Clovis Oncology Inc (CLVS) 2014 Q1 法說會逐字稿

Good day, ladies and gentlemen, and welcome to the first-quarter 2014 Clovis Oncology, Incorporated earnings conference call. My name is Kim and I will be your operator for today.

(Operator Instructions)

I would now like to turn the conference over to your host for today, Ms. Anna Sussman, Senior Director of Investor Relations. Please proceed.

Thank you, Kim. Good afternoon, everyone. Welcome to the Clovis Oncology first-quarter 2014 conference call. You should have received a news release announcing our financial 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's President and CEO, will discuss the highlights of the first quarter and provide an update on our clinical development program. Then Erle Mast, Clovis's Chief Financial Officer, will cover the financial results for the quarter in more detail and comment on the Company's updated 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 security 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 statement.

Now I will turn the call over to Patrick Mahaffy.

Thanks, Anna. Welcome, everybody. Thank you for joining us this afternoon. We look forward to providing updated data on each of our compounds in development at ASCO at the end of this month and continuing to advance our clinical development programs in the coming months.

In addition to the many studies we're currently enrolling, we will soon initiate two Phase 2 global TIGER studies for 1686 and EGFR-driven non-small cell lung cancer, a Phase 2 study of rucaparib in BRCA-mutant pancreatic cancer, and two Phase 2 studies of lucitanib in breast and squamous non-small cell lung cancer. Importantly, data from the ongoing Phase 2 expansion cohorts of 1686, together with data from TIGER2, are expected to serve as the basis for NDA submission to the FDA by mid-2015.

Let me start with 1686. In March we announced the most recent update of 1686 clinical data, which continues to demonstrate that 1686 is, in fact, a very active drug. Highlights of the data presented at ELCC include the following.

A 64% objective response rate was achieved in evaluable T790M-positive patients. And 91% of evaluable T790M-positive patients achieved disease control, defined by stable disease or a partial response.

Although we have not yet achieved the median duration of progression for each survival, or PFS, in the T790M-positive patients, we have observed a median PFS of greater than six months in the evaluable T790M-positive patients. And the trend suggests it could be substantially longer than six months. We are particularly pleased to see this kind of durability in 1686.

One of the issues with oncogene targeted therapies is that, while initial response rates can be promising, they can also be relatively short-lived. Our data to date have demonstrated both a consistency of response and an impressive initial duration of clinical benefit.

1686 is also very well tolerated. Only 1 of 62 patients treated with a therapeutic dose in the Phase 1 discontinued drug due to an adverse event. And we believe it is the only EGFR inhibitor to completely spare wild type EGFR signaling, and to shut down the mutant EGFR pathway active in tumor cells.

We and our investigators continue to believe that 1686 has the potential to be a very important drug. And we are determined to identify the best way to get this drug approved as rapidly as possible and into the hands of physicians to treat the patients who may benefit.

Enrollment is underway for the Phase 2 expansion cohorts in patients of EGFR-mutant non-small cell lung cancer. And we expect our two T790M-positive cohorts, together with data from TIGER2, to serve as the basis for an NDA submission by mid-2015.

These expansion cohorts will test the efficacy of 1686 in two patient subsets. The first in approximately 150 to 200 patients who are T790M-positive directly after progression on their first and only TKI therapy, similar to our TIGER2 study design. And the second in approximately 150 to 200 T790M-positive later-line patients after progression on their second or later TKI therapy or subsequent chemotherapy. Both cohorts are now storing doses of 500 milligrams, 625 milligrams and 750 milligrams BID.

Since we have observed meaningful efficacy at each of these doses, we no longer intend to pursue the 1,000 mg BID dose, as there was no evident increase in efficacy to offset the increase in dose-related toxicities. Given the pronounced efficacy of the drug and the potential for long-term administration, we are fortunate to have the luxury of testing multiple efficacious doses to ensure we choose the dose with the best balance of efficacy and tolerability.

