Good day, and welcome to the Kura Oncology Second Quarter 2022 Conference Call. Today's conference is being recorded. At this time, I would like to turn the conference over to Pete De Spain, Senior Vice President of Investor Relations. Please go ahead, sir.

Thank you, Sarah. Good afternoon and welcome to Kura Oncology's second quarter 2022 conference call. Joining me on the call are Dr. Troy Wilson, our President and Chief Executive Officer; and Tom Doyle, our Senior Vice President of Finance and Accounting. 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'll now turn the call over to Troy.

Thank you, Pete, and thank you all for joining us this afternoon. Last year, as we continued in dose escalation with our menin inhibitor ziftomenib in an all-comer population of patients with relapsed or refractory acute myeloid leukemia, we sought FDA feedback regarding the design of our registration-directed trial. In the context of those discussions, FDA advised we spend more time in our Phase 1 study to identify an optimal dose. Guidance we now know was part of a broader FDA initiative in oncology drug development aptly named Project Optimus. In agreement with FDA, we enrolled a Phase 1b study with two-dose expansion cohorts, 200 milligrams and 600 milligrams, each comprised of 12 patients with NPM1 mutant or KMT2A rearranged relapsed refractory AML. I'm pleased to report we've nearly completed our assessment of these patients in the expansion cohorts for efficacy, safety and tolerability, as well as pharmacokinetics and exposure, and we believe we've identified a recommended Phase 2 dose for ziftomenib. We're working diligently to gather the data package for submission to FDA and look forward to sharing the recommended Phase 2 dose for ziftomenib later this year, pending the agency's review along with top line data from the Phase 1b study with a more complete dataset reserved for presentation at a medical meeting in the fourth quarter. In the meantime, enrollment in KOMET-001 has continued and we're pleased to announce that we've enrolled an additional 18 patients in the Phase 1b study in less than three months that what we believe to be the recommended Phase 2 dose, an indication of the continued enthusiasm surrounding ziftomenib among investigators and patients. We continue to believe data from all patients treated at the recommended Phase 2 dose will have potential to contribute to the registrational patient population. In parallel with…

Thank you, Troy, and good afternoon, everyone. I'm happy to provide a brief overview of our financial results for the second quarter 2022. I invite you to review our 10-Q filed today for a more detailed discussion. Research and development expenses for the second quarter of 2022 were $24.3 million, compared to $21.1 million for the second quarter of 2021. The increase in R&D expenses was primarily due to increases in our clinical trial costs related to our ziftomenib program and personnel cost. General and administrative expenses for the second quarter of 2022 were $11.1 million, compared to $12.6 million for the second quarter of 2021. The decrease in G&A expenses was primarily due to the decreases in personnel costs and professional fees. Net loss for the second quarter of 2022 was $34.8 million, compared to a net loss of $33.7 million for the second quarter of 2021. As of June 30, 2022, we had cash, cash equivalents and short-term investments of $450.3 million, compared to $518 million as of December 31, 2021. Based on our operating plan, we continue to believe that our cash, cash equivalents and short-term investments will fund current operations through 2024. With that, I now turn the call back over to Troy.

Thank you, Tom. Before we jump into the question-and-answer session, let me lay out our anticipated milestones for 2022. For our menin inhibitor program, determine the recommended Phase 2 dose for ziftomenib in consultation with FDA and report top line data from the Phase 1b study later this year. Present updated data from KOMET-001 at a medical meeting in the fourth quarter. And for our FTI programs, initiate the Phase 1 KURRENT-LUNG study of tipifarnib plus osimertinib this quarter and submit a new investigational new drug application for KO-2806 in the fourth quarter. With that, Sarah, we are now ready for questions.

Thank you. [Operator Instructions] We'll take our first caller from Jonathan Chang, SVB Securities.

Hi, guys, thanks for taking my questions. First question, on timing of the top line ziftomenib data, can you provide any additional color on how you're thinking about when to disclose the top line data?

