Greetings, and welcome to Kura Oncology’s Fourth Quarter 2022 Earnings Conference Call. At this time, all participants are in a listen-only mode. A question-and-answer session will follow the formal presentation. As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, Mr. Pete De Spain. Thank you. You may begin.

Thank you, Rob. Good afternoon and welcome to Kura Oncology’s fourth quarter and full year 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. Dr. Stephen Dale, our Chief Medical Officer is also with us and available to answer questions. Before I turn the call over to Dr. Wilson, I’d 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. Let’s jump right in. In December, we were proud to report updated data from our Phase 1 trial of ziftomenib at the American Society of Hematology Annual Meeting. Ziftomenib is our once-daily oral drug candidate targeting the menin-KMT2A protein-protein interaction for the treatment of genetically defined AML patients with high unmet need. The data at ASH highlighted the encouraging safety profile and clinical activity of ziftomenib in patients with relapsed/refractory AML. Notably, the data included a 30% complete response rate with full count recovery among 20 patients with NPM1-mutant AML treated at the 600 milligram dose. To our knowledge, this represents one of the highest response rates reported to date for targeted therapies in a relapsed/refractory setting. A median duration of response had not been reached as of the ASH data cutoff on October 24. In addition to the strong observed clinical activity, ziftomenib demonstrated a favorable safety profile and encouraging tolerability, which resulted in designation of 600 milligrams once-daily dosing as the recommended Phase 2 dose and schedule following a positive Type C meeting with FDA. Building on the momentum of our Phase 1 data and FDA interactions, we recently announced the first patients dosed in our Phase 2 registration-directed trial of ziftomenib in NPM1-mutant relapsed or refractory AML. We expect to enroll a total of 85 patients in the United States and Europe. The primary endpoint is CR or CRh, and key secondary endpoints include duration of response, transfusion independence, safety and tolerability. Dosing the first patients in our registration-directed trial of ziftomenib marks a significant milestone for our menin program and is a testament to the hard work and dedication of our team. The speed with which we’ve begun enrolling patients in the trial also speaks to the significant interest in ziftomenib among investigators. NPM1-mutant AML accounts for approximately 30% of new AML cases annually, and represents a disease of significant unmet need for which no approved targeted therapy yet exists. Although untreated NPM1-mutant AML may present a more favorable prognosis upon initial diagnosis, the risk of relapse remains high and survival outcomes are poor after initial chemotherapy, particularly when other poor risk mutations, such as IDH 1 or 2 or FLT3 are also present. Notably, in our Phase 1 trial for ziftomenib, two-thirds of NPM1-mutant AML patients who achieved a CR at 600 milligrams had either IDH and/or FLT3 co-mutations, all of whom had failed prior treatment with IDH and/or FLT3 inhibitors. An additional NPM1-mutant patient who entered the trial with multiple co-mutations, including DNMT3A following two prior stem cell transplants, also achieved a CR with no evidence of minimal residual disease and remains on ziftomenib for more than 31 cycles as of the October 24 data cutoff. In addition to impressive activity as a monotherapy in patients with NPM1-mutations, we believe ziftomenib is well-positioned for future combination strategies. Our conviction is supported by several key competitive advantages including no evidence of drug-induced QTc prolongation, no predicted adverse drug-drug interactions, and oral daily dosing that should enable convenient administration with standards of care. Our team is working diligently to initiate the KOMET-007 and KOMET-008 trials to evaluate ziftomenib in combination with current standards of care in earlier lines and across multiple patient populations, including NPM1-mutant and KMT2A rearranged AML. We’ve designed these Phase 1 studies to assess the safety, tolerability and therapeutic activity of ziftomenib in combination with key regimens such as venetoclax and azacitidine, gilteritinib, and 7+3. Our approach is to establish a foundation where ziftomenib can be combined safely with various commonly used regimens, and then prioritize those combinations that represent the largest populations and greatest potential commercial