Ladies and gentlemen, thank you for standing by, and welcome to the Fourth Quarter 2019 Kura Oncology Earnings Call. At this time, all participants are in a listen-only mode. After the speaker's presentation, there will be a question-and-answer session. [Operator Instructions] Please be advised that today's conference is being recorded. [Operator Instructions] I would now like to hand the conference over to your speaker, Pete De Spain, Kura's Vice President of Investor Relations. Please go ahead.

Thank you, Sidney. Good afternoon, and welcome to Kura Oncology's fourth quarter and full-year 2019 conference call. Joining me on the call from Kura are Dr. Troy Wilson, our President and Chief Executive Officer; Dr. Marc Grasso, our Chief Financial Officer and Chief Business Officer; and Dr. Bridget Martell, our Acting 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 Web site for information concerning risk factors that could affect the company. With that, I'll now turn the call over to Dr. Troy Wilson, President and CEO of Kura Oncology.

Thank you, Pete, and thank you all for joining us this afternoon. Our mission at Kura is to realize the promise of precision medicines to help patients with cancer lead better longer lives. Over the past five years, we've made significant strides toward achieving that mission. We've advanced three wholly-owned drug candidates into the clinic. We've achieved clinical proof-of-concept in four separate indications with our lead candidate Tipifarnib. We've initiated our first registration directed trial of Tipifarnib, and we're now actively preparing for a second, and we continue to make progress with our two emerging pipeline programs, our ERK inhibitor KO-947, and our menin inhibitor KO-539. Recently, we've also taken a number of steps to better position the company for our next phase of growth. This includes an increasing investment in pre-commercial activities, expansion of our team of medical science liaisons, and importantly, the appointment of our Chief Commercial Officer, Kirsten Flowers. Kirsten joined us last month from Array Biopharma, where she built and led the commercial organization that delivers the impressive launch of Braftovi plus Mektovi for patients with BRAF mutant melanoma in the United States. Previously, she held several commercial leadership roles at Pfizer, including U.S. commercial lead for the launches of IBRANCE in breast cancer and INLYTA in renal cell carcinoma. Although Kirsten has been on board only for a short time, she's already proven to be a valuable addition to our executive leadership team as we refine our market insights and begin to build the capabilities and expertise required for commercial success and long-term growth. Last month, we also announced that Antonio Gualberto had stepped down as Chief Medical Officer. We want to thank him for his contributions, and wish him success in his future endeavors. With this transition, comes an opportunity to sharpen our focus…

Thank you, Troy. In December, we reported updated clinical data at the American Society of Hematology Annual Meeting in Orlando, showing robust and durable activity from Tipifarnib as a monotherapy, and relapsed our refractory Angioimmunoblastic T-cell Lymphoma or AITL. Our data presented by Dr. Thomas Witzig, a hematologist at the Mayo Clinic and a principal investigator in the trial, demonstrated an objective response rate of approximately 50%, and a heavily pre-treated patient population with a median of three prior regimens. Additionally, enhanced anti-tumor activity was observed in the 10 clinical trial patients, who carry mutations and the Killer cell Immunoglobulin-like Receptor or KIR, a CXCL pathway associated biomarker. These patients had an overall response rate of 70% and a complete response rate of 40%. We believe our data coupled with the high unmet medical need for these patients supports our efforts to expand the development of Tipifarnib beyond our initial focus in HRAS mutant solid tumors. As a reminder, peripheral T-cell lymphomas comprise up to 20% of all aggressive non-Hodgkin lymphoma and consist of many different subtypes of fast-growing lymphoma. Outcomes for these patients are poor; five-year survival is approximately 30%. Although several drugs had been approved in the relapsed and/or refractory setting, none has led to survival benefit. In addition, the National Comprehensive Cancer Network guidelines currently recommend clinical trials for these patients. On another note, before we continue, significant advances in the genetic landscape of T-cell lymphoma have led to revision of the World Health Organization classification and the introduction of new terminology. As such, we have modernized our terminology going forward in an effort to align with the latest WHO classification. For instance, instead of AITL, and AITL like lymphomas, you'll hear us refer to more comprehensive classification of advanced nodal lymphomas of T follicular helper or…

