Clovis Oncology, Inc.
Q4 2013 Earnings Call Transcript

Published: 28 Feb 2014

[Operator:]

Good day ladies and gentlemen and welcome to the Clovis Oncology Fourth Quarter and Year-End 2013 Financial Results Conference Call. My name is Cilia and I will be your operator for today. At this time all participants are in a listen-only mode. Later we will conduct a question-and-answer session. (Operator Instructions). As a reminder this conference is being recorded for replay purposes. I would now like to turn the conference over to your host for today Ms. Anna Sussman, Senior Director of Investor Relations. Please proceed.

[Anna Sussman:]

Thank you, Cilia. Good afternoon and welcome to the Clovis Oncology fourth quarter and year-end 2013 conference call. You should have received the news release announcing our results. If not, it is available on our website at www.clovisoncology.com. As a reminder this conference call is being recorded and webcast. Remarks may be accessed live on our website during the call and will be available in our archive for the next several weeks. The agenda for today’s call is as follows. Patrick Mahaffy, Clovis’ President and CEO will discuss the highlights of 2013 and provide an update on our clinical development program. Then Erle Mast, Clovis’ Chief Financial Officer will cover the financial results of the quarter and year in more detail and comment on the company’s outlook for 2014. Patrick will make a few closing remarks and then we will open the call for Q&A. Before we begin please note that during today’s conference call we may make forward-looking statements within the meaning of the federal securities laws, including statements concerning our financial outlook and expected business plans. All of these statements are subject to risks and uncertainties that could cause actual results to differ materially from those described in the forward-looking statements. Please refer to our recent filings with the SEC for a full review of the risks and uncertainties associated with our business. Forward-looking statements speak only as of the date on which they are made and Clovis undertakes no obligation to update or revise any forward-looking statements. Now I will turn the call over to Pat Mahaffy.

[Patrick Mahaffy:]

All right, thanks Anna. Welcome everybody. Thanks for joining us this afternoon. 2014 will no doubt prove to be an important year for advancing our clinical development programs which I’ll briefly review. We are also aware that there are a lot of moving parts in our rapidly evolving global clinical development plan for 1686 as well as clear opportunities to potentially accelerate our NDA submission. 1686 is our targeted covalent inhibitor the mutant of EGFR for the treatment of non-small cell lung cancer. 1686 targets both the initial activating EDFR mutation as well as the dominant resistant mutation, T790M. From what we know so far, 1686 is very well tolerated drug. We have shown that we are the only EGFR inhibitor that doesn’t hit wild-type EGFR in clinical studies. We have seen no evidence of TKI-related EGFR wild-type rash or diarrhea at any dose or formulation study. We believe this represent a significant point of differentiation for 1686 compared to other TKI approved currently in development. It is also a very active drug. In October 2013, we announced the most recent update of CO-1686 clinical data which included six recess partial responses observed at that time and valuable T790M positive patient dosed at 980 BID of the free-base formulation for a 67% objective response rate. [Eight] of the nine evaluable patient or 89% experienced TRs or tumor shrinkage greater than 10%. These patients were heavily pre-treated prior to receiving 1686, eight of the nine patients has progressed on EGFR TKI immediately prior to enrollment in the study. Six of the nine patients received two or more previous TKI lines. At that time 36 patients had been treated with 1686 across all dosing cohorts of the free base. There is no evidence of dose-related wild-EGFR driven toxicity that remains true today as well. Clearly, we believe the 1686 is potentially a very important drug and we are determined to identify the best possible way to get this drug approved rapidly and in the hand of physician and patients who need therapy. This can now become our focus as we have completed dose escalation with improve hydrobromide formulation of 1686. We have commenced enrollment of the Phase 2 expansion cohorts in patients with EGFR mutant non-small cell lung cancer and our two T790M positive cohorts are increasing from 80 patients to approximately 300 patients in total or 150 patients in each. These cohorts will test the efficacy of 1686 in two patient subsets in two-dose cohorts each. The first in approximately 150 perhaps up to 200 patients who achieved T790M positive directly after progression on their first and only TKI therapy similar to our TIGER2 study design and the second is approximately 150 T790M positive laser line patients directly after progression on their second or later TKI therapy or subsequent chemotherapy similar to our TIGER3 study design. The FDA has made a number of public comments about the importance of fully exploring dose in drug development. This is particularly important we believe for well tolerated targeted therapeutics or MTD-based dosing may not be ideal or in certain cases and maybe ours not possible. This program is designed to rapidly and properly ensure that we’ve explored dose beyond our stated doses of 750 mgs BID in large groups of patients. Importantly we have seen very encouraging activity in each of the HBr doses which makes it possible to fully explore those in these expansion cohorts. Of course that is particularly attractive to us since this data can also serve as the basis of an accelerated NDA submission. The maximum tolerate dose for 1686 has not been reached and will not be reached since we are planning to do further dose acceleration work. While a dose limiting toxicity of hyperglycemia has been observed in a minority of patients most of these patients have been asymptomatic and all the cases have been easily managed. We will continue to move forward with the TIGER program which includes three global registration studies for 1686 all in EGFR mutant non-small cell lung cancer. These include TIGER2 and T790M positive second line patient directly after progression on their first and only TKI. TIGER3 in more dense patients directly after progression on their second or later TKI therapy or subsequent chemotherapy and of course TIGER1 in newly diagnosed patients who have not had TKI therapy but may have received one type of chemotherapy before this study are randomize and begin to [inaudible] placebo. Our next presentation of 1686 data will be at the European Lung Cancer Conference in Geneva in late March. Dr. Heather Wakelee one of our investigators will present the 1686 data in an oral presentation during the advanced disease or targeted agent session scheduled from 9 AM to 10

