Good afternoon, everyone. Welcome to Guggenheim Emerging Outlook Biotech Summit 2026. My name is Yatin Suneja, one of the biotech analysts here at the firm. My pleasure to welcome our next presenting company, AnaptysBio. I will be having a discussion with the President and Chief Executive Officer, Daniel Faga. Probably will be Chief Executive Officer of two companies, soon. Dan, thank you so much again for your time. Always. I've done successfully before, by the way. Yeah, yeah. Co-CEO, why don't you make some opening comments? Obviously different parts of the story, a lot going on there, one on the spin-out side, but also from the clinical asset side. Just make some comments, and I have prepared some questions that I'm gonna sort of ask after your comments. Perfect. Yeah. Well, an exciting period of time we're walking into with, I think, a lot of a lot of catalysts across the different sides of the business. So you stole my thunder a little bit, but it's not a secret. We are creating two companies from Anaptys today. We announced last September our intention to separate our biopharma operations from the core royalty portfolio that we have in the company today. We are tracking towards a Q2 separation. It could slip a little bit from here, but our intent and priority in the company is to have the separation affected as soon as we can and move on with what we think is gonna create a lot of opportunity for investors on both sides of these houses. So we're gonna dividend out the biopharma business, which will have three clinical stage programs in it. We'll have rosnilimab, which finished the phase 2b study in RA last year, and we're looking to capitalize the phase 3 moving forward, in RA. We'll talk more about that. The CD122 program, we have two studies, one ongoing in celiac and one initiating imminently in EoE, both phase 1b studies. And then our third program is ANB101, which is BDCA2 modulator, which is in the phase 1 trial that's ongoing. So that's gonna get dividended out. Most, if not all, of the employees of Anaptys will move into the new business. It'll have a new name, publicly traded company, and we'll capitalize it with at least as much cash as we need to get through the CD122 trials, plus some run rate. We have more capital than that, and we will work through over time how to split the entirety of the capital up between the biopharma business and the royalty business we're leaving behind, which is anchored on two programs: Jemperli, which is a royalty from GSK. GSK just had their earnings last week. They're on a $1.5 billion run rate. And if you draw their growth rate through consistently quarter-over-quarter, it'll do $1.8 billion this year. And I think the catalysts exist where we could potentially see that happen. And then imsidolimab, which we have outlicensed to Vanda, who filed a BLA in GPP in December. They're seeking accelerated approval, but one way or the other, we should see an approval for the second commercial asset, this calendar year. Thank you. So let's take the royalty co first. So obviously, Jemperli is the key asset there. How one should evaluate the royalty stream there and then the value that it brings to you? I mean, is it just we use the consensus number, but it seems like consensus is also catching up to the sale? Just maybe help us understand that dynamic. Yeah. So I'm not sure consensus is a great way to look at this. Like I just mentioned, the growth rate is in the teens quarter-over-quarter, consistently through last year. There's no reason to believe that will change moving forward here in a negative way. Endometrial cancer is the lead indication, frontline endometrial cancer. We have overall survival data for Jemperli. Mm-hmm. Keytruda does not have survival data, and it's really driving the market share capture that we're seeing out of GSK. So that was approved in the U.S. in the middle of 2024, but it wasn't approved in Europe until January of 2025. And just standard cycles on reimbursement timelines, as Europe is really just starting to get into the numbers right now. So there's a lot of growth behind it in Europe, and then ultimately, beyond that, this year, we're gonna see rectal cancer data, pivotal trial, that we'll read out. The phase 2 had a 100% ORR rate. I think that there's a lot of anticipation that that drug works. It's just how well. Yeah. GSK did receive the government's national Priority Review Voucher, which leads to a 1-2-month review period when they eventually file. So they're guiding the data this year there. And there's also data that's gonna read out in dMMR colon cancer, which is the bigger colon cancer market. That's a phase 2 trial that I think is upside when it comes to forecasts. And the reason I'm saying not to rely on consensus is as of January now, I don't have the latest. Sure. Models are coming in. But as of January, consensus GSK analysts have negative growth as it relates to the run rate. Those numbers are wrong. When you look at the 2027 consensus numbers, $1.7 billion, there's a good reason to believe that this year's revenues will beat the 2027 consensus number. GSK has guided historically now for multiple years, greater than £2 billion, which is about $2.7 billion of peak sales. And what they're quoted as saying, and it's historic, that endometrial cancer and rectal cancer monotherapy will drive towards those peak sales on their own. Doesn't include colon, pMMR, or dMMR. Doesn't include head and neck. It doesn't include the possibility for combinations. So there's a lot of run rate here. We have IP out to 2025 or I'm sorry, 2035, 2036, just on composition of matter. So there's a long run rate here, big equity story. It's one of the reasons we think this company will trade really well. On On a