Pete De Spain - VP of IR Troy Wilson - President, CEO Antonio Gualberto - CMO, Head of development Marc Grasso - CFO, CBO

Jonathan Chang - STB Leerink Chris Shibutani - Cowen Joel Beatty - Citi Jay Olsen - Oppenheimer

Good day, ladies and gentlemen, and welcome to the Kura Oncology First Quarter 2019 Financial Results Conference Call. [Operator Instructions] I would now like to introduce your host for today's conference, Mr. Pete De Spain, Kura's Vice President of Investor Relations. You may begin.

Thank you, Sara. Good afternoon, and welcome to Kura Oncology's first quarter 2019 conference call. Joining me on the call from Kura are Dr. Troy Wilson, our President and Chief Executive Officer; Dr. Antonio Gualberto, our Chief Medical Officer and Head of Development; and Dr. Marc Grasso, our Chief Financial Officer and Chief Business Officer. Before I turn the call over to Dr. Wilson, I would like to remind you that today's call will include forward-looking statements based on current expectations. Such statements represent management's judgment as of today, and may involve risks and uncertainties that could cause actual results to differ materially from expected results. Please refer to Kura's filings with the SEC, which are available from the SEC or on the Kura Oncology website for information concerning risk factors that could affect the company. With that, I will now turn the call over to Dr. Troy Wilson, President and CEO of Kura Oncology.

Thank you, Pete. And thank you, all for joining us this afternoon. We've made considerable progress over the past quarter as we continue to focus on the operational execution of our initial registration-directed trial of tipifarnib. The treatment cohort of this global open-label non-comparative trial is designed to enroll at least 59 evaluable patients with HRAS-mutant head and neck squamous cell carcinoma. And I'm pleased to report that it's proceeding and on track. Meanwhile, we've enrolled additional HRAS-mutant HNSCC patients in our ongoing phase two trial which we call RUN-HN. We plan to provide an update from RUN-HN in the second half of the year. We expect that this update will include additional follow-up on ongoing patients in the trial as well as preliminary data on newly enrolled patients in both the HNSCC as well as other squamous cell carcinoma cohorts. Our goal with our registration-directed study is to generate a data package to support an application for marketing approval in HRAS-mutant HNSCC as soon as possible while we work to broaden tipifarnib's potential use to include other diseases of high unmet need. We've also made significant progress toward the identification of farnesylated protein targets as well as the potential mechanistic linkage between farnesyltransferase inhibition and CXCL12. Further supporting the development of tipifarnib in a number of CXCL12-driven hematologic and solid tumor indications. For more on this, I'll turn the call over to Antonio Gualberto, our head of development and chief medical officer.