Sure, Jonathan. Thanks for the question. As we indicated, Jonathan, our goal here is to determine the recommended Phase 2 dose in consultation with FDA. We're at a point where we are completing our assessment and preparing to submit the package to FDA that should happen shortly. What we don't have as much visibility into is the process and the timeline by which FDA reviews that. Unlike, for example, in the case of an IND submission there isn't a 30-day clock. We certainly believe that we're going to submit a package that should address all of their questions, we will stand ready if they have additional questions or need us to look at the data in any different way. At this point, I think that the best we can say is we're probably looking at late in Q3, it could potentially slip into Q4, just depending on the timing with FDA.

Got it. Thank you. And I guess, are you able to provide any color on the identification of the RP2D and the regulatory interactions. I guess, what boxes remain to be checked before officially declaring the RP2D?

Yes. So maybe just to take a quick step back, we undertook this Phase 1b study really as an exercise in dose optimization, and this was part of the FDA's initiative around Project Optimus, it's becoming standard for targeted therapies. I can tell you with our view now having conducted the Phase 1a and the Phase 1b that the Phase 1b was absolutely the right thing to do. We’ve gathered a tremendous amount of information about the clinical activity, the safety and tolerability, you know, the PK, in addition to how to manage the on target AE such as leukocytosis and DS. So it was absolutely the right thing to do. I think we're going to emerge from this in our view with a very strong data package supporting the recommended Phase 2 dose, we still want to jump the gun at this point. And it isn't so much Jonathan, a check the box exercise as it is. The FDA is looking for information relating to clinical activity, safety and tolerability, PK and exposure really across all the patients enrolled in the study to this point, but with a particular emphasis on the Phase 1b patients and integrating that and analyzing that to really make a strong recommendation that supports advancement as a monotherapy and that sets the dose for any and all future combination studies, that's why this is so critically important. And I can't stress enough, I think we did, although it took a bit longer, given the profile we have with ziftomenib and given what we were seeing absolutely the right experiment to do.

Got it. Thank you. And just last question for me. On the additional 18 patients enrolled in KOMET-001 since May. How many of these patients could we see data on for the top line disclosure and for the fourth quarter medical meeting presentation? Thank you.

Yes, it’s a good question, Jonathan. So it's been our intent from the beginning and this was actually guidance that we received from FDA to conduct the Phase 1b using the same endpoints as will ultimately be used in the registrational portion of the Phase 2. As such, the data that we're gathering is to use a -- for lack of a better word, it's sanctified, right? These are patients that we hope and expect will be part of the registrational totals. And we're certainly treating them as such, that's partly perhaps what -- it's helpful to help people understand is you really need to make sure the data coming from the sites is robust, it’s clean, you've checked it. This ultimately we hope will become part of the submission. That's true also Jonathan for the additional 18 patients and of course all subsequent patients we would enroll. So we're balancing here, is there incremental value in sharing additional data versus the time lost of them having to potentially replace those patients? You put at risk when you're sharing data from sanctified patients in a registration enabling study, you put those patients at risk if you keep doing data cuts. So at this point, I'm not expecting, Jonathan, that you're going to see more than the initial 12 patients in each cohort in the top -- both top line -- sorry, in the top line results. At ASH, you'll see of course the data from the Phase 1a and the Phase 1b, it's not our current expectation that we'll go beyond the initial 12 patients in each cohort. At this point, we might be able to speak qualitatively to it. But we don't want to -- we're doing everything we can to try to maintain momentum and close the gaps and we don't want to put those patients at risk.

Makes sense. Thanks for taking the questions.

Our pleasure, Jonathan. Thank you.

Thank you. And next we'll move on to Tiago Fauth with Credit Suisse.

Great. Thanks for taking the question. Congrats on the progress. So I understand you might be fairly limited in what you can share at this point. But to the extent that you can provide any qualitative comments, wondering about the enrollment proportion between the two genetic sub types, if that is consistent with prior competitor experience. I don't know if you can also talk about consistency of efficacy response between those two subpopulations. And perhaps just trying to understand a little bit better the future for the FTI franchise, so if you have 2806 expected to enter clinic in Q4, perhaps Q1 depending on how that shakes out with the IND filing? And you have recently initiated the combo trials for tipi, right, with both [chapter K] (ph) and EGFR? Do you expect to develop the same combo simultaneously? Would it make sense to establish proof-of-concept with tipi, and perhaps progressed with 2806 for our registrational trial. Curious if there is any characteristics that would make tipi a better candidate for us -- for giving combo or how that's going to evolve over time? Thanks.

