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Executives

Breanna Burkart – Director, IR

Patrick Mahaffy – President and CEO

Erle Mast – EVP and CFO

Analysts

Marko Kozul – Leerink Swann

Ravi Mehrotra – Credit Suisse

Clovis Oncology, Inc. (CLVS) Q1 2013 Earnings Call May 7, 2013 8:30 AM ET

Operator

Good day ladies and gentlemen and welcome to the Quarter One 2013 Clovis Oncology Inc. Earnings Conference Call. My name is Carol and I will be your operator for today. At this time all participants will be in a listen-only mode and we will conduct a question-and-answer session towards the end of this conference.

(Operator Instructions).

As a reminder this call is being recorded for replay purposes.

I would now like to turn the call over to Breanna Burkart, Senior Director of Investor Relations. Please go ahead.

Breanna Burkart

Good morning and welcome to the Clovis Oncology’s first quarter 2013 conference call. You should have received the news release announcing our first quarter 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 maybe accessed live on our website during the call and will be available an 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 of 2013 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 comments on the company’s outlook for 2013.

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 plan.

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 day 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 Patrick Mahaffy.

Patrick Mahaffy

Thanks Breanna. Good morning everybody. Thank you for joining us. We made pretty important progress during the past quarter in each of our clinical development programs and in particular I’m pleased to share with you for the first time details of our development as an improved formulation for CO-1686. During the first quarter we initiated a study in healthy human volunteers comparing the pharmacokinetic properties of the new tablet formulation which is a hydrobromide salt form the drug to our current capsule formulation.

I am happy to say that tablet formulation is consistently demonstrating much higher price in exposure levels and substantially reduce variability in humans compared with our current capsule formulation. I’ll speak more about this shortly.

For rucaparib, we believe we’re very close to identifying a dose we are nearing the end of the Phase I portion of our monotherapy study. And we take this opportunity to highlight our plans and expectations for the clinical development programs both 1686 and rucaparib for the remainder of the year.

CO-1686 is our oral targeted small molecule covalent inhibitor of the mutant forms of epidermal growth factor receptor or EGFR for the treatment of non-small cell lung cancer. 1686 targets both the initial activating EGFR mutations, as well as the dominant resistance mutation, T790M, and as a result it has a potential to treat non-small cell lung cancer patients with EGFR mutations both as the first line and as the second line therapy. Because 1686 was designed as their wild-type or normal EGFR it also has the potential because of lower incidence of toxicity such as skin rash and diarrhea that are normally associated with other EGFR inhibitors.

In March 2012 we initiated the first human clinical study of 1686 at a dose of 115 mgs per day we have continued to dose escalate for the year that we are currently dosing at 900 milligrams twice daily. As we discussed previously the current 900 mg BID dose of the capsule formulation we are beginning to see trough plasma levels above a therapeutic threshold for a reasonable period of time. We have already provided an update that included some cover on progressively better patient outcomes as we get to these higher doses including symptomatically and signs of clinical benefit.

Given the fact that ASCO was only four weeks away we’re going to limit our comments on this Phase I study but we do look forward to providing you a more detailed Phase I update in Chicago at ASCO in four weeks. It is important to note that in this ongoing Phase I study we have not yet determined the maximum tolerated dose or a recommended Phase II dose. What I’d like to do is discuss more specific details of our formulation efforts for 1686.

As I stated during the first quarter we initiated a study of 1686 and helping given volunteers comparing to PK properties of a hydrobromide salt tablet formulation with the current capsule formulation in use today in the ongoing dose escalation portion of the Phase I/II study. Based on data collected to-date the tablet formulation has demonstrated plasma exposures approximately three times greater than the capsule formulation dose per dose as well as greatly reduced variability. These data suggest that the tablet formulation could be administered significantly lower over doses to achieve higher and more predictable exposures in patients compared to the current capsule formulation.

Based on these very encouraging data we intend the transition to the tablet formulation for our 1686 studies beginning in about August of this year. Until that time we will continue to enroll patients in the ongoing Phase I/II study at the current dose of 900 milligram BID with the capsule formulation.

