Carlo Tanzi - Head of IR & Corporate Communications Roger Pomerantz - President, CEO & Chairman Eric Shaff - CFO.

Tazeen Ahmad - Banc of America, Merrill Lynch Dae Gon Ha - Leerink Partners Bill Tanner - Cantor Fitzgerald.

Good day, ladies and gentlemen, and welcome to the Q1 2017 Seres Therapeutics Earnings Conference Call. At this time, all participants are in a listen-only mode. Later we will conduct a question-and-answer session and instructions will follow at that time.

[Operator instructions] I would now like to turn the call over to Carlo Tanzi, Head of Investor Relations and Corporate Communications. Please go ahead..

Thank you, and good morning. A press release with the company's first quarter 2017 financial results and a progress update became available at 7 a.m. 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'll be making forward-looking statements about those future expectations, the timing, design and potential results of our clinical studies, including the ECOSPOR III study and its potential to qualify as a pivotal trial; the result of using cytotoxin assays in the ECOSPOR III study and dysbiosis as an underlying cause of disease.

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 Financial Officer. I'll now pass the call over to Roger..

SER-262 for primary C. diff infection; and SER-287 for ulcerative colitis in patients who are failing first-line therapies. Let's begin with SER-109 and recurrent C. diff infection. SER-109 is a biologically sourced, highly purified microbiome therapeutic candidate containing a consortia of bacterial spores found in healthy individuals.

Our objective with SER-109 is to develop a new, convenient, effective and safe approach to treat patients experiencing multiple recurrences of C. diff infection. Today's standard of care for treating a C. diff infection is treatment solely with antibiotics. While antibiotics are often able to treat the acute C.

diff infection, antibiotics also further disrupt the normal microbiome, resulting in a higher risk of further recurrence of this disease. Our therapeutic objective with SER-109 microbiome therapy is to catalyze repair toward a more healthy microbiome immediately following antibiotic use, meaningfully reducing the risk of a C. diff recurrence.

We believe that SER-109 could represent a clinically important improvement over the limited treatment options available today for these patients. We have made excellent progress with our SER-109 program in recent months. At last month's European Congress of Clinical Microbiology and Infectious Diseases, our Chief Medical Officer, Dr.

Shelley Trucksis, delivered an invited oral presentation discussing our learnings from prior SER-109 clinical development efforts. Our prior SER-109 clinical studies provide key biological and clinical data that we believe have meaningfully advanced our understanding of recurrent C.

diff infection and the mechanisms of our microbiome therapeutic drug candidate. These data also provide Seres with important insights that inform our future development efforts. In March, we announced that we had completed a highly successful Type B meeting regarding the SER-109 program with the FDA.

In our FDA dialogue, we reviewed detailed scientific and clinical data related to the program and our plans for a new SER-109 clinical study, ECOSPOR III. We have been very pleased with the level of engagement and the specific feedback we received from the FDA.

The FDA has demonstrated significant interest in the microbiome as an emerging therapeutic modality, and I will remind you that SER-109 has both breakthrough and orphan-drug designations from the agency.

Regarding the SER-109 specific feedback we obtained, importantly, the FDA agreed that our new study, ECOSPOR III, may qualify as a pivotal study with the achievement of a persuasive clinical effect and addressing FDA requirements, including clinical and statistical factors and adequately sized safety database and certain CMC parameters.

ECOSPOR III is planned to include approximately 320 patients with multiply recurrent C. diff infection randomized 1:1 between SER-109 and placebo. The size of the study was driven both by assumptions regarding SER-109 efficacy and study powering as well as our desire to obtain an adequate safety database.

All ECOSPOR III study subjects will be treated with standard-of-care antibiotics to address the qualifying acute C. diff infection, and subjects will then receive either SER-109 or placebo. ECOSPOR III will evaluate patients for 24 weeks, and the primary endpoint will compare the C.

diff recurrence rate in subjects who received SER-109 versus placebos at up to 8 weeks after dosing. We have obtained several important learnings from our previous SER-109 development efforts that we will apply to ECOSPOR III. Diagnosis of recurrent C. diff infection, both at study entry and for primary endpoint analysis, will be confirmed by C.

diff cytotoxin assays. We believe that the use of C. diff cytotoxin assays in the study will ensure that patients entering the study are truly experiencing an active C. diff recurrence. We also believe that use of the C. diff cytotoxin assay will increase the accuracy of in-study recurrence diagnosis for both subjects in the treatment and placebo arms.

