Earnings Call: Q1 2018

May 8, 2018

Good day, ladies and gentlemen, and welcome to the Q1 2018 Cura Oncology, Inc. Earnings Conference Call. At this time, all participants are in a listen only mode. Later, we will conduct a question and answer session and instructions will follow at that time. I would now like to turn the call over to Pete De Spain, Vice President, Investor Relations. Please go ahead. Thank you, operator. Good afternoon, and welcome to Kura Oncology's conference call. Joining me on the call from Kura are Doctor. Troy Wilson, our President and Chief Executive Officer Heidi Henson, our Chief Financial Officer and Doctor. Antonio Galvezto, our Head of Development and Chief Medical Officer. Before I turn the call over to Doctor. 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 report Accura's filings with the SEC, which are available from the SEC or on the Accura Oncology website for information concerning risk factors that could affect the company. With that, I will now turn the call over to Doctor. Troy Wilson, President and CEO of Kura Oncology. Thank you, Pete. At Kura, we're committed to realizing the promise of pursuing medicines and ultimately to helping patients with cancer lead better longer lives. We set out to assemble a pipeline of small molecule drug candidates that target oncogenes and cancer signaling pathways, then pair them with molecular or cellular diagnostics to identify those patients most likely to respond to treatment. Now less than 4 years from our founding, we are on the verge of our first registration directed study with our lead drug candidate Tipifarnib. Tipifarnib is potent, selective and orally bioavailable inhibitor of the farnesyltransferase enzyme that we licensed from Janssen. We're currently evaluating tipifarnib in multiple solid tumor and hematologic indications. Our most advanced indication is in HRAS mutant head and neck squamous cell carcinomas or HNSCC. In March, we provided a regulatory update following a successful end of Phase 2 meeting with the FDA. Based on the clinical activity we've observed in our ongoing Phase 2 RUN HN study, as well as encouraging feedback from the agency, we're now planning to conduct a global registration directed trial of tipifarnib in at least 59 patients with HRAS mutant HNSCC who have received prior platinum based therapy. We're calling this our AIM HN trial. The primary endpoint of AIM HN is overall response rate. Our trial design has approximately 80% power to detect the difference between a null hypothesis of 15%, which is the point estimate of second line therapy ORR for recurrent and metastatic disease and 30% an ORR considered of interest. Based on the feedback we've received from FDA, we believe this trial is positive, could support an application for accelerated approval. In addition, we were encouraged that FDA did not require patients to have received second sorry, to have received prior second line therapy, including immune therapy, despite the fact that several agents are approved for use in the second line in the U. S. This allows us to enroll any post platinum patients independently of line of treatment and gives us maximum flexibility in terms of enrolling patients both in the U. S. And abroad. Finally, given the extensive clinical data previously generated by Janssen and based on input from the agency, we believe our safety database should be adequate to support an NDA filing if the AIM HN study is positive. We are planning to initiate our AIM HN trial in the second half of this year. We anticipate the trial will require fewer than 100 clinical sites worldwide and take approximately 2 years to enroll. Pending a final statistical analysis plan, the trial could need as few as 15 confirmed responses in order to reject the null hypothesis and meet its primary efficacy endpoint. Thus, although we're projecting a 2 year enrollment period, the trial has the potential to become positive prior to the completion of enrollment as was the case for our RUN HN trial. In conjunction with the AIM HN trial, we're also preparing to initiate SEQ HN, a multicenter, non interventional screening and outcome study. There are 2 primary goals of SEEK HN. The first is to facilitate the identification of patients with HRAS mutations for potential enrollment into our AIM HN trial. The second goal is to characterize the natural history of patients with recurrent or metastatic HNSCC with HRAS mutations. We know for example that the response rates for the 3 agents currently approved for treatment of HNSCC in the second line are in the range of 13% to 16%, but the response rate for the HRAS mutant population is unknown. Although we're using a null hypothesis of 15% in our AIM HN trial, none of the first nine patients enrolled in our ongoing Phase II trial experienced a response on their last prior line of therapy. Thus, the