As we have described, a dose-limiting toxicity of hyperglycemia has been observed in some patients. However, clinicians can easily screen for it and treat it with Metformin, a commonly prescribed single agent oral therapy. As presented at ELCC, we also have seen rare occurrences of QTC prolongation in a small number of patients on study, which occurs as well with other TKIs, including many approved drugs.

With 1686 we see a clear relationship to dose. All cases are either transient or readily managed by dose reduction, and no clinical consequences have occurred. Given the profile of the drug emerging from this study, investigators are extremely enthusiastic about moving the 1686 program forward rapidly, and ensuring it can be approved and made available for the large number of patients for whom it may provide benefit. With their support and active engagement, we are rapidly advancing the TIGER program. This includes three global registration studies for 1686, all in EGFR-mutant non-small cell lung cancer. TIGER2 in T790M-positive second-line patients, directly after progression on their first and only TKI therapy, for which we are currently opening sites.

In the June-July time frame we expect to initiate the Phase 2 portion of TIGER1, a randomized Phase 2-3 registration study versus erlotinib in newly diagnosed EGFR-mutant patients. And TIGER3, a randomized comparative study versus chemotherapy in T790M-positive second-line patients directly after progression on their first and only TKI therapy, which is expected to initiate during the second half of 2014. We intend to start each of these studies at a dose of 625 mgs BID. As I mentioned, the next presentation on 1686 data will be during the lung cancer clinical science symposium in ASCO in late May. I expect that I will see many of you there.

Lastly, we initiated our Japanese Phase 1 study during the first quarter.

Let me turn to rucaparib. We are actively enrolling patients in two studies in the ARIEL program, including our registration-focused Phase 3 study. ARIEL2 is our global Phase 2 single-arm open-label study designed to identify molecular features that predict sensitivity through rucaparib using DNA sequencing to evaluate each patient's tumor. This study assesses and correlates rucaparib efficacy with the genotype and phenotype of each patient's tumor. And these data will inform the final definition of homologous recombination deficiency for the ARIEL3 registration study.

To our knowledge, we are the only company seeking to prospectively demonstrate a PARP inhibitor's activity in a molecularly selected population beyond germline BRCA mutation And if successful, we believe it will meaningfully differentiate rucaparib from its competitors.

ARIEL3 is our global randomized, double-blind Phase 3 registration study that compares the effective rucaparib versus placebo. This study will evaluate whether maintenance rucaparib therapy can extend the period of time for which disease is controlled after successful chemotherapy in platinum-sensitive ovarian cancer patients. The study will utilize prespecified step-down efficacy analyses, first in BRCA, then in the broader HRD population, as defined by the ARIEL2 study, then in all comers.

Later this quarter we expect to initiate the Phase 2 study of pancreatic cancer patients with BRCA mutations. This study is based on the striking partial responses observed in two germline BRCA-mutant pancreatic cancer patients treated with rucaparib, each of whom had failed traditional chemotherapy. As you know, there is significant unmet medical need for the treatment of pancreatic cancer. So, if successful, there is potential from this study for an accelerated approval. An update on the Phase 1 solid tumor study of rucaparib will be presented at ASCO in late May.

And, finally, to lucitanib. Lucitanib is our oral potent inhibitor of the tyrosine kinase activity of FGFR 1 and 2, VEGFR 1 through 3, and PDGFR alpha and beta. Lucitanib has demonstrated impressive response rates with manageable side effects in previous trials of heavily pretreated patients. We hold exclusive US and Japanese rights. And have a collaboration agreement with Servier, the holder of European and rest of world rights for the global clinical development of lucitanib.

We are initially targeting solid tumors with FGFR pathway activation, including breast and squamous non-small cell lung cancer. There are currently three Phase 2 monotherapy trials of lucitanib planned or underway. And the two Clovis-sponsored trials are expected to begin during the second quarter. These will include a Servier-sponsored European Phase 2 study in advanced breast cancer patients, known as FINESSE, which began enrolling patients in late 2013 our Clovis-sponsored US Phase 2 study in treatment refractory FGFR1 or 11q-amplified patients with advanced breast cancer; and a Clovis-sponsored global Phase 2 study in advanced squamous lung cancer patients with FGFR1 amplification.

