Good day ladies and gentlemen and welcome to the Syndax First Quarter 2017 Earnings Conference Call. At this time all participants are in a listen-only mode. Following manager’s prepared remarks, we will host a question-and-answer session and our instructions will follow at that time. [Operator Instructions] As a reminder this conference may be recorded. It is now my pleasure to hand the conference over to, Melissa Forst with Argot Partners. Ma'am, you may begin.

Thank you, operator. Welcome and thank you to those of you joining us on the line and the webcast this afternoon for a review of Syndax’s first quarter financial and operating results. I’m Melissa Forst with Argot Partners and with me this afternoon to discuss the results and provide an update on the company’s progress are Dr. Briggs Morrison, Chief Executive Officer and Rick Shea, Chief Financial Officer. Also joining us on the call today for the question-and-answer session is Michael Metzger, President and Chief Operating Officer of Syndax. This call is being accompanied by a slide deck that has been posted on the Company’s website. So I would ask you to please turn to our forward looking statements on Slide 2. Before we get begin, I would like to remind you that any statements made during this call that are not historical are considered to be forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the risk factor section in the company’s most recent Annual Report on the Form 10-K and other reports filed with the SEC. Any forward looking statements represent our views as of today May 8, 2017 only. A replay of this call will be available on the company’s website at www.syndax.com following the call. And with that please turn to Slide 3 and I’m pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer of Syndax.

. : We are pleased that enrollment for this cohort has accelerated and we now anticipate completion of enrollment in the third quarter, one quarter ahead of our prior expectation. Data from the first stage of our phase 2 trial will be presented at the 2017 ASCO meeting next month and we look forward to sharing those detailed results with you. We also recently announced that we’ve expanded our collaboration with Merck on ENCORE 601 to include cohort of colorectal patients that represent an important unmet medical need and I will present further details on this cohort shortly. Slide 5 details the rationale behind the therapeutic potential of combining entinostat with PD-1 antagonist. Most notably, pre-clinical data indicate that entinostat can modulate the critical tumor microenvironment by blocking the function of both myeloid-derived suppressor cells and regulatory T. cells has been shown to increase the anti-tumor activity of the anti-PD-1 antibodies in multiple pre-clinical models. Through these mechanisms we believe entinostat can reverse resistance to PD-1 antagonist and we're starting to generate the first clinical support for this hypothesis in our ENCORE study. Several posters were presented during the recent annual meeting of the American Association for Cancer Research that highlighted new data and insight into how entinostat alters the cancer cell and the tumor microenvironment to enhance immunotherapeutic approaches. On Slide 6 we showed the results of this one example of the posters that were presented, this is from a mouse lung cancer model. The far left panel shows the significant anti-tumor efficacy seen in this model with the combination of entinostat and the PD-1 antibody. The middle panel shows the ability of entinostat to reserve the immunosuppressive function of myeloid-derived suppressor cells taken from mice treated with entinostat. And on the far right panel shows that entinostat decreases…

Thank you, Briggs. Turning to Slide 17 for three months ended March 31, 2017, Syndax reported a net loss of 13.0 million or $0.71 per share compared to $12.9 million or $2.85 per share for the prior year quarter. Our research and development expenses in the first quarter of 2017 increased to 9.6 million from $4.8 million for the first quarter of 2016. The increase was primarily due to increases in clinical trial activities of $3.4 million, employee compensation expense of 0.8 million and legal and consultant expenses of 0.5 million. Our G&A expenses were $3.9 million during the first quarter of 2017, a decrease from the prior-year period of $4.3 million of G&A expenses. Decrease was primarily due a decrease in employee compensation of 0.7 million partly offset by increases in consulting expenses and other costs related to being a public company of $0.3 million. The decrease in employee compensation of 0.7 million was primarily due to decreases in non-cash stock compensation of 0.9 million and bonus expense of 0.2 million, partly offset by increased salary expense of $0.3 million due to increased headcount. Total common shares outstanding at March 31, 2017 were 18.25 million, on a fully diluted basis 21.8 million shares were outstanding. Additional financial details will be available in our quarterly report on Form 10-Q which we expect to file this week. Syndax ended the quarter with a cash balance of $92.8 million, which we believe is sufficient to fund development into the middle of 2018 enabling us to reach key corporate milestones. For the second quarter 2017, we expect research and development expenses to be in the range of $11 million to $13 million and total operating expenses to fall between $15 million and $17 million. For the full year, we expect R&D expenses to be between $52 million and $57 million and total operating expenses between $68 million and $73 million. We believe that we are in strong financial position and we will continue to make appropriate and measured investments in building the company's pipeline. Now I'd like to turn the call back over Briggs.