response rate of atres mutant patients to the standard of care may be less than 15%. Data in the literature have already shown a lesser response rate to standard first line therapy and poorer prognosis in HRAS mutant HNSCC patients as compared to HRAS wild type patients. And we expect to confirm those observations in our data set. For that purpose, CK HN is designed as a case control study matching our AIM HN patients with HRAS mutations against those who are HRAS wild type using factors such as age, line of therapy and type of treatment. This will provide us with a better understanding of the natural history of patients with HRAS mutations and their medical need. We took this innovative parallel design of Seq HN and AIM HN to the FDA and we were very encouraged by the feedback we received. If our AIM HN trial is positive, the agency is willing to consider the totality of the data, including the results of AIM HN, CK HN and our ongoing RUN HN trial to determine the appropriateness and nature of an approval and post approval commitments. We received similar input in 2 national scientific advice meetings in Europe. Rather than conducting we've now elected to run both studies under a single clinical protocol for operational efficiency. We are currently in the process of finalizing the updated protocol and expect to initiate seek HN concurrently with AIM HN in the second half of the year. An important element of our development strategy for tipifarnib in HNSCC is our ability to identify patients with HRAS mutations. This is the same challenge faced in the development of other targeted therapies, including inhibitors of TRK, ROS1 and RET, namely the need to screen and identify relatively rare patients among the overall population. In order to avoid any delay as a result of the new study protocol, we are already triggering many of the HRAS sequencing activities included in Seq HN, including contracting academic laboratories and central tumor DNA sequencing facilities in the U. S, Europe and Asia and developing patient and physician directed materials in collaboration with the Head and Neck Cancer Alliance and academic groups. We are also developing a travel assistance program for patients that is designed to support our ongoing RUN HN and also support AIM HN. We remain squarely focused on enrollment and will continue to pursue opportunities to support patient identification and screening as we prepare for the initiation of AIM HN and CK Chan. Meanwhile, development activities are underway to expand the potential opportunity for tipifarnib in solid tumor indications with aTRAS mutations beyond HNSCC. We've expanded our ongoing Phase 2 clinical trial of tipifarnib in HRAS mutant solid tumors to include an exploratory cohort of patients with other HRAS mutant squamous cell carcinomas. Given that the majority of investigators in our ongoing RUN HN trial specialize in head and neck cancers, we expect this 3rd cohort to enroll primarily patients with cutaneous squamous cell carcinomas that are also seen in head and neck clinics. We also recognize the potential opportunity for tipifarnib in HRAS mutant lung squamous cell carcinoma, a histology with a similar genetic pattern as HNSCC. Just last month at AACR, we presented new data showing that Tipifarnib is highly active in preclinical models of HRAS mutant lung squamous cell carcinoma. To evaluate this opportunity, we are collaborating with the Spanish Lung Cancer Group, a cooperative group that consists of more than 150 public and private oncology centers in Spain on a proof of concept trial of tipifarnib in HRAS mutant lung squamous cell carcinoma. We anticipate this investigator sponsored trial to initiate later this year. We continue to be very encouraged by the clinical and preclinical data we've generated supporting the potential of Tipifarnib as a treatment for solid tumors characterized by HRAS mutations. Our goal 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 its potential use to include other diseases of high unmet need. Now let's turn our attention to the opportunity for tipifarnib in hematologic malignancies, which represents an important and exciting second major focus of our development strategy with tipifarnib. At ASH in December, we presented new findings that identified activation of the CXCL12 pathway and bone marrow homing of myeloid cells as potential biomarkers of Tipifarnib's activity in certain hematologic malignancies including PTCL, MDS and myeloid neoplasia, CMML and AML. Based on these observations, we're now working to prospectively validate potential biomarkers in each of our 3 ongoing Phase II trials. In PTCL, we are evaluating tipifarnib in patients with angioimmunoblastic T cell lymphoma or AITL as well as patients with PTCL who have the absence of a single nucleotide variation in the 3 prime untranslated region of the CXCL12 