Patients in the ECOSPOR III SER-109 arm will receive a total treatment dose that is approximately tenfold higher than the SER-109 dose used in the prior Phase II study. The dose of SER-109 in ECOSPOR III will be administered over 3 consecutive days.

We expect, based on our previous microbiome data sets in humans, that administration of SER-109 at this higher dose and over multiple days will support more rapid engraftment of SER-109 after antibiotic therapy, thereby reducing the risk of C. diff recurrence.

Overall, we believe that changes implemented for ECOSPOR III will increase the study probability of success and expand the degree of efficacy we expect to see in SER-109-treated patients versus placebo. We have been making excellent headway preparing for the initiation of ECOSPOR III.

Expediting study start-up, enrollment and ultimate study completion are utmost priorities for the company. We are leveraging our prior clinical experience and taking numerous measures to speed enrollment. I would like to highlight some of our recent progress.

Our clinical team has finalized the ECOSPOR III study protocol, and the protocol has already been cleared by several institutional review boards. The study will enroll multiply recurrent C. diff patients who have experienced three or more C. diff episodes within the last 12 months. As previously mentioned, in all patients, the qualifying C.

diff episode for study entry will be confirmed by cytotoxin assay. FDA-approved C. diff cytotoxin assays are broadly available. Nevertheless, we have decided to use a central lab for cytotoxin assays in the study to ensure both consistency and accuracy.

We have completed substantial clinical site feasibility work and we have selected the large majority of planned ECOSPOR III investigator sites. ECOSPOR III subjects will include patients being treated as outpatients as well as inpatients located in hospitals, rehabilitation facilities and long-term care facilities.

We plan to utilize over 100 clinical sites, a far larger number than utilized in our prior SER-109 study, and these sites will be geographically distributed so that much of the U.S. population will have access to this study, and we will also now include a number of Canadian clinical trial sites.

I am very pleased with the rapid progress we've made preparing for the ECOSPOR III study and look forward to initiating the study in the middle of this year. I will now transition to discussing the important progress we have been making with our other microbiome therapeutic candidates. Let's begin with SER-262 program.

We have continued to advance the SER-262 Phase Ib study to prevent recurrence in patients with primary C. diff infection. This is the first-ever clinical trial to evaluate a human synthetic, multi-strain microbiome therapeutic candidate.

SER-262 is manufactured using bacteria grown in production fermenters in a process that does not require human donor material. SER-262 contains a consortium of 12 bacterial strains in spore form, rationally selected from Seres' field-leading proprietary bacterial library of over 14,000 well-characterized human microbiome strains.

The strains included in SER-262 were selected based on multiple criteria, and the final SER-262 composition was optimized from over 100 different consortia that were evaluated in diverse preclinical studies.

The SER-262 Phase Ib trial is a 24-week, randomized, placebo-controlled, dose-escalation study in patients who have experienced a first episode of C. diff infection.

Our objectives are to demonstrate that SER-262, as the first synthetic microbiome therapeutic candidate, has an acceptable safety profile, results observed in the microbiome changes and reduces the risk of recurrent infection in primary C. diff patients.

Our original SER-262 Phase Ib study design included 5 dose-escalating patient cohorts to evaluate single administrations of SER-262 doses ranging from 10 to the fourth spores to 10 to the eighth spores. Each patient cohort includes 10 treated patients as well as 2 placebo patients.

Based on our learnings from our prior microbiome clinical development efforts, but especially and directly from our recent SER-109 Phase II root-cause analysis, we are considering modifying the SER-262 study protocol to include additional cohorts with SER-262 administered over multiple days and/or at higher doses.

With these potential additional dosing regimens, we could evaluate the impact of multiple dosing on tolerability, microbiome changes and kinetics and recurrence rates with this potential first-in-class synthetic microbiome drug candidate.

Through the SER-262 Phase Ib study, we expect to gather important information on the dosing effects of our microbiome therapeutics. Specifically, we anticipate that we will obtain data on how the therapeutic dose impacts subsequent microbiome changes.

