All right, good morning. It's my pleasure to introduce Daniel Faga, President and CEO of AnaptysBio, as our next speaker. Dan, welcome. It's the first time for me to host you at the Goldman Sachs Conference, so thank you for being here. Before we kick it off with the Q&A, I'm gonna turn it to you for a quick opening remark.
Perfect. Thanks for having me here today. It's my pleasure to be here. We have a lot going on at AnaptysBio. We just came off of a really exciting week with six-month Phase 2b Data in our arthritis trial for our lead program rosnilimab. You know, bigger picture than that, our company is focused on developing antibodies that target overactive immune cells in autoimmune inflammatory disease. We have three clinical stage programs in development, two that were homegrown from our research engine, one that we unlicensed in. Our lead is rosnilimab, like I just mentioned. It's a PD-1 depleter. It targets PD-1, PD-1 positive immune cells. Like I said, in arthritis, they're overactivated, 80% of your T cells are expressing PD-1 in the joints per RA. Really amazing data that we just presented. We'll get into that.
We have a second trial that's ongoing as well for rosnilimab in ulcerative colitis. We will read out initial data before the end of this year. Enrollment's going really well. We're on track to have that completed soon. We have two other drugs, CD122 antagonists called ANB033. We started the Phase 1a last October, and we'll do an R&D event later this year to get through more details. And, ANB101, which is a BDCA2 modulator. We had $383 million in cash coming out of the first quarter. We have access to a huge royalty stream from GSK, and it is, they sell a drug called Jemperli, which is a PD-1 antagonist. It's selling quite well this year. The second drug, cabiralizumab, is a combination that GSK is running, a combination trial that reads out in the next few months, in second-line lung cancer. So we're well-capitalized.
We've accessed royalties to three clinical stage drugs. A lot, a lot happening in the company. It's exciting.
Congratulations on your Phase 2b Data that you guys updated last week. Before we jump into the data, maybe tell us a little bit about the key priorities and the catalysts that investors should pay attention to moving forward from now on.
Yeah, so we just announced the Phase 2b results in arthritis, and it is in a 424-patient study. It's a big study. We have the second study, in colitis that I was referring to. It's a 132-patient study, that's been ongoing for a year and a half. The initial results, the top-line results, we'll read out in the fourth quarter of this year. That's the next big catalyst on rosnilimab. Between now and then, I referenced a royalty read-through milestone for us from GSK. I'll give you more detail on that. It's a second-line lung cancer trial that's gonna read out of docetaxel versus docetaxel plus Jemperli versus docetaxel, Jemperli, and cabiralizumab. And cabiralizumab's a TIM-3 antagonist. Either way, whether it's the doublet or the triplet, there'll be royalty inbound.
What's exciting here, or the second-line lung cancer, is a chemo market. It's a graveyard. What we do know is 20%-25% of patients are still responsive to PD-1s after they progress on KEYTRUDA. A lot of patients go back to KEYTRUDA. This is a 750-patient phase III trial. Last patient was November of 2023, so it's been quite some time. I think this is a big sleeper catalyst for us. Ultra-high risk, but huge reward. That's upcoming in the next couple of months. Those are the next two catalysts for the story in the back half of this year.
Okay, got it. So why don't we jump into the data?
Mm-hmm.
The Phase 2b, the rules are otherwise as data. Why should investors be excited about it?
The arthritis is a market where there has not been a new mechanism of action approved since 2012, so quite some time. When we went into the development here two or three years ago, we heard from a lot of folks, "Lots of that's a crowded market. It's a mature market." We enrolled the trial quickly. Huge trial. It's, it's in the end, it's actually not that crowded. There's almost nothing in phase III development. You hear a lot about combinations in different autoimmune diseases. In arthritis, there's been no combinations developed because they were all toxic and didn't give enough efficacy value over the monotherapies themselves. What we just delivered was, in about three months, 70% of patients who took rosnilimab across doses achieved low disease activity, so controlled disease.