gene. Our MDS study includes a cohort of patients with neutropenia at steady entry and is evaluating CXCL12 pathway biomarkers as a method of patient enrichment. Finally, you may recall we announced at ASH our Phase 2 study of tipifarnibin CMML had achieved its primary efficacy endpoint. Although the results were preliminary, we observed a signal that supported the use of CXCL12 pathway biomarkers to stratify CMML patients who may benefit from treatment with Tipifarnib. On the basis of that data as well as our retrospective analysis of previous studies of Tipifarnib in AML conducted by Janssen, we have amended our Phase 2 trial in CMML to comprise MDS MPN overlap syndrome, a group of myeloid disorders that include CMML and a cohort of relapsed refractory AML patients with CXCL12 pathway biomarkers. Our strategy for tipifarnib in hematologic malignancies is to replicate the approach that has served us well in our ongoing trial in HRAS mutant HNSCC. Specifically, we're looking to confirm the clinical activity of tipifarnib, validate our biomarker hypotheses, secure patent and or regulatory exclusivity, optimize dose and schedule for each disease and generate clinical data that supports advancement to 1 or more registration enabling studies. In keeping with that strategy, we recently announced the issuance of US Patent 9,956, 215 methods of treating cancer patients with farnesyltransferase inhibitors. Similar to our recently issued patent covering the use of tipifarnib in HRAS mutant HNSCC, the 215 patent provides coverage of the use of tipifarnib as a method for treating patients with CXCL12 expressing PTCL or AML. Moreover, issuance of the 215 patent reinforces our commitment to unlock the value of Tipifarnib in genetically defined patient populations. Our goal is to provide initial data in 1 or more biomarker enriched hematologic indications by the end of 2018. Now let's quickly turn our attention to our 2 emerging pipeline programs, beginning with our ERK inhibitor KO-nine forty seven. We're advancing KO-nine forty seven as a potential treatment for patients with tumors that have dysregulated activity due to mutations or other mechanisms in the MAP kinase pathway. Our Phase 1 dose escalation trial of KO-nine forty that will enable us to evaluate KO-nine forty seven in genetically that will enable us to evaluate KO-nine forty seven in genetically selected patients whose tumors are sensitive to ERK inhibition. In that regard, last month at AACR, we presented preclinical data for KO-nine forty seven including the identification of 11q13 amplification as a potential biomarker of activity for KO-nine forty seven in squamous cell carcinomas. Amplification of chromosomal region 11q13 is a common genetic alteration in squamous cell carcinomas comprising approximately 20% of HNSCC and approximately 50% of esophageal squamous cell carcinoma. We're also advancing KO-five thirty nine, a potent and selective small molecule inhibitor of the menin MLL interaction that has demonstrated potential antitumor activity in genetically defined subsets of acute leukemia, including those with oncogenic driver mutations in NPM1 and DNMT3A. Together with the mixed lineage leukemias, these mutations represent approximately half of diagnosed cases of AML. Pending successful completion of IND enabling studies, we expect to submit an IND application for KO-five thirty nine in late 2018 or early 2019. This covers the update on our development programs. I'll now turn the call over to Heidi for a discussion of the financial results for the Q1 of 2018. Thank you, Troy, and good afternoon, everyone. I will provide a quick overview of our financial results here on the call and invite you to review our 10 Q filed today for a more detailed discussion. R and D expenses for the Q1 of 2018 were $11,600,000 compared to $5,500,000 for the Q1 of 2017. The increase in R and D expenses for the quarter was primarily due to an increase in clinical development activities related to tipifarnib. G and A expenses for the Q1 of 2018 were $3,400,000 compared to $2,100,000 for the Q1 of 2017. The increase in G and A expenses was primarily due to increases in non cash share based compensation and personnel costs. Net loss for the Q1 of 2018 was $14,600,000 or $0.46 per share compared to a net loss of $7,500,000 or $0.39 per share for the Q1 of 2017. As of March 31, 2018, we had cash, cash equivalents and short term investments of $138,200,000 which included $57,700,000 in net proceeds raised under our ATM facility in January 2018. That's compared with $93,100,000 as of December 31, 2017. We believe these funds give us the resources to advance our pipeline of drug candidates through a series of upcoming potential data catalysts and expect that our current cash, cash equivalents and short term investments will be sufficient to fund current operations into the first