royalty portfolio that's 8% up to $1 billion, it escalates to 25% at $2.5 billion of revenues, which their guidance is already north of. Already north of. How is the relationship with GSK? Any of the litigation that could delay the timing for the split? So there's ongoing litigation, which we can talk about a little bit, but it does not impact the separation. Okay. The separation of the biopharma business is completely independent. Yeah. Of litigation that is very specific to a contractual matter. Mm-hmm. On Jemperli only. Okay. So if you own one share of Anaptys right now, what happens after the split? What I'll say is if you own 1% of Anaptys. Uh-huh. You would own 1% of each business the day after the separation. I see. It's really a dividend. Of the relative ownership. There might be some exchange ratio that get. Sure. That's in there, the relative ownership on the on that dividend. So, you know, at some point, there'll be a Form 10 that'll be in the public domain as we get closer. Then they're on really a regulatory timeframe with the SEC of how the process goes from there. Got it. Really within a 2-month period once we get to that stage. Just one more question on this. With regard to the other company where you have the pipeline asset, is there a reason just to fund it through 122 data? Why not move all the cash there because the royalty doesn't require too much cash? So yeah. So the statement I agree on there is the royalty business is effectively going to be a virtual or semi-virtual business. Mm-hmm. We don't need a lot of capital to deploy to run that public entity. We do have non-recourse debt with a group called Sagard. Mm-hmm. Which we are projecting that will be paid off into middle of 2027. Mm-hmm. So you need about a plus or minus a year of capital. But the choice here as the CEO of one entity today. Mm-hmm. If you have a dramatically undervalued business as it relates to. Yeah. JEMPERLI on its own, not to speak of imsidolimab, that last year we bought back well north of 10% of the company in stock repurchases. If all this is, is it ultimately a cash-positive company on day one? And given where we're trading today, we should buy back every penny of stock we can. Okay. with the royalty. Now, the flip side, the biopharma company CEO. Yeah. Putting that hat on, wants every single dollar in the biopharma business. We're not gonna starve the biopharma business. We had $310 million of cash coming into the year. We will have cash if we put it all into the biopharma business, we'd have cash into 2028. And so it's really just a judgment call. Got it. Of finding the right balance there, creating value for both entities. If you're a shareholder today, you care about both of those points. Got it. Got it. Very good. So let's move to the pipeline, more exciting part, in my view. So the CD122, I think this is a year where we're gonna get a lot of data. You specifically chose CD122 over IL-15, which, I think two companies are going after. So if you could, and there is some new preclinical data that you have. So just maybe walk me through where you stand on CD122. How is the molecule differentiated? Where are you in terms of these studies that you're enrolling? Yeah. Running, sorry. Yeah. Well, it's nice a lot's happening, I'd say in the class or in the pathway IL-15, CD122. The CD122 antagonist blocked the signaling of both IL-15 and IL-2. So there's differentiation there that we're targeting cell types that, in specifically in certain diseases, you see overexpressed with the CD122 receptor, which is present in different forms, in different a dimeric or a trimeric receptor depending on the cell type, whereas the IL-15s are only doing one thing. One thing. Yeah. So there are different diseases that, I think, folks are looking at. The landscape here is there's one other CD122 player. There are two IL-15s that are in development as well. There's a consortium of diseases that folks, I think, are focused on. Vitiligo on one hand. Yeah. We are not there in Phase 1b. And celiac disease on the other. So we are developing the drug in celiac disease where there is proof of concept with IL-15s and CD122 programs, in gluten challenge studies. Mm-hmm. The whole purpose of these studies is you're taking patients who are relatively who have disease but do not have mucosal injury. You're giving drug or placebo. You're giving them gluten. On the placebo, you should be getting worse. You should see deterioration. You should see an increase in IELs. These are cells that are recruited into the epithelial layer. Yeah. Where there's damage, and they provoke the autoimmune cycle and really are what ultimately present and cause a symptomatic impact in celiac disease. We know these drugs work in that part of the pathology. CD122, the receptor, is also expressed on CD4 cells, which when you ingest gluten, APCs pick it up, present, activate CD4, IL-2, interferon gamma is expressed. And that's what instigates the IL-15 and CD8 cell biology. We should also be targeting activated CD4 cells. And our preclinical data shows this. Yeah. So we're excited about what CD122 targeting can do above IL-15 in this disease. The second disease that we're looking at is EOE. Eosinophilic esophagitis. Dupi works okay in EOE. It's the only approved biologic. 