We were satisfied at three months on the regulatory endpoints, but the higher order response rates of low disease activity and then even clinical remissions were compelling quickly, and then they were durable through six months. Then we showed off-drug, at least through eight weeks, off-drug, but in trending towards three months plus, you have off-drug response. We have a once-month dose driving high disease activity right out of the gate that is stable, and then we have the potential for every q8 week or better dosing in the long term. It is a profile that together, that if it can be repeated in phase III, is best in disease.
Yeah, you guys showed a lot of data there. I think the primary endpoint was the DAS28-CRP.
Yeah.
and then there's a lot of ACR20, 50, 70, 70s, CDAI, and then a lot across many different time points. Looking just maybe like the totality of data, how do you think that compares to the standard of care? And, and which one of these endpoints or time points that you wanna highlight?
Right. Your drug has to work fast, has to work deep, and has to be durable, right? I hit on a couple of these points. A standard phase III regulatory endpoint versus a placebo control is ACR20. What that means is you are 20%, you feel 20% better symptomatically and clinically. It is a relatively low bar. We had over 80% of the patients hit ACR20.
Mm-hmm.
And that was that sig. What's true in arthritis is early, early biologics drug TNFs, and these have been around for decades. Back then, these were the low bar outcomes that were measured, and there's decades of history on them for comparison. You have to be fast enough for patients to feel better. What clinicians and patients need is going out to six months in a year to control disease, remission of disease, that's differentiated but also stable. This is also true for colitis, but a third to half of patients ultimately lose response in the plus or minus one-year timeline on biologics. What we're trying to do here is drive those deep responses that are durable.
The reason we provided so much data is we're really hitting this from different standpoints. Patients need to feel good, but then know they're gonna have some very deep relief. We're hitting on all, on all angles.
Mm-hmm. How are you guys thinking about the phase III, going forward? What, what, which endpoint would you use, time point?
Yeah, so there's lots of ways to think about phase III. Stepping back strategically for us, you know, I talked about this colitis trial that's ongoing as well. We have, we're first-in-class program at this point. Our competitors, which I think we'll probably talk about through this discussion, have fallen off for different reasons. Ultimately, they're not as potent. They're not hitting the target as hard. And we have very differentiated responses because we are potent and we are hitting the target hard. I could dive into some of these things, but because we're in a first-in-class position and our mechanism of action here, PD-1 depletion, is applicable to so many autoimmune diseases, there's choice for us how to move forward. In plus or minus six months, we're gonna have a colitis readout.
The reason I'm giving all this context is we have a couple of paths forward that we're assessing right now that we wanna understand better before we commit to what the next steps are. One is, should we put a partnership in place? Whether that's around RA, UC, or both, we would look for one partner to do everything with us. That's a choice when you're first in class with a novel mechanism in areas where there isn't a lot of novelty.
Mm-hmm.
The second choice here is we look at what we have in colitis and we decide, should we move forward there on our own? The growth dynamics in that market are very different than in RA if you wanna be a second-line biologic player. They're more attractive in something like an ulcerative colitis where you have branded drugs in the front line, like a SKYRIZI. In RA, front line is generic biologics. The pathways are different. We have a choice in RA to move forward, but we wanna get to the colitis trial readout first and then decide where we're gonna play. It's not practical for a biotech company like us to go into big therapeutic areas on our own. Now the answer to your question, what would you do if you were in phase III for RA? Like I said earlier, you gotta be fast.
ACR20 is a regulatory endpoint versus placebo. You can only have placebo controls for three months in this disease. It is unethical to keep patients on placebo beyond that given there is so much choice. Ultimately, what you are also gonna be looking for are these remissions or low disease activity. You have different ways to think about, short-term, placebo control, but then also longer-term active comparator trials where you might look at something like low disease activity to be differentiated.
I see. Got it. In the Phase 2b trial, you also had a mix of biologic experience and also 90 patients. Any differences in response across these two different populations for your 400 mid- dose?