half of twenty twenty. With that, I will now turn the call back over to Troy. Thanks, Heidi. Before we jump into Q and A, let me quickly lay out our potential milestones for the remainder of the year. For tipifarnib, initiation of AIM HN and SEK HN in the second half, additional updates from our ongoing RUN HN trial in the second half, initiation of a proof of concept study in HRAS mutant squamous non small cell lung cancer through the Spanish Lung Cancer Group and biomarker enriched data in hematologic malignancies in the second half. For KO-nine forty seven, data from the Phase 1 dose escalation trial in the second half and for KO-five thirty nine, submission of an IND application in late 2018 or early 2019. With that operator, we're now ready for questions. Thank Our first question is from Jonathan Chang with Leerink Partners. Your line is now open. Thanks for taking my questions. First, can you talk about the reasons for confidence that the AIM HN study will enroll patients in a timely manner and the steps you're taking to ensure that, including the SEEK HN study in a number of clinical sites, etcetera? Sure, Jonathan. I'll take a crack at that and then Antonio can add his thoughts. As we've said previously, we've seen an increase in the rate of enrollment of HRAS mutant patients as we've been conducting this study. It took us approximately 18 months to enroll the first three patients, approximately 6 months to enroll the next three patients, 3 months to enroll the final three patients and that's the last data cut that we gave. And we continue to be pleased with the rate of enrollment. We have approximately 25 sites, clinical sites open now. So to your question about our confidence around enrolling AIM HN, we're guiding to needing fewer than 100 clinical sites. If you look at that as roughly, call it a tripling of the number of clinical sites, just to be conservative, we think that should bring us in on time within the enrollment projections that we've given you. Great. That's helpful. Thank you. Second question, can you help set investor expectations ahead of the Phase II TIPPE biomarker front for heme malignancies? So, yes, again, I'll take a crack at that, Jonathan. So as I said in the prepared comments, the program that we're running with the hematologic malignancies is very similar to what we used in the case of HNSCC. Namely, we're looking to satisfy those elements to confirm the clinical activity to validate the biomarkers that we've identified to secure patent or regulatory exclusivity, dose and schedule and then of course, perhaps most importantly, the clinical data. We're running studies as we've indicated in PTCL, in MDS and then in the myeloid neoplasia, which are 1 in CMML and 1 in AML. The PTCL study is probably the most advanced just from a timing perspective. You've seen an update on that data set at last year's ASH where we not only identified CXCL12 as a marker in PTCL, but we then identified CXCL12 pathway biomarkers as markers in the other diseases. That along with the data that we're generating gives us confidence that we're on the right track in terms of the clinical data. What we're looking to come back to you with is sufficient clinical proof of concept that's the equivalent of what we generated in the case of HRAS mutant squamous cell head and neck data, where you say to yourself, okay, there's a sufficient level of clinical activity here to justify then going to the next step of a registration directed study, as well as those other elements. And that's why part of why we were so pleased to see the patent issuance on the CXCL12 patent because that's sort of an important, I think box to check on the way to the clinical data later in the year. It's our finally, it's our goal to come with data for at least one indication, but it's still relatively early in the year and we're doing our best to move them all forward. I can add a little bit of color to the Readiness. So, we described the number 2s last year, CXCL12, UTR variations in the gene, expression of CXCL4, CXCL2, all those clinical biomarkers, all those tools have been already developed. They are at clinical grade. We can apply it in the studies. The appropriate changes in the protocol, appropriate amendments have been already conducted. Certainly, all the tools are ready to be deployed. Great. Thanks. And just one last one, if I may. On the menin MLL program, can you talk about reasons for excitement here? And what a development strategy could look like when this program enters the clinic? Thanks. Sure. So let's start with excitement first. The history of drug development in AML in particular, Jonathan, has been marked by 2 features. One feature is a lot of genetic heterogeneity. So the thought is there are a number of mutations that contribute to the disease. And the second is really the lack of sort of durable responses