In addition, while this is a relatively small Phase I study, we hope to see a dose response and observe C. diff recurrence rates in patients treated with the higher doses of SER-262. Overall, we expect the SER-262 Phase Ib data to inform our future development efforts for SER-262 as well as our other microbiome R&D efforts.

We continue to expect SER-262 Phase Ib top line study results in the second half of 2017. Now moving to the SER-287 program. We continue to execute our SER-287 Phase Ib multi-dose, placebo-controlled study in ulcerative colitis patients.

Specifically, we are evaluating SER-287 as an induction therapy in patients with mild to moderate ulcerative colitis who are failing prior nonbiologic therapy.

The rationale for evaluating microbiome therapy in ulcerative colitis is supported by several published controlled clinical studies which suggest that modification of the microbiome via repetitive fecal microbiota transplantation can result in a meaningful clinical response.

The SER-287 Phase Ib study is evaluating three treatment arms that include daily or weekly SER-287 administration over the eight-week treatment period.

The study will also evaluate vancomycin antibiotic pretreatment, the rationale being that reducing gastrointestinal bacterial levels prior to SER-287 administration may support engraftment of the microbiome therapeutic candidate.

The study will enroll a total of approximately 55 subjects, with 15 in each treatment arm and 10 subjects in a placebo arm. As a Phase Ib study in a clinically heterogeneous disease, the SER-287 study's primary endpoints focus on safety, tolerability plus pharmacodynamics, as measured by microbiome changes.

We hope to observe an acceptable safety profile and a normalization in study subjects' microbiomes following administration of SER-287. In addition, the study will also evaluate a number of exploratory efficacy measures, including various biomarkers and total Mayo Clinic scores.

The Mayo Clinic score is a widely used ulcerative colitis clinical score comprising 4 components and resulting in a 0 to 12 scale, with 12 being the most severe. The components of the Mayo score include measures of stool frequency, rectal bleeding, endoscopic evaluation and physician global assessment.

All endoscopies are centrally read in order to minimize site-to-site variability. Our objective with SER-287 is to develop an effective orally administered therapeutic option which is not immunosuppressive. There are approximately 700,000 ulcerative colitis patients in the U.S. alone.

We believe that our microbiome therapies may have the potential to address a substantial proportion of UC patients who are not well managed by currently available drugs.

In addition, there may be a substantial opportunity to better serve individuals suffering from UC not treated with currently available, later-line therapies because of safety risks including, but not limited to, immunosuppression, which can lead to opportunistic infections and opportunistic tumors associated with many of these drugs.

Enrollment of the SER-287 study is nearing completion, and we look forward to SER-287 study results in the second half of this year. I'll now pass the call to Eric to review our recent financial performance..

Thank you, Roger, and good morning, everyone. Seres reported a net loss of $25.5 million for the first quarter of 2017 as compared to a net loss of $19.7 million for the same period in 2016.

The increase in first quarter net loss was driven primarily by continued growth in clinical and development expenses as well as increased headcount and ongoing developments of the company's microbiome therapeutics platform.

The first quarter net loss figure was inclusive of $3 million in revenue recognized associated with the company's collaboration with Nestlé Health Science. Research and development expenses for the first quarter were $20.1 million as compared to $15.4 million for the same period in 2016.

The increase in R&D expense was primarily due to expenses related to our microbiome therapeutics platform, the clinical development of SER-109, SER-262 and SER-287 as well as the company's preclinical programs.

General and administrative expenses for the first quarter were $8.8 million as compared to $7.2 million for the same period in the prior year. The increase in G&A expense was primarily due to increased headcount, an increase in professional fees and facility expansion to support overall growth.

The decrease in cash balance during the quarter was $27.8 million. Seres ended the first quarter with approximately $202.2 million in cash, cash equivalents and investments. I'll now pass the call back over to Roger..

This has been a highly productive period for Seres as we have advanced our pipeline with continued progress in preparing for the start of a new study for SER-109, our lead clinical program. We have also continued to execute on our two ongoing Phase Ib studies for SER-262 and SER-287.

We will move our pipeline programs forward with determination and focus, and we are looking forward to an eventful year ahead. In the coming months, we expect to initiate a new potentially pivotal clinical study with SER-109.

