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. At this time, all participants are in a listen-only mode. After the speaker presentation, there will be a question and answer session. To ask a question during the session, you will need to press star one on your telephone. Please be advised that today's conference is being recorded. If you require assistance, please press star zero. 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. It's very nice for you to 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 gonna go through the presentation and on the study and then answer questions, just wanted to give a big picture of, you know, why are we doing DED. You probably heard me say many times that we begin with the end in mind, and 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 OTX-DED is because the market needs options for dry eye disease. One of those options, the option that works best at the moment for as far as active substances 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. What the market really needs is they need a steroid that doesn't have a preservative, which is what like OTX-DED, they need a steroid that's non-abusable. Since OTX-DED is physician administered and not patient administered, it's the doctor knows the dose the patient is going to get and how long they're gonna 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. For all of these reasons, preservative-free, non-abusable, buy and bill, we believe that OTX-DED, should we be able to get this product registered and on the market, has a significant potential from an economic standpoint, and also meets a significant need for patients to be able to benefit from a product like OTX-DED. With that as sort of the bigger picture and the backdrop, I'll hand it off to Michael 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? Thanks, Antony, and thanks everyone for joining this morning. I will walk you through some prepared slides that you can access on the investor website. Following that, we'll have the opportunity for some questions. Starting on slide two, to remind you what OTX-DED is and why we're interested, and Antony sort of set the scene. We commonly use steroids for the acute treatment of dry eye disease. Prior to Restasis, which is the only approved product, 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 of abuse, meaning patients can continue to use them even beyond when they're supposed to stop using them. The big opportunity here is to take a low-dose steroid and put it with our hydrogel, and we deliver that as a preservative-free therapy which lasts two to three weeks. It also, in addition to the steroid, because it's in the hydrogel platform, it also has the benefit of including the punctum, which also has some benefits for dry eye patients. And like all the products that we have, it biodegrades on its own 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 gives you an overview of the study design. It was a three-arm study with two different formulations of OTX-DED, a 0.2 milligram formulation and a 0.3 milligram formulation. We compared that in a 1-to-1-to-1 ratio with a hydrogel vehicle formulation. All patients had an insert placed. It was 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. We had a number of secondary endpoints as well, in addition to looking at the bulbar conjunctival hyperemia in the different zones. The primary endpoint here was at 2 weeks, and we had a follow-up period for safety out to 8 weeks. Moving to slide four. This gives you a little bit more data around the primary endpoint. We used 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. Essentially what you do is you grade a scale of zero to four, three different zones of the conjunctiva. When we say bulbar means the part of the conjunctiva that's touching the eye. You look at the temporal zone, which is sort of the outside zone. 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 sum them, you get a score of 0 to 12. For the primary endpoint, what we did is we looked at the worst zones. We took patients when they entered the trial, we assessed the worst zone, and then we followed that zone, but we also have data for all the other zones. This was all done through a central reading center. The primary endpoint is worst 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 Analog Scale for dry eye severity and frequency using a scale between 0 to 100. Moving to slide five, this gives you the demographics and baseline measurements. We enrolled 166 subjects in the modified intent-to-treat population. You might wonder, what's the modified part? In this population, the intent-to-treat population are all the patients randomized, and the modified part means they had to have had the insert placed. It's every patient who was randomized who actually had an insert placed in the study eye, that's the modified intent-to-treat population. The mean age was in the low 60s as expected. It was primarily female as expected. 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 two on a scale of 0 to 4, which was as we expected it would be. Mean eye dryness severity and frequency scores were in the low 70s, which means it was a pretty severe population. That's a pretty high number. Moving to slide six. Everyone always asks about retention. As expected, in this trial, retention rates were extremely high. The retention rates at the primary endpoint in the mid- to high 90s, and then it tapered off. 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 this study. Moving to slide 7. This is the money slide. This is the primary efficacy endpoint. This was pre-specified, looking at bulbar conjunctival hyperemia in the worst zone at day 15. You can see on the left is the mean values, on the right is the change from baseline values. You can see that we saw about a half unit change for the OTX-DED 0.2 milligram group and the OTX 0.3 milligram group. Then in the green, we pre-specified we'd actually look at the groups in a combined way, and that's the data combined. The advantage of that obviously is you get a little bit more power. That all compares to the vehicle hydrogel group, which had a change of about minus 0.2 units. 