value, primarily venetoclax and FLT3 containing regimens. In particular, we believe ziftomenib has the potential to combine more safely and effectively with FLT3 inhibitors relative to other menin inhibitors in development. Notably, up to half of NPM1-mutant AML patients also exhibit co-mutations in the FLT3 gene. We also believe that rational combination approaches will help to mitigate differentiation syndrome in the KMT2A-rearranged population, as has previously been demonstrated in the development of IDH inhibitors in combination with azacitidine. We’re very excited about the potential for our combination studies to further unlock the value of ziftomenib for patients with acute leukemias. We anticipate initiating the first of these studies, KOMET-001, in the first half of 2023. We continue to have strong conviction in ziftomenib and its potential to be the best-in-class menin inhibitor. And we continue to prioritize investment in the program, including significant investments in NDA preparedness, as well as combination studies. We look forward to sharing further updates on the program as the year progresses, including presentation of a more mature dataset from our Phase 1 trial of ziftomenib in NPM1-mutant AML at a medical meeting in mid-2023. Now, let’s turn our attention to our farnesyl transferase inhibitor programs. Over the past several years, we’ve pioneered the development of FTIs as combination agents to delay or prevent emergence of resistance to certain classes of targeted therapies in large solid tumor indications. Our preclinical data is supportive of FTIs in combination with a growing number of targeted therapies, including EGFR inhibitors and PI3 kinase alpha inhibitors, as well as tyrosine kinase inhibitors in renal cell carcinoma, and KRAS G12C inhibitors in lung cancer. Our next generation farnesyl transferase inhibitor KO-2806 was developed with these applications in mind. KO-2806 was designed to improve upon potency, pharmacokinetic and physicochemical properties of earlier FDI drug candidates. Last month, we were pleased to announce FDA clearance of the investigational new drug application for KO-2806 for treatment of advanced solid tumors. We intend to evaluate safety, tolerability and preliminary antitumor activity of KO-2806 in a Phase 1 dose-escalation trial, which we’re calling FIT-001, as a monotherapy and in combination with other targeted therapies in adult patients with advanced solid tumors. Clearance of the IND for KO-2806 marks an important next step for this program, and we look forward to starting FIT-001 in the third quarter. Meanwhile, we continue to evaluate tipifarnib in combination with the PI3 kinase alpha inhibitor alpelisib to address larger genetic subsets of HNSCC patients. In October, we reported the first demonstration that the combination of tipifarnib and alpelisib can induce a durable clinical response in a PIK3CA-dependent HNSCC patient at the EORTC-NCI-AACR Molecular Targets and Cancer Therapeutics Symposium. Notably, a patient with stage III squamous cell carcinoma of the tonsil with a PIK3CA mutation has achieved a durable partial response in our KURRENT-HN trial, and we have continued on study for more than 27 weeks as of the September 14 data cutoff. Treatment-related adverse events in KURRENT-HN are consistent with the known safety profiles of each drug and are manageable, with no dose-limiting toxicities reported to date. Our team is now focusing its efforts on identifying a recommended Phase 2 dose and schedule for the combination with a goal of determining the optimal biologically active dose in mid-2023. In an ongoing effort to prioritize those programs with the highest potential to create value for patients, health care providers and shareholders, we’ve decided to close our current lung trial and discontinue further development of tipifarnib in combination with osimertinib. We believe taking this disciplined approach enables us to enhance our focus on those development programs with the highest potential value, namely ziftomenib and KO-2806, while maintaining a strong cash position. Finally, in support of our ongoing corporate development strategy, we were pleased to announce a $25 million equity investment from Bristol Myers Squibb in the fourth quarter. The equity investment from BMS strengthens the relationship between our organizations and provides us with key insights and expertise. We’re pleased to have the confidence of the BMS team and excited to work with them to deliver innovative science with the potential to benefit patients. With that, I’ll now turn the call over to Tom for a discussion of our financial results.

