Thank you, Tess, and thanks to J.P. Morgan for having us at this year's conference. It's great to be in person to talk about Seres, our mission, our vision, and have the opportunity to connect. I'm pleased to be joined by my colleagues, Marella, Matt, and Terri, and together after the presentation, we look forward to answering your questions. Now, I will be making forward-looking statements in today's presentation, so I encourage you to review our risk factors in our most recent 10-Q. Now, I'd like to start with a brief overview of who Seres is, and perhaps this can serve as an outline for how we allocate time in this presentation. And it starts with Seres itself, where we have pioneered the live biotherapeutic drug modality using a consortia of bacteria to prevent disease.
That starts with SER-109, or what is now VOWST, where we had outstanding clinical success. This led to an FDA approval, making VOWST the first live microbiome therapeutic oral in our space. Our modality is one in which we can target a broad range of human biology, and we'll talk about mechanism and the science in depth. We've generated multiple positive clinical data sets with our programs, and we're focused on preventing infections in vulnerable patient populations. We own the entire value chain in-house. We discover, we develop, we manufacture. We have leading manufacturing and regulatory capabilities, and we designed VOWST from inception to approval. We believe that we're poised to do it again with SER-155 and other programs. We're happy today to talk about 155. It's our next program. We believe that it has blockbuster potential.
It had remarkable efficacy and a favorable safety profile in preventing infections in Allo-HSCT patients in our phase 1b study. It was recently awarded Breakthrough Therapy Designation, and we see a substantial opportunity to help patients not just with 155, but adjacencies from Allo-HSCT such as Auto-HSCT, and then 147, which we'll talk about in others. But for us, it's difficult to talk about Seres or even SER-155 without starting with VOWST. So VOWST is proof of concept for the outstanding potential for live biotherapeutics to save and improve patient lives. So VOWST had a dramatic clinical benefit, 88% efficacy in preventing recurrences of C. diff infection with a favorable safety profile. Now, keep in mind, this was and is an incredibly difficult-to-treat disease where companies have for decades tried to innovate on behalf of patients with limited success.
This is a therapeutic which is effective, it's oral, it's well tolerated, and a great deal of our experience with VOWST we think is highly relevant as we go forward with SER-155 and other programs. Now, it's important to talk about, for us, the recent transaction that we had with VOWST and our partner at Nestlé Health Science. With the majority of our rights in VOWST, we sold to Nestlé Health Science, including the transfer of about 80 employees. I would note that as part of this transaction, we emerged from it a more streamlined company, clean balance sheet, and really focused on the right skills and experience to create value on behalf of patients. I would note that this morning we announced an expected receipt of a $50 million milestone payment as part of the transaction, which is built into our cash runway.
Now, for us, we know that the health of the microbiome is connected to human health, and disruptions to a healthy microbiome, or what we call a dysbiosis, is related to serious diseases like C. diff, but certainly not only C. diff. And if you think about the mechanistic link between disruption of a microbiome and disease, think about the idea of the risk of pathogens, but also critically important, the susceptibility of the system to those pathogens. It's relevant for VOWST. It's relevant for SER-155, where pathogen overgrowth can result in infection, and preventing pathogen overgrowth can have a positive impact for patients who are vulnerable. It's relevant as we think about gut barrier integrity, preventing pathogens from translocating from the gut to the bloodstream.
It's relevant as we think about regulating immune response, and we've got some new data to share on our 155 study that I'll talk about in a minute. Now, as it relates to impacting biology, it's important to know how we deliver bacteria as therapy. So we designed a consortia of bacteria we are intending to repair and restructure a damaged microbiome. As I've indicated, the gut microbiome can become disrupted, leading to functional deficiencies and susceptibility to disease. In other words, you can lose microbes in your gut, and as such, the gut doesn't function correctly and is contributing to or is the primary driver of disease. Our consortia are delivered in a pill. The bacteria are intended to take up residence in the gut and replicate and basically use the gut as a bioreactor. Now, we'll talk about allo-HSCT. We'll talk about auto-HSCT.