Since as I’ve already noted the maximum tolerated dose or MTD has not yet been achieved we will resume dose escalation with the table formulation when it becomes available in the next couple of months. We currently expect to resume the dose escalation at approximately 300 milligrams BID with the table which relates to the exposure seen at 900 milligrams BID with the capsule.

At this point there is no single toxicity that we are seeing including any evidence of volatile EGFR in addition. So thus far we do not yet have insight into what dose limiting toxicity will be. Thus far 1686 appears to be a very well tolerated drug. We expect to achieve the recommended Phase II dose and will then initiate the Phase II expansion cohorts with the tablet formulation by the end of the year. The two cohorts include a study 1686 and approximately 40 non-small cell lung cancer patient who have progressed well on the treatment with EGFR directed therapy such as Tarceva or Iressa and have developed the T790M resistance mutation. We expect to initiate this study by the end of 2013.

Secondly a study of 1686 in an expansion cohort of newly diagnosed patients who’ll express the activating mutations of EGFR which we expect to initiate by early 2014. If by inhibiting both activating mutations of EGFR and its dominant resistance mutation T790M we are able to demonstrate a meaningful progression pre-survival benefit to compared to what has been seen to-date to Tarceva and other TKI therapies we would be in a position to move 1686 into the frontline or first line development program.

Pending data from the second line T790M positive cohort, our goal is to commence a registration study in the second half of 2014 in this population. We also plan to initiate a Phase I study of the tablet formulation in Japan early next year.

Turning now to rucaparib. Rucaparib is a oral, potent small molecule inhibitor of PARP-1 and PARP-2, which we are exploring as both a monotherapy and in combination with chemotherapeutic agents in ovarian cancer patients who are predisposed to PARP inhibitor sensitivity. We’ve been pleased with the progress in both our ongoing monotherapy in combination with chemotherapy Phase I/II studies as well as our investigator-sponsored monotherapy in combination chemotherapy trials. Our Phase I/II monotherapy study continues to advance and we believe we are close to the end of the Phase I portion of the study. Currently dosing at 480 milligrams twice daily we are pleased with the plasma levels the evidence of efficacy – disease control but that we have absorbed to-date.

Once we have achieved the recommended Phase II dosing schedule we will then expand into the Phase II portion of the study to assess the efficacy of rucaparib in patients with ovarian cancer, associated with germ-line mutations in the BRCA genes. We will provide an update from the Phase I portion of this Phase I/II monotherapy study at well as data from the Phase I study of rucaparib in combination with carboplatin at ASCO in June.

Again and as a reminder this is an ongoing Phase I and we have not yet determined the maximum tolerated dose or a recommended Phase II dose for rucaparib. In the second half of 2013 we look forward to initiating two studies through rucaparib one a single arm biomarker study in women with relapsed, platinum-sensitive, high-grade serous ovarian cancer to begin in the third quarter to inform the definition of Homologous Recombination Defects or HRD for the pivotal study and the pivotal study itself a global registration switch maintenance study in platinum-sensitive ovarian cancer patients with efficacy analyses pre-specified in populations defined by deficiencies in BRCA and in other DNA repair genes to begin during the fourth quarter.

Now I’ll turn the call over to Erle to discuss first quarter 2013 financial results and guidance for the year.

Erle Mast

Thanks, Pat. Good morning, everyone. Our full financial results are included in this morning’s press release. So I’ll direct my comments to highlights for the first quarter of the year.

We reported a net loss of $15.7 million or $0.60 per share for the first quarter of 2013 compared to a net loss of $19 million or $0.86 per share for the first quarter of 2012. This decrease in our net loss in the first quarter of 2012 was due primarily to a $4 million charge required in process research and development expense recorded in the first quarter of 2012 associated with the achievement of a development milestone for CO-1686.

Research and development expenses totaled $12.1 million for the first quarter of 2013 and this represented a 34% sequential decrease from R&D expense for the fourth quarter of 2012 and this decrease was due to the termination of development activities for CO-101 at the end of last year. And finally, our total operating expenses for the first quarter of 2013 included $1.8 of share based compensation expense.

