Good day ladies and gentlemen and welcome to the Syndax Fourth Quarter 2016 Conference call. At this time all participants are in a listen-only mode. Later we’ll conduct a question-and-answer session and instructions will follow at that time. [Operator Instructions] I’d now like to introduce your host for today’s conference, Melissa Forest. Madam, 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 fourth quarter and year end 2016 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 our 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 March 2, 2017 only. A replay of this call will be available on the company’s website www.syndax.com following the call. You can find the dial-in information for the replay in today’s press release as well as on the company’s website. I’d now ask you to turn to Slide 3 and I’m pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer of Syndax.

Thank you, Melissa. Good afternoon and thank you everyone who’s joined us on our conference call and webcast. I’d like to start by summarizing some of our key achievements in 2016, a year that proved to be transformational for Syndax. I’ll then review the progress we’ve made since our last earnings call and Rick Shea, our new Chief Financial Officer will then provide a financial update and following that we will take your questions. Slide 3 summarizes some of our major accomplishments last year. First, at about this time last year, in fact exactly one year ago today, we completed our initial public offering raising 50.5 million in net proceeds, allowing us to focus the remainder of the year on our clinical and business objective. Second, we made great progress in advancing our clinical program. Under the sponsorship of the Eastern Cooperative Oncology Group, American College of Radiology Imaging Network otherwise referred to as ECOG-ACRIN and the NCI, enrolment in our Phase 3 registration trial in hormone receptor positive due to negative breast cancer accelerated. And ECOG-ACRIN believes that the trial is on track to complete enrolment in the fourth quarter of this year. Together with three leading pharmaceutical companies as our partners, we also progress three immuno-oncology studies called the ENCORE studies. The ENCORE studies are proof of concept studies evaluating our Class 1 specific HDAC inhibitor, Entinostat in combination with three different checkpoint inhibitors in five separate clinical studies. Third, we also expanded our pipeline with the addition of SNDX-6352, a potential best in class anti-colony-stimulating factor 1 receptor or referred to as an anti-CSF-1R monoclonal antibody that we recently advanced into a Phase 1 clinical trial. So overall, as you can see, 2016 was really a very productive year for Syndax. I like to now turn to…

Thank you Briggs, turning to Slide 13, for the three months ended December 31, 2016 Syndax reported a net loss of $10.8 million or $0.59 per share. Net loss for the full year 2016, was $47.1 million or $3.22 per share. Our R&D expenses in the fourth quarter of 2016 increased to $8.5 million from $2.6 million from the comparable prior year period and for the year ended December 31, 2016, R&D expenses increased to $31.7 million, compared to $9.5 million for the prior year. These increases were primarily due to increased patient accrual cost in E2112, higher expenses associated with Phase 2 expansion of ENCORE 601 and the commencement of ENCORE 602 as well as the upfront payments in 2016 relating to the expanding of the pipeline with SNDX-6352. Our G&A expenses were $3.0 million during the fourth quarter of 2016 and $13.3 million for the year, similar to the prior periods in $2.4 million and $11.6 million. The number of common shares outstanding at December 31, 2016 was 18.2 million shares and with 2.9 million shares of commons stock equivalents outstanding, we had a total of 21.1 million shares outstanding on a fully diluted basis at December 31, 2016. Additional financial details will be available in our 10-K which we expect to file no later than mid to late March. We ended the year with cash of $105.3 million, which we believe is sufficient to fund our development programs into mid 2018 and which will enable us to reach our key corporate milestones. We believe that we are in a strong financial position, will continue to make appropriate and measured investments in building our company. I’ll now turn the call back to Briggs.

Great, thanks Rick. In closing I would like to acknowledge my colleagues at Syndax for their valuable insights into innovative cancer drug development and unfailing commitment to try to meet the needs of cancer patients with limited treatment option. I’d like to thank our collaborators as well as the patients, the trail sites and investigators involved in our clinical program. Our solid progress this quarter is a direct result of their collective involvement as well as efforts of the team here at Syndax. Again as you can see on slide 14, we believe we have a highly promising portfolio of potential investment class asset supported by a robust corporate strategic plan and a financial run way that takes us through several critical value and deflection points including the anticipated completion of enrollment in both are Phase 2 trial of entinostat and triple negative breast cancer and our Phase 3 registration trail of entinostat and hormone receptor positive breast cancer at the end of this year. We are also pleased by the progress we’ve made in enrolling ENCORE 601 and of course are pleased that the melanoma cohort achieved a minimum pre-specified efficacy hurdle. Of course we’re waiting to determine either of the remaining the two cohorts of ENCORE 601 will also successfully meet their respective go criteria for advancement. Finally of course, we are pleased to have advanced our second potential best in class program 6352 into Phase 1and we are look forward to sharing the results from those via single window on those trials towards the end of this year. We continue to remain externally focused with the respective business development opportunities that we believe offer an attractive risk reward profile for Syndax to add to its pipeline as evidenced by the decision to end license 6352. We are…

[Operator Instruction] And our first question is from Chris Marai with Nomura. Your line is now open.

