Good morning, everyone. My name is Gena Wang. I'm a Biotech Analyst at Barclays. Welcome to our 27th Global Healthcare Conference. It is my great pleasure to introduce our presenting company, AnaptysBio. With me on the stage, we have Dan Faga, President and Chief Executive Officer. Dan, please go ahead.
Good morning, everyone. My name is Dan Faga. I appreciate the opportunity to present here on behalf of the company. I'll walk through some slides for about 15 minutes or so and then turn it over to Gena for some Q&A. Today's discussion will contain statements that are forward-looking. AnaptysBio, we are focused on the discovery and the development of antibodies that target disease-modifying and overexpressed immune cells that are generally found in the state of disease of autoimmune or inflammatory disorders. We have three clinical stage programs ongoing right now. Our lead program is rosnilimab. It's a PD-1 depleter and agonist, and it's currently ongoing in two phase II trials for rheumatoid arthritis and for ulcerative colitis. A month ago, we presented initial top-line data in arthritis, and we'll have the full data set reading out in the second quarter of this year.
In ulcerative colitis, the phase II initial data will read out in Q4 of this year. I'll spend most of today's presentation going through these data from the RA study. Our other two programs, ANB033 is a CD122 antagonist. It's moving through the phase I-A in healthy volunteers, and we'll be entering our first phase I-B trial in patients later this year, where we'll hold an R&D event walking through this pathway of the IL-15 as well as IL-2 blocking as we target CD122 and reveal the disease that we're moving into for the phase I-B. Our third program is just initiating phase I-A this month. It's a BDCA2 modulator, which is a receptor predominantly found on plasmacytoid dendritic cells. We're excited about this mechanism of action.
Again, early days for it, and we'll talk more about this program through the course of the remainder of this year and into 2026. Overall, we have a best-in-class immune cell modulating antibody platform. AnaptysBio has been a company for approximately 20 years, and we're fortunate enough to have already developed programs that are highly differentiated in the space. We have a collaboration with GSK, which is a financial-focused collaboration, for a couple of programs that are focused in the oncology space. I'll speak a little bit about this later, but we have a very large royalty stream that's generated from this relationship. We're well-capitalized overall, $420 million of cash coming into the year and cash runway for at least three years to year-end 2027.
Diving into our data for rosnilimab, there's five key points, and I'll click into each one of these through the remainder of the presentation. We're really excited about what we presented a month or two ago. It's a 424-patient study in arthritis. Five key takeaways is we were statistically significant at week 12 in the arthritis trial across all three doses on the primary endpoint of DAS28- CRP, or the change in DAS28- CRP over time. Equally important is we were statistically significant in all three doses on ACR20, which is the registrational endpoint used in the phase III trials. Beyond that, our program showed robust and distinguished translational data relative to placebo. It really showed that the drug is doing exactly what we wanted to in a very targeted way, with 90% elimination in the first read of PD-1 high-expressing T cells.
That's at the top of the immune cascade. Downstream, we're seeing an equally strong reduction in the biomarker objectively on CRP. In placebo, you don't see a change. I think this is important. The drug is working, and it's working quite effectively in the first three months. Our program, our drug was safe and tolerable. Very few patients dropped out of this trial from a tolerability perspective, and the overall profile was benign. Importantly, beyond that, the data that we produced through the first three months was 69% of patients hitting low disease activity on the CDAI scale. This is best-in-disease data at three months. Further, and even more important, is these data are stable so far to date. 220 patients hit LDA out of 300 patients who were treated with rosnilimab in this trial by week 14.
As of this data cutoff, which was in early December, over 100 of those patients were out through 28 weeks or over six months, and they were stable. We'll come back to this in a little bit. This is the most important point. When you look at month six data as a treater, most patients are in low disease activity, and these data stack up to or are comparable or even potentially better than a JAK, which is the best in disease. This is a huge commercial market. Second-line plus in arthritis just in the United States is greater than $10 billion of revenue. These are post-TNF failures. What patients do right now is switch between classes. All of our doses were stat-sig. Two of those doses were once-monthly subcutaneous injections.