in the relapsed refractory setting. All of our data to date is preclinical, but we are excited by the fact that with the menin MLL inhibitor with KL-five thirty nine, we've generated very persistent responses in preclinical models and we've shown data relative, for example, to FLT3 inhibitors where you can see there's a qualitative difference in the robustness of the response. We also seem to see activity in AML tumors that have NPM1 mutations, DNMT3A mutations as well as the mixed lineage leukemias, those collectively, if you combine them are greater than 50% of the tumors of AML. So in our it's still early days of preclinical data, but we're really excited to the fact that that's going after sort of the two elements that have held back drug development in that disease in particular. Thank you. Sure. Our next question is from Joel Beatty with Citi. Your line is now open. Good afternoon. This is Sean calling in for Joel. Thank you for taking my questions and congrats on your recent progress. So for my first question, in your pivotal AIM HN study, can you talk a bit on your assumptions regarding how many patients that you plan to enroll on each prior treatment line of therapy? So Sean, the feedback that we received from FDA is that any patient essentially who is post platinum is eligible for entry into the study. And importantly, we don't have to take patients that have experienced either immune therapy or cetuximab. We would expect a majority of the patients in the US to likely have been treated with immune therapy because that is the approved standard of care. The situation may be different in Europe. I'm not sure we can give you much more clarity than that on how we would expect it to break down. But if you look at the last data update that we gave in February, you can see the patients are coming having experienced chemotherapy, cetuximab, various immune therapies, we would expect that I think that the population in the AIM HN trial will be similar in composition. Yes. I would say it's fair to say, maybe a little bit differently because we are the Phase II is slated mostly for U. S. Accrual. So it's fair to say that the expectations that the large majority of the patients will be second line patients, just considering the penetrance in of other therapies, particularly immunotherapy in other countries. Obviously, we will have accruals in the U. S. And then the expectation there that they may have second line treatment. But again, consider the distribution and the use of other therapies, our expectation will be the large majority of the patients to be second line patients. Great. That's helpful. And just as a brief follow-up, we noticed that when going through the RUN HN data that the 2 patients with the longest duration of response were both pretreated with cetuximab. And also in your recent slide deck, you kind of mentioned that cetuximab may enrich for HRAS mutations. Do you have any data suggesting that cetuximab may make a more homogeneous HRAS mutant tumor? Or maybe just at a high level, do you have any thoughts on this? So it's actually known that the it's actually published, know that the SRAS mutation in head and neck is a main mechanism of resistance to anti EGFR therapy. It resembles in many ways KRAS in the colorectal population. Whether that is a mechanism that is only specific to EGFR and not other therapies, it's hard to say. You may have seen also in our data set, patient with the RAS mutations that they were resistant to treatment within your therapy. Something that you know that it's important to take into account that it's hard to say where those FRASS mutations that develop resistant to the prior therapy are the novel mutations that have been published or in fact they were there all the time. And that I think is a real possibility. The only thing that this new therapy is doing is uncovering because that colon that is resistant may grow during the first or second line therapies. So we don't understand completely the biology, but in many cases, what we see with efraas resemble the behavior of KRAS in other indications such as colorectal and non small cell lung cancer. Our expectation is with time, it will as SRAS and Tipifarnib will follow the same direction that other targeted therapies that at some point treatment like cetuzumab may not be the best option for patients currently target the mutations, and that could be also the case for SRAS. Great. Thank you. That's very interesting. And then just my follow-up my final question. Regarding the developmental pathway forward in your heme malignancies, it seems like CXCL12 is a real focus. Do you foresee each of the heme malignancies getting kind of a tailored diagnostic or is the goal kind of a universal heme diagnostic? It's actually a very good question. So it's we do have to follow the data in the lymphoid setting, and the data that