Thank you, Troy, and good afternoon, everyone. I’m happy to provide a brief overview of our financial results for the fourth quarter and full year 2022. I invite you to review our 10-K filed today for a more detailed discussion. Research and development expenses for the fourth quarter of 2022 were $22.7 million, compared to $21 million for the fourth quarter of 2021. R&D expenses for the full year of 2022 are $92.8 million, compared to $84.7 million for the prior year. The increase in R&D expenses was primarily due to increases in clinical trial costs related to our ziftomenib program offset by decreases in clinical trial costs related to our tipifarnib program. General and administrative expenses for the fourth quarter of 2022 were $12.5 million, compared to $12.1 million for the fourth quarter of 2021. G&A expenses for the full year of 2022 are $47.1 million, compared to $46.5 million for the prior year. Net loss for the fourth quarter of 2022 was $33.1 million, compared to a net loss of $32.7 million for the fourth quarter of 2021. Net loss for the full year 2022 was $135.8 million, compared to a net loss of $130.5 million for the prior year. Net loss for the fourth quarter and full year 2022 included non-cash share-based compensation expense of $6.8 million and $26.3 million, respectively. This compares to $6.4 million and $23.6 million for the same periods in 2021. Our cash, cash equivalents and short-term investments were $438 million as of December 31, 2022, including the $25 million equity investment from Bristol Myers Squibb and a onetime $10 million draw from the Hercules loan facility. This compares to $518 million as of December 31, 2021. We believe that our cash, cash equivalents and short-term investments will be sufficient to fund our current operating plan into the fourth quarter of 2025 assuming no further draws on the debt facility. 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 this year. For ziftomenib, dose the first patients in the KOMET-007 combination trial in the first half of 2023. Present updated data from the Phase 1 trial in NPM1-mutant AML at a medical meeting in mid-2023 and dose the first patients in the KOMET-008 combination trial in the second half of 2023. For tipifarnib, determine the optimal biologically active dose in the KURRENT-HN trial in combination with alpelisib in mid-2023. And for KO-2806 dose the first patients in the FIT-001 dose-escalation trial in the third quarter of 2023. With that, Rob, we’re now ready for questions.

Thank you. At this time, we will be conducting a question-and-answer session. Our first question comes from Jonathan Chang with SVB Securities. Please proceed with your question.

Hi, guys. Thanks for taking my questions. First question on the mid-2023 Phase 1 KOMET-001 update, can you help set expectations around what information you plan to share and clarify whether this update is for NPM1-mutant patients only. And then the second question on the Phase 2 portion of the KOMET-001 study in NPM1-mutant patients. How has the early experience shaped your thinking around timelines for the study? Thank you.

Thanks, Jonathan, for the questions. So starting with the update that we anticipate in mid-2023, we do intend to focus that update on the patients with NPM1-mutant AML who were enrolled in the Phase 1 study, and the intent there is to provide an update on all the patients in the study. Obviously, one of the key questions at ASH was the durability of response and we’ll be in a position to provide a significantly more mature dataset. But as is customary, we’ll give a full clinical update on all the NPM1-mutant patients on the study. And recall there were 20 NPM1-mutant patients dosed at the 600 milligram dose. In terms of the experience in the Phase 1b and the timing for the Phase 2, I think that’s your second question. It’s still early, I mean, we’ve been very encouraged, we were deliberate to say that we had dosed multiple patients. When we first put the press release out, announcing the initiation of the study, and interest among and enthusiasm among the investigators has been robust. We’re still in steady startup that will take really the first fully through the first quarter here in the U.S. But every week that goes by we have additional sites coming online. And as you recall, when all the sites were up and running in the Phase 1b, we dosed 14 NPM1-mutant patients in 3 months. Here, we’ve got to get to steady state in the Phase 2, but we’ll have more sites from which to draw, and we expect to see robust enrollment.

Got it. Thanks for taking my questions.

Thank you.

Our next question is from Roger Song with Jefferies. Please proceed with your question.