Our net cash burn for the first quarter of 2013 totaled $14.5 million and we ended the quarter with $129.6 million in cash $26.2 million outstanding shares of our common stock. Now I’d like to discuss our financial guidance for 2013. We’ve updated our cash burn guidance for the year and now expect to burn between $60 million and $65 million for the year and to end 2013 with approximately $82 million in cash. Now the reason for the increase in our cash burn guidance for the year is the acceleration of clinical trial and drug supply cost form what we expected in 2014 into 2013 as we advance the clinical development programs for CO-1686 and for rucaparib.

Now I’ll turn the call back to Pat for some closing remarks and then we’ll open it up for Q&A.

Patrick Mahaffy

Alright thanks, Erle. So, our anticipated milestones for the remainder of the year. For 1686, we plan on completing the dose escalation portion of the ongoing Phase I/II study to establish the optimal dosing schedule transitioning to the tablet formulation of 1686 once it becomes available in the third quarter. To initiate the Phase II expansion cohorts to assess efficacy in second line T790M positive non-small cell lung cancer patients late this year and in first line non-small cell lung cancer patients in early next year. And overall advance the clinical development program in order to initiate a registration study in second line T790M positive patients in the first half of 2014.

Now, to rucaparib, we also plan to complete the dose escalation portion of the ongoing Phase I/II study to establish the optimal monotherapy dosing schedule, initiate the Phase II expansion cohort to assess efficacy in selected ovarian cancer patients; to advance the development of a companion diagnostic to identify the patients most likely to respond to rucaparib, and initiate both the biomarker study and a pivotal study in platinum-sensitive ovarian cancer patients in the second half of 2013. Lastly for our Mutant cKIT Inhibitor program with the rate we intend to identify a product candidate by the end of this year or during the first part of 2014.

In summary, we are pleased with the progress we’ve made in the development of these programs and we very much look forward to providing the Phase I updates from both of our clinical development programs at ASCO next month. With that we’d like to thank you for joining us today, oh and happy birthday to my son Ryan who turns 19 today. And with that I’ll be happy to any questions you ask.

Question-and-Answer Session

Operator

(Operator Instructions). Please standby for your first question which comes from the line of Cory Kasimov from JPMorgan. Please go ahead.

Unidentified Analyst

Hi, this is Whitney on for Cory. Thanks for taking the questions. Just wondering if you can give us little bit color on what data we’ll be seeing at ASCO, maybe how many patients will have data on for both drugs and the duration of treatment?

Patrick Mahaffy

Well you know all of a sudden, and try to be pretty circumspective of what we say is going to be presented at ASCO given anxieties, but, it could affect the presentations and so. On 1686 there will be data on approximately 40 patients that have been treated to-date, including of course with the very low doses that we started in the Phase I study, on rucaparib it is a slightly larger number, I think there will probably be data in the combination study around 35 patients or 40 patients in a similar number for the monotherapy class. When you will see is data on PK, safety and any observations of efficacy observed to-date at the time we present those data.

Unidentified Analyst

Okay. And what’s the to-date is that or I guess what the data cut-off to that?

Patrick Mahaffy

It will be middle to late May, I mean it.

Unidentified Analyst

Okay, okay pretty real-time then. Okay. And then I guess for rucaparib what kind of toxicities are you starting to see at 480 that are, making you think you’re close to finding the MTD there?

Patrick Mahaffy

I think it’s driven more by exposure levels, if we were to predict the MTD it would probably being nausea. We had one case at 360; we have not observed we get at 480. We have not seen any meaningful amounts of myelosuppression yet. So would probably will be nausea as the MTD, but we haven’t achieved the MTD yet, so I can’t say that uncertainty.

Unidentified Analyst

Okay great, thank you for taking the questions.

Patrick Mahaffy

You bet.

Operator

Thank you for that question. The next question we have comes from the line of Marko Kozul from Leerink Swann. Please go ahead.

Marko Kozul – Leerink Swann

Hi, good morning. My first question is also on 1686. Pat, I want to ask how we should read into the updates that you provide in this morning regarding continuing dose escalation with the bromide salt formulation and having clarity on starting the pivotal trial in 2014. Previously on the last call you indicated two more aggression was being observed would you say the objective for ASCO have been met? And my second question related is that, whether toxicity to-date has remained consistent with only grade, 1 grade, 2 toxicities observed so far?

