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Thank you for standing by. My name is Tina, and I will be your conference operator today. At this time, I would like to welcome everyone to the series therapeutic webcast to discuss recent clinical studies results. All lines have been placed on mute to prevent any background noise. After the speaker's remarks, there will be a question and answer session. To ask any questions, please press star 1 on your telephone keypad. To withdraw your question, press star 1 again. It is now my pleasure to turn the call over to Carlo Tansey, Kendall's Investor Relations. Please go ahead. Thank you, Operator. Earlier today, CERES announced promising results from the investigator-sponsored trial, or IST, of CR155, an immune checkpoint inhibitor-related endocolitis, or IREC, conducted at Memorial Sloan Kettering Cancer Center, or MSK. We have posted slides to the investor section of the series website, which we'll review on today's call. As noted, we will be making forward-looking statements on todays call, including regarding our pipeline, potential applications for our drug candidates, clinical development plans, potential partnerships and financing strategies, and other matters which are subject to risks and uncertainties, as described in the company's SEC filings, and as noted on this slide. Ceres undertakes no obligation to update forward-looking statements except as required by law. Speaking on today's call are Richard Kender, Executive Chairman and Interim CEO, Dr. Matthew Henn, Ceres President and CSO, and Kelly Brady, EVP and COO. Dr. Jonathan Pellilid, a bone marrow transplant specialist and cellular therapist at MSK, will also join the call. Morella Thorell, EBP and CFO, and Dennis Walling, SVP, Clinical Development, will be available for Q&A. I'll now pass the call over to Rich. Good morning. Thank you for joining us. We are excited to report promising new clinical data that we believe expands the opportunity for Ceres live biotherapeutics as a fundamental component of cancer care. Memorial Sloan Kettering Cancer Center, one of the world's leading institutions devoted to cancer treatment, has worked in collaboration with CERES for over a decade, and this partnership has advanced our understanding of the importance of gut microbes to human health and, importantly, has helped translate these learnings into improved outcomes for oncology patients. I want to thank the patients and the investigators involved in this study for aiding in these efforts. We believe the results of this IST support the potential of CR-155 to provide a differentiated, non-immunosuppressive approach to treat IREC, and importantly, to allow cancer patients to remain on their life-saving immune checkpoint inhibitor, which is often discontinued as a result of IRECs. With that, I'll turn the call over to Kelly to describe the ICI patient journey and share the study results. Kelly? Thank you, Rich. Starting on slide three, immune checkpoint inhibitors, commonly known as ICIs, are a widely and increasingly used class of cancer therapy because they are effective in a range of solid tumors. ICIs work by interacting with the immune system. The immune system has built-in breaks that prevent immune cells from overreacting. Cancer tumor cells exploit these breaks by expressing various proteins to hide from the immune system. ICIs unmask the cancer cells so that the immune sistem is activated and amplified and can recognize and attack cancer tumors. Unfortunately, the immune systems activated by ICIs can often also attack healthy tissue, including in the gut, leading to a serious side effect called immune checkpoint inhibitor-related enterocolitis, or IREC, also referred to as immune-mediated colitis. For the patient, IRECs typically result in diarrhea, abdominal pain, colitis or inflammation of the intestine, and blood in stool, and can significantly affect quality of life, and in some cases, progress to costly patient hospitalizations and serious or life-threatening consequences. IREC incidence rates vary by ICI type and regimen. Moderate to severe IRECs, classified as grades 2 to 3, occurs in approximately 25% of all ICI recipients, which in the U.S. alone equates to an estimated 75,000 patients, or one-quarter of the 300,000 pacients estimated to be on ICIs in 2026. And the use of ICIs is growing as the types and stages of cancer, which are eligible for treatments with ICIs, is also expanding. Devastatingly, while ICIs work well, guidelines stipulate that patients who are afflicted with moderate to severe IREC must halt their ICI therapy and initiate immunosuppressive corticosteroids. Moving to slide four, this is where SIR-155 could potentially fill a significant gap for patients and clinicians in need. There are numerous clinically meaningful toxicities associated with current standard of care immunosuppressives, including systemic immunosupression, increased infection risk, and metabolic complications. Additionally, the immunosuppression may negatively impact the anti-cancer effect of the ICI therapy and put cancer outcomes at risk for