Great. Thank you for taking the question. Maybe just quick two questions for ziftomenib. One is given the very strong data from Phase 1b, have you started a conversation with the FDA regarding the potential PDUFA timeline? And the second question is around the Phase 2 statistical assumption, given you’re enrolling 85 patients, what is the null hypothesis you tried to clear for enrolling these 85 patients? Thank you, Troy.

Yeah. Thanks, Roger, for both of those questions. So, on the question of PDUFA, maybe stepping back for a second. We intend to take advantage of every development and regulatory strategy we can to accelerate the development, to accelerate time to market and overtake our competition. And I don’t want to be specific on our interactions with the agency. As everyone recalls, we were very measured in giving guidance around our FDA interactions around the Type C meeting. I’ll just tell you that, again, I’ll reiterate anything that we can do to accelerate the timelines we intend to do. We certainly feel like we have a very strong dataset with a 30% CR rate with full count recovery. And NPM1-mutant relapsed/refractory AML is clearly a high unmet medical need. In terms of the second part of your question, Roger, around the Phase 2 design, the 85 patients is really driven by safety that’s our view on what’s needed to support a marketing application. Again, in the NPM1-mutant relapsed/refractory population, we haven’t disclosed the specifics of the statistical design, nor do we intend to. But, again, I’ll reiterate to you that we intend and we’ve built into our development strategy and our protocol, every opportunity to go more quickly if the data permits. So I’ll just leave it with that, and I don’t want to get too much more into the details. But we’re quite enthusiastic at the rate of enrollment, the rate of interest, and very much looking to continue the trend that was becoming clear in the Phase 1b.

Great. Thanks for the comment. I appreciate it.

Sure.

Our next question is from Peter Lawson with Barclays. Please proceed with your question.

Thanks, Troy. I guess, on ziftomenib, two questions. When can we see the combination data, like we see that by year-end? And then just as we think about the EU, do you think they’ll be comfortable with differentiation syndrome?

Peter, forgive me. Could you repeat the second part of the question? I want to make sure I understood it. The first part, I think was clear.

Oh, yeah. So as you think about kind of a global study, and you try it was in the EU?

Oh, EU. Got it.

How are you thinking about adding European sites, and if they’re comfortable with differentiation syndrome?

Yeah. Yeah. So let’s take that question first. As we alluded to in the prepared remarks, there’s strong precedent that of the ability to manage differentiation syndrome in combination with standards of care. That’s what we’re seeing with the IDH inhibitors. And if you look at the data, the differentiation syndrome was certainly mitigated. I think, in the discussions we’ve had with investigators, they’re very much of the mind that that should both allow us to mitigate the differentiation syndrome that we’ve seen in the Phase 1 and really unlock the full therapeutic value of ziftomenib. So there isn’t any real concern, the European sites, as you know, they just take longer to get up and running. It’s not unusual for some of the European sites to take 9 to 12 months. So now going to kind of the first part of your question, we expect that we’ll have – we’re very much working toward initiation of the 007 trial here in the second quarter. And I’ll just remind everybody that in the Phase 1, we observed responses as a monotherapy at both the 100 milligram and 200 milligram doses, where the starting dose in combination is at 200 milligrams. So, I think, we’re well within the window in terms of potential activity, I don’t want to guide, Peter, yet to disclosure – sort of timing of disclosure of data. I will say, we appreciate it’s a question on people's minds. We’re confident in our ability to mitigate any differentiation syndrome through combination, and we’ll look for an opportunity, if possible, to share that data later this year. I think it’s premature to be more specific on venue or timing, but it’s something we definitely are – it’s one of our goals.

Great. Thanks so much.

My pleasure.

Our next question is from Li Watsek with Cantor Fitzgerald. Please proceed with your question.

Okay. Thanks for taking my questions. I got a couple of questions on the combo study. I guess, you initiate the 007 study in, I guess, the second quarter. Just wondering what are the gating steps here? And how should we think about the enrollments in these two cohorts, is there any chance that we can see the combo data in the KMT2A cohort this year?