We'll spend a minute on CLD in this presentation, but we know that lower microbiome diversity is associated with increased infection and worse overall survival. We've done considerable work over the years to identify disease populations where disruption in the microbiome is a primary driver of disease. Currently, we're focused on immunocompromised cancer and liver disease patients where their treatment regimens, such as chemotherapies and prophylactic antibiotic use, have led to serious disruptions in their GI microbiome, and these functional deficiencies have been linked to diseases, so specifically, we're focused on allo-HSCT, auto-HSCT, and cirrhosis. These are medically compromised patient populations where a specific link between GI microbiome diversity, which is a proxy measurement for disruption, has been linked to survival.
In these patient populations, one of the most significant causes of mortality are infections that can result, among other things, in pathogen colonization, loss of barrier integrity, and immune function. Our programs going forward are SER-155 and SER-147, both of which Seres fully owns. We were thrilled to announce Breakthrough Therapy designation from FDA at the end of last year. Prior to J.P. Morgan, we announced that we had submitted our briefing book to FDA for our next intended clinical study, and I'll talk about that in a minute. We also have SER-147. Both of these programs are designed to reduce the incidence of serious bacterial infections and related complications in medically vulnerable patient populations.
Our immediate focus is preventing life-threatening infections, but as we continue to progress in these programs, we see the potential to treat immune-related diseases, particularly in light of our recent gut barrier integrity data and inflammation data, so let's dig a little bit deeper into Allo-HSCT, allo patients that are undergoing a cancer treatment regimen that significantly impacts their immune system and can leave them uniquely susceptible to serious and potentially fatal infections. There is substantial clinical evidence that the gut microbiome is disrupted in allo patients. Mortality rates have been estimated at about 10%. Morbidity is significant despite the common use of antibiotic prophylaxis, which often causes hospital readmission and increased time in intensive care units. We designed SER-155 to try to prevent bloodstream infections and associated complications that are harming these patients. Now, let's take a deeper look at bloodstream infections.
BSIs are a serious problem and, in fact, are increasing due to the rapid adoption of PTCy, or post-transplant cyclophosphamide, which has led to an increase in BSIs. It's a serious problem for these physicians to have their patients come off their underlying therapeutic tracks. These infections can be significant, they can be frequent, and they, in fact, can be fatal. And these are really fragile, complicated patients whose cost of treatment also can be very expensive. Infections, complications, fever can be the difference between a discharge and a readmission or even an ICU stay where there can be substantial financial consequences to the hospital and even to the system. So let's talk about SER-155 in our phase 1b study, which included two cohorts. We started with a leading cohort where we read out data in 2023.
The intention of this was to show that we could dose patients with high doses of bacteria. The primary goals were looking at engraftment of our organisms and safety, and we were pleased with both of those metrics alongside a reduction in expected pathogen overgrowth as compared to a reference cohort that we had established with Memorial Sloan Kettering over a number of years. The second cohort utilized a randomized double-blinded one-to-one placebo-controlled design to further evaluate safety, consortia engraftment, and early signs of efficacy, specifically the incidence of bacterial bloodstream infections among the other endpoints that are listed here below. Starting with safety, 155 was generally well tolerated throughout this period. Recall that these patients are highly immunocompromised. A major aim was to ensure that, as I said before, they could be dosed with a live biotherapeutic.
We're pleased with the safety that continues to be favorable across our platform. There were a number of meaningful outcomes on the efficacy side of this study. Patients that were administered 155 had a significantly lower rate of bacterial bloodstream infections compared to the placebo group as measured through HSCT day 100. Febrile neutropenia is another common complication experienced by allo patients lower in the 155 arm versus the placebo arm. Lastly, in clinical practice, these are patients who, when they experience a BSI or febrile neutropenia, are aggressively treated often with broad-spectrum antibiotics. As you can see in our study, we observed a meaningfully lower cumulative exposure to systemic antibiotics and antimycotics. It was principally antibiotics. We believe that these data show the potential benefit for SER-155.