Data on lucitanib will be presented in a oral presentation at ASCO in May. These data will be familiar to many of you but we were pleased to receive an oral presentation for what will be, for most US physicians, their first introduction to the drug.

Now let me turn the call over to Erle to discuss first-quarter 2014 financial results and guidance.

Thanks, Pat. Afternoon, everyone. We reported a net loss for the first quarter of 2014 of $30.7 million, or $0.91 per share, and net cash burn for the quarter of $19.6 million. Our financial results for the quarter included a number of unusual, or at least infrequently occurring transactions, but coincidentally the net effect of these items was not material to the overall financial results. But I wanted to review these transactions just to provide a little more clarity on our results.

During the quarter, we recognized revenue for the first time in the Company's history. Pursuant to our collaboration and license agreement with Servier for lucitanib, we earned a $13.6 million milestone payment as a result of the expiration of the opposition period for lucitanib's European patent. The receipt of this milestone payment triggered the recognition of certain expenses for the quarter.

First of all, a portion of the milestone payments that we receive from Servier are passed through to the original licensor of lucitanib. And, as such, we recorded a $3.4 million charge for the milestone payment to the licensor in the first quarter. Second, the milestone payment resulted in the amortization of a portion of an intangible asset that we recorded in the fourth quarter of 2013 as part of the purchase accounting for the acquisition of EOS. And this created a non-cash charge for the quarter of $3.4 million.

And then, finally, a $2.1 million income tax provision was recorded in the first quarter due primarily to projected taxable income that we will have in Italy for 2014, relating again to the receipt of the Servier milestone payment. I'd also note that the majority of this income tax expense is a non-cash charge.

The final transaction that I would highlight for the first quarter is the $5 million milestone payment that we made to Celgene for the initiation of the first Phase 2 study for CO-1686. This payment, combined with the milestone payment for the lucitanib licensor, resulted in a charge of $8.4 million for acquired end process research and development expense, which you will see captioned on our income statement.

The Company's net loss for the first quarter of 2013 totaled $15.7 million, or $0.60 per share. Now, as I mentioned, the transaction that I just highlighted basically offset each other and did not have a material net impact on our net loss. So, accordingly, the increase in the loss for the first quarter of 2014 as compared to 2013 is due primarily to expanded development activity for CO-1686 and rucaparib programs.

Research and development expenses totaled $24.2 million for the first quarter of 2014, and this compares to $12.1 million for the first quarter of 2013. An increase in expense this year is due to the initiation of the ARIEL2 and ARIEL3 studies for rucaparib, an increase in the number of patients enrolled in the Phase 1/2 study for CO-1686, the initiation of the TIGER2 and the Japanese Phase 1 studies for CO-1686, and increased manufacturing of clinical drug supplies for both the 1686 and rucaparib programs.

As a reminder, the development expense for lucitanib are currently being funded by Servier. So its addition to our portfolio had no impact on R&D expenses for the first quarter of this year.

General and administrative expenses totaled $5.3 million for the first quarter of this year, and that compared to $3.2 million for the first quarter of 2013. This increase is largely due to higher share-based compensation expense for employees engaged in general and administrative activities.

Total operating expenses for the quarter included non-cash charges of $9.2 million. And this relates to share-based compensation expense, amortization of the intangible assets that I referred to earlier, and the accretion of contingent purchase consideration associated with our EOS acquisition. As of March 31, the Company had $303.7 million in cash and 33.9 million outstanding shares of common stock. We continue to expect cash burn for 2014 will total approximately $120 million, and to end this year with approximately $200 million in cash.

With that, I'll turn the call back over to Pat for some closing remarks, and then will open it up for Q&A.