Thanks very much Rich. Looking forward, we expect several key upcoming milestones summarized in Slide 18 which include announcement of whether either of the two non-small cell lung cancer cohorts in ENCORE 601 have achieved their pre-specified efficacy criteria for advancement into the second stage of the trial. As I noted earlier, we've expanded enrollment in the refractory melanoma cohort of ENCORE 601 and given the rate of enrollment seen to-date we expect his cohort to complete enrollment by the end of third quarter of this year. We look forward to presenting the results from the first stage of the melanoma cohort of ENCORE 601 at ASCO next month as well as to our upcoming discussion with FDA to explore the feasibility of a pathway for accelerated approval of entinostat in this setting. We also expect enrollment completed year-end in ENCORE 602, our phase 2 combination trial of entinostat and atezolizumab in triple-negative breast cancer. We expect to complete enrollment in E2112, our phase 2 registration trial of entinostat in hormone receptor positive HER2 negative breast cancer and share the PSS analysis in the first half of next year. Finally, we expect to advance 6352 into a multiple ascending dose trial in the third quarter and anticipate presenting results from the ongoing single ascending dose in the fourth quarter. We look forward to sharing data from these trials at the most appropriate scientific congresses as they become available. I'd like to end my prepared comments by reiterating our excitement here at Syndax on the progress we're making with our portfolio of programs as shown again in my last slide and which includes two potential best in class molecules being tested in five ongoing trials across six different indication. Finally, we continue to be opportunistic with respect to business development opportunities that offer an attractive risk reward and a strong strategic fit for Syndax as evidenced by our successful in-licensing of SNDX-6352. In closing I’d like to thank all the fantastic employees here at Syndax, our collaborators and perhaps most importantly the patients, trial sites and investigators involved with our clinical program. With that I'd like to open the call to questions. Operator, can you please open the call to question?

[Operator Instructions] Our first question will come from the line of Bert Hazlett with BTIG. Please proceed.

Congratulations on the progress especially with the expansion of ENCORE 601 in melanoma. My questions are around that program specifically. Could you describe kind of what the intentions of the type B meeting are, what might represent an accelerated pathway of what that might look like? Could you do something with the existing trial to materially expand that and have that move into a registration type of a study, I guess is what I'm asking initially.

Hi, Bert. Thanks very much for the meeting - for the question. The type B we want to discuss with the FDA the overall further development of entinostat in melanoma, including a potential accelerated path and as you know with the accelerate - even if you were to get an accelerated approval path, what the sort of confirmatory trials would be, so we’ll try to discuss the broad overall development strategy. As I said in my prepared remarks, given that there is a significant unmet medical need, we do have a couple of thoughts that we'd like to discuss with them about an accelerated path. I probably can't say much more about what those options are other than to say that I don't think the single trial that we have ongoing right now would be sufficient. We hypothesize that we need to do something in addition to that.

I guess that dovetails into some of the discussions that's going to be presented at ASCO. Can you give you a little bit more granularity on whether specific types of patients might be discussed or the types of biomarkers that might be discussed? And could that be used to further enrich the trial design as you move forward with FDA - the discussion with FDA?

