Capricor Therapeutics, Inc. (CAPR) Earnings Call Transcript & Summary

Greetings, and welcome to the Capricor presentation of CAP-1002 open-label extension study results. [Operator Instructions] As a reminder, this conference is being recorded. I would now like to turn the conference over to your host, A.J. Bergmann, Capricor's CFO. Thank you. You may begin.

Thank you, and good morning, everyone. Before we start, I would like to state that we will be making certain forward-looking statements during today's presentation. These statements may include statements regarding, among other things, the efficacy, safety and intended utilization of our product candidates, our future R&D plans, including our anticipated conduct and timing of preclinical and clinical studies, our plans to present or report additional data, our plans regarding regulatory filings, potential regulatory developments involving our product candidates, potential milestone payments and/or our possible uses of existing cash and investment resources. These forward-looking statements are based on current information, assumptions and expectations that are subject to change and involve a number of risks and uncertainties that may cause actual results to differ materially from those contained in the forward-looking statements. These and other risks are described in our periodic filings made with the SEC, including our quarterly and annual reports. You are cautioned not to place undue reliance on these forward-looking statements, and we disclaim any obligation to update such statements. With that, I'll turn the call over to Linda Marbán, CEO.

Good morning, and thank you very much for joining us today. Today is a very exciting day not only for Capricor, but most importantly for the Duchenne community as we share with you the data from the open-label extension trial as part of the HOPE-2 clinical study. This is our standard forward-looking statement slide, which A.J. just shared with you. We are CAPR and NASDAQ listed. So today, I am joined by my colleague, Dr. Dan Paulson, our Vice President of Clinical Development; A.J., who you just heard, our CFO; Dr. Craig McDonald, our National PI and adviser to Capricor over these several years through the HOPE-2 open-label extension as a national PI of the upcoming HOPE-3 clinical trial. Dr. McDonald, as you well know, is a leader in the space in terms of clinical trial design and implementation in Duchenne muscular dystrophy. And Dr. Suzanne Hendrix, the CEO of Pentara Statistical Group; Suzanne has not only done the analysis for this open-label extension, but also a co-author and the lead statistician on the HOPE-2 program, which was recently published in The Lancet. So we certainly have a good team here today to share with you the data and to answer any questions you might have. So let me just remind you of the mechanism of action of CAP-1002. CAP-1002 is an allogeneic, which means off-the-shelf cardiosphere-derived cells product. It is a cell therapy that is not a stem cell. It does not work by grafting into host tissues or becoming part of a functioning or injure tissue. What it does is it secrete exosome. And as you may remember, exosomes are nanometer size with the bilayer vesicles that contain molecules such as microRNAs, noncoding RNA and proteins that drive biologic responses. The primary mechanism of action of CAP-1002 unlike anything else that is currently under investigation or available in the Duchenne muscular dystrophy space is its immunomodulatory capabilities. It antifibrotic properties and its pro-regenerative property, all of them leading to the disease-modifying behavior that you're going to see today. The cells are made from transplant qualified hearts. That means these hearts to be used for transplant but are not able to be done so due to technical reasons. The most common situation is that about 40% of hearts are not qualified for transplant and we are able [indiscernible] use these to make CAP-1002. So there will not be a supply or demand issue as demand increases and commercialization occur. So one of the great things about CAP-1002 is how easy it is to deliver to patients. It does not require a significant amount of time as patients get it once every quarter. It's about a 45-minute infusion that requires a simple oral premedication regimen prior to the infusion. As a result of this premedication regimen and the years of study has had a strong safety profile with no treatment-related SAEs reported through 94 infusions in the HOPE-2 open-label extension and several hundred infusions prior to that. So we have a very good safety profile, very easy to adopt treatment opportunity for patients with DMD and beyond. So let me just highlight the patients that CAP-1002 is being targeted at this current time. We are going primarily for those that are in the later stage of the disease process, those that are at the loss of ambulation. That means that they're dependent on a wheelchair to get around. Now that means that they have probably half their lives or more in front of them. And they have a tremendous amount of quality of life ahead of them, which we are working hard to preserve -- looking to preserve upper limb function. Upper limb function means that they can move their wheelchair. It means that they can watch TV by using a remote control. It means they can play on their phones, use their computers and tend to their personal needs such as brushing their hair or using the bathroom. So we are highly committed to this patient population for the more than 15 years of life that they probably or hopefully have ahead of them. And let's remember that over 50% of DMD patients in the United States alone are non ambulant. So because we are working with those patients that are primarily non ambulant. We needed to find a measure in which we could quantify progression of the disease or tenuation of disease progression that focus on the upper limb because they were unable to do, for instance, any type of ambulatory assessments such as the 6-minute walk or the North Star Ambulatory Assessment, which you may be more familiar with. The performance of the upper limb is a scale of 21 items that was developed by physicians, physical therapists and patients