Good afternoon ladies and gentlemen and welcome to Syndax’s First Quarter 2019 Financial Results Conference Call. [Operator Instructions] I would now like to turn the call over to your host, Ms. Melissa Forst with Argot Partners. Please go ahead.

Thank you, Operator. Welcome, and thank you to those of you joining us today for Syndax's First Quarter 2019 Financial Results Conference Call. Joining us this afternoon for prepared remarks will be Dr. Briggs Morrison, Chief Executive Officer; Michael Metzger, President and Chief Operating Officer and Rick Shea, Chief Financial Officer. And also joining us on today’s call for the question-and-answer session will be; Dr. Michael Meyers, Chief Medical Officer; and Dr. Peter Ordentlich, Chief Scientific Officer. This call is being accompanied by a slide deck that has been posted on the company's website, so I'd ask you to please turn to the forward-looking statements on Slide 2. Before we 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 factors, including those discussed in the Risk Factors section of the company's most recent quarterly report on Form 10-Q as well as other reports filed with the SEC. Any forward-looking statements represent the company's views as of today, May 6, 2019, only. A replay of this call will be available on the company's website, www.syndax.com following the call. And with that, I am pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer of Syndex.

Thank you very much Melissa and thank you to everyone for joining us on today's call and on the webcast. Slide 3 provides a high level summary of our current corporate priorities. As you progress through this year, we continue to focus our resources on two incredibly exciting opportunities. The first is we are anticipating a positive readout of E2112, our Phase 3 trial of entinostat in hormone receptor-positive breast cancer; and a subsequent filing of our first NDA and the corresponding launch of our first product. I want to again emphasize that our positive overall survival trial in hormone receptor positive HER2 negative breast cancer would be a landmark result and would be transformative for Syndax, its shareholders but most importantly for patients. We believe the entinostat opportunity in hormone receptor positive breast cancer carries blockbuster potential. The E2112 Data Safety Monitoring Committee recently completed their scheduled second quarter interim analysis and has informed us that the trial will continue as planned. This result is encouraging and consistent with our base case assumption. We will now turn our attention to the upcoming fourth quarter 2019 analysis. I'd also like to take a moment to congratulate Dr. Roisin Connolly on behalf of everyone here at Syndax for winning the ECOG-ACRIN Young Investigator Award this past Friday. As you may know, Roisin is the lead investigator for E2112 and we appreciate all the work that she's done to make E2112 a successful endeavor. Second, we remained on track to file an IND this quarter for SNDX-5613, our potential first and best-in-class menin targeted agent for the treatment of mixed lineage leukemia followed by the rapid initiation of our broad clinical program in acute leukemia. As we continue to learn more about the potential of 5613 in acute leukemia, we see this molecule becoming another important value driver for our company. We believe that the breadth of indications we will investigate with 5613 represents a second blockbuster opportunity. Now let me review these opportunities in a little more detail. Slide 4, summarizes the design of our Phase 3 trial of entinostat in hormone receptor positive HER2 negative breast cancer. The trial has randomized 608 patients to either exemestane plus placebo versus exemestane plus entinostat, and the focus of this trial is now clearly on overall survival. As we've noted before, overall survival interim analyses are conducted approximately every six months and positive outcome at any of the OS interim analysis or upon achieving the final number events needed to conclude the study would allow us to file for regulatory approval based upon the terms of our breakthrough therapy designation in hormone receptor metastatic breast cancer and a special protocol assessment process we went through with the FDA. The Data Safety Monitoring Committee recently informed us that based upon the second quarter interim analysis the trial passed a formal futility analysis and continue as planned. I like to remind everyone that each interim analysis evaluates both the possibility that the trial is futile through a formal futility analysis at each interim, as well as the possibility that the trial is positive based on a statistically significant improvement in overall survival. So we are pleased that the trial has not stopped for futility and we remain confident that the trial will be positive. The final analysis of this trial will be conducted once there are 410 survival events. We don't know when the 410th event will occur, but based upon the modeling we've done, we believe the final analysis could occur in November of this year or possibly in May of 2020. Slide 5 emphasizes the potential for the entinostat-exemestane regimen to be the preferred agent after CDK4/6 therapy for hormone receptor positive HER2 negative breast cancer representing a blockbuster market opportunity. We know that CDK4/6 therapies, most notably Ibrance, are being used increasingly as first-line agents, there's a clear unmet need for therapy that will be effective in a patient who has stopped responding to a CDK4/6 inhibitor. Our current estimate is that between 30% and 50% of patients in E2112 will have received a CDK4/6 inhibitor prior to entering the trial, and that's we will have a highly relevant dataset in the post-CDK4/6 patient population. This population of patients is substantial with an estimated 34,000 patients each year who go on to receive hormone therapy