune competency. So we haven't seen any safety issues, like I mentioned earlier, with this type of profile. I think importantly, we have hit the CD8 T cells, as is explained in this data, but in the bottom left, there's a negligible impact in CD8s overall. So this is going to have positive implications in disease. We saw similar results with CD4 cells, and importantly, we did not see any impact in total peripheral Tregs. First, in celiac disease, this is a potential blockbuster market where there are no approved therapeutics today. Over one million patients alone in the U.S. have diagnosis confirmed with celiac disease, and 250,000 patients in the United States are non-responsive to a gluten-free diet. So that's the market opportunity.
Payers understand the severity of this disease. They view this as another arm in the IBD portfolio of where disease is in a similar call point. So high disease burden, we believe there's going to be large price points. It's about a $5 billion-plus market alone just targeting that quarter million patients who are non-responsive to gluten-free diets. So the biological rationale, there's two pathways of autoimmunity that we see driving the inflammation in celiac disease. On the left-hand side of the page, patient ingests gluten. It could be trace amounts of gluten, which downstream gets picked up by an APC, antigen presented, and instigates the T cell cycle with CD4 TH1 cells. It upregulates IL-2 and interferon gamma. You see IL-15 secretion and incoming IELs which further perpetuate the autoimmune cycle.
As I explained earlier, CD122 targeting antagonists would impact directly the CD4 cells in this disease as well as the IELs. So we're hitting both sides of the pathology of the inflammation in this disease. In the purple box in the top right-hand corner, there is proof-of-concept in the space with the other IL-15s and CD122 programs where they've shown reduction of IELs in gluten challenge studies as well as prevention of villus atrophy as shown in lamina propria from both the CD4 and the IEL inflammation. There's been a lot of failure historically in celiac. These drugs that have not worked have really targeted the antigen, the gluten, in various timelines from ingestion through APC presentation. The IL-15s and the CD122s are the first drug classes that are targeting the inflammatory pathways, and the CD122 class is the only ones of those two.
They're targeting both sides of the inflammatory pathways. In addition to a lot of in vitro data showing on-target activity of cell types like IELs, we ran a mouse model of mice with celiac disease. What you're seeing on this page is the results of the histology from that study. On the left is sham. What you're seeing is villi that are fully functioning. In the middle was isotype control where we added gluten, and you're seeing the atrophy of the villi with the white space that's on the page. On the right, the same gluten challenge, but in addition to ANB033, which is preventing that deterioration. When we talk about the histology of this disease, what you're really looking at is atrophy of the villi, and then that's measured in a ratio, the villus height to the crypt depth ratio.
This is the histological endpoint that draft FDA guidance is looking for approval in this disease. The same data presented in that ratio on the right-hand side, the sham at two and a half with no impact. If you look on the right-hand column, again, no impact when you're giving gluten with the protection of the drug, but with isotype, you see reduction in that ratio. In addition, we saw exactly what you'd want to see with prevention of expansion of IELs when you're on drug, as well as prevention of an increase in CD4 T cells in lamina propria. Patients present in the real world not just with histological damage, but also with symptoms, and there's a range of that presentation.
Most phase I-B studies for drugs that are targeting this disease, you're running these gluten challenge studies in well-controlled patients that do not have histological damage where you can then administer gluten to see the destruction and the inflammation in the villi. You're also treating patients who are well-controlled in that they are not experiencing symptoms. What we are also doing, and I'll get into the trial design in more detail, is we're looking at those patients in a gluten challenge, but we're also running in a second cohort, patients who have damage, who have a VH:CD ratio less than two and have atrophy of the villi. The target population in a commercial setting, as I showed earlier, are going to be patients who have inflammatory damage to villi with a range of symptoms overall.
In our phase I-B, we're looking at two different types of patient populations, one of them much more on point with where we'd end up going in a phase II-B or in phase III trials for a commercial label. This is our trial in a typical design format. We're going to be enrolling 60 patients overall across the two cohorts, 30 in each. It is a placebo-controlled trial, one-to-one randomization. In the gluten challenge shown in cohort one, 30 patients will be administering drug or placebo at baseline, week two and week four, subcutaneously. Then at week four, you start daily, 14 days of gluten, and at week six, you then do a scope. You look at the endoscopy, and you're looking for placebo patients who have gotten worse, just like we saw in that mouse model, relative to drug patients who are preventing that damage.