Yeah, Li, so the sort of a follow-on from – thank you for the two questions. A bit of a follow-on from Peter’s question. So what we’re waiting for is just is the site activation and steady startup over the last several years, it’s just taken longer to get sites up and running, I think not only in oncology, but in a number of disease areas. That’s just – they’re overloaded. They don’t have enough staffing. I mean, we all sort of know what’s going on. Our sites are very motivated, they’re very engaged. We’ve had no challenges at all in getting sites interested to participate, now in three potential studies, the registrational study 001, the 007, and the 008. And I should have commented in response to Peter’s question, we actually will have European sites on the 001 study. They’re just going to come online a little bit later than the U.S. sites. Li, as you know, we’re basically what we’ve tried to do with the strategy with 007 and 008 is to make the funnel as large as possible, so that any potential patient with KMT2A or NPM1 on any regimen is eligible to come into one of those two trials. That’s one of the ways we’re looking to really maximize the value of ziftomenib in AML, and that’s really resonated with investigators. It’s likely, of course, that the venetoclax containing regimens will probably go more quickly, because those are the largest number of patients. But, we’re going to open the cohorts as quickly as we can. With regard to your question around timing, I’ll just repeat what I said to Peter, that the focus is very much going to be on a mid-year clinical update in the NPM1 population. And then as soon as it’s appropriate to provide an update on the combo either the KMT2A or the NPM1, we’ll look to do that in some form and fashion. I just can’t be any more specific because, again, the team is just cranking on getting the trial sites open, and the first patients on the study.

Thank you.

Sorry, and one other additional point that I’m just reminded of. Just for everybody’s benefit, we can of course combine data on KMT2A regardless of the combination regimen to show the mitigation of differentiation syndrome. So it’s not as though we have to wait for any one of those cohorts to enroll. They certainly the expectation is the combination will mitigate the signs and symptoms of differentiation syndrome. And we’ll look to show that it’s just with us not yet having patients on study, it’s a little hard to do. The crystal ball isn’t as clear as I’d like it to be.

Our next question is from Brad Canino with Stifel. Please proceed with your question.

Great. Thanks for the question. And Troy, it’ll really be a follow-up to what you just said. Because, I just want to get your working thoughts on the ziftomenib combination data and how quickly you think they can be used to serve as evidence that differentiation syndrome can be mitigated. And really, it’s a question of sample size. Do you think it would only take a handful of KMT2A patients to show that differentiation syndrome is lower and that you can drive those patients towards a response? I think the corollary there is on efficacy, how do you then think about parsing the contribution of efficacy from the components with a small end in that scenario?

Yeah, Brad, so two good questions there. On the – what does it take, it’s probably a little larger than a handful, just to be colloquial maybe a couple of handfuls. But if you’ve got – if you’re not seeing – or if you’re seeing sort of mitigated differentiation syndrome, i.e. grade 1, grade 2, you’re not seeing the more severe forms of differentiation syndrome; you can calculate the posterior probabilities and figure out what’s needed. The more patients you have, the more confidence you have. But, we were seeing a 30%-plus rate of differentiation syndrome, so it won’t take too long. In terms of the contributions of efficacy, that obviously will require more patients to parse them out. But I’ll just remind folks, neither 7+3 nor venetoclax are particularly effective at driving durable responses in these patients, particularly in the KMT2A patients. So you should get a signal fairly early on. And I’ll just remind you, Brad, we were seeing all of – many of the other correlates of disease control, blast count reduction, symptomatic improvement and so forth. So we’re pretty confident that this is going to solve the problem. And as far as the NPM1 is concerned, we’re in good shape there. We don’t really have to take anything beyond the traditional measures to manage the differentiation syndrome. This is really just a question now about KMT2A.