Yes, Thiago. Thanks for that. It's a three-part question, let me take each of the parts in turn. So on your first question of around enrollment, it ebbs and flows, I would say we see a pretty healthy balance between NPM1 and KMT2A rearranged patients. Again it ebbs and flows, kind of, at any given point in time. It seems enriched in KMT2A rearranged AML patients relative to what the overall epidemiology might suggest. You'd expect it to be roughly four or five to one, we're seeing more of kind of an equal weighting, if you will, but a lot of interest among physicians who want to enroll both populations. So I think we're going to continue to see strong enrollment as we transition into Phase 2 in those ultimate registrational cohorts. Relating to activity, what I can tell you there is our thoughts remain consistent that we're thinking of the cohorts as being approximately the same size, namely 50 to 75 patients each, that should tell you know that statistical design should tell you we're looking to meet or exceed really the same bogey, right? And that is 20% to 30% CRH rate, four to six months durability, transfusion independence as a secondary endpoint, we think that number of patients is probably in the right range to allow us to deliver successful Phase 2 cohorts in both the KMT2A and the NPM1. So that's as much as I think we could say. Of course, we'll have the flexibility to be data driven. On the third part of your question that relates to the strategy around the FTIs, you make an important point and you really -- we're really trying to solve several things simultaneously. So the first is data generation, I think our mindset has evolved to the highest…

Yes. Thanks again for taking the question. Appreciate it.

Pleasure.

Thank you. And next we'll move on to Peter Lawson, Barclays.

Great. Thank you. Thanks for taking the questions. Troy, just the 200 milligram dose, which do you think sets you better for first line in combination use? And then is there anything you're seeing in the data that makes you the menin data? Anything that makes you incrementally more positive for unconventional more negative?

Yes, it's a good question, Peter. So maybe to take a step back to the first part of your question, what we're really looking for first and foremost is safety and tolerability, right? This is still ultimately a Phase 1 study. Efficacy remains even though we are conducting a pursuant to registrational endpoints we're all in such a rush, but ultimately it is still a safety study. We feel like we have a good safety window at both doses. We have the ability to dose at either dose and potentially to move between them as needed, so that I think is first and foremost. We've been looking at clinical activity, PK and exposure, pharmacodynamic markers as well and we're looking forward to sharing that with you. You'll get a glimpse of it in the top line. You'll get a much more fulsome picture at ASH. I think it's a very nice setup for a monotherapy and potentially in combination. We're feeling, as I said, in response to Jonathan's question, it was the right experiment to run. One of the things that we've learned as we've transitioned from 1A to 1B is we see leukocytosis. We see -- it's rare, but we see cases of differentiation syndrome to the uninitiated, leukocytosis can look like progression. And you have a patient who's failed three or four lines prior therapy they go on a menin inhibitor, you start to see leukocytosis, which means it looks like the counts in the periphery are going up. What we've learned is that is not necessarily progression, that's actually the cells doing exactly what they are programmed to do when you block them in an MLL interaction, they're moving into the periphery and then they live there for a couple of weeks and begin to die off. So that kind of learning, Peter, is invaluable both as a monotherapy and setting up for success and then thinking about in combination. If you start to see things in combination, you need to really understand, okay, which element of the combo is it coming from? With respect to the second part of your question, our enthusiasm continues. I'm trying and hopefully I'm succeeding in just maintaining a very steady course. We remain encouraged about the potential for ziftomenib, we're looking forward to sharing the data. We are very, very much living this experience in Project Optimus. And we look forward to sharing the data with the FDA and hopefully gaining their alignment. I think we'll be in a good position come the top line data and ultimately the presentation at a medical meeting to be able to support the idea that there's a strong path forward here as a monotherapy and potentially we're very well set up in combination to be best-in-class. So time will tell.

Great. Thanks so much.

Our pleasure.

