Seres Therapeutics, Inc. (MCRB) Earnings Call Transcript & Summary

Ladies and gentlemen, thank you for standing by, and welcome to the Seres Therapeutics Conference Call. [Operator Instructions] Please be advised that today's conference is being recorded. [Operator Instructions] I would now like to hand the conference over to your speaker today, Dr. Carlo Tanzi of Investor Relations. Please go ahead, sir.

Thank you, and good morning. A press release announcing top line results from the SER-287 Phase IIb clinical study in patients with mild to moderate ulcerative colitis became available at 7 a.m. Eastern Time this morning and can be found on the Investors & News section of the company's website. I'd like to remind you that we'll be making forward-looking statements relating to the potential impact of microbiome therapeutics; the safety, efficacy, regulatory and clinical progress of our product candidates; plans, timing and potential impact of the release of additional preclinical and clinical data, including the SER-287 microbiome analyses; our cash position and our future development plans. Additionally, these statements are subject to certain risks and uncertainties, which are discussed under the Risk Factors section of our recent SEC filings. Any forward-looking statements made on today's call represent our views as of today only. We may update these statements in the future, but we disclaim any obligation to do so. On today's call with prepared remarks, I'm joined by Seres' President and Chief Executive Officer, Eric Shaff; Chief Medical Officer, Dr. Lisa von Moltke; Chief Scientific Officer, Dr. Matthew Henn. And during the question-and-answer portion of the call, we will also be joined by David Arkowitz, Chief Financial Officer. And with that, I'll pass the call to Eric.

Thank you, Carlo, and good morning, everyone. In a few moments, Lisa will review the top line clinical results from our SER-287 Phase IIb study in ulcerative colitis that we announced earlier today and Matt will discuss the microbiome and metabolomic data that remain pending from the study. The SER-287 Phase IIb study did not demonstrate clinical benefit in patients with mild-to-moderate UC. We are surprised and disappointed with this outcome, and we are especially disappointed for the UC patient community that we are ultimately working to serve. Today's disclosure represents the preliminary clinical information we currently have in hand. However, the Phase IIb study was designed to provide a rich data set, and we expect to obtain important additional results in the second half of the year. These results, including detailed microbiome and drug activity data, will provide us with valuable information that will help us better understand study conclusions and determine next steps for the SER-287 program. Furthermore, these data will also provide the team with valuable insights to drive the continued advancement of our microbiome development efforts for inflammatory diseases. UC remains an important target indication for Seres and we continue to see substantial promise for our microbiome therapeutic approach to provide new solutions for patients with this condition. Seres is, at its core, a data-driven science-based organization. As we have successfully done in the past with our SER-109 program in recurrent C. difficile infection, we intend to carefully scrutinize all Phase IIb study results, learn from the data and determine the optimal path forward for continued clinical development of our microbiome approach in ulcerative colitis. Specifically, we will look to understand why the SER-287 Phase IIb results are so different than the encouraging results from our prior Phase Ib study, and we are exploring all aspects of the trial. We remain steadfast in our belief that our microbiome therapeutics have the opportunity to play an important role in the treatment of many diseases, including ulcerative colitis. Our microbiome approach for UC is based on extensive scientific evidence that links the microbiome to inflammation and gut barrier integrity, which Matt will discuss further. We are pleased to have a second program, SER-301, in development for UC. SER-301 is a differentiated candidate that is based on our next-generation rationally designed approach. As we have discussed in the past, we expect that this type of microbiome therapeutic candidate based on specific strains of biologically active bacteria will be the basis for all of our future pipeline candidates. Seres is also well positioned from both a financial and operational perspective to continue to lead this new field of medicine forward. Earlier this month, we entered into a license agreement with Nestlé Health Science to co-commercialize SER-109, Seres' lead investigational oral microbiome therapeutic for recurrent C. diff infection in North America. The agreement provides Seres with a substantial upfront payment of $175 million, $125 million upon FDA approval, substantial additional development and sales milestones. And upon commercialization, Seres will be entitled to an amount equal to 50% of future commercial profits. This transaction adds to a balance sheet that was already strong. As of June 30, Seres had approximately $229 million in cash, cash equivalents and marketable securities. That cash balance does not include the upfront fee of $175 million that has been received by Seres following the agreement. The Q2 quarter ending pro forma cash balance inclusive of the upfront fee is over $400 million. We are very pleased with this transaction and with our ongoing collaborative relationship with Nestlé. In addition to being well resourced, we are fortunate to have an exceptional R&D team and differentiated core capabilities in place for both the discovery and GMP manufacture of microbiome therapeutics. We intend to leverage our capabilities to continue to aggressively identify and develop novel microbiome therapeutics for inflammatory diseases as well as a number of other serious conditions. I'll now pass the call over to Lisa.