Yeah, sure. So the ASCO presentation will be updated data on the 13 patients that were in stage one that we - the advocacy and safety data from that cohort that we used to make a decision to expand into the stage 2 melanoma cohort. We’ll have detailed information on the patient characteristics of those patients as they come into trial and we will have some information on bio marker status at baseline. I would hesitate to say that out of the 13 patients, we’ll be able to say too much about a subset that could play a role in accelerated pathway, but we can discuss that more once we actually have the data from ASCO.

Thank you. Our next question will come from the line of David Lebowitz with Morgan Stanley. Please proceed.

Thank you very much for taking my question. With respect to the breast cancer trial, would it be reasonable to expect that the overall survival data would be likely to be towards 2019?

That's right, David. I mean. The overall survival data as the trial was put together and modeled would come roughly 18 to 24 months after the completion of enrolment. So that’s in the 2019, early 2020 range.

Was there much granularity on what led to the enrollment, I guess, slowing somewhat in recent months?

Not a lot. I mean I would say that we had very good enrolment throughout last year, the beginning of the year, the enrollment seemed to slow a little bit and then has picked up in the last month. So it's a little bit uncertain exactly how it will play out over the course of the next few months, but in our discussions with ECOG, nothing specific came to light in terms of the variability of the enrolment month to month.

Sure. And I guess just jumping over to the combo trials to 601, could you go into a little more detail on the genesis of the decision to add a colorectal cohort?

Sure. As I said in my prepared comments, I think there is a couple of things. Because PD-L1 antagonist don’t really -- in the microsatellite stable population, the sort of general most common from a colorectal cancer, you don't see very much. We think we can -- if [indiscernible] is adding, we should be able to pick that up in a single arm trial with, it should be pretty straightforward. As I said, because the responses we've seen in the melanoma population and sort of relates to Bert’s question about the characteristics of those population, which was shared at ASCO, combined with some of the biology that we see in colorectal cancer, we think it’s a reasonable hypothesis that entinostat could actually work in some of these microsatellite stable patients.

Thank you. Our next question will come from the line of Chris Shibutani with Cowen. Please proceed.

Thank you. Appreciate the updates on the combination entinostat KEYTRUDA study, and it's been especially helpful to have kind of your threshold responses that you were looking for the program to move from Stage 1 to Stage 2. Can you provide us with some insights in terms of what you think in the totality of the study as you progress through Stage 2, what kind of response rates you might be thinking about once we do get to those total enrollment levels? And also in that regard, when we think about responses, can you comment as well about perhaps the durability of the types of responses we could see? Thank you.

Sure. So Chris the Simon two-stage design, if we open enrollment in all three of them and end up enrolling the total number of patients that we’ve described previously, the total number of patients were defined based upon the statistical hypothesis of what the response rate is we were looking for. So in the melanoma population, the way the trial is set up that total of 34 patients, if there is sufficient power to detect the response rate of about 25% or the pre-treated patients, the 56 patients gives us power to detect a response rate of around 15% and the 46 patients in the naïve is a targeted response rate of 35%. Probably in a subsequent time, we can go through sort of the rationale behind each of those, but their built off of both in some cases, what you would expect from a PD-1 alone or what is standard of care and sort of the lower bound of what we would need to see to be the standard of care. I think your second question about the durability of the responses, in general, what we're looking for is responses that have the durability of six, nine months or so. That's really I think the bar that people look for to say that there is something clinically significant going on. So we get -- the opening of the trials themselves do not have a bar related to durability, but at the end of the day, we would like to see as high as possible response rates that are durable.

Great, that's helpful. And those target response rates are consistent with what you've had in the previous deck, I just didn't notice it on this one. So, I'm just wondering if there was any change. But the new change is with colorectal cancer. Can you share with us what you think the target response rate could be for that cohort?

Right. So colorectal cancer, you’ll notice the stage one and stage two is the same as melanoma. So the target response rate there that we’re looking for is about 25% response rate, which again I think in the colorectal -- in the microsatellite stable colorectal cancer population would be I think a notable advance over the current therapies that are available to those patients.