We also look forward to two data-rich clinical readouts from our SER-262 and SER-287 microbiome programs in the second half of the year. In addition, we continue to make progress in our other R&D efforts, including those in inflammatory diseases, metabolic diseases, liver diseases and immuno-oncology.

We look forward to providing you with timely updates on these diverse but focused preclinical programs. Thank you for your continued interest in Seres, and we look forward to keeping you updated on our progress during the coming year..

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

Thank you. [Operator instructions] Our first question comes from Tazeen Ahmad with Bank of America..

Hi. Good morning. Thanks for taking my questions. Maybe just a couple.

About the new sites that you've picked for the next study, can you just remind us how many of these sites overlap with sites you might have used in the previous study? And can you also remind us what your previous analysis revealed about any discrepancies that might have existed in the procedures between the different sites? And then maybe for 287, can you talk to us about what you think the actual market opportunity is? Of the 700,000 UC patients in the U.S., how many of them are not getting to goal with their current therapies, whether it be related to efficacy or safety?.

Thanks, Tazeen, for two good questions. So operationally, when you look at the different sites for SER-109, I'll remind you that we're going to have over 100 in this new trial. We had approximately 27 in the previous trial and we're adding Canadian sites.

We're -- without going into exact numbers, we do have many of the sites which will be used again, and they have investigators. One of the nice things about this is that we have these sort of up and running already. We have the IRBs who know us that agree with -- quickly with the trials. We have nurses and clinics that are used to taking these patients.

So, as I said in my remarks, it should speed things up. We did not -- and this was part of our root-cause analysis, I think I had mentioned it on one call but I'll say it again, we did not see any differences in the sites based on performance or their ability to make diagnoses.

We did look at that, as anyone would in a root-cause analysis for a Phase II drug, but we did not see that. What I will remind you is that, objectively, the most important thing that we had sorted out was using cytotoxin versus PCR. And we think that is going to, again, make C. diff objective again and make the different sites having little judgment.

We're trying to make the calls on true recurrence based on this approach very tight. So, we're happy where we are, and we're glad we have many of the other sites that we've used in the prior Phase II now in the ECOSPOR III trial. To your second question on 287. So, ulcerative colitis has approximately, as I've said, 700,000 people in the U.S.

About 200,000 are failing first-line therapy. If you think about what first-line therapy is, it is not a biologic, it's not immunosuppressive. It's 5-ASA plus/minus boluses of steroids.

When you fail that, though, you go into immunosuppressant therapy, whether they're oral immunosuppressants like azathioprine or IV immunosuppressants like the monoclonal antibodies, the TNF and other targets.

So, we think the opportunity here in this first trial is for these patients before they have to make a decision whether they go into immunosuppressants or not. And this is all their goal is, is to try to stay out of being immunosuppressed for obvious reasons, as I mentioned, with opportunistic infections and tumors associated with it.

We feel that we expect SER-287 to be non-immunosuppressive; we don't see a reason for it to be.

And if it is efficacious in this population of the patients who are failing first-line therapy, we think that we offer them just a great opportunity to have a drug to keep them out of immunosuppressant biologics such as monoclonals or drugs such as azathioprine. But the other point I'll mention to your question is this is not where we would stop.

If we have a good Ib trial with 287 and we move forward, as we expect, to a Phase II trial, we will consider other lines of therapy in ulcerative colitis and, as I've said before, potentially even Crohn's. What we would say is that if you go in those other lines of therapy, it is somewhat longer treatment.

And what I'm thinking about is maintenance therapy. This is an induction trial. We would consider maintenance after that. We would consider other areas of ulcerative colitis, maybe later, people who are failing monoclonal antibodies. But right now, we're looking forward to seeing this data..

Okay. Thanks, Roger, for that very good explanation. Maybe just a follow-up on that. You're trying to get 55 patients into the study. You've been enrolling for some time.

Is the reason that it's taking a bit longer to enroll that you have a very specific profile of patients that you're trying to enroll? Or is it that there is some stickiness in current therapies and patients might be a little bit averse to trying something new?.

Yes, there are -- certainly, in some areas, there's stickiness in therapy. As a physician I know that and was probably guilty of it. But we have not seen that. We actually think this trial is moving quite well. The physicians have been incredibly open to using the microbiome drug. We've had no pushback.

