Good day, ladies and gentlemen, and thank you for standing by. Welcome to Syndax Fourth Quarter and end of the year 2018 Earnings Call. [Operator Instructions] As a reminder, this conference may be recorded. I would now like to turn the conference over to Melissa Forst with Argot Partners. Please go ahead.

Thank you. Welcome, and thank you to those of you joining us today for Syndax's fourth quarter and 2018 full year financial and operating results conference call. Joining us this afternoon for prepared remarks will be 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 are Michael Metzger, President and Chief Operating Officer; 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 please ask that you 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 is considered to be forward-looking in nature for 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 annual report on Form 10-K as well as other reports filed with the SEC. Any forward-looking statements represent the company's views as of today, March 7, 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 please turn the call over to Dr. Morrison.

Thank you very much, Melissa. And thank you to everyone who is joining us on today's call and webcast. As we closed out 2018 and entered 2019, we took the time to look back in what this management team has accomplished over the past 3.5 years. Our goal has been to build a pipeline of opportunities that will allow us to reach our mission, that will allow us to realize a future in which people with cancer live longer and better than ever before. And as we were closing out 2018, we concluded that we have too many opportunities for our company of our size and resources. And so through conversations with physicians, scientists, advisers and members of our board, we've prioritized our portfolio. The work was difficult. We've had many passionate advocates inside and outside our company for every one of our active programs, and we believe that all are active programs have potential to benefit patients. And yet, we had to choose the ones we thought had the most potential. Today I'm going to share with you the results of that prioritization effort and explain our reasoning. Slide 3 provides a high-level summary of our prioritization effort. As we progress through 2019, we'll be focusing our resources on 2 incredibly exciting opportunities. First, we are anticipating a positive readout of E2112, our Phase III trial of entinostat in hormone receptor positive breast cancer; and a subsequent filing of our first NDA and a corresponding launch of our first product. I would emphasize that a positive OS trial in hormone receptor positive HER2- breast cancer would be a landmark result that will be transformative for Syndax and its shareholders. We believe the entinostat opportunity in hormone receptor positive breast cancer carries blockbuster potential. This is an important opportunity for us, and it will require our focus and resources. Second, we anticipate a second quarter filing of the IND for SNDX-5613, our potential first and best-in-class targeted agent for the treatment of mixed lineage leukemias along with the rapid initiation of our broad 5613 clinical program. 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 for our company. We may have early clinical data from the program later this year. We believe that the breadth of indications we will investigate with SNDX-5613 represents a second completely distinct blockbuster opportunity. This, too, is an important opportunity for us, and it will require our focus and resources. Given these 2 tremendous opportunities, we've chosen not to move forward at this time with our entinostat KEYTRUDA combination trial in non-small cell lung cancer. It's a very difficult decision for us given the strong data we have seen the our ENCORE 601 program in both non-small cell lung cancer and melanoma, and yet, we believe our near-term focus on E2112 and 5613 is the right thing to do for our company. I will also note that we announced today that neither ENCORE 602 nor 603 met their primary endpoint. These results were not a material factor in our decision to refocus our resources, and I will say more later about why we don't think the results of 602 and 603 inform our view of the non-small cell lung cancer and melanoma results. Let me now turn to Slide 4 and give an update on our Phase III trial of entinostat and hormone receptor positive HER2- negative breast cancer, the first area of focus for 2019. Slide 4 again summarizes the trial design. The trial randomized 608 patients to exemestane plus placebo versus exemestane plus entinostat, and the focus of this trial is now clearly and unequivocally an overall survival. As we've noted before, OS interim analyses are done approximately every 6 months, so the next interim OS analyses will be around May and November of this year. Positive outcome at any of these interim analyses or upon achieving the final number of events needed to conclude the study would allow us to file for regulatory approval based upon the terms of our special protocol assessment with FDA. The final analysis of this trial will be conducted once there are 410 survival events. We don't know exactly when those 410 events will occur. But based upon modeling that we've done, we think that the final analysis could be November of this year, although it could drift into May of 2020. We remain very confident in the possibility that E2112 will achieve a survival benefit, and hence, our decision to keep our focus on this opportunity. Recall that it was the Phase II OS results that led to the granting of the breakthrough therapy designation by FDA. And as I have summarized previously, based on results of the Phase II trial, combined with the statistical design of E2112, we always believed the OS endpoint was more likely to be positive than PFS in E2112. Hence, the fact that PFS did not achieve a very high prespecified statistical hurdle does not in any way diminish our confidence in the possibility of achieving a survival benefit in E2112. We also know that OS is the most valued endpoint for patients, physicians, regulators and payers, and hence, a positive OS trial would enable both rapid regulatory review and potentially rapid payer access. Slide 5 emphasizes the blockbuster potential for the entinostat exemestane regimen to be the preferred agent after a CDK4/6 therapy for hormone receptor positive HER2- breast cancer. We know that CDK4/6 therapies, most notably, Ibrance, are being used increasingly as first-line agents, but there's a clear desire to understand what therapies will be affected in a patient who has stopped responding to a CDK4/6 inhibitor. Our current estimate is at between 30% and 50% of patients in E2112 will have received a CDK4/6 inhibitor prior to entering the trial, and that's when we will have a highly relevant dataset in the post-CDK4/6 patient population. This population of patients is relatively large, with an estimated 34,000 patients each year will go on to receive hormone therapy after failing first-line therapy and could therefore potentially be eligible to receive entinostat. We're also very excited about the upcoming IND filing for our genetically-targeted agent, SNDX-5613 and I would therefore