Ladies and gentlemen, thank you for standing by. And welcome to the Syndax First Quarter 2020 Conference Call. At this time, all participants lines are in a listen-only mode. After the speakers’ presentation there will be a question and answer session. [Operator instructions]I would now like to hand the conference over to your speaker today, Melissa Forst with Argot Partners.Thank you. Please go ahead now.

Thank you, operator. Welcome and thank you to those of you joining us on the line and the webcast this afternoon for a review of Syndax's first quarter 2020 financial and operating results.I am Melissa Forst with Argot Partners, and with me this afternoon to discuss the results and provide an update on the company's progress are Dr. Briggs Morrison, Chief Executive Officer; and Rick Shea, Chief Financial Officer. Also joining us on the call for the question and answer session is Michael Metzger, President and COO; 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 to the Company's website. So I'd ask that you please turn to the forward-looking statements on Slide 2.Before we begin, I'd like to remind you that any statements made during this call that are not historical are considered to be forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the Risk Factors section in the company's most recent quarterly report on Form 10-Q as well as other reports filed with the SEC. Forward-looking statements represent the Company's views as of today, May 7th only.A replay of the call will be available on the Company's website at syndax.com after the call. And with that, I am pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer.

Thank you very much, Melissa, and thank you to everyone joining us on today's call and webcast. Before we get started, I'd like to take a moment to acknowledge that we are actively monitoring the ongoing COVID-19 pandemic to assess any potential impacts to our business.Our number one priority is of course, the health and safety of our employees, as well as the patients and medical professionals involved in our ongoing clinical programs.At this time, we do not anticipate any interruption or delays to our ongoing clinical programs, nor do we expect any impact on our financial guidance. We will continue to monitor the evolving situation, and we'll provide updates as necessary.Let us now turn to Slide 3, which provides a high-level summary of our current corporate priorities, as we strive to realize a future, in which people with cancer live longer and better than ever before. As we had anticipated, 2020 is turning out to be a tremendously exciting and transformative year for our company.Since our last call in March of this year, we have presented the first clinical evidence that inhibition of the menin-MLL1 interaction by SNDX-5613, our Menin inhibitor can induce response in patients with MLL-r acute leukemias and we announced the successful addition of approximately $100 million to our balance sheet under attractive terms.Moreover, the final overall survival readout of E2112 will occur this quarter, bringing us closer to a potential near-term FDA filing, approval and launch in hormone receptor-positive metastatic breast cancer.Finally, we continue to collect data that will further clarify the potential of our anti-CSF-1R antibody, axatilamab to treat chronic graft-versus-host disease.So let's review each of these opportunities in greater detail. Slide 4 summarizes the design of the Phase 3 trial of entinostat in hormone receptor-positive HER2-negative breast cancer. The trial randomized 608 patients to exemestane, plus placebo versus exemestane plus entinostat and the focus of this trial is now on the final overall survival analysis.The final analysis will be conducted once there are 410 events, which, based on our modeling and recent discussions with ECOG, we believe will occur before the end of June this year. A positive outcome would allow us to file for regulatory approval in the United States, based upon the terms of our breakthrough therapy designation in hormone receptor-positive metastatic breast cancer and our special protocol assessment with FDA.Our team is prepared to submit a regulatory filing, should the trial be positive within about six months of receiving the data from ECOG, which would set us up to launch entinostat in 2021. The trial has 80% power to detect a hazard ratio of 0.75 and the maximum hazard ratio that would yield a statistically significant positive trial is approximately 0.82.Based upon the design assumptions, if E2112 achieved a hazard ratio of 0.82, that would indicate that patients receiving the combination had about a five month improvement in median overall survival.Slide 5 emphasizes the potential for the entinostat-exemestane regimen to be the preferred agent after a first-line aromatase inhibitor, which is typically given either as a single-agent or in combination with 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. Thus, we should have a highly relevant dataset in the post-CDK4/6 patient population.In our opinion, the rapid adoption of CDK4/6 inhibitors, such as Ibrance in the first-line setting, underscores the desire of physicians and patients to improve the outcomes associated with anti-estrogen therapies. In the setting of a positive E2112 result, we would expect entinostat to achieve similar widespread use.This population of patients is substantial with an estimated 34,000 patients in the U.S. 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.Importantly, we will be prepared to launch entinostat in the U.S. on our own. We are actively building out our internal commercial team to ensure we are well-positioned for the potential launch of entinostat in 2021, while currently entering into discussions with potential rest-of-world commercial partners.Slide 6 emphasizes the clinical potential of entinostat in hormone receptor-positive breast cancer. In preparation for launching entinostat, we have conducted qualitative market research with community physicians and breast cancer experts. We tested a conservative profile, essentially the minimum benefit that could provide a positive OS result in E2112.We consistently heard from both groups of physicians that there is a high need for novel agents in hormone receptor-positive breast cancer and that they find the potential ability of entinostat to resensitize patients to endocrine therapy to be a very attractive feature of entinostat.Not surprisingly, they uniformly saw overall survival as the most important efficacy endpoint and believe that an agent that could extend survival and lengthen the patients' time on hormone therapy with minimal impact to their quality of life made a very compelling profile.We remain confident in the potential for E2112 to be a positive trial and are eager to bring this potentially important new medicine to patients.Let me now turn to Slide 