Ocular Therapeutix, Inc. (OCUL) Earnings Call Transcript & Summary

Good day, and thank you for standing by. Welcome to the Ocular Therapeutix conference call announcing top line results for Phase II clinical trial of OTX-DED for short-term treatment of dry eye disease. [Operator Instructions] Please be advised that today's conference is being recorded. [Operator Instructions]. I would now like to hand the conference over to your speaker, Donald Notman, Chief Financial Officer. Please go ahead.

Thank you, Shannon. Good morning, everyone, and thank you for joining us on our conference call announcing top line results for Phase II clinical trial of OTX-DED for the short-term treatment of dry eye disease. The press release and presentation can be accessed on the Investors portion of our website at investors.ocutx.com. Leading the call today will be Antony Mattessich, our President and Chief Executive Officer. As a reminder, on today's call, certain statements we will be making may be considered forward-looking for the purposes of the Private Securities Litigation Reform Act of 1995. In particular, any statements regarding our regulatory and product development plans as well as our research activities are forward-looking statements. These statements are subject to a variety of risks and uncertainties that may cause actual results to differ from those forecasted, including those risks described in our most recent quarterly report on Form 10-Q filed with the SEC. I will now turn the call over to Antony.

Thanks, Donald, and thanks, everyone, for joining us on the call. Sorry to get you out of bed so early on a Monday morning, but data comes when data comes. So it's very nice for you be able to join us this morning for this very exciting release of our OTX-DED Phase II data. Before I hand over to Mike, who's going to go through the presentation on the study and then answer questions, just wanted to give a big picture of why are we doing DED. You probably heard me say many times that we are -- we begin with that in mind that our products are pulled forward by market need, not driven by the fact that we think we have a cool technology that we can develop a product for. The reason why we're developing DED is because the market needs options for dry eye disease. And one of those options, the option that works best at the moment for -- as far as active supplement go is steroids. Now they need a steroid, obviously, that has an indication, but that's really more of a necessary condition in order to be able to enter the market. But what the market really needs is they need a steroid that doesn't have a preservative, which is like OTX-DED. They need a steroid that is not abusable. Since OTX-DED is physician-administered and not patient-administered, the doctor knows the dose the patient is going to get and how long they're going to get that dose. The market also needs a product or would very much like a product where the doctor could have an ability to improve the office economics. With OTX-DED, like all of our products, it is a buy-and-bill product with an associated procedure code, which allows for the office to be able to control the economics of the product that they give to the patient. So for all of these reasons: preservative-free, non-abusable, buy-and-bill, we believe that OTX-DED should we get -- should we be able to get this product registered in all the market, has a significant potential from an economic standpoint. And also is it going to meet the significant need for patients to be able to benefit from a product like OTX-DED. So with that sort of the bigger picture and the backdrop, I'll hand it off to Mike Goldstein, our CMO and President, to be able to go over the details of the study and then talk about next steps as we head into Phase III. Mike?