Thank you, Troy. Among the compelling features of the tipifarnib problem when we licensed it from Johnson were the signs of durable anti-tumor activity upsurge across multiple hematologic indications as well as certain solid tumors. Despite this evidence of activity, the mechanism of action of farnesyltransferase inhibitors has remained elusive for decades. The data we had generated in HRAS-mutant HNSCC provided the strong evidence of activity in tumors driven by these exclusively farnesylated oncogene. However, many of the other tumors in which evidence of activity have been reported, such as lymphomas, myeloid leukemia, pancreatic cancer or breast cancer do not typically correlate as that mutations. In December 2018, at the American Society of Hematology Annual Meeting, we reported primary data from our phase two trial of tipifarnib, a later stage peripheral T-cell lymphoma. The data show a significant association between CXCL12 expression and clinical benefit as well as clinical proof of concept angioimmunoblastic T-cell lymphoma, an aggressive form of PTCL, often characterized by high levels of CXCL12 expression. At the same time, we reported results from an ancillary, non-clinical study which indicated that high CXCL12 expression is, in fact, a negative prognostic factor for a standard of care PTCL therapy. We also showed that tipifarnib can now regulate CXCL12 secretion in models of bone marrow stroma. The preliminary results reported attached validated our observation that the CXCL12 pathway is a therapeutic target of tipifarnib and provided a potential path to expand the development of tipifarnib well beyond HRAS-mutant solid tumors by using CXCL12 related biomarker to enrich for patients most likely to benefit from tipifarnib treatment. Importantly, CXCL12 and its receptors are known to contribute to metastasis. An elevated CXCL12 expression is known to be a poor prognostic factor in patients with certain tumors, including pancreatic cancer. We are increasingly encouraged by our growing body of CXCL12 related data. An outstanding question, however, still remains. What are the molecular mechanisms that relate the inhibition of the farnesyltransferase and sign with the observed anti-tumor activity of tipifarnib in patients with high CXCL12 expression? As previously stated, despite the fact of a number of large pharma companies and academic investigator, have work on farnesyltransferase inhibition for many years. Not the mechanism of such in the clinic have been defined. Last month, at the American Association for Cancer Research Annual Meeting, we reported new findings suggesting that the gene expression of the exclusively farnesyl prodding [indiscernible] is strongly associated with CXCL12 expression in bone marrow stroma. We believe this funding may help us identify a molecular mechanism connecting farnesyltransferase inhibition with a targeting of the CXCL12 pathway by tipifarnib. Individual analysis of a subset of patients from a previously conducted phase 2 trial in the lab refer to lymphoma identified CXCL12 expression as a potential buyer market of clinical benefit from tipifarnib in patients with diffuse large B-cell lymphoma as well as mycosis fungoides, the most common form of cutaneous T-cell lymphoma. These findings provide further evidence supporting the inhibition of the CXCL12 pathway to make it in for such immediate in the activity of tipifarnib in the clinic We believe that CXCL12 pathway biomarkers provide the common mechanistic basis to enrich for political benefit across multiple hematological and solid tumors indications. Now we look forward to providing additional data from the two cohorts in our ongoing phase two trial of tipifarnib in light estate PPPCO, including original response data from the AITL cohort and original data from the CXCL12 positive PTCL cohort. I am pleased to report that this data have been accepted for all our presentation. At birth, there would be a hematological association. And while congress and the international conference of malignant lymphoma, both in June. Meanwhile, we continue our efforts to further elucidate the biology of farnesyltransferase and the specific molecular mechanism for action of tipifarnib, including the identification of genetic mutations potentially associated with a limited CXCL12 expression. And we expect more to say on that either at ICML next month as well. With that, I will now turn the call back over to Troy.

Thank you, Antonia. I continue to be very encouraged by the progress our team continues to make with the tipifarnib development program. The discovery of CXCL12 related biomarkers offers the potential to significantly expand the therapeutic opportunity for tipifarnib as a treatment for patients with cancer. Our development strategy for tipifarnib in CXCL12 driven tumors follows a similar approach that has served us well for the treatment of patients with a HRAS mutant HNSCC. Namely, as we consider potential CXCL12-driven indications, we would seek to prioritize those for which there is the potential for rapid clinical development and an opportunity to move into earlier lines of therapy. Other key elements of this strategy include optimizing dose and schedule, validation of biomarkers that enrich for clinical benefit, evidence of durable clinical benefit, and securing patent protection and/or regulatory exclusivity. Ultimately, we believe CXCL12 pathway biomarkers could enable registrational strategies for tipifarnib in multiple hematologic and solid tumor indications with high, unmet need. In the meantime, we look forward to providing additional prospective data from our ongoing phase two trial of tipifarnib in CXCL12 positive PTCL next month followed by an update from our RUN-HN trial in the second half. Now let's quickly turn our attention to our emerging pipeline programs, beginning with our ERK inhibitor KO-947. KO-947 is a potent and selective small molecule inhibitor of ERK which we're advancing as a potential treatment for patients with tumors that have dysregulated activity in the MAP kinase pathway. Our preclinical data suggests that KO-947 has anti-tumor activity in KRAS or BRAS mutant adenocarcinomas as well as certain subsets of squamous cell carcinomas. We continue to evaluate dosing regiments for KO-974. Our goal is to reach a recommended phase two does or a maximum tolerated dose. And we believe we remain on track to accomplish that goal later this year. We would anticipate providing data on the phase one trial when available. Our third product candidate is KO-539, a potent and selective small molecule inhibitor, the menin-mixed lineage leukemia or menin MLL protein protein interaction. We've generated preclinical data that support the potential anti-tumor activity of KO-539 and genetically defined subsets of acute leukemia, including those with rearrangements or partial tandem duplications in the MLL gene as well as those with oncogenic driver mutations in genes such as NPM1. Our investigational new drug application for KO-539 has been cleared by FDA. And we're preparing to initiate our phase one clinical trial in relapse to refractory AML shortly. With that, I'll now turn the call over to Marc Grasso for a discussion of our financial results for the first quarter of 2019.