after failing first-line therapy and who could therefore be eligible to receive the entinostat regimen. We're also of course quite excited about the upcoming IND filing for our genetically-targeted agent 5613. Slide 6 shows the similarity between our menin program and other medicines that have attacked fusion proteins that are a result of chromosomal rearrangements. The first example of a recurring chromosomal rearrangement in oncology was the so-called Philadelphia chromosome, which results in the BCR-ABL fusion protein, and which led to the development of gleevec and other BCR-ABL inhibitors. Since then, there have been many examples of medicines that specifically attack such fusion proteins that result from a chromosomal translocation, including medicines against EML4-ALK fusions, NTRK fusions and RET fusions. In these chromosomal translocations, there were strong evidence that the resulting fusion protein is driving the cancer cell. Being able to precisely define these patients led to the development of medicines that demonstrate large treatment effects in specific patient populations and enabled a rapid clinical developments and regulatory path. I want to emphasize that our 5613 program is an example of a targeted therapy that was designed based upon our understanding of a specific chromosomal rearrangement that leads to a specific fusion protein known to drive the leukemic process. On Slide 7, we summarize the status of this program. The IND is on track to be filed later this quarter, with the Phase 1/2 clinical program to begin soon thereafter. Once the IND is approved, we'll be able to provide the final details of our Phase 1/2 clinical program. However, we can say that our goal is to enroll adults with MMLr Leukemias followed by children with MMLr Leukemias. And we also intend to enroll adults with NPM1 mut leukemia based upon the very compelling preclinical data that was presented at ASH this past December, which showed that 5613 has promising activity in that disease as well. Again, I want to emphasize that we see a rapid and straightforward clinical development path for 5613 similar to the path taken for patients with NTRK fusions or IDH1 mutations. We expect that the molecule should have single agent activity and it's quite possible that we could observe clinical activity early in the clinical development path, again unlocking significant near-term value for Syndax. As we continue to learn more about the potential of 5613 in acute leukemia, we see this molecule becoming an additional and important value driver. Let me now briefly turn to our entinostat ENCORE clinical trial program, in which we evaluated entinostat in combination with PD-1 pathway antagonists. I will remind investors that the ENCORE program was set up as a signal-seeking program exploring multiple tumor types with different immunologic characteristics. We've also look for biomarkers that could predict clinical benefit. Slide 8 shows that the immunologic environment is quite variable in different tumors. The ENCORE results today indicate that the beneficial effect in entinostat is strongly evident in inflamed tumors but not in the other immunologic settings. We believe this is an important conclusion of our work. Slide 9 summarizes our findings recently presented at AACR, consisting with prior data we see a strong signal of clinical benefit when entinostat is combined with KEYTRUDA in patients with non-small lung cancer patients, who's decease has progressed after both chemotherapy and a PD-1 antagonists. We've also identified a biomarker, peripheral blood class O monocytes that appears to predict clinical benefit in this population of patients. In addition, we've seen a strong and durable clinical benefit when entinostat is combined with KEYTRUDA in patients with melanoma, whose disease has progressed on after both PD-1 inhibitor and a CTLA-4 inhibitor. We're especially encouraged by the positive feedback we've received from therapeutic area experts and investigators, who like us recognize the potential of this combination to deliver a clinically meaningful benefit to patients who are currently lack alternative options. As we discussed on our last quarterly call, following the availability of positive E2112 OS results, we will determine whether to advance the entinostat-PD-1 combination programs into one or more registration trials. Let me now turn to turn Slide 10 in SNDX-6352, our potential best-in-class monoclonal antibody targeting the CSF-1 receptor. We initiated a trial testing in chronic graft versus host disease in the fourth quarter of last year. Chronic graft versus host disease is a frequent complication of hematopoietic stem cell transplantation, wherein the donor derived immune cells contribute to the initiation and development of fibrosis and manifestations of many of the advanced disease symptom. In preclinical models, blockage of the CSF-1 pathway with anti-CSF-1R antibodies can result in the depletion of donor macrophages, thereby preventing and reducing chronic graft versus host disease. We believe that chronic graft versus host disease represents an attractive opportunity and we look forward to sharing initial efficacy data in the second half of this year. Finally Slide 11 summarizes how the many transactions that we have completed to acquire both SNDX-6352 and the Menin-MMLr programs prove that we have an ability to strategically expand our pipeline. Our management team and board have established relationships that allow us to identify quality, differentiated assets, and the extensive clinical development experience of our team gives us a competitive advantage in closing agreements. We continue to expend significant efforts in this area, and we consider this capability to be a core strength of our company. I'd like to now turn the call over to Michael Metzger, our President and Chief Operating Officer to discuss our recent financing. Michael?