I appreciate that. If I can sneak in one on the FTI decision to deprioritize the EGFR combination, how should we read that in terms of the potential KO-2806 combination partners? Because you previously mentioned you’d be using new targeted therapy combo partners for that drug early on? Well, those combo partners being types where you’re trying to enhance overall response rates, and we can see that earlier or versus delaying response like an EGFR combo? Are there…

Yeah, Brad, I appreciate – yeah, sorry to step on your question there. I appreciate the way you ask the question, because you’ve already with your question anticipated the answer. So we’re seeing pre-clinically, the potential to combine FTIs and, most notably, 2806 with a number of different targeted therapies. And I listed EGFR inhibitors, PI3 kinase alpha inhibitors; you’ve now heard us reference TKIs, specifically in renal cell carcinoma and KRAS inhibitors. And to your specific question, one of the things that we’re always doing is taking in data, scientific data, clinical data, business data, and macroeconomic data. We realized that we want to get to clinical datasets that will show the ability for FTIs to realize the promise of the potential for additive or synergistic activity. We think there may be opportunities, Brad, to do that more quickly than was the case with osimertinib. So it was not in any way a lack of interest or enthusiasm on our part, but really a recognition that we need – we operate in a world, where we have to show data as quickly as possible. The amount of value that we can create per dollar and per unit time is a measurement of our success, and we want our shareholders to understand. We think we’ve got a winner with ziftomenib. We think that 2806 is looking very strong and coming on more quickly than we expected. So I think it’s appropriate particularly in these times to look at the portfolio and, say, where can you create the greatest amount of value in the shortest amount of time and the fewest dollars. And that’s exactly what we did.

Okay. Thanks, again.

Sure.

Our next question is from Tiago Fauth with Credit Suisse. Please proceed with your question.

Hey, this is Jeffrey Weiner on the line for Tiago. Thanks for taking our questions. So we’ve heard a lot about discussion about the relative value of an MRD positive CR versus an MRD negative CRh in the relapsed/refractory setting. So what’s your perspective on that? And are there any data that really addressed that question? And then is there any read-through to durability?

Yeah. So let me parse that for you, because there’s a couple of things that are mixed in there. The value of the CR versus the CRh is that you have full reconstitution of platelets and neutrophils. So if patients have incomplete responses, they’re at risk to either have infection or bleeding. So that’s why we keep underlining. We observed a 30% CR rate, not CRh, not CRI that’s meaningful from the standpoint of putting the patients in the best possible position. And the second part of your question is MRD negativity. There’s pretty good evidence that MRD negativity is a useful surrogate in terms of thinking about survival. It’s not yet at the point where it’s acceptable as a surrogate endpoint. But there’s definitely an effort underway, there’s even a consortium to do that. You want to be able to, if possible, to drive patients to MRD negativity; you can have MRD negativity with various, if you will, grades of complete response, you’d like to get as many patients as possible to MRD negativity. The question becomes, though, what are you using to measure it? Are you using flow? Are you using something more sensitive like PCR? And that’s where the devil is in the details. But I think we’ve been very impressed by the rate of MRD negativity that we’ve seen. We’ll look forward to getting that as one of the elements of the update mid-year really that’s going to serve as a comprehensive update on the entire NPM1 experience in the Phase 1 trial and MRD negativity will be part of that.

Great. Thanks for taking the question.

Sure.

Our next question comes from Eva Privitera with Cowen. Please proceed with your question.

Hi. Congrats on the quarter. And thanks for taking our questions. Clarification for the mid-year update for the Phase 1, do you expect to present data on patients who have gone on to transplant?

Eva, yeah, so thanks for the question. So we will provide an update of every NPM1-mutant patient in the Phase 1. So the short answer to your question is yes. For a patient who has gone on to transplant, we’ll – to the best of our ability, extend to data in the database. We’ll give you an update on all of the patient’s experience that we’ve seen. We’ve been very impressed with not only the depth of response, but the durability of response and look forward to providing that update at the time.

Great. And I have a follow-up on the further work on KMT2A disease. What are the plans for pursuing additional monotherapy work? And will this happen prior to going into combos or kind of happen concurrently?