[Erle Mast:]

Thanks Pat, good afternoon everyone. Our full financial results are included in this afternoon’s press release so I will direct my comments to highlights for the quarter and provide some additional analysis and commentary. We reported a net loss $29.2 million or $0.92 per share for the fourth quarter of 2013 and $84.5 million or $2.95 per share for the full year of 2013. Our research and development expenses totaled $22.5 million for the fourth quarter and $66.5 million for the full year 2013. R&D expense for the full year increased by $7.6 million compared to last year. Now this is the net effect of two factors; expanded clinical development activities for 1686 and rucaparib partially offset by the termination of CO-101 program beginning late 2012. As expected research and development expenses in the fourth quarter of 2013 increased over the third quarter of 2013 by $6.5 million. Now this growth is due primarily to the initiation of the ARIEL2 and ARIEL3 studies in the second half of the year as well as the manufacturing of additional clinical supplies for both the 1686 and the rucaparib programs. General and administrative expenses totaled $5.5 million for the fourth quarter of 2013 and $16.6 million for the full year. G&A expenses totaled for both the fourth quarter and the full year were impacted by transaction cost and fees associated with our acquisition of EOS this past November. Those costs totaled $1.6 million for the fourth quarter and $2.2 million for the full year 2013. Now our operating results for the fourth quarter were also impacted by non-cash expenses relating to the accounting for the EOS acquisition. We incurred non-cash charges totaling approximately $1 million in the fourth quarter relating to the currency translation of euro denominated contingent payment obligations as well as the accretion of these future contingent payments. And then finally our operating expenses for the fourth quarter and the full year of 2013 included $2.8 million and $9.5 million of stock compensation expense respectively. We ended 2013 with cash totaling $323 million with no outstanding debt and with $23.9 million shares of common stock outstanding. As we previously stated we expect cash burn of approximately $120 million for 2014. However we will continually evaluate this estimate as we see how enrolment in our clinical trials progress. And with that I’ll turn the call back over to Pat for some closing remarks and then we will open it up Q&A.

[Patrick Mahaffy:]

Great, thanks Erle. Let me zip through our anticipated milestones for 2014. For 1686 we have now initiated the expansion cohorts for the phase 1 2 study to swiftly build a larger data set for our T790M positive cohorts and expanded them to include approximately 300 patients in two dose cohorts each. These include approximately 150 to 200 T790M positive patients in two dose cohorts directly after progression on first and only TKI as well as approximately 150 T790M positive later line patients in two dose cohorts directly after progression on their second or later TKI therapy or subsequent chemo. We intend to initiate the Phase 1 study in Japan this quarter and to initiate the first three studies in the TIGER program all in non-small cell lung cancer which include the following. The TIGER2 registration study in T790M positive patients directly after progression on first and only TKI; TIGER3 registration study in later line patients directly after progression on second or later TKI or subsequent chemo and the Phase 2 portion of the TIGER1 registration study in first line EGFR positive patients. For Rucaparib we’ll continue enrollment of the ARIEL2 treatment study and ARIEL3 maintenance study in platinum sensitive ovarian cancer patients with BRCA mutations and other DNA repair deficiencies. And during the second quarter we intent to initiate Phase 2 study in Rucaparib in pancreatic cancer patients with BRCA mutations. Finally Lucitanib, during the second quarter we intend to initiate our Phase 2 studies of Lucitanib in selective patients in addition to the FINESSE breast cancer study currently under way by our partner, Servier. These includes the Phase 2 study in patients with treatment refractory FGF-aberrant breast cancer and the global phase2 study in patients with metastatic squamous non-small cell lung cancer with FGFR 1 amplification. In sum we expect to enroll more than a 1,000 patients in the Clovis-sponsored studies around the world in 2014. I am very proud of what our team has achieved in 2013 and look forward to even more important years as we continue to advance and aggressively advance our clinical development programs. All right thanks for joining us today and we are now happy to answer the questions you may have.