like to spend some time describing that program for you now. Slide 6 points out the similarity between our Menin program and other medicines that had been developed to attack 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, which led to the development of gleevec and other BCR-ABL inhibitors. Since then, there have been additional examples, where scientists have been able to develop medicine that specifically attacks such fusion proteins that result from a chromosomal translocation, including medicines against EML4-ALK fusions, NTRK fusions and RET fusions. These fusion proteins, which are the result of a chromosomal translocation, have been a very fruitful area of oncology drug development given the strong evidence that the fusion protein is driving the cancer cell. The development of such medicines is enabled by being able to precisely define the patients, leading to large treatment effects in specific patient populations in a rapid clinical development and regulatory path. I want to emphasize that our Menin program is an example of a targeted therapy that is designed based upon our understanding of a specific chromosomal rearrangement that leads to a specific fusion protein known to drive the leukemic process. Slide 7 shows a simplified view of the MLLr fusion protein. The left half of the fusion protein comes from a protein called MLL1, and the right half of the fusion protein comes from another protein. The fusion protein never appears in a normal cell. It is only found in leukemic cells. The left half of the fusion protein binds through a protein called menin, and our drug blocks that binding and, hence, blocks the ability of the fusion protein to work. This is -- we've studied that at the crystal structure level, as shown on the right panel on this slide. Menin interaction is shown schematically on Slide 8. On the left figure, you can see that the MLL1 fusion protein bound to menin assembling a large multiunit machinery that causes abnormal production of a variety of proteins that cause leukemia. On the right figure, you can see that SNDX-5613 blocks the ability of the fusion protein to bind to menin and stops the abnormal production of downstream proteins that cause leukemia. The cancer cells then normally differentiates and die. I want to again emphasize that 5613 is targeted to inhibiting the action of a specific fusion protein found only in cancer cells, which is like other medicines that have been designed to work against cancer-specific fusion proteins. On Slide 9, we summarize the status of this program. The IND is on track to be filed in the second quarter of this year, with the Phase I/II clinical program to begin soon thereafter. We will be enrolling adults with MLLr leukemias, followed by children with MLLr leukemias. We'll also be enrolling adults with NPM1 mutant leukemia based upon a very compelling preclinical data showing SNDX-5613 has promising activity in that disease as well as was recently presented at ASH this past December. I want to emphasize we see a rapid and straightforward clinical development path for SNDX-5613, like the path taken for patients with NTRK fusions or IDH1 mutations. We expect that the molecule should have the single-agent activity, and it's quite possible we could observe clinical activity very early in the clinical development path, again unlocking significant value for Syndax and its shareholders. 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 for our company. We therefore have chosen to focus our resources in developing this targeted therapy as rapidly as possible. Let me now turn to our ENCORE clinical trial program, in which we've tested entinostat in combination with PD-1 pathway antagonists, either PD-1 antibodies or PD-L1 antibodies. I'll remind investors that this program was set up as a signal-seeking program exploring different tumor that have different immunologic characteristics. We've also invested in looking for biomarkers that could predict clinical benefit. With today's announcement of the results of ENCORE 602 in triple negative best cancer and Encore 603 in ovarian cancer, we have now essentially completed the signal-seeking program. Slide 10 shows the immunologic environment is quite different in different tumors, with lung cancer and melanoma often being infiltrated with T cells, colorectal cancer and triple negative breast cancer being characterized as having T cells but for some reason they organize around the rim of the tumor and are excluded and ovarian cancer being generally categorized with an absence of T cells. We asked whether entinostat would enhance the activity of PD-1 pathway antagonist in different clinical settings based upon a variety of preclinical observations. It appears that the beneficial effective of entinostat is evident in the inflamed tumors and not in the other immunologic settings. I think this is an important conclusion of our work. Slide 11 summarizes our findings. We've seen a strong signal of clinical benefit when entinostat is combined with KEYTRUDA in patients with non-small cell lung cancer, whose disease have progressed after both chemotherapy and the PD-1 antagonist. We've also identified a biomarker, the peripheral blood class monocytes that appears to predict clinical benefit in this population of patients. In addition, we've seen a strong signal of clinical benefit when entinostat is combined with KEYTRUDA in patients with melanoma, whose disease has progressed after both a PD-1 inhibitor and a CTLA-4 inhibitor. Updates on both of these exciting programs will be presented at AACR. Indeed, we've been notified that each of these will be the subject of an oral presentation. Based on the data in our ENCORE studies, we previously communicated our intention to initiate a registration study in a biomarker-defined subset of non-small cell lung cancer patients, the ENCORE 607 study. And we believe the ENCORE 601 data also warrants moving forward in melanoma. We will be reviewing the updated data to be presented at AACR with our partners and remain open to partnering opportunities with entinostat in both non-small cell lung cancer and melanoma. However, as a result of our prioritization efforts, we've decided to defer the initiation of the non-small cell lung cancer 607 study as well as any melanoma registration study pending the results of E2112. Rick will discuss the impact of this decision on our financial guidance. Let me now briefly turn to Slide 12 in SNDX-6352, our potential best-in-class monoclonal antibody therapy targeting the CSF-1 receptor. As you may recall, the monotherapy, multiple ascending dose study in cancer patients is ongoing, as is the combination of 6352 with IMFINZI, AZ's PD-L1 inhibitor. And we anticipate selecting a randomized Phase II dose next quarter. Our chronic GVHD trial is also underway, and we anticipate initial efficacy data from that trial in the second half of the year. Finally Slide, 13 summarizes how the transactions that we have completed to acquire both SNDX-6352 and SNDX-5613 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 expand significant efforts in this area, and we consider this capability to be a core strength of our company. And with that, I'll turn it over to Rick for the financial update.