Thank you, Bridget. We believe that CXCL12 pathway biomarkers may have the potential to unlock the therapeutic value of farnesyltransferase inhibitors across a range of hematologic and solid tumor indications. One of the indications of particularly high interest is pancreatic cancer. The currently reported five-year survival rate for pancreatic cancer remains at a dismal 10% and there's an urgent need to identify new molecular mechanisms to drive anti tumor activity and improve survival. Recall, a year-ago, we reported a retrospective analysis of prior clinical data that appears to identify a potential association between CXCL12 expression and clinical benefit from Tipifarnib in patients with pancreatic cancer. Since then, we've continued to conduct additional preclinical work to validate Tipifarnib in a CXCL12 high sub population of pancreatic cancer patients. Recently, we generated preclinical data showing that Tipifarnib can block production of CXCL12 by activated pancreatic stellate cells. In addition, we've observed the potential for synergy between Tipifarnib and chemotherapy in preclinical models of pancreatic cancer. These data bolster our retrospective analysis for the prior clinical data and further support our decision to conduct a proof-of-concept trial of Tipifarnib in combination with chemotherapy in the second line setting for the treatment of advanced pancreatic cancer. Preparations are underway to initiate this trial in the second half of 2020. We're very encouraged by the high level of clinical activity observed thus far in both solid tumors and malignancies with four positive Phase 2 studies now achieved. We believe farnesyltransferase inhibition has the potential to deliver multiple expansion opportunities and long-term growth. Now let's turn our attention to our emerging pipeline programs beginning with our ERK inhibitor KO-947. KO-947 is a potent and selective small molecule inhibitor ERK, a protein kinase that represents a central node on the Mitogen Activated Protein Kinase or MAPK pathway,…

Thank you, Troy, and good afternoon, everyone. I'll provide a brief overview of our financial results here on the call and invite you to review our 10-K filed today for more detailed discussion. Research and development expenses for the fourth quarter 2019 were $13.5 million, compared to $12.1 million for the fourth quarter of 2018. R&D expenses for the full-year 2019 were $47.8 million, compared to $46.8 million for the prior year. The increases in R&D expenses for the year were primarily due to an increase in clinical development activities related to our registration-directed trial of Tipifarnib, offset by decreases in preclinical development for Ko-539 companion diagnostics and clinical supply manufacturing activities for Tipifarnib and non-cash share-based costs compensation. General and administrative expenses for the fourth quarter of 2019 were $5.5 million, compared to $4.6 million for the fourth quarter of 2018. G&A expenses for the full-year 2019 were $19.7 million, compared to $16.1 million for the prior year. The increase in G&A expenses was primarily due to increases in non-cash share-based compensation and personnel costs. Net loss for the fourth quarter of 2019 was $17.9 million, compared to a net loss of $16.1 million for the fourth quarter of 2018. Net loss for the full-year 2019 was $63.1 million, compared to a net loss of $64.4 million for the prior year. Net loss for the fourth quarter and full-year 2019 included non-cash share-based compensation expense of $2.4 million and $9.4 million, compared to $1.7 million and $8.7 million for the same periods in 2018. Our cash and cash equivalents and short-term investments were $236.9 million as of December 31 2019, compared with $179 million as of December 31, 2018. Kura has received a regulatory feedback regarding our proposed registration-directed trial and advanced T-cell lymphomas, we are updating our cash guidance. We believe our cash, cash equivalents and short-term investments will be sufficient to find our operating expenses and capital expenditure requirements into 2022. With that, I will now turn the call back over to Troy.

Thanks, Marc. Before we jump into the Q&A session, let me lay out our anticipated milestones for the year ahead. For Tipifarnib additional Phase 2 data and HRAS mutant solid tumor including HRAS mutant urothelial carcinomas in 2020 initiation of a registration directed trial and advanced T-cell lymphoma in the second-half of 2020, initiation of a proof of concept study and pancreatic cancer in the second-half of 2020, additional Phase 2 data in chronic myelomonocytic leukemia in 2020, and the potential for full enrollment in AIM-HN in the first quarter of 2021. For KO-947, open an expansion cohort of HNSCC and esophageal squamous cell carcinoma patients with 11q13 amplifications in 2020, and for KO-539, an achievement of a recommended Phase 2 dose by the end of 2020. With that, Operator, we're now ready for questions.