we have is in with T cell lymphomas. We do see CXCL12 as the main driver, and that may just follow the biology. There's a number of publication that show that how T cells are highly dependent on CXCL12. We don't understand completely the mechanism. It is possible that tipifarnib down regulates this production of CXCL12 is one of our hypotheses. In the other indications, we know the pathway is relevant. I mean, maybe possible that in some settings, you may see an overexpression of the ligand versus others that perhaps you see an overexpression of the receptor such as CXCR4. And there is something that we have previously presented at ASH. And it's part of our data set, but it's probably a predominant hypothesis in the myeloid indications, but we have only data currently limited to CMML and AML, other myeloid indications will have to be investigated. Excellent. Thank you for taking time for my questions. Sure. Our next question is from Konstantinos Iplakos with JMP Securities. Your line is now open. Hey guys, thanks for taking my questions. So switching gears if I may to KO-nine forty 7, you had a nice presentation at AACR that I wanted to touch on. So my first question, should we take the PDX models that you guys were looking at and namely HNSCC and esophageal SCC as sort of potential indications for 947 in the clinic? And then a quick follow-up, amplification of LQ13 was called out as a potential biomarker. Could you elaborate on that and sort of what that would look like going forward? Thank you. Sure, Constantine. Thanks for the question. I think you can certainly, HNSCC and the esophageal squamous cell carcinomas that are defined by that amplification are of interest to us from the PDX data. And that was that's the data I think you're referring to at AACR. It's certainly something that we'll be very interested in investigating at the appropriate point in time. Maybe I can let Antonio speak to the specifics of how that plays into the diagnostic. Yes. As you can imagine, there's a high degree of excitement in the company. This is something that have been an internal discovery. And as you can imagine, we consulted many experts where to go with an ERK inhibitor. And we got the expected input, BRAF, melanoma, perhaps KRAS. But we did a tremendous effort. We tested more than 200 PBX, trying to looking some cases for the serendipity, trying to find what will be the potential best indication for 947. We were very pleasantly surprised when we see these dramatic regressions in those tumors amplify with the 11Q13 amplicon. Obviously, we are now dedicating a lot of time to see what are the factors within the amplicon that are responsible for that effect. We have good candidates. It may be possible that the fact that it's an amplicon is because you need more than one gene for that pathway. I mean, again, we are generating data in support of these hypotheses. And obviously, that has the translation to the clinic. The 11q13 is, in many ways, an ideal biomarker. It's the DNA fragment. It's very clearly amplified. It can be detected by classical techniques by efficiency, but also the NGS will be able to identify. We're also very fortunate that it contains cycling D. As you can imagine, cycling D is in every panel. What actually, it gives already elect to us to whatever are the genes responsible in the amplicon, it will be amplified concurrently to Cyclin B. So you certainly can go to many of our clinical sites and use potentially cyclinb amplification as surrogate to allow the identification of patients that potentially can benefit from 947. So a great story, but potentially there that we are looking forward to pursue. Thanks very much. That was very helpful guys. Sure. Thanks Constantine. Our next question is from Chris Shibutani with Cowen. Your line is now open. Hi, this is Pam Barrett on for Chris Shibutani. Thanks for the update and congratulations on the progress. Can you help us understand the rationale for combining the potentially pivotal AIM HN trial with the natural history study, SEEK HN, under a single protocol and the steps that led that decision? And I might have a follow-up. Sure. Pam, good question. The simplest answer is one of operational efficiency. We realized that many of those activities that there was going to be a fair amount of redundancy if we were running them under 2 separate protocols in terms of redundant databases and so forth. And as we said, we're already triggering a number of the screening activities. So when we stepped back and looked at it, we thought both from an operational efficiency and a cost effectiveness, it was better to just combine them into a single protocol and be able to get both the screening information and the natural history. And then ultimately, for HRAS mutant patients identified, those patients can go into AIM for the treatment portion of the study. Excellent. That's