Hi, good afternoon guys, thanks for taking the questions and congratulations Richard on joining the team. I was wondering if you actually elaborate little bit potentially on Syndax 6352 anti-CSF-1R antibody recently licensed, I guess I was wondering perhaps how do you look at that clinical path forward giving any others targeted anti-bodies and molecules in the space and then what can we anticipate from the SAD trial update that you are going to provide, I mean I am just going to be potentially safety and healthy and is there anything specific you are looking forward to help differentiate you as best in class molecule. Thank you?

Right, Chris thanks very much for your question. So in terms of the clinical development strategy for 6352, at this stage we really only talked about the single ascending dose and the multiple ascending dose. We anticipate that little bit later this year, we will be able to share with you the details around what we - the clinical development strategy. I think I would start practice that comments I made in my prepared remarks that there is quite a bit of pre-clinical data showing the ability of this agent and class of agent to enhance the efficacy of not only check point inhibitors but chemotherapy, radiation therapy and cell therapy. So we believe there is quite a bit of opportunity form a development point of view and will say more about that in a subsequent call later in the year. In terms of the single any dose file, it is a single dose in a normal healthy volunteer, the main is we are looking to characterize the PK/PD and of course tolerability in a normal healthy volunteers. The potential information that we can get from that trail that could inform differentiation at this point is really the PK/PD relationship, dose level we need to go to get good pharmacodynamic effects and potentially some information from modeling of that data and what might be a dosing frequency.

Okay great, thank you and I was just wondering could there be any additional color you can provide perhaps on the phase 3 enrollment and how that’s going relative to your expectations? Thank you.

Yeah, so as I said, ECOG provides us regular updates on enrollment, at this stage of the games, the things are still progressing quite nicely and they remain comfortable and the enrollments should be complete by the end of this calendar year

Great, thank you.

And our next question comes from Tony Butler with Guggenheim Securities. Your line is now open.

Yes Briggs thanks very much. Two brief questions, one around 601. Is this neurohypophysis or Syndax hypothesis is that, if administered any reversal of resistance or the notion of reversal of resistance solely due to it is a fact, as diminishing Tregs in MDSCs as is anticipated or as is known or is there another mechanism, that’s point one and number two is, could you maybe address the notion of when you think about moving if in fact non-small cell lung also was to demonstrate some positive outcome, why didn’t you assume that this notion of reversal with resistance was not necessarily specific and I just wanted to - if you could address that or would you anticipate to be specific? It is not that you actually know that answer today but I am just trying to think about this from a hypothetical standpoint. Thanks very much.

Great, thanks very much Tony. So I think the question of the mechanism by which entinostat can reverse resistance is an interesting question and I think those who have surveyed show there is an actually a number of different mechanism so clearly the MDSC, the effect at the Hopkins had described on inhibiting both the function and proliferation of MDSC work that [indiscernible] quite extensively on Tregs, there is also of course data on HDAC and in general not entinostat, specifically on sort of reversing exhausting. There is data on up regulation of class 2 enhancement of NK activity, inducement of T-cell. I think recent data at ACR from some of the pre-clinical work looking at affects other mediators. So I think at this stage of the game it is hard to say exactly what the mechanism is. As we pointed out before we have been quite diligent in trying to get biopsies both before and after therapy in ENCORE 601 trial and particularly on the melanoma cohort, the investigation has been quite successful. So we hope to learn more by analyzing what happening in those tumors with treatment. So, I think stay tuned on more science to come how this is working. I think your question is about whether this reversal of resistance to a specific one as you say at this stage, speculation based up on the mechanisms that we just discussed. It is of course our hypothesis that this could extend to number of different types which is why we are doing experiments and lung cancer melanoma triple negative breast and ovarian where there may be slightly different operative immune suppressive mechanisms and again because it is not entire clear which one of those entinostat effects that’s why we are testing in multiple one. I would tend to agree with you that should we have evidence of reversal of resistance in two different tumor types and as we learn more about characteristics of the tumors in those patients, I think that will inform how much broader we think this mechanism could be operative.