Thank you. [Operator Instructions] Our first question comes from Jonathan Chang with SVP Leerink. Your line is open.

Hey, guys, this is David Ruch on for Jonathan. Thanks for taking our questions. I guess, first, could you provide any additional color on the partial clinical hold and the SAE that was observed, just kind of any color on what that was, and does this impact the condition, like, what are the conditions of the hold, I guess?

Sure. Thank you for the question. This is Bridget. You know, as with any clinical trial, we don't really discuss the clinical trial data outcomes whether it's safety or efficacy, but suffice it to say we're confident that this will be an iterative and collaborative discussion with the FDA, and we're confident that we'll move into our expansion cohort shortly.

Okay. Could you talk a little bit in general on how this impacts the development strategy overall and how you might be potentially thinking about combination studies down the road?

So, from a monetary perspective, before I get to the combination, I think the goal of any Phase 1 trial is studying a new chemical entity as a monotherapy, and reaching a recommended Phase 2 dose oftentimes by virtue of a dose-limiting toxicity, and so, based on that, we know that we have achieved that, and we can now look to combination therapies that would be in concert with the mechanism of this drug and both benefit patients and have a sufficient safety profile.

I think, David -- this is Troy, just to add to that, I don't think it changes at all our strategy from a development perspective, we've been consistent that we see an opportunity to evaluate KO-947 at a recommended Phase 2 dose and these 11q13 amplified patients. That is -- those patients were suggested by the extensive preclinical modeling that we did, that we've spoken to over the past several years. As Bridget mentioned, we need to work internally and with FDA to lift this clinical hold, and then we look forward to moving forward into those populations, but it doesn't change the development strategy really in any way. It is -- the goal is to identify a recommended Phase 2 dose and we've done that, we do need to work through this though with FDA.

Got it, understood, thank you. I guess, moving out from that, could you talk about if the AIM-HN study is positive? What are the next steps for Tipifarnib and squamous cell head and neck, and what are the opportunities for frontline expansion and kind of other expansion opportunities beyond SSCHN?

Sure. It's a good question, and I think we're guided by three different things. We are guided by what we've seen clinically both in RUN-HN and AIM-HN. We are guided by the evolving landscape of standard of care, and then we're guided by our preclinical data. You know, clearly there, I think one have to acknowledge that immune therapy and combinations with chemotherapy are moving to the frontline, and we've talked in the past about evaluating Tipifarnib in combination with various agents, including chemotherapy, targeted therapy, and potentially immune therapy. We're not yet at a point where I think we can articulate to you exactly what the clinical studies would look like, but it is something of interest to us. And as I mentioned in the prepared remarks, what we are also encouraged by is that we see a level of clinical activity as we look across solid tumors, whether it may be head and neck, urothelial, salivary, and so, we also want to be mindful of that, and this is going to be an evolution with the research and development group, as well as Kirsten's group, the commercial group to plot out the next steps. So I think we'll have more to say about that perhaps later in the year. At this point, though, we do definitely see an opportunity to move to additional indications and to earlier in the treatment paradigm, if and when AIM-HN is successful.

Got it. Thanks, Troy, appreciate that, and we will look forward to talk to you later.

Great, thank you.

Thank you. And our next question comes from Chris Shibutani with Cowen. Your line is now open.

Thank you very much. Two questions, on the reclassification, the new [true] [ph] terminology for the lymphoma genetic landscape T-cell there, should we think that reclassification possibly at all changes the potential denominator of patients that you might be thinking would be eligible for your therapies, or is that just true, true, not related? And again, your sort of biomarker guarded strategy still gives you the same scope of patients when you think about the ultimate, either clinical trial or commercial opportunity?

Yes, Chris, thanks for the question. So, the literature references suggest that there are 3,500 to 4,000 patients per year in the U.S. with PTCL, equivalent numbers in ex-U.S. territories. Our best estimate of the eligible patient population under the new classification, the nodal T-cell lymphomas of the T-follicular helper phenotype is approximately 30% of that population. It may be a little higher outside the U.S., but it probably doesn't change what we've been guiding to in terms of the eligible population. It's just -- the physicians and the KOLs who treat this disease are very active at, as you know, challenging for new therapies, new biomarkers, new ways of classifying patients, and so, this -- in our way of thinking, this actually, probably helps us, because again the entry criteria on to the study is a pathological diagnosis that's consistent with the WHO criteria. Then with a retrospective analysis of the biomarker and that way it's different than the AIM-HN study. Does that help to answer your question?