very helpful. And given that these are now combined and that these will be important trials moving forward for the second half of the year, can you give us any color on how that could affect expenses? Did you say expenses? Yes, it's actually. Yes. So, it will be less expensive than so there's two answers. It's less expensive than probably running them independently. We do often get the question of why do SEEK now. And the best answer for that is, we're already out there screening patients, looking, seeking to identify HRAS mutant patients. We have to identify and follow a number of the wild type patients until we can find an appropriate match because it's a case controlled match protocol for whatever mutant patient. But by doing it now, we'll already we'll have the proper consents, we'll have the data, we'll be ready to go as opposed to needing to realizing that we may have to do this 3 or 4 years from now when we're in the midst of discussions around the appropriateness and the nature of whatever an approval might look like. So personally, we think this is the right thing to do now, not so much to support the application for accelerated approval, but ultimately to help support discussions around the nature and appropriateness of the approval. And we don't think it should affect the timelines. As we've said, it hasn't changed the cash guidance or anything. If we can add to that, so we wanted to conduct both studies independently because we wanted to initiate there's a certain change in the standard of care that head and head tumors are not usually sequenced. So we wanted to facilitate as much as possible the sequencing of these tumors. And for that, we're going to launch all 6 months sooner, the sick agent much sooner than the end agent. However, that implies that you have to create 2 databases, you have 2 theaters going to the sites. So it's certainly duplication of efforts and a duplication of costs. At some point, kind of like the light bulb came on and we decided, well, we actually can unify both protocols. We can trigger every sequencing activity that was associated to the CKS currently instead of waiting for the triggering of the common protocol. So that actually solved or accomplished the objective that we wanted to increase as much as possible the screening of these patients and also save costs and save resources by unifying both studies and then one single protocol. Okay. Thank you. And we have a follow-up question from Jonathan Chang. Your line is now open. Yes. Thanks for taking the follow-up. I'm just curious, can you guys talk about how you're thinking about business development opportunities for your pipeline programs, including TIPI-nine forty seven and 539? Yes. Jonathan, we can answer that question sort of in general terms. So we are evaluating options all the time for business development. One of the key considerations with Tipifarnib is the clinical data and the intellectual property situation and how those 2 are tied together. We are pursuing a strategy where we're looking to check most, if not all of those boxes that I articulated, including patent and or regulatory exclusivity. We're making good progress in the U. S. We have applications pending in other countries worldwide. That very much fits into our business development strategy. If you look at our pipeline more broadly, we have activities directed to, if you will, thoracic cancers, head and neck and lung, and we have activities directed to hematologic malignancies with AML, PTCL, MDS and so forth. So, as we think about business development strategy across the pipeline, there are potentially opportunities to do either deals that are defined by a particular therapeutic area focus or disease focus or deals that are defined by region. And those are the sorts of considerations that we are taking account of now. I think business development has to be an important part of any company. It's hard to do everything you want to do by yourself. But that hopefully gives you some color on the way that we are thinking about the strategy with tipifarnib and then across the pipeline. Great. Thank you. Thank you. I'm showing no further questions. I would now like to turn the call over back to Troy Wilson for any further remarks. Great. Thank you, operator. Thank you all again for participating in our call today. I'm very pleased with the progress we've made over the past quarter and we look forward to providing additional updates in the months ahead. Tomorrow, we'll be at the Deutsche Bank Conference here in Boston and we look forward to seeing many of you there. If you have any additional questions in the meantime, please feel free to contact Pete, Heidi or myself. Thank you again and have a good evening everyone. Ladies and gentlemen, thank you for participating in today's conference. You may now disconnect. Everyone have a great day.