Thank you, Troy. And good afternoon, everyone. I'll provide a brief overview of our financial results here on the call and invite you to review our 10-Q filed today for a more detailed discussion. Research and development expenses for the first quarter of 2019 were $10.4 million compared to $11.6 million for the first quarter of 2018. The decrease in R&D expenses for the quarter was primarily due to a decrease in clinical development activities related to our phase two trials of tipifarnib, offset by an increase in clinical development activities related to our registration-directed trial for tipifarnib. We continue to strengthen the research and development team with key hires in the areas of clinical operations and regulatory affairs. General and administrative expenses for the first quarter of 2019 were $4.6 million compared to $3.4 million for the first quarter of 2018. The increase in G&A expenses was primarily due to increases in non-cash, share-based compensation and personnel costs. Net loss for the first quarter of 2019 was $13.9 million or $0.37 per share compared to a net loss of $14.6 million or $0.46 per share for the first quarter of 2018. As of March 31st, 2019, we had cash, cash equivalence, and short-term investments of $165.5 million compared with $179 million as of December 31st, 2018. We remain well-funded through our upcoming milestones and expect that our current cash, cash equivalence, and short-term investments will be sufficient to fund current operations into 2021. With that, I will now turn the call back over to Troy.

Thank you, Marc. This concludes our prepared remarks. But before we jump into Q&A, let me just quickly lay out our anticipated near-term milestones. For tipifarnib, additional data from our phase two trial in AITL and CXCL12 positive PTCL at EHA and ICML in June. Additional data on biomarkers associated with elevated CXCL12 expression at EHA and ICML in June. Additional data from our phase two trial in HRAS-mutant HNSCC and other HRAS-mutant SCCs in the second half of 2019. And additional data from our phase two trial in chronic myeloid monocytic leukemia in 2019. For KO-947, data from our phase one dose escalation trial in the second half of 2019. And for KO-539, initiation of our phase one trial in mid-2019. With that, Operator, we're now ready for questions.

[Operator Instructions] Our first question comes from Jonathan Chang with STB Leerink. Your line is now open.

Hi, guys. Thanks for taking the questions. And congrats on getting all presentations at EHA and ICML. First question, as we look ahead to EHA, can you help set investor expectations on the upcoming PTCL data in terms of how many more patients, how much more follow-up, etc. will there be versus the data we got at ASH? And what do you see as the benchmarks in PTCL? And what would you consider a win in the upcoming data?

Thanks, Jonathan. I'm going to ask Antonio to address your two questions.

Yes. Thank you. So, thank you, Jonathan, for the call. So, the data that we presented at ASH indicated proof of concept in AITL. If you recall at the time, we were still enrolling the CXCL12 positive cohorts. So, without getting into the detail, the intention is to provide it first with the cohort. And the only thing that I can tell you is that they certainly enzyme in some investigators and that it was sufficient to drive toward our presentations from a meeting [indiscernible]. So, certainly, there wasn't a strong interest from those in the field in the outcome of the data that was showing in their study.

Got it. And I guess how much new data will there be Abstract versus the ASH presentation or should we expected to largely be a placeholder for the upcoming presentation?

So, that actually is a good question. So, I can tell you that what you are expecting, basically -- or what I will be expecting -- maybe addressing your initial question -- is for the trial to have reached its objective. And if you recall, the intention was we saw some level of activity. We saw selection. And then we were attempting to reach proof of concept. We checked the level of selection. It is based on histology or based on the marker. And again, based on that outcome, the data has driven toward our presentations.

But Jonathan, just to answer your question, given the timing of those abstracts -- I don't know that I'd say they're placeholders. But the data has continued to mature since then. So, I wouldn't be expecting in June to see a more mature data set than perhaps what's described in the abstracts.

Got it. Thanks for the color. Maybe just one more question. Can you talk about the current status of the KO-947 ERK inhibitor phase one study? Where are you in the dose optimization process? And how close or far are we from seeing initial clinical data?

So, it's a good question. So, as it's quite a difficult target. There have been orders that they have abandoned those programs. So, the one thing that I can tell you is that we have sufficient confidence to continue escalating. What we want to make sure is that we have the appropriate regiment either for the extension cohort or a phase two. So, there are no reasons for us -- there are no stops in the escalations. We are just trying to optimize what is the best regiment. So, that may happen by the end of the year. But the intent is to get the recommended phase two goes and then select the patients based on the markers that were suggested by [indiscernible].

Got it. Thank you, very much for taking the questions.

Our next question comes from Chris Shibutani with Cowen. Your line is now open.

Yes. Thanks very much. On the menin inhibitor, can you give us a sense for perhaps a little bit of preview in how you're framing the clinical development there? I believe there's another one that's also approaching the clinic. And so, I think we'll be keen to observe what the different strategies and differentiation could be. Any additional insight would be helpful to keep us engaged and tease us a little. That would be great.

