AnaptysBio, Inc. (ANAB) Earnings Call Transcript & Summary

Good day, and thank you for standing by. Welcome to the AnaptysBio Rosnilimab Top-Line Phase IIb Rheumatoid Arthritis RA Data Conference call. [Operator Instructions] Please be advised today's conference being recorded. I would now like to hand the conference over to your speaker today, Dan Faga, President and CEO. Please go ahead.

Thank you, everyone, for joining us this morning. Over the past 3 years, our strategic focus at Anaptys has been to develop innovative and best-in-class antibodies that have the potential to drive a paradigm shift to how autoimmune diseases with high unmet need are treated. Rosnilimab, which represents one of these programs is a potent depleter and agonist that targets the PD-1 co-inhibitory receptors selectively expressed on the surface of PD-1 positive or activated T cells. Today, we are excited to share positive and statistically significant results for rosnilimab from our Phase IIb trial in rheumatoid arthritis, or RA, that potentially paves the way for a differentiated novel treatment option for patients who have not had the benefit of a new therapeutic class in more than a decade. Today's press release and this presentation contain statements that are forward-looking. Dr. Paul Lizzul, our CMO, will speak to the data; and Dr. Martin Dahl, our SVP of Research, will join us at the end for Q&A. We are highlighting today the exceptional study results that in the first 3 months exceeded our 6-month target product profile in RA. Importantly, rosnilimab demonstrate a favorable safety and tolerability profile. Equally as important, we achieved statistical significance on our primary endpoint, the DAS28-CRP at week 12 as well as on key secondary endpoints at both week 12 and week 14 even though we observed somewhat higher than typical placebo response rates. Approximately 7 out of every 10 rosnilimab treated patients in the overall study population achieved CDAI low disease activity or LDA at week 14. This is the highest response rate on this measure ever reported in a robust Phase II or Phase III study. The top half of this slide in the blue shaded columns showcases rosnilimab response data for CDAI LDA, ACR50 and ACR 70 from the bio-experienced patient subset of our trial week 14, which are, to date, consistent with what we are observing at the end of study treatment at week 28. We are comparing rosnilimab results to data from head-to-head all active studies after 6 months for the key RA competitors. Shown in the gray shaded columns from left to right are Rinvoq, a JAK inhibitor, Orencia, co-stim antagonist and Kevzara, an IL-6 inhibitor. Let's now put these data in perspective. In these active comparer RA studies, you typically see a significant boost to response rates when compared to the observed responses for the same drugs in placebo-controlled studies. Said simply, rosnilimab week 14, CDAI LDA, ACR50 and ACR70 response rates are either numerically equivalent or superior to the published data from all of these active comparator studies at time points up to and including 6 months. These conclusions are also applicable to our bio naive patient subset. What's more, the rosnilimab responders appear to show sustained CDAI LDA and ACR50 responses and potential deepening of these responses to ACR70 beyond 6 months. Needless to say, we are really excited about these trial results for rosnilimab and the impact it could have on patients living with RA. Now Paul will walk you through these data in detail.