Yes, thanks, Antony, and thanks, everyone, for joining this morning. So I will walk you through some prepared slides that you can access on the Investor website. And then following that, we'll have the opportunity for some questions. So starting on Slide 2. To remind you what OTX-DED is and why we're interested in, and Antony sort of set the scene. We commonly use steroids for the treatment, for the acute treatment of dry eye disease. And prior to steroids, which is the only approved products, these are mostly off-label steroid use. Issues with the approved therapies are that they all have preservative in them, and they all have the risk with use, meaning patients can continue to use them even beyond when they're supposed to stop using them. So the biggest opportunity here is to take a low-dose steroid and put it with our hydrogels and we deliver that as a preservative-free therapy, which lasts 2 to 3 weeks. It also, in addition to the benefit of the steroid, because it's in the hydrogel platform, it also has the benefit of fleeting the pump, which also has some benefits for dry eye patients. And like all the products that we have, it biodegrades and stands without the need for removal. The slide also, shows compared to our approved product, DEXTENZA, the OTX-DED product is actually slightly shorter in length, which means it's actually easier to put in. Moving to Slide 3. This tells -- this gives you an overview of the study design. So it was a 3-arm study with 2 different formulations of OTX-DED; a 0.2 milligram formulation and a 0.3 milligram formulation; and we compare that in a 1 ratio with the hydrogel vehicle formulation. So patients had an insert placed. This prospective, randomized, double-masked in the U.S., to get into the trial, you had to have dry eye for at least 6 months. The primary endpoint was looking at bulbar conjunctival hyperemia in the worst zone at day 15, looking at change from baseline, and we had a number of secondary endpoints as well in addition to looking at the bulbar conjunctival hyperemia in the different zones. And the primary endpoint here was at 2 weeks, and we had a follow-up period for safety up to 8 weeks. Moving to Slide 4. This gives you a little bit more data around the primary endpoints. So we use a validated scale called the CCLRU grading scale. This was developed in Australia. It's commonly used in many, many trials, both outside the U.S. and inside the U.S. And essentially, what you do is you create, on a scale of 0 to 4, 3 different zones of the conjunctiva. And when we say bulbar, bulbar means that the frontal conjunctiva is touching the eye. And so you look at the temporal zone, which is sort of the outside zone. If you look at the nasal zone, which is the zone closer to the nose. And we look at the frontal zone, which is the zone you see straight ahead. Each of those zones is graded between 0 and 4. And if you -- some of them, you get a score of 0 to 12. And for the primary endpoint, what we did is we looked at the worst zone. We took the patients when they entered the trial, we assessed the worst zone and we followed that zone, but we also have data for all the other zones. And this was all done through a central reading center. And so the primary endpoint is worse zone, we had a number of secondary endpoints looking at the other zones. In addition, we looked at several different symptoms. One of the symptom scores we looked at was looking at the visual analogue scale for dry eyes across severity and frequency using a scale between 0 and 100. So moving to Slide 5. This gives you the demographics and baseline measurements. So we enrolled 166 subjects in the modified intent to treat population. So you might wonder what's the modified part. So in this population, the intent to treat population of all the patients randomized, and the modified part means they had to have their part of the insert placed. So it's every patient who was randomized to actually have an insert placed in the studied eye, that's the modified intent to treat population. Average -- the mean age was in the low 60s, as expected. It was primarily female, as expected, and it was primarily Caucasian. The only imbalance here is there were slightly more African-American subjects in the active group compared to the vehicle hydrogel group. In terms of baseline characteristics, you can see the mean conjunctival hyperemia in the worst zone was just around 2 on a scale of 0 to 4, which is as we expected it would be. Mean eye dryness severity and frequency scores were in the low 70s, which means that it's a pre-severe population. It's a pretty high number. Moving to Slide 6. Everyone always asked about retention. As expected, in this trial, retention rates were extremely high with retention rates at the primary end point in the mid- to high 90s, and then it tapered off. And you can see by 2 months, it was just below 50%, which is, again, as we expected, given the hydrogel that we're using in the study. Moving to Slide 7. This is the money slide. This is the primary efficacy endpoint, this was prespecified. Looking at bulbar conjunctival hyperemia in the worst zone at day 15. And you can see on the left is the mean values; on the right, the change from baseline values. And you can see that we saw about a half unit change for the point of the OTX-DED 0.2 milligram group and the OTX 0.3 milligram group. And then in the green, we prespecified. We actually look at the groups in a combined way, and that's the data that combines. And the advantage of that, obviously, is to get a little bit more power, and that all compares to the vehicle hydrogel group, which had a change of about minus 0.2 units. And these differences between each of the groups and the combined groups was statistically significant, with a p-value of 0.004 for the 0.2 milligram group, 0.028 for the 0.3 milligram group and 0.004 for the combined group. And I should say, we are thrilled with these results. The study was not powered for statistical significance. So as you're aware, many of these dry eye patients studies are much, much longer -- not much, much longer, much, much bigger, and require a much bigger end to achieve statistical significance. So showing statistical significance in this smaller study is a testament to the robustness of the data, both from a separation from the vehicle as well as the standard deviation perspective. So moving to Slide 8. This gives you an idea of some of the secondary endpoints. So this is looking at both our conjunctival hyperemia