Thanks, Erle. Anticipated milestones for the remainder of the year -- for 1686 we've initiated the expansion cohorts for the Phase 1/2 study, swiftly built a larger data set for our T790M-positive cohorts, and expanded them to include approximately 350 patients in two dose cohorts each.

These include approximately 150 to 200 T790M-positive patients in dose cohorts directly after progression on first and only TKI therapy, and approximately 150 to 200 T70M-positive later-line patients in those cohorts after progression on their second or later TKI therapy or subsequent chemotherapy. I think I said two -- it's three does cohorts. Sorry.

In addition, we intend 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 therapy, the Phase 2 portion of the TIGER1 registration study in newly diagnosed EGFR-mutant me patients, and the randomized comparative TIGER3 registration study of 1686 versus chemo in T790M-positive patients directly after progression on their first and only TKI.

Turning now to 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 intend to initiate the Phase 2 study of rucaparib and pancreatic cancer patients with BRCA mutations.

Finally, for lucitanib, during the second quarter we intend to initiate our Phase 2 studies of lucitanib in selected patients, in addition to the FINESSE breast cancer study currently underway by our partner Servier. We include the US Phase 2 study in patients with treatment refractory FGF-aberrant breast cancer, and the global Phase 2 study in patients with metastatic squamous non-small cell lung cancer with FGFR1 amplification.

In summary we expect to enroll more than 1,000 patients in Clovis-sponsored studies around the world in 2014, which is rapidly emerging as a very important year for us. We look forward to seeing many of you at ASCO where I should note that we intend to host an investor analyst event late Saturday afternoon, May 31.

With that, thanks for joining us. We now open the call to Q&A.

(Operator Instructions)

Marko Kozul, Leerink Partners.

Good afternoon and thanks for taking my question and your progress. First question, can you give us, Pat, maybe some color on how enrollment is proceeding for the additional patients in the Phase 2 expansion cohort?

Without giving a number I'll just say that interest in the trial on the part of clinicians and physicians remains exceptionally high. At the sites open we have waiting lists to enroll into the trial that remain very large. And we anticipate that as more sites open into the expansion cohort and into TIGER2, the enrollment in these trials is going to go exceptionally fast. It is exactly on track with what we would expect it to be.

All right. Thanks. And then because you're planning a 1686 filing based on TIGER2, and Phase 2 expansion cohort patients, can you give us a rough sense of what the mix of data might look like or what each trial experience might contribute to the filing?

We're going to have a complete data set from the expansion cohorts, from each of the expansion cohorts. And we will have meaningful data from TIGER2 at the time we submit. It may be complete data. We do expect the expansion cohorts to fully enroll a little bit ahead of TIGER2 because they are underway now and TIGER2 hasn't started enrolling yet. It will shortly. We'll make that judgment at some level based on dialogue with FDA and based on all that we have in terms of data from the expansion cohorts themselves.

Thanks. And I'll squeeze in a quick QTc cardiac two-part question. First, do you plan on excluding cardiac disease patients from any of your trials that you are about to start, similar to another competitor? And, second, what do you estimate the proportion of patients either in the frontline or relapsing scenario that have underlying cardiac or morbid disease? Thanks.

We have not and do not intend to exclude patients for cardiac disease. In fact, we have very limited exclusion criteria in our trial given the tolerability of the drug.

Secondly, one can speculate on the number of patients with cardiac disease in our trial experience. It's probably at least 10% to 15%. In a broader population, in a larger population it would likely be somewhat higher.

Great. Thanks for taking the questions.

[Bob Ive], Alexa Capital.

Thank you for taking my call. My question mostly, all related to CO-1686. And the first one if you can -- a question -- there's non responders. Have you looked at those patients that don't respond? Do they have a new mutation or they just have a mutations at different pathways?

Andrew?