That’s very helpful, one last question if I may. It is really around, I only know one of the region having one response and resistance and IR resistant tumor [indiscernible] you know of others and that I believe it is only in one patient which is makes this even more interesting.

Yeah, I don’t know that we have done an extensive research know everything about every company that is out there. We are aware of that maybe you referenced but we are aware of other agents who have tried to do the same experiment that we are doing, trying to reverse resistance and do not see any responses. So at this stage of MI, I can’t site you other good examples but of course we keep, what was that old saying only the paranoid survives, so we worry about it and we keep looking and for now we are pressing on aggressively with our program.

Fantastic, thanks very much. Congrats.

And our next question comes from David Lebowitz with Morgan Stanley. Your line is now open.

Thank you very much for taking my question. I had a question on the threshold in the various cohorts, could you just run us through the rational and how those particular thresholds were selected?

So again, the so called sign in two stage design is setup where one enrolls, a certain number of - you try to limit the number of patients you enroll, in case the drug has no activity at all. If the drug does have any activity you want to be exposing large numbers of patient to it. So the idea for the - and having said that, if the drug does have activity then you have a hypothesized target rate that you are essentially trying to test for. So if we take the melanoma cohort as an example, at the end of the 34 patients, the total 34 that hypothesized response rate that we are looking for is 25% and we are trying to rule out a lower bound of considerable of 10%. So the way the sign in two stages are set up, is essentially you are looking for some preliminary evidence that you could exceeded that 10%, lower bound or what you are trying to exclude and if you have some evidence of that then you go to the 434, which again should give you a pretty good confident around a point of estimate of 25. So that’s sort of logic that we have applied to each one of these for the patients of non-small cell lung cancer are progressed on PD1 antagonist target response rate is 15% with lower bound of 5 and for the non-small cell lung cancer, patients who are naïve target response rate is 35 with lower bound of 15 approximately. So that’s sort of how we have come about it. But again I want to emphasis the stage one portion is really just if the drugs is not doing anything, just stop because it is not the right thing to do for patients and if there is any enroll more and if the statistics are around what the constant would be around your hypothesized point estimate. I guess one other point they just sort of - why pick those numbers. So if you say in refracting melanoma, there really isn’t anything, so if they fail both, if they [indiscernible] inhibitor plus PD-1 or PD-1 CTLA-4, essentially there is not really much for those patients. They might go on DTIC which has response rate of somewhere in the 5% to 7% range. So if you can rule out a lower bound of 10% we think you are clearly better that what would be the only sort of alternative for those patients. And again that’s sort of logic we use as we said, these lower bound and the point estimates for each cohort.

Excellent, thank you very much. That was very helpful.

And our next question comes from Robert Hazlett, BTIG. Your line is now open.

Yes, thanks and congratulations on leading the threshold just to continue along the thought, so is your expectation then if you do reach that 25% threshold in melanoma, then you would advance the registration direct studies or is there an ability to even expand further the second stage of the Simon two stage design where you might have an expedited route to registration.

Right, so I think Robert, the so I want to be very clear that we have not had any conversations with regulators about half way to registration. I think what I would say in general terms, when you are studying a patient pipe relation, life is refracting melanoma patients where they really aren’t good available therapies and standard would be something like DTIC and then I think that’s part of whether sort of 25% came from, if you are in that range and you can rule out a lower bound of 10% then we are relieved that it is clinically important for those patients and could potentially be something that a regulator might be willing to look at. But I don’t want to but we have not talked any regulatory agencies about path there. So I don’t want to leave you with an impression that we think that isn’t likely we will let you know once we have appropriate regulatory interaction.

Okay so, what would then was that as a backdrop what would - assuming you achieve the threshold in the 34 patients, what would logical step be then, even away from regulatory discussion?

Right, so I think, drug development is always hard to separate from a regulatory decision because that’s part of the barrier for us in order to make the available, the patients you got to get through regulatory discussion. So we would fairly want to think about enlarging the sample size to get a better estimate of response rate, the durability of response and the safety in that. Patient population again, I would point out that, these are designed as signal seeking proof of concept trial and the fact you could potentially reverse resistance of advance patients of course may be rapid path from a development point of view but it also raises the question of do you want to study your agent in an earlier line of therapy you wanted to study in first line which we have not undertaking yet. So that’s something else that we are thinking about.

Okay, thank you and again touching on number of points you brought up there, do you have any comment on the particular types of patients in the melanoma study that show response or where you showed activity.

As I said we can’t really talk at all about the data that sort of difficult for presenting at scientific congress. But we do - as I said we have been trying to get biopsies, pre-treatment and post treatment and from those that biopsy data it is possible that we will be able to make some at least together small l number of patients, general options about you seem to be responding.

