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Edited Transcript of SNDX earnings conference call or presentation 6-May-19 8:30pm GMT

Q1 2019 Syndax Pharmaceuticals Inc Earnings Call

WALTHAM Jun 8, 2019 (Thomson StreetEvents) -- Edited Transcript of Syndax Pharmaceuticals Inc earnings conference call or presentation Monday, May 6, 2019 at 8:30:00pm GMT

TEXT version of Transcript

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Corporate Participants

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* Briggs W. Morrison

Syndax Pharmaceuticals, Inc. - CEO & Director

* Michael A. Metzger

Syndax Pharmaceuticals, Inc. - President & COO

* Michael L. Meyers

Syndax Pharmaceuticals, Inc. - Chief Medical Officer & Senior VP

* Peter Ordentlich

Syndax Pharmaceuticals, Inc. - Co-Founder & Chief Scientific Officer

* Richard P. Shea

Syndax Pharmaceuticals, Inc. - CFO & Treasurer

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Conference Call Participants

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* Chris Shibutani

Cowen and Company, LLC, Research Division - MD & Senior Research Analyst

* Christopher N. Marai

Nomura Securities Co. Ltd., Research Division - MD & Senior Analyst of Biotechnology

* Harshita Polishetty

B. Riley FBR, Inc., Research Division - Analyst

* Ishmael Izakiel Gyimah Asante

Morgan Stanley, Research Division - Research Associate

* Joel Lawrence Beatty

Citigroup Inc, Research Division - VP & Analyst

* Madhu Sudhan Kumar

Robert W. Baird & Co. Incorporated, Research Division - Senior Research Analyst

* Robert Cummins Hazlett

BTIG, LLC, Research Division - MD & Biotechnology Equity Research Analyst

* Melissa Forst

Argot Partners, LLC - VP

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Presentation

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Operator [1]

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Good afternoon, ladies and gentlemen, and welcome to the 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.

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Melissa Forst, Argot Partners, LLC - VP [2]

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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 would ask you to please turn to the forward-looking statements on Slide 2.

Before we begin, I would like to remind you that any statement 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 reports 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'm pleased to turn the call over to you, Dr. Briggs Morrison, Chief Executive Officer of Syndax.

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [3]

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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 2 incredibly exciting opportunities. The first is we are anticipating a positive readout of E2112, our Phase III trial of entinostat in hormone receptor positive breast cancer and the subsequent filing of our first NDA and the corresponding launch of our first product. I want to again emphasize that a positive overall survival trial in hormone receptor positive HER2-negative breast cancer would be a landmark result and will 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 and 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 '19 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-Akron 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 remain 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 III 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 6 months and positive outcome at any of the OS interim analyses or upon achieving the final number of events needed to conclude the study will allow us to file for regulatory approval, based upon the terms of our breakthrough therapy designation in hormone receptor metastatic breast cancer and the special protocol assessment process we went through with the FDA.

The Data Safety and 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'd 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.

Now that CDK4/6 therapies, most notably Ibrance, are being used increasingly as first-line agents, there's a clear unmet need for a therapy that will be effective in patients who have 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 thus, 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 attacked the 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 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, and 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 summarized the status of this program. The IND is on track to be filed later this quarter, with the Phase I/II clinical program to begin soon thereafter. Once the IND is approved, we'll able to provide the final details of our Phase I/II clinical program, however, we can say that our goal is to enroll adults with MLLr leukemias followed by children with MLLr leukemias. And we also intend to enroll adults with NPM1 mutant 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 TRK 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 an important value driver.

Let me now briefly return to our entinostat ENCORE clinical 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 also look for biomarkers that could predict clinical benefit. Slide 8 shows that the immunologic environment is quite variable in different tumor types. The ENCORE results to date indicate that the beneficial effect of entinostat is strongly evident in inflamed tumors, but not in the other immunologic settings. So we believe this is an important conclusion of our work.

Slide 9 summarizes our findings recently presented at AACR. Consistent with prior data, we see a strong signal of combo benefit when entinostat is combined with KEYTRUDA in patients with non-small cell lung cancer, the disease has progressed after both chemotherapy and the PD-1 antagonist. We've also identified a biomarker peripheral blood classical monocyte 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 both the PD-1 inhibitor and a CTLA-4 inhibitor. We're specially 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 currently lack alternative options. As we discussed on our last quarterly call, following the availability of positive E212 OS results, we will determine whether to advance the entinostat PD-1 combination program into 1 or more registration trial.

Let me now turn to Slide 10 and SNDX-6352, our potential best-in-class monoclonal antibody targeting the CSF-1 receptor. We initiated a trial testing 6352 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 symptoms. 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 -- the transactions that we have completed to acquire both 6352 and the Menin-MLLr program 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 the competitive advantage in closing agreements. We need to expend significant effort 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?

