Pete De Spain - Vice President, Investor Relations Troy Wilson - President and Chief Executive Officer Heidi Henson - Chief Financial Officer Antonio Gualberto - Head, Development and Chief Medical Officer

Jonathan Chang - Leerink Partners Konstantinos Aprilakis - JMP Securities Pam Barendt - Cowen

Good day, ladies and gentlemen and welcome to the Q1 2018 Kura Oncology, Inc. Earnings Conference Call. [Operator Instructions] 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 Dr. Troy Wilson, our President and Chief Executive Officer; Heidi Henson, our Chief Financial Officer; and Dr. Antonio Gualberto, our Head of Development and Chief Medical Officer. Before I turn the call over to Dr. Wilson, I would like to remind you that today’s call will include forward-looking statements based on current expectations. Such statements represent management’s judgment as of today and may involve risks and uncertainties that could cause actual results to differ materially from expected results. Please refer to Kura’s filings with the SEC, which are available from the SEC or on the Kura Oncology website for information concerning risk factors that could affect the company. With that, I will now turn the call over to Dr. Troy Wilson, President and CEO of Kura Oncology.

Thank you, Pete. At Kura, we are committed to realizing the promise of precision 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 farnesyl transferase enzyme that we licensed from Janssen. We are 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 have observed in our ongoing Phase 2 RUN-HN study as well as encouraging feedback from the agency, we are 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 are 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 no 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 have received from FDA, we believe this trial, if 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 are 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 are also preparing to initiate SEQ-HN, a multi-center non-interventional screening and outcome study. There are two primary goals of SEQ-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 three 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 are using a null hypothesis of 15% in our AIM-HN trial, none of the first 9 patients enrolled in our ongoing Phase 2 trial experienced a response on their last prior line of therapy. Thus, the response rate of HRAS 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 poor prognosis in HRAS mutant HNSCC patients as compared to HRAS wild-type patients and we expect to confirm those observations in our dataset. For that purpose, SEQ-HN is designed as a case-control study matching our AIM-HN patients with HRAS mutation 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 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, SEQ-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 two national scientific advice meetings in Europe. Rather than conducting SEQ-HN and AIM-HN as two separate studies, we have now elected to run both studies under a single clinical protocol for operational efficiencies. We are currently in the process of finalizing the updated protocol and expect to initiate SEQ-HN concurrently with AIM-HN in 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 track, Ross 1 and rat, 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 contracted academic laboratories and certainly tumor DNA sequencing facilities in the U.S., Europe and Asia and developing patient and physician directing 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 SEQ-HN. Meanwhile, development activities are underway to expand the potential opportunity for tipifarnib in solid tumor indications with HRAS mutations beyond HNSCC. We have 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 specialized in head and neck cancers, we expect this third cohort to enroll primarily patients with cutaneous squamous cell carcinomas that are also seen in head and neck clinics. We also recognized the potential opportunity for tipifarnib in HRAS mutant long 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 consist 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 have 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 neoplasias CML and AML. Based on these observations, we are now working to prospectively validate potential biomarkers in each of our three ongoing Phase 2 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 in a single nucleotide variation in the 3-prime untranslated region of the CXCL12 gene. Our MDS study includes the cohort of patients with neutropenia at study 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 tipifarnib in CMML has 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 and 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 the 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 are looking to confirm the clinical activity of tipifarnib, validate our biomarker hypotheses, secure patent and/or regulatory exclusivity, optimize dosing schedule for each disease and generate clinical data that supports advancement to one or more registration-enabling studies. In keeping with that strategy, we recently announced the issuance of U.S. patent 9,956,215 methods of treating cancer patients with farnesyl transferase 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 one or more biomarker enriched hematological indications by the end of 2018. Now, let’s quickly turn our attention to our two emerging pipeline programs beginning with our ERK inhibitor KO-947. We are advancing KO-947 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-947 in solid tumors is ongoing. We are working to define a dose in schedule that will enable us to evaluate KO-947 in genetically selected patients whose tumors are sensitive to ERK inhibition. In that regard, last month at AACR, we presented preclinical data for KO-947, including the identification of 11q13 amplification as a potential biomarker of activity for KO-947 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 are also advancing KO-539, a potent in selective small molecule inhibitor of the menin-MLL interaction that has demonstrated potential anti-tumor 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-539 in late 2018 or early 2019. This covers the update on our development programs. I will now turn the call over to Heidi for a discussion of the financial results for the first quarter 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&D expenses for the first quarter of 2018 were $11.6 million compared to $5.5 million for the first quarter of 2017. The increase in R&D expenses for the quarter was primarily due to an increase in clinical development activities related to tipifarnib. G&A expenses for the first quarter of 2018 were $3.4 million compared to $2.1 million for the first quarter of 2017. The increase in G&A expenses was primarily due to increases in non-cash share-based compensation and personnel cost. Net loss for the first quarter of 2018 was $14.6 million or $0.46 per share compared to a net loss of $7.5 million or $0.39 per share for the first quarter of 2017. As of March 31, 2018, we had cash, cash equivalents and short-term investments of $138.2 million, which included $57.7 million in net proceeds raised under our ATM facility in January 2018, that’s compared with $93.1 million 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 2020. With that, I will now turn the call back over to Troy.