Thanks, Eric. We advanced SER-287, an oral microbiome therapeutic candidate consisting of a consortium of highly purified Firmicutes spores, into a Phase IIb study based on several lines of evidence. This included clinical data from several groups indicating that fecal microbiota transplantation could result in clinical benefit for UC patients as well as our own encouraging Phase Ib clinical microbiome and metabolomic data. Additionally, preclinical data have demonstrated the ability of bacterial preparations to result in favorable activity in animal models with UC. SER-287 progressed into a Phase IIb study with a total enrollment of 203 subjects with active mild-to-moderate UC. The 3-arm study evaluated 2 dosing regimens of SER-287 against placebo during a 10-week induction period. One active arm used the successful daily dose from the Phase Ib study and the other active arm utilized the same dose for the first 2 weeks, followed by a lower dose for the remaining 8 weeks. Both active arms began with 6 days of vancomycin preconditioning designed to support SER-287 engraftment. The inclusion criteria focused on subjects who had an inadequate response or were intolerant to conventional UC treatments. The primary endpoint was clinical remission after 10 weeks of induction treatment, and the study was also designed to evaluate a multitude of secondary and exploratory endpoints, including a body of data that remains pending. The study enrolled participants from approximately 100 sites in the U.S. and Canada, whose demographics were well balanced on age, race, time since UC diagnosis, location and extent of disease and concomitant UC medications. Clinical remission was analyzed and defined by a 3-component modified Mayo score. Clinical remission rates were 10.3% for the full induction dose, 10.6% for the step-down induction dose and 11.6% for placebo, demonstrating no meaningful differences between the treatment groups. Similarly, there were no meaningful differences observed across 3 treatment groups for endoscopic improvement, endoscopic remission or symptomatic remission. And from a safety perspective, both dosing regimens of 287 were generally well tolerated. Treatment-emergent adverse events were observed in 67.6% of those on the induction dose, 46.2% of those on the step-down dose and 50.7% of subjects on placebo. The majority of observed adverse events or AEs were of mild or moderate intensity. The most commonly observed AEs were worsening of UC, diarrhea, nausea and abdominal distension. Four participants on active treatment reported serious treatment-emergent AEs, which were worsening of ulcerative colitis, colonic dysplasia, congestive heart failure with a decreased hemoglobin and a case of appendicitis. One patient on placebo also reported a serious treatment-emergent AE, a worsening of ulcerative colitis. We did have a suspected unexpected serious adverse reaction or SUSAR reported by an investigator for one study subject who had previously completed 10 weeks of daily therapy on the step-down regimen and was then receiving once weekly SER-287 in the exploratory maintenance arm. Six weeks into the once-weekly dosing arm, the patient was hospitalized after developing dyspnea, dry cough and sore throat. Although a number of potential ideologies were identified, the investigator elected to discontinue study drug treatment and the patient was discharged. Based on the lack of clear evidence supporting SER-287 efficacy in UC, we are halting additional activities in the exploratory maintenance arm as well as the open-label portion of the study that had been active for induction period clinical remitters. We are conducting various analyses, including extensive patient subpopulation examination to better understand the Phase IIb study results and why these data are so inconsistent with the prior Phase Ib results, where we saw evidence of clinical benefit. There were some differences in study design and patient inclusion criteria that may have had a role, but it is too early to provide any specific commentary on this. We also expect to learn additional information from the pending microbiome and metabolomic data that may help explain the results. We would specifically like to learn more about the Phase IIb SER-287 engraftment profile and how this compares to what we observed in the Phase Ib. We have conducted a rigorous well-executed study. Our organization places a high importance on obtaining interpretable clinical results from appropriately sized trials, and I would like to acknowledge the efforts from our clinical team and study sites. We expect to continue to learn a great deal from the Phase IIb study and we expect to be able to apply these learnings to our future microbiome therapeutics, including potentially to our ongoing SER-301 study. One specific point we are currently evaluating is whether there may be opportunities to obtain more clinical and biological information from the SER-301 Phase Ib study that would help our team make robust data-driven decisions regarding the future development of that program. I'll now pass the call to Matt to discuss the pending study data and our ongoing SER-301 study.

