Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q1 2024 Earnings Call Transcript

Corvus Pharmaceuticals, Inc. (NASDAQ:CRVS) Q1 2024 Earnings Call Transcript May 6, 2024

Corvus Pharmaceuticals, Inc. isn’t one of the 30 most popular stocks among hedge funds at the end of the third quarter (see the details here).

Operator: Good afternoon ladies and gentlemen and welcome to the Corvus Pharmaceuticals’ Business Update and Reports First Quarter 2024 Financial Results Conference Call. At this time, all lines are in a listen-only mode. Following the presentation we will conduct a question-and-answer session. [Operator Instructions] This call is being recorded on Monday, May 06, 2024. I would now like to turn the conference over to Zack Kubow of Real Chemistry. Please go ahead.

Zack Kubow: Thank you, operator and good afternoon everyone. Thanks for joining us for the Corvus Pharmaceuticals’ first quarter 2024 business update and financial results conference call. On the call to discuss the results and business updates are Richard Miller, Chief Executive Officer; Leiv Lea, Chief Financial Officer; Jeff Arcara, Chief Business Officer; Jim Rosenbaum, Senior Vice President of Research and Ben Jones, Senior Vice President of Regulatory and Pharmaceutical Sciences. The executive team will open the call with some prepared remarks, followed by a question-and-answer period. I would like to remind everyone that comments made by management today and answers to questions will include forward-looking statements.

Forward-looking statements are based on estimates and assumptions as of today and are subject to risks and uncertainties that may cause actual results to differ materially from those expressed or implied by those statements, including the risks and uncertainties described in Corvus’ annual report on Form 10-K, and other filings the company makes with the SECTOR from time-to-time. The company undertakes no obligation to publicly update or revise any forward-looking statements except as required by law. With that, I’d like to turn the call over to Leiv Lea. Leiv?

Leiv Lea: Thank you, Zack. I will begin with a quick overview of our first quarter 2024 financials and then turn the call over to Richard for a business update. Research and development expenses in the first quarter of 2024 totaled $4.1 million, compared to $4.6 million for the same period in 2023. The net loss for the first quarter 2024 was $5.7 million, including non-cash income of $0.2 million related to Angel Pharmaceuticals, our partner in China. This compares to a net loss of $7.9 million for the same period in 2023, which included a $1.7 million non-cash loss related to Angel Pharmaceuticals. Total stock compensation expense for the first quarter of 2024 was $0.7 million, compared to $0.5 million for the same period in 2023.

As of March 31, 2024, Corvus had cash, cash equivalents and marketable securities totaling $22.1 million, as compared to $27.1 million at December 31, 2023. Today, we closed a $30.6 million financing that included a premier group of biotech investors as well as some members of the Corvus leadership team. Including the proceeds from this financing pro forma cash at March 31, 2024, was approximately $52.7 million, extending our cash Runway into Q4 of 2025. I will now turn the call over to Richard, who will discuss our clinical progress and elaborate on our strategy and plans.

See also Top 20 Copper Producing Countries in The World and 40 Perfumes Celebrities Actually Wear (but aren’t paid to).

Q&A Session

Richard Miller: Thank you, Leiv and good afternoon everyone. Thank you for joining us today for our business update call. Since our Q4 update in mid-March, we have continued to make progress against two key value drivers that we are focused on for 2024. First for our planned registrational Phase 3 trial of soquelitinib for patients with relapsed peripheral T cell lymphoma, we remain on track to begin enrollment in the third quarter, and our confidence in this trial continues to grow as two additional patients in our Phase 1b trial recently achieved objective responses at first follow up. Second, our placebo controlled Phase 1 trial of soquelitinib for patients with moderate-to-severe atopic dermatitis. We began patient enrollment in April, which keeps us on track to report early data from the trial before the end of the year.

In addition to these two priorities with soquelitinib, today we are reporting encouraging initial data from our Phase 1b/2 trial of Ciforadenant, our adenosine A2A receptor antagonist in frontline metastatic renal cell cancer, or RCC. Based on the significant deep response rate seen in the initial set of patients, the protocol pre-specified statistical criteria for expanding the study has been met and the Kidney Cancer Research Consortium, or KCRC, is enrolling additional patients. Combined with our ongoing business development efforts aimed at further unlocking the potential of ITK inhibition in a broad range of oncology and autoimmune indications, we believe Corvus is positioned to continue building value and advancing our unique pipeline to help improve clinical outcomes for patients.