Thanks, Heidi. Before we jump into Q&A, let me quickly layout our potential milestones for the remainder of the year, for tipifarnib initiation of AIM-HN and SEQ-HN in the second half, additional updates from our ongoing RUN-HN’s 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-947, data from the Phase 1 dose escalation trial in the second half and for KO-539 submission of an IND application in late 2018 or early 2019. With that, operator, we are now ready for questions.

Thank you. [Operator Instructions] 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 are taking to ensure that, including the SEQ-HN study and number of clinical sites, etcetera?

Sure, Jonathan. I will take a crack at that and then Antonio can add his thoughts. As we have said previously, we have seen an increase in the rate of enrollment of HRAS mutant patients as we have 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 are 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 have given you.

Great, that’s helpful. Second question, can you help set investor expectations ahead of the Phase 2 tipi data and hematologic malignancies in the second half of this year and put this into context in terms of the progress being made on the biomarker front for heme malignancies?

So, again I will take a crack at that, Jonathan. So as I said in the prepared comments, the program that we are running with the hematologic malignancies is very similar to what we used in the case of HNSCC. Namely we are looking to satisfy those elements to confirm the clinical activity, to validate the biomarkers that we have identified, to secure patent or regulatory exclusivity, dosing schedule and then of course perhaps most importantly the clinical data. We are running studies, as we have indicated in PTCL, in MDS and then in the myeloid neoplasias, which are one in CMML and one in AML. The PTCL study is probably the most advanced, just from a timing perspective. You have seen an update on that dataset 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 are generating gives us confidence that we are on the right track in terms of the clinical data. What we are 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 is 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. 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 are doing our best to move them all forward.

I can add a little bit of color to the readiness. So, we described the number last year. CXCL12, you see variations in the gene, especially CXCL4, CXCL2, all those clinical value markers, all those tools have been already developed. They are at clinical grades. We can’t apply it in the studies. The appropriate changes in the protocol appropriates amendment have been already conducted. And 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 two 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 KO-539, we have generated very persistent responses in preclinical models and we have shown data relative, for example, to FLT3 inhibitors, where you can see there is 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, it’s still early days of preclinical data, but we are really excited that 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.

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

This is Shawn calling in for Joel. Thanks 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 Shawn, 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 the majority of the patients in the U.S. to likely have been treated with immune therapy, because that is the approved standard of care. The situation may be different in Europe. I am not sure we can give you much more clarity than that on how we would expect it to breakdown, but if you look at the last data update that we gave in February, you can see how the patients are coming, having experienced chemotherapy, cetuximab, various immune therapies. We would expect – I think that the population in the AIM-HN trial will be similar in composition.

Yes. I will say it’s fair to say – maybe a little bit different, because we are – the Phase 2 is slated mostly for our U.S. accrual. So it is fair to say that the expectations that the vast majority of the patients will be second line patients just considering the penetrance in further therapies, particularly immunotherapy in other countries. Obviously, we will have accruals in the U.S. and then the expectation that they may have on second line treatment, but again, consider the distribution and the use of further therapies our expectation will be the last remaining 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 two patients with the longest duration of response are both pretreated with the cetuximab. And also in your recent slide deck, you kind of mentioned that cetuximab may enrich for HRAS mutations. Do you have any data suggest on cetuximab may make 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 part of it, it’s not that the HRAS mutation is the main mechanism of resistance to anti-EGFR therapy, irresistible in many ways KRAS in the colorectal population, whether that is the mechanism that is only specific to EGFR and not to other therapies, it’s hard to say. You may have seen also in our dataset patients with HRAS mutations that they were resistant to treatment with immune therapy, something that it’s important to take into account that it’s hard to say where those HRAS mutations that develop resistance to the prior therapy are de novo 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 immunotherapy is doing is uncovering, because that clone that is resistant may grow during the first or second line therapy, so that we don’t understand completely the biology, but in many cases, what we see with HRAS resemble the behavior of KRAS, another indication such as colorectal and non-small cell lung cancer. Our expectation is with time it will – HRAS and tipifarnib will follow the same direction that other targeted therapies that at some point treatment like cetuximab may not be the best option for patients currently targeting mutations and that continues to be the case for HRAS.