[Operator:]

(Operator Instructions). The first question comes from the line of Cory Kasimov JPMorgan. Please proceed.

[Cory Kasimov:]

Hey, good afternoon guys and thank you for taking the questions. I have a lot of them but I will narrow it down to just few here. So I guess first thing first on the Phase 2 expansion strategy you are announcing today, what led to the change in the path forward for just one month ago at your R&D day was this based off of interactions with the FDA or pushed from investigators or what was it?

[Patrick Mahaffy:]

I think we landed on it for a variety of reasons. So first I want to say it did not involve interaction with FDA with any regulatory agency. So just put that aside. So we landed on it as what’s not to like about this. We have a lot pressure from investigators who have a number of slots and patients waiting to get into this trial and were already worried that at 80 they were going to run out of slots. So pressure from investigators is real for us right now. Two we have a really active drug that has shown really good evidence of activity across multiple doses and we know that FDA is increasingly telling sponsors they like to see a full exploration of dose in the context of their development programs. Again though we didn’t hit in NTB this is the perfect example of where we can provide FDA what they have requested, a much more complete exploration of dose. And finally we’ve known all along that it was the realm of the possible to consider a more accelerated timeline for our NDA submission that was of course depended on generating data that would have met what we believe to be appropriate requirements. We think we are doing that. And so for us all of that adds up to a really clear path, to increase the size of the expansion cohorts, to consider them for accelerated approval and to explore dosing in that context although while keeping our investigators very happy with what we are doing.

[Cory Kasimov:]

Okay and are you able to say what two doses you are talking forward?

[Patrick Mahaffy:]

We are going to discuss that more fully in Geneva.

[Cory Kasimov:]

Okay and then on Geneva are you able to have…

[Patrick Mahaffy:]

Including selling [inaudible] it sounds like….

[Cory Kasimov:]

No I understand okay and then on Geneva can you tell us at least roughly speaking how many patients we might see data on ELCC?

[Patrick Mahaffy:]

We, – yes we could, no, we won’t. We don’t know exactly the date of the cut- off we will have a reasonably robust patient population for Geneva.

[Cory Kasimov:]

And then I guess one for Erle and then I can hop back in the queue at the others. But on the financial side of things this decision to substantially increase and accelerate development of 1686, not really sure how this doesn’t impact the burn guidance for this year something else slowing down?

[Erle Mast:]

No, it’s not slowing down Cory it’s a good question and so much of our burn should have earn in cash is just driven about how our clinical trials enroll. And I think given we’re at the beginning of the year what I’d like to do is we still have not changed our guidance as we get through reporting for Q1 and we have a better sense on the timing and the enrolment pace and we will update that. So it’s nothing more than we are at the beginning of the year and I’d like to see how the first three months play out before we revise our guidance.

[Patrick Mahaffy:]

Yeah that’s completely true and it’s sort of it’s a bit of a moving target. The other thing you should know is for evaluating given the breath of this expansion cohort now. Whether we may dial back to number of patients we enrolled in each of TIGER2 and TIGER3, so we’ll evaluate that over the course of the next couple of months.

[Cory Kasimov:]

At this point TIGER2 is smaller and sampler size it seems like than your expansion cohort in Phase2 is that correct?

[Patrick Mahaffy:]

Two things, TIGER2 is a single dose and so you they highly complementary programs to say the least.

[Cory Kasimov:]

Okay, all right thank you for taking the questions.

[Operator:]

The next question comes from the line of Brian Klein of Stifel. Please proceed.

[Brian Klein:]

Great, thank you for taking my questions. Just a few here, first on dose-limiting toxicity with hyperglycemia, where exactly was the threshold that led you to call out to DLT? And secondly were you seeing that only of the highest dose test or did you see that at other doses as well?