7 and SNDX-5613, our genetically targeted agent. On our last call, we highlighted two premier publications, one in Cancer Cell and one in Science that provides a scientific rationale and preclinical validation of our ongoing clinical trial.Those publications did not involve the use of our development candidate, SNDX-5613. Therefore, we were quite excited to be selected to present the preclinical profile of SNDX-5613 at the AACR New Drugs on the Horizon Session last month. I will not review the details of that presentation, it is available on our website, but I will summarize a few key points.First, our molecule is a potent and specific inhibitor of the menin-MLL interaction. The only off-target activity of note is its relatively weak binding to the HER channel. And second of clinical relevance, SNDX-5613 is metabolized by CYP3A4.On Slide 8, we summarize the detailed experiments that were conducted to derive a model of the plasma exposures we think will be needed in patients to drive efficacy.We were, of course, pleased that, as shown on Slide 9, the second patient in the trial and the first patient in the trial with an MLL-r rearrangement had plasma exposures that exceeded the levels we anticipated would be required for efficacy and indeed went on to achieve a complete response. Importantly, clinical activity was observed rapidly by day 28 of therapy.No dose-limiting toxicities were observed and the only treatment-related adverse experience was a grade-two QTc prolongation. Of note, this patient was on a concomitant medication that inhibits the activity of CYP3A4, which may account for the disproportional PK exposure relative to what we had anticipated.Full details on additional patients are included in the AACR presentation that's available on our website.The updated first-in-human trial in the Accelerated Understanding of Menin Inhibition or AUGMENT program is the AUGMENT-101 trial and is shown schematically on Slide 10. This first-in-human clinical trial is a combined Phase 1 and Phase 2 trial.The Phase 1 portion is a dose-escalation trial designed to identify the maximum tolerated dose and a recommended Phase 2 dose of SNDX-5613 in two independent cohorts of patients with relapsed or refractory leukemia.Arm A enrolls patients who are not on a strong CYP3A4 inhibitor and Arm B enrolls patients who are on a strong CYP3A4 inhibitor at the time of enrollment. The first 28 days of dosing serves as the period in which safety is evaluated for determining dose escalations.As required by the FDA, patients do not need to have a specific genetic abnormality to enroll in the Phase 1, 2 study. As of the time of the AACR presentation, we have completed our evaluation of cohorts one and two in Arm A and are evaluating a single patient at dose level three.No dose-limiting or grade-two toxicities have been observed to-date. And at the time of the AACR presentation, in Arm B, we had no dose-limiting toxicities and have expanded to a three-plus-three design given one grade-two toxicity.Our intent is to define a recommended Phase 2 dose for each cohort. Once the recommended Phase 2 doses are established, a Phase 2 trial will proceed to enroll three distinct expansion cohorts, each of which consists of a specific genetically-defined relapsed or refractory acute leukemia.The three cohorts are, adults with MLL-r Acute Lymphoid Leukemia, or ALL, adults with MLL-r Acute Myeloid Leukemia, or AML, and adults with NPM1 mutant AML. Our intent is to have specified dosing guidelines for patients in Phase II derived from these two cohorts in Phase 1.The Phase 2 portion will further characterize the safety of SNDX-5613 and will provide an initial estimate of the complete response rate as the primary measure of therapeutic benefit. Additional updates from the Phase I portion of the AUGMENT-101 trial are anticipated in the fourth quarter of this year at a medical conference. We do not anticipate any further updates before the fourth quarter.In addition, we are eager to advance this molecule into the pediatric population as a key component of our overall strategy. We will have more to say about the details of the pediatric timing and approach on our future call.We know pediatric leukemias with MLL-r rearrangements represent a significant unmet medical need and we are eager to work with the pediatric oncology community to bring SNDX-5613 to their patients.Let me now turn to Slide 11 and axatilamab, formerly known as SNDX-6352, our potential best-in-class monoclonal antibody therapy targeting the CSF-1 receptor. Results from the multiple-ascending dose trials exploring axatilamab alone and in combination with durvalumab in patients with solid tumors were presented last week during the virtual AACR meeting.These results demonstrated the tolerability and robust pharmacodynamic biomarker modulation of axatilamab and underscored its ability to promote rapid and sustained depletion of circulating pro-inflammatory monocytes at all dose levels tested.As you know, we initiated a trial testing of axatilamab as monotherapy in chronic graft-versus-host disease and the rationale for using a CSF-1R inhibitor against this disease as shown on Slide 12. Chronic GVHD is a frequent complication of hematopoietic stem cell transplantation, wherein donor-derived immune cells contribute to the initiation and development of fibrosis and the myriad manifestations of the disease.In preclinical models, blocking the CSF-1, CSF-1R pathway with anti-CSF-1R antibody can result in the depletion of donor macrophages, thereby preventing and reducing chronic graft-versus-host disease. We believe chronic GVHD represents an important clinical opportunity.Last year, we released the initial data from our Phase 1 trial, which is diagrammed on Slide 13. The Phase 1 portion is a dose-escalation trial designed to identify the maximum tolerated dose and a recommended Phase 2 dose of axatilamab for the treatment of chronic graft-versus-host disease.We have released the data from the first five patients enrolled in the first three cohorts and have now modified the trial to include a Phase 2 cohort at the one milligram per kilogram dose. We will continue the Phase 1 trial to formally define the recommended Phase 2 dose and may open one or more additional Phase 2 dose cohorts, as well.Finally, Slide 14 summarizes the transactions that led to the acquisition of the Menin-MLL-r and axatilamab programs. We believe that we will be able to continue to expand our pipeline through the acquisition or in-licensing of quality differentiated assets.We believe we have the necessary skill to evaluate and identify high-quality assets and the clinical development experience to bring these compounds through valuable inflection points. We expect to remain among preferred partners of such transactions.I'll now turn the call over to Rick to review our financial results. Rick?

