Yep. Okay. We all good? Ready to go? All right. All right. Good afternoon, everyone, and welcome to our next session at the H.C. Wainwright 28th annual global investment conference. My name is Matt Keller. I am a vice president in the equity research department, and it is now my pleasure to introduce our next presenting company, Seres Therapeutics. Presenting for the company, we have Rich Kender, CEO. Sorry, Kelly Brady, CEO, excuse me, and Matt Henn, president. Go ahead, guys. Great. Thanks a lot, and good afternoon, everyone. Joined here by my colleagues, and let me just start by saying thanks to H.C. Wainwright for the opportunity to connect with all of you today and talk about Seres' unique technology. I will be making some forward-looking statements, and please keep that in mind. Now to the more exciting stuff. For millions of years, microbes have evolved with humans. We know increasingly day in and day out with all the work that has been done over the past couple of decades, how intricate and important they are to health and disease. The metabolites and the proteins that these microbes produce have profound impacts on multiple host pathways that have disease relevance, and we continue to learn more and more about that really on a nearly weekly basis. Seres has pioneered a novel technology to basically be able to harness that therapeutic potential of these microbes and all those metabolites that they make. We have a track record of achieving very ambitious goals. We were the company who were able to bring forward VOWST, which was the first ever biotherapeutic licensed by the FDA, that in this case, to treat Clostridium difficile disease. We have a history of innovating at the company, and I think that is strongly evidenced by getting two breakthrough therapy designations from the FDA. As you know, a designation that is given to strong clinical results, where you are addressing an unmet medical need. In addition, we have clinically demonstrated, and I will talk more about this in just a little bit, the ability of our biotherapeutics to actually target the mucosal epithelial barrier interface, which is a unique area to target for many diseases. Importantly, we've been able to continue to demonstrate placebo-like safety profiles for our drugs, which gives us a lot of flexibility in how we think about how we use our drugs. In addition, this is all built on a platform that's been being built up over the past decade plus, where we can now explore at very high resolution the relationship of individual microbes, the metabolites and peptides they produce, and human disease. This has now been integrated with AI technologies, which is also now allowing us to even refine how we undergo target identification, optimization of our drugs to hit those targets, as well as providing unique insights into how we think about manufacturing and clinical development strategies such as patient stratification. We are focused in the area of oncology and in inflammatory and immune diseases. I am going to talk in just a bit about some of those areas. Importantly, what I want you all to take home is we have two phase II programs. Our drugs, what are they? They are consortia of bacteria. We actually use the bacteria themselves as the drug. These bacteria are optimized, and the composition are optimized to produce a very specific set of metabolic metabolites to impact these disease pathways, and they are formulated for oral delivery. I have already talked about our ability to have translated on the epithelial barrier, and I have also already commented on the safety profile of our drugs. We have three core disease areas that we are currently focused on. The first is for our SER-155 asset. We have two programs. On the left side of this, no, right side of the slide. Whatever you guys say. On the right side of the slide here is our allogeneic hematopoietic stem cell transplant program. This is our SER-155 drug. In hematopoietic stem cell transplant patients are at high risk of infections. They are highly immunocompromised patients, some of the sickest of the sick patients. These infections can actually derail their transplants. Importantly, are the leading cause of mortality in this patient population after the cancer itself. We have designed this drug to be able to address those bloodstream infections. In the middle of our other program for SER-155 is our immune-related enterocolitis program. Those of you who are familiar with KEYTRUDA, OPDIVO, YERVOY, so checkpoint inhibitor therapies, one of the significant adverse events in those patients is this irEC, so immune-related enterocolitis. What is enterocolitis? It is essentially diarrhea, severe diarrhea and colitis that causes these patients to have to come off their cancer therapy and actually start broad systemic corticosteroids that are immunosuppressive and can have negative impacts on the cancer therapy itself. In this patient population, we are targeting moderate to mild disease, which occurs in about 25% of these patients. Lastly, our other core program is our inflammatory bowel disease program. In this case, our SER-603 program. Here we are addressing the efficacy ceiling that you observe in these therapies, which is due to efficacy hitting a bar in these patients, and as well durability of responses, and that is an area that we are working as well. I will talk a little bit more about each of these programs briefly. Our allo- HSCT program, as I noted before, is phase II ready. And that is based on our phase I-B results, where we demonstrated a 77% relative risk reduction in bloodstream infections in this placebo-controlled study. Importantly, we also observed reductions in febrile neutropenia, as well as reductions in healthcare utilization, as well as antibiotics. The drug was well-tolerated. I want to stop on that point for