Yeah, thanks for bringing that up. It was a 424-patient trial. About 40% of the patients were experienced on prior advanced therapy. That could have been TNF, JAKs, IL-6, Orencia, rituximab, or a combination of all these things. We were allowing up to two modalities, so you could have had third-line by class patients in as well. 40% were second and third line. In all mechanisms, at least in RA, and you see this in all these autoimmune diseases, really, you do see a step down in efficacy between naive advanced therapy and experienced advanced therapy. We did see some of that, but whether you look at our data, for naive patients to advanced therapy, it looked JAK-like or better numerically.
In experienced patients, it looked JAK-like or numerically better than, specifically, RINVOQ on all active comparator trials where there's a bias in their results where patients knew they were on drug. We've looked as good or better, low disease activity on ACR 50 and ACR 70. The whole composite here looks differentiated. There is a slight lower bar once you move down therapy. To get some perspective on this, for the advanced patients, 500,000 patients get treated into the advanced therapies. 20%-25% are cycling through four more classes to salvage, which is rituximab. That's a $2 billion market on its own. There's a huge market in terms of the step down. What happens here is patients need therapy. They lose remissions if they're lucky enough to get to them over the course of time.
Huge market opportunity, huge number of patients that move through these lines of therapy. Yeah, the response rates are lower, which is what's so impressive with our data is there are relatively high response rates in those advanced treated patients.
Now thinking about the phase III, will you also enroll a similar mix of biologic experience in patients with prior JAK and JAK patients?
Uh, and then is there like, like is there a target, in terms of the proportion of the, the patient who had biologic versus JAK or, or naive?
Yeah, so a couple of different questions there. Just, you know, back to our Phase 2b trial, I mentioned we had a, we had a mix. About 30% of patients did have prior JAK experience, which I think in itself is impressive when you're comparing to JAKs themselves that you're treating patients that whether with a JAK or without a JAK, the data was pretty much the same when you, when you slice and dice. The trial was big enough where you can start to look at these populations separately, and it's, the numbers are big enough where you have some, you have some meaning there in these subpopulations.
For phase III, like I was alluding to, it really depends on are you looking to develop a drug that can be approved across all lines of therapy regardless of where it's contracted and the formulary position is, or are you looking to design a phase III program where it's more focused in the third or fourth line? I think that's gonna give you different answers on what endpoints you're looking at, at what time points, and the way you're gonna set up your program, right? We ran one Phase 2b trial, but a program could be one, two, three, four different trials together driving towards an approval on a label. I think those decisions still need to be made, what would be the right development strategy for phase III, and that could be different depending on who does it.
In a big pharma's hands, if we were to partner, you might look at something different or you might look at multiple options. If it was just us going forward in RA, you might look at something that's more specific to third and fourth line. I think a big decision for us is gonna be, yeah, you'll have your placebo control trial for three months, so then there'll be some long-term extension. Do we have an active comparator trial in there? What's the right active comparator?
Right.
It's a little too early to speak to some of those specifics. Like I said earlier, strategically for us in the background, whether it's colitis, whether it's RA, it's the same drug stuff since there's scale fast to happen. There's planning for the exact questions you're talking through depending on whose hands this is. Do we partner the drug now? Do we partner in a year? Do we move forward in UC? Do we move forward in RA? All these options are on the table. What we've said is partnering is rational at some point. If the UC data looks compelling, that could be the first place that we would look to go on our own.
I see. Also, the dose carrying forward to phase III, have you put some thoughts around that? I think you guys tested three doses. The mid and the high dose look relatively similar.
Yeah.
How do you think about that?
Yeah, that's a great feature. Just to walk through what the doses were, like you said, three active doses versus placebo. The low dose is 100 milligram monthly. The mid was 400 milligram monthly, and the high was 600 milligram every other week. Coming into this, we were hoping that the once a month looked like the every other week and that we would have a once a month profile, right? That's where we ended up. It's great that the mid and the high dose look that way. We could see in SARA for phase III planning, we know we have a once a month drug out of the gate. There's no loading. There is differentiation between that mid and low dose that were the two monthly doses.
