Good morning and thank you all for joining the GlycoMimetics call. At this time, all participants are in a listen-only mode. Following management’s remarks, we will hold a brief question-and-answer session and at that time the lines will be open for you. [Operator Instructions]. I would now like to turn the call over to Shari Annes of the Investor Relations group at GlycoMimetics. Please go ahead.

Good morning. Today, we will highlight the key achievements of the third quarter and provide a summary of our financial results. In addition, with our ASH abstracts now released, we will also use the call to highlight what we'll present in December, including new data from the recently completed Phase I/II clinical trial of uproleselan in AML. The press releases we issued yesterday on the ASH abstracts and earlier this morning on our Q3 financials are available in the News section of the company's website at www.glycomimetics.com. This call is also being recorded. A dial-in phone replay will be available for 24 hours after the close of the call. The webcast replay will also be available in the Investor Relations section of the company's website for 30 days. Joining me on the call today from GlycoMimetics are Rachel King, Chief Executive Officer; Brian Hahn, Chief Financial Officer; and Dr. Helen Thackray, Senior VP of Development and Chief Medical Officer. We will start today's call with comments from Rachel. And after that, Helen will comment in more detail on the latest data from our AML Phase I/II trial. And then, Brian will provide an overview of the company's financial position. We will then open the call for Q&A. I'd like to remind you that today's call will include forward-looking statements based on current expectations. Forward-looking statements contained on this call include, but are not limited to, statements about the development plan for uproleselan, or upro, formerly known as GMI-1271; and for rivipansel, GlycoMimetics' product candidate licensed to our collaborator, Pfizer; and our other pipeline programs. Such statements represent management's judgment and intention as of today and involve assumptions, risks and uncertainties. GlycoMimetics undertakes no obligation to update or revise any forward-looking statements. Please refer to GlycoMimetics' filings with the SEC, which are available from the SEC, or on the GlycoMimetics website for information concerning the risk factors that could affect the company. I'd now like to turn the call over to Rachel.

Thank you, Shari, and thank you all for joining our call. This morning, we'll provide a progress report on our Phase III program in relapsed/refractory AML with uproleselan, as well as on our collaborations with the NCI and HOVON. Importantly, with the ASH abstracts published yesterday, we also want to provide you with our perspective on the broad data set we'll be showing at the ASH Annual Meeting. We've had a very busy past few months across all aspects of the business. Of note, we initiated recruitment in our GMI-sponsored Phase III program in relapsed/refractory AML, with enrollment of the first patient expected shortly. We're working diligently in the US, Europe, Canada and Australia, with a plan to have all territories enrolling patients in early 2019. With regards to the NCI collaboration, we've also made excellent progress. I'd like to emphasize that this randomized controlled registration trial will include a Phase II interim analysis based on event-free survival, or EFS, after the first 250 patients have been enrolled. As you know, EFS supported the approval of Mylotarg in 2017, suggesting that this could be a meaningful endpoint for evaluation in this population. If positive, we anticipate discussing the data with FDA to establish if it's sufficient for an expanded label claim for uproleselan in this newly diagnosed setting. You can now plan the study design posted on clinicaltrials.gov. With respect to our HOVON collaboration, we're continuing to work towards the initiation of this study in Europe in early 2019. With that background, I'd now like to turn your attention to ASH. I'm thrilled to report that this year's six abstracts were accepted for presentation during the conference, including an oral presentation on the final data from our Phase I/II trial of upro in AML. As you know, ASH is the most important meeting of the year for the clinical hematology, oncology research community. As such, it's gratifying to see the breadth and depth of our portfolio selected for presentation during this meeting. I'll now ask Helen to walk through the scientific data published yesterday in the posted ASH abstracts. Helen?