patients. Approximately 40% of these patients do not respond to systemic steroids and require escalation to biologics treatment, which may also be immunosupressive. This is why clinicians are seeking safe, non-immunosuppressive solutions to treat IREC and get their patients back on the drugs to fight their cancer as quickly as possible. SEER-155 is an oral treatment designed to repair the mucosal epithelial barrier and reduce the gastrointestinal inflammation which underpins IRECs, and which Matt will discuss later, and to do so without any negative interference with the immune system. Now that you have the context of the large unmet patient need, on slide 5, we've summarized key results of the study. First, we saw an impressive 80% immunosuppressive-free clinical response rate, with 12 of the 15 participants treated with SIR-155 achieving at least a one-grade response in diarrhea, a common measure of IREC severity, by day 15. As expected, based on our prior clinical study experience, SIR-155 was generally well-tolerated with no serious drug-related adverse events. Importantly, we also observed pharmacology results that support the clinical outcome, notably improved mucosal epithelial barrier function and reduced gut inflammation. In a second indication, the first being in the strong study results from our Phase 1b of SIR-155 in allo-HCT patients, which you may have previously seen. The design of this study is described on slide 6. It was an open-label Phase 1B trial conducted by MSK evaluating SIR155 and 15 participants with grade 2 or grade 3 IREC. as a reminder that is moderate to severe, who had not yet received immunosuppressive therapy for their IREC. MSK is an institution with substantial expertise in managing immune-related gastrointestinal toxicities associated with checkpoint inhibitors. The study's main clinical efficacy assessment was immunosupressive-free clinical response at day 15, defined as at least a one-grade improvement in diarrhea symptoms without corticosteroid or biologic immunosuppressive therapy. Safety and tolerability were also evaluated. Dosing of SIR-155 was a convenient two capsules once a day for 12 consecutive days. As noted on slide 7, the enrolled population reflected a clinically representative IREC population and included participants with a range of underlying cancers and most at later stages 3 and 4. A wide range of prior ICI treatment regimens, including PD-1 inhibitors such as Keytruda, Opdivo, Zyniz, PD-L1 inhibitor such as Infinzi, Baventio, CTLA-4 inhibitors such as Yervoy M. judo and LAG-3 inhibitors, such as Upduilag, were represented in this study. Notably, 60% of participants entered the study with debilitating grade 3 diarrhea, reflecting a severe form of IREC. There was strong compliance with the SIR-155 dosing regimen. we will speak about ICI therapy interruption next. As you can see on slide 8, IREC diarrhea grades range from low grade 1 to moderate to severe grades 2 to 3, to progression to grades 4 to 5, resulting in life-threatening complications or deaths respectively. While grade 1 is managed with only symptomatic care, importantly, as noted previously, the treatment guidelines for grade 2 or higher dictate halting the patient's ICI therapy. This practice was borne out in the ISP, as we noted that 14 of 15 study participants, or 93%, had their ICI therapy interrupted prior to study entry as a result of their IREC. Additionally, a post-hoc observation in the study found that a portion of participants returned to their ICI therapy through day 43 of the study, and CERES expects to analyze ICI administration in a future study. Grades 2 through 4 IREC also require medical intervention with the current standard of care, which is immunosuppressive therapy, such as corticosteroids or biologics. Patients with more severe forms of IREC can require hospitalization, and this can certainly have a significant impact on the patient's quality of life. Digging a bit deeper into the results on slide 9, as noted earlier, at day 15, the primary endpoint, 80% or 12 of the 15 participants achieved immunosuppressive-free clinical response following SIR-155 dosing. Further, 33% or 5 of the 15 participants, which represents 42% of the 12 responders, achieved immunosuppressive-free complete clinical remission, defined as full resolution of diarrhea symptoms down to grade zero without immunosupressive therapy. A few more details worth noting are the speed of response, 11 of 12 responders showed improvement by day 8, and the magnitude of response. Eight of 12 respondents improved by two or more grades by day 15. Slide 10 shows the day 43 clinical results. Importantly, all 12 responders at day 15 remained at the same diarrhea grade or better as of day 43. Five of 15 participants maintained immunosuppressive free response, two of whom remained in clinical remission, which is a grade zero, and three of whom remain a grade one. We believe these results are highly encouraging because they suggest that CR155 improves IREC symptoms without requiring immunosupression over a period of time. The 7 of 15 remaining day 15 responders