Thank you. We'll move on next to Roger Song with Jefferies.

Great. Thank you for taking the question. Maybe just a couple clarifications from Troy, so first of all, I see what you said is the 6th May you're starting to enroll additional 18 patients in the RP2D arm alone, so maybe just -- can you clarify that's the case maybe that imply you already decide RP2D in May based on the profile you have been seeing that time?

Yes, Roger. And I'm going to be very different here to the FDA on this. The protocol as was originally agreed to with the FDA gave us the flexibility to enroll 12 patients at each of the two doses and then to continue enrollment in either cohort, depending on the way the data went. And so we've done exactly that. We've enrolled the 24 patients that where we've nearly completed the assessment, we've continued enrolling at what we believe to be the optimum dose. I want to choose my words carefully out of respect for the agency, we'll be able to come back and tell you that is the recommended Phase 2 dose once we have their alignment. But obviously, we feel at this point that the data is trending in the right direction that we want to try to both give every patient the best chance for clinical benefit or benefit risk, if you will. And as I said in response to the earlier question, to try to close any gaps on enrollment and maintain the momentum for the program.

Excellent. Thank you. Okay, and the next question is related to the regulatory interaction. Understanding you have now final -- your data analysis for those 24 patients, but have you got any kind of advice or having any discussion with the FDA regarding this RP2D package? And kind of decide what kind of data you want to include in that package?

Yes, that's a very good question, Roger. So as part of the discussions when we were agreeing with FDA on the design of the Phase 1b study, they were very clear at what they were looking for as far as the data coming out of the Phase 1b in terms of assessing benefit risk. And I have characterized that in kind of the three columns of efficacy data, safety and tolerability, PK and exposure. And then any other data we want to include to help support the benefit risk at what we would feel is the appropriate recommended Phase 2 dose. Nothing there has changed. We have regular interactions with the FDA, I don't want to get into the specifics, but nothing on that guidance has changed at all. Where we are is this data has to be again sanctified, right? These are patients that we hope and expect will ultimately be able to be included in a registrational package. So as we're pulling data out of the site, as we're pulling it out of the vendors, we have to make sure it's clean. We have to make sure it all ties out. I don't think the answer is going to change, Roger, between now and when we ultimately submit the package. But the FDA is looking for a level of credibility, of excellence, of professionalism that we intend to meet or exceed. And they were clear with their instructions on what they're looking for. We're going to deliver them that. We're also going to then Roger as every company I suspect does, we'll prepare for any other questions they might have, right? So they get the data. Do they want to look at it in different way? Do they maybe have a question about cutting it this way or that way. This is the kind of scenario planning that you do and our team is all over that. We'll be ready to provide the FDA any additional information that they need or any further analysis to help support the recommended Phase 2 dose. We found them to be very collaborative and to be very clear on what they need and we're hoping we can move through this as efficiently as possible.

Yeah, that's very good. Great, maybe just very quick last one. Maybe just to confirm this additional 18 patient on the optimal dose additional 18 patient won't be part of this RP2D package or FDA not requiring or not asking for the data from those 18 patients?

Yes. So just to be clear, Roger, the FDA had -- I'm going to rely on my legal background here. The FDA has jurisdiction over every patient on every study, right? So they can ask whatever they want to ask. And particularly as it pertains to safety, if there are safety updates, you're obligated to share that with them. But let's go back to the point of the exercise, we believe that the 24 patients, who comprise the Phase 1b population at the 200 milligram and 600 milligram dose are going to be what's needed. We'll provide any additional safety updates as needed. But we're not expecting to have to keep doing data cuts. Obviously, if the FDA asks, we're of course going to work with them and comply, but that's not the expectation going in.

Very good. Okay, great. I think that's it from us. Thank you. Thank you, Troy.

Thanks, Roger.

Thank you. And next we'll move on to Li Watsek with Cantor Fitzgerald.

Hey, guys. Thanks so much for taking my questions. I guess one question on ziftomenib. I mean, you finished enrollment in May and now in August, I guess for, you know, differentiation syndrome, we know that typically occurs early in treatment. So, I guess, is it safe for us to doing that, like, there's less risk now for seeing, I guess, serious cases?