60%-70% of patients respond to weekly subcutaneous administration of Dupi. Dupi targets Th2. Yeah. CD4 cells and ILC2s. So does CD122. It's expressed, and it's expressed densely on ILC2s cells. So you're asking about the preclinical data. We've run a spontaneous eosinophilic model where you're trying to prevent the recruitment of eosinophils. You're trying to prevent the increase in ILC2s. We're flooring those. We're completely preventative in that model relative to other mechanisms. So we know we're targeting the biology that Dupi targets. We're also targeting CD8 biology. So for patients who are not responsive to Dupi, guess what? There's an influx and increase in IL-15, and you're seeing CD8s present, particularly in that subset of patients, which is a big subset. Mm-hmm. So we're hitting both sides of the biology in EOE as well. Translation across both of these types of diseases, there's a host of number of areas we can go, explore with these programs beyond just two huge market opportunities in celiac and EOE on their own. Got it. So just if we just step back, I understand these two areas you're going. Like, conceptually, how are you thinking about indication prioritization? Because we are s I mean, these are T-cell-driven diseases. It's not that Th2-driven diseases are not T-cell-driven, but a little bit different. But we are seeing expansion there also with atopic dermatitis. So is that sort of on the cards, or you just stay with the area that you have identified? Yeah. Well, we know a lot about atopic dermatitis at Anaptys. Yeah. AD, right, we know targeting Th2 cells through Dupi and other mechanisms, IL-13 blockers, has an impact in AD. Novartis is one of the other IL-15s. They're running an AD trial. They're talking about AD being a CD8-driven disease. There may be a component of that. I see. There, we're seeing Teva now talk about. Yeah. Atopic dermatitis as an expansion indication. That might work. We know there's gonna be an impact on CD8 cells. We'll let them run those experiments. As I just described in EOE. Yeah. We should see similar biology in ILC2s, Th2, and CD8s. So it's an area that we're able to go run fast in, in the phase 1b. We could always move into AD, but if we do so, it's gonna be on a broader premise of CD4 and CD8 biology as well as ILC2. Got it. Not just a CD8 angle. Got it. For the product itself, I think Teva has made some comment that they might be looking for quarterly dosing. Like, how do you envision the dosing frequency for your, for this mechanism for CD—well, for your drug? So what's, I think, great about this class so far, right, a marker that I think historically, people have been paying attention to, the NK cells. Mm-hmm. We do see long-term PD in terms of the impact of CD122 expressing NK cells, which is somewhere in the range of 60%-80% of all NK cells. NK cells that don't express CD122 still have immune competency function. So we don't see a safety issue by doing this, but we do see long PD in the periphery. We are also modeling it consistently that way in tissue. And as an example of this, in our celiac trial. We have two different cohorts. I was talking a little bit about the gluten. Yeah. Challenge side earlier. The other cohort that we're using to treat celiac disease is on patients who have mucosal injury. So defined by a VHCD, villous height-to-crypt depth ratio, less than 2. Those with greater than 2, we're giving them gluten. We're gonna induce injury. Those who are less than 2, they already have injury. They're presenting, and we're looking to induce healing in the mucosal by seeing that VHCD ratio improve and go up. So the reason I just brought us down this path is in that trial, it's a 1:1 ratio versus placebo. We're dosing subcutaneously at week 0, week 2, week 4. Then we're gonna wait till week 12 and do a biopsy and see, have we improved the inflammatory environment? Have we induced healing? There's an 8-week delay there. Mm-hmm. The reason we'll do that is 'cause we do think, based on the preclinical data and the Phase 1A data, that we have the PD where we can look at dosing, where you're induced, induction quickly, and then looking at month 3. So I'm not out there saying we're gonna have every 3-month dosing or longer, but we clearly are seeing similar activity where we should be at an IC90 above the threshold needed through week 12 just by dosing through week 4. So we have the opportunity here for different dosing profiles over time. Yeah. We'll be able to get a hint of that from the phase 1b study in celiac. Got it. What is the like, how do you envision the treatment in celiac disease? Like, what is the end goal? It's just that patient can have this accidental exposure, or they just like, how will it be adopted in the sort of real-life setting? Yeah. Like, there's, there's probably horizons to this, but. Mm-hmm. A reasonable place to start in a disease that has no therapeutics available to these patients. Stepping back, we think there's well north of 2 million patients in the United States that have celiac disease. Over 1 million are diagnosed today. Approximately 250,000 patients in the U.S. alone are not compliant to a gluten-free diet. Mm-hmm. Even when they're gluten-free, they still have symptomatic impact. And that comes from trace exposure to gluten that instigates this cycle. That 250,000 patients is the patient population on day one. And this is in a market that will grow, particularly when you're getting close to and then have a therapeutic actually proven disease. Yeah. So in other words, there's no reason to go get a biopsy to know you have celiac disease today. There's no way to treat it. It's no different than a gluten-intolerant patient. You need a gluten-free diet. There's just nothing else you can do as a patient today. So when you think of the world in that sense, you have this 250,000 patients that we know right now have inflammatory damage. We wanna show that, in a world where you're exposed to gluten, that they can get better. Mm-hmm. That's step one. That's the therapeutic benefit we think of treating with the CD122 program. That's why that second cohort I just walked through is so important. We should see statistical significance in the gluten challenge, but