Yes. So, as you know, we appear to be ahead of others. We have an IND that was submitted or had been cleared by the FDA. We're on a [indiscernible] basis. It's a question of how soon you're bringing studies. But I can tell you that that will happen shortly. We don't have major delays. This is just a quick turn off, IND paperworks, contracts, etc. And the standard dose escalation has some variation behind. But there are no major differences in what you will expect on a phase one dose escalation if they're a factory AML population and the nature intend is not to select molecularly. Although, at some point, we will look for those AML rearrangements and NPM1-mutant population where you are expecting to get activity. I don’t know if this answers your question. -- Well, go ahead.

Yes, no that's helpful. I think as we think about how AML the landscape has changed progressively over the past few years with most of the regions. Many of the physicians and also folks in drug development are thinking about it in terms of potential for combinations. And I'm wondering if you could speak to the pathway and whether you're not you believe that it makes sense to contemplate potential combination even at a pretty early stage of your development and if so is there a logical potential set of other agents to combine with when you think about either kind of mechanistically or as you anticipate what the clinical paradigm could be. And I realize that that's evolving but insights there particularly there got a combination, that'll be helpful.

Yes. It's a very good question. So, I will say that you don’t need to turn your back on the monotherapy for the simple reason that they are not a specific therapies against the adult NPM1 mutated population. Now, is also through that NPM1, maybe concurrent to our new vision and you may have find patients for him for example that have NPM1 mutations and T3 mutations you know. So, that gives you percentage on combination, although not as exciting you should need to consider combination with the standard-of-care. So, the way I will put it you want to get your recommended phase to dose in line of therapy and pending whether you get or not early responses, you can consider combination both with the standard-of-care or we target it agents for those that are maybe targeting the co-mutations that may appear within NPM1.

Great. And then, lastly for Troy just on IP related except the -- I think in your current slide deck you talked about some of the patent extent state efforts that you'd had including where you outlined that you believe that you have for HRAS-mutant after 2036 and CXCL12 expressing up to 2037. From a pragmatic standpoint is are those the rough timelines that you're encouraging investor community to think about in terms of what the IP could go out to in terms of exclusivity? Thanks, very much.

Sure, Chris. So, maybe just taking a step back before I answer your question. That what we brought to the table is an ability to connect the biomarkers, the disease and the dosing schedule. And if you look at the patents that have issued and the patent applications that are pending, that's the theme that runs throughout. That’s the sort of inventive step if you will. And we've been I think quite successful at getting patents issued not only in the U.S. but now they're beginning to issue in outside the U.S. we are guiding as we show in the corporate presentation, we are imagining patent protection under multiple overlapping patents how as you say it at a 2037 or 2038 in the U.S. potentially even longer in Europe. And I think where there is reason for optimism. There really has never been a drug like this that how well it was in development, the exact molecular mechanisms were not known. And so, that's given us a lot of sort of fertile ground and I think you'll continue to see interesting developments from our patent portfolio throughout this year and into next year. So, it's definitely something that is marching along very much hand-in-hand with the development strategy as that's playing out successfully.

Great, thanks. Well, certainly there see for data so we look forward to those mid-summer updates. Thank you, guys.

Our next question comes from Joel Beatty with Citi. Your line is now open.

Hi, guys. This is Sean Egan calling in for Joel. I think I got one for Troy and then one for Antonio. First of all a clarification question. For AIM-HN, the registrational study. If you hit the 15 confirmed responses or reject now, just kind of wondering how you will roll that data out and what'll happen with that study kind of going forward. Or you'll continue to enroll patients to I don’t see if you reach your target objective response rate. And then for Antonio, I know a more comprehensive update on the pancreatic study is forthcoming but I'm just kind of wondering how you will be able to leverage your recent pain analysis as a means of enrichment. Is pain an objective enough to use as like in an enrollment criteria or have you made any progress kind of tethering that to your KRAS or BRAFs.

Sean, thanks for the questions. I'll let me take your questions around AIM and then Antonio can address your the questions relating to the pancreatic data from ASCO GI. So, with respect to AIM-HN, you're correct, the study's intended to enroll at least 59 evaluable patients. However, as we've said if the there are 15 confirmed objective responses, the study illuminates the null hypothesis and is a positive study. At that point we would expect that the DSMB would notify the company that the trial had met its primary efficacy endpoint. We would in turn need to notify FDA and we would likely also announce that publicly. It would be our expectation that the trial if enrollment was not complete, the trial would continue to enroll patients but that would give us an opportunity to begin a dialogue with the agency around next steps towards submission very much in the manner in which our Phase II trial in HRAS-mutant had not achieved proof-of-concept prior to the completion of enrollment and we were able to go and have an end of Phase II meeting with the agency. It's a very analogous situation.

