Good morning and welcome to the Seres Therapeutics Conference Call. As a reminder, this conference call is being recorded and will be available on Seres website for replay. I would now like to introduce your host for today, Carlo Tanzi, Vice President, Investor Relations and Corporate Communications. Please go ahead.

Thank you, Victor. Thank you and good morning. A press release with the company's fourth quarter and full-year 2017 financial results and a business update became available at 7 AM Eastern Time this morning and can be found on the Investors & Media section of the company's website. I'd like to remind you that we will be making forward-looking statements relating to the prioritizing our assets, our development plans, the ability of ECOSPOR III to support SER-109 approval, the promise and potential impact of any of our microbiome therapeutics or clinical trial data, our plans to initiate clinical studies of SER-287 and in immuno-oncology, the timing and results of any clinical studies and the sufficiency of cash to fund operations. Actual results may differ materially. 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, I'm joined by Dr. Roger Pomerantz, Seres' President, CEO and Chairman, and Eric Shaff, Chief Operating and Financial Officer. Before I pass the call to Roger, I'd like to mention that we'll be participating in two upcoming conferences including Cowen in Boston on March 18, and Oppenheimer in New York on March 23. We will also be planning to host an R&D Investor Day in New York [ph] City in May. Roger?

Thanks, Carlo, and thank you all for joining us. During the past year, Seres has continued to make excellent progress in our efforts to advance our microbiome pipeline. Seres has focused on developing new therapeutics for serious human diseases where dysbiosis of the gastrointestinal microbiome is thought to play a central role. We believe that microbiome therapeutics has the potential to address multiple disease states and our R&D efforts target therapeutic areas where compelling preclinical and clinical data indicate that the microbiome is important, such as infectious diseases, metabolic diseases, and inflammatory and immune diseases, including immuno-oncology. Let's begin with a recap of Seres' key accomplishments during the past year and we will then discuss our plans to maximize Seres' assets in 2018 and beyond. 2017 was a productive year for the company with three very important accomplishments. Number one, we launched a Phase 3 pivotal trial of SER-109 for patients with multiple recurrent C. diff infections. Number two, we reported highly encouraging SER-287 Phase 1b clinical study results in ulcerative colitis and number three, we initiated a field leading immuno-oncology focused microbiome therapeutic program in collaboration with MD Anderson and the Parker Institute for Cancer Immunotherapy, two leading institutions in the field. Now let's begin with SER-109. To remind you, based on encouraging preliminary clinical study results, SER-109 has received both breakthrough and orphan drug designations in the U.S. for the treatment of multiply recurrent C. diff infection. Early last year we announced our learnings from a comprehensive analysis following our SER-109 Phase 2 study. In summary, we determined that SER-109 was biologically active as measured by the engraftment of SER-109 bacterial species in patients' microbiomes. However, we also identified two key factors that we believe impacted the outcome of the Phase 2 study. These were; number one, the…

Thanks Roger and good morning everyone. Seres reported a net loss of $89.4 million for the full-year of 2017 as compared to a net loss of $91.6 million for the prior year. The company had a net loss of $29 million for the fourth quarter of 2017 as compared to a net loss of $25.3 million for the same period in 2016. The fourth quarter net loss was driven primarily by clinical and development expenses, personnel expenses, and ongoing development of the company's microbiome therapeutics platform. The fourth quarter net loss figure was inclusive of $3.1 million in recognized revenue associated with the company's collaboration with Nestlé's Health Science. Research and development expenses for the fourth quarter were $24 million as compared to $20.3 million for the same period in 2016. The R&D expense was primarily related to Seres microbiome therapeutics platform, the clinical development of SER-109, SER-262 and SER-287 as well as the company's immuno-oncology preclinical program. General and administrative expenses for the fourth quarter were $8.8 million as compared to $8.5 million for the same period in the prior year. G&A expenses were primarily due to headcount, professional fees and facility costs. The decrease in our cash, cash equivalents and investments balance during the quarter was $21.3 million. Seres ended the fourth quarter with approximately $150 million in cash, cash equivalents and investments. We have revised and extended our projection regarding cash guidance. Cash resources are expected to fund operating expenses and capital expenditure requirements excluding cash inflows or outflows from future business development activities or potential incoming milestone payments through Q1 2019. Seres is eligible to receive a substantial milestone payment that is not considered in the financial guidance update associated with the planned initiation of the next SER-287 clinical study. I'll now pass the call back over to Roger.

