Syndax Pharmaceuticals, Inc. (SNDX) CEO Briggs Morrison on Q4 2019 Results - Earnings Call Transcript

Syndax Pharmaceuticals, Inc. (NASDAQ:SNDX) Q4 2019 Results Earnings Conference Call March 3, 2020 4:30 PM ET

Company Participants

Claudia Styslinger - Argot Partners

Briggs Morrison - Chief Executive Officer

Rick Shea - Chief Financial Officer

Michael Metzger - President and Chief Operating Officer

Michael Meyers - Chief Medical Officer

Conference Call Participants

Madhu Kumar - Baird

Bert Hazlett - BTIG

Ed White - H. C. Wainwright

David Lebowitz - Morgan Stanley

Joel Beatty - Citi

Jackson Harvey - Nomura Instient

Operator

Good day, everyone. And welcome to Syndax Fourth Quarter 2019 Earnings Conference Call. Today's call is being recorded. At this time, I would like to turn the call over to Claudia Styslinger of Argot Partners. Please begin.

Claudia Styslinger

Thank you, operator. Welcome, and thank you to those of you joining us on the line and the webcast this afternoon for a review of Syndax's fourth quarter and full year 2019 financial and operating results.

I’m Claudia Steinwender with Argot Partners. And with me this afternoon to discuss the results and provide an update on the company's progress are, Dr. Briggs Morrison, Chief Executive Officer and Rick Shea, Chief Financial Officer. Also joining us on the call today for the question-and-answer session are Michael Metzger, President and Chief Operating Officer and Dr. Michael Meyers, Chief Medical Officer.

This call is being accompanied by Syndax that has been posted on the company's Web site. So I would ask you to please turn to our forward-looking statements on Slide 2. Before we begin, I would like to remind you that any statements made during this call that are not historical are considered to be forward-looking within the meaning of the Private Securities Litigation Reform Act of 1995.

Actual results may differ materially from those indicated by these statements as a result of various important factors, including those discussed in the Risk Factors section in the company's most recent quarterly report on Form 10-Q, as well as other reports filed with the SEC. Any forward-looking statements represent our views as of today, March 3, 2020 only. A replay of this call will be available on the company's Web site, www.syndax.com, following this call.

With that, I am pleased to turn the call over to Dr. Briggs Morrison, Chief Executive Officer of Syndax.

Briggs Morrison

Thank you, Claudia and thank you to everyone joining us on today's call and the webcast. Slide 3 provides a high-level summary of our current corporate priorities as we strive to realize a future in which people with cancer live longer and better than ever before. We made great progress in 2019 on all three of our program. Since our last call in November of 2019, we have announced clinical data demonstrating proof of concept for the use of our anti-CSF-1R antibody, axatilamab, is the treatment of chronic graft versus host disease. We've announced two premier scientific publications that add to the compelling preclinical data supporting the potential of our menin inhibitor to be an effective therapy in acute leukemia, and we announced the addition of $55 million to our balance sheet.

I think 2020 will be a tremendously exciting and transformative year for our company. First, we know that the final overall survival readout of E2112 will occur this year, bringing us closer to a potential near term FDA filing, approval and launch in hormone receptor positive metastatic breast cancer. Second, the Phase I AUGMENT-101 trial of our highly selective rationally designed menin inhibitor, SNDX-5613, is underway and we expect meaningful data from that program this year. And finally, we will continue to collect data that will further clarify the potential of our anti-CSF-1R antibody, axatilamab, to treat chronic graft versus host disease. So let's review each of these opportunities in greater detail.

Slide 4 summarizes the design of the Phase III trial of entinostat in hormone receptor positive HER2 negative breast cancer. Trial randomized 608 patients to exemestane plus placebo versus exemestane plus entinostat, and the focus of this trial is now on the final overall survival analysis. Final analysis will be conducted once there are 410 events, which based on our modeling and recent discussions with ECOG, we believe will occur in the second quarter of this year.

A positive outcome would allow us to file for regulatory approval in the United States based upon the terms of our breakthrough therapy designation in hormone receptor positive metastatic breast cancer, and the special protocol assessment process with FDA. Our team is prepared to submit a regulatory filing, should the trial be positive, within about six months of receiving the data from ECOG, which would set us up to launch entinostat in 2021. Trial has 80% power to detect the hazard ratio of 0.75 and maximum hazard ratio that would yield a statistically significant positive trial is 0.82. Based upon the design assumptions, if E2112 achieve the hazard ratio of 0.82 that would indicate that patients receiving the combination had about five month improvement in median overall survival for about 22 months in the control group to 27 month in the entinostat arm.

