Pieris Pharmaceuticals, Inc. (NASDAQ:PIRS) Q4 2018 Results Earnings Conference Call March 12, 2019 8:00 AM ET
Allan Reine - Senior VP, CFO & Treasurer
Stephen Yoder - CEO, President
Louis Matis - Senior VP & Chief Development Officer
Conference Call Participants
Umer Raffat - Evercore
Pam Barendt - Cowen and Company
Matt Phipps - William Blair
Joe Pantginis - H.C. Wainwright
Greetings, and welcome to the Pieris Pharmaceuticals 2018 Fourth Quarter and Corporate Update Conference Call. At this time all participants are in a listen-only mode. A brief question-and-answer session will follow the formal presentation. [Operator Instructions] As a reminder, this conference is being recorded.
It is now my pleasure to introduce your host, Allan Reine, Chief Financial Officer for Pieris Pharmaceuticals. Thank you. Mr. Reine, you may begin.
Good morning, everyone. And thank you for joining us for our year-end 2018 conference call and corporate update. On the call today, we have Steve Yoder, our President and CEO; and Lou Matis, SVP and Chief Development Officer, who will be available for Q&A. You can access the press release released this morning on the Investor Relations page of our website at www.pieris.com.
Before we begin, I'd like to caution that comments made during this call may contain forward-looking statements involving risks and uncertainties regarding the operations and future results of operations of Pieris, including statements related to the timing and progress of our clinical trials and preclinical programs, our partnerships and our financial position. And actual results or events may differ materially from those expressed or implied by such forward-looking statements.
Factors that might cause such differences are described in our filings with the SEC, including our annual, quarterly and current reports. The information being presented is only accurate as of today. And Pieris undertakes no obligation to update any statement to reflect future events or circumstances. But today, we are providing the company's year-end cash position and an update regarding recent and anticipated future corporate developments. Our 2018 full year audited financials will be released with our annual report on Form 10-K, which we anticipate filing by Monday, March 18.
As part of our year-end close process, we are addressing a unique matter associated with a recent U.S. tax reforms impacting licensing income derived from our wholly owned German subsidiary. And we have taken additional time to analyze this matter with our tax advisers and auditors to ensure optimal tax treatment for the Pieris group. At this juncture, we would regard these efforts as extra blocking and tackling and see nothing that would prevent a timely filing.
We can, importantly, provide an update regarding our year-end cash and investment position, which was $128.1 million as of December 31, 2018, compared to a cash and investments balance of $82.6 million as of December 31, 2017. While we will not be able to answer any specific questions related to our financials today, they will be included in our annual report on Form 10-K.
With that, I will turn the call over to Steve for our corporate update.
Thank you, Allan. And thank you to everyone for joining us today for this 2018 year-end earnings call. I will begin by giving a brief overview of our company before providing highlights for 2018 and our plans for the future.
At Pieris, we are harnessing the power of our Anticalin platform to develop next-generation protein therapeutics. Anticalin proteins are engineered derivatives of human lipocalins and a defining novel drug class proprietary to Pieris.
Lipocalins, which are naturally abundant in the body and serve to bind and transport various molecules, have distinct advantages that we believe make them suitable for therapeutic applications. They are small and monomeric, two characteristics that render them well suited for a variety of treatment options, including inhaled delivery or a topical approach to treating respiratory disorders.
2018 was an important year for Pieris as we focused on execution across our clinical and preclinical pipeline, setting the stage for many important catalysts this year. Last year, we completed and reported initial results from the single ascending Phase I trial of our lead respiratory program, PRS-060, for moderate-to-severe asthma. And at the beginning of the third quarter of 2018, we initiated a multiple ascending dose trial for that program with the objective of interrogating PK/PD for PRS-060 in its trial beyond assessing safety and tolerability of this drug candidate.
Beyond our respiratory franchise, we continue to enroll patients both in our Phase I dose escalation trial for PRS-343, which is our lead immuno-oncology drug candidate for HER2-positive tumors, and also our Phase I trial of PRS-343 in combination with atezolizumab, which is an approved PD-L1 inhibitor. Finally, we completed dosing of all patients in our Phase IIa trial of PRS-080 for anemia in 2018.