Now, just to dig a little bit deeper, looking specifically at the metrics, 10% BSIs in the 155 arm versus 43% in placebo. So that's an over 30% absolute reduction between the arms, 77% relative risk reduction between the arms. Even though this study was not designed for statistical significance, this result actually was significant. The placebo arm, which is really standard of care, is about what we had expected in this arm. As we think about the next study and next steps, I think we have the benefit of considering a smaller delta, but still something that physicians will find of considerable value. Importantly, as we think about antibiotic exposure, significantly lower exposure to systemic antibiotics and antimycotics, almost exclusively, as I said before, antibacterials. Significant reduction in days on antibiotics, approximately 10 in the 155 arm versus 21 in the placebo arm.
As you think about antibiotic resistance, this was a particularly meaningful result for us and for our KOLs. We recut the data one more time just to adjust for days on therapy, and as you can see, the trend continues to hold. Now, in summary, what I'd say is we're very pleased with these data from our 1B study. The data, particularly on the efficacy side, exceeded our expectations for a positive outcome and really suggests to us that SER-155 has the potential to meaningfully reduce bloodstream infections in this patient population. Based on this data, we are eager to advance SER-155 to the next stage of development for allo-HSCT patients and also to explore other adjacencies, and we'll talk about that in a second. But before I do, just point out a couple of items on the pharmacology side of things.
We tend to run data-rich studies, and we care deeply about the engraftment of our consortia of bacteria. We found that our organisms engrafted, or as I mentioned before, took up residence in the GI tract as we had hoped and expected, and we actually saw that that engraftment, in fact, was durable. Now, we have some new data that we talked about in a press release that we put out last week, and we're excited to report that the clinical pharmacology continues to support the idea that the mechanism of action that we were designing 155 for, we're actually seeing in practice, and it also supports our, we believe, our capability to design drugs to target multiple pharmacologies simultaneously. We talked about in the past the engraftment. These are new data from the study that looked at the evaluation of multiple plasma biomarkers of epithelial barrier integrity and inflammation.
So specifically, first, fecal albumin levels were significantly reduced during the peritransplant window in 155 subjects, suggesting that 155 repairs and protects the epithelial barrier from damage, preventing translocation of pathogens. Albumin is an established biomarker of gut barrier integrity. Albumin is made in the liver, excreted to the bloodstream. When the barrier is damaged, albumin can leak from the bloodstream into the gut and then thus into the feces. I would also note we also observed a reduction in multiple biomarkers of pro-inflammatory responses compared to placebo, with additional reductions observed in systemic inflammatory markers. I would lastly note that these results were accepted for the 2025 Tandem Meetings. We have an oral presentation and best abstract in ID and a poster.
I would say that these data are further suggestive to us and supportive to us of the mechanism, not just in SER-155, but as we think about our technology more broadly. Very excited by this. Now, let's talk about HCPs. HCPs tell us that they want a solution like SER-155 that can decrease infections and keep patients on track. When considering the idea of helping HCPs do their jobs of getting the transplant to take and ensuring that the patient survives, the feedback is that SER-155 would be adopted broadly into standard of care. The value driver is reducing infection, valuable to HCPs, valuable to patients, valuable to the system. Specifically, our research and interactions with HCPs suggest that a relative risk reduction of 50% of BSIs would be seen as transformative and likely would support the inclusion in standard treatment protocols.
We actually have some new non-clinical data to share as well. We recently completed some market research with U.S. payers, including both health plans and PBMs with about 130 million lives that are covered. As you can see on the slide, payers recognize the high unmet medical need and the costly nature of these transplant patients, and the profile of SER-155 is received positively, especially with a relative risk reduction of about 50%. Finally, because 155 is given orally and not simultaneously to the transplant itself, payers confirm that the drug would be dispensed outpatient and, as a result, reimbursed through the outpatient drug benefit and not in the hospital.
Overall, this feedback, both the HCP feedback and the payer feedback, align well and suggest to us the substantial opportunity with 155 to help patients avoid these life-threatening infections with a novel modality, which is addressing the limitations of existing standard of care. Now, before I move to talk about next steps, I would just say that because 155 is novel, there aren't great comps, but Merck has a drug called Prevymis, which is intended to prevent viral infections. There are some lessons that are relevant to us as we think about and look at Prevymis, including the fact that infections, of course, are severely and costly, but there's a recognized value in preventing them, and as a result, we've heard that HCPs and patients don't tend to have issues with access.