Patrick Mahaffy

So as for, whether we have achieved – what we had hoped to achieve by ASCO, yes – yeah I guess at some level we would have thought we would have achieved the dose by now, we had not, that in the end a good news; we have not achieved the dose, because we are not seeing toxicities that would hinder our ability to continue to dose escalate.

As – so I’m actually very pleased with what you’re going to see at ASCO, I’m particularly pleased that in a very short period of time compared to other two of transition to an improved formulation of TKIs. We are going to move in real-time to a formulation that has a meaningful improvement in pharmacokinetic properties not the least of which was the improvement in exposures, but also the fact that there is variability that you often see with fully observed TKIs has been reduced and it’s been reduced primarily by bringing up the absorption in all patients.

So it isn’t just that we’re getting higher absorption in a slow number of patients, in all patients we get their absorption, which has great impact on our ability to dose that an effective dose for the majority of patients treated. So, we’re really pleased with this transition and happy that we’ll be able to continue to dose escalate with this improved formulation, ideally achieving a dose by the end of the year putting us in a position to rapidly enroll the expansion cohort and clearly putting us in a position to initiate based on data, the registration study in the second half of 2014.

I won’t speak much to details of the ASCO presentation, Marko you will see the presentation there. We will only reiterate that we do not see evidence of wild-type EGFR inhibition and that we tell we’re able to continue to dose escalate we clearly have not seen any evidence that we’ve achieved in MTD.

Marko Kozul – Leerink Swann

And thanks for that. You know based on what you know today about 1686, do you have any preliminary socks on what a pivotal trial it might look like?

Patrick Mahaffy

Well we have – we have a couple of options and they’re going to be based less on what we see to-date, with trouble mind use of the drug that we have not yet achieved in the Phase II dose. But what we see in the expansion cohort, the two options that we believe would be available to us are as follows; one is in the event we see an encouraging response rate and I don’t know what encouraging means exactly, there are different numbers that investigators or even people currently would say, but clearly if we had a response rate that sorted with the three, we think there is a realistic chance that we would follow the path that Pfizer took with crizotinib, which is an accelerated approval based on a relatively modest number of patients caller on 200.

In a single arm study looking at response rate for this very clear unmet medical need, in the event the response rate would be lower than that, which I’m not predicting, but if we’re in the 20 say, I think is more likely a registration study would be a head-to-head against chemotherapy, I think that chemotherapy would probably be (inaudible). And the end point would be a negotiation with FDA whether they would accept PFS as an endpoint in that second line study or whether they require survival or whether they would accept PFS as an endpoint for accelerated approval and require complementary survival study.

What we hope obviously is that we would be able to follow that crizotinib path on a single arm study, which of course would be somewhat faster. In any event we will run the head-to-head study against crizotinib, because that would be required as the confirmation of the study.

Marko Kozul – Leerink Swann

Terrific. Just one more quick one then I’ll jump back in queue. Can you talk a little bit about the market opportunity you say for 1686 the market that would potential address?

Patrick Mahaffy

Well I can talk about patient population, there are in the United States and Europe about 15% of lung cancer patients developed that non-small cell lung cancer, because of mutations in EGFR. Half of those – so 7.5% or about 15,000 a year develop the T790M mutation as the cause of their failure on Tarceva or other TKIs.

In Japan and in other Asian territories for reasons that are not clear to me like anybody that I know, the epidemiology is different, 30% to 35% of patients with non-small cell lung cancer developed that cancer because of mutations on EGFR and again half of those or 15% ultimately fail on TKIs more likely Iressa in Asia, because of T790M mutation.

So in the second line setting we addressed an annual population in the United States of 15,000 or so a larger number than that in Europe just because of the population being larger. And in Asia the kind of unusual skewing of the population which is at least the size of not larger than that of the United States, but actually markets being larger when you include all of Asia, because the epidemiology is different.