We have a competitive administrative profile on top of a very big market opportunity in front of us. Now let's turn to some data. What you see on this slide here is our primary endpoint, the change in DAS28 over time. The gray line is placebo. The three solid blue lines are three doses. What you can see is separation starting as early as week four. The blue lines separate and accelerate away through week 10, through week 12, and further on to week 14. The dotted blue lines are the responders. Those 220 patients at week 14 that hit low disease activity, you can see separation for the responders versus the overall population starting around week eight through week 14. You see those responders who were able to stay on drug in this trial past week 14 through 28.
You see a very stable DAS28 curve over time. Again, those dotted lines in aggregate represent 220 of the patients of the 318 that were touched with rosnilimab. As it relates to placebo, you see a deceleration there between week eight to 10 and, importantly, 10 to 12. As placebo patients come off drug into week 14, you see that line recede. Now I'm turning to the responders, those 220 patients. This is a responder curve. Each data point on here represents the percentage of those 220 patients that hit additional high-order response rate. On the top is ACR50. On the bottom is ACR70. The vast majority of patients who hit LDA at week 14 also hit ACR50. The big takeaway from this page is this is a lot of patients here, robust setting.
Post-week 14, these patients held on to their higher order and responses. This is differentiated in this disease. This is a disease where you look at other biologics. Most patients fall off drug between 8 and 12 months. That is because not only do a lot of them not hit this type of outcome of ACR50, ACR70, or LDA, they lose their response over time. We are not seeing that. These are the translational data on this slide. In the top left is our data from the phase II-B trial. There is a dark red line. This is representative of all the doses, but we are showing as the aggregate 400 mg monthly dose, so the middle dose. It is the same outcome for all three doses. The dark red line in the top left is the PD-1 high T cells. You are seeing a 90% elimination of them in the first read.
This is consistent with prior clinical trials, including the phase I and what we predicted based on our preclinical data. In the orange line, you're seeing a 60% reduction overall of the PD-1 positive expressing cells. I think, importantly, here in blue, you're seeing a neutral to increase in Tregs over time. The bottom left is placebo. You're not seeing any activity. That would be what was expected here. You're not getting immunological benefit on placebo in this drug, regardless of some of the subjective endpoints. Patients do see some benefit over time. You have to remember, in this trial, these patients are on background methotrexate, so it's not true placebo. In the top right, we're now comparing to Eli Lilly's peresolimab in their phase II-A data. What you see here is they announced only their first 12 weeks of results.
The red line on the page is a 60% reduction of PD-1 high T cells. Compare that to our 90% reduction. We have a 50% improvement. We have a more potent drug than peresolimab. I think, importantly, when you compare back to the left side of the page, that red line out to week 38, which is now 12 weeks off a drug, the PD of our program is still better than Eli Lilly's peresolimab's deepest response in the first read of 60%. We have long PD here. What I'm setting up now is I flip to... What I'm setting up here right now is if you compare our clinical data set over time, I was mentioned earlier that we have 69% of patients at low disease activity at week 14.
In Eli Lilly's phase II-A trial, they only had 55% at their high dose, 44% at their low dose. We're talking about stability of results on all of our slides. Eli Lilly's phase II-A trial, they started to lose response, consistent with a lot of other drugs. That 55% on an ITT basis moved down to 37% at month six. Three months off drug, they're down at 22% of the ITT population in response. As I mentioned earlier, our 69% at week 14 out through 28 weeks, we're generally stable. A huge difference relative to where our competitor was. Now, as I think most investors are aware, Eli Lilly will not be pursuing RA moving forward with their program. They announced that in November.