Slide 5 emphasizes the potential for the entinostat-exemestane regimen to be the preferred agent after a first-line aromatase inhibitor, which is typically given either as a single agent or in combination with CDK4/6 inhibitor. Our current estimate is that between 30% and 50% of the patients in E2112 will have received CDK4/6 inhibitor prior to entering the trial. Thus, we should have a highly relevant dataset in the post CDK4/6 patient population.

In our opinion, the rapid adoption of CDK4/6 inhibitor such as Ibrance in the first-line setting underscores the desire of physician and patient to improve the outcomes associated with antiestrogen therapy. In the setting of a positive E2112 result, we would expect entinostat to achieve similar widespread use. This population of patients is substantial with estimated 34,000 patients in the U. S. each year who go on to receive hormone therapy after failing first-line therapy and who could therefore be eligible to receive entinostat regimen.

Importantly, we will be prepared for launch entinostat in the U. S. on our own. We are actively building out our internal commercial team to ensure we are well positioned for the potential launch of entinostat in 2021, while concurrently entering into discussions with potential rest of world commercial partners.

Slide 6 emphasizes the clinical potential of entinostat in hormone receptor positive breast cancer. In preparation for launching entinostat, we have conducted qualitative market research with community physicians and breast cancer experts. We tested a conservative profile, essentially the minimum benefit that could provide a positive OS result, and we consistently heard from both groups of physicians that there is a high need for novel agents in hormone receptor positive breast cancer, so that they find the potential ability of entinostat to resensitize patients to endocrine therapy to be a very attractive feature of the drug.

Now surprisingly the uniform we saw overall survival as the most important efficacy endpoint, and believe that an agent that could extend survival and lengthen the patient's time on hormone therapy with minimal impact to their quality of life made a very compelling profile. We remain confident in potential for E2112 to be a positive trial and are eager to bring this potentially new important medicine to patients.

Let me now turn to Slide 7 and SNDX-5613, our genetically targeted agent. Since our last call, two premiere publications have circulated related to menin inhibition; one, in Cancer Cell, detailing the preclinical results of one of our molecules in MLLr leukemias; and one in Science, detailing the preclinical results are one of our molecules in NPM1 leukemia. These premiere publications provide the scientific rationale and pre-clinical validation of our ongoing clinical trial, which is outlined on Slide 8.

The first-in-human trial in the accelerated understanding of menin inhibition or AUGMENT program is AUGMENT-101. The first-in-human clinical trial is a combined Phase 1 and Phase II trial. The Phase 1 portion is a dose escalation trial designed to identify the maximum tolerated dose, and a recommended Phase II dose for SNDX-5613. Patients with relapsed or refractory acute leukemia will be enrolled, and will take SNDX-5613 daily by mouth until they experience either progressive disease or unacceptable toxicity. The first 28 days of dosing will serve as the period in which safety is evaluated for determining dose escalation. As required by the FDA, patients do not need to have specific genetic abnormalities in order to enroll in the Phase I study.

The first cohorts follow an accelerated dose titration with only one patient required per cohort upon encountering a pre-specified level of toxicity, the trial will convert to a standard 3+3 design. We announced in the fourth quarter of last year that dosing has commenced, and the trial is progressing nicely. The PK analysis is a key component of the Phase 1 trial. Our preclinical data indicates that the menin-MLLr interaction needs to be continuously inhibited in order to achieve optimal efficacy.

We believe that safely achieving adequate target coverage in the Phase 1 trial could bode well for establishing efficacy in the Phase II trial. We have been carefully examining the drug exposure and patients to assess whether we are achieving adequate target coverage. Once the recommended dose is, Phase II dose is established, the Phase II trial will proceed to enroll three distinct expansion cohorts, each of which consists of a specific genetically defined relapse or refractory acute leukemia.