In the population you were asking about earlier, the experienced, biologic-experienced population, there was a distinct difference between the clinical efficacy endpoints, these high-order response rates, between low dose and mid dose. That gets backed up from translational data, which I haven't spoken to yet, but one of the, two of the things that you can measure here that are easy are the PD-1 high-expressing T cells. What happens to them when you hit them in the periphery and in the synovium? In the blood and at the site of inflammation. All doses did pretty good in the periphery. I mean, there was a small dose response there where you saw about 90% plus elimination of the PD-1 high-expressing T cells.
In the synovium where you have to draw antibody into tissue, the mid and the high dose had 90+% elimination of PD-1 high T cells. The low dose did not. They were not depleting out, you know, those specific cells we're targeting that are driving disease activity. We have a differentiation on why we think we're seeing deeper clinical responses between the mid and high dose versus below in these harder to treat patients. We think it's clear from the translational data. Between the two, we do see a dose response there, and that was important.
Right. Right. Right. And then the placebo ACR20 at week 12 was slightly lower than RINVOQ's. I think partly it was due to you guys saw a higher placebo effect at week 12. I think it was 50% in your trial versus like 34% in RINVOQ's Phase 2b in the biologic experienced patients. How do you plan to minimize or mitigate any placebo effect in phase III?
I'm glad you picked up on that because the Phase 2b trials for RINVOQ are long forgotten to some degree. We were trying to stress how quick we were acting relative to RINVOQ. You know, people think the JAKs are very quick acting. They are. So was rosnilimab. What you saw in our trial on ACR20, again, the lower bar of people feeling just better, you saw separation from placebo for us starting at week four, through six, through eight, it grows, and then into 10 and 12. We had an absolute high number, but in that first one to two months, we looked the same or better than the JAKs on a placebo-adjusted basis. At week 10-12, and this has to do, I think, with a lot of what you're seeing in all RA trials.
Mm-hmm.
We do see a higher placebo rate start to come up over time, but the curves are very different on how you got.
Mm-hmm.
How you got there. J& J actually just put out a poster today, their PD-1 program, and they had higher placebo than us at week 12, and they were not that sick, just showing, highlighting the differences between potency of our drug and their drug. Coming back to the JAKs, a few percentage points on placebo-adjusted response in ACR20 isn't what's gonna drive commercial uptake. You need to know your drug works. We work fast. We look like the JAK on an absolute basis. Again, placebo, just for context, placebo is not placebo here. All patients are on background methotrexate in this trial. You are on an active product, so there is a different response.
Yeah. Yeah.
The reason I'm walking through this is we were stat-sig at all doses.
Mm-hmm.
We did show differentiation. You need to see that in a phase III trial. What I keep coming back to is are you hitting low disease activity, a much, much higher bar.
Mm-hmm.
Than an ACR20. That's gonna drive the, the commercial utility. You're probably looking at additional endpoints than just ACR20 in your phase III as well to drive the, the commercial label.
Right. Got it. How do we think about safety? This is a new class of drugs, the PD-1 depleter. What is sort of like the on-target class effect that you believe it has? For the drugs specifically, anything you want to point out and how you think that could play out in the longer term?
Yeah. For PD-1, which is receptor-on-activated T cells, the physiological role is immune homeostasis. It's immune control, right? In these autoimmune diseases, you're out of balance, right? These T cells are overreactive. In a healthy control, 15% of your T cells are PD-1 expressing or activated, and maybe 3% or 4% are PD-1 high expressing.
Mm-hmm.
In the synovium of an RA patient, 80% plus are PD-1 expressing. A lot of them, the majority of them are PD-1 high activated.
Mm-hmm.
When you're depleting out 90% of those PD-1 high expressing T cells.
Mm-hmm.
You're, in effect, it's very, very targeted, only those cells. You're bringing control back to a homeostatic state. All we're really doing is bringing these patients to a, in the, in the tissue environment, to what you would look like in a healthy control. It is on-target. You end up having broad downstream effects.
Mm-hmm.
Right? A lot of what's approved today is hitting various cytokine pathways and blocking them. JAKs hit all of them and more.
Mm-hmm.
We're very, very targeted in what we're doing as far as these downstream effects. The reason I walk through that, it's a novel class, but we know very well how this mechanism works and that you're not going overboard in terms of depleting everything out where you aren't, you don't have any activated T cells.