Thank you, Briggs. The results of our operations in Q4 full year 2018 and the comparison to the prior year periods are included in our press release, so I won't repeat them in these remarks. Additional financial details are available in our Form 10-K, which we have just filed this afternoon. Turning to Slide 14, we ended 2018 with $80.9 million in cash and 26.8 million shares outstanding. The net change in cash for Q4 was a decrease of $8.7 million. The operating cash burn of $14.8 million was offset by $6.1 million of net proceeds from our ATM, and we currently have $31 million available to [sell off] the ATM. Looking ahead, Slide 14 shows our updated financial guidance for both Q1 and for the full year of 2019. For the first quarter of 2019, we expect R&D expenses to be $11 million to $13 million and total operating expenses to be $15 million to $17 million, which includes approximately $1.5 million of noncash stock compensation expense. For full year 2019, 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 noncash stock compensation expense of $6 million and interest income runs approximately $2 million, so our net cash burn for 2019 is expected to be $52 million to $56 million. This projected cash burn for 2019 is approximately $8 million lower than our previous guidance due to the pause in initiating entinostat I/O registration studies in either non-small cell lung cancer or in melanoma, as Briggs discussed, and to further focusing our operating activities on our highest priority programs. Our current cash, along with 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 SNDX-5613, our targeted menin inhibitor. So now I'll turn the call back over to Briggs.