maintained their clinical response at day 43. These patients received non-systemically acting gastrointestinal targeted immunosuppressants for mild residual or moderate recurrent symptoms. Importantly, these data suggest that C155 has potential to help patients avoid the use of high-dose systemic corticosteroids and address the unmet medical needs in IREC. Turning briefly to safety, on slide 11, SIR-155 was well-tolerated through day 43. There were no serious adverse events assessed as related to SIR155, and no bloodstream infections were reported. Two participants experienced non-serious adverse events assessed as possibly related to vancomycin and SIR-155, and those events were moderate in severity and resolved. In summary, taken together, we believe these clinical and safety results support the potential of SIR155 as a differentiated, non-immunosuppressive therapeutic approach in IREC, which could allow patients to remain on their ICI cancer drugs and potentially benefit to a greater degree from the immune therapy. With that, I'll hand the call over to Matt. Matt? Thank you, Kelly. Moving to slide 12. In addition to the clinical observations, we were also pleased with the pharmacology and translational results from this study, which provide important biological support for the observed clinical activity of 0155. I'll start by explaining more about the functional properties that 0156 was optimized to target and how the clinical pharmacology results support that it's working as intended. Notably, in cancer patients, different stressors, for example, chemotherapy, or as in the case of immune checkpoint inhibitor therapy, the activation and amplification of T cells and macrophages can damage the cells that create the mucosal epithelial barrier in the gastrointestinal tract, and this damage leads to gastroentestinal inflammation and the further exacerbation of such by various inflammatory cellular products and potentially harmful bacteria present in the gut. In addition, in certain high-risk patient populations, mucosal epithelial barrier compromise can lead to infections. SEER-155 is a live biotherapeutic that was designed to prevent the translocation of gastrointestinal pathogens and resulting bloodstream infections in allogeneic hematopoietic stem cell transplant or alloHSCT patients. Mechanistically to achieve this, the SIR155 bacterial consortia was optimized to include bacteria that CERES has identified to be potent producers of metabolites that promote mucosal epithelial barrier integrity and that can modulate immune responses without immunosuppression and, in addition, include bacteria that can prevent the colonization of harmful bacterial pathogens in the gut. Importantly, the targets of CERES biotherapeutics are key upstream drivers of inflammatory and immune diseases that existing drugs do not target. In CEREs previous Phase 1b study of CIR-155 for the prevention of bloodstream infections in alloHSCT patients, biomarker data demonstrated clinical translation on all of the above-noted mechanisms of action, including protection and repair of the mucosal epithelial barrier and immune modulation linked to anti-inflammatory outcomes. In that study, these pharmacology data supported the observed clinical results, a strong 77% relative risk reduction in bloodstream infections for those participants who received SIR-155. Results that led to the FDA granting breakthrough therapy designation to SIR155 and also the acceptance of these study results for publication in Nature Medicine in a coming future issue. MSK was a collaborator on our SIR-155 Phase 1b AlloHSCT study, and the results from this study, along with the significant unmet medical need for a new solution in treating IREC, motivated the IRECE investigator-sponsored study. Turning to the IROC study pharmacology results on slide 13, consistent with prior SIR 155 studies, the majority of SIR-155 strains colonized and took root in the gut, i.e. engrafted, across all patients. The engraftment profile was consistent with what we have previously observed in the allo-HCT setting. These data support and reinforce the robustness and reproducibility of SRI-154 pharmacokinetics. Turning to the drug's pharmacodynamics, SRI 155 could be a highly differentiated therapeutic option for IRAC that addresses current standard of care limitations. The translational analysis from this study support that rationale. At baseline, participants showed evidence of epithelial barrier disruption and severe gastrointestinal inflammation as evidenced in the biomarkers fecal albumin and fecal calprotectin, respectively. Fecal albumin is a biomarker that indicates protein leakage from the bloodstream into the gut lumen and provides direct evidence of mucosal epithelial barrier compromise. Fecal calprotectin is a well-established clinical biomarker of immune activation that indicates the presence of activated neutrophils in the intestinal mucosa. At study entry, participants had elevated fecal albumin and calprotctin levels that are characteristic of individuals with colitis. Following SIR-155 treatment, both albumin and