Thank you, Dan. Let's start with a recap of the overall design of the Phase IIb study. We enrolled a moderate to severe RA patient population with active disease. Participants were randomized to receive 12 weeks of treatment of either 100 milligrams subcutaneous rosnilimab every 4 weeks, 400 milligrams every 4 weeks, 600 milligrams every 2 weeks or placebo. All of these patients, regardless of study arm were required to be on a stable background conventional DMARD, such as methotrexate. The approximately 60% bio-naive and 40% bio-experienced trial participants were balanced across the 4 treatment arms, meaning that we stratified enrollment for this criteria at baseline. Our primary endpoint analysis was conducted at week 12 with key secondary endpoints at both week 12 and week 14. At week 14, rosnilimab-treated patients who achieved low disease activity defined as a CDAI score of less than or equal to 10 continued with their assigned treatment through week 28 in a blinded all active treatment period. If a patient did not achieve low disease activity by 3 months or they were on placebo, they were required to discontinue from study treatment. For this reason, only the low disease activity responders were eligible to stay on rosnilimab from week 14 onward through the remainder of the study out to 28. In our trial, we will be looking to further confirm that these responders have sustained or even deepened their response through 6 months of total treatment. With regard to study disposition, 424 patients were randomized equally across 3 active dosage arms and placebo with approximately 106 participants in each arm. Discontinuation rates in the active arms were low and balanced across arms. Importantly, rosnilimab was safe and well tolerated with very few patients discontinuing treatment due to an adverse event. We enrolled a typical moderate to severe RA population. The average patient was 57 years old with 22 tender joints and 15 swollen joints and a mean baseline DAS28-CRP score of 5.63. There was a mean baseline CDAI score of 38 and approximately 95% of the population was severe, defined as having a CDAI score of greater than 22. These baseline characteristics fall within the range of what would be expected in a typical moderate to severe RA study. In addition, 31% of patients were enrolled in the U.S. and 69% in Canada and Europe. We observed consistent and balanced baseline characteristics across geographies as well as across both the bio-naive and experienced cohorts. Now keep in mind that the typical RA patient when compared to the general population lives with a two- to threefold increased risk of significant comorbidities such as infections, MACE and malignancies. To compound things further, these patients were typically on background immunosuppressive therapies such as methotrexate and steroids, which can also drive higher infection rates. Additionally, approved classes of therapies, such as TNF, JAKs or CD20s have black box warnings indicating that they can further exacerbate the risk of these comorbidities. Now let's take a look at rosnilimab safety data in this trial to date. Overall, rosnilimab was safe and well tolerated with mostly mild or moderate AEs that were balanced relative to placebo. This profile is consistent with what we have seen in prior studies. There is no particular safety signal observed to date. There were no treatment-related severe AEs or SAEs and the few events reported were not concerning. Importantly, we observed no malignancies, no MACE and no anaphylaxis or systemic hypersensitivity associated with rosnilimab. And there was also no elevation of serious infections versus placebo. The most common events observed were headaches and upper respiratory tract infections. So taken all together, these safety data are quite encouraging as you don't often see such a muted safety and tolerability profile in RA patients. Importantly, we are further encouraged by the safety profile for those trial participants who have already made it beyond week 12 as it also remains consistent with these observations. This is great news. Before we review the clinical data, let's look at initial translational data showing the clear, objective and meaningful immunological impact of rosnilimab at all doses. We observed early and rapid reduction of PD-1 high and PD-1 positive T cells in the blood that is sustained through the entire study dosing period. The graph on the top left displays results from the 400-milligram monthly dose, which is representative of the results we saw in the other 2 doses. We observed an approximate 90% reduction in PD-1 high T cells including TPH cells regardless of the baseline T cell count. This is consistent with what we previously reported in Phase I and Phase II studies. Few PD-1+ Tregs were present and were reduced proportionately to PD-1+ positive T cells overall. Taken together, we observed stable total T cell counts with an increase in total Tregs, leaving patients with a favorable T cell composition reflective of healthy immune homeostasis. In contrast, no reduction of PD-1+ pathogenic T cells were observed in the placebo arm. These data show that rosnilimab is a potent depleter of PD-1 high T cells in the periphery, which is known to correlate with active disease in both RA and UC. Equally important, we observed an approximate 50% reduction in CRP from baseline, an objective measure of inflammation in rosnilimab-treated patients through the entire study period, and this was not observed on placebo. A decrease in CRP demonstrates an objective reduction in inflammation supporting rosnilimab made an impact beyond directly targeting T cells, such as on macrophages, which are major producers of inflammatory cytokines such as IL-6 and TNF-alpha. This observation supports the long-term impact of rosnilimab on diseases such as RA and ulcerative colitis. We look forward to sharing additional exciting translational data from both the blood and synovial tissue in the next few months. Now let's turn our attention to the clinical efficacy data. As Dan mentioned, the overall study was a success, and the primary endpoint, mean change from baseline in DAS28-CRP, was statistically significant at all doses at week 12. There was continued improvement on rosnilimab, as you can see, we are still on the steep part of the curve heading into week 14, suggesting that maximal efficacy has not yet been achieved at that time. This is exciting. Given the mean change in DAS28 improvement observed here at week 14, it's already equivalent to or even better than reduction seen by other therapies such as the JAKs. We begin to see separation from placebo at week 8 and initial statistical significance that we can as well as a flattening of the placebo response curve within the variability of small changes observed between visits. Rheumatologists are open to keeping patients on a therapy if they are seeing ACR20 improvement in month 3 with the anticipation of possibly achieving even deeper responses like low disease activity by month 6. At week 12, we achieved statistical significance on all doses for ACR20, which is a standard registrational endpoint and is a validated composite measure that correlates with patients feeling notably better. It is really remarkable to see a large majority of the population achieving ACR20. We see greater than 70% ACR20 rates at week 12, which is similar in magnitude to Rinvoq, a JAK inhibitor used in clinical practice. The results on CDAI LDA are also important because it's a validated threshold that correlates with slowing the progression of joint erosion. Even more exciting is the magnitude of CDAI LDA response that we already see at this relatively early time point of week 12. In fact, approximately half of the rosnilimab treated patients achieved LDA at week 12. This result is quite impressive and actually would be even if it were only observed by week 24. Now looking at additional higher order response rates. Typically, you see modest improvements in ACR50 and 70 at 3 months, whereas the expectation is that patients will need prolonged treatment to achieve these thresholds if they can achieve them at all. On the left, it's encouraging to see early deeper clinical responses across the overall rosnilimab-treated population already at week 12. While we did observe somewhat higher than typical Phase II placebo rates on ACR50 and 70, we achieved numerical superiority at each dose and statistical significance at one dose on ACR50. On ACR70, you would not expect to see statistical significance at this early time point in a Phase II study, and we're encouraged by the absolute response rates being north of 20% as shown here. What's particularly encouraging and important are the ACR50 and 70 importment shown in the middle and right columns regardless of prior treatment experience. And in the approximate 3-month time frame, we also still appear to be on the steep part of the response curves for both measures, and this is consistent with what we observed in the DAS28-CRP, where we saw a step-up in efficacy from week 10 to week 12 and to week 14 and as I'll show you on the next slide, they are sustained through week 28. As Dan shared earlier, these ACR50 and 70 absolute response rates at week 14 are also quite remarkable. Furthermore, when looking at both ACR50 and 70 responses over time for the 69% or 220 patients treated with rosnilimab across all doses who achieved CDAI LDA at week 14, it's exciting to see a sustained response growth out to week 28. What's even more exciting is the potentially deepening of ACR70 responses seen through month 6 as well. Now keep in mind that these are early week 28 data. Our trial is still ongoing and not all responding patients who remain on drug have completed treatment through week 28 as of the cutoff date. You'll also note the dash black trend line in the background capturing the average of all the patients across the 3 rosnilimab doses from baseline through week 28. As you can see, while there are some expected week-to-week variability in the data, there is continued upward momentum from month 3 through month 6, the time point at which clinicians need to see higher order responses to keep their patients on therapy. So taken all together, we believe that these data present a compelling efficacy profile for rosnilimab not just through 3 months, but potentially through month 6 and beyond. Additionally, these 220 responding patients appear to sustain DAS28-CRP improvements through week 28. As a reminder, the trial design only allowed for CDAI LDA responders at week 14 to remain in the study and continue to receive active treatment. All of the nonresponding patients regardless of their potential to further improve through month 6 were required to exit the treatment phase at this time. This artificially caps the potential peak response rates achievable at week 28. While these week 28 data are early, we are encouraged by the consistency of this long-term trend across multiple endpoints. The data set coming in Q2 will include all CDAI LDA responders up through week 28. Additionally, we'll present further translational data, including insights from synovial biopsies. We also anticipate presenting full clinical data later in 2025 at a medical conference. So as you have heard throughout this presentation, we are excited about these data, especially because of the promising efficacy and safety profile that can potentially make a significant difference for millions of RA patients. Now let me hand it back to Dan.