So, thank you for the reference. I mean, that the data that we presented at ASCO GI brought some excitement to the pancreatic investigators. So, you are referring to paying actually where you say that's a connection with CXCL12 expiration on these mostly potentially you will suggest kind or like locally a balanced population that is a good setting. But we have further some analysis of the now if you recall that there was a relationship between CXCL12 expiration and that a little frequency of KRAS. And that can also be very helpful on the metastatic setting that could be potentially earlier path for registration. So, our intent is that to more potentially in a med medical need setting, it could be potentially a second line and to select the patients based on molecular tools. So, we can mainly see a selection of patient for example in KRAS lower than 5% a little frequency that give you 30% of the population is a big chunk of patients and potentially then apply CXCL12 related marker to the time when where you it's a little bit better on how you can identify the patients that are developed the responses or better clinical benefit. So, we do have with those tools and the strategy and we are currently in discussion, we say about with KOLs and our intent is to initiate a pancreatic study proof-of-concept this year.

Great, thank you so much for taking my questions.

Sure.

Our next question comes from Tyler Van Buren with Piper Jaffray. Your line is now open.

Hi guys, this is Alex on for Tyler. Two questions for you. First, given the significant opportunity for tipifarnib, how are you thinking about which indications to prioritize for internal development or for partnership? And secondly, on the 947 program with the recent excitement in programs that target KRAS and bearing in mind of course we don’t have any clinical data yet. How would you compare the potential for single agent activity between KRAS and ERK in addition or in other words would you expect one to be more powerful than the other. And secondly, would it make sense for the KRAS inhibitor program to combine with your ERK inhibitor in combination therapy to improve clinical outcomes? Thanks.

Sure. So, those are two pretty meaty questions. With respect to your first question on prioritization of indications, it's a great question, it's something that we were talking about a lot internally. I think we're quite encouraged by the way in which the CXCL12 hypothesis seems to be playing out. We've shown that prospectively validated AITL retrospective looks at AML, pancreatic, potentially DLBCL. And now we're going to see, again, prospective data initially in PTCL, and then later in the year in CMML. All of those indications have in common that the CXCL12 pathway seems to be driving the disease. One of the things that we've tried to focus on -- and we alluded to this in the prepared remarks -- is you want to get that initial anchoring indication that allows you to drive a smaller trial with a higher likelihood of success and gives you really a foothold to be able to become either part of the standard of care or displace the standard of care. I think we're increasingly encouraged that we see multiple opportunities for that. And we'll have more to say probably a little bit later in the year after we're able to share with you an update on our PTCL studies, as Antonio mentioned, at EHA and the congress in Lugano. With respect to your second question, it's a good question. And there are two very, very different agents. And so, it's hard to draw comparisons, particularly in the absence of data. The promise of the KRAS inhibitors, the G12C inhibitors, is that you are inhibiting an oncoprotein directly. And as a consequence of that, you have the potential for a reasonable therapeutic window. You do have to worry about mutations and resistance. ERK, on the other hand, is a central actor. We're inhibiting the wild type protein that is really a chokepoint for dysregulations in that pathway. And we've talked about it in the past. But there are two distinct ways forward. One is you identify with ERK populations where you can drive meaningful single agent activity. The other is that you identify opportunities where you can drive clinical benefit in combination. As far as we can tell, we're still optimistic that both of those are possible. We would, of course, want to gravitate toward single-agent monotherapy for the reasons that small companies can just do that more tractably. Is there an opportunity to combine a KRAS inhibitor and an ERK inhibitor? Certainly. But I think there's an opportunity to combine an ERK inhibitor with a number of different agents. But as Antonio mentioned, key to that is that you really have to understand what is your recommended phase two dose and how best to use your agent. And then you can figure out how best to deploy it in a combination setting. So, we're very much keeping that question in the forefront of our mind as we work to finish out this phase one setting and hopefully position 947 for the next step of development.