Cohort two, VH:CD less than 2.0, already have that damage. Similarly, week baseline, week two, week four, subcutaneous dosing versus placebo. Then we wait. We wait till week 12 to do the scope, and we're looking to see if we've induced healing relative to placebo. Expectations here, we should have statistically significant differentiation versus placebo in cohort one, and we're looking for numerical benefit relative to placebo in cohort two towards that healing. We're also going to be looking at the PRO CDSD, which is the second co-primary endpoint that we would anticipate in a phase II or phase III trial for approval. That's been validated and aligned with the FDA. Second disease, EoE, we announced this weekend we'll be initiating a trial later this quarter. The market here is large and growing.
We estimate that in 2025, based on claims data, DUPIXENT, which is the only approved drug in this disease, will sell about $2 billion just in EoE alone in a market that's approximately 5 billion patients large right now, and as dupi has been approved over the last three years, diagnosis is growing in this disease. Again, dupi is the only approved drug. It's a once-weekly administered biologic, so another cartoon on how the biology of the disease works. On the right, there's one side of the inflammatory pathway that targets CD8 cells, which we target directly with the CD122 antagonists. Up to 30% of patients who are non-respondent on dupi show an increase in CD8s and IL-15 production. On the left-hand side of the page is where dupi is working in this disease. An allergen instigates EoE. CD4 cells are activated again.
ILC2s are recruited as an innate cell expressing IL-13, IL-5, which instigates and pulls through eosinophils. By targeting both aspects of the biology here, we should be able to treat patients who would be or would not be responsive on DUPIXENT. There has been failure here as well in this disease. There have been a number of mechanisms that have targeted eosinophils directly. They've been depleting them. There's a failure last year in a trial with the mast cell driving target, which impacted mast cells in the disease. The core principle here is you need the upstream of the eosinophils to have an impact on the direct inflammation. Like I said earlier, we think we're doing both what DUPIXENT does well and what they don't do well across the spectrum of patients that present with this disease.
I'm going to walk through this mouse model in a second, but there is proof-of-concept with another IL-15 that by just targeting the CD8s, you see reduction downstream of eosinophils. That was shown by Calypso, which Novartis acquired a couple of years ago. What we're showing in this page is really important data. It's Aspergillus-induced eosinophil model. In blue is ANB033. In the top left and bottom left, you're looking at the prevention of eosinophil recruitment relative to isotype in black. You can see other mechanisms on this page, much less impact. Importantly, we're also preventing that increase in ILC2 as shown in the bottom middle panel relative to isotype. Very quickly on rosnilimab, best-in-disease data from a 424-patient robust phase II-B trial that was executed last year. These data were presented at ACR in the fall by Dr. Paul Emery. The medical community has celebrated this data.
It's the first positive trial in RA in many, many years with a new biologic class. More importantly than showing statistical significance on all doses on ACR20 and DAS28 is over time, we start deepening our responses in terms of low disease activity being achieved as well as remissions through six months and then off drug at nine months. This drug was tolerable and safe across the board in this large study as well as in other trials that have been run by rosnilimab. This is a huge market, $20 billion market in the United States after TNF failure, $5 billion-$10 billion market in third and fourth line. So what we're doing right now is we're assessing a path forward for rosnilimab. We're looking to fund through either strategic collaboration, strategic financing, or other asset sources of capital to advance through a phase III program in arthritis.
We have an end-of-phase II meeting by the end of Q1, which will help define the size and the scope of what the phase III program is as well as the cost to run the trial. And expectations here as a base case are that this program would separate out with us into the biopharma business, but at some point in the future, we do need a strategic partner to commercialize it. So we're going to look to solve some of that over the next six to nine months. So in summary, the biopharma business is a catalyst across the board with the movement forward in rosnilimab, ANB033 in celiac disease and EoE in terms of data in Q4 in celiac across both cohorts. EoE is getting going, and we'll have data in 2027.
There'll be a lot of data as well as in the space of the IL-15s and CD122s this year. AMB101, and I don't have time to get into much right now. The phase I-A is ongoing. It's a BDCA2 modulator. There's competitive data from Biogen that'll read out in the back half of the year, a couple of phase III trials in SLE. We have a more potent version of that molecule with longer half-life with broader depletion profile of plasmacytoid dendritic cells, which is the target cell for that molecule. And with that, I'll take some questions.
Thank you, Dan.