for the total score. So this is summing the nasal, the temporal and the frontal scores at day 15. And here, again, you can see a robust change in the active group compared to the vehicle hydrogel group, with the active groups being just under a 1-unit change and the vehicle hydrogel group being minus 0.13 units. Again, highly statistically significant with the 0.2 milligram group being, I mean, a p-value of 0.002; the 0.3 milligram group being at a p-value of 0.014, and the combined group having a p-value of 0.002. And then you might wonder, if you go to the next slide, you might wonder, Slide 9, might wonder about each of the different zones. So we were just lucky in the worst zone, and the frontal zones. So this gives you a score for the nasal zone, the temporal zone, the frontal zone. And, again, the story is the same with a nice separation between the active groups and the vehicle control group, and these differences were statistically significant for all the points, with the 1 exception being the frontal zone 0.3 milligram group only have a p-value of 0.184, which, frankly, has that been the whole result, we've been thrilled with that. So really, really strong data here, looking at overcoming conjunctival hyperemia. So moving to Slide 10. You might wonder about the symptom score. So this is the -- shows you data from the visual analogue scale severity score. At the bottom, you can see the baseline data, and you can -- against the patients started in the low 70s, which indicates a very severe population. And you can see today that day 8 and day 15, we saw a very large improvement in both the 0.2 milligram and 0.3 milligram groups compared to baseline. But we also saw a very large vehicle response, which is likely related to the benefit of the punctal occlusion. I would say that this is a larger response than one might expect just from punctal occlusion but may indicate how well the hydrogel does in terms of including the punctal. So what about safety? So if you move to Slide 11, this gives you an overview of safety events. And there were no real differences noted between the active group and the vehicle control group in terms of number of treatment-emergent adverse events or number of ocular treatment of emergent or adverse events. For non-ocular treatment emergent adverse events, there were no ocular serious adverse events. There were 2 serious adverse events non-ocular seen in the trial. Both were in the vehicle group. One was a subject who had cellulitis, who was hospitalized for this. One was a subject who had COVID pneumonia, who was hospitalized for this. We also had 3 -- so most events were considered mild or moderate. There were 3 severe adverse events in this trial, 2 of them were the aforementioned cellulitis and COVID pneumonia. The third was a subject who had epiphora in the 0.2 milligram group, the -- this lasted for approximately 1 month, at which point the inserts were removed. So moving to Slide 12. This shows you the most common ocular treatment emergent adverse events in this trial. There weren't many, so this is all -- the whole list of those ocular treatment emergent adverse events that were greater than 1%. So we saw eye itching at 1.8%. We saw increased epiphora, which was 8.1% in the OTX-DED treated group and 6.6% across the trial. And we saw elevation of eye pressure, which was 3.6% in the OTX-DED treated groups. And again, there were no ocular serious adverse events, and there were no cases of dacryocanaliculitis seen in this trial. In terms of -- moving to Slide 13, in terms of systemic adverse events, the only one that occurred with a frequency of more than 1% was arthralgia. And as I mentioned before, there are 2 serious non-ocular adverse events, which were unrelated. So turning to Slide 14. In conclusion, we're thrilled to have found that we saw a statistically significant improvement in the primary endpoint of bulbar conjunctival hyperemia in the worst zone for OTX-DED relative to the vehicle hydrogel for both the 0.2 and the 0.3 milligram group. We saw this despite the fact that the trial was not powered to show statistical significance. Data from numerous secondary endpoints, looking at bulbar conjunctival hyperemia, scores supported the conclusions for the primary endpoint with very refining data, really, in all areas. And all of these were statistically significant, except for the frontal zone of 0.3 milligram group not shown. We also did a number of different sensitivity analysis using different methods of imputation, including LOCF, MCMC and FCS, and all showed similar results to the primary endpoints. Both doses seem to perform well, with no dose response seen, and I'm sure that will be a question. We expected that because the rate of delivery of the drug between the 0.2 and the 0.3 milligram groups, which was designed to be very similar, with the main difference being the 0.3 milligram group would last longer than the 0.2 milligram group. In terms of symptoms, we did see a large improvement from baseline in all 3 groups, but did not see much separation between the active groups and the vehicle group. And we have done some preliminary outlier and post-hoc analysis, which shows potential opportunities to differentiate between the OTX-DED active groups and the vehicle hydrogel groups. And finally, we -- in this trial, we observed OTX-DED to have a favorable safety profile that was generally well tolerated, with very low rates of ocular pain, discomfort and irritation. And the most common adverse event seen, as expected, were epiphora and IOP elevation, and we saw no ocular serious adverse events. So again, super excited with these results. Next steps are, we need to continue to interrogate the data. We need to look at the full data set. We need to spend more time understanding the data around symptoms, and there are a number of analysis we can do, including an outliner analysis looking at different demographics, looking at different inclusion/exclusion criteria, in an effort to find the most appropriate population to use in the Phase III trial. There's also going to be some ongoing discussions about the most appropriate comparator. In this trial, we used a vehicle hydrogel that really had sort of the same characteristics as the OTX-DED in terms of durability. There's an opportunity to use a hydrogel that biodegrades in a clinical manner, which would be more representative of a true placebo effect. So again, I'm super excited about the results of this trial and happy to answer any questions.