Now I will provide more detail on our progress, starting with soquelitinib for PTCL. While we are no longer enrolling new patients in our Phase 1 trial, the data continues to evolve as patients on therapy complete their scheduled follow up assessments. In the most recent data cutoff from May 3, 2024, we had two additional patients that achieved an objective response at their first follow up visit. The first was a complete response confirmed by PET CT scan, and the second was a partial response with over 80% tumor volume reduction. These patients both had multiple sites of disease and had failed two prior therapies. Both of these patients are continuing on therapy. With these additional valuable patients, the objective response rate, or ORR for the Phase 3 eligible patients is now nine out of 23 or 39%, including five complete responses and four partial responses.

Although not studied head to head, the complete response rate for soquelitinib at 22% is approximately double that seen with belinostat or pralatrexate, the standard chemotherapies for PTCL that we will be comparing to in our Phase 3 trials. Similarly, the ORR disease control rate, progression free survival, and overall survival for this group compares favorably to the results seen with belinostat or pralatrexate. The median PFS for our patients, which is the primary endpoint for the Phase 3 trial, is 6.2 months. This is substantially better than reported results for the standard agents, which is 1.6 and 3.5 months for belinostat and pralatrexate, respectively. The durability of our responses is impressive with some of the earlier enrolled patients maintaining their responses for more than 24 months.

We plan to begin patient enrollment in our soquelitinib registrational Phase 3 clinical trial in relapsed PTCL in the third quarter of 2024. We are working with or are in advanced discussions with a number of leading centers in the United States and Canada. We anticipate about 40 centers will participate in the trial. The vast majority will be in the United States. Now for an update on soquelitinib for atopic dermatitis, the first immune disease indication we are evaluating. In April, we initiated patient enrollment in the first patient cohort of the trial. There is high interest in our trial from physicians due to several attractive features of soquelitinib. First, this is a first in class drug with a novel mechanism of action. Soquelitinib acts upstream by blocking Th2 and Th17 cells and thereby results in inhibition of many different cytokines involved in disease.

Second, it is an oral therapy and in our cancer studies has been shown to have very good safety profile and third, it may have broad utility across many different autoimmune and inflammatory diseases and this trial may prove provide proof of concept for the treatment of other immune diseases. The trial is designed to enroll 64 patients with moderate to severe atopic dermatitis that have progressed on at least one prior therapy. The study is randomized, placebo controlled and blinded to patients and treating physicians. There will be four sequentially enrolled cohorts of 16 patients, with patients in each cohort being randomized three to one to different dosing regimens of soquelitinib or placebo given for 28 days. The primary endpoint is safety and tolerability and efficacy is measured using investigator global assessments and the clinically validated measurement of improvement in eczema area and severity index score, also known as EASI.

It should be noted that while the trial is double blind, the company is not blinded. We plan to evaluate the data in an ongoing manner as successive cohorts complete enrollment. We also will be measuring the levels of various serum cytokines at baseline and on treatment. These measurements may provide useful biomarkers. Based on current enrollment trends, anticipated site activations, and follow up timelines, we believe data from the initial cohorts will be available before the end of 2024, with study completion in early 2025. Outside of our PTCL and atopic dermatitis trials, we are still planning a soquelitinib solid tumor trial as a single agent and in combination with nivolumab in relapsed RCC, and we remain active with our corporate partnering discussions.

Our business development strategy is to find partners with development and commercialization expertise in immune diseases as well as seek regional partnerships in oncology that would be complementary to our focus and expertise in cancer. I’m excited to update you on the progress with ciforadenant, our adenosine A2A receptor antagonist. We have been one of the leaders in the development of adenosine A2A receptor antagonism for the treatment of cancer. Over the past few years, published preclinical and clinical studies have demonstrated the antitumor activity of ciforadenant as a monotherapy and when given in combination with checkpoint inhibitors. In particular, in our preclinical studies published in 2018, we found that anti-CTLA-4 antibody combination with ciforadenant produces striking antitumor efficacy in several animal models.