Thank you.
I'll ask the first couple of questions, but to the extent there are any questions in the audience, feel free to raise your hand, and I can call on you. Dan, the slide said the split between biopharma co and royalty co as early as 2Q, but you were pretty definitive in your statement, in your comments, that it would be in 2Q.
We're targeting to have this happen by 2Q. So since we've announced the separation September today, there's a lot of background work in financial audit to break down a company, review processes with the SEC. It's not definitive that's Q2, but we do believe we'll be through that regulatory process to be ready to spin and separate in the second quarter. The business decisions that still need to happen, are we definitively putting rosnilimab into the biopharma business or not? We're not going to artificially try to get a financing done ahead of that, but we do have an opportunity to potentially do so and leave some of the economics behind in the royalty business. The second decision that has to happen is how we're going to capitalize each of the businesses with some subset of $310 million we have coming into the year.
Okay, and so there is a scenario where rosnilimab then goes completely to royalty co or stays at biopharma co? It depends on the timing of the potential.
But the base case to set expectations would be biopharma co.
Biopharma co.
But for clarity there, we will not be using royalty proceeds or the cash on the balance sheet today to fund the phase III program.
Can you walk us through some of the push-pull levers in this litigation that you have with your partner, GSK, on JEMPERLI, and some timelines we should consider, and to the extent that this ongoing process with GSK might impact the timing of your split or not?
Yeah. So just the last part of that question, the separation of the biopharma company is not impeded by JEMPERLI or anything related to JEMPERLI, which would include the litigation. The biopharma business will be completely independent of what's going on with JEMPERLI. From background on Anupam's question as it relates to litigation with GSK, last summer, through normal course of business with GSK, we were notified that GSK had gone ahead with a pivotal trial with one of their ADCs developed with both JEMPERLI as well as KEYTRUDA. We view that to be in breach of the contract that we have with GSK on how they are able to develop drugs in the PD-1 sphere. Through the working teams, we're not able to get to resolution. The contract defines a dispute resolution process.
There's a letter that's in the public domain that we sent to GSK on October 7th as defined by that process to the head of R&D at GSK, saying that we are in dispute with this trial amongst other trials that we've now discovered that they've been running with other PD-1 programs. While we were negotiating in good faith, we were surprised that GSK did preemptively file litigation with us on November 20th. We were ready for that situation, even though we weren't expecting it to happen. We did file a counterclaim, which really outlined the rationale for three material breaches of our contract. One being that Tesaro was either induced or encouraged by GSK to not follow the exclusivity obligations that they're obligated to by developing only Tesaro mAb as the only PD-1 at the company. The second is with material disclosure obligations that they were deficient in.
And the third is a breach of the optimum commercial return that the contract defines that Tesaro is obligated to follow in development relative to the rest of the portfolio and any other PD-1. So we have a number of different claims there. The trial date has a fuse on it. It's scheduled for July 14th and 17th. This is not going to go on forever. We have also filed a motion to dismiss on the initial claim that GSK is alleging, which is that we have repudiated our contract, which means we're walking away from our obligation, which is really to collect royalty checks and receive information.
So as a matter of law, our motion to dismiss is saying that that repudiation is not possible since we're engaging in a process to either find resolution and/or continuing on with the duties of collecting those royalties and interacting in a joint review committee. So there's a few things happening, but at the end of the day, if GSK is found to be a material breach on one of these claims, the contract is very clear. There's a reversion right of JEMPERLI back to AnaptysBio.
Okay. Yeah.
Hey, Anupam. Who was the driving force behind the separation, and what's the rationale behind the separation?
The question is, who was the driving force behind the separation, and what is the rationale for the separation?
So the royalty business and biopharma business principally are going to have very different business strategies, one being a cash consumption to develop and discover further drugs, royalty management business, which would have a very low cost of capital and a very low cost base. We think we'll trade at a very different level over time than if we keep these entities combined. That's the rationale for separation: different business strategies and different investment philosophies.
So who's driving this? So there's a mispricing assumption here that these assets are mispriced as a joint entity.
We are trading at $15 a share the day before we announced the separation, and we were up 50% the day we announced it. I think the clarity that we're going to protect and return the future equity growth and ultimately in long-term yield of that royalty relative to investing into earlier stage riskier assets, there was a difference in views on investors that look at each of those assets. So the separation inherently has creative value, and the arbitrage there is really discount rate difference of both entities.