[Operator Instructions] Our first question comes from Jon Wolleben with JMP Securities.

Congrats on the data. Just a few for me. Maybe can you tell us a little bit more about what's a clinically meaningful change in hyperemia? It seems like both active and vehicle groups got to kind of a very slight to slight score. So is this a meaningful change in terms of what a patient sees or thinks or feels, and what a physician wants to see as well?

Yes. Good question, Jon. Thanks for your question. So from a regulatory perspective, the definition of clinically meaningful is that you show statistical significance. So that's an important point. From a clinical perspective, a half unit change on the baseline of essentially 2 is a meaningful and noticeable change. And what I didn't say is -- so this data was all done using the central reading center. We also had investigators assess patients in real-time throughout the trial, and they also noticed a nice benefit from -- in terms of the improvement of the conjunctival retina scores.

That's helpful. Can you provide some more details on the IOP elevation? The magnitude, any consequences, how it resolved with treatment or without?

Yes. Again, thanks for the question. So the overall rate was low at 3.6%. In general, the elevations were low, so there were 4 patients that had elevations in this trial. 3 of the 4 had very low elevation. I think it was 3 to 5 millimeters, something like that, it did not require treatment. One patient did have a more significant elevation of approximately 10 millimeters. That patient was treated with an eye drop, and it resolved over time, so no need to remove it. It was treated with an eye drop. Of note, that patient also had elevated baseline eye pressures at the initial visit in the mid-20s. So that's a patient that was susceptible to developing an IOP elevation. So I'm not saying it was predictable, but that you could have suspected from a clinical perspective that, that would be patient with the higher risk.

Okay. And maybe one last one for me before I jump in the queue. Mike, you touched on this a bit about how you're thinking about next steps. But can you tell us if you think you have the right doses here, or is it just going to be the 0.2 milligram dose as you move forward? Do you think there needs more exploration? And then, I'm guessing hyperemia is going to be the sign moving forward, but what other symptoms did you look at that could come to play here?

Yes. Well, a good loaded last question, by the way. So yes, I do think we have the right dose here. I think we saw a nice dose effect with both the 0.2 and the 0.3 milligram group. I think we could take forward either of them. We haven't determined which one we would take, or if we would only take forward one of them. But I think both are viable candidates to move forward. I think the issue, really -- and in terms of the sign, bulbar conjunctival hyperemia is clearly the sign. It was a really robust effect. So the issue, really, is figuring out and really interrogating data around a symptom. And I think there are sort of 2 aspects to that. One is figuring out what's the best symptoms forward to use. And so in this case, we use visual analogue scale, dryness and visual analogue scale eye dryness, severity and frequency. There are a number of other scales that can be used and some of those we did use in this trial, including the OSDI and the speed scores, and we need to look through that data to understand sort of the best endpoint to use. But the other aspect, I think, that's important is the comparator. So here, the vehicle hydrogel group performed extremely well, which, not totally unexpected, one of the treatments that we use for dry eye patients is punctal occlusion. And one of the reasons we do that is it makes people feel better. So what was a little surprising, again, was the effect was larger than you would see in the literature for just punctal occlusion. And that could be a true placebo effect on top of a real effect or could even be that -- and this is an important point. The hydrogel -- the way the hydrogel works when you place it in the canaliculus is it comes in contact with water and expands, and it kind of fills the space. Sort of like one of those little animals that you put into water, it fills the space. And because of that, you get a very, very good occlusion of the punctum. And it could be that we're seeing a more robust effect because we're getting a better occlusion of the punctal than you would with, say, a silicon plug where fluid can still sort of drain around the sides. So all that needs to be sorted out. But I think, again, I think from a formulation perspective, the 0.2 and the 0.3 milligram groups are both very viable moving forward.

Our next question comes from Dane Leone with Raymond James.