Further research has revealed the probable mechanism for this synergy, which involves modulation of the tumor microenvironment, specifically the blocking of myeloid derived suppressor cells. In other words, we believe that anti-CTLA-4 antibodies are a much better combination partner for A2A antagonist than anti-PD-1s. These findings led to our collaboration with the Kidney Cancer Research Consortium. This group of institutions brings the leading physicians and researchers in kidney cancer whose goal it is to discover improved therapies for patients with renal cancer. Our Phase 1b/2 clinical trial, which is led by Dr. Kathy Beckermann from Vanderbilt University Medical Center, is evaluating ciforadenant as a potential first line therapy for metastatic renal cell cancer in combination with ipilimumab and nivolumab.

The study is now open at MD Anderson, Vanderbilt, Duke and the University of Pennsylvania. The clinical trial is currently in the Phase 2 portion and overall is designed to enroll up to 60 patients. There are currently over 27 patients enrolled. The trial employs a stringent efficacy endpoint, deep response rate. Deep response rate is the CR rate plus the PR rate only counting PRs that achieve greater than 50% tumor volume reduction. Note the usual criteria for PRs is 30% tumor reduction. Data from the KCRC has shown that deep response rate correlates with long-term progression free survival and overall survival and in their previous studies is 32% with ipilimumab and nivolumab. In an interim analysis, our protocol defined pre-specified statistical threshold for efficacy is the demonstration of at least a 50% increase above the 32% deep response rate seen with previous ipi-nivo combination trials in renal cell cancer conducted by the Kidney Cancer Research Consortium.

This means we need to exceed a deep response rate of 48%. As of May 2, 2024, the interim analysis that was conducted indicates that we have met the statistical threshold for efficacy, so the trial continues to enroll patients. We are excited about these results given the positive clinical implications for patients. In addition, they are consistent with our laboratory and preclinical findings and we believe may represent a novel immunotherapy approach. Summarizing the outlook for the remainder of 2024 with our recent financing, our current cash gives us runway into late 2025, allowing us to achieve several near-term milestones, including starting our registrational Phase 3 clinical trial of soquelitinib and PTCL in the third quarter generating interim results from our soquelitinib Phase 1 atopic dermatitis trial before year end, followed by final data in early 2025, reporting additional data from the ciforadenant Phase 1b/2 clinical trial later this year and initiating a Phase 2 clinical trial with soquelitinib in solid tumors in the fourth quarter, with initial data anticipated in the second half of 2025.

We look forward to providing updates on our programs in the coming quarters. I will now turn the call over to the operator for a questions-and-answer period. Operator?

Q – Unidentified Analyst:

ralatrexate:

Richard Miller:

ralatrexate:

Unidentified Analyst: Okay, that’s helpful. And with the new responses, how much this is going to increase your sort of preliminary PFS and OS. I know you reported previously 6.2 months in PFS, 28 months in OS. So is it going to increase significantly?

Richard Miller: So the current ORR now, overall response rate is 39%. Just to remind you that. And by the way, in lymphoma we use the Lugano criteria, which is 50% for PR. And I should add that the PR that I just mentioned has about 87% reduction of tumor. One tumor was totally gone. I suspect he could be on his way to a CR very soon. The PFS, we expect the PFS to improve as these last few patients moved through the median.

Unidentified Analyst: Okay, understood. And regarding the data from the Phase 3 trial, when do you think we will have a first glimpse on the readout? I know this is randomized trial, blinded trial, but when do you think we’ll have the first look at it?

Richard Miller:

ralatrexate: There is an interim. There is a point that we conduct an interim analysis, which is when half of the events occur, the events being the PFS events, but that occurs so late in the study that we would probably wait for the end of the study to make a final determination. Now, having said that, we do have an outside data monitoring committee, and I guess if the results were so persuasive or compelling, you would possibly have an ethical reason to discontinue the study.

Unidentified Analyst: Okay, makes sense. And the last one, if I may.

Richard Miller: Let me just say, so I think you’ll have data from this trial in 24 months.

Unidentified Analyst: Okay. So, like 2026. Okay. So I’m trying to understand, these drugs seems to be working, and, but there is 40% who don’t respond essentially, 39% based on DCR. So is there any way to come up with some other potential biomarkers to screen patients who would be more likely to respond or somehow choose patients? Yeah.