Thanks, very much, Rick. I would like to close our call with a clear summary of our company priorities. We believe that a positive OS result in 2112 will be transformative for Syndax and creates significant shareholder value. Although we believe that a positive 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 SNDX-5613, our menin MLLr inhibitor. We expect that the molecule could have single-agent activity, and it's quite possible that we could observe clinical activity early in the clinical development path, again, unlocking significant value for Syndax. We are prepared to get through the initial proof of concept data from this program, which could take us into mid- to late 2020. We remain extreme excited about our data in lung cancer and melanoma. Updates from both of those programs will be the subject of oral presentations at AACR. And we believe it is prudent to pause our further development spending in I/O until such time that we receive the positive results of E2112. Rick has outlined our financing plans, and we want investors to be clear that we are not currently forecasting registration programs in lung cancer or melanoma in our financial guidance. For SNDX-6352, we remain on track to select and recommend a Phase II dose in solid tumors in the second quarter of this year and anticipate having initial efficacy data in chronic GVHD later in the year. Finally, we continue to aggressively look for additional molecules or technologies to bring into our portfolio. I believe 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 would 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] And our first question comes from the line of Christopher Marai with Nomura Instinet.

I was wondering if you could help elaborate a little bit on the recommended Phase II dose data that we might be seeing for 6352 in combo with PD-L1. What other data are you going to provide there beyond a recommended Phase II dose? Will you also look at target engagement measures, other measures around sort of the -- like I said, patient tumor microenvironment, et cetera? And then I have a follow-up.

Right. So Chris, this is Briggs. It's the -- I think you've probably seen some of the PK/PD data that we presented from the normal healthy volunteers. We'll be confirming that in the combination trials with PD-1 and the recommended Phase II dose. So I think that's the main.

And Chris, this is something -- we'll certainly be presenting data on both PK as well as important PD parameters, such as CSF-1 levels, IL34 levels, target engagement, monocyte depletion. Those will all go in predetermination of what the appropriate RP2 data is.

Great, got it. That's very helpful. And then I guess just another one, if I may. Regarding the path forward for some of those entinostat I/O programs, I understand the whole point of -- look, I guess that's sort of pending the results of entinostat in breast cancer. In the event that entinostat does not produce an OS result in breast cancer, would you be open to reopening -- reevaluating these programs and entinostat specifically in the I/O programs or not? How should we sort of think about that?

Yes. So I think Chris, our base assumption is that based on the strong Phase II data, that 2112 will be positive. So we haven't really given too much guidance around what would happen if that wasn't the case and what we would do with the I/O program.

And our next question comes from the line of Chris Shibutani with Cowen.

For 5613, I look forward to you guys introducing that into the clinic. Can you help us a little bit frame the opportunity? In particular you talked about potential best-in-class and the options of treatment. So could you just give us a sense for the MLL-rearranged as well as the NPM1 leukemias? What kind of percentage we believe of the AML population these may be? And then when you're thinking about the initial monotherapy use, on what line or what stage of clinical treatment are these patients that you're thinking about in this initial Phase I/II work that you're doing?

Chris, so again, I think you nicely laid out there essentially 3 different populations that we've been talking about. There's MLLr, rearranged leukemias that occur in kids, which is generally ALL. And then there's the mixed-lineage leukemias that occur in adults, which is roughly -- which is generally AML. For the pediatric ALL, the worldwide incidence is probably about 1,000 patients a year, about 10% of ALL. If you've ever heard of an infant being born with ALL, about 80% of those are these MLLr, rearranged leakemia. So that's the pediatric ALL. In adult AML, it's about 6% to 10% of AML, about 5,000 patients a year. The NPM1 mutant population represents about 1/3 of all AML, so that gives you some rough numbers around the size of the opportunity. In terms of the patient population that we would study, of course, we'll be studying relapsed/refractory patients in, again, pediatric MLLr rearranged leukemias, adult MLLr rearranged leukemias and adult NPM1 leukemias.