calprotectin biomarkers showed early, durable, and concordant reductions over time with significant reductions in both measures achieved by day 43, reflecting consistent improvement across two mechanistically linked dimensions of IREC disease. These biomarker improvements were directionally consistent with the clinical observations and provide additional support for SIR-155's potential biological activity in this disease setting. Importantly, the pharmacological and translational results suggest that SIR155 may act on core disease-relevant biology rather than simply produce a symptomatic effect. As noted on slide 14, CIRES has pioneered a new drug modality and accessed the vast therapeutic potential of microbes. We have a track record of success with achieving FDA licensure of VALST and are advancing innovative technologies as supported by multiple breakthrough therapy designations. More importantly, we view the IREC study results as supporting the potential of SIR-155 and series live biotherapeutic technology across diseases characterized by microbiome functional disruption and resulting mucosal epithelial barrier dysfunction and inflammatory dysregulation. We are focused currently as a company on addressing unmet medical needs in oncology and inflammatory and immune diseases where we think our drugs are uniquely positioned. As noted on slide 15, mucosal epithelial barrier disruption is increasingly recognized as an important driver across multiple inflammatory, immune, infectious, and oncology related conditions. By therapeutically modulating the gastrointestinal microenvironment, supporting mucosal healing, and reducing inflammatory responses of immune cells, in other words, inducing immune homeostasis, rashly designed live biotherapeutics may address clinically meaningful disease biology in ways that are distinct from conventional immunosuppressive therapies. Over time, this biology could have relevance beyond IREC, including in other oncology settings, inflammatory bowel disease, the focus of series CR603 program, infection-associated complications, and additional inflammatory and immune disorders. In closing, as noted on slide 16, we believe the results of the investigator-sponsored trial reviewed today are an important milestone for series that represent a potentially meaningful opportunity for patients undergoing cancer therapies. Immune checkpoint inhibitor drugs have revolutionized cancer treatment and are sizable, valued at over $50 billion globally in 2025, and growing drug class. Estimates of the annual growth rate of ICIs range from mid to high double digits over the next 5 to 10 years, driven by broadening eligibility for ICI therapy across multiple cancer types, earlier intervention and use of ICIs in combination with other cancer therapies, and increasing global cancer rates. Unfortunately, many patients develop debilitating immune-related enterocolitis, which the current standard of care does not meet the medical needs and can lead to disruption of life-extending cancer treatment. SIR-155 could offer a unique solution to IREC with a demonstrated potential to broadly achieve immunosuppressor-free treatment and prevent the halting of life saving cancer therapies. With that, I'll turn the call back to Rich. Thank you, Matt. As we evaluate next steps in the development of CR155 for IREC and in our Phase II Ready program for LOHCT, we believe this study data will strengthen our ongoing engagement with potential strategic counterparties and financial partners, including those interested in finding solutions to both improved outcomes for oncology patients and enhance the use of ICIs, as well as those who want to address broader inflammatory and immune diseases. Before we open the line for questions, I would like to introduce Dr. Jonathan Pellett from Memorial Zone Kettering and express my appreciation for the great work he and his colleagues are doing to advance cancer care and improve patient outcomes. Dr. Pellitt, I know I speak for everyone at CERES in appreciation for you taking the time to join this call. Thank you very much, Rich. Happy to be here. Thank you. Dr. Pellett, I'd like to ask you to comment on MSK's experience with ICIs and IREC, and given your experience working with CIRES on clinical studies, to share your thoughts on the potential for CIR-155 in IRECs and beyond. Sure thing. You know, we've been, as was mentioned, we have been collaborating for many years working on this. And the gut barrier is really where the microbiome and the immune system meet one another with just a single cell layer between them. And this is a really critically important part of the body for human health in cancer treatment and infectious disease and in and many other inflammatory diseases, but it's really largely inaccessible to many drugs, and the drugs that are used often have a lot of side effects. But I think that CR155 as a live biotherapeutic is really novel and unique in its ability to target and modulate the gut community of bacteria and the biology that's happening in the intestine. And there are really two clinical settings where