The only thing I will add is that strategies are not necessarily mutually exclusive. So, you can work on tipifarnib on the pancreatic indication. That could be most likely a combination and will require randomized trials. Some may take several years. But it will give you a large, commercial opportunity. And in parallel, you can pursue an AITL or diffuse large B-cell lymphoma subset as monotherapy that translate to registration. For a company like us, having one registration line up after another have it determines value. So, you could do both strategies in parallel and pursue anchoring indications that you can respond. Then you can do label [indiscernible] at the same time that you have this big, commercial opportunity that is also developing in the background.

Great. Thank you.

Our next question comes from Jay Olsen with Oppenheimer. Your line is now open.

Oh, hi. Thanks for taking the questions. Maybe if I could ask you to look ahead into the future, assuming the tipifarnib gets approved for an E transmutant population, could you help us understand what percent of that population is going to be treatable and what we should expect for a penetration level since this is a very targeted indication? Should we expect to see a high penetration level?

I only say we're expecting high penetration for the simple reason that in a setting of a certain line where you are expecting 5% response rate, if you are reaching 50% response rate on a setting in which those patients have no responses, you are immediately displacing the standard of care. And seeing that the standard of care could be immunotherapies, they are not necessarily cheap. You are not displacing [indiscernible]. So, I can say that you can expand vertically, moving all the way to the front line, trying to pursue a new [indiscernible] setting. And then you can expand horizontally on those settings in which maybe the allele frequency is not the best for monotherapy. But you can add to the combination with immunotherapy. You can add to the combination with the 2CMAP. And then you are being carried by those visions because the reality is that either the mutation has very high frequency from the get-go and is driving the tumor or appear later as the mechanism of assistance. So, think of that is published. Hard for those progressions from C2CMAP. They are RAS mediated. At least half of those, they are going to be HRAS. So, you can delay the resistance to the standard of care. So, that gives you at least 5%-10% of the population if you don't do selection. If you do directly combination, obviously, it's much larger potential.

Okay. Great. Thanks. That's very helpful. And then maybe as a follow-up, just thinking about this CXCL12 population, you had identified at AACR CXCL12 expression is a potential biomarker of clinical benefit in patients with DLBCL and the subset of CTCL. And apologies if I missed this. But are these indications on the horizon for development? And how will you prioritize them?

So, first of all, just going to reiterate that are very excited that the dates are coming at EHA and ICML. And this has been shared by a number of investigators on KOL. And that give us a big head in lymphoma. So, the thing that we would only [indiscernible] lymphoma. The data enabled on data mycosis from going this gave us the opportunity. So, sorry. Just backing up, even within peripheral T-cell lymphoma, we know that -- and this has been shown by Tom Wicksett that skin lesions where this had been, in the original data that he presented in 2011. So, that together we're now reprocessing CTCL. That show you that there's also activity in cutaneous T-cell lymphoma. That actually doubled the population of T-cell lymphoma. Diffuse large B-cell lymphoma is obviously more interest. Why? Because it's five times the size. There's more competition. But it's obviously a higher medical need and a very large population. So, we need to decide effectively do we do [indiscernible]. Do we do very targeted registration is something that we are still discussing internally and with others. But we are going from a beachhead to a large opportunity. There will be companies that they will just develop in this area of lymphoma by itself.

Yes. Jay, just to add to Antonio's comments, what we're trying to do is to demonstrate very clear phase two proof of concept in these indications. So, we started with HRAS-mutant head and neck. You saw AITL at ASH last year. We're highlighting, obviously, the presentations in June. And to the back half of the year, the CMML data, those are giving us beachheads into these CXCL12 positive indications. And then, as Antonio mentioned, we said it a couple of times in a couple of different ways. I put this in our basket of high-class problems. Can we pursue accelerated registrations as a monotherapy and, in the meantime, be laying the groundwork for these potentially much larger indications? Rest assured, we're doing both. And we're doing it in the context of tipifarnib being the only drug candidate we know of that has a clinical proof of concept on the CXCL12 pathway. So, we're trying to be thoughtful and stake out a near-term, an intermediate-term, and a long-term opportunity. And that's what's increasingly coming into focus.

That's great. Thank you for the details. It's super helpful. Thanks for taking my questions.

At this time, I'm showing no further questions. I'd like to turn the call back over to Troy for any closing remarks.

So, thank you all once again for participating in the call today. We'll be at the Deutsche Bank Healthcare Conference in Boston tomorrow and the Bank of America Merrill Lynch Healthcare Conference in Las Vegas next week. And we look forward to seeing many of you there. In the meantime, if you have any additional questions, please feel free to contact Pete, Mark, or myself. Thank you again. And have a good evening, everyone.

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