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. I should say, you know, we were thrilled with this result. The study was not powered for statistical significance. As you're aware, many of these dry eye studies are much longer, much bigger, and require a much bigger N to achieve statistical significance. Showing statistical significance in this smaller study is testament to the robustness of the data, both from a separation from the vehicle as well as a standard deviation perspective. Moving to slide 8. This gives you an idea of some of the secondary endpoints. This is looking at bulbar conjunctival hyperemia for the total score. This is summing the nasal, the temporal, and the frontal scores at day 15. Here again, you can see a robust change in the active group compared to the vehicle hydrogel group, with the active group seeing 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 having a p-value of 0.002. The 0.3 milligram group being at a p-value of 0.014. The combined group having a p-value of 0.002. Then you might wonder if you go to the next slide. You might wonder, slide 9, you know, might wonder about each of the different zones. Were we just lucky in the worst zone, in the total zone? This gives you the score for the nasal zone, the temporal zone, the frontal zone. The story's the same with a nice separation between the active groups and the vehicle control group. These differences were statistically significant for all the points, with the one exception being the frontal zone, 0.3 mg group, only had a P value of 0.184. Which frankly, had that been the whole result, we would have been thrilled with that. Really strong data here, looking at bulbar conjunctival hyperemia. Moving to slide 10, you might wonder about the symptom score. This shows you data from the Visual Analog Scale severity score. At the bottom, you can see the baseline data, and you can again, the patient started in the low 70s which indicates a very severe population. You can see the data at 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. We also saw a very large vehicle response, which is, you know, likely related to the benefit of punctal occlusion. You know, I would say that this is a larger response than one might expect just from punctal occlusion, but may, you know, indicate you know how well the hydrogel does in terms of occluding the punctum. What about safety? If you move to slide 11, this gives you an overview of the safety events. 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 emergent adverse events or non-ocular treatment emergent adverse events. There were no ocular serious adverse events. There were two 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. Most events were considered mild or moderate. There were three severe adverse events in this trial. Two of them were the aforementioned cellulitis and COVID pneumonia. The third was a subject who had epiphora in the 0.2 mg group. This lasted for approximately 1 month, at which point the inserts were removed. 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 full list of those ocular treatment emergent adverse events that were greater than 1%. 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. We saw elevation of eye pressure, which was 3.6% in the OTX-DED treated groups. 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. As I mentioned before, there were two serious non-ocular adverse events which were unrelated. Turning to slide 14, in conclusion, you know, 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 0.3-mg 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 strong data, really in all areas. All of these were statistically significant except for the frontal zone 0.3-mg 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 seemed to perform well, with no dose response seen. I'm sure that'll be a question. We expected that, because the rate of delivery of the drug between the 0.2 mg and the 0.3 mg groups, which was designed to be very similar, with the main difference being that the 0.3 mg group would last longer than the 0.2 mg group. In terms of symptoms, we did see a large improvement from baseline in all three groups, but did not see much separation between the active groups and the vehicle group. 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. Finally, we've in this trial, we observed OTX-DED to have a favorable safety profile. It was generally well-tolerated with very low rates of ocular pain, discomfort, and irritation. The most common adverse events seen, as expected, were epiphora and IOP elevation, and we saw no ocular serious adverse events. Again, super excited with these results. You know, 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. There are a number of analyses we can do, including an outlier 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 DEXTENZA in terms of durability. There's an opportunity to use a hydrogel that biodegrades in a quicker manner, which would be more representative of a true placebo effect. Again, super excited about the results of this trial and happy to answer any questions. Thank you. As a reminder, to ask a question, you will need to press star one on your telephone. To withdraw your question, press the pound key. Please stand by while we compile the Q&A roster. Our first question comes from Jonathan Wolleben with JMP Securities. Your line is open. Hey, good morning. Congrats on the data. Thanks for taking the questions. Just a few from 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. 