Thanks, Lisa. Our R&D team continues to be optimistic and compelled by the prospects for a microbiome therapeutic approach for the treatment of ulcerative colitis based on external and internal research over the past decade-plus that demonstrates that individuals with IBD, including both ulcerative colitis and Crohn's individuals, can have a gastrointestinal microbiome that differs from those of the healthy individuals. As discussed at our UC investor event earlier this year, a disrupted diseased microbiome can lead to breakdown in mucin and the dominance of proinflammatory bacteria, such as those in the family Enterobacteriaceae that interact with human epithelial cells to promote the production of proinflammatory cytokines. Furthermore, research suggests that these microbiome differences have impacts on host cell and tissue functions that are of relevance to IBD. In contrast, commensal microbes and microbe-associated metabolites in a healthy individual help to maintain immune homeostasis and suppress inflammation. These microbes and associated metabolites can promote mucosal and epithelial barrier integrity and impact the differentiation of various immune cell populations, including T cells, macrophages, dendritic cells and B cells and can signal the production of various cytokines. In addition to evaluating SER-287 safety and efficacy, the Phase IIb study was designed to capture a rich data set of microbiome, metabolomic and other translational data. Analysis of these data was gated by unblinding of the study. Over the coming months, we will be executing on predefined microbiome endpoints and conducting additional data analyses to inform drug activity and pharmacology in the Phase IIb study. These assessments will be similar to those conducted in the Phase Ib study and published in January of this year in the journal Gastroenterology. With these data, we will be examining a number of scientific questions that we anticipate will facilitate interpretation of study outcomes and our IBD programs more broadly. These assessments will include engraftment of bacterial drug species, changes in microbe-associated metabolites and changes in other metabolites as well as transcriptional data from intestinal biopsies to evaluate the upregulation or downregulation of disease-relevant host pathways. As we have done in the past, we will further leverage this sizable, rigorously collected high-value interventional human data to inform and support our broader microbiome therapeutic efforts. I'll close by speaking briefly about our SER-301 UC program. SER-287 and SER-301 are both consortia of bacteria found in the gastrointestinal tract of healthy individuals. However, important compositional and potential therapeutic differences exist between these investigational drugs. SER-287 is a donor-derived product, whereas SER-301 utilizes Seres' next-generation technology and is a rationally designed cultivated consortium of bacteria. Complex diseases such as mild-to-moderate ulcerative colitis may require a more specific approach distinct from that represented by donor-derived products. The bacteria in SER-301 are targeted at and specifically selected to reduce proinflammatory activity, improve epithelial barrier integrity and reduce TNF-alpha-driven inflammation in intestinal epithelial cells and modulate UC-relevant, anti-inflammatory innate and adaptive immune pathways. The design of SER-301 has leveraged the company's reverse translational platforms and capabilities that can evaluate at high resolution how microbes in the gastrointestinal tract are interacting with one another and human cells and tissues to impact disease pathways. These platforms can interrogate the mechanisms of action of microbes both directly in humans and in combination with nonclinical assays and models to rationally select specific strains and confirm lead candidate activity. Using these platforms, the SER-301 consortium was optimized by combining insights from across our entire clinical portfolio, informing bacterial species engraftment and mechanistic functional properties such as the production of desired microbe-associated metabolites and additionally, based on rich knowledge of the functional, safety and manufacturing properties of individual bacterial strains in our broad strain library. SER-301 is currently enrolling mild-to-moderate UC patients in a Phase Ib study in Australia and New Zealand. I'll now pass the call back to Eric for final remarks.

Thanks, Matt. As an organization, Seres is well aware of the nonlinear and iterative nature of drug development. This is especially the case when advancing a novel therapeutic modality. As a team, we talk about humility as a key ingredient in successfully pioneering a new field of medicine. At the same time, we have confidence in our tools, insights and capabilities and have seen magnificent results for patients by facing adversity and complexity head-on. We are confident that Seres has the resources and the scientific and clinical expertise to thoroughly interrogate the SER-287 study data. Based on this information, we will determine and implement any necessary adjustments to our microbiome development plans. Several years ago, Seres faced a significant challenge with the SER-109 Phase IIb setback. Following those data, our organization completed a detailed scientific analysis that revealed several areas that we believe could increase our probability of success. We subsequently implemented study changes that led to a highly positive outcome, and we are now working towards a BLA submission for SER-109, which we expect to become the first ever approved microbiome therapeutic. Our belief in the potential of our microbiome approach as an important emerging treatment modality remains strong. This is supported by the weight of scientific evidence linking the microbiome to multiple diseases, the capacity of our technology to modulate the human microbiome and perhaps most importantly, the definitive Phase III data we've obtained with our lead SER-109 program. We know that microbiome therapeutics absolutely have the capacity to transform patient outcomes for serious diseases. Looking ahead, we intend to continue to execute on our mission to apply our technology to making a real difference in the lives of patients. With that, operator, we'll now open the call up to questions.