We don't have data yet to inform that question. One of the reasons for that is that even the patients who aren't responding typically are staying on drug -- IE, they have stable disease. And obviously in the context of progression, which is obviously what brings them into the trial in the first place, then stable disease is a good result.

And so, while stable, they also don't get on-study biopsies. There is an optional biopsy at study exit but typically few patients will take up that opportunity. And, so, today we just don't have information to inform your question.

Now, obviously as the utility of plasma testing increases over time, it potentially will become a lot easier for us to start to get some insight into why patients may either not respond fully to drug or progress upon drug. So that's something we're optimistic about going forward, but today we don't have the data.

Okay. And then the other questions -- maybe I missed it -- I thought the FDA finding would be based on TIGER2 and TIGER3 data. Now it seems like mostly you are saying it's going to be based on TIGER2 and data expansion study. Is there a change there or maybe I missed something?

You're not entirely wrong. Things have accelerated here. And, so, we had intended for what was originally TIGER3 to be analogous to the expansion cohort in later-line patients. We and our regulatory team don't believe that an additional focused dedicated Phase 2 trial in that population is necessary beyond what we will learn from and submit based on the expansion cohort in the later-line patients.

So, TIGER3 is now the confirmatory study for this accelerated approval path. And TIGER3 is a comparative study in second-line patients versus chemotherapy. And the TIGER3 study will initiate in the second half of this year. It will ultimately be a part of a submission to FDA and other regulators because it's our confirmatory study. But it will not be a part of our initial registration package.

Okay. And my last question about this a QTc promulgation, can you help us understand what is the requirement for a thorough QTc study for cancer drug, or maybe just for TKI drugs with some QTc concern?

I want to make sure I got that question correctly. So, I wonder if you could ask it again.

I'm just wondering whether I think, for a GP drug, I thought that the FDA probably require a thorough QTc study. I'm just wondering what for cancer drugs.

I got it. The question is do we need a full QT study? We don't believe we do. At some level, the answer to QTc prolongation is now embedded in the data that we presented at the LCC and obviously we will continue to present over the course of the development of the drug.

So, we do not believe that a dedicated QTc study is going to be required. Funnily, that would have probably been more likely had we not seen QTc to prove that it didn't exist. So, our view is that a QTc study is not going to be required.

You're right to differentiate. This is hardly a drug that it will be prescribed by general practitioners for an overall healthy population. This is a drug being prescribed, as other TKIs are with QTc, in very advanced cancer patients.

Just in light of the QTc, that grade 3 study, do you plan to increase in QTc monitoring going forward?

No.

Okay. All right. Thank you

Cory Kasimov, JPMorgan.

Good afternoon, guys. Thanks for taking the questions. Two of them for you. First of all, regarding the Phase 2 portion of the TIGER1 study in newly diagnosed patients, do you plan to provide regular updates on that part of the trial before it advances to Phase 3? What I'm asking is when is the earliest we may be able to see data in that setting?

Yes, we will provide updates at scientific meetings. It is open label to us and therefore we are able to see the data and provide it to you.

Given that enrollment will begin, let's call it June/July, I think the most realistic scientific meeting at which you will see data is probably ASCO 2015. That feels realistic. It's possible that we might decide to participate again in, I think it's in March again next year, at ELCC. But you should not anticipate data from that study. It would just be too immature this year. So, I would target ASCO 2015.

Okay. And then what are your thoughts about submitting for breakthrough status, especially now that AZD-9291 has it? And how much do you think that matters in the grand scheme of things?

It's a very nice thing to have. It doesn't really change timelines in any meaningful way relative to the already accelerated approval path, which has been very successfully and rapidly used by companies like Pfizer for crizotanib, et cetera, prior to breakthrough. I think from all the dialogue we've had with companies that have it, is that it allows for a very frequent interaction at a high level with the FDA. That is a real benefit, and we would like to have that benefit. A

As I've said to everybody, given our path, which is clear, and our timelines, which are clear, the time at which we would really benefit from that breakthrough is second half of this year. So, we have targeted trying to get breakthrough status in the second half of this year. We definitely are going to ask for it at some point. We've always known that it would be better to ask for it when we have absolute confidence we will get it. So that's what I would be pointing to, Cory.