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? Yeah, good question, John. Thanks. Thanks for your question. From a regulatory perspective, the definition of clinically meaningful is that you show statistical significance. That's an important point. From a clinical perspective, a half unit change on a baseline of essentially two is a meaningful and noticeable hyperemia. What I didn't say is 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 in terms of the improvement of the conjunctival redness 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? Yeah. Again, thanks for the question. So the overall rate was low at 3.6%. In general, the elevations were low. So there were four patients that had IOP elevation in this trial. Three of the four had very low elevation. I think it was 3-5 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. Of note, that patient also had elevated baseline eye pressures at the initial visit in the mid-twenties. That's a patient that was, you know, susceptible to developing an IOP elevation. I'm not saying it was predictable, but you could have suspected from a clinical perspective that that would be a patient that would be at higher risk. 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, do you think you have the right doses here? Is it just gonna be the 0.2 milligram dose you move forward? Do you think there needs more, like, exploration? Then, I'm guessing hyperemia is gonna be the sign moving forward, but what other symptoms did you look at that could come into play here? Thanks. Yeah. Well, that was a loaded last question on the way out. So yeah, 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'd take forward. We'd 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 the data around a symptom. I think there are sort of two aspects to that. One is figuring out what's the best symptom score to use. In this case, we use Visual Analog Scale dryness and Visual Analog 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. The other aspect I think is important is the comparator. Here the vehicle hydrogel group performed extremely well, which, you know, not totally unexpected. One of the treatments that we use for dry eye patients is punctal occlusion. One of the reasons we do that is it makes people feel better. What was a little surprising, again, was the effect was larger than you would see in the literature for just punctal occlusion. That could be a true placebo effect on top of a real effect, or it could even be, and this is an important point, that the hydrogel, the way the hydrogel works when you place it in the canaliculus is it comes in contact with water and it expands, and it kind of fills the space, you know, sort of like one of those little animals that you put into water and it fills the space. Because of that, you get a very, very good occlusion of the punctum. It could be that we're seeing, you know, a more robust effect because we're getting a better occlusion of the punctum than you would with, say, a silicone plug where fluid can still sort of drain around the sides. All that needs to be sorted out. I think again from a formulation perspective, the 0.2 and the 0.3 milligram groups are both very viable moving forward. That's really interesting. Thanks again, and congrats on the data. Thanks, John. Thanks, John. Our next question comes from Dayan with Bryan Garnier. Your line is open. Thanks for taking the questions and congratulations on the data. A couple from 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 experience with Reproxalap and the ongoing clinical studies there. 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? 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. I actually think the regulatory pathway is pretty straightforward. It's not an easy pathway, but it's pretty straightforward. You have to show two adequate and well controlled trials. You have to hit statistical significance for a sign and symptom in two adequate and well controlled trials. That's the target. You know, we could argue that this is one adequate and well controlled trial, so that would be a discussion with the FDA. If so, that could count as one of the signs. I'm not saying it will, but it's possible that could. That means we still have to hit, you know, at a minimum, sign in another adequate and well controlled trial and symptoms in two adequate and well controlled trials. In terms of other ancillary endpoints, you know, there aren't any, you know. We know that bulbar conjunctival hyperemia is an acceptable sign endpoint. It is the endpoint that was used in the ICOW's trials for regulatory approval. We're very comfortable with that as the sign endpoint. As mentioned in the discussion with John, there are a number of different symptom endpoints that we can look at. 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, you know, a similar grader 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. You know, as a backup, that's certainly an option. I think the preferred option is to use the central reading center. I think I answered all the questions. I think I did. Is there anything else you have, Dayan? I have more, but I'll jump back in the queue. I just one follow-up to what you just said. Just reading kind of between what you've said here, since you know you did note you will need two successful studies on symptoms, is that more the premise of thinking about changing what the vehicle is in the pivotal studies that you know given how the control performance was in this study, you know there would be maybe a better opportunity to differentiate if you had a shorter acting vehicle on- Yeah. On symptoms. Yeah. I would say, again, two strategies. 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 comparator is an important potential strategy here. Great. Thank you so much. Thanks, Dayan. Our next question comes from Joseph Catanzaro with Piper Sandler. Your line is open. Perfect. Thanks so much for taking my questions, guys. Maybe a couple for you, Mike, just following up on this, placebo effect and vehicle. 