Thanks Eric. As we conclude our remarks, I would like to spend just a few minutes discussing Seres' R&D efforts and our plan to maximize the value of our pipeline during 2018 and beyond. Since Seres was founded over five years ago, substantial progress has been made in the emerging field of microbiome therapeutics. Our company has directly led the opening and initial progress of this new field in medicine. The scientific evidence supporting the role of the microbiome on human health continues to grow and there is now compelling biological and increasingly clinical data linking the microbiome with many serious human diseases. Our clinical data has demonstrated for the first time that the modulation of the human microbiome and impact of chronic inflammatory condition, ulcerative colitis. We are still in the early stages of discovering the full role and therapeutic potential of the human microbiome. We remain absolutely convinced that in the coming years as maturation of the microbiome field continues we will see additional compelling clinical microbiome therapeutic data in many other serious human diseases as well. Seres has had a longer-term strategic goal to extend our leadership position in those aspects of microbiome drug development to best position the company to capitalize on these advances in the field. Seres now has world-class capabilities that include proprietary expertise related to computational biology, microbiology, preclinical modeling of bacterial compositions and microbiome drug manufacturing. Seres has also accumulated significant intellectual property, as well as specialized know-how, ranging from highly technical drug development approaches to regulatory policy. We expect our differentiated capabilities to continue to benefit the company as microbiome science further grows and matures. As a result of the company's strong technical capabilities, Seres drug discovery engine has been very active and the company now has a broad array of…

Operator, let’s open up the line for questions.

Yes sir. [Operator Instructions] And our first question comes from the line of Chris Shibutani from Cowen and Co. You may begin.

Thank you very much. For Seres 262 could you just help us understand what it is that you feel will become the most important next step? It seems as if from an efficacy standpoint it wasn't powered to demonstrate, but perhaps you could comment at all whether you were seeing any kind of trend? And also it seems that the placebo group was fairly modestly sized, but also made it difficult to make some conclusions on efficacy? I'm just trying to understand how confident you are in dosing and it also seems as if you're not emphasizing this program as your top three priorities going forward, just help us frame 262 status and how you're really interpreting the data what you learned. Thank you.

Yes, sure Chris. I just want to take a moment, I have to, to congratulate your kids on the medals in the Olympics. We all watched it here, well done. Now getting to SER-262, one thing I would not do is say that this is, this program is not being highlighted. Remember we haven't finished the program yet. We don't have data on the last cohort and a lot of microbiome. We've found that this is an interesting drug and as you pointed out a drug - I've seen a lot of Phase 1b trials where I used to be the Chair of the Merck, Early Development Committee, and most of - it's very rare to have one that's powered to show real statistical significance. But we did this, so that we could have learnings in a lot of area, that include efficacy, that include engraftment and that include safety. Remember the FDA, no one's ever done this before and the safety that we've shown again in this climbing cohort study is very important as we and maybe in the future other companies move rationally design fermented drugs to the market. Now let's talk about efficacy though and what we did learn and I'm going to put on my infectious disease physician hat. The data that came out when you look to 262 with Vancomycin versus Metronidazole is not something that you can find in the IV literature, where it always goes from 25% to 30%, Vanco is around 25% depending on whether you have sick and old patients where there's higher recurrence, when we saw 4% versus 31%, that was highly interesting to us. It is clearly not dispositive because the placebo cohort was modestly sized as it usually is, but this gives us a hint of interest that we have not seen in the literature and we're seeing engraftment that we've seen which again correlates with that. I would put that as an interesting point because the robustness and the speed, the kinetics of engraftment in Vanco patients versus Metronidazole does co-segregate with the low recurrence rates with Vanco. I don't want to get ahead of my skiis because in our 1b the placebo for a trial like this where the literature says it's about 25%, it's not powered to do that. But I can tell you that was surprising and interesting data and we're going to continue to look at that and decide how we evaluate this drug and whether to move it to a larger study. But we brought this forward now because we had meaningful data from meaningful number of cohorts and the story here is interesting to us.

Great, thank you for the comment and I appreciate the progress updates.

Thanks Chris.

And our next question comes from the line of Bill Tanner from Cantor Fitzgerald. You may begin.

Hey Bill.

Hey Roger, how are you? And I just had a quick question on 262 but I wanted asked a more thought provoking question perhaps on 401, so on 262 Roger, I think you mentioned that there were no recurrences in the placebo and again appreciating the fact that this is a small study, but just harkening back to the experience with 109 and the diagnosis of active disease, I'm wondering how you're pondering addressing that to make sure you're getting the right people in the study?