So you make 2 statements on Slide #9, potential best-in-class. Can you help us understand what data you've seen so far, be it preclinical or anything early, that would support how you're defining that? And then with fast to market, we're certainly seeing in the AML so much development of novel treatments over the last 3 or 5 years or so. Can you talk about standard screening protocols? So in existence already are these mutations that are being screened for?

Sure. So again, we think -- we're only aware of one other molecule that is approaching the clinic for this particular target. We really like our molecule. We think it's very clean, very specific, very potent, and hence, the hypothesis that it could be best-in-class. I think that -- what was your second question?

So potential fast to market. Can you talk about standards of screening. Is that what it is today?

Yes. So I think the short answer is yes. NPM1 mutations are standardly screened for -- in patients with leukemia. And the MLLr, again, it's a chromosomal rearrangement, so whether you do even just a chromosomal spread or you do [most] specifically for, these are identified today. So what we've heard from all of our investigators, again, these will relapsed/refractory patients, but they know at a time the patients are diagnosed that they have these genetic lesions. And so we don't think we'll have much problem identifying the patients that would be candidates for our therapy.

And in terms of the background therapies, the potential monotherapy benefit, would we assume that these patients are not getting some of the standard, for instance, 7+3 chemo in the AML setting? Or just clarify a little bit more what you mean by monotherapy.

Sure. Right. So this would be relapsed/refractory patients. So both for AML, we would anticipate that they would have been treated with 7 and 3. And for the MLLr AML, they tend not to stay in remission very long, so they will have a relapse. We wouldn't be at all surprised if they had received other therapies that are available, whether it's a [3] inhibitor, venetoclax, the things that are around for AML. So that's all up to the physician. They could come in just having relapsed from their 7 and 3 or some re-induction regimen, but they would be relapsed/refractory patients. And again, I think from a single-agent point of view, it's really what we're looking for is clinical activity at the single-agent in patients who have relapsed/refractory disease. Not that different from what I think Agios had with their IDH1 inhibitor.

Our next question comes from the line of Robert Hazlett with BTIG.

This is actually Jake Colby on the line for Bert. I was wondering, what will really give you the confidence to resume development of entinostat PD-1 combinations?

Yes. So Jake, thanks very much for your question. This is really a sort of prioritization effort given the resources that we have available to us. So it's not that we don't have confidence. And as I said, it's kind of interesting that we have 2 oral presentations at AACR. So obviously, the organizers there thought that we had some pretty interesting data. So it's not that we don't have confidence. It's really just our prioritization around our resources. So I'd say when 2112 is positive, if we had more resources, we would go back and revisit these potential investments. But at this point, they're not in our financial guidance.

Great. Okay, that's helpful. And I guess on SNDX-5613, how should we think about kind of trial size and maybe any other kind of comments you can make on potential trial design here? And then how would you define showing proof of concept for the program?

Sure. But I won't say too much more about the details of the trial. I think after the IND is approved and we have a clear agreed-upon detailed trial design, then we'll talk more about it. I think in the AML space, the standard definition of efficacy is a complete response, so we're looking for patients to have complete responses for their AML. And again, I think if you look at the Agios story, it's a good surrogate for the kind of program we'd like to envision.

And our next question comes from the line of David Lebowitz with Morgan Stanley.

Would you be able to, I guess, help run us through the reason why the entinostat PD-1 combos might work in inflamed tumors in a better way than excluded versus non-inflamed?

Yes. David, thanks very much for the question. I'll let Peter Ordentlich take that question, our Chief Scientific Officer. Peter?