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Michael A. Metzger, Syndax Pharmaceuticals, Inc. - President & COO [4]

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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 3 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 served to limit the amount of dilution to our existing shareholders at a 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'll now turn the call over to Rick to review our financial results. Rick?

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Richard P. Shea, Syndax Pharmaceuticals, Inc. - CFO & Treasurer [5]

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Thank you, Michael. Results of our operations for Q1 2019 and a 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 Q1 was an 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 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 noncash stock compensation expense.

For the 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 noncash 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.

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [6]

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Thanks very much, Rick. At the 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 are 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 the 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 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 programs.

With that, I'd like to open the call for questions.

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Questions and Answers

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Operator [1]

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(Operator Instructions) Our first question comes from the line of Bert Hazlett from BTIG.

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Robert Cummins Hazlett, BTIG, LLC, Research Division - MD & Biotechnology Equity Research Analyst [2]

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I have 2. First on the Menin-MLLr program. There was some discussion 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?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [3]

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What your second question, Bert?

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Robert Cummins Hazlett, BTIG, LLC, Research Division - MD & Biotechnology Equity Research Analyst [4]

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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?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [5]

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Okay. So I'll take the first one and 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 I think Bert's question is around the monocytes and it's applicability to melanoma.

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Peter Ordentlich, Syndax Pharmaceuticals, Inc. - Co-Founder & Chief Scientific Officer [6]

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Yes. 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 long cohort.

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Robert Cummins Hazlett, BTIG, LLC, Research Division - MD & Biotechnology Equity Research Analyst [7]

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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?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [8]

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Bert, this is Briggs, I'll take that. So I don't know we have 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 for other biomarkers. So it is certainly something that is a consideration, but until we decide whether to go forward with either one of those programs, we probably don't have to say too much about exactly what the details would be of that program. But it is a consideration.

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Operator [9]

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

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Madhu Sudhan Kumar, Robert W. Baird & Co. Incorporated, Research Division - Senior Research Analyst [10]

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So first one is when we're looking back at ENCORE 301, kind of looking at the protocol, it appears that the protocol allows patients who are on entinostat plus exemestane to 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 the entinostat arm stayed on entinostat therapy post progression?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [11]

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So your question, Madhu, is about ENCORE 301?

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Madhu Sudhan Kumar, Robert W. Baird & Co. Incorporated, Research Division - Senior Research Analyst [12]

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Yes.

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [13]

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Yes. I don't know. Peter, do you know the answer of that question?

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Peter Ordentlich, Syndax Pharmaceuticals, Inc. - Co-Founder & Chief Scientific Officer [14]

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All patients came off at the time of progression. I don't -- nobody was continued on theentinostat after disease progression.

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Madhu Sudhan Kumar, Robert W. Baird & Co. Incorporated, Research Division - Senior Research Analyst [15]

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

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [16]

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

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Peter Ordentlich, Syndax Pharmaceuticals, Inc. - Co-Founder & Chief Scientific Officer [17]

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Sure, it's a good question. And we've thought about that quite a bit as we got our data and the BOLERO-2 data readout and a few other trials of the exemestane. It wasn't too far off if using the -- I think it was the investigator-assessed or the central-assessed BOLERO, 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 those 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 furthermore 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.

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Madhu Sudhan Kumar, Robert W. Baird & Co. Incorporated, Research Division - Senior Research Analyst [18]

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Okay. Great. If I can squeeze one more in. So thinking about the Menin-MLLr inhibitor, so now that they're 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 inhibition of the Menin-MLLr interaction?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [19]

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

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Operator [20]

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

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Chris Shibutani, Cowen and Company, LLC, Research Division - MD & Senior Research Analyst [21]

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With 5613, it is obviously one of the molecules that's going to go into the clinic. And I think there are several other 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 will be helpful for context.

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [22]

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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 [Ciro'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 2, is I think too early to be able to say because we don't know exactly which molecule they are taking forward. But I would say that at some point, it will be great for people to be focused on the differentiation between 2 active agents. So 6 months from now, when we have good efficacy data and maybe they also have a little bit that is probably more relevant question.

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Chris Shibutani, Cowen and Company, LLC, Research Division - MD & Senior Research Analyst [23]

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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 this current plan in the event that for instance, the E2112 does not read out until mid-2020? If you feel the need to perhaps once done, make other considerations because I noted 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, [probably about there]?

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Richard P. Shea, Syndax Pharmaceuticals, Inc. - CFO & Treasurer [24]

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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.