Yes. No, it does seem to be moving more of a classification difference, didn't know whether or not it had any implications for how we should be thinking about the opportunity, and we'll certainly continue to follow that. If I could ask a follow-up question, AIM-HN enrollment, some clear goals for the patient numbers at a minimum and the timelines, which I think you reiterated now to be first quarter of 2021. You also mentioned that you have some additional fresh eyes on potentially the situation particularly with Bridget and Kirsten, with Kirsten's pedigree coming from an Array certainly is something that I think with a commercial viewpoint could be potentially valuable. Can you tell us about any of the new insights or strategies that you're perhaps putting into place that continue to perhaps give you a confidence in being able to make those timelines? I think in the past, you talked about kind of trying to figure out how patients who are either in the Phase 2 versus the Phase 3 study, often there were questions of perhaps sicker patients, whether they were eligible or not. How are you balancing those factors, particularly with the new voices at the table that you have? Thanks.

Yes, thanks for the questions. So may be to take the questions in reverse, so we are delighted to have Bridget in this expanded role, partnering with not only with Kirsten, but with Kathy Ford, our Chief Operating Officer, and we are -- I said it in the prepared remarks, and I'll reiterate it, it is our highest priority at the company, and we are focused on number of aspects of that study, including numbers of patients screened, given that we are screening in the frontline, you know, we have to be mindful of the impact of kind of the evolving treatment landscape in the frontline, and it's very much -- it's the number one thing we talk about at the company. At this point, I'm not sure I can give you a lot more clarity. We are at a point now where nearly every site is open, that is going to be open, there may be a straggler or two, we continue to try to get more out of our sights in terms of screening patients, and to doing the best we can deliver on the timeline that we've articulated, but I can't get much more into the specifics at this point. Yet I do think, and again, I said this in the prepared remarks, and I'll emphasize it, it's been -- I think terrific to have Bridget come in and have the team really come together, and not only look at AIM-HN, but across the entire pipeline with lots of ways of creating value, lots of kind of interesting inflection points throughout the year, and I've been -- just as CEO just really gratified to see the extent to which the team has pulled together to say, "How can we do better, do different and better if needed?" So I think we'll be in a stronger position going forward through the rest of this year and into next year.

Great, thanks. It's great to see the bench strength improved, and we'll keep an eye on that trial and moment. Thank you, Troy.

Thanks, Chris.

Thank you. And our next question comes from Tyler Van Buren with Piper Sandler. Your line is open.

Hi, guys, good afternoon. I had another one on AIM-HN, especially with the encouraging updates on enrollment and pre-commercial activities. So, can you just confirm that it's still 15 responses required to reject the null hypothesis, and if the 15th response comes tomorrow, can you start the rolling NDA submission immediately, are you guys in a situation where you can do that, and how long would that take in terms of timelines, and specifically also mentioned eligibility for NDA rolling submission, how is that determined?

Right. So, Tyler, thanks for the question. You've got a few things kind of packed in there. So, you're correct, 15 confirmed responses are what are needed to reject the null hypothesis. Those have to be centrally adjudicated and reviewed by the Data Safety Monitoring committee. So if and when that happens, we are we are assuming that the DSMB will notify the company that the company has to both notify the agency, and the investigators on the study. We would then anticipate that we would make that information public. I think it's -- let me just say it's premature I think to talk about the timing of the submission. We were gratified to get the fast track designation. I think that's a recognition by FDA of the unmet medical need and the clinical activity that was demonstrated in Phase 2, we continue to push to take advantage of any sort of regulatory advantage that would be available, not only in head and neck, but now you'll see in T-cell lymphoma. That's a bit of a work in progress, but I don't want to look too far into the future, and our focus at the moment is on that execution point that you mentioned, and we'll keep it there. We are trying to set the company up for success if and when AIM-HN is positive.

Okay. That's helpful. And maybe just a quick second one on menin MLL, can you just give us any sort of color where you are in terms of the dose ranging or what dose cohort you're at, and also if you expect any responses or significant political benefit in this initial non-enriched patient population?