[Andrew Allen:]

The threshold, this is Andrew Allen, the Chief Medical Officer, the threshold for great free toxicity which is the definition for DLT is a fasting plasma glucose a change 50 milligrams per deciliter or greater, so that’s the threshold and we’ll give you the toxicity by dose stage in Geneva.

[Brian Klein:]

Great, thanks and then in terms of the expansion cohorts versus the TIGER program, do you expect enrolling patients in the expansion cohorts will impact your timelines for enrolment in TIGER2 and TIGER3?

[Patrick Mahaffy:]

No, I don’t. We’ve got sites all over the world and the expansion cohorts are predominantly in the United States. The TIGER2 and TIGER3 involve a number of Asian and European sites and so there is not very much overarch at all. And finally we have the ability in the United States to involve the community as well. We’d like to be real involved in the community setting for TIGER2 because the vast majority of TIGER2 appropriate patients are in a community setting. So I think our timelines will not be affected at all.

[Brian Klein:]

Great, thanks for taking my questions.

[Operator:]

Question from the line of Marko Kozul, Leerink. Please proceed.

[Marko Kozul:]

Hey guys, good afternoon and congrats on the progress. On your expanded expansion strategy many of your catalogs have been advocating either consider back selling the ongoing 1686 trials given significant patients interest beyond capacity. So just to follow up to some of the other questions, how quickly do you think you can enroll these expanded patients for the expanded portion of the studies?

[Patrick Mahaffy:]

I think what we want to do is at the time of Geneva provide you an early forecast and if not at Geneva then certainly by ASCO provide you a timeline. Let’s get enrolling now and I prefer to provide you that timeline when you have a little better clarity.

[Marko Kozul:]

Terrific and everything we know…

[Patrick Mahaffy:]

Really everything we know there is a lot of patients out there, there is a lot of remained by investigators. And we have clearly told you we believe that is very encouraging this will accelerate the timeline for our MDA submission in an adequate.

[Marko Kozul:]

Terrific and my second question with duration of response data for the hydrobromide salt formulation that will be seen at the LCC. If the emerging duration response is trending well beyond six months data say to seven eight, nine months. How should we think about that in terms of the listing the front line market opportunities?

[Patrick Mahaffy:]

Well, I think that – I think it’s pretty simple. I mean you can math if you want, and assume that we are going to get to a similar PFS as the placebo or Lucitanib, 10.5-11 months and then you can try to add the math of what we see in T790M population. That’s one metric you can use, that’s not a complete story about the drug patients for long time. But I know that if we have seen a very limited duration of benefit would be worrying and so my view is I will be worried about if it was bad. I am going to kind of optimistic about it if it’s good. Andrew would you?

[Andrew Allen:]

Yeah, I think increasing that community believes that multiple clones of cancer are present at the outset of disease and one clone will dominate kind of Darwinian competitive system depending upon the drug that’s in environment, of course there is drug environment in this disease it’s activating patients that clearly have clones and replicate the fastest and therefore to dominate the clinical chemo that patient presents with. But the belief is, there is resistant clones including across T790M are probably present in all of these patients pretty much from the beginning and they grow quietly and frankly unaffected by use of – because it’s a minority clone, its growth is invisible clinically. Now when you introduce a TKI which kills of the [790] clones now of course you have created a situation in which that resistant clone will slowly become the dominant clone as we know it takes about 10 months or so on average for that resistant clone to go through and terminate the account benefit of erlotinib in the front line setting. Then we come in with our drug and obviously we are suppressing that resistant clone, we now presumably creating an opportunity for third 1686 resistant clone to go through whatever that might be. So if believe this is happening in parallel and these clones are growing relatively independent to each other and it’s reasonable to simply add the PFS you are seeing in the second line setting on top of what you see in front line setting, and obviously, the longer the second line PFS becomes therefore the greater the expected hazard ratio when we compare ourselves against erlotinib in the front line setting. So I think we are gaining market and that is a very reasonable set of assumptions and obviously we will test those in the TIGER1 trial.

[Marko Kozul:]

That’s very helpful. Andrew, thank you. And just last one on rucaparib. Can you give us some details on the two [inaudible] patient treated so far? How should we interpret the comment you had about striking response and how long these patients been in the study? Thanks.