I would now like to review our pipeline in more detail. Our lead respiratory asset, PRS-060, is an inhalable IL-4 receptor alpha antagonist in development for the treatment of moderate-to-severe asthma. PRS-060, which targets the same pathway as FDA-approved, systemically administered dupilumab, is designed for local administration into the lungs through inhalation.
We are developing PRS-060 in collaboration with AstraZeneca as part of a five program respiratory alliance in which Pieris retained co-development and co-commercialization options for PRS-060 and two other programs.
As our lead program, PRS-060 serves as a proof-of-concept for the inhalable administration potential of our platform in addition to the promise of being a multibillion commercial opportunity.
Last year, we completed the single ascending dose Phase I study for PRS-060 and announced that the drug candidate was safe and well tolerated in 48 healthy volunteers across a broad range of nebulized doses.
PRS-060 is the first Anticalin protein to be administered to human subjects via inhalation and we believe represents the high potential of the Anticalin drug class to drive the development of a novel respiratory franchise.
For PRS-060, we continue to enroll subjects with mild, controlled asthma with prescreened elevated levels of fractional exhaled nitric oxide or FeNO in a placebo-controlled multiple ascending dose Phase Ib study with the objective of ascertaining a meaningful PK/PD profile for the drug candidate.
More specifically, we are evaluating the safety, tolerability and PK profile of this drug candidate along with its capacity to reduce FeNO in subjects dosed with PRS-060 versus placebo.
Elevated FeNO is a well-established marker of lung airway inflammation. And the ability of PRS-060 to reduce FeNO could reflect effective IL-4 receptor alpha target engagement locally in the lung, demonstrating PRS-060's therapeutic potential and better informing a Phase IIa dosage regimen.
We expect to report the full dataset from these Phase I studies at upcoming medical meetings alongside our partner, AstraZeneca. Assuming successful completion of the ongoing Phase Ib study, AstraZeneca will sponsor the Phase IIa study, which will focus on moderate-to-severe asthmatics. Once the Phase IIa study is complete, we may exercise our options to co-develop this drug candidate and separately to co-commercialize PRS-060 in the United States.
In addition, Pieris initiated an additional discovery stage program in its alliance with AstraZeneca in the fourth quarter, bringing the total number of active programs in the alliance to three. AstraZeneca may initiate up to two additional programs within this alliance. And beyond this, we continue to advance the two proprietary discovery stage respiratory programs initiated last year and intend to initiate additional proprietary respiratory programs throughout 2019.
I would now like to turn our attention to the immuno-oncology pipeline. Our lead oncology asset, PRS-343, is a fully proprietary 4-1BB/HER2 bispecific designed to preferentially activate tumor-specific T-cells in the tumor microenvironment. We continue to enroll patients in our 343 Phase I dose escalation trial for HER2-positive solid tumors with the objective of ascertaining the appropriate exposure levels of the drug candidate as measured by the desired PD response.
We intend to report comprehensive data from the PRS-343 Phase I monotherapy dose escalation study later this year. We also continue to enroll patients in our Phase I dose escalation trial of PRS-343 in combination with atezolizumab, an approved PD-L1 inhibitor, and we also intend to report data from that study later this year.
Additionally, we continue to make progress across our partnered immuno-oncology programs. We recently exercised our opt-in right to co-develop and retain U.S. rights for PRS-344, a PD-L1/4-1BB antibody Anticalin bispecific molecule, which is the lead program in our five program immuno-oncology collaboration with Servier.
We recently achieved 2 preclinical milestones for the drug candidate's development, triggering two milestone payments totaling €2 million. Along with Servier, we plan to jointly initiate a first-in-human clinical study of the drug candidate later this year.
We also continue to make meaningful strides in our other anchor immuno-oncology alliance, a three program collaboration with Seattle Genetics, which we signed in February of 2018.
To date, we have generated and characterized the first tumor-targeting bispecific for further evaluation and development by Seattle Genetics. We're pleased with the continued advancement of our partnered programs and look forward to reporting progress on those programs as they mature.
And now to conclude. I would like to give a brief update on PRS-080, which is a potent antagonist of hepcidin, the master negative regulator of iron metabolism. While a non-core asset, PRS-080 demonstrates the excellent drug-like properties of the Anticalin drug class.
And in the fourth quarter of 2018, we dosed the final patients in a Phase IIa study in dialysis-dependent patients with functional iron-deficient anemia. This study evaluated five weekly doses of PRS-080 versus placebo at two different dose levels, 4 milligrams per kilogram and 8 milligrams per kilogram.