They ran a phase II-B trial, and what they also spoke to last week publicly for the first time is in their phase II-B trial, they saw consistency with what they saw in phase II-A, which is a decline of response over time and incremental toxicity. Importantly, there's not a class effect on safety. That's another thing we heard last week from Eli Lilly, and I know that's one of the potential theoretical concerns. Let's not talk about the safety of these drugs and what happens in RA. The comorbidities of RA are two- to threefold higher than healthy controls when you take into account infections, MACE, malignancy. If you look at the commercial landscape, Humira, Orencia, Rituximab, and then obviously the JAKs, generally speaking, they all have black boxes. Again, they're all on background methotrexate, these patients. They're immunosuppressed. A lot of them are on steroids.
You see higher rates of infection in this disease just because of the comorbidities where they're exacerbated on drugs. Now let's compare that to the PD-1 program, at least our data sets. From what we know right now of peresolimab, this is a relatively benign profile as it relates to placebo. Infections are about the same across all doses. We saw no MACE, no malignancy, no increase in severe infections. This is a great safety data set. What this allows us to think about in the future is not only monotherapy development, but also combination development as we think about phase III and beyond in this disease and others. This data set is consistent on the safety profile of what we know is in this space with other competitors over time, relatively benign.
The reason for this is it's a very targeted therapy, really only interacting with these PD-1 high expressing T cells that are found exacerbated in diseases like RA. In healthy controls, 2% or 3% of your T cells are PD-1 high. In disease, about 40% are PD-1 high and 80% are PD-1 expressing. It's a gross difference. We're targeting what's driving the disease on target, but we're not interacting with naive T cells, which are the majority of the T cells in a healthy control. The whole idea here is to bring these patients back to homeostasis. You're seeing that play out in the safety of the patients, safety results of the patients. All right. Now let's bring this home. What this slide is showing is a comparison. It's the highest bar that's available in the data sets to date in RA.
The blue-colored bars are our data across three high-order response rates: LDA on the left, ACR50 in the middle, ACR70 on the right. We're comparing this to active comparator trials, Rinvoq versus Orencia, which have the highest response rates reported in this disease until what we've now seen. Further higher bars, we're reporting our week 14 results relative to their week 24 results. Now, put this in context. All patients know for these gray bars, they all know they're on an active drug. It's a similar equivalent to being on an open label. The handicap for us here is that at week 14, if you didn't respond, you were removed from the study. This is only now responders moving forward for us.
A hypothesis is, and you saw the slide earlier on the DAS28 change over time, is that patients who maybe didn't hit LDA at week 14, some percentage of them probably would have gotten there over time if they're allowed to stay in the study. We believe that these data are even handicapped and potentially could have been better out to week 28, knowing that our data results to date are stable. This holds up really well. The most important thing, if you're treating patients in this disease, is are your patients feeling better at week 12? We showed that 70% of patients were in ACR20. That grew to 80% over week 14. The vast majority of patients are feeling better. Drug is tolerable.
What would happen in the commercial setting is you would stay on this drug and drive towards low disease activity or even remissions over time. These data hold up very well to anything in the commercial landscape. We hit our TPP by beating all the other biologics. Not only did we approach the JAKs, we look equivalent and potentially even superior to the JAKs. Again, this was a 424-patient study, quite robust and representative of the size of a study that would look like in the phase III. The commercial landscape. In RA, you have a mature market. Patients cycle off a TNF between three or four other classes before they're in salvage. That's a $10 billion market post-TNF today. We would play very well into the second or third-line setting and with this type of a profile, once-monthly injection, sit in front of the JAKs.
That's the commercial vision. Second, we're moving forward in a second trial I mentioned earlier in ulcerative colitis. Translationally, we saw data that I just presented with the reduction of PD-1 high T cells that, in the setting of UC, is correlated with remission of disease. That's just in the periphery. We should see a drug effect in the site of inflammation, no different than the synovium in RA, but also in the lamina propria of UC patients where there is an overexpression of these PD-1 high and PD-1 expressing T cells. Quick word on the ulcerative colitis trial. It's ongoing, currently enrolling 132 patients, two active arms versus placebo. This is a three-three design to month six. Non-responders would stay on this drug through month six, so hopefully we see peak response at that point in time. We were unable to do that in the RA design.