Thanks a lot, Paul. RA is a well-established $20 billion U.S. and global market. And in the U.S. alone, approximately $10 billion of this revenue is generated annually in the subset of bio-experienced patients who cycle between largely undifferentiated biologics. There is clearly a need for something new. Building off the Paul's summary of clinical results in RA, our data presented today further boosts our confidence in succeeding in our ongoing Phase II ulcerative colitis trial for 3 reasons. First, rosnilimab safety and tolerability satisfies the profile needed to be prescribed in both moderate and severe UC patients. Second, multiple drug classes are approved in both RA and UC, such as the JAKs and TNS with consistent efficacy results. As a reminder, there is strong overlapping biology in these 2 diseases that are relevant for rosnilimab including a return to low numbers of TPH cells that are strongly correlated with clinical remission of UC. And third, the translational data presented today suggests depletion matters. We've shown that rosnilimab significantly reduces those pathogenic TPH cells in the periphery. Also, rosnilimab showed an approximate 50% mean decrease in CRP, which is associated with the reduction of inflammation beyond T cells. These initial findings bode well for the anticipated topline UC results now anticipated in Q4 2025. We ended 2024 with approximately $420 million. I also want to provide 2 additional perspectives about the strength of our financial position. First, our cash runway guidance through year-end 2027 includes completing the rosnilimab Phase IIb trial in RA and the Phase II trial in UC. Importantly, given that UC topline results are now expected later this year, most capital commitments to facilitate Phase III enablement in either of these indications will come after the UC topline data are available. Second and equally important is our cash runway guidance excludes any potential inbound dollars from business development or future royalties and milestone payments due from our long-standing immuno-oncology financial collaboration with GSK. As a reminder, this collaboration covers JEMPERLI, a PD-1 antagonist discovered at Anaptys and launched by GSK a few years ago and cobolimab, the TIM-3 antagonist also discovered at Anaptys, which is in Phase III development. Based on GSK's Q4 2024 results, we believe JEMPERLI is potentially tracking to achieve $1 billion in revenues either this year or next. And once this occurs, a onetime $75 million payment will be due to us from GSK. Finally, we think there remains a significant financial upside in JEMPERLI royalties over the next decade. Beyond the additional rosnilimab catalyst in RA and UC, we have 2 additional clinical stage programs. ANB033, a CD122 antagonist and ANB101, a BDCA2 modulator. These programs further strengthen our pipeline with important Phase Ib data catalysts upcoming. In closing, I want to thank all the patients and clinicians who participated in and supported our Phase IIb trial. Also, thank you so much to our team at Anaptys, who work tirelessly every day to find ways to transform patient health. Now we will turn over to the operator for Q&A.