Great. Thank you. It’s very interesting. And then this is my follow-up final question regarding the development of pathway forward in your heme malignancies, it seems like CXCL12 is a real focus. Do you foresee each of the heme malignancy is getting kind of a tailored diagnostic or is the goal kind of universal heme of diagnostic?

It’s actually very good question. So 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 a main driver and that may just follow the biology. There is a number of publications 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 hypothesis. In the other indications, we know the pathway is relevant and it maybe possible that in some settings, you may see an overexpression of the ligand, but you saw there is some – perhaps you see an overexpression of the receptor such as CXCL4 and there is something that we have previously presented at ASH and it’s part of our dataset, but it’s probably a predominant hypothesis in the myeloid indications, but we have only data currently limited to CMML and AML all the myeloid indications will have to be investigated.

Excellent. Thank you for taking my questions.

Our next question is from Konstantinos Aprilakis with JMP Securities. Your line is now open.

Hey, guys. Thanks for taking my questions. So switching gears if I may to KO-947, 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 947 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, because you elaborate on that and so what that would look like going forward? Thank you.

Sure, Konstantin. 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 are referring to at AACR, but certainly something that we will 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 diagnostics.

Yes. So, if you can imagine there is a high degree of excitement in the company. This is something that have been an internal discovery. And if you can imagine we consulted many experts, where to go, we got ERK inhibitor and we got the expected input, BRAF, melanoma, perhaps KRAS, but we did a tremendous effort. We tested more than 200 PDX, trying to – looking for business for the serendipity trying to find what will be the potential base indication for 947 and we were very pleasantly surprised to see this dramatic regressions in those tumors amplify we did 11q13 amplicon. Obviously, we are now dedicating lot of time to see what are the factors within the amplicon that are responsible for that effect we have good candidates. It maybe possible that the fact that recent amplicons, because you need more than one gene for that pathway and again we are generating data and support to all of these hypotheses and obviously that have a translation to the clinic. The 11q13 is in many ways an ideal biomarker. It’s the DNA fragment. It very clearly amplify – it can be detected by classical techniques [indiscernible] but also the NGS will be able to identify. We are also very fortunate that it contains cycle B. As you can imagine cycling B is in every panel or actually it is already elect to us to whatever other genes responsible in the amplicon, it will be amplify concurrently to cycling B. So, you certainly can go to many of our clinical sites and use potentially cycling B amplification of a surrogate to allow the identification of patients that potentially can benefit from 947, so a great story potentially there that we are looking forward to pursue.

Thanks very much. That was very helpful, guys.

Sure. Thanks, Konstantin.

[Operator Instructions] Our next question is from Chris Shibutani with Cowen. Your line is now open.

Hi, this is Pam Barendt 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 SEQ-HN under single protocol and the steps that led that decision and I might have a follow-up?

Sure. So 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 two separate protocols in terms of redundant databases and so forth. And as we said, we are already triggering a number of the screening activities. So, when we stepped back and look at – we looked at and 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.

Yes. So it will be less expensive than – so there is two answers. It’s less expensive than probably running them independently and we do think we do often get the question of why do seek now. And the best answer for that is if we are already out there screening patients, 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 are already – we will have the proper consents, we will have the data. We will be ready to go as opposed to needing to realizing that we may have to do this 3 to 4 years from now when we are 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 have said, it hasn’t changed the cash guidance or anything.

If we can add, so we wanted to conduct both the studies independently, because we wanted to initiate – there is a certain change in the standard of care that, that [indiscernible] tumors are not usually sequenced. So we wanted to facilitate as much as possible the sequencing of those tumors and for that we wanted to launch all 6 much sooner, the SEQ-HN, much sooner than the AIM-HN. However, that implies that you have to create two databases, you have two CRAs going to the site. So it’s certainly a duplication of efforts and a duplication of cost. And at some point kind of like the light bulb came on and we decided what we actually can unify both protocols. We can trigger every sequencing activity that was associated to the SEQ-HN currently instead of waiting for the triggering of the current protocol, so that actually solved, while complete objective that we wanted to increase as much as possible the screening of these patients and also save cost and save resources by unifying both the studies under 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 call. I am just curious can you guys talk about how you are thinking about business development opportunities for your pipeline programs including tipi, 947 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 two are tied together. We are pursuing a strategy where we are looking to check most, if not all of those boxes that I articulated including patent and/or regulatory exclusivity. We are 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 of focus or a 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. And I am 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 am very pleased with the progress we have made over the past quarter and we look forward to providing additional updates in the months ahead. Tomorrow, we will 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.