Yeah.
What we're also not doing is we're not blocking the activation of T cells. The reason I just walked through that is there's a drug called ORENCIA, which is the only other immune cell modulator that's on the market. It's been out for 20 years, sold by Bristol Myers . There is no link to any broad serious infections to malignancies or anything with that, and they're blocking activation.
Mm-hmm.
All we're doing is targeting the activated cells, which is why we're acting faster than a drug like ORENCIA, right? What does this mean in terms of the actual data we've seen, the safety data we've seen? 424-patient trial. In the first three months where we were placebo-controlled, we looked like placebo. There was no imbalance of infection. Again, everyone's on background methotrexate. Half the patients are on steroids, so you're already immunosuppressed. That's a big deal. No serious infections, no malignancy, no MACE. When you look out over a six-month period on an adjusted basis, 100 patient-years, you continue to see no imbalance to what you see in placebo. Another way to think about this is tolerability of the drug.
Mm-hmm.
Less than two percent of patients dropped out of this trial due to AE. That's a very, very low number. In the commercial landscape, I mentioned ORENCIA, the other immune cell modulator. It's the only one that doesn't have a black box. JAKs, HUMIRA, IL-6, rituximab, blowing out your B cells, driving.
Mm-hmm.
Driving infection. They all have black boxes. That's the landscape. Not only are we confident with what we're seeing so far, I think on a relative basis, there's a huge headroom here, compared to what's already commercially available. When we talk about best-in-disease profile, it's the speed and efficacy at deep depth of exit at six months, but it's also the safety and tolerability that all combined are a profile of what we think this market needs.
Right. In late last year, Lilly discontinued their PD-1, out of the Phase 2b, due to, I think they said, like, overall benefit risk profile.
Yes.
Any of that, the discontinuation, is there any negative review or, or how are you guys looking at it for?
It's, I mean, it's really a positive read-through for us. I mean, we're, we just saw this with J&J and the, you know, abstract a couple weeks ago, and the poster just posted overnight, at EULAR over in, in Europe. Those drugs aren't as potent. So J&J's translational data they provided was limited, right? But what they did show was PD-1 reductions in the periphery, and they show a 60% reduction.
Mm-hmm.
We're showing greater than 90% reduction, full coverage, right, of what we're trying to do. T heir absolute efficacy at three months on these high order response rates like CDAI, LDA, those use activity. We were better than them. And then over time, they saw a loss of response. This is in their phase 2a study. They saw a loss of response. That's what's gonna happen when you're taking out some of the T cells. You get a benefit, but then you have the rest of those T cells proliferating and still driving activity. If your drug's not potent enough, you're not gonna get a full response. We're not surprised to see them lose efficacy over time. When you look out six months, which is truly what matters commercially here, their response rates were 37% LDA.
When you look at six months for us, we're closer to 60%. And that's in a trial that was handicapped where there's a gating factor where we couldn't even see matched response for both of these trials. We were almost twice as powerful as them out six months. We were stable. We have a very, very different drug. When Lilly says we don't have the right benefit risk, it's pretty clear they don't have the right benefit.
Mm-hmm.
Over time to have a drug that would be competitive in a mature market.
Mm-hmm.
Johnson & Johnson, their safety profile looked benign, just like Lilly's in phase 2a and ours to date. They showed, again, just hit this morning, it looks like you're approximating a graph that doesn't have numbers. Looks like 50-60% elimination of PD-1 high T cells in the periphery. There's another poster that'll drop tomorrow, but in the abstract, it showed about a 40-50% reduction in the synovium. We're at 90%. These drugs just aren't potent enough. They're not driving the same depth of response and durability of response.
I see. Got it. And what's the overall aspiration for the drug? There's a lot of, you know, you can imagine there's a lot of different classes of different TNFs, T cell modulators, IL-1, IL-6, CD20s, and the JAKs and so forth. What’s the, you know, when you look at your target product profile, what's that aspiration of what, what?
Yeah.