[Operator Instructions] Our first question comes from Joseph Thome with TD Cowen.

Congratulations on the great data this morning. Just a quick question between the week 12 and week 14. Obviously, great to see the response is increasing. But there was quite a big jump between the -- specifically on the ACR50 and ACR70 responses. I guess is there anything to call out between these 2 time points, anything to flag other than just overall deepening responses. And then one follow-up, if I can. Can you just comment a little bit on the type of infection that you were seeing throughout the study look like one of the arms maybe had a slight more -- nothing too crazy, but just if you could just comment on that, that would be great?

Paul, want to kick it off?

Yes, sure. On infections, typical nonserious ones like upper respiratory or sinusitis, so really nothing to say there. On the week 12 to week 14, there was no change between those visits in terms of number of subjects that were at those visits. As you will recall from the study design, patients had to achieve LDA at week 14 in order to continue into the study. So potentially, there could be some small chance of bias introduced there, and that was similar to the design that Lilly had to conduct for their Phase IIa study. But I think what you're seeing there is a continuing deepening of response on the active as people continue to improve on drug and I think you're seeing a normalization of that placebo rate over time with that curve flattening.

Next question comes from Yasmeen Rahimi with Piper Sandler.

Congrats on the data. I think there's quite a bit of CV, like I would love to get some clarity on that, what -- from the protocol between week 12 to week 14. So specifically, I guess the question is what happened? So you noticed, right, that -- I guess one question is that the placebo patients were then transitioned at week 12 to get on drug. I guess the question is why do we have a placebo still at week 14? And then another question that we would like to ask is, could it be that that design element of 12 to week 14 could have introduced some sort of bias that led to it? I think if you could just kind of walk us through, again, what did you do at week 12? What did you do at week 14? And how could the design change not introduce a change in efficacy? So if you could just walk us in detail through that would be really helpful as many clients wonder that aspect.

Sure. So similar to the Lilly design, week 12 was the primary endpoint. At week 14 subjects came in and had a determination of low disease activity, whether they were placebo or active, and they had to achieve LDA at week 14 to continue through the study.

