Good day Ladies and Gentlemen, and welcome to the Kura Oncology Incorporated Second Quarter 2016 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. [Operator Instructions]. As a reminder, this conference call is being recorded. I would now like to introduce your host for today's conference, Mr. Robert Uhl with Westwicke Partners. Sir, you may begin

Thank you, Chanel. Good afternoon and welcome to Kura Oncology's second-quarter 2016 financial and operating results conference call. Joining me on the call from Kura Oncology are Dr. Troy Wilson, President and Chief Executive Officer; Heidi Henson, Chief Financial Officer and Antonio Gualberto, 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 the risk factors that could affect the Company. I will now turn the call over to Dr. Troy Wilson, President and CEO of Kura Oncology.

Thank you, Robert. Good afternoon, everyone and thank you for joining our teleconference. On today’s call we will provide a corporate update, including a discussion of our drug, discovery and development pipeline as well as financial results for the second quarter. After that Heidi, Antonio and I will all be available to take your questions. We’ll touch on some specific updates on our Tipifarnib development efforts later in the call, but before we did so, I wanted to take a few minutes to provide some context on two trends that shaped our approach to drug discovery and development. The first is an increased understanding of the molecular basis of cancer. Over the past several decades, scientists have identified hundreds of mutations, amplifications and translocations in DNA that may contribute to cancer. Some of the defects occur in the aero correcting machinery of the cell, others were in the signalling machinery which leads to the transmission of aerosignals. Some defects allow cells to become invasive, disrupting more healthy cells in tissues and finally some defects make the cancer cell immortal [ph] so that it’s resistant both to the body’s natural defense mechanisms as well as anti cancer therapies. At Kura Oncology, we are working to understand how specific molecular defects drive the activity of cancer cells and how we might use our small molecule drug candidates to address these defects. The second trend is how we identify these molecular level defects to prioritize the right therapy for the right patient. We witnessed wide spread migration of multiplex genetic testing from the research lab into the clinic. The promise of genetic testing is that if we can understand the molecular basis of cancer we can direct the patients to a targeted therapy specific for their disease. As a result nearly at nearly…

Thank you, Troy, and good afternoon, everyone. Total operating expenses for the second quarter of 2016 were $6.8 million compared to $5.9 million for the second quarter of 2015. The increase in expenses is primarily due to the expansion of our research and development activities and the costs of being a public company. R&D expenses for the second quarter were $4.9 million compared to $4.4 million for the same period in the prior year. Meanwhile, G&A expenses for the second quarter were $1.9 million compared to $1.5 million a year earlier. Our net loss for the second quarter of 2016 was $6.7 million versus $5.6 million for the second quarter of 2015. During the second we put in place a $20 million term loan facility of which $7.5 million was drawn down during the period. As of June 30, 2016 we had $80.1 million in cash, cash equivalents and short term investment and approximately 21.4 million shares of common stock outstanding. We expect that our current cash, cash equivalent, short-term investments will be sufficient to fund our current operations into 2018. With that, I will now turn the call back over to Troy.

Thank you, Heidi. In summary, we are encouraged by the preliminary data from our Phase II trial on HRAS mutant solid tumors. We believe the data provide initial validation of a molecular strategy for the identification of patients who may receive clinical benefit from treatment with Tipifarnib. With several additional trials ongoing, we look forward to further evaluating Tipifarnib and its activity among the additional patient populations. For those of you tracking our progress, the important milestones to watch out for as we move to the rest of the year, our initiation of the Phase II clinical trial for Tipifarnib in patients with GMML planned for the second half of 2016. Submission of the IND for the ERK inhibitor, KO-947, that is anticipated in the second half of 2016. As well as nomination of a development candidate for the menin-MLL program that is anticipated in the second half of 2016. With that, operator, we're now ready for questions.

[Operator Instructions] Our first question comes from the line of Mike King of JMP Securities. Your line is now open.

Good afternoon, guys. Thanks for taking the questions. Troy, I just wondered if you could tell us little bit more about the patients with head and neck cancer. Would this – I mean, another HRAS positive but just wondering if would this be a similar population for Keytruda or can you tell us if they had -- previously had Keytruda maybe just little color in that regard would be helpful?

Sure, Mike. Thanks for the question. I'm going to actually ask Antonio to address your question.

Sure.

So, we're circling on our left to investigate company send the data on the characteristic of the patients in any upcoming meeting. Probably what is important to tell you is that these are refractory patients that are progressing other therapies, patients in which we will not have an expectation to see a response or the responses seeing that setting will be less 10% which certainly not able to come on present time of the relationship with immunotherapies.

Okay. But the response rates you're citing are those that would be associated with patent-based chemotherapies or rituximab and the like, is that correct?

Yes. That is correct. Those sized standard therapies; my understanding is that unnecessary participant in immunology studies.