Yes, thanks for that question. So we think based on what we've learned, and we'll actually show some of this at AACR, that there's some pre-existing priming or some type of immune activity required in order to see benefit with entinostat. And based on some of the gene expression work that we've done, particularly in the lung cancer cohort, we have some better understanding of what some of those resistance pathways may be and some of -- the way that entinostat may be able to inhibit those. And it just seems that in these harder-to-treat tumors, where the immune activity in general seems to be low, like ovarian and triple negative, we just may not have that pre-existing signal for which entinostat may be able to work on. I think that's reflected by the relatively low efficacy of the immune checkpoints overall in those types of tumors. So I think it's a combination of existing resistance pathways that entinostat can target as well as some pre-existing immune reactivity.

And I guess, could you -- if you could just run us back through -- I know E2112 OS is coming up on the next analysis. Based on what occurred in the Phase II trial, what is, I guess, a similar timeframe that as far OS analysis, that the Phase III could theoretically conclude?

Yes. So I think briefly, the trial could conclude at this upcoming readout in May or it may require going to the full 410 event. I think we're at that point in the evolution of the trial. Remember that there are also futility analyses, which the trial has continued to progress. So based upon that, it could be as early as May or it may take to the final 410 event.

And our next question comes from the line of Joel Beatty with Citi.

The first one is about the focus of your pipeline. It looks like based on the press release, the emphasis is on E2112 trial as well as the Menin program. And then I noticed that CSF-1 program is not on that list. So could you help us understand the difference in focus you see from the early-stage CSF-1R program compared with your focus on the Menin program?

Joel, thank you so much for the question. Again, I think when we look at the -- we like both programs. The CSF-1R program, the single-agent work being done in GVHD will continue. There's not really new work that we or new resources we have to dedicate to that program. It doesn't -- it's not a large burn of our existing resources. I think as we gear up for 5613, that is new resources that we want to make sure we have in place and that people have a focus. And again, as I sort of indicated in my prepared remarks, these diseases that are driven by chromosomal translocations tend to be quite fruitful, so we just want to really make sure we keep our focus on the Menin program. I think if we see activity in GVHD, we'll, again, reevaluate the prioritization. I think the prioritization work that we do is ongoing constantly as new data becomes available. So I think that might help you in thinking about the decisions we've made.

I appreciate it. And another program on the E2112 trial, still some uncertainty on when it will read out. And I imagine that part of what affects that is the P-values that are remaining when compared with what's already then spent. Can you help us understand that and how -- what P also is left and how [is it] among the remaining potential readouts?

Yes. I don't think we've ever disclosed how the P-value gets -- what the thresholds are at each of the interim analyses. What we can say is that the -- you may remember the trial was set up where .002 of the alpha went to PFS, 0.48 goes to OS. There's a very small amount of alpha that's spent on each of the interim, but we've never talked about what the actual threshold is through each of those interims.

Okay, got it. Then maybe one last question, on partnering. It sounds like it's still an important focus for looking for additional assets. Could you help us maybe just on a high level on what you're looking for? What will make one potential asset more attractive than another?

Yes. So I always joke with my team that the only molecules you want in life are the ones that work. So if it works, we'd be interested in it. So I think we're -- we have sort of a prioritization list on sort of how we think about different molecules and sort of interestingly, we set that prioritization list up a number of years ago when we first joined the company. And tumors that are driven by chromosomal rearrangements and no infusion proteins is actually #1 on our list, and that's why we're so excited when the Menin program became available. So there are a variety of targets that we would be interested in. But I don't think I'd say much more than that.

And our next question comes from the line of Madhu Kumar with RW Baird.

So first one, thinking about E2112. So you've previously talked about preclinical data for CDK4/6 drug, their indiscernible] not affecting entinostat/exemestane response on this. So kind of thinking about the flip side, have you examined whether later line chemotherapies in HR-positive breast cancer respond differently after entinostat plus exemestane? Should it be worse than exemestane alone?

I don't think -- Peter, I don't think (inaudible) will be able to look at that from the Phase II fixed data. And I don't know, either Peter or Michael, if you know the answer to that.