What we hope and believe based on the preclinical data we have so far and the tolerability we have seen thus far is that this drug very clearly has an opportunity to be positioned as a first line therapy that would replace existing therapies, because one we hope it can heal at longer duration, progression free survival by inhibiting the dominant resistance mechanism from emerging mutation from emerging. And secondly because, if we are able to maintain this good tolerability it clearly would be far better tolerated than crizotinib or Tarceva or other TKIs.

Since those two drugs today Tarceva and Iressa total at least 2 plus billion dollars in annual revenues. We think we have every opportunity with more absolute pricing to be a very large drug in the event that we address that population adequately.

Marko Kozul – Leerink Swann

Pat thanks for taking the questions. I’ll jump back in queue. Thanks.

Operator

(Operator Instructions). Next question we have comes from the line of Ravi Mehrotra (Credit Suisse). Please go ahead.

Ravi Mehrotra – Credit Suisse

Thanks for taking my question. Firstly Pat, please test my best wishes on survive for his birthday.

Patrick Mahaffy

I bet you are going to get to that.

Ravi Mehrotra – Credit Suisse

Okay and I think that’s a good sight for night. On the Phase I/II dose escalation for 1686, you previously talked about QD versus BD for the old formulation. For the new formulation you’re still looking into that, can you give us any granularity on sort of the shape of the PK curve so we simply divide by three as you flagged in your press release for the new formulation. And I guess taking with the tablet formulation can you just walk us through what steps are required for you to actually start using that, is it it’s stability attached further stability attached or just manufacturing ramp up, I’ll come back to you with more after you’ve answer those.

Patrick Mahaffy

Well let’s see if I remember them first of all. So, it – will also be BID the half size is about the same as it is the same as it is for the current formulation so we anticipate going late to BID dosing. Secondly it’s always more complex than just dividing by three but dividing by three is good enough we’ll present some of these data we would intend to present some of these data at ASCO and provide a more detailed update of the PK profile but dividing by three is pretty safe right now as a place to start in terms of determining the profile of the drug.

And then as to timing it’s driven not my stability or other test really it’s about getting manufacturing completed for one and two just the timing of IRB approvals to change the formulation which we anticipate will take place in around July. So, the goal is to get into patients with the tablet formulation not necessarily at all centers because IRB approval kind of come in a staggered way. But by the middle of through August we would hope to being studies in patients as the 300 mgs or so BID with the tablet formulation.

Ravi Mehrotra – Credit Suisse

Okay just two quick follow-ons any developments on the – Roche like diagnostic test are you still expecting a PMA with the NDA rucaparib the HRD study how many patients were involved into that – would you just likely put everyone who has gone over rucaparib into that and finally if you can just tell us whether the payoff for 1686 that will be great?

Patrick Mahaffy

What was the last question Ravi, I don’t think I heard it?

Ravi Mehrotra – Credit Suisse

No something about PR then, well it’s right, right?

Patrick Mahaffy

Yeah it’s absolutely and I honor the effort I do. So, first as to the HRD study we’re going to enroll about 200 patients in that study and that will begin in the third quarter. Ravi, as I just giggling about your second question I forgot your first. Yeah with Roche everything is on track we continue to work with them on the diagnostic and we anticipate that what is now been analytically evaluated will be clinically validated over the course of our registration study and then the file the PMA at the time we file the NDA for approval.

Ravi Mehrotra – Credit Suisse

Okay look forward to seeing you at ASCO.

Patrick Mahaffy

We do.

Operator

Thank you. The next question we have comes again from Marko Kozul from Leerink Swann. Please go ahead.

Marko Kozul – Leerink Swann

Thanks for taking the follow-ups. I wanted to ask have you any thoughts or understanding as to how indolent T790M tumors might be in other words early stage patients generally respond or fail to respond to Iressa and Tarceva therapies in certain timeframes. Given the senses to whether we should expect T790M patients to follow this pattern of time to response or might the book of responses be observed with a different time course? Thanks.

Patrick Mahaffy

I think it’s true early for us to answer that question. I think that’s the question that is it will be usefully answerable when we get to a dose and we are treating patients in the expansion cohort. It feels too early our patient population is highly variable I mean the medium number of cycles or therapies these patients have been on treating higher therapies is around five. So we’ve got a pretty advanced pool of patients that is common in our Phase I study. I think our Phase II/I will be at a dose two of the tablet formulation and three will be a much more strictly defined population of pure second line patients who have only had and then failed Tarceva or another TKI. So, I am not trying to dodge you of course Marko I just don’t feel I enough information to answer it.