Thank you. Our next question will come from the line of Tony Butler with Guggenheim. Please proceed.

Thanks very much. A couple of questions, if I may. Briggs, when you think about, if we go back to the expansion of 601 in CRC, so the notion is -- I sort of had it before was that you had a fairly high immunogenic response in microsatellite in stable CRC. You also had high permeability in a melanoma patient. So the question is you're looking at lots of mutations and yet you're choosing an area in microsatellite stable colorectal cancer, which likely has fewer mutations, which is unusual, but I'm struck by the [indiscernible] article for -- at least that from the Spanish group, which states that you -- there is an assumption that you may get increased expression of T cells chemokines and I'm curious -- you need to get an increased expression of T cell chemokines. And I'm curious what those might be because they actually end up referencing the same paper which talks about HDAC inhibitors in lung adenocarcinoma. So really, two questions, one about fewer mutations, why? And then the second about what T cell chemokines need to be increased? Thanks.

Yeah. So thanks for your question Tony. The question about the mutational load and using that as a predictor of response to PD-1, you're correct that the microsatellite, the MSI high population has a high mutation load and seems to have a notably positive response to PD-1. But I wouldn’t say that the mutational load is a definitive marker of who is going to respond and who is not going to respond. So, and you are correct that the microsatellite stable population tends to have a lower mutational load than the MSI highs. In some of the preclinical work that was done even in relatively low mutational loads, you still a beneficial effect of entinostat. And so I think what we're testing more I think in the colorectal population is the role of the immunosuppressive cell types, MDSCs, and Tregs. And so, as you know, there is one particular type of, it’s called the inflamed type of colorectal cancer and it’s inflamed with essentially immunosuppressive cells that has Tregs, MDSCs, Th17 cells and so it’s inflamed presumably because there are antigens that are recognizable, but has sort of an immunosuppressive mutation types. SO we think that’s the population, that particular type is probably the most obvious way entinostat would work. There are other types as you noted that are sort of cold, they're not inflamed and that’s the hypothesis that you need to stimulate a certain T cell chemokines to -- and there was the paper you referenced that [indiscernible] can help do this. I don’t remember off the top of my head exactly which T cell chemokines that they referenced, but so there is different theories on how intense that could help the different immune phenotypes and so we’re not selecting for each of those. They represent significant spontaneous population. So we think by enrolling sort of an unselected population, we can start to take a look at these different immune phenotypes and colorectal cancer and see if in fact entinostat affecting some of the immunosuppressive factors.

Thank you. Our next question will come from the line of Joel Beatty with Citi. Please proceed.

Hi. This is Sean calling in for Joel. Congratulations on the quarter. I was wondering if you could provide a little more color on the potential [indiscernible]. What types of signals are you expecting from [indiscernible]?

Right. So we’re actually doing some preclinical work on that combination now and hopefully in the near term, we will be able to give you, learn ourselves exactly what's happening with that combination. Theoretically, as I outlined, I think there's a possibility of hitting the TAMs, MDSCs and the Tregs. So we’re testing that first preclinically. I think we haven’t said much about the development of 6352 either at monotherapy or at which combinations we would do, we do think about doing a combination with entinostat, but I think it’s better for us to give you a broader picture of what we’re going to do with 6352, which will probably be a little bit later in the year.

Thank you. Our next question will come from the line of Hartaj Singh with Oppenheimer. Please proceed.

Yeah. Hi. Thanks for my question. I just had a couple. One, I just want to ask on the insights you got from the melanoma cohorts and then gave you sort of insights in the colorectal cancer, any thoughts about similar or maybe analogs or insights you got to the lung cancer cohorts, and I know you're waiting for those later this quarter, Briggs, but just any thoughts there and what sort of insights might translate over from the data you're presenting at ASCO in melanoma into lung cancer?