Richard Miller: Well, we are working on that. We’re looking all the time for mutations and baseline immune status, et cetera. But you’ll remember that several months ago, we implemented, and on conference calls, I talked about the immune status at baseline, the absolute lymphocyte count, then using a number of prior therapies. I’m happy to report that since we’ve implemented those eligibility criteria, we have seen, I would say, not only more responses, but I would say the kinetics of the responses also have been faster. So I think that those moves that we made several months ago or maybe a year ago now, really have made a difference and those moves were based on our better understanding of the mechanism of action. So I expect that in a Phase 3 trial, we already know this, Phase 3 trial, we’re going to get better patients.

They’re going to have better immune status to start with. Phase 1 trials usually get sicker patients just by nature of the fact that they’ve exhausted any other therapies that are available. So I would expect that our results could get better. And we are continuing to look at different markers. But so far, I don’t know, other than the baseline immune status, I don’t know if we have a specific molecular marker.

Unidentified Analyst: Understood. Thank you. Thank you so much, and congratulations with the progress.

Operator: Your next question comes from the line of Jeff Jones from Oppenheimer. Your line is now open.

Jeff Jones: Thank you, operator and congrats on the news, guys. That’s great and congrats on the financing as well. One question on soquelitinib, there are a number of responders in the Phase 1 that were cutaneous T cell lymphoma patients. Can you remind me if cutaneous T cell lymphoma patients are going to be included in the Phase 3 and what impact that might have on the PFS?

Richard Miller: There are a couple of patients who are included in 23 that had cutaneous T cell lymphoma. Both of those patients had transformed cutaneous T cell lymphoma. That portends a very bad prognosis when you get what’s called large cell transformation. That’s not your typical CTCL is my point. CTCL patients are not going to be enrolled in our Phase 3 trial because it really is a different disease. It’s treated with different drugs and it can be a chronic disease early. In people who have just skin disease can have disease for many years. That’s not the patients we’re talking about in this trial. But Jeff, I think you raised a good point, which I forgot to mention. We see responses in cutaneous lymphomas, anaplastic lymphoma, peripheral T cell lymphomas, something called angioimmunoblastic, or now known as T follicular helper cell lymphoma.

These are very histologies, very different histologies under the microscope. They have different patterns of spread in the body and they have different genetic mutations. The fact that we see activity in this very diverse group of lymphomas, of T cell lymphomas, is really, again, consistent with our mechanism, which is to induce a host antitumor response and one of the motivating factors that we think we can extend this into solid tumors. That was the reason we started doing preclinical work with solid tumors. That data has been presented and confirmed by others, and this is the reason why we’re also excited about looking at this drug in solid cancers. Did I answer your question, Jeff?

Jeff Jones: Yes, you did. That was really helpful. I appreciate it. I’ve always wondered a little about those cutaneous responses, which are obviously, generally good responses.

Richard Miller: Jeff, hold on. The responses that we see in these cutaneous patients, it’s not fair to call them that. They have cutaneous disease. They have circulating tumor cells. They have lymphadenopathy. Sometimes they have visceral disease. The responses that we’ve seen in the responding patients is not just cutaneous, it’s throughout the body.

Jeff Jones: Okay, fair. Sorry, that was poor language choice on my part. In the atopic dermatitis study you mentioned, I believe patients had been on two prior lines of therapy. Are there going to be, are you including patients who have previously had dupilumab and failed, or are you not being that specific?

Richard Miller: We’re not being that specific, and they have to have failed at least one prior therapy, one prior, either systemic or topical therapy. Some of the patients, we assume that some of the patients that come in our trial will have failed dupi, but it’s not required. They will have also failed others. I think we got a recent patient who failed the JAK inhibitor, for example. So really, we have to put this, this trial was really intended to show, of course, that the drug is well tolerated in a patient population like this, and we’re looking for activity. You know, obviously, subsequently, we’ll be trying to figure out how does it stack up against some of these other agents. But right now we’re confirming mechanisms, safety, and yes, we are measuring efficacy against the placebo.

Jeff Jones: Got it. No, I appreciate the clarity. And then last question on cifo, I know that you had said 27 patients were enrolled, but you didn’t specify how many were included in that interim efficacy analysis?