Congratulations on the data. A couple for me as well, I guess. Could you just maybe speak more specifically to what you anticipate the regulatory pathway is going to be heading into a Phase III, and what the ask may be, maybe within the context of the experiment -- experience with reproxalap and the ongoing clinical studies there? And then secondly, when you think about the actual clinical effect relative to vehicle, what do you think the ancillary endpoints are going to need to be as you think about going into a pivotal study, assuming you would still use hyperemia as the primary? And then lastly, just probably an easier question. As you scale up into a Phase III study, would you still be able to use central reading for the primary endpoint of hyperemia?

Okay. Lots of good questions there. So I actually think the regulatory pathway is pretty straightforward. So it's not an easy pathway, but it's pretty straightforward. And you have to show 2 adequate and well-controlled trials. You have to get statistical significance for assigning symptom into adequate and well-controlled trials. So that's the target. And we can argue that this is one adequate and well-controlled trial, so that would be -- especially with the FDA, and if so, that could count as one of the signs. I'm not saying it will, but it's possible that, that could, but that means we still have to hit at a minimum, sign in another adequate and well-controlled trial and symptoms and 2 adequate and well- controlled trials. In terms of other ancillary endpoints, there aren't any. We know that bulbar conjunctival hyperemia is an acceptable side endpoint, is the endpoint that was used in the [indiscernible] trials for regulatory approval. So we're very comfortable with that as the sign endpoint. And as mentioned in the discussion with Jon, there are a number of different symptom endpoints that we can look at. And in terms of using the central reading center, yes, we think it is viable to use the central reading center. We think it's preferable to use the central reading center where you can get a similar grade or grading all of the images in a consistent manner. That said, as mentioned before, when we did look at investigator assessment at each site, we still did see a benefit of the drug over the vehicle. So as a backup, that's certainly an option. But I think the preferred option is to use the central reading center. So I think I answered all the questions. If I did, or is there anything else you asked here, Dane?

I have more, but I'll jump back in the queue. Just one follow-up to what you just said. Do you -- just reading kind of between what you've said here, since you didn't know, you will need 2 successful studies on symptoms. Is that more the premise of thinking about changing what the vehicle is in the pivotal studies that, given how the control performance was in the study, there would be maybe a better opportunity to differentiate if you had a shorter active vehicle on symptoms?

Yes, I would say, again, 2 strategy sets. That's one strategy, the other strategy is to interrogate the data and understand the population to stratify or fortify the population. But yes, I think considering the competitor is an important potential strategy here.

Our next question comes from Joe Catanzaro with Piper Sandler.

Maybe a couple for you, Mike. Just following up on this placebo effect and vehicle. And I'm wondering if mechanistically, it makes sense that, that placebo effect would be very apparent on the symptoms endpoint and eye dryness and not be as apparent if present at all on the hyperemia signs endpoint, if that makes sense to you? And I have a follow-up.

The answer is, yes. So we know that punctal occlusion does make people feel better, that's why we do it a lot. But we also know there's no mechanistic reason that should improve eye redness, and it really didn't. So yes, I would say the data made sense and was expected. The unexpected part was the magnitude of effect of the vehicle hydrogel in terms of improvement. So that was larger than I would have -- if you had asked me before the trial, I would expect that was larger, but it was directionally what I would have expected.

Okay. Got it. And maybe as a follow-up to that, can you remind us the vehicle or placebo controls that were used in the DEXTENZA trials and why you couldn't sort of take same approach here with DED? And then I noticed about 40% of patients retain the insert out to 40 days. Is the insert still eluding drug at that point? Are you able to detect DEX in the [indiscernible] until 56 days?

So 2 good questions. One is the vehicle we used here is similar to the DEX -- to the vehicle used in DEXTENZA trials, but the endpoint patient symptoms is different. So there, we're looking for the complete absence of pain at day 8, which is a different -- sort of a different estimate. In terms of -- is the drug continuing to elude out to 2 months, not much, if any. So the 0.2 milligram group is really designed to release most of the drug by 2 weeks with a slow taper -- with a slight taper after that, and the 0.3 milligram group really released drug for about 3 weeks with a slight taper after that. So we don't expect to see any or much drug by 2 months. That said, we did do a durable PK analysis, that data we don't have yet. That will be part of the full data set, so we'll be able to verify what if those assumptions are true. But as designed, we would not expect much drug, if any, at a 2-month timeframe.