We reported preliminary data from the study on our previous earnings call and now plan to report the full data from that trial in the first half of 2019. We also plan to share the full data set with ASKA Pharmaceutical, at which point ASKA will decide whether to exercise its right to develop and commercialize PRS-080 in Japan and other Asian territories.
So in summary, 2018 was a year defined by clinically focused execution and the advancement of several preclinical assets. We concluded two clinical studies, we initiated two clinical studies and we significantly broadened our respiratory franchise.
As for our year-end financials, we look forward to making them available to you in our Form 10-K expected to be filed by Monday, March 18, and would like to emphasize that our year-end cash balance demonstrates our prudent cash management and is a cash position that allows us to reach significant clinical milestones.
Thank you for joining us on the call today. We would now like to open the call for your questions.
Thank you. [Operator Instructions] Our first question comes from the line of Umer Raffat with Evercore. Please proceed with your question.
Hi. Thanks so much for taking my questions. I had a couple, if I may. First, perhaps one for Steve and Allan, if you could speak to the FeNO changes we should expect in a controlled environment that these patients will be kept in. I don't know if it's four seasons in Australia, but that was the first question.
The second one was if you could contextualize for us the bar for success on FeNO, again obviously, given that we would probably expect placebo patients to decline as well in the controlled environment.
And I ask that specifically in the context of is there a certain placebo-adjusted percentage number that you would have in mind and/or are you thinking up more of an absolute FeNO reduction parts per billion? That would be really helpful. Thank you.
So Umer, thanks for the questions. Yes, those are great questions and I'll frame how we're looking at the current - the progression of PRS-060. And as you know, Allan has done a lot of work in this space looking at all of the relevant parameters for third-party molecules, particularly biologics. So I'm going to let him answer all of those questions you've asked.
Yeah, Umer, I think if you look at the recent data that assesses FeNO reductions in controlled asthmatics, it can really be gleamed from a UCB, Vectura study of their IL-13 fab [ph] fragment, which was presented at AGS in May in 2017, where they did demonstrate a statistically significant reduction versus placebo at the high dose level tested, what they did at 20-milligram via dry powder inhaler and also post hoc benefiting the 10-milligram dose group.
What they show there is a placebo reduction of about 33% - an adjusted mean reduction of about 33% to 37% in the placebo arm. And remember, the reason that FeNO goes down in a trial like this is because the patients are actually treated in a facility, and that's over a 10-day period. And that's done so that you eliminate the exposure to environmental allergens and take out that variability on that FeNO measurement.
So we'd expect those placebo to come down. And then obviously, we're testing for difference in drug versus placebo. If you do kind of FeNO measurements in a normal asthma trial looking at mild or moderate-to-severe, you actually see FeNO kind of stay around where it is at the baseline in the placebo group. So this is a different way to look at that measure.
In terms of what success looks like, we have predefined criteria with our partner AstraZeneca on what that threshold of success is in that trial. We're not going to release that at this time.
However, I would say if you look at the study for - that UCB, Vectura study, where they did see a statistically significant reduction, they saw relative - a relative difference versus placebo of about - in the low 30% range. So we think that's a reasonable target to look at.
Got it. And just to sort of clarify a minor point there, Allan, one of the things we noticed in the Vectura data was even though they went in with mild asthma patients, they ended up having to amend the trial to include patients with low-dose steroid.
Has there been any protocol changes in this study and/or I know that was a exclusion criteria to begin, but was that - did that continue to be the case for the double enrollment?
Yeah, we - there have been no protocol changes having to do with background therapies in our trial. So enrollment has not been an issue for us.
Got it. Thank you very much.
Thank you. Our next question comes from the line of Chris Shibutani with Cowen and Company. Please proceed with your question.
Thank you. This is Pam [Barendt] on for Chris. Hi, guys. Can you help set expectations for the pace of the PRS-060 program following the data release or results later this year? Thank you.
Thanks, Pam. Thanks for the question. Look, at the outset, I'd say that, as it is a partnered program with AstraZeneca, we are not at liberty to talk a lot about the disclosure pace, the progress of the trial in specific detail. And as you know, the Phase Ia was rapidly enrolled and completed in a timely manner. And the data were top line last year. And we look forward to disclosing those data at an upcoming medical conference as far as the ongoing Phase Ib trial.