[Operator Instructions] Your first question comes from the line of Joseph Thome with Cowen.

Maybe the first one, did you see any challenges in compliance or drop rates in the study? Have they been kind of impacted by the COVID pandemic? And then second, when we do see the SER-301 data, has the SER-287 data readout kind of increased the bar that you need to see in that Phase I or to advance the study or kind of how are you thinking about the benchmark that you want to see in that, just an update.

Yes. Joe, thanks for the questions, and maybe I'll ask Lisa to start with the first one. I mean, obviously, getting to the finish line through the pandemic was a challenge that required a lot of tenacity. But maybe I can ask Lisa to comment on the first and then I'll take the second.

Yes. We actually have seen that the compliance within the study and actually even the retention for the study looked quite good. Now what we do need to see is that microbiome data because that's analogous to the PK, if you will, and that will give us an idea of, a more concrete idea of whether people actually took the drug as they reported and whether it engrafted.

Yes. And Joe, maybe on the second question, I think it's probably a little bit early to talk about if the bar or how the bar might change for the 301 readout. What I will say is that, as always, we'll follow the data. And if there are learnings that accrue from the SER-287 microbiome analysis that we can build into the 301 study, we absolutely will look for those opportunities. It's a Ib study, and we're certainly not so far along that we can't make adjustments if those adjustments are appropriate or will be helpful. So as we go through this next phase of analysis, that certainly will be something that we'll be looking at.

Your next question comes from the line of Mark Breidenbach with Oppenheimer.

First, I was wondering if you could tell us how many different donors were used to manufacture drug product for ECO-RESET and how that compares to what was done in the Phase Ib trial? And kind of aside from the donors used to source the material, can you point to any material changes in manufacturing or release criteria between the 2 studies?

Yes. Mark, let me start with the question. So there were multiple donors that were used in the Phase Ib study. There were multiple donors that were used in the Phase IIb study. We don't have full information which we will have later, including and through our microbiome analysis to dig deeper into the donor aspect of things. I will say that there were multiple donors used throughout the study. The remissions that we saw from the 2 active arms were spread reasonably evenly throughout the study. So with the information we have, it doesn't look like there was a donor effect at first pass. But certainly, that's something that we'll take a look at. I think you had another question.

Just in terms of other changes in manufacturing or release criteria.

Yes. So I would say, in general, there were minor process changes between the Phase I and the Phase II. But the intention or the design behind the II versus the I was really to replicate the signal that we saw in the high dose from the I. So those changes were, in general, minor. Certainly, we'll look at those, any changes from the I to the II as we move forward. And there were no changes in formulation.

Okay. Got it. And just maybe one follow-up, probably pointed at Matt. I'm wondering if you can expand at all on or give us more comments on the compositional overlap between SER-301 and SER-287. And just remind us if SER-301 can include vegetative non-spore-forming strains that would be excluded from SER-287?

Yes. Sure. So SER-287 and SER-301 are related but are differentiated with potential therapeutic differences. So SER-287 contains a broad diversity of Firmicutes species that has a specific subset of bacteria in the donor stool samples and is manufactured, as you know, by fractionation, purification from donor materials. SER-301 in contrast is a cultivated targeted set of bacterial species that were optimized for engraftment in the GI and the pharmacological properties that our clinical and preclinical research have identified as potentially important drivers of a treatment effect. And I'd be happy to expand upon those optimizations. But SER-301 is a rationally designed consortia where all the strains are cultivated. And as you noted, Mark, some of the strains are delivered in the form of spores and some are delivered in a lyophilized form.

Your next question comes from the line of Chris Shibutani with Goldman Sachs.

Can you comment about, I believe, the Nestlé relationship? I believe they had access as well to the ulcerative colitis opportunity OUS. And obviously, you recently announced the commercialization agreement for 109. Are the individual components completely independent of each other? And with the recent commercialization agreement, is there anything formal in the contract in terms of a standstill as far as the relationship that set up the ownership? To be explicit, the ability of Nestlé to acquire Seres as a function of how you set up the commercialization agreement.