Marko Kozul – Leerink Swann

I appreciate that. May be one on the competitive landscape, Pat could you talk a little bit about of the candidates that are specific for T790M patients such as AVD 92, 91 and Afatinib and then the other similarities or differences would be terrific and also do you have any sense as to why the AVD 92, 91 all the sites are actually less mainly in Asia, because of the environment?

Patrick Mahaffy

Well I mean I can speculate so first of all we don’t know a lot about the AV compound we don’t know more than you do because they have never presented it at any scientific forum. So, we don’t have any sense of the preclinical data or how it behaves or how it’s corrected. I have heard from an investor who have currently heard from AstraZeneca that it is similar to the gatekeeper compound so that implies to me it is a covalent inhibitors of EGFR which is intriguing.

As to why they’re in Asia, well first of all there is a large population of patients with these mutations in Asia as I discussed earlier so it’s not totally surprising. And secondly their relationships are probably pretty strong in Asia because ERISA is really used primarily as the dominant TKI in Asian territories. So, it doesn’t really surprise me but I can’t say anymore than that it’s all speculation.

As to the competitive landscape beyond AstraZeneca, I’ll just reiterate that Afatinib which now is has been front of the FDA for first line mutations of EGFR and showed about 11ish month progression-free survival versus 4.5 or so for chemotherapy. Thus in preclinical model show activity against T790M. However they have not been able to show that in patients because they have a greater in addition for wild-type EGFR as they do for T790M and while they can dose over that and might with great toxicity they can get to in effective dose for T790M in patients as a monotherapy and it just have not been able to.

There are data that have shown a response when you combine Erbitux with the Afatinib and T790M positive patients that response also includes patients who do not have the T790M mutation. So there is some mechanism at play there that perhaps we don’t fully understand. One thing we do understand is that is a wickedly toxic combination and would may never become – be available for patients and if it did would be limited to those who can tolerate the synergistic EGFR wild-type in addition that causes brutal diarrhea and rash. So, from my standpoint we remain in the lead in the development of an inhibitor of T790M with a compound with merits you can clearly evaluate based on the vast number of preclinical presentations we’ve made in the early signs that we’ve shown you from the Phase I study in humans.

Marko Kozul – Leerink Swann

Thank you for that. May be just one on rucaparib. Some of the other products are generating excitement moving into breast cancer, well rucaparib is very squarely focused on ovarian cancer why don’t you ask about any plans you might have in the future to go beyond ovarian and other tumor types and second to that the foundation medicine in companion diagnostic, would this only be applicable to ovarian cancer it might be use further indications as well? Thanks.

Patrick Mahaffy

What we’re doing with foundation is very specific to ovarian. The applicability of the two breast, I do not know but the genes we’re looking at HRD genes have been associated with ovarian and the biomarker validation study we’re doing will be clearly associated with ovarian responsive to rucaparib. So, there may be a great amount of overlap but right now you can think of that is been limited to ovarian cancer.

We have not determined where to go in addition to ovarian. We have purposely chosen thus far not to pursue a trial in breast. We are intrigued by certain other tumor types where HRD may play a role most notably prostate but it’s very early days for us and we will limit certainly in 2013 and probably for a while our development activities to ovarian this is a very robust program we have with the biomarker validation study as well as with the Phase III study so that will be our focus for now.

Marko Kozul – Leerink Swann

Pat thanks for taking the questions.

Operator

Thank you for standing by in the Q&A session ladies and gentlemen. I would now like to turn the call back over to Breanna for closing remarks.

Breanna Burkart

We thank you for your interest in Clovis today. This call can be accessed via a replay at our webcast at clovisoncology.com beginning in about one hour and will be available for 30 days. Again, we appreciate your interest and time. And thank you and have a good day.

Operator

Thank you for your participation in today’s conference. That concludes the presentation. You may now disconnect. Thank you and enjoy the rest of your day.

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