We have to make sure that we have the proper patients in the study. We're being as careful as possible. And remember, they're evaluated with a long evaluation, including endoscopy upfront. So, it has nothing to do with enrollment or doctor stickiness in this the case, but we are making sure that the patients are well evaluated before they come in.

And we are close, as I've said, to completion..

Okay. And then a last question for me on the 109 study.

Have you talked about what you want to power it for?.

Yes. So, we've said before that we're looking -- we have it overpowered. We were allowed by the FDA to do that, which is a great thing. And we have a -- over -- a 95% or a little overpower in this study. Remember, 320, we want excellent statistics. We want to excellent powering.

We're -- we've made this trial so that if the data is persuasive, there will be the parameters for the FDA to consider it a pivotal trial. Statistics is just one part of that..

Okay. Thanks Roger..

Thank you, Tazeen. Good questions..

Our next question is from Joseph Schwartz with Leerink Partners. Your line is now open..

Hi guys. Thanks for taking the question. This is actually Dae Gon dialing in for Joe. Two quick ones for me.

With regards to the entry criteria for the Phase III ECOSPOR III trial, can you maybe go into a little more detail about the market opportunity there using the stringent diagnostic protocol? And sort of following up on that, not to get into the weeds here or anything, but just wanted to see if you will be providing a single cytotoxin assay to all the clinical trial sites to minimize any kind of variability between the commercial vendors.

And also, how many replicas will each site be conducting to make sure they're not seeing any false positives or negatives?.

Yes. So sorry, you might have missed this. I said in the remarks, we're going to use a central site, so -- for accuracy and consistency just, to your point. So, there will be several replicates, just as done in any of these diagnostics, and it will be done in a central site.

And we're -- we've shown that we're able to do it quickly so that it does not hurt diagnosis and treatment. So that's how we're going to deal with it. I can tell you that FDA-approved cytotoxin assays are available everywhere, and they were used everywhere for decades. It's just that PCR, for reasons that have more to do with primary C.

diff and epidemiology, took over the standard of care as first-line diagnostics in many centers. We believe that, that will not be a problem, obviously, in the trial, as we do a central site, nor when we expect to market the drug as this is available throughout the country. I -- your other question, I think you had one more that I missed.

What was the other one, Dae Gon?.

Yes.

So, using the entry criteria for the Phase III, what do you think is the market opportunity?.

Oh, yes. Yes. No, that's another great question. So again, we believe this is not a stringent test. This is the test that was used all the time. When I trained, we only used cytotoxin assays. So, we don't expect this to be a stringent test. What we do expect it to be is truly find patients that are -- that have failed antibiotic therapy and have recurred.

We don't think this is going to have a meaningful decrease in what we think is a robust, albeit orphan market. Because we also have an epidemic that's growing at north -- a CAGR of north than 3%.

And if we find the right patients with the increasing epidemic, we think we can make a meaningful impact to both the patients and to the epidemic as it spreads by stopping these recurrences. I hope that helps..

Great. Sorry. One more quick follow-up, if I may.

So, given the root-cause analysis and the comprehensive nature of it, I wanted to see if you had any clues to how the phages and the dynamic between bacteria and phage may have created any problems at all?.

That's a great question. You should come work for us. We are very interested in the virome of -- as it's called, of the intestine. As you pointed out, it's not just stages. There are other viruses that are endogenous to our microbiome, and we are very interested in that and have some research going on.

Right now, I don't have anything to say about it, but it does show the complexity of the microbiome. I would point out to you that there are no viruses or phages in our drug because they are depleted by -- when we isolate the spores to near purity. So, it would only be the interactions that happen in the host.

We have no data for that having an effect in this drug. But it's an interesting question..

Great. Well, thank you very much for taking our questions..

Thanks for the good questions..

Our next question is from Bill Tanner with Cantor Fitzgerald. Your line is now open..

Thanks for taking the questions. Roger, I had a couple for you on 109. And I don't know if you want to speak in any detail or even generally on your SAP for the planned pivotal, but I was just wondering if there's an opportunity that the data might be looked at from a responder analysis.