And our assessment is that with a clear value proposition for SER-155, 155 would likely follow similar conditions. So just to summarize, high unmet medical need, 40,000 transplant patients worldwide in allo. These patients are incredibly costly. And from a commercial model, there's an efficiency here that there's a high concentration of these transplant centers treating these patients, many of whom we know from our first clinical study. And we believe that the commercial potential is considerable, right? So 40,000 worldwide allo procedures, more auto procedures, roughly 10 times that number in terms of broader blood cancers. And certainly, as we think about the mechanism of action of 155 and the vulnerability of patients in auto or blood cancers, we think that these adjacencies are logical. We think that they're tractable, and they can create a blockbuster opportunity.
Certainly, you can envision that as we think about the clinical results and ways to move forward, we're doing so with a regulatory lens towards moving with efficiency. Now, with that lens, we're seeking an accelerated path with SER-155 given the unmet medical need, the exciting early signals of efficacy, and the safety profile of the program. We never get ahead of the FDA, but we have submitted a briefing book. Our proposal is to move to a single pivotal registrational study for efficacy. We have breakthrough designation. We've considered ways in which we can build expansion into adjacent patient populations into the next study, including features like an interim read. Lastly, we're considering opportunities for a strategic partnership.
Obviously, we're doing the critical work to prepare for the next study in terms of preparing sites, manufacturing, and clinical material, but we do think that there's a set of scenarios where working with others, not just to finance the company, but also to provide expertise, relationships, knowledge, particularly ex-US, can bring value to the program and to the system. Now, before we close, just quickly on SER-147, which is our next program in development. 147 is a cultivated bacterial consortia in spore form. It's designed to reduce pathogens causing gut-seated infections, including bloodstream infections and spontaneous bacterial peritonitis in patients with chronic liver disease. There's a significant unmet need in this population with few medicines in development to address the high rates of infection. In our assays, SER-147 reduces the abundance of E. coli and other pathogens causing infections in liver patients.
And with a very focused lens towards SER-155 and moving forward, we're working towards IND readiness for SER-147, but our focus right now is on SER-155. Now, just to summarize, as we think about VOWST, where we've made a profound difference in patients' lives, SER-155, with our exciting 1b data breakthrough designation, where we will soon establish the regulatory and clinical path forward, the adjacencies within SER-155 from allo to auto to potentially other blood cancers and the substantial opportunity therein, and then SER-147, which is built on the same idea, and then additional opportunities where we think that our technology and our platform may be uniquely positioned to help patients. So I'm over, but I'll conclude by saying that this is a critical year for Seres and our work on behalf of patients.
Thank you again to J.P. Morgan for having us at this year's conference, and we're happy to take questions. I invite my colleagues to join in the Q&A session.
Great, thank you, Eric. I have my colleague, Caroline Pötsch-Hennig, on the stage with me. She will be asking questions as well, but I thought I would kick us off. Just to level set, can you expand a little bit more upon the mechanistic rationale behind SER-155, which allows it to promote epithelial barrier integrity?
Sure. Maybe I can start, then I'll ask Matt to comment, but there's really three dimensions of our approach with 155. So the first is thinking about pathogen overgrowth and pathogen domination. And there's a deep literature to suggest that pathogen overgrowth is connected with infection itself. The second is protecting gut barrier integrity, and we talked a little bit about that. And the third is systemic inflammation, but maybe Matt can expand on that.
Yeah. So in those three particular pillars, keep in mind, these are patients that undergo very intensive chemotherapy, prophylactic antibiotic use, a whole set of insults, and that really leads to this disruption in the microbiome, meaning that they lose key commensal bacteria that provide certain functional properties that have an impact on the epithelial barrier and on the inflammatory state. So SER-155 is designed to include various bacteria that produce metabolites that we have identified at the company to be very potent modulators of the epithelial barrier, as well as modulators of multiple different anti-inflammatory pathways. So what we're doing is we're bringing inflammation down at that epithelial barrier to basically prevent it becoming disrupted and broken, so to speak. And that allows us to prevent bacteria moving from the gastrointestinal tract into the bloodstream.