This is, as I'd like to say, kind of a contrived patient population. Our intended-to-treat population is obviously not going to be mild asthmatics with elevated FeNO. This is a really great way to short-circuit to get to the optimal dose for Phase IIa and get a real, hopefully, derisking perspective on target engagement PK/PD very early in the process. For Phase Ib, that doesn't happen every day. I'm really excited about that in a broader sense.
I would say that the Phase Ib study, despite that "contrived" population, enrollment is going very well. And we have been working across multiple Phase I sites. We have not encountered any enrollment issues whatsoever to complete the timelines that we have set together with AstraZeneca.
We remain committed to timely completing the trial and timely reporting the results at an upcoming medical conference, subject to final alignment with AstraZeneca on the precise venue and the messaging. But as we sit here today, everything remains on schedule, and we look forward to sharing the details with the investment community in due course.
Thanks so much. And a similar question for 343 and 344, can you provide some color on the pace there, particularly for 2019? Thank you.
Sure, I'm going to let Lou talk about those timelines. So I'm going turn it over to Lou for that.
Yes, so this is - I'll start out with 344. That program is moving well towards an IND filing and initiation of the clinical trial in this calendar year, later this year, together with Servier.
And with respect to 343, enrollment continues to go well in the single-dose escalation study. We anticipate, as we stated, that we will be presenting the data later this year. As we go through each dose and cohort, we're looking, of course, at the drug exposure.
And correlating that drug exposure at the same time in all of these patients with evidence of a pharmacodynamic effect by looking at changes in the tumor microenvironment with respect to immune activation and at the same time looking for evidence of clinical response. And so we will be reporting on that later this year as well.
Beyond that, the combination trial with atezolizumab also continues to enroll very well. At the same time, we'll be looking at similar parameters and obviously evidence to a synergy with our drugs' activation form being tumor-targeted fashion, together with PD-1, PD-L1 pathway inhibition.
Thank you very much.
Thank you. Our next question comes from the line of Matt Phipps with William Blair. Please proceed with your question.
Good morning, guys. Thanks for taking my question. On PRS-344, obviously you seem pretty excited about this program. There's also quite a few other companies moving forward with similar - at least similar targeting assets.
I wondered if you could talk enough a little early about the clinical development path. Specifically, if you decide to go into more PD-1 amenable indication for melanoma or lung, how could you really determine the benefit of the added 4-1BB signaling? Or do you plan on looking at maybe refractory tumor types of those that don't respond very often to PD-1 monotherapy?
Hey, Matt. Good morning. Thanks for the question. Again, I'm going to let Lou tackle this one.
Yes. So thanks, Steve. I think that there's no doubt that this is a very, very exciting bispecific. And that's evidenced by the fact that we are not the only company by any means developing this particular bispecific targeting the PD-1 pathway and 4-1BB simultaneously.
One reason that it's a very exciting combination is due to the fact that there's really an abundance of preclinical scientific evidence indicating that there is synergies - significant synergy in tumor models between 4-1BB activation and PD-1 pathway inhibition.
In addition, I think this is implied by your question, there are - basically, almost every single tumor type has a certain amount of PD-L1 expression in subsets of patients. And so this drug is amenable to development across a wide range of different tumor types.
That said, we're not really at liberty to, at this point, to give you specific information on how we're going to initiate the clinical development with respect to tumor types in particular and previous therapy that the patients may have had in particular to look for evidence of benefit that you wouldn't have seen with either PD-1 pathway inhibition alone or co-stimulation alone. But as we move forward toward an initiation of a clinical trial in the second half of this year, that will become clearer.
And if I may, just add to a follow-up, I think it's a good time to just remind everyone, particularly since we have not yet disclosed data for 343, why we remain enthusiastic around 344 and why I think Servier is also very enthusiastic around 344. And there are a couple of reasons for this.
Number one is that although this, of course, is a local expansion of - intended to be a local expansion of T-cells through the tumor-mediated 4-1BB cross-linking, like 343, we also believe that with a PD-L1-based approach, we're able to also get local activation in the drain lymph nodes by engaging in immune cells [ph] there such as dendritic cells, number one.