Yeah. So I’m glad you asked the question. If we were not at this point intending on pursuing monotherapy further. For the primary reason that we believe in order to maximize the benefit to patients, we need to pursue in the case of KMT2A, we need to pursue ziftomenib in combination. It will allow us to drive – we believe deeper and more durable responses; it’ll mitigate the differentiation syndrome. It’s also probably obvious to folks, it will also support a global marketing application, although it’s not off the table that you can do a single-arm study, for example, in Europe, it’s highly unusual. And so these combination studies set the table for ultimately a global development – global filing, both in the KMT2A and the NPM1. So we’ll get there just as quickly as we can, but all of our efforts going forward with KMT2A will be in combination.

Perfect. Thank you.

Sure.

Our next question comes from Reni Benjamin with JMP Securities. Please proceed with your question.

Hey, thanks for taking the questions and squeezing me in. Just, I guess, starting off, Troy, can you talk a little bit about a clinically meaningful median duration of response? I think in the Phase 1, we had seen somewhere around 4 to 5 months or so. And – but we’re looking at different doses, and we have different genetic types. I guess, within the NPM1 population, what do you feel really drive kind of uptake? And we’ll give you kind of the go ahead that you want? And then also, I guess, it’s my second question, as you know just building on Brad’s kind of benchmarking of efficacy and the combination studies, as you think about prioritizing these studies, just within 007 is like echo or it’s right. How do you go about doing that, if the efficacy is meeting your benchmarks? Do you focus on frontline? Do you just spend everything you can on both frontline and relapsed/refractory? Any sort of thoughts as to how you start to funnel these studies into registrational combination study?

Yeah. So two good questions, Reni, and let’s take them in turn. So as far as we know and the kind of the guidance that we’re using, 4 to 6 months of duration of response in the relapsed/refractory population is approvable. Now, you’d like to do, obviously, you want to do as good as you can, you want to give these patients the longest duration possible, but the bar to approval is probably 4 to 6 months. And you were right, kind of in the – we were – the data was immature. But we were getting into the right zip code at the time of the ASH presentation. I look forward to providing an update sort of mid-year here this year. Consider that the NPM1 overall survival is a median of about 6 months without menin inhibitors. So if you’re talking about four to 6 months duration of response, that’s a good improvement that’s where that number comes from. The second piece of your question is kind of how do a prioritization. And I would say the following, in your scenario, where multiple regimens look good. This is – I’d like to say several of you’ve heard me say, let’s put that in our bucket of extremely high-class problems, right? If we’ve got multiple regimens that look good, you don’t have to register all of them. We will continue to be good fiduciaries and prioritize those combinations that we believe are going to drive the greatest commercial value. And you already know what they are, it’s clear. Venetoclax containing regimen with or without azacitidine, let’s see how that plays out, would you need the triplet or the doublet. And then, of course, the FLT3 containing regimens, because at least in the relapsed population, a significant number of the NPM1-mutants are also FLT3 new mutant, co-mutants those are probably ran the two greatest populations. But if we got a handful of 10 to 20 patients worth of safety and activity data to support other regimens that just helps broaden the utility, broaden the knowledge base and the comfort among the hematologist, oncologist, who ultimately are out in the community using ziftomenib. So we’re going to do just enough that we give everybody comfort that that zifto is almost – it’s an amazing drug, right? It’s highly mutant selective, extremely efficacious, and yet it’s also extremely tolerable. The patients say to us, the only reason I know on the drug is I take a pill once a day in the morning. If we can couple that up with the commonly used regimens, we think we’re in great shape.

Perfect. Thanks for taking the questions.

Our pleasure.

We’ve reached the end of the question-and-answer session. I would now like to turn the call back to Dr. Troy Wilson for closing comments.

Thank you, Rob, and thank you all once again for joining our call today. We’ll be participating in both the Cowen and the Barclays Health Care conferences over the next several weeks, and we hope to see many of you there. In the meantime, if you have additional questions, please feel free to contact Pete, Tom or me. Thank you all once again and have a good evening.

This concludes today’s conference. You may disconnect your lines at this time. And we thank you for your participation.