Yeah. I would say yes Hartaj, there is what we're seeing in melanoma could help us think about back to I think one of the earlier questions of subpopulation of non-small cell lung cancer. So we're thinking about that.

Got it. Great, Briggs. And then the other question is just on E2112, a question was asked earlier about overall survival. I know you've said that both endpoints are primary endpoints. Can you just sort of walk us through as well as you can or sort of quickly on how -- what sort of our statistical methodology that you'll be utilizing for sort of testing those hypotheses and then how will you walk through these two that are not co-primaries, if I remember correctly, but the primaries and then how you sort of go through the secondaries, et cetera?

Right. Yeah. Thanks very much for the question. So you are correct. They're not formally co-primaries, because the formal co-primary means you have to hit on both. So they are two primary endpoints and they’re not, very simply, they are not hierarchical statistical testing. It’s actually, alpha is split between PFS and OS. So certain amount of alpha goes to PFS and a certain amount of alpha goes to OS, which is why you can win on either.

Got it. And then is it -- I assume that when PFS is completed and you expect to see that in the first half, will you have a chance to look at OS at that point or will you just look at PFS or I guess ECOG will look at PFS and then wait till you get to a certain point to look at OS?

So there is a first interim look at OS. It will occur in the same time as the final PFS analysis. So when the DSMB looks at PFS in the first half of next year, they will also do the first interim look at OS and then OS is reviewed, there are additional interim looks every six months. Based upon our assumptions of putting the trial together and how these events will read out, we think it’s unlikely that OS would be statistically significant at that very first look at the same time as PFS, which is why in an answer to the earlier question, we tend to think a bit about 18 to 24 months later. If for some reason, the PFS benefit were, I mean the OS benefit were greater than hypothesized, of course, you could find that earlier, but based upon the assumptions of the trial, we don’t think it will read out at that first interim look.

Got it. We can still follow the PFS assuming it’s positive?

Exactly.

Thank you. Our next question will come from the line of Mike King with JMP Securities. Please proceed.

Good afternoon, guys. Thanks for taking the question. A lot of my questions have been asked and answered. So I guess, Briggs, only thing left for me would be to ask you on 6352, what is going to help us understand how the profile differentiates against other CSF1R inhibitors when you show us the data, and do you have any thoughts as to if that -- if the data top-line may come out later this year or is that something we should anticipate next year, maybe just a little bit of color on those topics?

Sure. So the ongoing clinical trial is a single ascending dose trial in normal healthy volunteers and what we’ll be able to get from that trial is obviously PK and PD and some safety data. So I think in terms of, from that trial in terms of the only things that we would be able to potentially inform differentiation would really be dose and dose frequency. So as we get a better sense of the PK and PD of the molecule, we’ll be able to, from a competition, if there is some modeling of what we think the dose and dose frequency would be, then that would be one thing that we can say potentially by the end of the year. Beyond that, I don’t think we can get that much more out of the single ascending dose trial.

Would there be any biomarkers that you could look at that could predict clinical activity?

Well, we have pharmacodynamic biomarkers in the trial. So we’re looking at effects on non-classical monocytes and the duration of the effect on non-classical monocytes. So we’ll have, I think, a pretty good view of the ability to block CSF1 and IL-34 and what effect that has on downstream pharmacology and how long that lasts. But again, it’s normal healthy volunteers. So we won’t have information that correlates that to efficacy until we move into the trials of cancer patients.

Okay. But you'll be able to read out that you've got the expected on-target activity?

Exactly.

Okay. And then I guess a bigger picture strategic question, just as far as your thought process behind the combinations of entinostat with the checkpoints, BAVENCIO in ovarian centric and TNBC, and I know that these other checkpoint modulators have shown activity in those particular tumor types, but I think that most clinicians would agree that these drugs are more alike than dissimilar. So from Syndax sort of upside or optionality point of view, how does -- how do you guys benefit from continuing with these trials with different checkpoints in disparate tumor types? Thank you.