Thank you, Briggs. As summarized on Slide 12, we completed an important equity financing on March 29, raising $27.5 million in new capital. This financing sets us up for success over the next 12 to 18 months and accomplishes three important goals for Syndax. First, as Rick will detail in his remarks, the financing extends our cash runway, enabling us to operate well beyond critical program milestones for entinostat and hormone receptor positive metastatic breast cancer and proof of concept in the 5613 program. Second, we structured the financing as a significant premium at a significant premium to market and through the warrant structure set up the opportunity to raise additional capital as our stock price appreciates. This creative structure serve to limit the amount of dilution to our existing shareholders at the time when we believe our stock is undervalued. And third, this offering gave us the opportunity to add top quartile investors to our list of significant shareholders. We are quite thoughtful about how we build our shareholder base and we are delighted to have new shareholders, who are aligned with our vision for building long-term value. I will now turn the call over to Rick to review our financial results. Rick?

Thank you, Michael. Results of our operations for Q1 2019 and the comparison to the prior year period are included in our press release, so I won't repeat them in these remarks. Additional financial details will be available in our quarterly report on Form 10-Q, which we intend to file later this week. Turning to Slide 13, we ended the first quarter of 2019 with $92.7 million in cash and 31.6 million shares outstanding. The net change in cash for Q4 was a increase of $11.8 million. The operating cash burn of $16.4 million was more than offset by $27.4 million of net proceeds from the offering, and $0.8 million of net proceeds from our ATM. Looking ahead, I'd like to provide updated financial guidance for both Q2 and for the full year of 2019. For the second quarter of 2019, we expect R&D expenses to be $9 million to $10 million and total operating expenses to be $13 million to $14 million, including approximately $1.5 million of non-cash stock compensation expense. For full year 2019, our guidance is unchanged. We expect R&D expenses of $46 million to $50 million and total operating expenses of $60 million to $64 million. Operating expenses for 2019 are expected to include non-cash stock compensation expense of $6 million and offset by interest income of approximately $2 million, so our net cash burn for 2019 is expected to be $52 million to $56 million. So our current cash, along with this reduced spending will allow us to operate the company to achieve key milestones for our prioritized programs, specifically OS results for E2112 and early proof of concept for our targeted menin inhibitor. Now, I'd like to turn the call back over to Briggs.