Thank you, Rachel. The data that will be presented at ASH is quite extensive, especially as it relates to the uproleselan Phase I/II abstract and the supporting data on E-selectin as a mechanism of resistance in AML. I'd like to begin by underscoring some of the key takeaways. First, I'd like to emphasize that the new data set from the Phase I/II study includes data from the final locked database. It includes extended follow-up for survival in patients past the time point initially specified in the protocol. We opted to amend the protocol to extend the duration of follow-up and to provide a final data set that now includes fewer patients with censored data for survival, the result of which is our increased confidence in the key efficacy endpoints that underpin our GMI and NCI-sponsored registration programs. Secondly, we now present – for the first time – data on measurable residual disease, or MRD, in each of these AML cohorts as we believe uproleselan selectively disrupts the relationship between leukemic cell and the bone marrow micro environment. We would expect to see a higher percentage of those patients who achieve complete remission to be MRD negative. I'm pleased to report that this is exactly what we see in our clinical trial. Over 50% of the evaluable patients in both the relapsed/refractory and newly diagnosed cohort achieved this stringent level of disease response. Thirdly, correlative data on E-selectin ligand expression on leukemic blasts and leukemic stem cells show that this target is highly relevant, particularly in the relapsed/refractory patient population with higher levels of E-selectin ligand expression correlating with both response and survival in this cohort of patients treated with uproleselan. These data on expression, combined with the data on MRD negativity, further support our underlying hypothesis that E-selectin is a…

Thank you, Helen. Taken together, the new ASH data on the potential benefits of inhibiting E-selectin strongly support our late-stage AML program with uproleselan. We hope that you will agree this is a compelling data set that underscores the breakthrough potential of the work that we and our consortium of collaborators are conducting in AML. As for timing, we expect to announce the enrollment of our first patient in our own study in relapsed/refractory AML shortly, followed by initiation of the NCI and HOVON consortia studies in early 2019. Across our GMI-sponsored, NCI-sponsored and HOVON-sponsored programs, we expect to have over 850 patients treated in Phase II/III clinical programs evaluating uproleselan, which we believe will result in a comprehensive data set for this drug. As you know, upro has received breakthrough therapy designation in relapsed/refractory AML from the FDA. If the results from each of these studies are positive, we expect that the totality of the data with upro could support broad label across the continuum of care in AML. I'd now like to comment on other data you'll see at ASH and also to say a few words about rivipansel. Also accepted at ASH for poster presentation is an abstract that points to the potential use of upro to dramatically enhance the reconstitution potential of mobilized hematopoietic stem cells. We think this is a novel approach to boost the engraftment of stem cells in autologous transplants, but also to potentially boost the efficacy of ex vivo gene therapy approaches, which rely on mobilized HSCs as the starting material. Additionally, we'll be presenting data in two other posters, highlighting two novel compounds in the GlycoMimetics pipeline that we've not previously discussed in public forums. Our poster on GMI-1687, a highly potent antagonist of E-selectin, points to the potential of 1687…

Thank you, Rachel. As of September 30, 2018, GlycoMimetics had cash and cash equivalents of $219.8 million compared to $123.9 million as of December 31, 2017. The company successfully completed a follow-on public offering of 8,050,000 shares, netting proceeds of $128.4 million during the first quarter. The company's research and development expenses increased to $9.7 million for the quarter ended September 30, 2018, as compared to $5.8 million for the prior-year quarter. The increase was primarily due to an increase in clinical trial expenses related to the start-up of the Phase III registration trial and higher manufacturing expenditures for uproleselan to meet clinical trial drug supply obligations for our late-stage clinical programs. The company's general and administrative expenses increased to $2.8 million for the quarter ended September 30, 2018 as compared to $2.4 million for the prior-year quarter. The increase was primarily due to higher patent and other legal expenses. In summary, GlycoMimetics is in an excellent financial position to carry out its planned initiatives and to advance applications for its unique technology platform. I'll now turn the call back over to Rachel.

Thank you, Brian. Before we open the call for your questions, I want to say that I believe we've uniquely been successful in progressing truly differentiated drug candidates from discovery well into late-stage development, an achievement which I hope will reward patients and our shareholders in the near term. With that, I'd like to open the call for your questions.

Thank you. [Operator Instructions]. And your first question comes from the line of Stephen Willey with Stifel. Your line is now open.

Yeah. Good morning. Thanks for taking the questions. I guess, Rachel, just – or maybe, Helen, just kind of curious as to the extent to which you expect to see patients with FLT3 mutations in the Phase III relapsed/refractory trial. I guess, I ask the question just given all of the clinical development that's occurring in that space right now. And then, secondly, I know that there was kind of a discussion regarding whether or not you would think about screening patients for E-selectin ligand expression as kind of a gating criteria for enrollment and the trials that you're running now are in all-comer patient populations. But just given the abstract data here, do you think that there's an opportunity to maybe perhaps even just prespecify as a secondary endpoint activity in those patients with E-selectin ligand expression at baseline?