What are you guys trying to achieve?
It, you just named a lot of drug classes that are approved in a lot of areas.
Right.
Here's what's true about autoimmune disease, systemic autoimmune disease. You're going to have exacerbated or overreactive PD-1 high expressing T cells in that cycle driving disease activity. There is a large number of places we could play. We took two initial proof of concept bets, one in arthritis where Lilly already had some early proof of concept there. We're running this trial on ulcerative colitis. We're really excited about that as well.
Mm-hmm.
The lamina propria is the inflamed tissue in the gut, similar to synovium. Half the cells there are overexpressed PD-1 positive T cells, right? We know there's target in the tissue to go hit. That's now rheumatology. We have IBD. There's other therapeutic areas that you can take this to. What we announced with our Phase 2b update in arthritis last week was we're gonna drive towards the UC data coming up. We're gonna pick an area to move forward in phase III. If ulcerative colitis hits the TPP, that's probably gonna be the choice. We do have an option in RA as an alternative.
Mm-hmm.
We did say we're gonna be looking at additional indications in other diseases starting phase IIs. There's this drug, the composition of matter here is out in the 2040s. We have lots of time to develop the drug.
Mm-hmm.
In a number of different areas, and there's always a race once you get out to market where.
Mm-hmm.
Where clocks start to tick.
Mm-hmm.
We have the time right now to sit and explore other rheum diseases, other GI diseases, and potentially beyond that. Like I said earlier, we're never gonna be a Japanese or European commercial player at Anaptys, right? Ultimately, we're gonna find support. That is a question of timing and return on equity. When you have a first-in-class now and best-in-class drug with years ahead of you before any other PD-1 depleters move into clinical development, we could take advantage of that time. We're gonna move as fast as we can.
I see. So your UC data is coming in Q4?
Yes.
Why are you so excited about UC, and why you select that indication to go after RA? What gives you confidence that you can penetrate the target tissue?
Yeah. Similar rationale how the mechanism of action aligns to the disease pathology, disease path, biology here. I mentioned that the lamina propria has a lot of the PD-1 high expressing T cells. We have correlations between the reduction of those cells in clinical remission. A drug like ENTYVIO, Enfaport Beta- 7, what they're doing, what that drug does is it blocks that receptor, blocks activated T cells from penetrating from periphery into the tissue. It's the same cells. We're depleting those cells. There's correlation of the reduction of those PD-1 high T cells in the blood to clinical remissions in UC. It's similar how other mechanisms work. We have animal model data, translationally from our arthritis trial. We showed in not just the reductions in the tissue and the blood of the PD-1 high cells.
We saw, in the gene expression panels, reductions of T cell activation pathway, B cell activation pathway, as well as the production paths in TNF, IL-6 is what we showed, but the genes that code for IL-12, IL-12 RB, which codes for IL-12 as well as IL-23. So mechanisms that are known to work. We're seeing translationally insight that also read through. Our trial's 132 patients. It's two active arms versus placebo. The highest dose in the colitis trial is higher than the high dose in the arthritis trial. We know that at the mid-dose, 400 milligrams monthly, we're getting 100% or close to elimination of PD-1 high cells in the synovium. Part of this is just making sure you're dosing high enough to get antibody.
Mm-hmm.
It's harder to get into the gut than it is the synovium.
Mm-hmm.
At that mid-dose, we already know we're 100% in the synovium. See, when you scale for these things ahead of time, you adjust for the fact it's harder to get antibody into the gut tissue.
Mm-hmm.
We feel comfortable that we'll have the antibody there, and we're excited about what we just saw in arthritis.
Right.
We should have on-target activity that's potent enough.
I see. Got it. I UC is also very crowded, just like RA. There's the IL-23s and oral small molecules and so forth. What, what's the bar for success when you think about, you know, your internal go and no-go decision?
Yeah. I think there's a lot happening in development right now in UC, right?
Mm-hmm.
Whereas in RA, there's not.
Yeah.