Thank you, Briggs. The results of our operations for the first quarter of 2020 and the comparison to the prior year quarter are included in our press release. So I won't repeat them in these remarks. Additional financial details will be available in our first quarter Form 10-Q, which will be filed today.I would like to point out that our operating loss for the first quarter was $15.2 million, but a non-cash charge of $3.9 million was recorded in the quarter due to the adjustments of the strike price on our series 1 and series 2 warrants, bringing our reported net loss attributable to shareholders to $19.1 million and this is described more fully in our 10-Q.Turning to Slide 15, we ended the first quarter with $99 million in cash and 36.1 million shares and prefunded warrants outstanding. This cash balance included the proceeds from a $35 million equity offering and a $20 million term loan we closed in February.Earlier this week, we closed on another equity offering of 5.6 million shares at $18 with net proceeds of $93.7 million. And following this recent equity offering, the total number of common shares and prefunded warrants is now 41.7 million.Looking ahead, I'd like to provide financial guidance for the second quarter of 2020. Our financial guidance for the second half of 2020 will be issued after we get the results of the E2112 study. We expect our operating expenses for the second quarter of 2020 to increase over the first quarter of 2020.R&D expenses for the second quarter will increase primarily due to increased development activities for SNDX-5613, our Menin inhibitor. Second-quarter G&A expenses are expected to be similar to the first quarter's G&A.For the second quarter of 2020, we expect R&D expenses to be $12 million to $14 million and total operating expenses to be $18 million to $20 million, including approximately $1.5 million of non-cash stock compensation expense.Given our cash from the recent equity offering and our operating expense guidance, we expect to end the second quarter of 2020 with approximately $175 million of cash, which gives us the financial flexibility to take advantage of key development milestones well into 2021.Now, I'd like to turn the call back over to Briggs.