The three cohorts are adults with MLLr; acute lymphoid leukemia, ALL; adults with MLLr, acute myeloid leukemia, AML; and adults with NPM1 mutant AML. The Phase II portion will further characterize the safety of SNDX-5613 and will provide an initial estimate of the complete response rate as the primary measure of therapeutic benefit. We know that a lot of people, patients, physicians and investors, are eager to see initial data from the AUGMENT-101 trial. We expect to report initial clinical data from the trial in the fourth quarter of this year.

Given that AUGMENT-101 is an open-label trial, meaningful interim data, including PK, PD or efficacy maybe available earlier in the year. In addition, we are eager to advance this molecule into the pediatric population it's a key component of our overall strategy. We'll have more to say about the details of the pediatric timing and approach on our future call. We know that pediatric leukemias with MLLr rearrangements represent a significant unmet medical need, and we're eager to work with the pediatric oncology community to bring SNDX-5613 to their patient.

Based upon pre-clinical data and the underlying biology of the pathway, we are expecting evidence of single-agent activity. As a result, there could be a rapid and straightforward clinical development path for 5613, perhaps like the path taken for agents addressing patients with FLT3 or IDH mutation. As we continue to learn more about the potential of 5613 and acute leukemia, we see this molecule becoming an additional and important value driver for Syndax.

Let me now turn to Slide 9 and SNDX-6352, our potential best of class monoclonal antibody targeting the CSF-1 receptor. Let me first note that we now have a generic name for this molecule, axatilamab and going forward, we will refer to this molecule with this generic name and retire the SNDX-6352 designation. We are conducting a trial testing axatilamab as monotherapy in chronic graft versus host disease.

Chronic graft versus host disease is a frequent complication of hematopoietic stem cell transplantation where an donor-derived immune cell contribute to the initiation and development of fibrosis and the myriad manifestations of this disease. In preclinical model, blockade of the CSF-1, CSF-1R pathway with anti CSF-1R antibodies can result in the depletion of donor macrophages, thereby preventing and reducing chronic graft versus host disease. And we believe that chronic graft versus host disease represents an important clinical opportunity.

At the end of last year, we released initial data from our Phase I trial, which is diagrammed on Slide 10. The Phase 1 portion is a dose escalation trial designed to identify the maximum tolerated dose and a recommended Phase II dose of axatilamab for the treatment of chronic graft versus host disease. We have released data for the first five patients enrolled in the first three cohorts, and have now modified the trial to include a Phase II cohort at the 1 milligram per kilogram dose.

We will continue the Phase I trial to more formally define the recommended Phase II dose, and may open one or more additional Phase II dose cohorts as well. Slide 5 reprises the results seen in the first five patients as of mid-December, only four of which the patients were evaluable for response as of that cut out. Our investigators are quite excited to see clinical activity at all doses, and the initial results suggest good durability of out of that.

Slide 12 is a picture that brings on the impact this medication is having on the disease. As we discussed the specific results of experts in fibrotic disease, they have commented on the improvement in both inflammation, you can see the redness subsiding and the benefit in improving the ulcers as well. We are now considering exploring several additional inflammatory and fibrotic diseases for axatilamab, and we'll have more to say about that in a future call.

Finally, Slide 13 summarizes the transaction that led to the acquisition of the menin MLLr and the SNDX-5352 programs. We believe that we will be able to continue to expand our pipeline through the acquisition or in-licensing of quality differentiated assets. We believe that we have the necessary clinical development expertise to bring these compounds through valuable inflection point, and expect to remain among the preferred partners of such transactions.

I will now turn the call over to Rick to review our financial results.

Rick Shea

Thank you, Briggs. The results of operations for the fourth quarter 2019 and for the full year, and the comparison to the prior year quarter and year are included in our press release so I won't repeat them in these remarks. Additional financial details will be available in our Annual Report on Form 10-K, which we intend to file this week.

Turning to Slide 14, we ended 2019 with $59.8 million in cash and $31.6 million shares and free funded warrants outstanding, the net change in cash for the fourth quarter was a decrease of $12.5 million. The net loss for the quarter of $14 million was offset by non-cash stock compensation expense of $1.5 million.

Looking ahead, I’d like to provide financial guidance for each of the first two quarters of 2020. Our financial guidance for the second half of 2020 will be issued after we get the results of the E2112 study. We expect our operating expenses for the first two quarters of 2020 to increase over the quarterly operating expenses we reported for the second half of 2019. R&D expenses will increase primarily due to increased development activities for SNDX-5613 our menin inhibitor and for axatilamab, our anti-CSF-1R antibody. We do expect G&A expenses also to increase, primarily due to increased entinostat pre-commercial activities.