we should directionally start to see that we're inducing healing in these patients who already have the damage. That's the commercial market we wanna further interrogate in a more robust phase 2b study as a next step. Got it. What are the symptoms? Like, are there particular symptoms that you should focus on or that's worth touching on in these two studies in these two cohorts? So the regulatory environment here, there's draft guidance. What are the endpoints that matter? You're looking for histology improvement, which VHCD ratio will hit. Then you need a PRO. Yeah. We're looking at one of the two validated PROs in our phase 1b trials in both cohorts. It's called the Celiac Disease Symptom Diary. It measures severity and frequency of things like nausea and vomiting that are tracked on a daily basis. We're looking at a full composite of symptoms that these patients experience. Got it. Got it. For the EOE as a second indication, like, how big will that study be, and the sort of test study design and timelines? So we'll give more details post the initiation of the trial, which, you know, as I just kinda said earlier. Okay. Is imminent. But the two points to note here, there's been plenty of failure in EOE. Yeah. You could target and deplete EOE. It doesn't have an effect on symptomatic and clinical benefit. Yeah. Eosinophils get recruited in this disease. That's not driving the inflammatory effects. So when we are looking at the study design, yes, we have to show the two things that are also the FDA-approved coprimary endpoints: eosinophils reduction but also symptomatic impact. So we're powering the phase 1b study to show both of those outcomes in the results here. Okay. We'll give more information, once we get the trial going on what the exact design looks like. But data won't be until 2027. We don't. Yeah. Won't be data this year. We just gotta get the trial going. Okay. Got it. For celiac, when is the data coming? Q4 of this year. We're on track for. Enrollment's going fine? Yeah. Okay. Then, on 101, the BDCA2 modulator that you have, like, how like, what are the next steps there, areas, or indication that you could prioritize with that mechanism? So, I think the competitive catalyst that is of most interest right now is there's a first-generation BDCA2 that is in three phase 3 trials. Yep. being developed at Biogen. They have two of them that'll read out this year in SLE and one phase 3 trial that'll read out, it sounds like, earlier 2027 in CLE. And they did just mention on their earnings call a couple weeks ago that they'll have phase 2 data in CLE at an upcoming conference. So I think there's gonna be more data in this space this year. Mm-hmm. We have a more potent molecule that has a longer half-life. The PD effects are showing a differentiated depletion profile of the target cell where BDCA2 is present, which are plasmacytoid dendritic cells. Yeah. Which, in these diseases, there's a huge amplification of, and you don't really see this cell type in healthy. Yeah. Healthy individuals. So I think those are obvious places that we will look to play at Biogen successful. If they're not successful, we will have to rethink how we're thinking through. Okay. But there are other diseases that make sense. So I think it really comes down to the quality of the data and what they say. Okay. We have a differentiated drug that we believe if they're successful in those diseases, we'll have a differentiated profile over time. So we've. Specifically stage 2? We've done a lot of preclinical work, and that work has so far been validated in the Phase 1a study that's still ongoing. So I know there's data we eventually have to show to prove what I'm saying. Yeah. But that's what we're seeing so far. Got it. Yeah. I mean, I think they even got the breakthrough designation, I believe, recently. Okay. Then the rosnilimab. What's the status there? Would you, yeah, just, like, partner in discussion? What, how should we think about Phase 3 and RA? Thanks for asking. So operationally, we have an end-of-phase 2 meeting with the FDA, later this quarter. And that's an important step 'cause it'll help define the size of the program. Yeah. If an RA program's likely gonna be more than one trial. So there's a number of dynamics that we need to get further information on. That's really important because it's gonna have a direct correlation to the size of the program but also then the dollars, how much it's gonna cost to go from here through an approval in RA. What we've stated we're looking to do is find, either/or strategic capital, financial capital, or a combination to advance the phase 3 program in RA. Okay. That's the principal focus right now. The base case is that the drug will be, in the biopharma business, although we do have the option to, finance the drug and then, potentially leave economics behind in the royalty business. Okay. But the base case is it goes in the biopharma business. Given what I was saying earlier, the priority is to get the separation done. We're not going to do a deal for the wrong reasons just to get one done ahead of the separation. I see. The separation is priority one. Getting the rosnilimab funding together is priority two. Got it. One more question. On the 033, I think you're the only subQ in clinic, right? That we're aware of. That's correct. SubQ. Yes. Yeah. Yeah. So that. Yeah. So, like, relative to the other CD122 program, we have a higher affinity. We have a differentiated binding epitope. Both in combination, we think, yield more potency. And then we are using a subcutaneous administration. Got it. In our trials. For very good. Dan, thank you so much. Thank you so much. It's all I had for you. Appreciate it. All right. Thank you very much. Thank you very much.