[Patrick Mahaffy:]

The presentation we presented at the R&D Day, these is the patient with the germline BRCA 2 mutations who receive [inaudible] front line chemotherapy which is now the likely standard of care, it’s full drug regimen carries pretty substantial toxicity but it’s shown the greatest overall survival benefit when used in the front line setting. These patients progressed after four cycles of full dose and they progressed on therapy and then developed a very nice partial response on the rucaparib mono-therapy. The duration of the actual response was around six months, they were on drug with high quality of life for nearly a year. So that was the first case which obviously captured our attention and then we have a more recent case of patient who progressed on gemcitabine mono-therapy also given as front line treatment for pancreatic cancer and that patient has not entered partial omission, she is still in it. So we don’t have duration yet. Again we are very compelled by this mono-therapy very well tolerated drug leading to clear clinical benefit in patients who progressed on aggressive cytotoxic chemotherapy that’s obviously the striking signal that we are choosing not to ignore.

[Marko Kozul:]

I appreciate taking questions. Thanks.

[Operator:]

The question from the line of Peter Lawson, Mizuho Securities USA. Please proceed.

[Peter Lawson:]

Just following on the rucaparib second patient, how long has he been in partial remission?

[Andrew Allen:]

We will update I think probably at ASCO year we will give confirmation on the fly for individual cases.

[Peter Lawson:]

Got you. And then just to be clear, the difference between the expansion and the TIGER2 and TIGER3, so the expansion of both of those were very similar to those. The difference is that larger dosing and different geographic mix, is that right?

[Andrew Allen:]

All of that’s accurate.

[Peter Lawson:]

Okay. And we find out about dosing in Geneva?

[Andrew Allen:]

You will.

[Peter Lawson:]

And then on just data timeline, Phase 2 data for CO-1686 when do you think we should see some of that?

[Patrick Mahaffy:]

From the expansion cohorts?

[Peter Lawson:]

Yes.

[Patrick Mahaffy:]

Most realistically at ASMO, there will be an update at ASOC on the dose cohorts that we will be following in the Phase 1 portion, so you will see data for those dose cohorts obviously in Europe and at ASCO. I think the earliest data which you will see – I know, the earlier data we should see data from the expansion cohorts in one of the fall meetings, I guess it would probably be ASMO at the end of September, but obviously deadline hasn’t been occurred yet. So, it will be one of the four meetings.

[Peter Lawson:]

Got you. Okay. Thank you so much.

[Patrick Mahaffy:]

You bet.

[Operator:]

(Operator Instructions). The next question comes from the line of Charles Duncan, Piper Jaffray. Please proceed.

[Unidentified Analyst:]

Hi guys. This is Corey in for Charles. Thanks for taking the questions. Most of have been answered I had a question about a recent patent issue in Europe between Puma and Boehringer, if you guys can comment on implications for 1686 in Europe and possibly the U.S.?

[Patrick Mahaffy:]

Well, I can give you the answer, I want to give you. My colleagues are telling me not to get involved with nasty, nasty words. So I won’t go there. Anna, you are welcome. Those of you modeling potential royalties for Puma should install this number for every year going forward, zero.

[Unidentified Analyst:]

Okay.

[Patrick Mahaffy:]

There is a [maturing] time for that patent what they didn’t tell you is that, of all the claims that BI aggressively sought to have thrown out, the first 22 they were all thrown out. They didn’t tell you that this could be the subject of a new appeal that would look at a small number of remaining claims. They didn’t get around to telling you that in United States you can look at the files that are publicly available, but the only claims related to T790M is specific to neratinib, neratinib, it’s the only drug by the way, not the only but one of the many who have proven itself to have exactly zero responses in T790M positive lung cancer. This is so embarrassing it will have no impact on our organization.

[Unidentified Analyst:]

Okay, great. Thank you. And a question kind of broad one on the I guess Rucaparib, the foundation essay I am not too super familiar with it, is there a failure rate, I guess if there is what is that?

[Patrick Mahaffy:]

So that obviously will be a technical figure, right, but it’s low single-digits. The key opportunity for the failure of any molecular diagnostic test is the quality and quantity of tissue that is submitted and the good news about the ovarian cancer is that typically at first line of treatment expensive circle deep uterine surgery where all the evident disease inside the pelvic and peritoneal cavity is removed, and therefore there is abundant tissue from that tumor available in laboratory of the hospital where that patient receives that treatment, and therefore for us to request some of that tissue [inaudible] patent-embedded and send it to foundation is actually very straight forward. And so for the ARIEL3 trial there is no requirement for further biopsy all we need for tissue they will almost inevitably will be sitting in the path lab. So, that obviously a very good news from the patients point of view, he doesn’t need, he should be able to get this high quality data on just about all of them. But obviously everything has a failure rate, so it’s not a 100% success but again low single-digit is our expectation.