Thanks very much, Rick. I'd like to close our call with a clear summary of our company priorities. We believe that a positive OS result in E2112 would be transformative for Syndax and create significant shareholder value. Although the final OS readout for E2112 could occur by the end of this year, we are prepared for a potential later final readout in mid-2020. We're also very excited about the prospects for 5613, our menin MLLr inhibitor. We expect that the molecule could have single-agent activity, and it's quite possible we could observe clinical activity early in the clinical development path, again, unlocking significant near-term value for Syndax. We remain excited about our data in non-small cell lung cancer and melanoma, as recently presented at AACR. Nonetheless, we believe it was prudent to pause our further development spending in I/O until such time that we receive the positive results of E2112. For 6352, we remain on track to select a recommended Phase II dose in solid tumors, end of this quarter and anticipate having initial efficacy in chronic graft versus host disease later in the year. Finally, we continue to look for additional molecules or technologies to bring into our portfolio. We have a proven track record of delivering on this pillar of our strategy, and I believe this is a core strength of our company. As always, I'd like to thank the team here at Syndax, our collaborators and most importantly the patients, trial sites and investigators involved with our clinical program. With that, I'd like to open the call for questions.

[Operator Instructions] Our first question comes from the line of Bert Hazlett from BTIG. Your line is open.

Thanks for taking the question. I have two, first on the Menin-MMLr program. There was some discussions at AACR with regard to differentiation syndrome that was seen with many of the AML therapies, and maybe that, that was an unrecognized or under recognized phenomenon with many of those therapies. Would you expect to see differentiation syndrome early on with the Menin program you have? And if so, can that be considered maybe an on target AE for the program?

What's your second question, Bert?

Second question is regarding the biomarker activity of entinostat. Is there an ability to translate the biomarker that you've selected for non-small cell lung cancer in melanoma?

Okay. So I'll take the first one, then I'll turn over to Peter Ordentlich to take the second one. So the differentiation syndrome, so again, if we look at the biology of what we think is happening when we treat leukemic cells with the MLLr inhibitor, you do turn off expression of genes involved in leukemogenesis and the cells are believed to differentiate before they die. So it wouldn't shock us, if we saw some evidence of the differentiation syndrome that you see with IDH inhibitors and others. Whether that is any kind of surrogate for efficacy, I'm not so sure, I think we would much rather rely upon the accepted regulatory end point of complete responses. And I'll turn your second question over to Peter, if you want to just comment Peter about the, I think Bert’s question is around the monocytes and its applicability to melanoma.

Yes, hi. The short answer is yes, we see similar trends in the baseline monocytes in terms of response, prediction in the melanoma cohort as we do in the lung cohort.

And if you – just as a follow-up, if you choose to continue these programs, would you expect to enrich in some way based on that biomarker in melanoma?

Bert, this is Briggs, I’ll take that. So I don't think we've made that decision yet, I mean, that was obviously part of the reason we were letting the melanoma data mature a bit further, both, so that we could better characterize the durability and that we could characterize the potential of using monocytes or other biomarkers. So it's certainly something that is a consideration, but until we decide whether to go forward with either one of those programs, we've probably don't have to say too much about exactly what the details would be of that program. But it is a consideration.

Okay. Thank you.

Our next question comes from the line of Madhu Kumar from R.W. Baird. Your line is open.

Hi guys, thanks for taking my question. So first one is when we were looking back at ENCORE 301, kind of looking to the protocol, it appears that the protocol allows patients who are on entinostat plus exemestane can continue on drug through progression as a maintenance therapy, while patients who progressed in the control arm had to come off therapy and go on to standard of care. Is that the case? And if so, what fraction of patients in entinostat arm stayed on entinostat therapy post-progression.

So your question Madhu was about ENCORE 301.

Yes.

I don’t know, Peter, do you know the answer to that question?

All patients came off at the time of progression. I don't – nobody who was continued on it, on the entinostat after disease progression.

Okay, great. And then when you guys think about ENCORE 301 in terms of the entinostat – it’s in the exemestane placebo arm, how do you think about that arm’s performance relative to other exemestane placebo arms and other clinical trials? And kind of how do you reconcile the performance of that arm in ENCORE 301 versus for example, BOLERO-2 and other exemestane the kind of monotherapy clinical trials?