So, let me add a couple of comments, and then I'll turn it over to Helen for further detail. As far as your point on FLT3, I think it's interesting that you raise that. We also agree that that was a very interesting observation from the data set that the FLT3 mutated patients did have higher levels of E-selectin ligand. And I think that's an important observation, suggesting, again, the importance of this marker, particularly in high-risk disease. And with respect to the screening, I think the simple answer is we don't think that we need to. But let me turn it to Helen for further detail on both of those.

Yeah. So, for FLT3 disease, this is certainly a highly resistant type of disease and, certainly, also then results in patients being refractory or having early relapse or late relapse. So, you would expect to see patients with FLT3 mutations in the relapsed and refractory population. We think that we would expect to see some of those patients in the Phase III trial and we will have that in the data set and would expect to assess that patient population in subgroup analyses to report what we see. We also think that the uproleselan could very well be paired with FLT3 inhibitors. There's several that’s now on the market and also in trials, and this could reasonably be paired with those to improve and deepen the response seen with FLT3 inhibitors. So, we'll look at patients both in the context of the Phase III trial in relapsed/refractory disease and we will look at opportunities to put this together with inhibitors in subsequent trials. With regard to screening or gating for enrollment on the E-selectin ligand, we have remained very confident that we've seen, in our data set, all patients we've assessed, all patients in our trials who we have assessed for the E-selectin ligand, we've seen expression of the ligand on their blasts. So, we believe that it is relevant to all patients. And, therefore, we don't see a need to gate for enrollment in the trial. We also agree that this it is an interesting finding and one that we would, we think, shows strength in the correlation with remission, strength in terms of giving confidence in the outcomes that we're seeing based on the mechanism of the drug. We will assess the E-selectin ligand in the context of our Phase III trial. And so, we will have that data and have an opportunity to look at subgroup outcomes and correlate with expression, but, again, we don't feel that that is necessary for gating. I would point out one other thing, and that is that there are other benefits seen with uproleselan beyond achieving remission. So, while we think remission is important and we see that we've gained confidence in the mechanism with these data, we also see that the ability to be medically well enough, to go on to consolidation, to then deepen remission and consolidation with the addition of uproleselan, and to generally improve the response, but also maintain the patient in health well enough, for example, with reduction in mucositis, you would see them then go on to transplant at a higher rate and you would expect all of those things to improve the overall survival outcomes beyond just the remission rate.

That's helpful. And then, just with respect to the MRD assay that you're going to be using in the Phase III, is that also going to be flow based? I know that there's a lot of different methodologies that are out there right now with respect to either flow or next-gen sequencing. I'm just curious as to which you are selecting for the purposes of Phase III development.

Yeah. So, we are certainly looking at MRD in the Phase III study. We are going to look at it by several different methods and we're doing that in a centralized fashion. So, we'll have data both on a flow-based assay and on DNA-based assay such as NGS. And that data then will be available at the end of the study for comparison between the groups, but also looking at both methods. They are rigorous methods, and so I think the data will continue to be strong.

I think it's also important to emphasize that both with respect to MRD and E-selectin ligand that these assays are going to be centralized and well controlled in the Phase III trial. So, we're going to be gathering data in a very rigorous fashion for the Phase III on both of those endpoints.

Great. Very helpful. Thanks for taking the questions.

Thank you. And our next question comes from the line of Irina Margine with Cowen and Company. Your line is now open.

Hi. Good morning, guys. Just wondering, to follow up on the previous question, what are the rates of MRD negativity in these patient populations based on natural history data? And then, I have one more.

So, I'll take that. The rates of MRD negativity are changing as the sensitivity of assays improves. Generally, rates of MRD negativity are not higher than 40% to 50% in most populations when the current rigorous assays are used. So, for example, specifically, sensitivity of assays presently is generally in the 1 times 10 to the minus 4 level of sensitivity or better. And that is the level at which we have measured this in our trial and that we're reporting at ASH. And so, with that level of sensitivity, usually, MRD negativity is 40 or so percent, maybe up to 50% in some populations. Where we've seen data in the higher-risk populations, it does not reach those higher levels. And so, we have been very encouraged, extremely pleased to see MRD negativity, in this context, over 50% in both groups and actually quite high.

Understood. Thank you. And then, on rivipansel, could you remind us of the differences in the primary endpoint between the previous Phase II study versus the Phase III that will read next year? And sort of when that data comes out, what would constitute a clinically meaningful effect in your view? What should we be looking for in that data?