Number two is at the appropriate exposure levels, we would also believe we could get the checkpoint inhibition blockade of PD-L1 inhibition. As we know, there are multiple indicated PD-L1s on the market and a lot of clinical activity with other PD-L1 antibodies. So that's an extra synergy on the I-O front within the same drug.
And then lastly, as Lou mentioned, we have a much broader tumor population that we could probe beyond HER2-positive solid tumor, which is, of course, what we're focusing on for PRS-343. So collectively, those three things make this a very different approach compared to 343.
And then as you mentioned, there are a number of companies working in the space on that specific type of bispecific approach. We're aware of that. We think that bodes well for us because it continues to validate the approach. And I would remind everyone that we think one of the powers - powerful techniques of our technology is to more broadly interrogate for the optimal biology, given the extreme formatting flexibility that we have.
And we are able to screen for those types of properties preclinically. And we believe we have the drugs that could drive for the desired biology after looking at a number of different formats. So I think that's hopefully helpful biology context vis-à-vis 343 in addition to the clinical development strategy that we outlined for you all.
Thank you. Our next question comes from the line of Joe Pantginis with H.C. Wainwright. Please proceed with your question.
Hey, guys. Good morning. Thanks for taking the question. Just a quick question on 343, if you don't mind. First, can you disclose at what cohort you're dosing right now in the monotherapy study?
And then secondly, and Lou mentioned this earlier with regard to potential synergy with atezo, maybe even though it's somewhat rhetorical, can you give a little more detail as to the mechanisms of synergy with atezo? Thanks a lot.
Sure, Joe. Thanks for the two questions there. Again, I'm going to let Lou talk about the dosing - current dosing strategy and then also the atezo combo synergy that you mentioned.
Yes. So as I said earlier, the dosing is - has been going very, very well. I can say we're certainly at very high dose, one of the higher dose cohorts at this point in time. And again, recruitment continues to go very well. And while we can't exactly say which cohort we're at, things are moving forward. And we'll be in position to present the data later this year, as we indicated earlier.
And again, the major purpose of an activity as we go through this is to correlate at these different doses the level of exposure of the drug during the dosing period and correlate that with evidence of immune activity, especially within the tumor microenvironment, where we're doing very comprehensive biomarker analyses, both with respect to activation at the tumor microenvironment at a cellular basis, for example, CDA T-cells, which is an excellent marker response for the tumor within the tumor microenvironment, and at the same time, do very detailed genetic analysis, including nanostring analysis of the tumor microenvironment as well.
Now as far as atezo, atezo is obviously blocking PD-1/PD-L1 pathway. And there are a number of reasons why one might expect that there will be synergy there. For one thing, most activated T-cells within the tumor microenvironment are expressing PD-1 on their surface, which is engaged with obviously - or cause checkpoint inhibition and also express 4-1BB, which when expressed on tumor cells within the tumor micro - T-cells within the tumor microenvironment is a marker for an enriched population of actual tumor-specific T-cells.
So it stands to reason that if you block the PD-1 pathway and basically take away the inhibitor effect of PD-1 signal, at the same time you're activating co-stimulation with 4-1BB, which has basically a multiplicity of beneficial effects on the T-cells, on the tumor-specific T-cells, including enhanced cytolytic [ph] activity, enhanced generation of antitumor inflammatory cytokines and so forth, you would expect a synergy.
And that's been demonstrated, as I mentioned earlier, multiple times preclinically, for example, in models where both co-stimulation of T-cells through 4-1BB in concert with taking off the brakes of checkpoint inhibition gives you very dramatic enhancement of the tumor responses.
Thanks, Lou. And actually, I think it might be also - I'll be happy to give a little bit more color on the first question because we haven't - we're not going to comment on specific details.
However, what I wanted to do is to remind everyone, we have the ability to over-enroll in our single ascending dose - or our escalation trial for 343, which is a multi-ascending dose, of course. And we see the benefit of enrolling more patients in higher doses beyond the minimum of three patients. And also there's great flexibility in the current protocol as written to explore different exposure levels.
And so while we're not commenting on any data until we have a comprehensive dataset later this year, as we said, there are no showstoppers so far. And based on the totality of data generated to date, we believe it is a reasonable investment to continue to ascertain the PD and the clinical potential of 343 at these various exposure levels as Lou had mentioned.
Okay. Thank you.
Thank you. Our next question comes from the line of David Hoang with Jefferies. Please proceed with your question.