Right, yes we're pretty sure that's fool us once shame on me, fool us twice, anyway we made the study after the 109 came forward based on Cytotoxin, so that we're very convinced that when we see recurrences they are recurrences here. So it's a great question and I'm glad I was able to get that. I should have mentioned it earlier. The other thing I would just point out which I didn't have a chance to mention in Chris's question is again when you look at the Vanco and the Metronidazole difference that's very compelling, but I didn't get to state something else and that is it's not just engraftment as I mentioned briefly and I want to just talk about that for a second. It's the global restructuring of the microbiome that we hoped we would see, but didn't know we would see, with such a small amount of organisms. Remember there are only 12 in SER-262 and to engraft is one thing, to lead to a restructuring globally of the microbiome when it does engrafted and to lead to this restructuring that allows augmentation, meaning other organisms coming in, a lot like we saw with SER-109 with 50 strains, is a huge learning and something again that was hoped for, but until now not proven.

Okay, that's helpful. Then as it relates to 401 and again I mean, obviously this is a very, very early stage program, but as you're thinking about down the road endpoints, I mean would you contemplate that it might be an improve - if you're talking about what the checkpoint inhibitors in improvement and the response that's already seen with a checkpoint inhibitor along with their proof or? And then secondly, there are myriad indications for some of these and with the contemplation be that you might show a beneficial effect of microbiome modulation with a couple of the indications. And then maybe the FDA would consider extrapolating that experience to the rest just trying to think about ultimately, what the label of that would look like?

Yes, all I would say to start is, I might remove one of the very, very, very early programs that I would point out that we expect it with the FDAs approval to be in patients this year and I think the rapidity of that is based not only on Seres, but on this great collaboration. The partners help us accelerate it. But to your point, there are - even though we've called it immuno-oncology, we are not talking about CAR-T, we're talking about checkpoint inhibitors, and there's only two checkpoint inhibitors at least the ones that are approved. We haven't said which one we'll use, but you can make some guesses. We do believe that you would start in the best studied of the oncological problems, metastatic melanoma first, and try to turn some higher number than a third of President Carter like patients that have had somewhat Lazarus effects with this drug to a higher level, that is what our goal is here. But early on we want to see things that would suggest that the goal is obtainable in a large study. That includes, do we change T regulatory cell tone? Do we have infiltration of active T cells into the tumor? Do you see some tumor regression? That's the other reason metastatic melanoma, although a horrible disease is good for this initial study. It's not only been the best studied with, with checkpoint inhibitors, but it's on the skin. You can take biopsies, you can look for T cells, you can judge easily regression and that's the other thing that makes it important. But certainly, if you'd see something there, you would not stop there. Obviously there are other immuno responsive tumors, you know my time at Merck with Keytruda we learned about what it could do with non-small cell of the lung, renal cell carcinoma, I'm naming some of the classic immunologically affected tumors. We would look at those down the road, but you see why we'd start with metastatic melanoma.

And if I could just sneak one last one in Roger, just as it relates to, I guess manipulating the microbiome, I'm guessing this is going to have to be done empirically, but you've got clearly a different patient subset or characteristics and you might have four UC or four C. diff and…?

You’re asking a great question and thank you for that. Remember though, we are partnered with Jennifer Wargo as well at MD Anderson and so we know a little bit about the different signatures that may be important, not just in animal models. We have the animal models ourselves here at Seres for immuno-oncology work in the microbiome and we'll bring some of that interesting work out probably later in the spring. But we also have the work with Jennifer Wargo. So we have now human hints of how to design a future drug. We may use a biologically sourced one in the first one, but again we think that animal models are helpful, but the real data in human microbiome is in humans.

Yes, got it. Okay, thanks very much. Good luck with everything.

Good questions. Thanks.

And our next question comes from the line of Joseph Schwartz from Leerink Partners. You may begin.

Hey, Joe.

Hey Roger, actually this is Degon [ph] dialing in for Joe. So I had a couple of questions on 262 and then 287 as well. So just getting a little more granular in the 262 can you maybe provide us a little more color on what you saw on the patient baselines or where there any imbalances between the placebo and the treated cohorts. And when - you've already conducted the first five cohort microbiome analyses. I was just wondering did you see any dose dependent engraftments and what kind of variabilities did you see? Where there any particular [indiscernible] for example that stood out across all of your microbiome analyses or were they variable in an all sense, what can you provide in terms of clarity?