So, the primary endpoint for the RESET trial, Pfizer's trial with rivipansel, includes a simple checklist that assesses points needed for discharge. It is very similar to the endpoint that we use for the Phase II trial and, therefore, reflects assessment of readiness to discharge in its very similar manner. It's a simple checklist and includes things such as discontinuation of IV opioids and readiness for discharge from the hospital as reported by the patient and the physician. So, that's quite similar to what we saw and what we measured in the Phase II trial. You would then expect to see – what we've heard is that about 24 hours or a day of – a day less of hospital time is clinically meaningful to the patients. And so, you'll be looking for something around that. What we know in the Phase II trial is that we saw an extended difference in the time to discharge from the hospital. It was greater than that. And so, we'll be looking for a day in Phase III, perhaps greater.

Yeah. And I want to add just a couple comments to that. I think there's – one important point about the Phase III is that the endpoint is it's simple, it's standardized, it's rigorously collected. And I think those are all important benefits of the way that the Phase III has been designed relative to what we've learned in the Phase II. And I'd also add on what Helen said that we were very encouraged in the Phase II study that we saw so much improvement in clinically-relevant endpoints. And, again, that's what's been collected in the Phase III data around clinically-relevant endpoints. And, ultimately, that's what's most meaningful to patients, to physicians and to payers. And we're very pleased that we were able to collect data in a very rigorous way around those endpoints, which we think are going to be the most meaningful ones.

Great. And then, maybe I can squeeze just one quick last one. Based on your understanding of the size of the market for sickle cell disease hospitalizations, what do you think is the rivipansel price that's implied by the $1 billion peak sale estimate that Pfizer has released?

Well, I can't speak to the specific pricing assumptions that Pfizer is making on that, but I think that, if you look at the fact that there's roughly 100,000 hospitalizations in the year in the US, it doesn't take a very high number to get to $1 billion if you look only at the US. So, I think that given the numbers of hospitalizations across these major markets, I think there is an opportunity to price the drug in a way that's going to be clinically and pharmacologic – both in terms of clinical and pharmacoeconomic reasons, I think, would be well justified. It's also possible that the hospitalizations actually underrepresent the need for the drug. There are even more patients who present in the emergency room and are not actually hospitalized. And we know that patients are reluctant to seek out care because they don't like going to the hospital. So, it's also possible that a drug that is able to interrupt a crisis once it's underway could potentially drive patients to seek out care. So, I think there are a number of dynamics in the market that could favor the adoption of rivipansel.

Great. Thank you so much. And I’ll see you guys at ASH.

Thanks.

Thank you. And our next question comes from Peter Lawson with SunTrust. Your line is now open.

Thanks for taking my questions. Rachel, just on rivipansel, what do you think we need to really see for that kind of blockbuster potential that Pfizer talks about in that Phase III data? Is it one less stay in hospital? If you can kind of help us kind of frame that of what's needed to be seen.

Yeah. Well, as Helen indicated, we're generally hearing from the community that reductions of a day of hospital stay would be considered both clinically meaningful and pharmacoeconomically meaningful. And so, I think that that type of improvement would certainly drive use because patients want to get out of the hospital faster. Doctors want to get them out of the hospital faster. And, remember, one of the really, I think, compelling observations that was made in our Phase II study was the very significant reduction in the use of opioids. We saw an 83% statistically significant reduction in the use of narcotics in the Phase II study. And I think that that's another benefit, particularly in the context of the crisis that the nation is facing currently with opioid use, I think is also very compelling in terms of the potential adoption of the drug. So, I think there are a number of factors that could contribute to the use of the drug. And the fact that there is really nothing in that setting currently available for those patients.

Got you. Thank you. And then, just the additional cycles of uproleselan in the pivotal, how quickly do you think that plays out? And when do you see the benefit? Does it play out in OS or is it deepening responses? Any guidance around that would be great. Or when could we potentially see the interim for that data?

Well, we're not doing an interim analysis in our Phase III. So, when you see the Phase III data, you'll see the reflection of the full benefit of the drug, including any benefit that we've seen in consolidation cycles. The interim analysis that we've described is an interim analysis planned in this study being conducted by the National Cancer Institute. And, again, to distinguish our studies in relapsed/refractory patients, you'll be seeing a final analysis in the OS for those patients. In the NCI trial, you'll be seeing an interim analysis for EFS. And so, we're looking at different endpoints in those different populations. But I would expect that both of those endpoints could reflect the benefit of the consolidation rounds.