Yes. Peter, do you want to take that one too?

Sure, thank you. It's a good question and we’ve thought about that quite a bit as we got our data and the BOLERO-2 data read out and a few other trials on the exemestane. It wasn't too far off, if using the – I think was the investigator assessed that or the central assessed BOLERO-2, I can’t quite remember right now. But the differences between what we had for our control arm and what that exemestane control arm read out were not that different in terms of magnitude. So the investigators we spoke to at the time were not very much concerned by that. And in fact, based on the fact if you recall in 301, we were enrolling patients actively progressing on their prior non-steroidal aromatase inhibitor. So the thought was that dose tended to be more perhaps resistant to their aromatase inhibitor activity. So overall, the investigators were not very surprised at what we had for the median outcome. I can’t really comment on sort of the more recent trials where exemestane had read out as a control arm, just the patient populations may have shifted a bit. But at least – at that time there really wasn't much concern that ours was underperforming that significantly.

Okay, great. If I can squeeze in one more in. So thinking about the Menin-MMLr inhibitor, so now that they kind of IND filing or kind of clinical trial plan is pretty well formed. What do you guys think is the best PD biomarker for showing innovation of the Menin-MMLr interaction?

Yes. So Madhu, I don’t think we've said much about the PD assays, we're working diligently on those, as I sort of answered two Bert’s question. I think to be candid, the thing that would get us most excited is to see clinical complete responses.

Okay, great. Thanks for taking my questions.

Our next question comes from the line of Chris Shibutani from Cowen. Your line is open.

Thank you very much. With 5613, it is obviously one of the molecules that’s going to go into the clinic and I think there are several of its compounds or at least one that is in the clinic as well. Can you help us think about how we should think about potentially differentiating either the compounds themselves or the approach that you're taking? It’d be helpful for context. Thank you.

Yes, thanks a lot Chris. So it's – I think at this point in time it's a little hard to put too much – to say too much about the differentiation, I assume the molecule you're referring to is Cour’s molecule. We know that they had their IND approved. And from what they have said publicly, I believe that their program, they’re probably studying similar populations to the ones we're looking at, both MLLr, NPM1 mutants, I think they also said they would do a little broader search maybe in their early program as an all-comer population. But from what we can tell – from what's publicly available, I think their molecule hits the same target that ours does. And figuring out exactly what the differentiation is between the two, it’s, I think too early to be able to say because we don't know exactly which molecule they're taking forward. But I would say that at some point it would be great for people to be focused on the differentiation between two active agents. So six months from now when we have good efficacy data and maybe they also have a little bit, that is probably a more relevant question.

Great. And then the recent financing that you did, certainly brought on board some smart money on your behalf. Can you talk about how confident you feel about your current plan in the event that for instance the E2112 does not read out until mid-2020, if you feel that need to perhaps once done like other considerations because I noticed that you also did talk about continuing to be on the search from a business development front. It would be helpful to understand in the event we get-off to mid-2020 for [indiscernible]. Thank you.

Yes, Chris, it’s Rick Shea. Given the guidance that we provided for cash burn in 2019, we should end 2019 with cash in the low-to-mid $50 million range without doing anything further, which at that time would give us slightly more than a year's worth of cash prospectively. So given E2112 time frame of probably Q2 2020, we should be in pretty good shape to have a result and to still have a reasonable amount of cash. But certainly, it'll be something that we'll have to pay close attention to at the time.

Great. Thank you. Look forward to getting an update, when you guys [indiscernible]. Thank you.

Thanks Chris.

Our next question comes from the line of Christopher Marai from Nomura Instinet. Your line is open.

Hey, good afternoon. Thanks for taking the question. Maybe first question just on entinostat, I’m assuming success, I was wondering if you could delineate for us some of the plans you've made with respect to commercialization for the compound. And from – on this point and then future points, what the plans would be to continue to progress commercialization? And then secondly, with respect to that in different geographies, would you be open to potentially partnering the assets? Can you walk us through some of your thought processes there around commercialization? And then one follow-up if I May. Thank you.