Yes, Chris, thanks for the question. Let me try to provide as much color as I can. So as a reminder, we did a global deal in 2016 where Nestlé licensed rights to 109, 287 and 301 ex North America, right? We, as you may remember, announced a deal just a matter of weeks ago with Nestlé where we licensed the North American rights to 109 as part of a co-commercialization agreement. So they now have global rights to SER-109 with the prior agreement structure for ex North America and with a co-commercialization structure in North America. To answer your question, there is not a standstill agreement as part of that next or the most recent agreement that we have with Nestlé.

And then can you comment at all even preliminarily about what this update on the ulcerative colitis program has for your view on operating expense outlook perhaps for the next 6 to 18 months or so?

Yes, Chris, I think it's a little bit early to comment on that. I think, as you know, we had been focused prior to this outcome on what is a really compelling set of opportunities, including continuing to support 109 forward towards the BLA and ultimately commercialization. We are continuing with 301, the Ib study in Australia and New Zealand. We've got our 155 study, which is moving towards the clinic. And we had before and continue to be excited about the opportunity to invest in the earlier stage pipeline. And I would say that, that was our focus before this outcome, and that continues to be our focus. So we feel we're in a very good position financially and operationally. Obviously, the Nestlé deal further supports what was an already a strong balance sheet. But we also are mindful of how we allocate capital and we'll continue to have a responsible approach to that as we go forward.

And finally, keeping true to form from the last call, I asked whether you could provide any insight on the timing of the 301 readout and then I would ask you once again. So here we are, I'll ask once again, some insight, 301 readout.

We don't, Chris. But I think as we said before, as we have done in the past, our practice has typically been as we get deeper into a study we'll provide a greater range once we see a slope of the curve. And then over time, we further refine that range or have done so. I would imagine that we might do something similar with 301 here.

Your next question comes from the line of John Newman with Canaccord.

I just wondered, given that this study was conducted during COVID, which was obviously a difficult time for all clinical trials, do you have any indication that there was any imbalance in the endoscopy measurements taken at the end of the study? Just because if I understand correctly, if a patient were to miss that, they would be considered a failure even if they were actually seeing a significant effect from the drug. I'm just curious if you noticed anything there?

John, thank you for the question. And I'll ask Lisa to comment. Again, it's hard to ignore the pandemic in the sense that when the pandemic began, we were still really in the midst of probably the earlier side of our enrollment curve. And when endoscopy is kind of shut down broadly, we had to think about the path forward. Ultimately, we were able to get to the finish line. We think it was a rigorous study, including the way that we set up the protocol that Lisa can talk to in terms of essentially red endoscopies and so forth. But maybe I'll ask Lisa to comment.

Yes. Based on the top line data we've seen so far, it looks like the execution was really smooth throughout. And we'll be looking, of course, for any kind of pattern as we dig deeper into it. But again, I think we were quite pleased with the way the sites and the clinical team executed, and we're quite thankful for their efforts.

And if I could ask one additional question. I know that you're looking at the preliminary data. Was there any indication that even though it wasn't really allowed in the study that physicians were using steroids in their patients during the study?

We have nothing to indicate that, that was happening. No.

Your next question comes from the line of Chris Howerton with Jefferies.

I guess maybe just 2 for me. First, perhaps for Lisa, with respect to the remission rate in the placebo arm, it's frankly a little lower than I might have expected. So I'm curious if you have any thoughts what might have been driving that? And I guess, if you agree with my perspective, first of all. And then the second question that I have was just if you could provide whatever details you can on the current 301 study design, that would be really helpful.

Sure. We agree that the placebo rate was lower than a lot of studies that you see in this space. We had always anticipated that because of the central reading and the rigor with which we controlled a lot of various factors that the placebo rate would be somewhere in the 5% to 10%. And so what we saw was pretty close to what we had expected. And again, we really think that the rigor of the central read, which also included comparing that with a local read was a big factor there. With regard to the design of the 301 study, we've discussed in a number of venues that it's composed of 2 parts. The first is a safety evaluation. And then the second part is a placebo-controlled, again, safety, but looking at signals for efficacy.

Okay. Great. And maybe if I may, just a quick follow-up with respect to the placebo response. The 5% to 10% range we've certainly seen historically, but in a more severe patient population. So I guess I'm just pressing a little bit on the point of mild to moderate patient population. Is there anything there that would have indicated maybe this was a tougher to treat patient population than one might have anticipated initially?