Okay, thank you so much.

Thanks.

Thank you. And our next question comes from the line of Jotin Marango with ROTH Capital. Your line is now open.

Good morning. Thank you for giving us a very dense abstract with the Phase I/II data. My questions on rivipansel were answered, so I'll just focus on AML. The most interesting features of the abstract, in my mind, are the MRD data and the selectin expression because these are completely new. So, let me focus on that. There seems to be a stronger effect on the MRD in the relapsed group, although both of the groups got chemo, different types of chemo and the upro. So, I would have expected a lower exit MRD in the treatment naïve group. So, anyway, I was going to ask yourselves about this trend. Do you think this is something specific to upro or is it the assay? Why are we seeing this dichotomy in the MRD?

I think it's actually not a dichotomy. I think it's an issue of numbers. In the relapsed/refractory group, we have a greater data set. We have patients who are high risk. We have an ability to see them, the effect in a slightly greater data set. And we're seeing that with MRD negativity. We're also seeing it with correlation of the E-selectin ligand expression and the outcomes. In the treatment naïve group, we have fewer patients who are evaluable for MRD. There were 9 who were evaluable out of 25 treated. Greater than half of those did achieve MRD negativity at the time of induction response, which we find extremely encouraging. And I think we just need to see that in a larger trial in order to confirm the outcome. So, we do expect that the drug is – the potential is there for achieving MRD negativity to these greater levels of sensitivity. And I would point out also that these MRD data are before the consolidation cycles are given. And so, once a patient achieves remission, they would then continue to receive consolidation and have the opportunity to deepen that response. We've not seen that in the treatment naïve group so far because we did not have an opportunity to assess MRD after consolidation. And I think we would expect that to improve the [indiscernible] remission and, therefore, the outcomes in the treatment naïve group in the randomized trial.

Got it. Okay. So, that actually brings – transitions nicely to my second question, which was about consolidation. So, this was allowed in the study with upro added. Anything you could tell us about the profile of the consolidation in responders? Was it in the same rates or the same number of cycles that you would have expected in this type of patients?

So, we offered consolidation by protocol amendment in the Phase I/II once we had established safety of the combination with induction. We, therefore, were able to achieve experience with a few patients with consolidation of uproleselan in the Phase I/II, which then allowed us to add it for the Phase III. We did have several patients who went through consolidation with uproleselan in the Phase II portion of the trial. More of those were in the relapsed and refractory group. A few of those were also in the treatment naïve group. And so, we have, I think, at this point, data on a few patients, all of whom did well from a safety perspective with consolidation, some of whom also did very well from a disease perspective with consolidation and we're able to bridge to transplant. That data set in the Phase II is really just in very few patients at this point, sufficient to give confidence that it's a very appropriate course to follow for treatment in the Phase III, but not sufficient to draw a conclusion as to the outcomes of consolidation from numbers in the Phase II.

Understood. Okay. And lastly, a question about the selectin levels, which could lead to very interesting directions in the future, I think, label or not. So, I'm looking at the abstract, and you have put in there these two charts, which are interesting to me. They show this linear relationship, linear sort of Y equals X on the selectin expression and blasts and then leukemic stem cells. And, I guess, my takeaway from that is that the expression is – goes hand in hand. It's not lower or higher in those stem cells than in the blast. And correct that takeaway if I'm wrong. So, my question is, does that linear relationship hold after treatment with upro? Do you have any data, the implication being does upro then sort of selectively target the leukemic stem cells or not? Thank you.