So Chris, let me let Michael Metzger take that question.

Yes. Hey, Chris. So in terms of commercialization, I think we've been pretty open about the fact that we've had discussions over time with potential partners to optimize the opportunity for the drug which has a global launch. And our reach probably doesn't extend outside of the U.S. in terms of our own commercial aspirations, but we do have aspirations to potentially launch the drug either on our own or in partnership with a large Pharma in the U.S. as well. So we have opportunities, I think partners are – as we are waiting eagerly for the data to emerge. And at that time we think we'll have multiple opportunities to partner either regionally or globally. And in terms of what our work is internally has been so far, I mean, we're not – we have not undertaken to build a sales force as of yet. I think small company likes Syndax typically waits a little bit longer to hire a field force, so that would – that's not something we've done. Clearly, it's not forecast in our burn. We have done some pre-commercialization work as you would expect. And I think we're well prepared on that front to take the next step when the data comes in, and we'll update everybody at that point.

You want to comment on geography?

Yes. And so I think the comment about geographies as I said, we are interested – most interested in launching and being represented meaningfully in terms of sales and marketing in the U.S. and then certainly we have partners in Japan and Korea and China now, but the rest of the geographies are open and so, we would be potentially open to a partnership outside the U.S. or also in some part globally where they would take all of the other geographies, including part of the U.S., and help us there as well. So we have some options to flex depending on how we make out.

Thanks, Michael. Just with respect to that, maybe could you further elaborate on aspirations to have your own salesforce? I mean, obviously if you have success with menin down the road, it could be advantageous, obviously different indications. So how should we be thinking about that? How's his Syndax thinking about that?

Yes, I know it's a great question. I think if we're fortunate enough to have breast cancer in our portfolio on its own, it's a big indication. Companies have launched in breast cancer, small companies have launched in breast cancer and have grown up through that process, roughly round numbers of 100 reps or so, 150 reps can do well in this indication. So that's not unattainable for a small company like Syndax, the menin inhibitor, obviously focused on leukemia, but they're all oncologists and so there is some overlap there, and there are some certain specialists who we would – and academic centers that we would focus on. So that's probably a smaller need in terms of a sales and marketing and headcount to cover the leukemia space. So certainly doable and it would be a great outcome if we had both drugs to promote in one bag. And so we're – yes, we'll be actively thinking about that when the time comes. Certainly something we aspire to.

Got it. Thank you. And then with respect to menin, just a follow-up on a few of the other questions, it sounds like we're looking for the next data set to include response rate data and then if that's correct, could you maybe remind me about roughly how many patients we might see in that first data clinical update once you get that in the clinic and things rolling. Thank you very much.

Yes. So Chris, let me just comment on that, until the IND is accepted and we know exactly what the Phase 1 or Phase 2 program looks like. I think we'd rather hold off on giving too much – we just can really say very much about how many patients in, when and things like that. So we'll say much more about that once the IND is accepted and we know exactly what the FDA is agreed to in terms of our clinical program.

Got it. Thank you so much.

Our next question comes from the line of David Lebowitz from Morgan Stanley. Your line is open.

Hi, this is Ishmael on for David. Thank you for taking our question. Piggybacking the IND for 5613, can you just give some guidance on when we should expect to hear more strategies on the monotherapy versus the combination opportunities and more specifically considering the mechanism for the menin inhibitor, which combinations would be logical to consider? Thanks.

Sure. So I think, obviously the IND is filed really just on the monotherapy and I think what we'll be able to convey in more detail after the IND is accepted is what the initial program would be in monotherapy. There's a variety of different combinations that could make sense and that we're thinking about and exploring. But I don't think we'll be in a position to say much more about the combination program until probably little further down the line.

Okay. Thanks for the color. And separately for the Phase 1 for 6352, the data presented in the second half. Can you remind us of what type of efficacy data we should expect to see from the study? Thank you.