Okay. Got it. And if I could just squeeze one last question in. I think I noticed on one of the slides there was about a 20%, 25% screen failure rate. What were the primary reasons for those screen failures?

So in any dry eye trial, there are a number of inclusion/exclusion criteria that are used at 25% rate. I would actually say, overall, it's pretty low. But the main criteria were that you had to have a certain score for bulbar conjunctival hyperemia at least to get into the trial, and so I think that was a big issue. You also have to have a certain symptoms for at least 30 to get into the trial. There's a certain [indiscernible] you had to get into the trial, a number of others, but it was mainly around the degree of redness. Not every patient with dry eye has redness, and the idea is that redness is a marker of inflammation, which is a marker of an acute player with dry eye. So that's really who we're targeting, those patients were acute players who need short-term steroids in order to treat their dry eye. So it's really around the redness.

[Operator Instructions] Our next question comes from Anita Dushyanth with Berenberg Capital.

Congrats on the data. Mike, just as a follow-up on the point you mentioned earlier. I just wanted to know that, besides the 0.3 milligram gel lasting longer than the 0.2, the other outcomes, were they sort of expected from the dose? Or is that something that you were probably kind of different from what you had expected between the 2 doses?

So in general, we expected the 0.2 and the 0.3 milligram groups to behave in a similar manner, with the 0.3 milligram group lasting longer. And in general, we did see that across the whole data set. I would say the one surprise, or a little surprise would be that the 0.3 milligram group symptom perspective did not do as well as the 0.2 milligram group. I don't believe that to be a real effect. I think that's related to a function of a smaller end, but we need to dive in deeper in the data and try to figure out what's driving that difference.

Okay. Okay. That's helpful. And then for the next steps in the Phase III, the rationale for choosing either of those doses, would the duration of the 0.3, would that be one of the criteria that you'll be looking at? Is that one of the -- I mean, do you think that 3 weeks -- the drug lasting for 3 weeks would make more sense? What's your thoughts on those?

Yes, it's a good question. I think there are a number of factors to consider when deciding what the best dose would be between the 0.2 and the 0.3 milligram group. One of which is duration, which would favor the 0.3 milligram group. Again, we haven't made that determination yet. I think we need to look at the full data set and take all the factors into consideration, but I think the bottom line really is that both are viable to move forward into Phase III. But we wouldn't move all forward, but both would be viable. And so there are pluses and minuses of each, which we will aim and then make a decision.

Okay. And then just regarding the Phase III trial, there would be 2 studies for assessing DED?

So, yes, it's a good question. So as I've mentioned earlier with the discussion with Dane, so you need 2 adequate and well-controlled trials to hit a sign and symptom twice. And so the most efficient way to do that is in 2 trials with co-primary endpoints. There is a strategy that says to do 4 trials. One was signed, one was signed, one was symptom, one was symptom. I don't think that would be the approach we would take, I think we'd be looking to do 2 trials. And we'd also -- like as I sort of alluded to earlier, we would like to have a discussion with FDA. It's possible that this trial would be considered one of the adequate, well-controlled trials for the sign. But again, that's a discussion that has to take place. But I would look at a minimum of 2 trials, yes.

Our next question comes from Yi Chen with H.C. Wainwright.

Based on the current results, how many patients do you think would need to be recruited for the pivotal study? And in the current environment, how quickly can the study complete enrollment?

Yi, so we haven't done the power calculation, that obviously, is a function. So it won't be driven by the sign data, which is quite robust and would not require a particularly large trial. It will be driven by the symptom data and the choice of the vehicle comparator. So we obviously need to assess what's the effect, difference and we know what the standard deviation is. So in general, trials looking at symptoms, if you look at the order of data of those trials were on the order of 800 or 900 patients, so -- and that was probably -- I'm sure that was driven by the needs for symptoms. So we haven't come with those power calculations yet for us, but that sort of gives you a ballpark of where it is. In terms of enrollment, we would expect this to enroll quickly. This trial, which we ended up with over 160 patients enrolled, incredibly quickly. We think even if it's a large trial, there's the opportunity to enroll very quickly.

Thank you. And I'm currently showing no further questions at this time. This concludes today's conference call. Thank you for participating. You may now disconnect.