one second. A drug where we dosed bacteria that were commensal with human subjects into some of the most immunocompromised patients in the world, had a placebo-like safety profile. Speaking, I think, strongly to the safety profile of these particular drugs. In addition, importantly in this study, we saw clinical translation on our ability to actually protect and repair the epithelial barrier, which is that key lining between your gut and the inside of your body, which is a primary driver of inflammation, and I will talk a little bit more about that in just a moment. Why is this important? First, the FDA thought the results were highly compelling, and the drug has breakthrough therapy designation. As I noted before, bloodstream infections are one of the leading causes of mortality in these particular patients. KOLs designate bloodstream infections on a scale of one to seven, a six in terms of importance of unmet medical need. Every time one of these patients gets an infection, it costs the healthcare system approximately $240,000. As I noted, we are phase II ready. We actually importantly have agreement with the FDA on the phase II study design, as well as line of sight to how an interim analysis in this particular study, and compelling efficacy there could potentially expedite the clinical development path for this program. Moving on to our irEC program. In this particular program, we ran a phase I investigator-sponsored study with our longtime collaborators at Memorial Sloan Kettering, built on the data that came out of SER-155 where we saw protection of this epithelial barrier. We had reason to believe that we could address this diarrhea and colitis in these patients. Because what happens in this patient population is the immune activation from the cancer therapy, can actually start to attack that epithelial barrier and drive different inflammatory responses. How they deal with that, as I noted earlier in this talk, they deal with that with immunosuppressive treatment, which has impacts on the cancer therapy itself. We saw an 80%, demonstrated 80% immunosuppressor-free clinical response, in this patient population. I think what I also really want to point out here is that we saw many patients, five of the 12 who responded, actually go into clinical remission, where they have grade zero. The other of those 12 go into grade one. To put this in perspective, irEC is on a scale of one through five, for diarrhea and colitis, and basically grade two to three is considered mild to moderate. Patients have to come off that treatment, that cancer therapy when they hit two to three and undergo these corticosteroids. To put this in context, if you get to grade four, that's life-threatening. Grade five, you're essentially dead. This is a significant issue that we think has a broad opportunity. As we all know, immune checkpoint inhibitor therapies are the most prominent cancer therapy, represent approximately a $50 billion global market currently with 300,000 patients in the U.S. alone and close to one million worldwide currently on these ICI therapies. Briefly, our inflammatory bowel disease program. In this particular program, we are looking to, as I noted earlier, improve the response of current IBD drugs, as well as identify biomarkers which allow us to target patients who are not responding to those particular current biologics on the market. I can say that we've made headway on both of these particular programs. At least two outcomes for this trial. As I'm showing here on the left side of the slide here, this is preclinical data where we've designed a composition SER-603. What we can do is actually get an inflammatory condition in these mice shown here by the pink. If you give them our drug 603, or sorry, you give them a biologic, anti-inflammatory that represents current types of technologies out there, in this case an anti-TNF, you can see you can ameliorate that inflammation to some degree, but you can't completely ameliorate that. In combination with 603, which is designed to indication stack or mechanism stack on top of that, you can achieve these greater reductions. This is where this particular program is at. As I noted, this is a preclinical program where we anticipate having a drug candidate nominated this year, and we are actively in IND-enabling studies for this program. Very briefly, let me talk about our epithelial barrier target, and what we're doing here. As I noted earlier, the epithelial barrier is this key interface between your gastrointestinal tract and the inside of your body. Many things can compromise this barrier: chemotherapy, antibiotic uses, diet, all kinds of insults can have an impact there. That leads to bacteria going across that barrier, as well as inflammatory compounds and all kinds of inflammatory cascades. What Seres has developed is technology which allows us to address basically the inflammatory bacteria or the problematic bacteria in your gut, and in combination, using a single drug, i.e. target multiple mechanism action, actually protect and repair this intestinal epithelial barrier. As I've said, we've actually translated on that mechanism. What's important here is we're operating upstream of where all other current therapies operate. Every other therapy is immunosuppressive, dealing with the downstream responses where we're hitting the root cause of the disease. Let me just wrap up briefly by talking about our strategy moving forward, so that we leave enough time for questions. Our goal moving forward is to partner our phase II-ready allogeneic stem cell transplant program, as well as drive towards partnership on our irEC program as well. Our two 155 phase II programs. In addition, to basically continue to, and identify capital to move forward our earlier stage programs. With that, I will open it up to questions. Thanks.