Thanks very much, Rick. As I hope you have appreciated from my prepared remarks, 2020 is a busy year for Syndax with several very important and exciting data readouts close at the end. We believe that a positive OS result in E2112 would be transformative for Syndax and create significant shareholder value. We anticipate a final readout very soon.We also believe that SNDX-5613, our Menin-MLL-r inhibitor, is now significantly derisked. We have many questions to answer, but we believe we have the skill and resources needed to advance the program and potentially enable early regulatory clarity.And finally, we are excited about the early results we are seeing with axatilamab in chronic graft-versus-host disease and look forward to presenting updated data from this program at the end of the year. With our recent highly successful financing, we are comfortable that we have the financial resources to get us through these key upcoming milestones.Finally, we are optimistic that we will continue to identify and bring in novel molecules to deepen 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 wonderfully talented team here at Syndax, our collaborators and most importantly, the patients, trial sites and investigators involved with our clinical programs. In addition, I'd like to thank our committed long-term investors who are helping us build this great company and to welcome the new investors who joined in that effort with our recent financing.With that, I'd like to open the call for questions. Operator?

[Operator instructions] And your first question comes from the line of David Lebowitz.

Thank you very much for taking my questions. Going into the menin Phase 1 studies, did you anticipate that the CYP3A4 inhibitors would impact the PK of the therapy? And I guess when you are moving toward the second stage at some point, will you be bifurcating any doses dependent upon whether or not the patients are on these inhibitors?

Hi, David. Yes. Thanks for your question. So, we did indeed anticipate that the combination of 5613 with a drug that is known to inhibit – strongly inhibit CYP3A4 would lead to higher plasma exposures. In preclinical models or preclinical assays, the drug is primarily metabolized by CYP3A4. So, that was anticipated. We obviously have to characterize that in patients in terms of its magnitude, and that's what we're doing carefully now with the arm A arm B separation.In terms of what we would do in Phase 2 with regard to dose, after we finish the dose escalations in arm A and arm B, if it turns out that the magnitude of the increase due to CYP3A4 inhibition is rather modest, then we may say there is just a recommended – one recommended dose.If that increase in exposure is more notable, then we may have a dose that we recommend for Phase 2 and a dose adjustment if patients are on a strong inhibitor, an approach that's not uncommon for drugs that are metabolized by CYP3A4.

That makes sense. And in general, these patients - what is their prognosis versus patients that don't have these mutations?

Well, so the – if you take patients with acute myeloid leukemia who have MLL-r rearrangements, that tends to be a bad prognostic group of patients. They are generally treated as aggressively as a physician can treat them, because they know they have a bad prognosis and unfortunately, even with that aggressive therapy, they still do worse than your average patient with AML.Patients who have NPM1 mutations, there's a spectrum. Some patients have only an NPM1 mutation with no other mutation. And those patients tend to do somewhat better than your average patient with AML. And then, there are patients who have an NPM1 mutation with additional mutations and those patients tend to do again, worse than your average patient with AML.

Thank you for that. Thanks for taking my questions.

Your next question is from the line of Christopher Marai, Nomura.

Hi. Good afternoon. Thanks for taking the question. It's Chris Marai from Nomura. I was wondering if you could perhaps elaborate on the opportunity in NPM AML with respect to this menin inhibitor. Obviously, you've got some pretty good data in the fusion setting, but I am wondering how you expect that to kind of map out as you go into the NPM1 mutants. And then secondarily, as you think about sort of the registration path forward for the agent, do you expect NPM1 AML to be sort of a separate registration path from the rearranged patients? And I have got a follow-up. Thank you.