Sure. So again, just to clarify, I don't know that we've specifically said we'll have a scientific presentation of data. The trial is set up as a dose escalation trial in patients with GVHD. So it's a combination of both getting safety and efficacy. There'll be small numbers of patients and we're using the sort of accepted chronic graft versus host disease efficacy or Michael, you can comment on what the tool we use for assessing efficacy.

Yes, it's a standard tool used to assess GVHD. So it's not at all associated with any tumor type or basic anticancer response, its specifically for GVHD patients and it's based on multi-organ systematic responses, based on the consensus instrument.

Okay. Great, thank you.

Our next question comes from the line of Harshita Polishetty from B. Riley FBR, your line is open.

Hey, good afternoon everyone. Just one question from me, with regard to your menin inhibitor and MLLr and NPM1 mutant leukemias, you've indicated that you are targeting patients who have failed initial therapies. So I was hoping you could provide some additional color on what the initial induction therapy is for these patients. I mean, I think you have previously mentioned that these patients are treated with essentially first-line option for AML or ALL, but the challenge is that they obviously don't respond well. So any additional info on what the response rates and duration of response looks like for these patient subsets in first-line would be helpful. Thank you.

Yes. Hi Harshita, thanks so much for your question. So I’d just to clarify, so all of these patients are treated with conventional therapy today. The practicing physicians will generally know who their MLLr patients are and their NPM1 mutant patients are both from standard chromosomal analyses and from sequencing. And so they will receive standard induction therapy. And for the most part go into remission just as would any patient newly diagnosed patients with one of these diseases. The main challenges that they have a high relapse rate and so we would anticipate, again, we'll have more details once we have the IND approved, but we would anticipate treating patients who have failed standard therapy or therapies. And again, that is a little bit of a moving target of course, there are new agents being tested in both ALL and AML. So exactly what regimens patients have previously had and failed before they come onto our trials, I think we'll be able to say more about that once the IND is approved.

Great. Thank you Briggs, that's helpful.

[Operator Instructions] Our next question comes from the line of Joel Beatty from Citi. Your line is open.

Hi. Thanks for taking my questions. The first one is on the Phase 3 breast cancer trial for entinostat, could you discuss, what makes the Q2 2020 analysis, definitely the final analysis, is there a potential that it could go past that or is it in the protocol that will be the last analysis?

Right. So Joel, the way what the protocol specifies is the final analysis for the trial is when there are 410 events. So the final analysis is an event driven analysis. Based upon our modeling of when we think the 410th event would occur that's where we say it could be as early at the end of this year or it could be in the spring of next year. So it's not – the protocol doesn't specify a time that the trial will be analyzed, it specifies the number of events. So it's just a question of how long it takes for the 410 events to accrue.

Got it. Thanks. Then another question on the trial, could you discuss the bar set for the futility analyses and then also the alpha that's been spent so far and what remains further remaining of overall survival analysis. Thanks.

Yes, so I don't think, there's a publication that describes the overall design of the trial and the statistics that went into the trial. But I don't think in that publication they specifically describe the rules around futility. So I'm not sure that that's in the public domain, you can imagine some of the standard rules that people use at any point that hypothesize hazard ratio is below the 95% considering all the point estimate, some people use that as evidence that you're not going to ever achieve a positive trial. But I don't think the formal rules have been described in the public domain for this trial. So I think the – I forgot your second part of your question.

I think you have answered the futility part and then also on the alpha spent so far and what remains?

So the alpha spent overall for all of the interim analyses doesn't add up to very much. I don't know that we've ever described exactly how much is spent at each interim analysis, but if you go through all of those and you have to go to the final 410 events, it's a relatively modest amount of alpha spent.

Right. Got it, thank you.

We have no further question at this time. I will now turn the call back to Dr. Morrison.

Great. Well, thank you everybody for joining the call. I thank you for all of your questions. We assume we'll meet up with many of you in Chicago later this month. And again, if you have any other questions along the way, please feel free to contact us.

Ladies and gentlemen, this concludes today's conference call. Thank you everyone for joining. You may now disconnect.