Absolutely, I can help you with some of that. I mean, obviously full data will be done when the trial is done. But like in 1bs we have data for each cohort and this was a meaningful time I think to start the conversation and bring the preliminary data out. To those points, there were no real imbalances and it's important that the numbers that got both either Metronidazole and Vancomycin were about the same. The major confounding variable that could not be known at the beginning of the trial was the difference that we saw with Vancomycin and 262 and Metronidazole and 262, that was a statistically significant unknown. We are not making a huge deal out of that because we want to see it in a – it would have to be in a much larger placebo stat sig trial, but when you see that it is a major reason why you can see a difference in these treatment groups and we find that highly interesting that it correlates the difference as I said before with what we saw with both the kinetics of engraftment and the restructuring and robustness of engraftment. That is probably from me the take home message from this small trial and I'll tell you I'm surprised by it. Again I don't want to go too far because you have to have a large placebo group to show this primary C. diff does not have the recurrence rate of multi recurrent. We knew it when we went into this. We knew that we had to design this to take a look and we found something that's what 1bs are supposed to do. We didn't, we not only were able to show safety and PK, PD which is for us is engraftment and restructuring the microbiome and but we were also able to show this interesting finding that will be taken into account with any development in this field again.

So just harkening back to 109, one of the key learnings was that dose dependent efficacy...?

Yes, oh I'm sorry, I didn’t answer that. I forgot that point. I apologize, so yes there was a dose dependence here. Remember it's a very different drug. This is synthetically made, is the spores are different. We're not going to add it's sort of proprietary or how the difference in engraftment takes place with synthetics and biologics, but here what we found was that there was engraftment and restructuring even at quite low levels. We'll have more data as we complete it, but I will give you that and that again shows that this is different than biologically sourced. And even at 12 we had variable engraftment, but engraftment at all levels and we'll have more data when we can put it all together.

Okay, I look forward to seeing that. So moving on to 287, you said you've been in constant dialogue and now you're planning on your next clinical study in mid 2018. So I guess going back to the points you've made about clinical remission and clinical response, just trying to get a sense of have you met with the FDA to discuss those finer points? I understand that the August draft guidance from 2016 does point to clinical response, but had they kind of substantiated that in your interactions since your data read out?

Yes, I don't like to talk about what the FDA is saying as we're negotiating with them, but so let me talk about what KOLs are saying which is they understand that it's different. They applaud the fact that the FDA is no longer using response, making the field more objective. We've had great dialogues with the FDA and we expect to be able to bring in not too distant future a very coregent clean trial. I can tell you as well besides the KOLs we're getting a lot of interest from - incoming interest from large pharma, obviously and you see where there's been a lot of drugs that have not done well, not only those that are marketed, but those that are in development and remission rates. Ours is a small trial, but we like our data in comparison.

Yes, absolutely. One last question if I may. On the point about the 26-week post treatment when you've had 0 out of the 11 patients experiencing a flareup, did you conduct a microbiome analyses on that to see if the sustained microbiome can be seen?

We did and we actually reported a little on that. It's out a month, there was no change in the microbiome engraftment. We don't know - we weren't able to recruit the patients at the six-month mark. We will try to do that in the next trial, but at a month after dosing there was no regression. And that's an important point and it sort of hit me at one point is that we're used to seeing maintenance because with monoclonal or a small molecule when you stop it with a T1 half it's gone. But with the microbiome drug, it's a live drug and it keeps living. If you're as – at least of what we've shown at a month. If that is the same, that might help us think about reorganizing how the field looks at giving maintenance. Again I don't want to get too far ahead of my skiis, it's only 11 patients, but with no flares and with that hypothesis, that empirical hypothesis that may hold true for microbiome drugs as opposed to small and large molecules again an interesting set of data.

Great, I appreciate all the answers. Thanks again and congrats on all the progress.

Thank you very much.

And our next question comes from the line of Terence Flynn from Goldman Sachs. You may begin.

Hi Terence.

How are you doing Roger? Maybe first just on 109 the Phase 3 just was wondering if you can give us any update on where enrollment stands and any more sense of the timelines and when we might see data there? And then my second question is for 287, you mentioned the milestone payment for starting the next trials are not included in guidance, can you tell us if the size of the milestone payment would differ if it's a Phase 2 versus a Phase 3 trial? Thanks.

Why don’t we let Eric answer the financial one, then I'll go to 109.

Yes, so Terence the answer is yes, that's one of the reasons that we haven't provided specificity on what that milestone is, so as we get closer and as our discussions continue, I think we'll provide more guidance later in the year.