Well, actually, to begin to answer that question, I'm going to point you to some data that was generated in – some preclinical data that was presented at last year's ASH abstract, which did show that chemotherapy in the absence of an E-selectin antagonist actually selects for the cells that are best able to resist chemotherapy, being those that bind to E-selectin ligand. So, what we think happens in the absence of treatment with uproleselan is that the cells that are best able to sequester are able to survive and then become the source of relapse. And the fact that these correlations have been shown in our clinical samples between the blast and the leukemic stem cells suggest that those cells that survived are the leukemic stem cells, the ones most able to propagate the disease. So, I think it's a very interesting observation. And, actually, adding to that and to the point you made at the beginning about the dense abstract, I think it is true and we're very encouraged by the fact that, over time, we've continued to build the supportive data case around the critical role of the E-selectin ligand in the persistence of leukemia. And I'll point you to an abstract that's actually not published by GlycoMimetics, but rather by a group in Europe that looks at the question of E-selectin on leukemic stem cells in CML and also shows an important correlation. So, I'll point you to Daniela Krause’s abstract, which is also at ASH this year. So, I think your point at the very beginning is really, in our view, the takeaway, which is that the new data we have on MRD and on E-selectin ligand does continue to build an important supportive case for the importance of this target. And we think that the studies that we've designed now in Phase III are well designed to capture those important potential benefits.

Very helpful. Thank you, Rachel. Great data. See you all at ASH.

Great. Thanks, Jotin.

Thank you. [Operator Instructions]. And our next question comes from the line of Biren Amin with Jefferies. Your line is now open.

Good morning. This is David Fong [ph] on for Biren.

Good morning, David.

So, just one question based on the data you're showing at ASH this year. The final Phase I/II data on upro, I think the OS is 8.8 months. It looked like it came in just a bit from last year's ASH, which I think you showed 9.4 months. So, does that impact your thinking at all of the stats and the powering around the Phase III or sort of what the expectations are for the benefit that you hope to see of upro over the standard chemo in Phase III?

Hi, David. This is Helen. That's a good question. In short, we don't see it as a difference in overall survival, and I can explain why. It also, therefore, does not change our approach for the Phase III. In fact, I think it gives us more confidence in the approach we're taking for the Phase III. The median OS reported is an estimated median OS by Kaplan-Meier. What we have now is a data set with more patients for whom the actual data is known, the event is achieved, rather than being censored in the data set. That tightens the confidence intervals and gives us more confidence in the numbers. And, in fact, then the median estimate we see is not different. But with a tighter confidence interval, there's more confidence that that truly represents the OS that is being seen. That then allows us to have more confidence in the approach that we took to powering for the Phase III and in use of OS as the endpoint for the Phase III. So, I think we're in a great position with that data. We have a tighter, more robust, richer data set now with the final data set. And we feel quite confident that we have the right design then for the Phase III.

Great, thanks. And maybe just one follow-up one. When we think about the early pipeline and the assets there, how should we think about – or, I guess, have you guys thought about prioritization of that? And when might we see a little bit more color on the next assets to be advanced into the clinic?

Well, I think one of the real substantial opportunities that we have at GlycoMimetics is that we've had such a productive research organization that has continued to generate these novel compounds. We do actually have a third in the clinic currently, which is the 1359 compound that targets both E-selectin and CXCR4. So, we'll be saying more soon about what we intend to do with that, having recently completed a Phase I in healthy volunteers. As far as the earlier-stage assets, the 1687 that we mentioned for the first time now, I think, is an extremely interesting molecule, very much more potent than uproleselan and subcutaneously available. So, that gives us an important potential follow-on for that compound. And moving into the galectins gives us opportunity to get not only into oncology, but also into some of the fibrosis space with those. So, we're going to be actively pursuing, enriching the preclinical data set around those preclinical assets and we'll be moving them into the clinic as we're able to. I think it's important to also emphasize, though, that for the company's operational focus in the very near term, it’s on what we’ve currently outlined, which is our comprehensive development program in AML. But we do feel that the expanding pipeline over time will give us further opportunities to move those into the clinic, either on our own or through partnering.

Great. Thanks for taking the question.

Sure.

Thank you. Ladies and gentlemen, this concludes today's Q&A session. I would now like to turn the call back over to Rachel King for any closing remarks.

Thank you, operator. And thank you, everyone, for your questions and for taking the time to listen to the call. We believe the company is now well positioned to deliver key clinical data readouts over the next several years, in particular, with major news in the second quarter of 2019 with the top line data from the ongoing Phase III trial of rivipansel in sickle cell disease and followed, starting in late 2020, with ongoing data readouts from our wholly-owned uproleselan program. We're excited to have a platform which continues to provide potentially game-changing therapeutic opportunities and we're pleased to have a strong balance sheet that we believe can finance the planned initiatives that we’ve discussed today. We'll be at both the Stifel and Jefferies conferences later this month in New York and London, respectively, and we look forward to continuing to update you on our progress. Thank you.

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