we've seen that we can already make an impact. As your colleagues mentioned, in the prior study that we collaborated on, which was placebo-controlled, we showed that we could reduce the risk of bloodstream infections during bone marrow transplantation. And in the current study, we now have this really promising signal about attenuating the inflammation, the colitis, and the diarrhea that can complicate cancer immunotherapy. You know, this was briefly mentioned earlier, but I just want to underline the point that the current standard approach to this complication of the cancer therapy, which is steroids, are really an inadequate answer for our patients, mostly because of the immunosuppression that they can cause and the risk of infection but also because of treatment interruptions. So the cancer patients are not only feeling miserable from their diarrhea but they have to pause their life-saving treatment for their underlying cancer. So the idea that we could administer an optimally designed consortium of bacterial strains that can produce the right blend of metabolites, promote the barrier function of the gut, outcompete pathogens, and potentially reset homeostasis in the gut is really exciting because this can potentially allow our patients to stay on their life-saving cancer treatment and deal with this very serious side effect while avoiding the side effects and the immunosuppression of the steroids. I'll just mention one other thing, which is that I think there are a lot of other clinical settings where if we could improve gut barrier function, it could really be transformative, even outside of the very specific clinical settings that we've currently studied this drug in together. Inflammatory bowel disease, patients in the intensive care unit, the neutropenia that accompanies conventional cancer treatment with chemotherapy and cellular therapy, just name just a few. So I think there's enormous potential here. Thank you, Dr. Pellett. We appreciate your thoughts. Operator, we can now open the line for questions. Reminder, to ask a question, simply press star 1 on your telephone keypad. Again, that's star 1 to ask your question. And we'll pause for just a moment to compile the Q&A roster. Our first question comes from the line of John Newman with Canaccord Genuity. Please go ahead. Hey, guys. Good morning. Congrats on really, really interesting data here. Could be a start of a new treatment paradigm to manage this issue. You know, you may have mentioned this on the call, but I'm just curious, in your study, were there any patients that were actually able to resume their immune checkpoint inhibitor therapy during the study? Hi, John. Thank you for the question. Yes, we, as a reminder, and we did mention it, that of the 15 patients who enrolled on this study, 14 of 15 participants had their immune checkpoint inhibitor interrupted at study entry. Though it was a post-hoc observation, we did observe that a portion of participants were able to return to their immune checkpoint inhibitor through day 43. And we did not observe that the immune checkpoint inhibitor had an impact on the diarrhea response at either day 15 or day 43, and we will absolutely look at ICI administration and analysis as part of our future study planning. Thanks, John. Sure. I just had one additional question. I'm just curious as to what the next steps are here for the program. And, you know, in particular, I'm curious, in the future, might you consider a study where you start the administration of CR155 in conjunction with the checkpoint inhibitors rather than here where it seems like you have treated only the patients that have IREC? Great question, John. I will start, and then I will ask some of my colleagues, potentially Mirella, Matt, to jump in. So first of all, based on the promising phase 1b data that we talked about today, and as we consider the clinical development path and life cycle management for SIR-155, we would strongly consider studying 155 as a prophylactic medication to prevent IREC with the goal of allowing patients to stay on ICIs without toxicity. As we think about the immediate next studies, we are aware, though, of course, that prevention trials sometimes are larger. So as we think about the immediate next steps, which are supported by the robust efficacy we saw at day 15, the strong safety, the strong PKPD, we have anticipated a modestly sized phase 2 trial of approximately 100 to 150 patients that would look at treatment of IREC with STEER 155, utilizing similarly timed endpoints for a timely readout, and in collaboration with our strong cancer centers like MSK and other relationships that we have. And so we feel confident that we are able to do that. And we feel confident that, you know, we have the regulatory efficiency as in the FDA relationship, the background of our breakthrough designation for STEER 155 in alloHCT. Now we have the experience of a second de-risked indication for STEer 155, and we have manufacturing efficiency as well with the work we've done for allo HCT. So we think this sets us up for a well-powered phase two for treatment of IREC, but