Of course, as Eric already talked about, we're reducing those bacteria themselves as well.
Regarding your new biomarker data that you presented last week, can you just orient us to the baseline fecal albumin levels and the magnitudes of reduction seen in both the arms? What are the levels generally seen in healthy patients compared to those who have undergone allo-HSCT?
Yeah. So as was noted earlier, albumin is generally generated by the liver, and it circulates in the blood, and it has various implications there, particularly with osmotic regulation. When the barrier becomes compromised, it moves into the gastrointestinal tract, and you can start to detect it there. So there's not a specific clinically relevant level of albumin that's been established that can be linked to various other clinical outcomes. But we know that when fecal albumin is observed in the feces and increases, you can confirm that that's established that that is a leaky barrier. And then what's most important here is you got to look at it in the context of placebo, which is what we've done, right? And we see a substantial, significant reduction in fecal albumin relative to placebo in 155 treated subjects.
Okay. Great. And so how soon after your engagements with the FDA do you think you'll be able to initiate your proposed trial? Do you expect that to be the only interaction you need, or will there be subsequent interactions after that?
I guess I'd start by saying we were very pleased to get breakthrough therapy designation, and we actually had breakthrough with what was then SER-109, what is now VOWST. It was an interesting time working with CBER during the pandemic, through the pandemic, and I think the team deserves a tremendous amount of credit for really advocating on behalf of patients when there were a lot of things happening in the world that were not focused on the 109 or recurrent C. diff patients themselves. We're looking to move as quickly as possible. We do expect to have interactions with the FDA with a breakthrough meeting in the first quarter. As we said, we submitted the briefing book. We expect to hear back shortly, and we're hoping to have clarity in Q1 as to the next steps in the study.
There may be questions that go back and forth, but we're doing the things that we think we need to do and to put ourselves in the position to go, not just from a regulatory perspective, but also thinking about, from a clinical ops perspective, making sure that sites are identified and ready and expansion versus the 1B study, ensuring that we're manufacturing clinical material for that next study. Now, whether the study is a phase two or a pivotal study, those steps are relevant in either case, and we can modulate whether the FDA comes back with us asking us for one direction or the other. But we're looking to move as quickly as possible into the next study after we get clarity from the FDA.
Okay. Great. And how are you thinking that the data from the phase 1B, I guess, will translate into your next trial?
Yeah. Yeah. So with some of the commercial assessment work that Terri has done with our interactions with KOLs, we have thought about the idea of a 50% relative reduction in BSIs. Obviously, we were significantly higher than that in our phase one study. So we do think that there's a design of a pivotal study with a 50% reduction, or let's call it a 20%-ish absolute reduction between active and placebo, which allows us to design a study which is tractable from a size perspective. And in fact, with the idea of potentially an interim read that could allow us to theoretically stop for efficacy, stop for futility, or resize, we're trying to build an efficient path which gets to a result as quickly as possible, but in the highest quality possible way as well.
Maybe I can add one additional point there, which obviously this is a phase 1B study where we saw stat-sig efficacy signal, but of course, that's supported by underlying drug pharmacology, and so I think it's a unique opportunity to have a situation where you've got the phase one with supportive pharmacology as well, and that gives us increased confidence in the clinical result that we've observed and the numbers.
So I think the bottom line is we think we can take down the delta a little bit from what we saw in the 1b and still have a profound result if we're successful.
What are the key risks?
The key risks in the study?
In kind of the next development stage here from a clinical study perspective?
Yeah. You know, I think that it's hard to identify one risk. There are different ways in which these patients are treated across different centers, which is why I think we've been very careful in how we select centers, high-quality centers which have comparability across treatment regimens. So from a variability perspective, we feel like we did a great job of selecting sites in the first study, and we would look to have the same approach in the second study. Beyond that, maybe I might invite my colleagues to think about other.