For each of the first and second quarters of 2020, we expect our R&D expenses to be $12 million to $14 million per quarter, and total operating expenses to be $17 million to $19 million per quarter. That includes approximately $1.5 million per quarter of non-cash stock compensation expense. Our cash at year end was about $60 million and in Q1 2020, we added $35 million to an equity financing and we drew $20 million of debt on a term loan, so our pro forma cash heading into 2020 is $115 million.

And given our cash operating expense guidance for the first half of 2020, we expect to end Q2 2020, the first half of 2020 with more than $80 million of cash, which gives us the financial flexibility to take advantage of key development milestones well into 2021. I'll now turn the call back over to Briggs.

Briggs Morrison

Thanks very much, Rick. And I hope you've appreciated from my prepared remarks, 2020 is a busy year for Syndax with several very important and exciting data readouts close at hand. We believe that our positive OS result in E2112 would be transformative for Syndax and create significant shareholder value. We anticipate a final readout in the second quarter of this year.

We also believe that SNDX-5613 our menin MLL-r inhibitor is well-poised for near term proof of concept data. We believe that safely achieving adequate target coverage in the Phase I trial could de-risk this program with single-agent activity in patients with either MLLr or NPM1 mutant leukemia, providing clinical proof of concept and enabling early regulatory clarity and planning for next steps.

And finally, we are very excited about the early results we are seeing with axatilamab in chronic graft versus host disease, and look forward to presenting updated data from this program at the end of this year. With our recent highly successful financing, we are comfortable that we have the financial resources to get us through these key upcoming milestones. Finally, we are optimistic that we will continue to identify and bring in novel molecules to deepen our portfolio. We have a proven track record of delivering on this pillar of our strategy, and I believe this is the core strength of our company.

As always, I would like to thank the wonderfully talented team here at Syndax, our collaborators and most importantly, the patients, trial sites and investigators involved with our clinical program. In addition, I'd like to thank our committed long-term investors who are helping us build this great company and to welcome the new investors who joined in that effort with our recent findings. With that, I’d like to open the call for questions.

Operator

Question-and-Answer Session

Thank you. [Operator Instruction] Our first question comes from Madhu Kumar with Baird. Your line is now open.

Q - Madhu Kumar

So thinking about the chronic graft versus host disease programs. Would you imagine the expansion cohort will still require ibrutinib-treated patients? Or do you imagine that it will be a kind of wider swath of the graft versus host population?

Briggs Morrison

Madhu, it will be a wider population of patients. As you recall we first started the trial, we were acquired maybe post-ibrutinib that inclusion criteria has been softened considerably. So now it is a wider population of patients.

Madhu Kumar

And then thinking about the menin MLL program, in terms of PK and PD data. Would you wait to get to dose-limiting toxicities right now kind of PK/PD data? Or would you want to, if you saw an activity that looked like we're getting good continual menin MLL inhibition and good kind of pharmacogenetics that you'd want to report that and ahead of really completing the dose escalation?

Briggs Morrison

Again, as I pointed out in my prepared remarks, Madhu, I think there's PK/PD and efficacy. If we had a sufficient number of patients that we feel like we've actually adequately characterized the PK and proportionality and the ability to cover the target and let's say, we had that in advance of a significant number of patients with efficacy data, we could potentially present that PK data.

Operator

Thank you. Our next question comes from Bert Hazlett with BTIG. Your line is now open.

Operator

Our next question comes from Bret Hazlett with BTIG.

Bret Hazlett

I’m intrigued by the commercial launch preparation discussions that are underway. Could you just remind us, assuming success in 2112, what the gating items would be for, first of all, the filing and then actually commercialization of it?

Briggs Morrison

So let me first take the filing piece and then I'll turn it over to Michael to talk about some of the commercial work we're doing. So as I said in my prepared remarks, we anticipate that within about six months of getting the data from ECOG, we would be in a position to submit the NDA. And then it would depend on FDA decision on whether the timing of how long that review would take, but our base assumption is we'd be in a position to launch the product in 2021. And then maybe I'll turn it over to Michael just to give a couple of comments and we're getting ready commercially to be prepared for that.