Yes. Well, we would agree that it's tough to treat population just because you don't have as much dynamic range to move, right? And so getting patients better if they're not really, really sick is a higher bar. But we have looked where we can find comparable populations. And if you look, for example, at the steroid literature, you can see that you find things below 10%. Cochrane database has some data as well that it can be in that range. So we think that, that was a reasonable target to look at.

Your next question comes from the line of Keay Nakae with Chardan.

Yes. Just anything in the baseline characteristics between this study and the Phase Ib that were meaningfully different, whether that be the Mayo scores or the eventual endoscopic subscores?

Yes. Maybe I'll start just with a general thought. I'll ask Lisa to comment on a high level as to the changes between the 2 studies. The one thing I would say is that, whereas we certainly are aware of the differences between the 2 studies. I think it's too early for us to comment on what may or may not be meaningful, and that really is the intent behind the microbiome analysis that will come next. But maybe, Lisa, you can just comment high level on the differences between the 2.

Yes. I would say that broadly, the populations were quite similar. They were mild to moderate population. But as Eric alluded to, we know that there have been some differences, probably the major one is for the field, the definition for the Mayo score, the modified Mayo score for clinical remission was updated by the FDA back in 2016. And with that came more specificity around certain parameters that are part of the Mayo score as well as dropping the physician's global assessment as part of that score. So that's a modification that is potentially significant. But as Eric said, we'll know more as we look at the data.

And maybe I'll add one more comment, which is I know in our prepared remarks, we talked about the 109 experience. And I think it's worth reiterating. On the heels of that data, the top line data release for the Phase II for SER-109, it's not like the next day we said, if we were to adjust the dose and the diagnostic algorithm, then we're going end up with a great result. I mean, it was the product of a rigorous objective scientific investigation that analyzed and then disregarded a number of things and then came up with these 2 key elements based on real data that built conviction that we could increase our probability of success based on those 2 major adjustments. So whereas we don't know what drove the differences between the I and the II today. We do know that taking a similar process is the right next step for us, and that's what we're going to do.

And just in terms of releasing the findings from the additional analysis, will this be done in one lump sum or could we see it roll out in different subsets of analyses in the second half of the year?

Yes. I prefer not to speculate. Sometimes we need to see different pieces together to really understand in totality what they mean. So when we've got something that we think is meaningful this year, then certainly, we will work with urgency to make sure that, that happens and that we share it.

[Operator Instructions] Your next question comes from the line of Gobind Singh with JMP.

I guess I had a follow-up with one of my previous colleagues, one of their questions. I've been thinking about the patient population that was in this trial versus maybe what was in the Phase Ib. I believe, if I remember correctly, the Phase Ib allowed treatment naive and then also treatment refractory to 5-ASA in the background med. In this trial, I believe it was all refractory patients. So I guess was Phase Ib including more treatment naive than obviously what was in this trial? And could that have been part of the reason why the efficacy was different?

Maybe I'll ask Lisa to comment on the question.

Yes. Well, we'll know more as we dig into it. But you're correct that the Ib study allowed for patients who were naive to treatment and what IIb did not. The Ib also allowed for low-dose steroids. The IIb did not. So there are a couple of differences. But I think broadly, the characteristics around a lot of the demographics are very similar. So we'll know more later.

Can you share what's the background or what percentage in the Phase Ib was treatment naive?

I think it was about 10%. It's actually in our paper. It's published in the paper. I'd have to check for the exact number, but it was not a large percentage. And just keep in mind, this is a bigger study, and it's a couple of weeks longer, but the big difference between any Phase I and Phase II is just simply the size.

Yes. I see. And I know one of the goals of this study was to also look at combination use, perhaps with like 5-ASA and so forth. And I know in the Phase Ib, I believe that was also allowed. Is there any chance there is something maybe one of the treatment arms had more combinations than the placebo or anything like that, that you can talk about in terms of just the baseline and how they came in?

Yes. Based on the top line results, the arms were very well balanced across not only con-meds, but endoscopy scores and a number of other important factors.

At this time, there are no further questions. I would like to turn the conference back to management for any additional or closing remarks.

So thank you, operator, and I want to thank everyone for joining our call today. We look forward to continuing to keep you updated on our progress. With that, we'll conclude, have a good day. Thanks.

Thank you for participating in today's conference call. You may now disconnect your lines at this time.