The markets, the commercial markets, UC is lagging behind right now in terms of the breadth of biologics that are available for patients. The growth in UC, in the next four, five, six years, it's gonna be at least as big as the RA market in second line beyond therapy, we think. SKYRIZI is penetrating into front line as a branded drug over HUMIRA, over biogenetic TNFs, over ENTYVIO, right? You're seeing a change there. The outcome for patients is ultimately surgery, which you want to avoid and costs a lot of money. You have great pricing, pricing corridors through lines of therapy given surgery is a high-cost last resort alternative that you do not have in RA.
Mm-hmm.
The growth dynamics are favorable for a new class of biologics. It's really the IL-23s, B19s. You have the T1As emerging, and then what? There's actually not a lot new. You're seeing knee-betters of all those classes. You're seeing orals, which would be less efficacious.
Mm-hmm.
Different administration. You're seeing half-life extension.
Mm-hmm.
Antibodies, but they're all different versions of the same thing. You're seeing these mechanisms being combined. It's actually lacking in novelty of different ways to treat patients in UC. We're really excited about that as an opportunity to play there into a market where you're going to have class switching no different than you had in RA. Just for awareness, even the T1As, they had great data at three months. You had 5-10 percentage points better on clinical response. When you get out to 52 weeks and you look at remission, they look no different than everything else. They start slightly higher. They come right back down. One-third to half of patients on these biologic classes lose remission between 6 and 12 months. That's an issue. If we can have a drug that looks like what we just showed in RA.
Mm-hmm.
Where patients feel better over three months, and our primary endpoint here is change in MMS score versus placebo at three months. If we can drive those deeper responses at six months, things like endoscopic remission that look like just other biologic classes, you only have to be better in this market because of the class switching that we're moving into.
Mm-hmm.
You're at least as stable as these other drugs, which are a pretty low bar. That's already a profile with a new class that's gonna hunt. There's upsides to that at six months on remission, endoscopic remission.
Mm-hmm.
If you could, sustain those remissions over time. We are excited based on what we saw in RA that translates for.
Mm-hmm.
The UC in the same type of a profile that'll be very different than the other classes that exist.
I see. Got it. We're almost out of time. I just wanna squeeze in one more question before I turn it to you for final remarks. So, besides, like, looking at your early pipeline, your O33 asset. So that space is heating up, right, that IL-15s, CD122.
Yeah.
It's heating up. How do you, you know, think about that, and then how do you compare these programs, and then, and what should we care about or look forward to?
Yeah. So, thanks for asking. ANB033 is a CD122 antagonist, and that is a dynamic receptor that blocks IL-15 and IL-2 on various immune cells that are expressed in disease: CD8-positive cytotoxic T cells, TEMRA cells, resident memory T cells, and NK cells. I agree with you. There's a lot of interesting activity with IL-15 antagonists. They're doing partial, right? They're only hitting IL-15. Teva has a program. Novartis Calypso has a program, where they're in phase IIs in celiac disease, vitiligo, alopecia. We'll see where Novartis plays, and we think they've alluded to they'll come out soon with the breadth of their phase IIs that they're looking to move into. The CD122 we think is a more potent way to hit at similar diseases. There's a couple out in the landscape. Footprint, affinity, all these things are gonna matter.
We're gonna have an R&D event in the back half of the year to walk through this mechanism in a lot more detail relative to IL-15s, show data that will report the differentiation from other CD122s that exist, as well as reveal our initial Phase 1b indication, which we'll have already initiated by the time we end up having this event. That's all to come. We're excited about it. We think there's a big opportunity. It's another one of these pipeline or product-type opportunities where it's not just one phase B that I think we'll end up moving forward in. Big opportunity there. Second, the second story, and it's great to have different ways to invest in the company.
Yeah. Very much looking forward to all these data coming out. Thank you so much for coming. It's a pleasure to host you at the Goldman Sachs Conference. I'll turn it to you for final remarks.
Perfect. No, exciting days for us. We just showed some great data. We have other big readouts coming up. Like I said, we're well financed at this point in time. We have an additional value stream in these royalties that are coming in that you can really think of the business a lot of different ways on value creation. I really appreciate your time. Thanks for having me.