Yes, Li. I'm glad you asked that question. So just to remind everybody, we were earlier this year on a partial clinical hold related to a case of differentiation syndrome. At that point, we implemented some revised guidance around how to manage differentiation syndrome. And it's been our experience Li as the trials continue to enroll that although we do see differentiation syndrome, it's relatively rare and infrequent. But in cases where you see it, the severity of the DS appears to be less now than it was prior to the implementation of the revised DS guidance. And our goal along has been, this is – so leukocytosis and differentiation syndrome are on mechanism AEs, right, if you will. The cells are doing exactly what you're programming them to do. What we are -- our goal is to try to provide the investigators, the clinicians with the tools to keep any cases of DS or leukocytosis at grade one, grade two, kind of mild to moderate, keep it away from the more severe grades. I think we've been more successful in that as the trial has gone on. We've learned a lot and of course, the physicians who have the greatest facility are the ones who have the most experience with the drug, not unlike what we've seen, for example, with venetoclax and tumor lysis syndrome. It took a while for the -- for investigators to develop an expertise and understanding of what to look for and how to mitigate it. So I would say not only, Li, are we seeing less perhaps less frequent, but certainly less severe DS and that's trending in the right direction. That should also only get better as we move into certain combinations with cytoreductive agents, because that's one of the means of mitigating DS is to provide something like cytarabine as a way of managing counts. So that's what I think we're optimistic that we're on track to be as good as if not better than our competition, that the arrows are at this point, it’s an ongoing trial, but the arrows are going in the right direction.

Okay, great. Thank you for the color. I guess my second question is about TP combination. I mean you mentioned from the Phase 1, I guess current head and neck study, you've seen some preliminary, I guess, activity. So I wonder if you can expand a little on that? I guess what have you seen so far that gives you the confidence that the activity is real? And maybe remind us what a benchmark is? You know, so I guess A, you mentioned that you might, I guess, present some data later this year. Can you give us a sense of what we should expect?

Sure. So good question, another three part question. Let me take one each of them in turn. So typically, we've worked me -- this is me and several others here, we've worked in and around the MAP kinase and PI3 kinase pathways for a long time on different agents. By and large, the industry has not been successful at combining inhibitors of the MAP kinase pathway and the PI3 kinase pathway due to overlapping toxicity. So first and foremost, the fact that we're seeing an acceptable safety and tolerability profile is a big -- I think a big advance, so that wasn't clear. That's where I would have assigned the greatest amount of risk, because you know preclinical models are only so good at predicting toxicity. We're at a point where we are in dose escalation and we remain encouraged by what we're seeing as far as safety and tolerability, that's usually been kind of the stopping point for most combinations on these pathways. But the equally important and perhaps more intriguing is we're seeing early evidence of clinical activity. So what do we mean by that? Well, that's, if you will, tumor regression that's the clinical endpoint. Now when we talk about proof of mechanism, what we're looking for is examples in a handful of patients that really recapitulate the preclinical data that we've published. You can see it in our corporate presentation, it’s available on the AACR presentations on our website, you see synergistic activity combining alpelisib and tipifarnib in each of the four subsets in head and neck cancer. The two HRAS-dependent and the two PIK3CA-dependent. You see synergistic activity across all four subsets. Even early in dose escalation, Li, we're seeing some early evidence that is trending in the right direction. And I'll just remind you…

Great. Thank you so much.

Thank you. And next we’ll move on to Reni Benjamin with JMP Securities.

Hey, good afternoon everyone. Thanks for taking the questions and congrats on the progress. Maybe Troy just starting off with this FDA review again. I'm trying to just get a better handle. Are you looking for them to confirm kind of your -- the RP2D that you have selected? And the go forward strategy? Or are you looking for something more guidance oriented, right? So you give them both the data sets and you -- it's more of like a collaborative effort to decide what the go forward RP2D should be?