we will absolutely be considering opportunities to expand this in the future to prophylactic approach, which would be a huge asset for this cancer population. John, let me add one quick point here, too. So keep in mind, as we've noted, you know, our technology really works on the upstream causes of inflammation and barrier compromise. And so when you start to think about that potential, not just as a treatment paradigm, but in the context of prevention, it becomes very, very powerful because we're upstream of where a lot of different drugs operate. And maybe I'll ask Dr. Pellett as well to comment on the clinical value from thinking about future prevention opportunities. Thank you, Matt. I would say that I think a preventative approach would be very welcome in our field, especially with something that is well tolerated. There's also another opportunity baked in with that idea. There are a lot of studies coming out lately that correlate microbiome features in the gut with the response of tumors to the checkpoint drugs in the first place. So, if something like CR155 would be deployed with an intention to prevent colitis, there could be opportunities to study effects on tumor responses at the same time if patients would be getting this kind of microbiome modulation the entire time they're getting checkpoint blockade. So it's a tremendous opportunity, and I think it could be very interesting. Great. Thank you very much. and your next question comes from the line of matthew keller with hc wainwright please go ahead yeah good morning uh congrats on the data and thanks for taking our questions so mine have to do particularly with the durability i was wondering maybe you guys could provide a more color or what your thoughts are on why some patients may have experienced a more durable more responsive than others. And then a follow-up to that is, how do you think the biomarker data that you guys collected fit into that observation as well? Yes, thanks so much for the question, Matt. I will start off with some comments, and then I will turn it over to Matt to speak to the biomARKER results. So first, again, I want to emphasize that we are encouraged with the robust response we saw at day 15, especially in absence of immunosuppressive. And the magnitude of that response as well in that majority of patients had two-grade response and it was occurring early. We also see that a third of participants remained in immunosupressive free response weeks after completing SIR-155. And as we noted as we went through the slides, A portion of those participants that achieved immunosuppressive free response at day 15, when they received an immunosupressive, the immunosubpressives they received after day 15 were only non-systemically GI-targeted immunos suppressives. And that was for either mild residual grade 1 or some moderate recurrence. It was well-managed, and then those patients got back to their responses at day 43. So this suggests a trend that 155 may support a reduction of reliance on these high-dose systemic immunosuppressants. And as with any phase one study, as you may imagine, we are digging into each and every patient's clinical journey, looking at their engraftment, their symptoms, their immune checkpoint inhibitor return, if it did occur, the biomarkers to inform dosing for the next study, as well as the efficacy endpoints after SIR-155 administration. So we remain encouraged and have some work to do to continue to analyze these patients. Matt, do you want to speak to the PKPD results and the biomarker results in context of Matt's question? Yeah, thanks, Kelly. Matt. Good morning. And thanks for your question. You know, CERES has always invested and done the work to build translationally rich clinical studies, and the biomarker data, I think, is particularly important generally and in specific with your question, so as I noted on the call, we really saw highly elevated levels, particularly of fecal calprotectin at study entry, and as I said, we see the reduction in that over time. What I think is interesting is that we saw those reductions in the fecal calprotectin, a well-established marker of inflammation, very, very rapidly and quickly soon after dosing. And importantly, even in the patients that required immunosuppressive treatment later by the non-systemic corticosteroids, as Kelly had mentioned, we didn't see further improvement in their calprotection scores when they were put on those immunosupressives. So in other words, it looks like SIR-155 already got them down to levels of fecal calprotectin that would be considered at the level of actually mucosal healing based on clinical precedence. So we're really encouraged by the calprotctin results from the study, and we think they strongly support the clinical observations. Yeah, it totally makes sense. Thanks for that. Very interesting data. Thanks again, guys. And with that, I will now turn the call back over to management for closing remarks. Thank you very much. We hope everyone has a great day. Thank you again for joining us today. This does conclude today's conference call. You may now disconnect.