Okay. Great. Thank you.

Brian Klein, Stifel.

Great. Thank you for taking my question. Regarding your upcoming presentation at the ASCO, can you give us a sense of how many patients worth of data we are going to get to see, and if your presentation will include any patients from the expansion cohorts?

Yes, great question. Our current thinking is that it will be an update of the Phase 1 experience. So, I think you should assume that it will be an updated data set on 62 to 65 patients or so that are at the therapeutic dose in the Phase 1. This is all of the 900 BID freebase patients and all doses of the HBr formulation.

Great. Thank you. And will that include also any expansion cohort patients?

No, I don't believe so.

Okay. I just wanted to confirm. And then not to beat a dead horse on the QTc but just wondering if that was related at all to dose, and if therefore you would not expect to see any QTc promulgation in the lower dosage you are testing? Thank you.

We wouldn't say that we wouldn't expect to see it at lower doses. We did see some of it at lower doses and it was reported at the ELCC. However, we do think it is clearly dose related and the QTc prolongation is a more frequent occurrence as we get to higher doses. Andrew, anything you would add to that?

No, that's accurate.

Great. Thank you very much.

Ravi Mehrotra, Credit Suisse.

Hi, thanks for taking the question. This is actually [Kun] asking a question on behalf of Ravi. I just wanted to follow-up on the data requirements for the potential NDA filing in mid 2015. When you say more meaningful data, could you provide a little bit more color? Are you referring to the fact that maybe patients from TIGER2 may not have reached the primary endpoint? Or is that you are waiting for more mature data on certain durability end points? Thanks.

It is along the lines of, if we have a really good data set from the expansion cohorts -- and remembering that that's a large number of patients so it meets any requirement FDA has about minimum exposures, and it's an end of patients that is consistent with submissions by others who have successfully achieved recently accelerated approvals -- we clearly will submit. We will submit, as well, with whatever data which may be nearing maturity or not quite mature yet from the TIGER2 experience, with the knowledge that FDA may request an update of those data over the course of their review.

Okay. Thank you.

Terence Flynn, Goldman Sachs

Hi. Thanks for taking the question. First, can you just tell us a little bit about the dose you're planning to use in TIGER1 and TIGER3? And if you haven't yet decided that, what information is going to drive that decision? And then just one more on dose, regarding the decision not to move forward with 1,000 mg. Can you tell us specifically what new information drove that decision, because I think at ELCC you were guiding to going forward with 1,000?

We were. As you know, we are generating data at a pretty meaningful clip here, at multiple doses. And one of the benefits of exploring these multiple doses is we are getting to see efficacy across dose levels. And we clearly now can say that the toxicities that we see are dose related.

So, in our effort to identify the balance of efficacy and tolerability, we've been aided by being able to look at a larger data sets that we had even at the time of the ELCC. And what has emerged is two things that are really important. One is that at each of the doses we're studying, 500, 625 and 750, we see clear and profound evidence of activity that is, in general, pretty consistent.

In addition, we now can really clearly see that QTc and hyperglycemia, the tolerability is dose related, and those effects are dose related. So, we haven't seen a benefit in terms of efficacy at 1,000 mg BID relative to our other doses. But we know we're going to see increased toxicity.

So we don't get an advantage out of going higher, and we get not disadvantage efficacy-wise going lower. So, it's clear why we would do this. We have chosen -- I think I said in the script -- the dose for each of the TIGER 1, 2 and 3 protocols, and that's 625 mg BID.

Okay. Thanks. And then could I just ask one on rucaparib, just remind us of the design of the trial there and then what you guys think the bar is for an accelerated approval? Thanks.

For which study, Terence? Do you mean for pancreatic cancer?

Pancreatic, yes.