I'll mention two in. Obviously, manufacturing of a drug and releasing a drug is always a risk, but this is a case where Seres has done this before, as well as brought one drug all the way through to commercial. And this is a group at the agency that we've been engaged with for a very long time, over a decade, and have a very good working relationship with. So I think that risk is mitigated. The second obvious, of course, is bloodstream infections being the primary endpoint. We could have those infection rates change, but there's actually been a really important trend in the field where you've seen the uptake of post-transplant cyclophosphamide. And this is a drug that's been a strategy that's been rolled out in this hematopoietic stem cell transplant population to actually increase incidences of graft versus host disease.
There's been a meaningful consequence of that where actually infection rates are going up. And we even saw that through the course of our running our phase 1b study where near the end, nearly all patients were getting post-transplant cyclophosphamide. So if anything, infection rates are actually increasing in this patient population, which gives us increased confidence in the numbers that we're modeling the trial design around.
Thinking bigger picture, how are you starting to think about the structure of a potential partnership for SER-155?
Yeah. So we care deeply, of course, about the resourcing element of a partnership and supporting the program, supporting the company, and allowing us to move forward. But there's multiple ways in which we think we could work with someone else who could add value to the program itself. As an example, we expect this to be a global study. So it's possible or maybe likely that a partner might have relationships with centers, KOLs, regulatory authorities in geographies outside of just the U.S. where we could move more quickly, more effectively, and ultimately from a clinical or regulatory perspective in a higher quality way than we might be able to move ourselves.
The other side, of course, is on the commercial end of things where someone who has real expertise in the field and can think about some of the metrics that we think about and tie them together to planning for a commercial state. We think those are examples of how someone might actually add significant value to the system and the program.
Great. And just one last big picture question from me. I know you had mentioned a couple areas of expansion that you kind of touched upon for SER-155. How are you thinking about potentially prioritizing those expansion areas?
Yeah. Well, I think in general, there are multiple ways in which we think we can apply our technology to help patients. And our aspirations for helping patients are not just aspirations. We are changing lives and have changed lives with VOWST. As I said before in the prepared remarks, this is an incredibly difficult disease where there really has not been innovation for patients in a long period of time. We even have therapy which is effective. It's oral. It's safe. And we think that the lessons that we learned through that journey and the technology itself is absolutely applicable to patients undergoing Allo-HSCT auto-HSCT, but broad areas beyond those fields. At the same time, what I can tell you is that from a resource perspective, we are incredibly focused on allo-HSCT, and we have to get that right. We intend to get that right.
And our license to move beyond that will be predicated on executing on this study in the best possible way. So with a difficult financing environment and finite resources, we are absolutely focused on doing the best we can with allo and with success we expect to be able to expand beyond.
Okay. Great. So I'd love now to turn to SER-147. So to set the stage here, can you just describe the biology of the mechanism and the rationale behind this product?
Sure. Maybe I'll ask Matt to speak.
Yeah. So there's similarities. So let me first say that Seres has been a data-driven company from the get-go, and we've built a platform which allows us to really understand those underlying mechanisms by which the microbiome and changes to it are having functional implications on the host. So if we look at cirrhosis patients, what we see in those particular patients are some similar dynamics to what we actually see in hematopoietic stem cell transplant patients. These are immunocompromised patients that have had multiple insults to their gastrointestinal tract. And as a result, they are susceptible to pathogen overgrowth, barrier damage, etc. So while there are similarities between 155 and 147, there are also some distinctions.
In the case of cirrhosis patients, they're susceptible to and particularly susceptible to spontaneous bacterial peritonitis, and that is also a susceptibility to pathogens that are different than the pathogens that you observe in hematopoietic stem cell transplant patients. One key difference between these drugs is the bacterial pathogens with which they're optimized to target and how to do that. The second key difference is actually chronic liver disease patients have an environmental condition given various treatments that they're on that make engrafting bacteria into the gastrointestinal tract. Some special considerations you have to take into account there that we have learned over the years. And so there are also formulation differences as well as bacterial strain differences that take that into account.
Okay. And what profile are you looking to deliver in your IND enabling work?