Additional questions from the audience? So maybe just also a clarification question on rosnilimab and RA in the update that you're going to be providing. So it's basically you're looking for a partnership, or are there other ways to finance a phase III?
Yeah. I mean, there's a number of examples. There's actually one just over the weekend that's relevant in the IL-15 space of Royalty Pharma giving capital to Teva just to go develop a drug within the portfolio. There's no restrictions on a biotech company having the same asset type of financing. At the end of the day, we are going to need support commercializing in arthritis. I've been saying this consistently for almost four years now, and so we're at one of those crossroads that we're going to move forward in arthritis. We're looking for a shared way to develop the capital. Ultimately, we're going to need support in the longer term. That could be strategic capital. That should be a strategic partnership. That could be asset financing or a combination of these things.
We're open to a lot of options, and we're focused on a return of equity to move the drug forward.
Maybe just switching gears a little bit to 033 and celiac disease. You walk through the trial design here. Maybe you can walk us through how much data we're going to get in that initial release? We're going to learn a lot here in the first half about the mechanism and things like that. But as of today, when you talk to KOLs, what would be a win scenario that could get you excited to move to the next phase?
Yeah. So while there's no therapies approved for celiac disease today, there is draft guidance of the types of endpoints you're ultimately going to have to show for approval. And those endpoints exist in the trials that we're running in both cohorts. So while there's different time points at which we're looking at the scopes for either prevention of villus atrophy or healing of the villi, we are going to end up presenting VH:CD ratio and the histology. We are going to show the translational data, importantly, reductions of IELs. We should also be looking at biomarkers. We'll be looking at interferon gamma. We'll be looking at the impact on IL-15. And then as it relates to the PROs, we are going to be assessing and using one of the PROs that the FDA has described and has validated. It's called the Celiac Disease Symptom Diary.
It's a daily score on both severity and frequency of the typical acute symptoms you see within celiac. So that composite information on the efficacy side in both different cohorts is what we'll end up presenting.
Questions from the audience? I've got one final one. You disclosed EoE as another indication for 033. You walked us through the market potential in the slides as well as a little bit of preclinical data. How did EoE come to beat out your whiteboard of other indications beyond the couple of things that you discussed here?
Yeah. Thanks for the question. So in celiac disease, let me kind of start there. There's proof of concept through IL-15s and other CD122s, but there's a direct impact on multiple pathways of inflammation that I was trying to stress. On the CD8 side, IELs are principally made up of CD8 cells. We're hitting that directly. On the CD4 side, it's a TH1 axis of targeting TH1 CD4 cells. We're also able to look through our trial design at dosing through a month, but then looking at endpoints at month three to look at a longer-term PD effect of this drug. So we're looking at both the immunology based on the biology as well as a real understanding of the dosing profile and potential over time. And just as a counterpoint there, Teva is already talking about quarterly dosing with their IL-15.
There is long-lasting PD that we're all seeing preclinically and for us as well in our phase I study that we're trying to prove out here with different designs. In EoE, we're exploring, importantly, a type of disease that I don't think you could fully target with an IL-15 that shows the power of blocking both IL-15 and IL-2 signaling on different immune cell types. In EoE, there's also a CD8 side of the equation, and Calypso has already shown that by targeting the CD8s in EoE, you are reducing downstream eosinophils. There's proof of concept data out there from 2024 that exists. Importantly, and this is why I walked you through the ILC2 data, ILC2s as well as TH2 CD4s that DUPI is specifically targeting, you're not going to be able to hit those cells and have an interaction there with an IL-15 blocker.
With CD122, you can. So if we're able to show an outcome here in EoE where we think there's a huge market, you only have DUPIXENT, and we're able to target where DUPIXENT is successful and where we think DUPIXENT failures aren't, we're getting the full spectrum of where this disease is presenting up in the upstream pathways of inflammation. If you see positive outcomes there, there are a number of other diseases where ILC2s are important drivers of disease. We could then take this beyond just EoE, where you're in a world that IL-15s also can't chase you. So that's a whole nother way. If an IL-15 is successful, we believe you could go use a CD122 and potentially be better. But there's also other diseases like EoE where I don't think IL-15s apply.
So we're very intentionally selecting diseases here where we could showcase the breadth of where a CD122 could be effective.
All right. Thank you, Dan.
All righty. Thank you. Appreciate everyone's time.