Yeah. So I think Mike, your hypothesis that these agents are more similar than different seem to be playing out as clinical data and all of them accumulates. I think from our point of view, and it goes back to the question about how we would develop the drug for example in melanoma. There is a scenario where one could think about combining entinostat with any PD-1 or PD-L1 that has an indication and a tumor type that you’re studying. And so by having safety data with entinostat combined with each of these, that enables us to think about that type of a trial design. While it’s true that I think that from an efficacy point of view, they seem to be more similar than different from a safety point of view, we just want to make sure that that’s true. Remember, they’re all slightly different antibodies. So we’re generating safety data with three in our ENCORE trials and then there is data being generated with ipi/nivo in a NCI sponsored trial. So I think it would be helpful for us to have safety data with all of the agents. So depending on what we do from a development point of view, there could be a possibility that combine entinostat with multiple agents within one trial.

Okay. And is it fair to say that it would also lead to sort of a generalizable effective entinostat that it could work with any checkpoint and any tumor type as long as there has been demonstration of activity with one of those?

I think the philosophy that you’re stating is the one that we’re interested in. There is always the regulatory definition of how generalizable is that and that depends of course on which ones you’ve studied. So again, being able based upon safety database able to study multiple ones in combination with entinostat, that improves our chances of having a more generalizable label.

Thank you. Our next question will come from the line of Christopher Marai with Nomura. Please proceed.

Hello. It’s actually [indiscernible] for Christopher Marai. And my question is regarding the 601 cohorts, will any of them provide any biomarker data to help us dish out entinostat effect on suppressive rather than [indiscernible] and will any of these data be present at ASCO?

So the answer to your first question is yes, we’ve been fortunate working with our investigators to get biopsies in a subset of the patients before they were treated with entinostat and after they were on therapy. And so we are accumulating all of that data now. To be honest, we’re still in the phase of analyzing all that and I don’t know exactly what we’re going to have ready to present at ASCO versus what we’ll have analyzed to be able to present later in the year. But we are collecting quite a bit of information and we will at a minimum at the ASCO will be able to describe what all those biomarkers are that we are doing, just data is coming in real time and we just don’t know whether we will have all correlate and analyze and ready to present at ASCO or whether we’ll have to wait till later in the year.

And should we expect clinical data at ASCO presentation?

You’ll definitely see clinical data on the first 13 melanoma patients.

And I have a second question kind of a follow-up for the question about the combination of CSF1R with entinostat, so a recent paper in nature highlighted the class 2 HDAC inhibitor modality to a repolarization of times, and what is showed in this paper that cotreatment of anti-CSF1R abolished this effect. Taken into consideration that and the difference between the classes, class 1, how do you think about this relation to entinostat and the ability to combine it with CSF1R antibody?

Right. So I think if I remember the paper you’re referencing as I think you had said it was a class 2 HDAC inhibitor, not a class 1 HDAC inhibitor, and we certainly seen in other preclinical experiments, when you look at for example Tregs that a class 1 inhibitor, in fact specifically entinostat has effects on Tregs that HDAC inhibitors do not presumably because the PAN HDAC inhibitors, their class 2 or class 3 activity is blocking that. So we're running our own experiments, specifically with entinostat and with a veering counterpart of 6352 so we can understand exactly how our selective class 1 inhibitor does that. It would not be unprecedented that there have been distinctions between a class 1 HDAC inhibitor and ones that pick class 2.

Thank you. Ladies and gentlemen, this concludes our question-and-answer session for today. So now it’s my pleasure to hand the conference back over to Briggs Morrison, Chief Executive Officer for closing comments and remarks.

Thanks very much operator. Thank you everybody for your participation in the call. Thank you for all of the wonderful questions and we look forward to catching up with people at ASCO.

Ladies and gentlemen, thank you for your participation on today's conference. This does conclude the program and you may all disconnect. Everybody, have a wonderful day.