Yes, Ren, I appreciate the question. We're not -- we're looking for FDA. We're looking for FDA's input, but we're looking for FDA to analyze and hopefully to agree with our recommendation. We're going to give them a recommendation and let them respond to that rather than seeking their input, sort of, making it a jump ball if you will. We're not going to do that. Just to remind everyone, FDA needs to agree with any registrational plan, which means they have to agree with the registrational dose. And so this is the predicate to starting the registrational portion of the KOMET-001 study or starting any combination study. But to your specific question, Ren, we will put to them here is what we believe is the minimal safe and efficacious dose pursuant to Project Optimus, here's the data supporting that and seek their feedback and address any questions. That's the way we're intending to do it.

Got it. And then in -- as part of this discussion, will you be talking about the registrational study and getting kind of like the FDA blessing on that? Or is that a subsequent discussion after this is completed?

No, you're absolutely right, Ren. So it's option one in your options. We will look to gain alignment from the FDA on the path forward in the registrational study as a monotherapy.

Perfect. Okay. And then just switching gears real quick to the current lung study that will be started. Can you talk a little bit about -- from the preclinical work, do you have a sense how exactly or what type of specific resistant mutations seem to be impacted by tipi? I seem to recall that like T79 -- T790M, C -- I think it's 797S mutations are the typical mutations that we’re looking for that confer resistance to OC. Just kind of trying to get a sense about that? And then I know that you're going to be measuring ctDNA as a biomarker for efficacy, but can you also use that as a biomarker to follow resistance?

Yes. So both really good questions, Ren. So what we're -- what this seems to be evolving to, is let's step away from EGFR and even for osimertinib for just a second. The -- you often asked the question, if you have a potent signal transduction inhibitor like osimertinib or KRAS for example, why don't we see CRs right? Why do we see PRs? This is a question I've been asking myself for the better part of 15-years as I've been working across various targets. And one potential mechanism is there are a subset of cells that are called drug tolerant cells. When you hit them with a potent signal transduction inhibitor like osimertinib, there's a sub population that you just don't kill. And the reason A, reason you don't kill them is those cells actually fundamentally rewire, they actually redifferentiate and they are able to cycle in the presence of osimertinib. And the reason -- and the way that they get into that drug tolerant state is through a farnesylated protein, one of the row proteins. When -- once they've developed some sort of resistance mutation Ren, then they redifferentiate and then they can take off in the presence of osimertinib or another EGFR inhibitor. Osimertinib happens to be the 800 pound gorilla, which is why it's the one we've started with. But that redifferentiation and that extent of drug tolerance is also farnesylation dependent. So now when you combine osimertinib plus tipifarnib, in patients who haven't seen osimertinib, what the preclinical data says happens is you prevent those drug tolerant cells from entering a state of drug tolerance. So they become more susceptible to osimertinib. Now I don't know if clinically we're going to be able to drive CRs, we have some preclinical data that suggests in some…

Got it, which as leads me to focusing on what you're going to look for, particularly for a go no, go decision, because it seems like median PFS would be way too long?

Yes and no. So I'm sorry, you reminded me that in my long winded answer, I didn't answer your ctDNA question. So we will be looking at ctDNA, AstraZeneca and the clinical investigators understand the ctDNA profile for everyone else on the call this is circulating tumor DNA. And what it allows you to do is you don't have to do a solid tumor biopsy, you can do its blood based, you can both watch disappearance of the mutant allele. So in this case T790M, you can also watch for reemergence of resistant alleles. And it's a way to kind of gauge ho -- it's equivalent to MRD negativity, if you will, in the AML instance. We're going to be looking at that Ren, if things start to go in the right direction, I think, will accelerate. But ultimately PFS is the right endpoint. And the downside of that is OC has a very long PFS. The upside is it's a huge opportunity and one where a 2806 osimertinib combo, we think potentially provides really a significantly better clinical benefit over osimertinib alone. There will be -- we're asking ourselves the question, Ren, and I want to acknowledge -- we recently retired Kirsten Flowers to be both Chief Commercial Officer and Chief Corporate Strategy Officer, we are looking for other instances of this where we can go -- get an endpoint even faster. So can you, for example, take KRAS, for example, could you go from six to eight months median time to relapse to extend that out maybe 10-months or 12-months. I would say stay tuned on that, a lot of preclinical work going there, but that would go alongside and help support this idea. And we've come just such a long way from targeting HRAS to now targeting the row proteins, rev this whole family of uniquely farnesylated proteins that drive drug resistance. It's a nice story. It’s -- and we look forward to sharing more of it probably early next year on the other side of the menin update.