Okay, and then shifting gears entirely, I would like to just ask a general question about trajectory of R&D spend, it was little lower in the fourth quarter, than in prior quarter. Do you have any comment about the trajectory as we move through 2017? Thanks?

Sure, I will let Rick take that question.

Yeah, I would clearly, as we explained, these clinical trials, the R&D spending will be ramping up into 2017. I think any different Q4 is probably is just a cost of these expenditures depending on a cool rates and when activities are kicked off, the manufacturing activities and that sort of thing. So I don’t think there was anything particular in the Q4 again certainly, we haven’t provided precise guidance on our spending levels for 2017 but the spending will be increasing.

Okay, thank you very much and congratulation on the progress.

Thanks Bert.

And our next question comes from Joel Beatty from Citi. Your line is now open.

Hi and good afternoon. Thanks for taking the question. Can you tell us a little bit more about the difference in diming between melanoma announcement today and two lung cancer cohorts and going? What was their difference in enrollment time or they are different courses of the diseases, could have explained that.

Yeah, I think it is actually a combination of both Joel, there was little latter completion of enrollment in the non-small cell lung as cohort and again when we had projected the end of the first quarter, the I guess to be very transparent on the thinking behind that, if you think about the time it takes to respond to PD-1 inhibitor so the mean time to respond I think in many of the large trails is somewhere in the 12 week time frame so we thought a patients were in and they had a six week scan and 12 week scan that potentially you could be able to score those patients relatively early. You may remember from the data that we presented response, they take a little bit longer to develop than you might expect from PD-1 alone. So I think it is a combination of enrollments and perhaps taking a little bit longer for responses to be confirmed in the lung cancer pipeline.

Okay thank you.

And our next question comes from Hartaj Singh from Oppenheimer & Co. Your line is now open.

Hi, can you hear me?

Yeah, Hartaj how are you?

Hey sorry and I apologize at this time there is kind of some background noise, I’m not in a good place. Just couple of very quick questions one is with the increasing use on melanoma of the [indiscernible] combination and non-small cell lung cancer in this thing, increasing testing of PDL-l expression. Just any thoughts like would melanoma - just how to think about your trial there and potential you know if it moves on further and the same thing if you decide to move on but the two lung cancer trails. The orders that mean the PDL-1 testing further trial and then second is CSF-1, is there any specific human types that right now you think that could be manual for and will it be mono or combo down the line, thank you.

So first of all if we come about Uruguay [ph] and I apologize I have always been trained to use generic names so I call it [indiscernible] but either way. We do have patients number of trails where we failed the combination as well as those who have failed maybe an individual mono therapy. I think as you finish out the cohort we will be able to have data on failing the double it as well as PD-1 mono, it appears that mono is probably using it a little less nowadays given that PD-L1 have shown superiority to - at least in mono therapy. And so if - it sort of goes back to the earlier question about the mechanism and how broadly active this is, if we see activity in failures in melanoma then I think it is mechanism you potentially could see the same thing in lung cancer, other tumor types where people are studying that combination. I think the question about PD-L1 testing is of course quite relevant you see in melanoma that PD-L1 testing plus some other bio markers can actually separate out those who are more or less likely to respond. Of course we know that’s true now in lung cancer. We’re getting PD-L1data on every patient in our trial, so we’ll be able to make some comments on that. But clearly in - lung cancer first line, PD-L1 testing is becoming - from our understanding pretty sort of kind of a care. So we’re doing that and we’ll be able to give some information on sort of where our drug works or doesn’t work relative to PD-L1 status, it’s actually a quite important variable. I think your question about where is CSF-1R work with tumor types, there’s - based upon the presence of tumor associated macro phages, if you want to use that as sort of your indication of where you think an agent that affects tumor associated macro phages might work. There’s actually quite a few tumor types including breast cancer, certain lung cancers, melanoma, ovarian cancer, it’s actually quite broad and so again that’s one of those things to answer your question of testing of can you assess the tumor associated macro phage signature or environment in tumors as you think about the right population of patients to treat. We’re working on that as we get ready to move into patients with cancer.

Thank you.

At this time I’m showing no further question. I’ll turn the call back over to Briggs Morrison, CEO for any closing remarks.

Thanks everybody again for joining us for the call. I want to again thank all of the employees at Syndax who’ve done just a fabulous job keeping our programs moving along. And again thank the investigators and patients and clinical trailers who’ve been working with us. And thank you very much for all of you for your questions. We’ll see you in upcoming conferences.

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