It's a single-arm study in patients who have progressed on approved chemotherapy. And the patients have evidence of a BRCA mutation which can either be a germline or a somatic mutation. And, as you probably know, more and more patients with pancreatic cancer are having their tumors sequenced now in the hopes that they will find something actionable. And it's possible that the somatic BRCA mutations, which appear to be reasonably common -- collectively, about 10% of pancreatic ductal adenocarcinoma seems to have a BRCA mutation, the majority of that is somatic mutation, not germline -- it's possible that those are the CR actionable mutations. And that's what we're exploring in our single-arm study.

There's a run-in phase where we are treating around 20 patients, looking for those necessary signals to give you confidence that the response rate is likely to be meaningful. And then there's an adaptive design where we are basically looking for increasing statistical certainty around a response rate that needs to be north of 20% for sure. Obviously, I think if it was at 20% there would be discussion as to whether that was adequate.

But bear in mind that even in the front line, response rates to cytotoxic chemotherapy in pancreatic cancer are in the 10% to 20% range. So 20% as monotherapy to a well tolerated oral agent in second line may well be sufficient for an accelerated approval. There's no precedent here so obviously we're speculating with these numbers. But I think 20% is a floor. If we are 30% or higher I think it's believed to be likely that an accelerated approval would be highly viable given the unmet need.

As you know, these patients, unfortunately, in the second line have a terrible outcome with a median survival that's just in a matter of a few months, typically three or four months. And most patients don't actually get second-line chemotherapy because they are not sick enough. So, if we are able to see response rates in the order of magnitude I've described, with decent durability, meaning north of four or five months, then I think we are opportunistic that that would represent a meaningful advance for that group of patients.

Great. Thank you.

Peter Lawson, Mizuho Securities USA.

Patrick, these back to back CO-1686 and AZD-9291, what date are you going to be providing, what format -- response rates, safety profile, durability? What should we be expecting from you?

I think you will see an update that is consistent in format. Maybe not exactly the same but consistent in format as we have now provided in Sydney at the World Lung Meeting and at ELCC in Geneva just a month or so ago. And you are right, it will be a pretty complete update now from the Phase 1 experience, with our focus on tolerability, of course; response, at the therapeutic doses, as we described in Geneva; and what we see as a very exciting emerging evidence of durability first described at ELCC.

Thank you. And then the Astra data and the exclusion of cardiac patients, are you seeing anything in your data that suggests why they are doing that?

We don't see anything in our data that suggests why they are doing that. And we haven't seen their data which suggests why they might be doing that. So, we don't really have -- we can only hypothesize. There's nothing in our data about our drugs that suggests we need to consider any type of exclusion criteria along those lines. But you're including cardiac patients in a general population of cancer patients.

We know we are.

Okay. We do not exclude them and we know we have included them. So, yes.

Got you. Thank you. And then I may have missed this on rucaparib, what did you say was the next update of data?

The Phase 1 data will be presented at ASCO in a month.

Great. Thank you so much.

Yuron Werber, Citi.

Hi. This is actually [Tennan] in for Yuron. I have one quick question on QTc prolongation in 1686. Specifically I was wondering if that data was corrected. And if so, if you could elaborate on the correction method that was used? Then just a quick follow-up relating to whether or not 1686 hits the HERG channels, or if you had any data surrounding that, and if that is something that you could share. Thank you very much.

1686 does not inhibit HERG channels meaningfully in the standard in vitro assays. And the correction method used routinely is Fridericia correction factor. We've also done the calculations with Bazett and with the linear aggression, sometimes called Framingham, approach. And the results have been fairly similar between all three methods.

Thank you very much.

Thank you, everyone. That's about all we have time for today. We'd like to thank you for your interest in Clovis Oncology. If you have any follow-up questions please call me at 303-625-5022. This call can be accessed via a replay of our webcast at clovisoncology.com beginning in about an hour, and it will be available for 30 days. Thank you for your interest and time. And have a good evening.

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