Got it. There's one final question for us. Translational continues to, I guess, gain in more and more popularity. We're noticing more papers, kind of, focusing in on this mechanism of action, especially in different diseases, including neurological ones, like Alzheimer's and the like. I know that you guys don't necessarily want to branch out there, but I'm kind of curious, do you have any BD discussions? Do you have any inbounds with interest, kind of, to partner your FTI library?

So, yes, so I don't want to speak to specific discussions, Ren. The papers that you're describing out of the University of California in Santa Barbara are very provocative, relating to the tau proteins and for an installation. One of the things that we're doing, Ren, is I don't know if it's 2806, but I'll just say colloquially it could be 2807 is a brain -- blood brain penetrant -- blood brain barrier penetrant FTI. So let me not sort of talk yes of the partnering discussions. Once you have a hammer and you show that in this case you show you can block FT farnesyltransferase. People, you know, Francis Burrows and our translational team have a huge number of collaborations ongoing. The osimertinib 1 came from intern in France, who came to us really with insights into farnesylation biology specific proteins and they needed the molecular expertise, they needed the drugs which we provided. We have other examples of that. So I would say stay tuned.

Great. Thanks for taking the questions.

Pleasure.

Thank you. [Operator Instructions] And next one, we will take Eva Privitera with Cowen.

Hi. Thanks for taking our questions. Back to the upcoming topline disclosure for zifto. I know you had previously mentioned that it will include composite CR. Can you remind us if it will also include MRD status? Or any of the PK and exposure data?

Yes, Eva, thanks for the question. So the -- as far as the top line data, we're expecting CR, CRH, CRC rates. We haven't yet decided to be perfectly frank on MRD status. We're very encouraged by what we're seeing, but we just -- that's one where we haven't made a determination. If you don't see it in the top line, you'll see it at ASH. I think the PK and exposure really isn't appropriate for a top line cut, that's probably more appropriate for a more fulsome discussion of the clinical data at ASH. So I'd probably hold that off until then.

Great. Thank you. And will the efficacy be broken down by genetic subtypes?

It will. Yes, it will and you'll see it certainly I think both in the top line and in ASH.

Great. Thank you. And just one more point of clarification. You had mentioned in your remarks that you expect 50 to 70 patients in each of the registrational cohorts for each genetic subtype. Would this be in addition to the 30 from the Phase 1b at the RP2D, since those patients can be counted for the registrational data?

Yes. So I think Eva the question is, we're going to need to have 50 to 75 patients who meet the criteria for inclusion, right? That's the focus. And that’s literally falls out of the 20% to 30% CR, CRH rate that we're aiming for. The patients that have been rolled up to this point are a mix of the two genetics. So we know in total we're going to need approximately 50 to 75 patients per cohort. We're obviously trying to get as many as we can. But sometimes patients will get knocked out for -- or the FDA won't allow you to count them. So oftentimes, you'll overenroll a bit just to ensure that that happens. But we just -- my -- that's our way of saying. And related to this question of are you seeing kind of equivalent activity between the two genotypes? The best way we think to answer that is to say, we're planning on running similarly sized cohorts. So that should tell you something, right, without getting into the specifics.

Perfect. That's very helpful. Thank you.

Our pleasure. Thank you, Eva.

Thank you. And there are no further questions. So that will conclude our question-and-answer session today. I would now like to turn the conference back over to Dr. Troy Wilson, President and Chief Executive Officer for any additional or closing remarks.

Thank you, Sarah. And thank you all once again for joining our call today. We'll be participating in the Wedbush Path Grow Healthcare Virtual Conference next week, look forward to seeing a number of you there. In the meantime, if you have additional questions, please feel free to contact Pete, Tom or me. Thank you again and have a good evening everyone.

Thank you. And that does conclude today's teleconference. We do appreciate your participation. You may now disconnect.