Richard Miller: I think there are 18 patients in that. You’re right, because some of them haven’t come back for their first visit yet. So this protocol, by the way, was prepared by the KCRC, and they have, there are sort of blocks of, I forget how many patients each, eight or nine patients each. And there’s a criteria, efficacy threshold that you have to pass to continue. The results so far are really pretty good. And in fact, we’re organizing a meeting at ASCO to think about discussing things like adding a control arm or where do we go from here?

sunitinib:

Jeff Jones: Got it. Just one clarification. You had mentioned in your remarks, I think 27 enrolled. And then going over this threshold of deep responses to expand that trial, did you mean just up to the 60 expand further up to the 60 planned or is there a potential expansion beyond those 60 patients?

Richard Miller: No, there’s no expansion beyond the 60. When I mentioned expanding, I think at some point it would be nice to add a control arm, maybe ipi-nivo alone, ipi-nivo placebo. But that raises the whole question of, do you want to do a randomized Phase 2, or do you want to go right to a Phase 3?

Jeff Jones: Yes, understood. All right, thank you very much, guys. That’s it from me.

Richard Miller: Thanks.

Operator: Your next question comes from the line of Graig Suvannavejh [Mizuho Securities]. Your line is now open.

Graig Suvannavejh: Good afternoon. Thanks for taking my questions. I have two in particular. One, maybe I’ll start with your second asset. I know you mentioned that you were able to pass, like the bar for success, for moving forward. I don’t know if you — I might have missed this, if you quantified how much better beyond that bar, that you had seen from, I guess, your 18 valuable patients, so I’m wondering if you can perhaps shed more color on that. And then secondly, just on your current cash, and congrats on the recent raise, but if you could clarify whether that cash gets you through the Phase 3 for soquelitinib? Thanks.

Richard Miller: Okay, Graig, let me take the first one first. So the statistical threshold was a 50% increase. So the statisticians, 50% increase above the 32%, which is obviously 48%. If you meet that, you have a difference with a P value of 0.1 on only 18 patients. That’s a pretty stiff hurdle. 50% increase is a big hurdle and so we exceeded that. I can’t give you the exact number because the KCRC doesn’t really want to disclose that yet, and I understand why because these numbers jump around in a small study, but we’re better than 48% deep response rate. Okay? And again, I want to emphasize 50% improvement in deep response rate, that’s a stiff hurdle. And the reason we wanted that is we didn’t want to waste time on something that didn’t have a significant probability of working. So we made it, nor did they. So we’ve deliberately made these hurdles pretty strict. Now, your second question. I’ll let Leiv answer.

Leiv Lea: So, Graig, associated with our financing, we also sold warrants. Now, these warrants, first of all, have an exercise price of $3.50, but more importantly, maybe they expire June 30 of 2025, so a little over a year from now. So if all those warrants were exercised, we’d raise about $60 million. So the $30 million plus the $60 million, should those warrants be exercised, would get us through the Phase 3 trial.

Graig Suvannavejh: Okay. Thank you for that clarification. Thanks again.

Operator: Your next question comes from the line of Roger Song from Jefferies. Your line is now open.

Liang Cheng: Good afternoon. This is Liang Cheng on for Roger Song. So, thank you for taking our questions. I guess a few questions from us. First one is the soquelitinib, the modified inclusion criteria, so about the absolute lymphocyte count about 900. So if I remember it correctly, there a big overlap between this 900 plus ALC count, between the patient population. So could you clarify what, in general, this population looks like?

Richard Miller: So the 900 absolute lymphocyte count we determined based on the early part of the trial where we were taking anybody who failed any number of prior therapies. And we recognized that those patients above 900 did better, much better. And then we recognized that those were the patients who had no more than three prior therapies, less than or equal to three prior therapies. And so that’s the criteria that we’re using because they’re less immunocompromised. Those are what’s been used on the patients that have been reported in today’s press release. It’s the number of prior therapies greater than or equal to one, less than or equal to three. I don’t recall, I’m sorry. Go ahead.

Liang Cheng: Do we know, in general, how many patients meet this criteria?

Richard Miller: Oh, in our trial, the percentage of patients that will meet this criteria are very high. Again, in a Phase 3 trial, we’re already hearing from doctors. We’re going to get patients right after they failed their first line therapy, maybe a second line therapy. I would expect the number of eligible patients to be nearly 100%.

Liang Cheng: Got it. Thank you. So our second question is about AD studies. So it mentioned there we could expect some early data read out in by year end. So how, just in general, how much data should we expect from there?