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Operator [25]

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

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Christopher N. Marai, Nomura Securities Co. Ltd., Research Division - MD & Senior Analyst of Biotechnology [26]

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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 this point and then future points, what the plans would be to continue to press commercialization? And then secondly with respect to that in different geographies, would you be open to potentially partnering the asset? Can you walk us through some of your thought process there around commercialization? And then 1 follow-up if I may.

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [27]

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

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Michael A. Metzger, Syndax Pharmaceuticals, Inc. - President & COO [28]

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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, as you know, is a global launch. And our reach probably doesn't extend outside 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, we're not -- we have not undertaken to build a sales force as of yet. I think a small company like 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 forecasting 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.

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [29]

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You want to comment on geography?

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Michael L. Meyers, Syndax Pharmaceuticals, Inc. - Chief Medical Officer & Senior VP [30]

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Yes. And so I think I -- the comment about geographies, as I said we're 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, in China now, but 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 the other geographies including part of the U.S. and help us there as well. So we have, as I said earlier, some options to flex depending on how we make out.

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Christopher N. Marai, Nomura Securities Co. Ltd., Research Division - MD & Senior Analyst of Biotechnology [31]

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Just with respect to that, maybe could you further elaborate on aspirations to have your own sales force? 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 and how is Syndax thinking about that?

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Michael L. Meyers, Syndax Pharmaceuticals, Inc. - Chief Medical Officer & Senior VP [32]

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Yes, I know, it's a great question. And I think 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. And so that's not unattainable for a small company like Syndax. The menin inhibitor obviously focused on leukemia, but they are all oncologists and so there is some overlap there and there's some -- certain specialists who we would -- and academic centers that we would focus on. So that's probably a smaller need in terms of 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 -- we'll be actively thinking about that when the time comes. Certainly something we aspire to.

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Christopher N. Marai, Nomura Securities Co. Ltd., Research Division - MD & Senior Analyst of Biotechnology [33]

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Got it. And then with respect to menin, just a followup 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 clinical update once you get that in the clinic and things rolling?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [34]

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Yes. So Chris, let me just comment on that. Until the IND is accepted and we know exactly what the Phase I or II program looks like, I think we'd rather hold off on giving too much -- we just can't really say very much about how many patients and when and things like that. So we will say much more about that once the IND is accepted, and we know exactly what the FDA has agreed to in terms of our clinical program.

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Operator [35]

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

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Ishmael Izakiel Gyimah Asante, Morgan Stanley, Research Division - Research Associate [36]

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This is Ishmael on for David. Piggybacking on 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?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [37]

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Sure. So I think the -- 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 till probably little further down the line.

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Ishmael Izakiel Gyimah Asante, Morgan Stanley, Research Division - Research Associate [38]

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Okay. And separately for the Phase I 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?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [39]

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Sure. So again, just to clarify, I'm -- I don't know that we have 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.

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Michael A. Metzger, Syndax Pharmaceuticals, Inc. - President & COO [40]

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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. It's specific to GVHD patients, and it's based on multi-organ systematic responses based on the consensus instrument.

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Operator [41]

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Our next question comes from the line of Harshita Polishetty from B. Riley FBR.

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Harshita Polishetty, B. Riley FBR, Inc., Research Division - Analyst [42]

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Just one question for me. With regard to your menin inhibitor and MLLr and NPM1 mutant leukemias, you've indicated that you're 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 think you have previously mentioned that these patients had treated with essentially first-line options for AML or ALL, but the challenge is that they obviously don't respond well. So any additional info on what the response rate and duration of response looks like for these patient subsets in first line would be helpful.

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [43]

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Yes. Harshita, thanks so much for your question. So 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. They're -- the main challenge is 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.

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Operator [44]

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(Operator Instructions) Our next question comes from the line of Joel Beatty from Citi.

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Joel Lawrence Beatty, Citigroup Inc, Research Division - VP & Analyst [45]

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So the first one is on Phase III breast cancer trials for entinostat. Could you discuss what appears -- what makes the Q2 '20 analysis definitely the final analysis? Is there a potential that it could go past that or is it in the protocol that, that will be the last analysis?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [46]

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Right. So Joel, the -- what the protocol specifies is that the final analysis for the trial is when there are 410 events. So the final analysis is based -- 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 as 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.

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Joel Lawrence Beatty, Citigroup Inc, Research Division - VP & Analyst [47]

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Got it. And 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 for the remaining overall survival analysis?

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [48]

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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 is in the public domain. You know there -- you can imagine some of the standard rules that people use, if at any point the hypothesize has a 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.

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Joel Lawrence Beatty, Citigroup Inc, Research Division - VP & Analyst [49]

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

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [50]

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So the alpha spend 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.

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Operator [51]

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

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Briggs W. Morrison, Syndax Pharmaceuticals, Inc. - CEO & Director [52]

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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.

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Operator [53]

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