Michael Metzger

Bert, I think as Briggs mentioned in his prepared remarks, the pre commercialization work is a focus for us, has been for some time and we'll continue with that through getting data and then up to a potential launch. Obviously, putting together the commercial team and the leadership around the commercial launch in the U. S is important, so we'll be working hard on that.

Hiring the field forest in the U. S., we had talked about launching the drug and be prepared to launch the drug on our own in the U. S., so that will require of course a focused field forced to do that. And lastly finding a partner for ex-U. S. will become a priority for us as well so we can have a global launch of the product to do so optimally. But all those work streams are sort of in process, and will be augmented around the time of phase.

Bret Hazlett

Can you remind us of how advanced the breakthrough designation in the U. S., but the path to potential acceptance of the 2112 data by the EU or other regulatory authorities? And how advanced those discussions are for rest of the world?

Briggs Morrison

So I think from a regulatory point of view, having a trial that shows improved overall survival relative to a standard second or third line agent, we think is a registerable package in the EU. We have not had a lot -- very recent discussions with them from a regulatory point of view and our intent would be to do that once we have the results of the trial. As I said, I think we would -- we will be prepared to launch the drug ourselves in the U. S., but we are concurrently looking for a commercial partner who can help us with the launch outside the U. S.

Bret Hazlett

Just shifting to 5613 briefly. Do you expect the low doses to be able to constantly inhibit the menin MLLr interaction?

Briggs Morrison

So again, as you know you always trying to project PK exposures. Based upon what you saw pre-clinically based upon those projections, it is possible that even at the early dose escalations, we would have sufficient coverage. And it goes back to Madhu’s question of you know seeing enough of that PK data to feel comfortable that we can cover the target. But based upon modeling from preclinical work into what we think will be PK in human, it's possible that one of those early dose levels we should be able to cover the target pretty well.

Operator

Thank you. Our next question comes from Ed White with H. C. Wainwright. Your line is now open.

Ed White

So just a question on axatilamab, I was just wondering if you have -- the third patient in Cohort 3 was not dilated yet as of the day of the update. Will we have to wait to the end of the year to see that patient updated? And also can you tell us how many patients have been enrolled in Cohort 4 and in the Phase 2, and what we should be expecting to see when you do release the data later this year. Thank you.

Briggs Morrison

Short answer is yes, you will have to wait till the end of the year, but we don't think it's that useful for people for us to regularly sort of update the data. So I think in general what you should think about for the end of the year is the completion of the Phase I portion of the trial, studying various doses and dose schedules. And some number of patients on the extended 1 milligram per kilogram dose. I don't think we really guided yet how many. But I think by the end of the year, we should have a good number of patients on that expanded cohort, as well as the completion of the Phase I. We think the best way to update people on the profile -- the emerging profile is at an appropriate medical conference and so that's why we've guided towards the fourth quarter of this year presenting that updated data.

Operator

Thank you. And our next question comes from David Lebowitz with Morgan Stanley. Your line is now open.

David Lebowitz

When you look at the menin program, I guess what do you see as the step after Phase 2 expansion? Once you select dose in Phase 1, you move to the Phase 2 portion. What do you see as the theoretical step beyond that point?

Briggs Morrison

So we think one potential avenue is a single-arm registration approach. So if you look at some of the other agents that have targeted agents for acute leukemias, they've been able to register the drug based upon a single-arm trial, looking at complete response rates and durability of those responses. So that is an avenue that we think, depending on how active the drug is that that could be a potential. Obviously, the next step would be to think about how we can combine this agent with standard of care for patients with AML.

And so we're giving some thought to that, both in the MLR population combining it either with induction chemotherapy or as maintenance after transplant, there's a variety of different designs we thought about. And in the NPM1 space, remember that NPM1, there's about 15% of patients who have just an NPM1 mutation with no other co-mutation, but the majority do have other co-mutations, some of which there are agents for, like the FLT3 inhibitor. So you could think about combinations with a FLT3 inhibitor already or an IDH inhibitor, we’re again, integrating into standard chemotherapy for the other patients. So I think there's a number of avenues but the most, the one that we would we’re hopeful for is that we could actually get the drug registered on a single-arm trial, should their response rate be of sufficient magnitude to allow that.

David Lebowitz

And what would you, I guess need to learn from the dose escalation portion before you proceed with moving in the pediatric direction?