Hi, Tyler, this is Bridget. I can address that question for you. So, we are in dose escalation in the Phase 1 portion of the trial. It is an all-comer AML as we have stated before. However, investigators do know that we are targeting a certain population. So, they will choose their patients as appropriate on to the dose escalation trial. We don't disclose currently where we are in that dose escalation, we can just say that it is progressing as planned.

Great. Thank you so much, guys.

Thanks, Tyler.

Thank you. And our next question comes from Jay Olson with Oppenheimer. Your line is now open.

Oh, hey guys. Congrats on all the progress and new additions to your leadership team. I wanted to follow-up on the positive feedback from the FDA at your end of Phase 2 meeting and comments they made about the registration study in AITL? Was there any color provided in terms of the two primary endpoints as to what the benchmark would be for either the ORR in patients, who carry the cure mutation, or the ORR in all patients in the study?

Sure, Jay. This is Troy. Thanks for the question. So, we now refer to that trial as the trial formerly known as AITL, because the T Follicular Helper Phenotype, including AITL is a bit of a mouthful. We'll come up with an appropriate name for the trial in the future, but as we mentioned, so the design of that trial is consistent with what has been used for other agents that have been approved in PTCL, and what would be expected for a level of activity in a second-line setting. We mentioned that each of the two independent objectives has a 9% null hypothesis. So that's a reasonably low bar. We would obviously want to see a higher level of activity both in terms of objective response and durability if we want to displace the existing therapies, and we're encouraged, because in a patient population that has experienced a median of three priors, so a fourth-line setting, we're seeing a 40% to 50% response rate with the ability to drive that to 70% in the KIR mutant subset and a 40% CR rate. So, there is the potential we think to drive a higher level of activity and displace the other agents, but specific to your question, those two arms each have a 9% null and the guidance that we got was that success eliminating the null hypothesis on either arm, or either endpoint, I should say, I misspoke, would be sufficient to eliminate the null hypothesis and potentially support an application for accelerated approval. Does that help you?

Yes. That's perfect. Thank you. And then, maybe as a follow-up as you get closer to commercialization of Tipifarnib, can you talk about how you envision the timing of all the various indications you're pursuing and how you want to sequence those potential approvals and manage the lifecycle of Tipifarnib?

So, Jay, that's a great question, and probably one that I'm going to give you an unsatisfactory answer to, but let me just say where we are following the science, we are following what we see in the clinic and we are informed by the commercial opportunities. So, we chose HRAS mutant head and neck and now nodal T-cell lymphomas of the T Follicular Helper Phenotype as initial indications, because they offer a fast-to-market strategy, and you could -- the potential for accelerated approval. We see an opportunity to expand into T-cell lymphomas and potentially other heme malignancies, potentially the opportunity to move into second-line pancreatic cancer. That will obviously take time, but if you look back up, and several of you on the phone have been following this story almost from the beginning. It wasn't more than a couple of years ago that we we couldn't conclusively tell you that Tipifarnib was a CXCL12 pathway inhibitor. Now, I think we can tell you that. We can tell you that we see knocked down of both message and protein and pancreatic stellate cells, and encouraging preclinical data and clinical data. So that encourages us. We are talking and working internally on a strong standalone plan to take Kura forward as well as considering optionality by combinations and other things, and we will give more light to that over time. At this point I think we're going to continue to do what has served as well, which is follow the science and focus very much on execution.

Great. Thank you very much taking the questions.

Sure.

Thanks.

Thank you. [Operator Instructions] Our next question comes from Joseph Pantginis with H.C. Wainwright. Your line is open.

Hi, guys, this is Pasquale from the line of Joe. A few questions from me, so my first question, so for the Tipifarnib trial in metastatic urothelial carcinoma, what kind of update should we expect in terms of additional treated patients, and also what frequency of HRAS mutation are you looking at?

Yes, first of all, thank you for the question. So that study, that urothelial HRAS -- that HRAS mutant urothelial carcinoma steady is an investigator-sponsored study being conducted at the Samsung Medical Center. It's not under our control. It's actually fully was designed and was directed by Dr. Park at Samsung. So, Dr. Park is the one who will make the determination of how many patients. We guided in the prepared remarks that we would expect a more complete dataset to be presented and/or published later this year. Again, it's Dr. Park's study, it's not ours, so we can guide to that, but we can't control it, but I think we're optimistic things go well to see that data presented a bit later this year. In terms of your question about the HRAS mutant frequency, estimates vary anywhere from 5% to 15%, depending on the literature reference that you look at. So, it's a meaningful percentage of urothelial carcinoma, and I think we'll have more to say once the kind of the full dataset has been presented from Dr. Park.