Yes. Yes, let's not get lost here a little bit. I mean this is a placebo-controlled trial, placebo was real in week 14. When you look across these data, week 10, week 12, 14, you see a flattening of that placebo curve across the totality of the data. And like Paul went into in detail here, through month 3 and beyond, we are in the steep part of the dose response curve here for rosnilimab. That's pretty clear. And we got to also not get lost in the details too much. We have all patients out at week 14 at this point. The trial in 220 patients, treated rosnilimab were responders. And I think what's also important to see here is that -- not only are these responses impressive at 3 months, they're real, they're durable and supported by these data are immunologically, we went through the translational data, particularly relative to placebo, there's a huge difference in immunological outcomes here on rosnilimab-treated patients and placebo. So it's a well-controlled trial. The data is real, and it's sustained over 6 months. And when you speak here with physicians in the community. That's what's going to matter is the absolute, as we mentioned, this TPP now for years, the absolute response rates noted that we separate from placebo at week 12, the absolute response rates here are what matter in this disease to the rheumatology community and they're stable out over 6 months.

Our next question comes from David Risinger with Leerink Partners.

So let me add my congrats on the data as well. Could you just talk a little bit about the exceptional efficacy of the 100-milligram once a month and the lack of differentiation of 1,200 milligrams a month with the highest dose utilized twice per month. And then just one more, please. If you could please comment on the SAEs of cholecystitis and pericardial infusion as well?

Sure. Thanks for the questions. I'll take the first one, I'll transition over to Paul on the AE profile. So this was a dose-ranging Phase II trial. And from one hand, we're really pleased to see that the lowest dose, which is a single once-monthly subcu injection was highly effective. We've said -- we've shown the data over the last couple of years that these low dose of 100-milligram, it hits the IC90 and given the potency of our antibody and this, to some degree, is what we're hypothesizing but given the potency of our antibody, we are seeing a full immunological effect. And so we walked you through the translational data. We're showing the 400-milligram on the slide, it's the same for the 100-milligram monthly as well as the high dose. But what you're seeing there is an immediate at the first read reduction of those PD-1 high T cells by over 90%. That's happening at the low dose. So at the end of the day, we put 3 doses in. We knew the low dose should be active given the IC90. And we're really pleased to see that hard-hitting depletion in a targeted way minimally has resulted in pretty comparable efficacy. As we think about next steps here and where we can go with this, that type of profile, a once-a-month dose, is going to be commercially really important and obviously competitive. And if we're somewhere between and we're not picking dose here today, there's still a lot of work to do. We have to finish the trial. There will be more translational insights, but we're somewhere between that low dose and that middle dose. We have not only once monthly, but also just one injection subcu. So we're pretty excited about these results, and this is why you run a broad dose-ranging study to begin with. Paul, why don't you take the AE question?

Yes. So the question was on the patient with cholecystitis and that had a pericardial fusion, typical course of a patient having a stone. They were hospitalized, had that taken care of and during the course of their hospitalization developed that complication as part of the surgical. So it's really not related or anything to do with the drug itself.

Our next question comes from Martin Fan with Wedbush Securities.

Congratulations on the data. I wanted to dive in following from David, quick question on the CDAI LDA rate at 12 weeks. It seems to be a little bit low in the 600-milligram Q2-week arm at 38%. I was wondering if you could speculate on why that might be the case when the ACR and DAS28-CRP responses did seem to show at least something of a dose response. And I was wondering, did it seem to -- because it seemed to catch up at 14 weeks, were there any outliers in geography or higher therapy at that week 12 time point?

No. So across the board, the results were very consistent on all the endpoints in geographies and as well as in the bio-naive and bio-experienced populations, really nothing there to report. And on CDAI, I think you're just seeing a little bit of the variability that can occur between endpoints and the data. There's really nothing to point to that would suggest the difference in assessments.

Yes. And I'm just going to repeat it one more time here as we're moving through month 3 into month 4, you are in a severe deepening of this curve and responses at all of these doses. And again, don't get caught up in very small variability across the doses here. All of these doses are effective. We hit stats and/or a numerically superior to where placebo was and when you look at week 14, all of these doses are consistent on the CDAI scale as we reported, they're consistent in ACR50 and they are deepening on ACR70 on all of these doses. Due to the trial design, unfortunately, nonresponders, i.e., that didn't hit the CDAI score of LDA at week 14, they were pushed off the study. And so to some degree here, we're limited at the peak response rate that we're seeing with this drug because nonresponders that didn't hit LDA may have responded further over time. So we have a rate limit ceiling due to the trial design that the FDA asked us to run. And that's why we're focused here. It's not just one data point. We did hit that on a placebo-controlled trial, but this data is getting better and is artificially limited as to how good it potentially may be. But again, consistency at week 14 out through month 6.