Briggs Morrison

Actually not that much, so we're working with the pediatric groups now. As I said, the MLLr/ALM in kids and AML in kids are area of high unmet need. So you know, I think if we can even get a little bit of PK data from the adults that maybe enough to start the pediatric program. But we'll say more about that in a future call.

Operator

Our next question comes from Joel Beatty with Citi. Your line is now open.

Joel Beatty

The first one is on the AUGMENT-101 trial. Can you give a rough sense of how many cohorts of data we might see if the data presentation ends up being in Q4?

Briggs Morrison

So I think, Joel, the reason we sort of guided to Q4 is we're hopeful that we could have finished the Phase 1 portion of the trial, and know what the MTD is and know what the recommended Phase 2 dose is. How many cohorts it takes to do that is not entirely clear. If you look at the literature in these dose escalation trials, it’s somewhere around four or five cohorts to get to your recommended Phase 2 dose. But I think part of the reason we tried to guide to the end of the years, we think the Phase 1, we would hope that the Phase 1 portion will be done and that we would have the recommended Phase 2 dose, if Phase 2 cohorts may have actually already opened by the end of the year, but that's to be determined.

Joel Beatty

And then one other question on the CSF-1R, actually on the graft-versus-post program, the CSF-1R. obviously, it looks really impressive responses, even though it's just small data set so far. Can you help give context of what gives you confidence that these responses you're seeing are due to the drug as opposed to other therapies that the patient maybe on?

Briggs Morrison

So the way that the trial is designed is the patients have to be stable on their current -- as you know, there are a number of different agents that people use, whether it's steroids, calcineurin inhibitors, ibrutinib, rux, et cetera. So whatever agent they're on, they have to be on that stable regimen for a period of time and so that we can actually evaluate what our drug do. Once they are treated with our drug if they have a response then the investigators are allowed to start tapering off the other drugs that they are on. But there's a requirement that there’ll be no change to their existing therapy when we put them on our test therapy.

Operator

Thank you [Operator Instructions]. Our next question comes from Christopher Marai with Nomura Instient. Your line is now open.

Jackson Harvey

Hello, this is Jackson Harvey on for Christopher Marai. My first question is on AUGMENT-101. Given that it's an unselected patient population. Can you give us some early insight into the distribution of new patient types that are currently enrolled, or what you expect to enroll? And then for the PD measurements, how should we expect PD to be reported in patients that do not have the relevant mutations? Thank you.

Briggs Morrison

So as I said, they're not required to have either MLLr or NPM1 to go into the Phase 1 portion. Having said that the investigators who are participating know how the drug works are clearly aware of all the preclinical data, and we've gotten certainly feedback from their bias towards putting on patients who have one of those two known genetic abnormalities. So we can't say for certain where that's going to end up. But I think we are optimistic that this patient population will be enriched for patients who have one of the two known genetic lesions. I can't tell exactly how enriched, but I think it will be enriched.

The question for pharmacodynamics is one that our team continues to work on. Your question with how you assess pharmacodynamics in patients who don't have the mutation, to be honest, we're still working hard on pharmacodynamics in patients who do have a mutation. So I think that's why I highlighted in my comments more about PK. I think we have a really good understanding of PK exposures we need for efficacy. There are some assessments that we can do of, having to do with understanding how the transcriptional activation of certain genes by the MLL/menin interaction. We can look at changes in menin. We can look at changes in binding of menin to the chromosome. But you are correct that it’s harder in patients without the mutation where we rely more on PK.

Jackson Harvey

And if I can sneak in one more question on axatilamab. I'm just curious about the -- if you're seeing a differential response based on the organ system involved, and whether these Phase 2 expansions could be registrational? Thank you.

Briggs Morrison

Yes, I think it's too early to say whether we're seeing different responses. I think that the initial data we showed was five patients, only four of which were valuable. So it's little hard to say that. So that's what I think the Phase 2 portion is for us to try to characterize that. So I think it's still a little early to say.

Operator

Thank you. And I'm showing no further questions in the queue at this time. I'd like to turn the call back to Briggs Morrison for any closing remarks.

Briggs Morrison

Thanks very much, operator. Thanks everybody for joining us on the call. I guess today is a voting day in part of the country. We just recommend you wash your hands after your vote, and we look forward to keeping in touch.

Operator

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