Richard Miller: I think you can expect data from the first couple of cohorts. And as you recall were, our first dose is 100 mg b.i.d., which is a pretty good dose. It’s a dose that we know occupies the target, maybe 50% or so, give or take. It’s not the best dose, but it’s a pretty good dose. The second cohort gets 200 mg, and then we have 200 b.i.d. So I think that we very well may see some signs of efficacy in the first cohort. I would expect in the second cohort we would see it. Obviously, I think it would be better in subsequent cohorts than the first cohort. But we’re also looking at these biomarkers, the serum cytokines that we know we affect and how they’ll change. So I’m hoping that sometime by the end of the summer, we’ll start to get a feel for the clinical activity of the drug and also its effect on circulating cytokines.

Liang Cheng: Got it. So, since you talked about dosing regimens, just in general, how should we think about this circulating dosing regimens in AD, considering if there’s a different indication compared to the dosing in T cell lymphoma?

Richard Miller: Okay, so we know, and we’ve tested this not only in T cell lymphoma patients, but in other normal people in vitro. We know what it takes to saturate the T cell ITK in the T cells. So, as you recall, it’s a covalent drug, similar to the way ibrutinib work, but except this is to a different target, so that once the drug binds to the target, it doesn’t come off. So we know what it takes. We have a really good pharmacodynamic marker to know that we’re blocking the T cells, or at least occupying the T cells. Now, we don’t know for sure that the same pharmacodynamics will apply in AD as in lymphoma. I mean, the occupancy will be the same, but what it takes to affect your immune response, that we don’t know. And that’s why we’re looking at different doses in this study.

The reason to look at different doses is what does it take to affect the immunology in these patients? And also, of course, looking for or as low as possible, the lower the dose, one would think, the safer it would be. So that’s why this is a Phase 1 study. But, I mean, this is basic chemistry. Soquelitinib reacts with the ATP binding pocket of ITK, and that’s the fact. That’s what happens. And once that’s occupied, that enzyme isn’t going to work, unless until a new one is made. So of course, as you know, the rationale is that atopic dermatitis patients have an intense Th2 helper T cell component in their disease. And we think if the drug gets there and it binds covalently to ITK, we know that we block Th2 cells. We know we block Th2 cytokines.

We think that will have an impact on the disease. But the purpose of the trial is to show that.

Liang Cheng: Sure. Maybe I can squeeze another question here. So, regarding the ITK inhibitors, I know you have a couple more coming up in the pipeline. So, what are some key differences between this one, the soquelitinib, and the other candidates?

Richard Miller: So, first of all, we have over a dozen other ITK inhibitors that we’ve been evaluating. Some are completely different chemical structures. Some are covalent, some are non-covalent. But the interesting biological feature is some seem to affect some T cell subsets more than others. And we find that to be quite interesting, quite novel, and provides for I think, some very strong intellectual property.

Liang Cheng: Got it. Thank you. That’s all from us. Thanks again.

Operator: Your next question comes from the line of Li Watsek from Cantor Fitzgerald. Your line is now open.

Rosemary Li: Hi, this is Rosemary on for Li. Thank you so much for taking our questions and congrats. So, just two quick ones from us. For atopic dermatitis, do you have a benchmark in terms of improvement in eczema area and severity index?

Richard Miller: No, we don’t have a benchmark.

Rosemary Li: Okay. Okay, thank you. And then for a second question for your next and ITK inhibitors, do you plan to generate any human data for BD discussions or just, like the clinical?

Richard Miller: I’m sorry. I can’t understand the question. Can you repeat it?

Rosemary Li: Oh, sorry. So, for your next gen ITK inhibitors, do you plan on generating any human data before going for BD discussions?

Richard Miller: Well, we’re doing both in parallel. We’re now selecting some of these backup or second generation ITK inhibitors. They’re in their IND enabling studies. We’re scaling them up. We’re moving down parallel tracks.

Rosemary Li: Okay, thank you.

Richard Miller: Okay, operator, I think that exhausts our questions here for now. I want to thank. Hello any other questions that I missed?

Operator: There are no further questions at this time. I will hand the call over to Richard Miller, CEO of Corvus. Please continue.

Richard Miller: Thank you, Operator. I want to thank everyone for participating in today’s conference call. We look forward to updating you on subsequent calls and appreciate your interest. Take care.

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