Next question comes from Derek Archila with Wells Fargo.

Congrats on the data. Just one from us. I just want to get an understanding in terms of the placebo response that you're seeing at week 14 on the ACR measures and how that compares to some of the week 14 data we've seen from [indiscernible].

I would say that the data between the 2 studies are similar and you did see some changes in results from between week 12 and week 14 and the Lilly data set as well. I think going back to ours, we're seeing consistency here, I think, on the placebo. Again, we're seeing flattening of that curve stabilizing over time. Separating from active starting at week 8. And then as Dan mentioned, we're seeing this continuing ongoing deepening of activity as you go from week 8 to 10 to 12 to 14 and beyond with the active. I think the other point here with regards to placebo is that, as I mentioned earlier, also on objective measures, we're not seeing any impact there. So you're seeing very clear impact on objective measures on active. You're seeing nothing happening on placebo and objective measures and on subjective measures that include many of these endpoints with some attributes, there's some inherent variability there, but you're seeing that stabilize over time.

Our next question comes from Alex Thomson with Stifel.

Congrats on the data as well. I guess on week 12, could you comment at all on the trends you're seeing across the naive versus experienced populations? Are you seeing better responses across endpoints in the naive patients as well here? And then maybe on some of the other potential secondary end points, could you talk a little bit about the trends that you're seeing on some of the other components of ACR50 and 70 like HAQ, et cetera?

So we don't have all the components yet on all these individual attributes. Obviously, this is topline data and we're still collecting and going through the information. But across the board, I would say, consistent results in the overall population at week 12 and week 14 across multiple endpoints. No dose response observed to date which is great news that the low dose is performing, and we wouldn't not necessarily unexpect to see that given what we know about PK and PD. And in addition to that with regards to the naive and experienced population, I would say, as expected, you do see some higher performance in the naive relative to the bio-experienced that wouldn't be surprising and unexpected, and I think we're seeing that consistently as well.

Our next question comes from Yatin Suneja with Guggenheim.

Congrats on the data. So the question for me is what would be the size and scope of a pivotal RA program? And how long might it take to conduct that? And then maybe as a follow-up, what additional safety data, if any, would you need for a long-term PD-1 agonism?

Sure. I'll frame some perspective here as we're thinking about what Phase III is. Clearly, these are large Phase III programs as you think about either RA, UC. And from a safety database, fortunately, across both of these studies, it really works together into Phase III and what you're going to need for the drug, not just for a specific disease. As we think about Phase III, these are also large commercial markets themselves on a global basis. As we're planning for Phase III [indiscernible], we've been saying for multiple years that it's not feasible for us to move rosnilimab forward in parallel through multiple Phase III programs to commercialize globally in 2 different therapeutic areas like rheumatology and GI. So this is a good problem to have if and when we get there across the 2 different drugs. And we have a lot else to do here in 2025 before Phase III is actually initiated. We need to finish the RA Phase IIb trial through the 6-month data. We have -- we're really far along. We're almost there but not quite done. We need to enable or meet with regulators to enable that Phase III. We just announced today that the Phase II results from the UC program will be in Q4. We have to complete that trial across the active doses there as well. Again, as a reminder, that trial is not only 6 months, it actually extends out to a year to generate additional efficacy and safety data over time. So there's a lot happening here through the course of this year as we think about how to best enable the program for success in 1 or 2 of these therapeutic areas for Phase III initiation 2026.

Our next question comes from Anupam Rama with JPMorgan.

A quick broad question, which is as you look at the totality of the data, would you really focus us on the biologics experience or naive population following on the last question in terms of next steps? And then just like -- I know like just this might be annoying, but for like a clarification question, right, which is at week 14, you've made comments that all patients were accounted for. But at the same time, like the slides say at week 14, a portion of patients were responders or LDA patients were responders, right? So I think the real controversy is like how do we -- are all patients accounted for at week 14? And then if they are, how do we explain some of the sort of bounces that you see in the data between week 12 and 14?