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. Thanks, and I have a follow-up. The answer is yes. We know that punctal occlusion does make people feel better. That's why we do it a lot. We also know there's no mechanistic reason it should improve eye redness. You know, it really didn't. Yeah, 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. That was larger than I would have, you know, if you had asked me before the trial what do I expect, that was larger, but it was directionally, you know, what I would have expected. Okay, got it. 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 the same approach here with DED? Then I noticed about 40% of patients retain the insert out to 40 days. Is the insert still eluting drug at that point? Are you able to detect Dex in the tear film out until 56 days? Thanks. Two good questions. One is the vehicle used here is similar to the vehicle used in the DEXTENZA trials, but the endpoint on patient symptoms is different. There we're looking for the complete absence of pain at day eight, which is a different sort of assessment. In terms of is the drug continuing to elute out to two months? Not much, if any. The 0.2 milligram group is really designed to release most of the drug by two weeks with a slow taper, you know, with a slight taper after that. The 0.3 milligram group really released drug for about three weeks with a slight taper after that. We don't expect to see any or very much drug by two months. That said, we did do a tear film PK analysis. That data we don't have yet. That'll be part of the full data set. We'll be able to, you know, verify if those assumptions are true. As designed, we would not expect much drug, if any, at the two-month time point. Okay, got it. 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? You know, in any dry eye trial, there are a number of inclusion/exclusion criteria that are used. At a 25% rate, I would actually say overall is pretty low. The main criteria were that you had to have a certain score for bulbar conjunctival hyperemia at least to get into the trial. I think that was a big issue. You also had to have a certain symptom score of at least 30 to get into the trial. There's a certain Schirmer score that you had to get into the trial, a number of others. It was mainly around, you know, 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, you know, a marker of an acute flare with dry eye. That's really who we're targeting is those patients. Acute flares who need short-term steroids in order to treat their dry eye. It's really around the redness. Okay, got it. Thanks for taking my questions. Thanks, Jeff. Thank you. As a reminder to ask a question at this time, please press star then one on your touchtone telephone. Our next question comes from Anita Dushyanth with Berenberg Capital Markets. Your line is open. Hi, good morning. Congrats on the data, and thanks for taking my question. Mike, just as a follow-up on the point you mentioned earlier, I just wanted to know that, you know, 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, you know, probably kind of different from what you had expected between the two doses? 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. In general, we did see that across the whole data set. I would say the one surprise or little surprise would be that the 0.3 milligram group from a 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 really just a function of a smaller N. We need to dive in deeper in the data and try to figure out what's driving that difference. Okay. Okay, that's helpful. Then for the next steps in the phase III, the rationale for choosing either of those doses, would the duration of it, 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? Yeah, it's a good question. I think there are a number of factors to consider, you know, when deciding what the best dose would be between the 0.2 and the 0.3 mg group, one of which is duration, which would favor the 0.3 mg group. Again, we haven't made that determination yet. I think we need to look at the full data set and, you know, take all the factors into consideration. But I think the bottom line really is that both are viable to move forward into phase III. We wouldn't move both forward, but both would be viable. There are pluses and minuses of each, which we will weigh and then make a decision. Okay, thanks. Just regarding the phase III, so if there would be two studies for assessing DED? Yeah, it's a good question. As I mentioned earlier with the discussion with Dayan, you need two adequate and well-controlled trials to hit a sign and symptom twice. The most efficient way to do that is in two trials with co-primary endpoints. There is a strategy that says do four trials, one with sign, one with sign, one with symptom, one with symptom. I don't think that would be the approach we would take. I think we'd be looking to do two trials. 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 and well-controlled trials for the sign. you know, again, that's a discussion that has to take place. I would look at a minimum of two trials. Yes. Great. Thank you. Thank you. Our next question comes from Yi Chen with H.C. Wainwright. Your line is open. Thank you for taking my question. Based on the current results, how many patients do you think would need to be recruited for the pivotal study? In the current environment, how quickly can the study complete enrollment? Thank you. Thanks, Yi. We haven't done the power calculation. That'll obviously be a function. It won't be driven by the sign data, which you know 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. We obviously need to assess what's the effects difference and we know what the standard deviation is. In general, trials looking at symptoms, if you look at the Aldeyra data, those trials were on the order of 800 or 900 patients. That was probably. I'm sure that was driven by their need for symptoms. We haven't come up with those power calculations yet for us. 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. Okay. Thank you. Thank you. I'm currently showing no further questions at this time. This concludes today's conference call. Thank you for participating. You may now disconnect.