Thank you so much, Troy. So, another question from me, I mean, I saw your IP slide in on your corporate presentation is very nice. So I was wondering, if you can provide color on your ongoing novel Farnesyl Transferase Inhibitor program and specifically, what kind of -- what is the status of the preclinical work, any success in identifying potential novel Farnesyl Transferase Inhibitors, and have you ever [filed] [ph] for novel composition [indiscernible] IP?

Yes. So, you have a few things packed into that question, Pasquale, let me see if I can unpack them and answer your question. So, if we take a step back before we get to the novel FTI, one of the things that I think we've done, we've absolutely delivered on is the ability to unlock the biological insights of Farnesyl Transferase Inhibition. So, when we brought this program in from Janssen, it was clear that Tipifarnib was active, it was -- it had a reasonable tolerability profile, but there was not a good molecular level understanding of what was driving the clinical activity. We now have two sort of major mechanisms; one, HRAS mutant solid tumors, the other, CXCL12 hematologic and solid tumors, and we're going to continue to flash that story out throughout this year. I don't want to say too much, but we really view ourselves as the leader in Farnesyl Transferase Inhibition and that is understanding the molecular mechanisms, understanding opportunities as a monotherapy, understanding rational combinations, and we've been very successful both in the U.S. and now increasingly ex-U.S. at getting patent offices to issue fairly broad patents covering not only Tipifarnib, but any Farnesyl Transferase Inhibitor in certain settings, and that's because we did what no company working previously was able to do, and that was to assign the molecular targets. With that -- that took, as you can imagine, kind of an alignment of planet to get that right, but here we are. Now, we're at a point where we understand the opportunity, we understand the farnesyl transferase targets, and there are things we think we can improve upon, even with a drug that is as well-positioned as Tipifarnib. So, we've started a second-generation compound. I've made this reference before, one of the analogies I make is to formally Celgene that worked with initially Thalidomide and then Revlimid and then Pomalidomide, and simultaneously worked out IMID biology and developed a very robust franchise. We'd like to be in a position to do something similar in farnesyl Transferase Inhibition. I can't really speak to where the program is at, but this is -- we obviously have crystal structures, we have a number of highly-potent compounds, both ours and others, and I think it's a good opportunity for a very efficient drug discovery effort, and I hope that we'll have something more to say, either later this year or early next year.

That's wonderful. Thank you for additional color. Last question from me, so what kind of update should we expect for the Tipifarnib trial in chronic myelomonocytic leukemia?

Sure. Yes, that's a good question. So if we a step back, we initially reported data in CMML that one -- we had an initial Phase 2 study where we were looking to exclude KRAS and NRAS mutant patients from those patients with CMML, because it had been established that KRAS and NRAS were not driver oncogenes that could be addressed with Tipifarnib or a Farnesyl Transferase Inhibitor as a monotherapy. That study was successful. We then -- once we identified the molecular inside of the CXCL12, CXCR4 interaction, we took a look at T-cell lymphoma, add additional lymphomas, as well as into leukemias, and thought should we be enriching on the basis of the CXCL12 pathway, and continued to run the study, but not looking at NRAS or a KRAS and NRAS, but at CXCL12 and CXCR4. So, we'll provide an update on that study. Our expectation is sometime we hope kind of midyear to second-half of the year.

Perfect. Thank you so much, Troy, and congrats on the progress.

My pleasure.

Thank you. And I'm not showing any further questions. I'd like to turn the call back to Troy Wilson for any further remarks.

Okay. Thank you, Operator, and thank you all once again for participating in our call today. We're going to be at a number of upcoming investor conferences, beginning with SVP Leerink tomorrow in New York. We will look forward to seeing many of you there, and in the meantime, if you have any questions, please feel free to contact Pete, Marc, or myself. Thank you, and have a good evening everyone.

Ladies and gentlemen, this concludes today's conference call. Thank you for your participation. You may now disconnect.