Yes. So I'm just going be crystal clear on this. Every patient in the trial, unless they dropped out, which was very, very few, we disclosed the dropouts in the trial. Every patient, on rosnilimab is treated at week 14. 220 of those patients hit low disease activity. That is a very high bar and the relevance in this trial is that if you hit low disease activity at week 14, you were then eligible to stay on the trial for 6 months. If you did not hit low disease activity at week 14, you were removed from the trial as well as all placebo patients were removed from the trial after week 14, and they're followed up for 2.5 months. So there should be no controversy between week 12 and 14 in terms of patient numbers. They're all there at both of those time points.

Our next question comes from Emily Bodnar with H.C. Wainwright.

So I guess I just want to confirm how you're thinking about next steps. It sounds like you're planning to complete the UC study and then potentially just pick one of these indications to move into Phase III. And then if you could just comment on the adverse events that led to treatment discontinuation of rosnilimab and if any of those were related to study drug?

Do you want to take that second question first, Paul? Treatment discontinuations why we have the few that we did?

They were not related to study drug and yes, it was very low balance across the board. And with regards to AEs, you had one or 2 subjects across each of the arms discontinuing. So I mean, we had a very low discontinuation rate that was consistent, similar, even better to what you're seeing across other trials. So really nothing to discuss about discontinuations.

Yes. And let's take a step back here a little bit. So where are we going with this? Yes, what I'm implying is there's no way we as a company are moving both these forward in UC and RA, and we have to get there in UC first on our own through Phase III, it's not practical financially, operationally. So I've been saying that for years. What we delivered on here today and what this market needs, which is validated by just countless discussions and surveys of KOLs, community docs, payers, patients is a new class of therapy, one that's safe, tolerable, drives the disease into low activity state and is durable through 6 months and beyond. That's what we're looking to achieve here and rosnilimab just delivered that. What these data are suggesting is that a physician can say to their patients that at least 7 out of 10 chance they'll achieve that treatment goal of LDA in as early as 3 months, and they have the potential to sustain or deepen that response in the longer term. And as I mentioned earlier, you could do that in a single onetime monthly subcutaneous injection. That is an exceptional profile here that we're sitting on. It's supported by clear translational data that show the mechanism is potent and impacting disease biology exactly as we predicted. So we're really excited about the totality here of the efficacy data, the safety data, the supporting translational data and not only does it seem like what we just showed is differentiated in RA. We believe this is transferable to UC. Those are 2 of the largest pharmaceutical markets in the world, there's the potential here to expand into further additional rheumatology or GI diseases or beyond. We're going to learn a lot more about that through further translational data in Q2. This program deserves to be and will be developed further in RA, likely in GI and in other diseases. We're not going to do all this on our own. So the question for us sitting here today is not if but when to find help. We're also not a global pharmaceutical company. So we're incentivized here with a first-in-class, best-in-class molecule. We look over our shoulder, there's no competitors in sight for years. It's a great position to be in. And from our standpoint, we're stressing that we have the capital needed to get through a number of events over the next few years and pick and choose our time when to find that partner, right? So that's the mandate here. And if that doesn't happen in the next 6 to 9 months, UC is something we can and will move forward in the Phase II on our own, and we can commercialize in the U.S. But the profile here, I think, is going to be attractive to folks. And so there's going to be interest.

Our last question comes from Ellie Merle with UBS.

It's Sam on for Ellie. Congrats on the data. I guess just given today's data, are there any learnings around which patients are most likely to respond to rosnilimab? And then how should we think about implications from today's data for the UC study?

Just one quick observation. We're showing this on the translational data side, and this is even across the doses. We're showing a pretty complete reduction of TPH cells across doses for rosnilimab-treated patients. And as we're showing you, 70% of patients at week 14 already hit low disease activity, and we don't believe it's going to be limited to that when we run broader trials that all patients continue on drug for 6 months. That's our hypothesis right now. You're asking a really important question. We don't have the answers to that yet. And these are some of the things we're hoping to assess as we get to additional biomarker data, not just in the periphery, but also in a very robust set of synovial biopsies that we've collected in this trial. We'll be assessing that through steady completion in Q2 and that's really going to help us answer that exact question. So something we're excited about. I can't promise that sitting here today, but it's something we look forward to reporting back on.

Thank you. Ladies and gentlemen, thank you for joining and participating in today's conference call. This does conclude today's presentation. You may now disconnect, and have a wonderful day.