Chris, thanks for your questions. So, first, in terms of the NPM1 population, if we look at our preclinical data, we see a robust anti-leukemic effect, both in the MLL-r population and in the NPM1 population, if you will, the negative control for that is, for example, BCR-ABL ALL where we don't see any activity.So we do think there is a good evidence from the preclinical data that the drug should also work in NPM1. We have not enrolled – and as you saw at the AACR presentation, there was not an NPM1 patient enrolled yet. We believe that the investigators participating have been – many of them have a particular interest in MLL-r.And so, I think that's where that enrichment has come from. But we do hope to get patients with NPM1 and if nothing else, the Phase 2 portion, of course has a dedicated NPM1 cohort.In terms of the registration path, it's uncertain at this point of whether the path would be for a broad label for a variety of lesions or if there were different labeling language for patients with MLL-r versus NPM1. I think our base assumption is that, they would be labeling for MLL-r and NPM1.

Okay. That's helpful. And then, just, with respect to your dose-escalation trial, it seems you got higher than anticipated exposures due to CYP inhibition in some patients at low doses. And I was just wondering where you are in that dose escalation? And how many more dose levels do you think you have to get through to reach similar exposures without patients with the CYP inhibition augmented exposure? Thank you.

Right. So arm A of the trial is patients who are not on a strong CYP3A4 inhibitor and as I mentioned in my prepared comments, we've cleared dose-level one and dose-level two, and we are now on dose level three.If you look at the plasma exposures for patient number two, who was on dose-level two, but had sort of a disproportionate exposure relative to the first patient, we could sort of maybe hypothesize that dose level four or five might be equivalent exposures in the absence of a strong inhibitor. So, what dose level might be getting close to a recommended Phase 2 dose, it could be the level we're at, it could be four, it could be five.On the arm with CYP3A4 inhibitor, again, at the time of the AACR presentation, we have not seen any dose-limiting toxicities. So we will continue to dose escalate there. We, of course, are and that second patients saw very nice exposure. So we may not have as many steps to go up there. But time will tell.

Excellent. Thank you. Appreciate the color. Congratulations.

Your next question is from the line of Chris Shibutani.

Thank you very much. Briggs, again, congratulations on the AACR data update. I have two questions. One, you made clear that the preclinical data that's been shared so far has been on the tool compound 469.Can you give us a sense for, number one, whether we'll be seeing some preclinical data on 5613? And how you would characterize 5613's profile to just be distinguished from 469 in ways that you will hypothesize may translate to something in the clinic, which I recognize is a challenging transitional question, but I'll ask it anyway.

Right. So Chris, as you pointed out, the publications have all been with 469. 5613 is in the same structural class as 469 and was chosen from a variety of molecules, because of its biopharmaceutical properties. The first portion of the AACR presentation was our – a fairly detailed description of the preclinical profile for our development candidate for 5613.That was really why we were excited about being able to present. So, I think there, you can get a pretty good view of the preclinical profile of the molecule. And as I said, I think the thing that differentiated, from our point of view, pre-clinically was really the biopharmaceutical properties. And thus far, at least 5613 is turning out to have the biopharmaceutical properties that we predicted.

Great. And then, turning to where we are today, your line about skill and resources are at hand to enable “early regulatory clarity”. Having the sort of maybe greater confidence of the resources that you do have on hand now, particularly on the balance sheet, specific ways in which maybe you are changing or modifying or thinking differently about the level of aggression that you pursue clinical development with 5613? And does that at all change as a result of the E2112 outcome?

Yes. So, I wouldn't say that our – I think we've tried to be appropriately aggressive on the development of the menin inhibitor. We were – we thought it had a very attractive preclinical profile. We've tried to move the trial along quickly.As I mentioned, we are in the process of working with pediatric oncologists to try to put together a pediatric plan. So I don't think the plan has changed. I think, obviously, the financial resources to make sure that plan gets executed are now a bit more stable, and nor do I think that that plan changes dramatically based upon the results of 2112.Obviously, if 2112 is positive, there is a tremendous focus of the management team to get ready for the filing and the launch. But that will not detract from the team who is committed to the menin program.If per chance 2112 is not positive, I do think the company is in very good shape, having both the menin program and the GVHD program, which we find both of those programs are quite promising, and the resources we have would be dedicated to those programs.