Let me make sure I understand the question. What type of information are we planning to include in our IND?
Yeah. Just kind of touching upon, I guess, what profile are you hoping to see in your preclinical work and what would be, I guess, included?
Sure. Yeah. So we're in the process of compiling those data, which obviously include the preclinical data from all of our functional screening data where we can show that the consortia are optimized for the particular bacteria that we want. The bacteria are able to repair and protect the epithelial barrier. Of course, we now have additional data from the clinic that helps support that and a host of other factors. And then as well, of course, the type of information that goes into there is patient population selection and rationale for the patient population, which in our case is based on looking at those chronic liver disease patients and those that are highly disrupted. And then, of course, all the manufacturing specifications and release specifications that are required for an IND.
Okay, and then looking ahead, how would you characterize proof of concept for this asset and what would a potential trial design look like?
Maybe Matt can start, but I would just say that we're not quite at that phase. Certainly, we're working towards IND readiness, but we have not disclosed the elements of a SER-147 study. I think there's work that we need to do to get there before we're at that point, and as I said before, our focus really is on SER-155, but maybe Matt can comment further.
What I'd say is that there's a very established literature out there that shows how different levels of disruption are associated with different stages of liver disease, and this has been shown in very large cohort studies. So what I can say is that we're building off of that knowledge and have been doing work internally to sort of identify where the right place to go is and most importantly, where the greatest clinical need is. It's a situation that's very comparable to hematopoietic stem cell transplant patients where these are very expensive patients once they get taken off track, and there are certain points along the way where that's important which we take into consideration.
Yeah. If I can just follow up for a second here, just so that I'm clear, can you talk a little bit more about what exactly you're looking for in a structure with a partner or partners? Do you want them to basically take charge of clinical development in your pivotal trial? Are you going to keep clinical development? Are you going to help with clinical development? What is the ideal scenario for you?
Yeah. So I would say that, Tess. There's not a defined recipe that we have to think about. I think that with that said, there's elements that we think are critical. There are certain capabilities that I think we are uniquely positioned to support going forward. As an example, manufacturing is something that is, it's certainly not commoditized. It's hard to envision that someone does that besides us, right? So as we think about a partnership, there's elements like our past partnership with Nestlé on VOWST where we will take the lead on certain elements of the science, certain elements of the manufacturing process, and it's hard to envision a scenario in which that doesn't happen.
I will say that from a clinical development perspective and a regulatory perspective, we have strong in-house capabilities that have a proven track record of success with VOWST, and we think it's absolutely relevant for 155, relationships with the FDA, all relevant to how we think about moving forward. We also think about what we could do, as we said before, beyond 155 and allo. So if there are ways in which someone can provide resources to us or capabilities to us that allow us to broaden our mandate a little bit, then that would be really interesting to us too.
Thank you.
Yeah.
Okay. And just last question for me, but can you just talk about your current cash position and your cash runway and how you're prioritizing spend?
Sure, so we updated our guidance in a press release last week where we said we had extended runway from cash into Q4 to cash into Q1 of 2026, and maybe I can ask Marella to comment further.
Can you hear me? Is this working?
No.
Okay. I think we're good now. Yes. As Eric said, with prudent management of costs and some success under our ATM, we have extended the runway. Importantly, as Eric said, our prioritization is really around advancing the work necessary to be able to go into the next phase with 155 and allo on the optimal timeline. So manufacturing, engagement with CRO, selection, the work that they're doing with respect to potential sites that we might engage. So where resources permit and it's prudent, we'll make additional investments in the pipeline and in 147 IND enabling work, but SER-155 readiness is our definite priority. And we were pleased. Included in the guidance around the runway is the installment payments that we're expected to receive from Nestlé this year. We are pleased to be able to announce this morning that, as expected, we got our $50 million installment payment.
We are expecting another approximately $25 million, less a settlement of some employment-related matters in July of this year, and there are a bit of ongoing obligations relative to the VOWST transaction, but again, our focus is really 155 advancement.
Okay. Great. Thank you so much. I hope everyone has a great rest of the conference.
Thank you for having us.
Thank you.