And I guess, responder speaking more to engraftment, or if you're confident -- I mean, I would presume that you're confident that the changes to the dosing, the amount and the number of doses, would lead to higher engraftment. And then the second question on that would be you mentioned that the patients enrolled would have experienced 3 or more C.

diff episodes. Wondering if you could speak to what that might -- what the result might be there as you look at labeling, and then the recommendations..

Those again, several very good questions. If you look -- I wouldn't go through what we've discussed with the -- about the SAP with the FDA, but I would say that, again, we are looking for both an effect on the microbiome as well as a clinical response.

We're not going to -- I don't like putting words in the FDA's mouth, but we doubt this will be a biomarker for it but -- at this point, but we certainly think this is the mechanism of action. I would just correct one thing you said. It's not just engraftment and the amount of engraftment of 109 species. It's the speed, it's the kinetics of engraftment.

What we've shown as -- is that the die is cast early in this disease. It's really -- as we've said, it's a race to repair, from our 2 trials that we've learned. So, it's not just that we need more robust engraftment in everyone; we need it to happen rapidly before C. diff starts over. That's the race between C.

diff and the reconstitution and repair of the microbiome. So, we think, as we've shown in our root cause analysis, the effects are not only in quantity of engraftment but speed of engraftment. And I hope that answers that question.

What was your second one again?.

It was -- the subjects that are being enrolled have had 3 or more C. diff episodes, and I'm wondering....

Yes, let me talk about that. As you know, the definition by both IDSA as well as the FDA of what is multiply recurrent means one occurrence and at least 2 recurrences, so 3 episodes of C. diff. That's the definition. That's how you got defined as multiply recurrent. Before that, no.

So that would be what we would look for in a label of this drug to treat this orphan condition. What's important is that the number of recurrences that -- or the percentage of recurrence that happen after each recurrence increases in a stepwise fashion, from 25% to 40s or -- then to 60s then to 80s to 100%.

And so, it is important that you have to have this definition of multiply recurrent, but you can have patients quite far into this recurrent cycle. I can tell you that both in our Ib and our II trials, the average is -- was around 4. But that's an important point.

We believe that, that will be important in the label and there will be a definition of what multiply recurrent is. That does not mean that the drug will not be studied in the future, once marketed, in other indications in C. diff..

Okay. That's helpful. And I'm glad you mentioned the word kinetics because that was part of the question I had on 287. Just wondering -- and you mentioned that the repetitive FMT has been shown to be somewhat effective for UC. So, I'm curious how much of it really is the kinetics important as you're thinking about with 287.

And modeling, it would -- I mean, are you modeling it after what you might see with repetitive FMT? And I guess, this isn't necessarily germane to 286, because your prior remarks would make it sounds like it's germane also to 109 in C. diff..

Oh, it's -- we know it's related to C. diff and the race to repair. The question is how is important kinetics in ulcerative colitis. I don't know that. I will empirically think that it is less than in the race with an infectious agent. This is a chronic inflammatory disease. Remember what the colon looks like in these two diseases.

After they're treated with antibiotics, the colon is not greatly actively inflamed. It's the recurrence that is -- you're worried about. In ulcerative colitis, these are failing patients. They have inflammatory colons. And now you're trying to engraft a microbiome drug repetitively but engraft in an inflamed colon. That's why we did a few things.

Again, looking at what we've seen in animal studies but also in the FMT literature, we gave the drug repetitively once a week for 8 weeks and once a day for 8 weeks in one arm, which is about fiftyfold of what we gave in a 109 trial of a biologically sourced spore-based product.

So, we're taking this into account because of the inflammatory nature of what we are working with in ulcerative colitis.

Why are we adding an antibiotic, vancomycin? Again, there is some human data, there is some animal data in our hands and in others that there may be better engraftment in this inflammatory -- ongoing inflammatory colon if you pretreat with an antibiotic that makes space in the dysbiotic microbiome of the UC patients. That's why we have four arms..

And so, this then, in UC, may be more about keystone species than about kinetics?.

It may be. That's my hypothesis just based on empiric understanding of each of the disease states. Let's see what we find out..

Okay. Thanks very much..

Our next question is from John Newman with Canaccord..

John, you there?.

And I'm showing no further questions. Ladies and gentlemen, thank you for participating in today's conference. You may all disconnect. Everyone, have a great day..