Placebo non-responders would cross over at three months. They would move to the high dose of the drug. At six months, responders stay on for a year. We will now see in this trial one year of durability as well as one year of safety. We are really excited about this. We think the translational data from RA read well into the study design. The disease biology and what we are doing here is similar to what we just did in RA, and the bar is lower. You do not need to be JAK-like. This is a growth market. We are in the future. You are going to see patients moving through biologic classes just like the mature RA market. A lot of opportunity here. Initial results will be presented in Q4 of this year. Lastly, on our cash position, like I mentioned earlier, $420 million of cash coming into the year.
We have a $75 million milestone due from GSK on a drug called Jemperli, a PD-1 antagonist, which has been on the commercial market for three years. When that drug hits $1 billion of sales, that's very possible this year, if not this year in 2026, based on Q4 growth rates from last year. The trend line here is really strong. You can see in the bottom right corner, Wall Street consensus in blue, $1.3 billion of peak sales is about half of what GSK is guiding to, which is north of $2.5 billion. We have an 8% royalty up to a billion. This escalates to 25% royalty up to $2.5 billion. Big value creation just in the royalty backbone on top of our current strong cash position. We do not need to tap into this royalty anytime in the near future.
We can continue to watch and see this value accrue in the background while we continue to develop out the portfolio of rosnilimab in the earlier two programs. Thank you.
That's great. Thank you, Dan. Maybe I will start with a question that you did show tons of also the data. Maybe the RA data, 28-week data, what can we learn from the data? Maybe like what are the data points you will be presenting and then the patient and then follow-up, and then what can we learn?
Yeah. We're really excited about what we can present and the full analysis that's coming up in Q2. We've seen only 100 of those 220 patients out to week 28. We'll have all patients out through week 28. I alluded to this from the translational data. What we're also potentially able to see here is, given the PD of this drug, the potential for sustained durability three months off a drug. Now, we're not projecting that you're going on drug holiday forever here, but compared to what happens in this commercial landscape where most patients fall off after a year because they lose response while on drug, potentially here we're seeing sustained response for the majority of our patients even off the drug.
If we can show that, I think the hypothesis here is that if you're staying on the drug, you will have stable disease over time well out through a year. I think that'll be comparable to other drugs that have been developed in this space. Second, again, we don't know the answer to this today, but those non-responders at week 14, they still may have had a lot of improvement. They all received drug up through 14 weeks. After that point, they did not come back for further treatment, but they did come back for further assessment. There is a potential where we could see increased response rates just from the non-responders coming back. Third, we're going to have a lot of translational data. We only had pretty top-level results right now with the T cell impact.
What we still have to show and look for is the cytokine impact in the periphery. We also have a robust set of synovium biopsies that were done where we could look at the effect of what's happening with immune cells at the site of inflammation as well as the cytokine activity. It is a pretty fulsome update. I think right now we have a great data set that could probably only get better from here.
Great. I think you mentioned a little bit maybe there's some confusion about week 12 versus 14 data. Maybe if you can clarify a little bit and then help us understand how should we interpret the week 12 versus week 14 data?
Yeah. I think you almost first have to step back from week 12 and 14 and look at those curves starting at week eight. We see separation. The PD of this drug, we're hitting full translational effect on the T cells through the three-month period. CRP, the biomarker, we're hitting a very meaningful effect through three months that holds. What we're seeing in terms of the outcome of the clinical activity starting at week eight is separation from placebo. You're accelerating to week 10, into week 12, into week 14. What I was just mentioning earlier, these non-responders that didn't hit LDA by week 14, we do think that some bolus of those patients potentially could have continued responding if we had more time with them. We didn't hit peak response by week 14. I think it's the key takeaway, but we do see an acceleration through that timeframe.