And then finally, on the graft-versus-host, do you anticipate that the data that we're hoping to have at the end of the year will put you in a position to make a go versus no-go decision? I think historically, you guys have had very good discipline about being able to make those kinds of decisions, given the opportunity set and resources you have. Thanks.

Yes. Thanks for that comment, Chris. We do hope that, by the end of the year, data we have will allow us to make a decision of whether we want to go into a registration trial for GVHD. But as you pointed out, we'll try to be pretty disciplined in looking at the data and deciding whether it warrants further development.

Great. Thanks for the updates.

Your next question is from the line of Joel Beatty.

Hi guys. This is Shawn Egan calling in for Joel. Thank you for taking my question. Two from me today. First, on 5613. I know at the AACR presentation, it was noted that five pediatric patients were dosed and you mentioned that you are looking to pursue that indication as well.I guess from a high-level from a scientific or a genetic perspective, the disease is fundamentally different between adults and children, And how is it best to think about the potential of 5613 in the pediatric population? And I have a follow-up, as well.

Right. Excellent. Thanks for the question. So, I think going into this, we thought that the pediatric population might have a slightly higher probability of the drug working simply, because the MLL-r ALL, in particular, in children tends to be otherwise genetically silent. You don't see a lot of other co-mutations. You just see the – what we hypothesized was the MLL-r driver.So, if any thought, it might have a slightly better chance. Of course, older adults who've had other chemotherapy or have had a chance for their tumor to develop other mutations may in fact be a little less likely. But time will tell. But I don't think we think of the pediatric population as being less likely than the adult population.

Okay. That's helpful. And then, on axatilamab, can you remind us of what organ systems you've observed that benefit in and the longest duration of response? And based on the organ systems, are there any insights to be gained into what other indications you could pursue after – on the graft-versus-host disease?

Yes. So again, it's only five patients, and at the time that the data was released, there were only four patients that had made it through the evaluation period. So I think it's a little hard early on to say, which organ systems we will and which organ systems we won't.We've clearly seen organs benefit in the gastrointestinal system, hepatic GVHD and you may see in our corporate deck very impressive benefit to a patient who had skin graft-versus-host disease. The preclinical data would suggest that both skin and lung seem to be particularly amenable.But, I think that does relate to the earlier question of we'll be able to make a go, no-go decision, part of that will be dependent on what organ systems we see a benefit in and the durability of those. As you may know, in the GVHD world, the NIH consensus criteria for evaluating efficacy scores - efficacy at about six months after starting dose.So one does need to see a good degree of durability. And your question about which organ systems, that's yet to be determined as we enroll more patients.

Great. Thank you so much, Briggs.

The next question is from the line of Peter Lawson.

Hi. Thanks for taking my question. So Briggs, just on 5613. Just your thoughts around which arms could potentially generate better efficacy or safety when we think about AML and ALL versus NMP1. Any thoughts around that would be great?

Right. So, we tend to – as the preclinical data would suggest that it's really the MLL-r translocation and whether it's ALL or AML. The time course of response and perhaps the type of response may vary a little bit between ALL and AML. But, generally speaking, we see benefit independent – it's really about the MLL-r.So, I think, thinking about MLL-r ALL versus MLL-r AML, I don't think we think, again, what time will tell. We have to do the clinical experiments. But I don't think we think of those as being too different. NPM1, I think – I think the question – the valid question still is, does the drug work in NPM1?Nobody has yet shown efficacy in patients with NPM1 mutant AML. Again, our preclinical data suggests that we should, but until we do, that one is still, I guess one could say that's not validated yet in that disease and we'll keep trying to find patients who we can validate it.Again, based on preclinical data, we would expect the efficacy to be comparable across all three arms in the Phase 2 portion, but time will tell.

Great. Thank you. And then just on the data we’re expecting in 4Q from the program, I mean, would that be press release? Is it data at a conference or an Analyst Day? Just anything around the timing or venues would be great. And do you think we could potentially have an NPM1 patient by then?