We didn't -- preclinically though, the experiment hasn't been done as to what happens to those types of therapies after treatment with entinostat in the Phase II clinical trial. That was looked at in terms of the balance of the immediate posttreatment as well as overall posttreatment therapies, and those were quite well balanced. But the actual response to those individual therapies was not captured. So we don't know how they did. We just know what they got.

Okay. Then thinking about SNDX-5613, a really kind of simple basic science question. What does the [indiscernible] MLL1 interaction do in normal tissues? And does that biology inform potentially relevant PD biomarkers?

Yes. So MLL1 actually is not that -- the normal MLL1 protein is not that widely expressed in adult tissues. It tends to be -- it's found in embryonic hematopoiesis. So that actually is one of the other reasons why there may be some specificity here because the amino-terminus interaction with menin, at least the MLL1 interaction, you don't see very much in adult tissues.

Okay. So then kind of based on the known kind of interaction base transcriptional effects, is there anything that biology can inform kind of a good biomarker to show the drugs hitting the target in patients?

Yes. Maybe Peter, do you want to talk a little bit about that?

Yes, I'm happy to. It's a great question and one, obviously, that we're interested in. And there's been some very nice work published both with menin inhibitors as well as knockdowns of MLL1 or deletions of the N-terminus. And those all point to certain gene expression signatures, of which several are highlighted and published on the haux [ph] and the MACE 1 [ph] Others involved in hematopoietic differentiation. And so those all potentially represent genes of interest to look at as well as differentiation markers as well as a chromatin modifications that are mediated by these complexes. But obviously, it's a good question and one that's top of our mind as we set up the development to look for these types of assays.

And our next question comes from the line of Harshita Polishetty with B. Riley FBR.

So in regards to your menin inhibitor, as a follow-up to the questions that have been asked, this has been historically difficult to target due to the protein-protein interaction. Briggs, you touched up on the (inaudible) of this molecule in the opening remarks as well as the market opportunity in earlier questions? But I wanted to kind of take a step back and was hoping to gain further insight on the historic failures and challenges of targeting menin and how 5613 addresses these challenges. And if you have any early insights on the differences between yours and [cure's] candidate.

Harshita, thanks very much for your question. I will say when I first heard about the program, so they told me they had a small molecule that disrupted protein-protein interactions, I was as skeptical as you are. Obviously, it's not a very standard thing. What's interesting here is that there are nice crystal structures of the actual amino-terminus of MLL1 binding to menin. It turns out to be a very small 4 or 5 amino acid contiguous segment that sits in the pocket of menin, so it's been well-characterized at the crystal structure level. And it turns out to be highly druggable. So I think it is, and again, we'll be happy to send you some of the references. I think it is one of those "protein-protein interactions" that actually are eminently druggable, and I think we have very good preclinical data to show that. I think the question on how our drug molecule compares to the [cure] molecule, we don't know exactly which molecule they are taking to the clinic, so I think it's a little premature for us to comment on that. We really like our molecule. We're excited about the program. We'll surely, of course, be watching them carefully, but I think at this stage, it's a little bit hard to know how to compare them.

And our next question is a follow-up question from Christopher Marai with Nomura Instinet.

Just on the menin program, I was wondering, obviously, given the pediatric population that's impacted by these diseases, what's your plan for bringing the molecule into kids versus adults? And how should we expect that to progress as you progress the compound for the clinic?

Yes. Chris, so we are extremely interested in the pediatric population. As I said, MLLr ALL is really an unfortunate disease for these little kids, and so we're working hard on pediatric formulation that will allow us to dose both kids and infants. And as part of our discussions, we're trying to lay out a plan that would allow us to move relatively rapidly and seamlessly from initial Phase I trials in adults into the pediatric population. We'll say more about that, of course, once the IND is approved, and we have an agreement from FDA on what that program will look like, but certainly, that's our anticipation at this point.

And I show no further questions at this time. I would like to turn the call back over to Dr. Morrison for closing remarks.

Great. Thank you very much, everybody, for joining us on the call. If you have any additional questions, we'll be happy to take them, and we look forward to further communications from the company. Thanks again.

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