Placebo patients at week 12, just like any other assessment, they come in, get assessed, they got their dose of placebo just like you would have gotten active drug in a blinded fashion. Going into week 14, sites were notified that a patient on placebo would not be staying in for further treatment. However, the independent assessor, the patient per protocol, were unaware of this. Going into that visit, they were assessed, and after the assessments were done, the patient was notified that they were no longer going to be in the trial, and i.e., they were on placebo and were removed from the study at that point in time for further placebo treatment. It was a blinded study. This study design was pushed on us by the FDA. Eli Lilly had the same.
There could be a potential for some bias, but the reason we are comparing to week 24 data in active comparator studies is on a theoretical worst-case scenario. If you consider our longer-term data open label, just compares to active comparator studies where everyone knows they're on a therapy and the data holds up. Importantly, there over six months is stable, both immunologically through translational and objective endpoints like CRP, as well as these higher-order magnitude thresholds that you don't see, generally speaking, on placebo over time.
Okay. Good. Now, quickly switch off your UC data. For Q, we will see tons of data. Maybe what is your bar or threshold you'll be looking for regarding the primary endpoint?
Yeah. We have yet to set specific quantitative numbers, but qualitatively here, we have a disease state where historically you'd take one or two advanced treatments and you move to a surgery. What's happening here in this landscape is now there's more options that are coming and will be coming available. Patients aren't moving to surgery. What we're seeing emerge is a true second, third, and fourth-line market post-Entyvio or TNF exposure. The way we ran our trial, we'll have a mix of bio-experienced and bio-naive patients. We'll be able to see all comers across both subpopulations. What we're looking for here, unlike in RA where you really need to be approaching a JAK to compete in the maturity of that market, we're going to be looking for something that's bio-equivalent, bio-like to therapies like Skyrizi, the IL-23p19s, or potentially the TL1As.
What's happening here with our drug is a very different mechanism of action coming down from the top, hitting the T cells and broader activity well upstream of things like IL-23. Different mechanisms of action give physicians and patients a very different choice as they move through lines of therapy or that second or third line. Big growth market, big opportunity relative to other biologics. I think you also have to put in perspective, it's highly differentiating to have no loading doses and being a one-time, once-monthly injection subcutaneous relative to everything else that's out there.
Last question. We have one minute. I think in the past you say you only maybe keep one internally. If UC also positive, how do you decide which one you want to keep internally? I assume the other you wanted to look for the partnership.
Yeah. If you asked me two to three years ago, what we were most excited about actually was ulcerative colitis, both in terms of disease biology, the animal model data we have, now the translational data. I think from a commercial perspective, importantly, we can go launch in ulcerative colitis given the growth dynamics in the United States independently. We can't move two phase III programs forward on our own, but if UC looks great, it's an obvious choice for us to move to phase III in that program because that's the independent path forward. That said, we're going to look to do what's the best return on equity for this drug. That could be just moving forward in UC and expanding in GI, other diseases, but it also could mean looking for a partnership where it could expand and move forward in phase III in multiple indications.
I think with our cash position and these options for an independent path forward that would create equity value for investors, we're going to have a choice on what to do. When you really step back from it, we do not have competition in the clinical development. We are the only PD-1 depleter that's in development for these diseases. Eli Lilly's not moving forward. They're not moving forward because they have declining efficacy with a less potent asset. J&J also isn't moving forward with their program anymore. What's out in the marketplace right now is they have manufacturing issues in terms of their cell line, the stability. We're in a great place where a first-in-class now program with anything else behind us that's a depleting PD-1 antibody still in preclinical development.
It gives us a lot of flex as we think strategic about what to do with the program in the future.
Great. Thank you very much. We look forward to the several data update later this year.
Thank you very much.
Thank you.
Appreciate the opportunity.
Thank you, everyone.