So, what we've guided is, that it would be at a medical conference in the fourth quarter. And there is a hematology conference that's typically held in the fourth quarter. If it's held this year virtually or live, none of us know at this point. But that's sort of where I think most likely there would be an update. Whether we'll have NPM 1 patients enrolled by then is a little hard to tell.I think there is a little bit of potential that new patients coming onto the trial at this point may actually be a little further enriched for MLL-r since we've already seen efficacy there. And those patients don't have a lot of options. So we are speaking with our investigators and do hope to get patients with NPM1 mutations on. But there is the potential that in fact, there will be more enrichment for MLL-r given the activity that's already been seen.

Great. Thank you so much. Thanks for taking the question.

Your next question is from the line of Madhu Kumar.

Hi. Thanks. This is Jack dialing in for Madhu. I know you touched on this in the opening remarks. But with respect to COVID, I was wondering if you could comment as to how the dose escalation of axatilamab trial is going? Have you seen any effects there, I guess?

I would say, of our three programs, that's the one that perhaps there is a little bit of an impact. They are outpatients with acute leukemia who need to be treated immediately. We've been able to continue to enroll patients.And our guidance that there'll be updates on completed Phase 1 and early data from Phase 2 by the end of the year. We still feel very comfortable with. But the enrollment may have slowed just a tad in that study.

Awesome. Thanks so much for taking the question.

Your next question is from the line of Bert Hazlett.

Yes, thanks. Congratulations on all the progress. Just want to follow-up on a little bit of the discussion you were having earlier with regard to the expansion of the patients in AUGMENT. Briggs, do you think you would ever just focus the expansion on MLL-r patients specifically, given the data you have and save NPM1 for a later time? Or are you still committed to the full expansion in all three groups?

Yes. Bert, thanks for the question. Just for the - the three arms run concurrently, but independently. So all three arms would be open. We would be enthusiastic about filling all three as fast as possible. If for whatever reason one of the arms filled up more quickly and there was promising and exciting data in that arm.It goes to one of the earlier questions, it wouldn't preclude a potential regulatory path in one population while the other one continues to enroll. But I don't think we would intentionally slow down any of the arms. All three will be open and we would work just as hard to get patients into all three arms.

Okay. And then just with regard to the recent raise and the strategic flexibility that they provide you, you had some other programs with entinostat. Would there be a consideration at this point of a reconsideration of further entinostat data or prosecution of the activity there, assuming success in 2112?And/or how aggressive are you being with regard to additional licensing? I know you've had material success there. But does this additional bolstering of the coffers help you with that? Thanks.

So, first, I would take the entinostat question. We have intentionally decided to wait until we see the results of 2112. We, as you know, we had – we thought some pretty promising data in combination with pembrolizumab, both in lung cancer and in melanoma. We consciously decided to put that on hold and focus the attention of the company on what we thought were our best opportunities, including the breast cancer trial and the menin program.And then, GVHD hit, so we've been focused on that. If 2112 is positive, I think there is two buckets of things we would think about in terms of further investment in that molecule. One would be additional life cycle management opportunities in breast cancer, of course. So you already have one positive Phase 3.The question is, are there other trials in different populations of breast cancer patients where we could test the drug? And then, we would also have the question of are there other – do we go back and relook at the data we had had in both lung cancer and melanoma and see whether those are worth investing in. And then we'd have to trade-off, which are the best uses of our capital.So, that's the way we think about that if 2112 is positive. I think if 2112 is negative, we'll have to do a lot of deep analysis to decide whether we would want to do anything more with entinostat, having not had a positive Phase 3 trial and having these wonderful opportunities with both menin and 6352. So that's something we have to look at should we - should it turn out that 2112 is not positive.

Okay. Thank you.

[Operator Instructions] I am showing no further questions at this time. I would now like to turn the conference over to Briggs Morrison, CEO.

Thanks very much, operator. And again, thank you, everybody, who has joined us on the call and the webcast today. As I said, I thought that 2020 would be an exciting and transformative year for our company and we are on that path. So, thank you all for your interest and perhaps the next time we talk to you, we'll have results from 2112.

Ladies and gentlemen, this concludes today’s conference call. Thank you for participating. You may now disconnect.