Hi, everyone. This is David on for Biren [ph]. So I have a few question, maybe some logistical - just some logistical ones first. Can you remind us what meetings make sense in terms of presentation of the 060 mild asthma data and then whether the dry powder inhalation formulation is ready for Phase II and when the Phase II might commence?
Sure, David. Thanks for the questions. In general, for respiratory disease, I think, in general, there are two major medical conferences. They're not the only two, but they're two major medical conferences for the respiratory space that kind of bookend the year, in the spring and the fall.
The springtime is the American Thoracic Society, ATS, specifically in May of the calendar year. And then in the fall, September is the European Respiratory Society meeting, ERS, which this year is in late September.
I think, in general, in line with AstraZeneca corporate communication strategy for their existing respiratory pipeline, I think you should be thinking about those conferences as target conferences in general to disclose data.
As far as the DPI concern, our strategy remains to initiate the Phase IIa study with the DPI formulation. And remember that while we are sponsoring the current Phase Ib trial, AstraZeneca will sponsor the Phase IIa study.
As has been our practice, we plan to disclose only those the first patient in the study. However, we will not be able to be more specific on the Phase IIa start at this time due to the fact that we have this collaboration with Astra. We're not authorized the disclosure of that. And they actually are ultimately in charge as the sponsor of the trial.
However, I can say that both parties remain very excited about the program. And we continue to push this forward as a high-priority asset for both companies.
Great. And I think just one follow-up. In terms of the signal of activity, you're able to achieve the FeNO reduction which you hope to see in mild patients. Is there any read-through to the moderate-to-severe population based on that outcome? And any read-through to other endpoints such as FEV1?
So yes, thanks. So that's a great question on the fundamental biology. So Lou can start. And then if Allan wants to add on to that, he can do so as well.
Yes. Obviously, these are separate populations. But then we've done quite a bit of thinking and strategizing on this. I think it's very clear that FeNO is a very significant marker of pulmonary inflammation and correlates quite well with the progression of disease, even in severe asthmatics, such that, for example, if FeNO remains elevated in severe asthmatics new current therapy, that portends a long-term decline in pulmonary function, such as FEV1, for example.
So we think, in general, although we're very careful to be cognizant of the fact that these are different populations, FeNO is generally a very good marker of pulmonary inflammation. It's continued elevation predicts a progression of asthma. And that's for the severe asthmatic population.
So in that sense, we think it's - in this particular population, being able to significantly reduce FeNO levels due to treatment is clear evidence that our drug is working within the line to block the receptor - well, four receptors in such a way that information has decreased.
Yeah. And I would just add on to that, I mean, if you look at the approved drugs in asthma, especially if you think about the severe asthmatic populations, so you have Xolair, an anti-IgE, and then the IL-5s that are approved, neither of which – four of those drugs, none of them have any effect on FeNO. And that's expected, I guess, given their mechanism of action.
But then you kind of compare that to dupilumab, which has a very significant effect on FeNO. If we kind of back out, one study we actually see probably normalization of about 70% of FeNO-high patients using IL-4 receptor alpha.
And that clearly has - going after that target, IL-4 receptor alpha, which we're doing with PRS-060, clearly has seen the best reduction in exacerbations in those patients plus the far superior effects on lung function, namely FEV1, with a Phase III program saw a 0.25 to 0.23 liter improvement in lung function, which is very clinically meaningful and substantial.
And if you look at even an inhaled receptor alpha in pitrakinra, which was studied back in 2010, if you look at their study that we looked at in the mild population at very high doses, it did have a nice effect on FeNO. But the lower doses that were eventually tested in the Phase IIb did not have that same effect on FeNO or result in lung function, although they did see a really nice 74% reduction in exacerbations.
So we really think that FeNO and especially lung function correlation exists, been seen in the dupilumab trials as well. So we're really excited of the importance of FeNO even if we're able to see that reduction in a mild patient population and how that may translate to the moderate-to-severe patient population.
Got it. Thanks. That’s helpful.
Thank you. There are no further questions at this time. I'd like to turn the floor back over to Mr. Yoder for closing comments.
Thank you. I only want to thank everyone again for your attention today and for your continued support of Pieris. We look forward to keeping you updated on our progress, and we wish everyone a great day. Thanks.
This concludes today's teleconference. You may disconnect your lines at this time. Thank you for your participation.