[Unidentified Analyst:]

But I noticed on the R&D side that, there was a failure rate, that’s not your data but 23% for FGF essay and it seem high. I wonder so...

[Patrick Mahaffy:]

Again the context in that is so, a lot of the HGF essays right now being done in lung cancer. In a lung cancer you are in a very different universe where you are relying because of difficulty to do lung cancer biopsies, you typically rely on very smooth fragments of tissue obtaining bronchoscopically as a source material and obviously that has a much higher failure rate because sometimes you don’t have either epithelial tissue to or enough tumor tissue to do the next gen to continue work. Again, as I explained in ovarian cancer we don’t have that problem, I have to say.

[Unidentified Analyst:]

Okay. And then the foundation, last question, the foundation essay just looking at in addition of to the BRCA mutations loss of Heterozygosity.

[Patrick Mahaffy:]

Yes it’s a what foundation does is sequencing and they sequence several 100 genes as well as a series of snips, single nuclear type polymorphism which are evenly spaced throughout the Genome and it’s the snip sequencing that tells you whether a patient has developed substantial amounts of LOH or Loss of Heterozygosity. So it’s that LOH analysis plus the BRCA sequencing analysis that are central to our classification.

[Unidentified Analyst:]

Okay, great. That’s all. Thank you.

[Operator:]

A question from the line of Yaron Weber, Citi. Please proceed.

[Unidentified Analyst:]

Great, thanks for taking the question. This is Christian for Yaron. Two questions first in your press release you mentioned filing NDA in 2015 but you do not specify what drug I assume you are referring to 1686 but can you please clarify that?

[Patrick Mahaffy:]

It would be 1686, yes sorry about that.

[Unidentified Analyst:]

Thank you. And then my second question is for Andrew regarding lucitanib you call that a little bit on profile of the drug and how you think it may differ from other similar drugs in development. It looks like the pre-clinical data especially the IC50 don’t translate into clinical activity what are your thoughts on that?

[Andrew Allen:]

Yeah it’s a great question and I think what we have learned as a community is that the IC50 for this class of drugs do not tell you exactly what the drug will do in the clinic and the obvious example is there are several molecules which had VEGF R2 as one of the high profile targets. Where in-vitro the IC50 had single digit non-amenable against that receptor but when these drugs are administered to patients you see no hyper tension or trivial amounts of hypertension. And it’s largely accepted that hypertension is very good pharmacodynamic marker of VEGF R2 inhibition. And so erlotinib is good example of drug that has in-vitro high potency against VEGF R2 with the hypertension rate in single digit. So I think you have to judge each drug on its clinical data. And what we’ve learned is that if you take pure or relatively pure VEGF R inhibitors and you put them into women with breast cancer you really don’t see a great deal of activity and I am sure you know several drugs have been testing in Phase 2 settings and one or two in Phase 3 and have really not shown any meaningful response rate, nothing beyond single-digit or even 0% response rates. Similarly pure relatively pure, FGFR inhibitors also even in SGF selected breast cancer patients also as far as we can tell have no objective responses. But they are not fully public but they have been presented at scientific meetings over the last couple of years and we – nominated but we know that both AstraZeneca and Novartis they have included FGFR1 on for breast cancer women in that clinical trials and have not seen any objective responses. So pure drugs don’t seem to work in this setting and what’s distinctive about lucitanib is that the toxicity tells it’s the VEGF receptor 2 and the efficacy is clearly different from pure VEGF R inhibitors and strongly suggest that we’re hitting FGF R1 at least in women with breast cancer where we see 50% objective response rate. So that’s the distinctive nature of lucitanib and that’s why we are so excited to be able to buy it last year and very excited to take it forward in breast cancer now where SGFR receptor amplification appears to be present both from the get go in a subset of women but also appears to be emerging as a very important driver of acquired resistance in many different types of therapy in breast cancer. We are really excited to be pushing forward with this drug.

[Operator:]

With no further questions I’ll turn the call back over to Ms. Anna Sussman for closing remarks.

[Anna Sussman:]

Okay thank you very much and thank you for your interest in Clovis today. If you have any follow up question please call me at 303-625-5022. This call can be accessed during – via replay of our webcast at clovisoncology.com beginning in about an hour and it will be available for 30 days. We appreciate your interest and time. Thank you have a good evening.

[Operator:]

Ladies and gentlemen, that concludes today’s conference. Thank you for your participation. You may now disconnect. Have a nice day.