Right. Okay. And then if I could switch gears to ERK for a moment. I think you're probably aware that selumetinib unfortunately had a negative trial that was announced yesterday, I just wonder how that if any of the – in anyway has caused to rethink about approaching tumors that had MAP Kinase Pathway activation?

Sure. So it’s unfortunate that its population of high unmet need, Mike, but two points of differentiation of our ERK inhibitor relative to other ERK inhibitors for which they has published data as well as MAPK inhibitors. The first is the potency. KO-947 has – we think among the best potency as you look from in Vitro into cells and then ultimately in human whole blood. The second is as I mentioned, you see this prolonged pathway inhibition on a variety of different dosing schedules. And one of the reasons that we chose to move forward with intervenes form of administration is it may offer us the opportunity to provide greater exposure with acceptable tolerability. And clearly this pathway is critically important to a number tumors, non-small cell lung among them. Our view as you really have to inhibit the pathway as stronger and as hard as you possibly can. And as you know we have in IV and in oral formulation we privatize the IV formation for that reason. We've also done an extensive campaign in patients drives xenograft models to try to identify models that are uniquely sensitive to ERK inhibition, and we found some of those models have mutation in members of the MAP Kinase pathway, but other don't have mutations but have other dysregulations. And we're going to continue to look very closely at that pre-clinically and then those are candidates ultimately for expansion cohorts if we're able to find a dosing schedule that will allow us to move forward with 947. So I think in some it's unfortunately. It's particularly unfortunate for that compound, but I think if reinforces the strategy that we're taking with 947, the preclinical data is very promising and we're working as hard as we can now we moved into clinic.

All right. Thanks for asking that answer in such a thorough way. If I could just maybe jump back minute a jippy. I just wondering if you can offer your thoughts about the differences in response in head and neck versus salivary and perhaps your thoughts on the importance of stable disease as a indicator of potential clinical benefit? Thank you.

Sure. I'll comment and then I'll maybe invite Antonio to add his thought. I think we're encouraged by the activity that we've seen in both head and neck cancer and salivary gland cancer. These are with HRAS mutation. These are both cancers of high end met need. We were not terribly surprised that we saw disease stabilization in one setting and regressions in the setting of head and neck. I think we're quite we're quite excited by the activity that we're seeing in head and neck, but its consistent with the hypothesis to drive oncogene and its consistent with the preclinical data that we’ve seen and it tells us, you know this is the first agent we think that is sort of meaningfully inhibited one of the RAS isoforms. So that's -- you know to us that’s something to be quite happy about. We obviously you know -- we are looking to position Tipi for the most efficient pivotal study we can and given the signal that we are seeing in head and neck cancer and the unmet need, you know that’s what makes us so excited about head and neck, but clearly there is also activity in salivary gland cancers and I think you know we’ve validated that HRAS is an oncogene and Tipifarnib is a way of inhibiting that oncogene in such a way that you can provide clinical benefit to patients. I don’t know -- I'll invite Antonio maybe to add his thoughts.

Yes, in the case of head and neck the responses are essential. We obviously currently now are working on the question of differentiation. You mentioned before the Cetuximab based therapies we know of that the HRAS mutation on the [Indiscernible] agent they are not overlapping. The question about PD-1 and immunotherapy is something that we are currently working on. But certainly we are quite enthusiastic to see responses and very good overall responses 11, 12 months in this city. The question of salivary gland is actually much simple. So salivary glands have no standard therapy. The patients basically become Phase 1 patients. They have no other treatments is Platinum-Based major responses in the single digit, so certainly an opportunity for us in the setting in which survival is measured in months to have patients that have been one year on this study.

All right. Thanks again for taking the questions guys.

Sure. Thank you Mike.

Thank you. [Operator Instructions] our next question comes from the line of Joel Beatty of Citi. Your line is now open.

Hi, and thanks for taking the questions. The first is, for the next presentations that you enrolled in the second cohort, would you’ll be looking to enrol you know all -- for HRAS solid tumors or looking to enrol specific types of cancers where you saw these plans or some other method of selecting patients.

A good question, Joel I’ll let Antonio answer that question.

Obviously we are quite excited by the [indiscernible] responses in head and neck. So we are currently discussing amendment of the protocol with the investigators and we solved that fairly quickly.

Thank you. And maybe one more follow up. Could you just discuss how the drugs have been tolerated to date, if there have been some dosing amendments as they [Indiscernible] looking forward there.

Yes they already may have been quite tolerated there are no changes with the profile that we had described previously.

Okay. Thank you.

Thank you. And I’m showing no further questions at this time. I would now like to turn the call over to Mr. Troy Wilson for closing remark.

Thank you again for participating in the call today. If you have any questions, please feel free to follow up with me or Heidi and otherwise we wish all of you a great evening and thanks again for dialing in

Ladies and gentlemen, thank you for participating in today’s conference. This concludes today’s program. You may all disconnect. Everyone have a great day.