And I'm going to just add one medical scientific point to that. Remember as we talked to the FDA and obvious affects that milestone payment, one of the things as I said in my little discourse here is that we now have like 300 patients that have seen drugs with no serious As tied to them. One of the reasons that we go slow in development is obviously "primum non nocere", first do no harm. If we can show that this is and I think we're showing it now is a safer modality. That's why as I said in my little discourse, we may be able to move the needle in the speed of developing drugs for patients who are waiting without putting at risk patients on trials. Then I'll get to 109 Terence now I didn't forget it. Obviously we've opened up Canadian sites. We're continuing to enroll. We are - stay tuned, we haven't said anything yet because we still have changes in the slope of the curve, but enrollment goes on and we may have some more to say in the spring.

Thanks.

Okay.

And our next question comes from the line of Mark Breidenbach from Oppenheimer. You may begin.

Hey, good morning Roger.

Hey Mark.

Couple of questions on 262 and may be one on 401 as well. It sounds like may be the inclusion of two different antibiotics in the Phase 1b trial is confounding the signal, or a signal that might be hiding in there. And I'm just wondering first of all why for Fidaxomicin is also not included as an option in this trial? And is it safe to assume going forward that will be limited to Vancomycin?

Yes, so let's talk about that. Remember this is primary C. diff. They are good questions, let me clarify. So everything is pretty clear. Primary C. diff used to treat it only with Metronidazole. Vancomycin has been added to guidelines and it's been moved up in the last few years. so Fidaxomicin is almost not used because of its price and because of a number of other reasons in primary it's mainly for the first, second, third recurrences. This isn't a confounding variables of just Vanco and Metronidazole. I believe that - and we believe that this is one of the most interesting parts of this study and quite informative, because when you see a recurrence rate of 3% and we didn't decide on this, this is what the - you have to let the investigators use what standard of care and Vanco or Metronidazole are standard of care out there. And many people think they're about the same in primary C. diff. What we have is data now. It's early, it's small, we don't have a large enough trial for stat sig in comparing to placebo. But statistical significance between Vanco and 262 and Metro and 262 was statistically significant and I think was interesting. So, rather than a confounding variable, we think that this is a very important learning and informative. And again we've seen even in the newest guidelines of IDSA, Vancomycin has sort of been moved up in the place even in primary C. diff. With its use in 262 and the effects that are co-segregating with this effect in the microbiome which I think I'd like to have various data sets, especially when something is in a 1b trial and it's usually not powered for placebo, we think that that is something, as I said before, interesting and not known before and something that we're going to use as we move forward in finishing this trial and determining path forward.

Okay, that's helpful. And you had mentioned that you are seeing a dose dependency in engraftments. We have been in these early cohorts, I was just wondering if the multi dose score, it sounds like we have maybe some early data from at least a couple of those [indiscernible] if that’s seems to be making a difference or not?

Again, remember when you see 262 microbiome dose dependent signal is more prominent in Vanco patients. Again you have to separate these because you have faster and better engraftment with Vanco throughout the doses, even at the lowest doses. So this is, again it's not confounding, it's something that supports the fact that there seems to have been in this small trial and the statistics there do say so that there was a real difference in Vanco as compared to Metronidazole and you saw it even when you looked at the microbiome and microbiome dose dependency.

Okay, fair enough. Just a final question on 401. You had mentioned that the study arms from MD Anderson trial, I just wanted to confirm, so it's placebo, it's an FMT effectively from a PD1 responder and it’s a score based product, that’s all taken from the same donor?

Yes, the only difference I have to make there is that we have not used the term FMT. That second which we have not defined yet because we want to get through the FDA in specificity, but it's just all we said there is that it's a microbiome drug from a normal patient then of a normal human not a patient that was a responder to checkpoint inhibitors.

Okay, got it. Okay, so these will be coming, the two treatment arms will be coming from different donor there?

Yes, one will be one that responded well to checkpoint inhibitors, one will be one that doesn't have metastatic melanoma and has no underlying illnesses.

Got it. Okay, thanks for that clarification. Okay, that's it from me. Thanks guys.

Hope that helps. As I've been told there are no further questions, I will thank you for continued interest in the microbiome and in Seres Therapeutics. We look forward to sharing our continued progress with you throughout the year and I will now end today's call. Thank you all.

Ladies and gentlemen, thank you for participating in today’s conference. This does conclude the program and you may all disconnect. Everyone have a great day.