themselves and what they do is they basically take and turn activities of daily living into some measures that can be quantified. So for instance, I will call your attention to lifting light and heavy can that would be analogous to drinking a cup of coffee or a bottle of water. And as all others of these are exactly of that same type of paradigm where they can be quantified, measured analyzed and qualified based on scientific measurement, but also relate directly back to the quality of life of the patient. So we have used the performance of the upper limb to measure skeletal muscle function and hope to [ send ] our first clinical trial. HOPE-2, the Phase II study published in The Lancet and now the HOPE-2 open-label extension. And now I'm going to walk you through the data and to keep your eye on the ball in terms of this very important measure of upper limb function and activity of daily living. First, I'd like to just refresh your memory on the data from the HOPE-2 clinical study. This data was published in The Lancet earlier this year, and we were very pleased to see that the performance of the upper limb 2.0 had a statistically significant improvement in treated patients compared to placebo patients. So as you may recall, HOPE-2 was a randomized, double-blind, placebo-controlled trial in which patients were randomized either to receive 150 million cells of CAP-1002 quarterly in the infusion protocol I shared earlier or the same type of paradigm for placebo. The performance of the upper limb PUL 2.0 is the data that I'm going to be showing you today, the primary efficacy endpoint of the HOPE-2 clinical trial was a performance of the upper limb mid-level 1.2, and all the details of that study, as I said, can be found in The Lancet paper. What I want to highlight for you today, however, is the ejection fraction improvement in HOPE-2. We saw 107% slowing of the disease process of this very important measure of cardiac function in the treated patients compared to the placebo patients. What this means is that we are actually slowing the progression of the cardiomyopathy which currently is the #1 cause of death in these boys and young men. So as you can imagine, while skeletal muscle performance is of great importance, also maintaining life by maintaining their heart function is probably the most important thing that's on their mind. And I just wanted to highlight this very important bioactivity of CAP-1002 in the treated patients. We did not measure cardiac function in the open-label extension, and I'll explain why in this slide shown here. So I want to take you through this slide, and I want you to highlight for you the 3 phases that I'm going to be talking to you about today. One is the HOPE-2 clinical trial. I just showed you some data from that, and remember that was the randomized double-blind placebo-controlled portion of that study. Then patients went into a relatively long, what we call gap phase, which was a little over a year, the average was 392 days. This was the time from the end of the HOPE-2 study when we were getting the open-label extension portion of the study up and running, analyzing the data and bringing all potential patients back in for the open-label extension. So we did several things, which we thought were very important in building this open-label extension study so that we can have more data to support CAP-1002 and DMD. The first thing is, is the patients have never been unblinded. So to this day, patients don't know their original treatment group. We were able to do this by suggesting that all patients was -- that they were placebo-treated or in CAP-1002 could be eligible for the open-label extension study. 13 patients out of the original 20 took this opportunity and they were nearly evenly divided with 6 CAP-1002 patients and 7 placebo patients, one patient [ withdrew ] early on. The average age was 13 years, by now all were non ambulant and all were on a stable regimen of corticosteroid. So on the next slide, I'm going to start walking you through the data that we acquired through this open-label extension study in which we built a statistical analysis plan and very carefully collected and analyzed the data. We used the full PUL 2.0, the data that you just saw in the previous slide as a measure of skeletal muscle function, and I'm very, very pleased to share this data with you over the next few slides. So shown here in this slide is probably the most important data that [ Glen ] showed you today. What it shows is what happens to the patients that were on placebo and then what happens to those patients when they're off any type of treatment and then what happens to them when they go on CAP-1002 now in these patients for the very first time. So what you can see is shown in red, and the thick line is when they're in the placebo phase, the first year of HOPE-2 the second year, which is the dotted line is the gap or the time off of any type of therapy. And then the third here shown in blue is when they have had CAP-1002 made available to them. And what I'd like to call your attention to, which is probably the most important thing is that the red line, the time that the patients were on placebo were off therapy mirror natural history of the disease. And this has been published and well known by Marika Payne as well as [ Anna Maughan ] and colleagues to show the natural history decline of non-ambulant patients with DMD. And what we show is that our patients within the HOPE-2 and HOPE-2 open-label extension study show that same paradigm. But then you see what I call the hockey stick type of paradigm here, which is an actual delay in the progression of the disease. And you'll see in the next few minutes by nearly 70% but I'd like to also call your attention to on this slide is that the change happens within the first 3 months of treatment. So it's soon as the patients go on CAP-1002, the patients start to slow down the progression of their disease. And that is the reason that we must work very hard to get this therapy to all patients with DMD as quickly as possible. Now what happened to the other group to the patients that were originally on CAP-1002, that's highlighted in this slide here. And I'd like to call your attention to the 2 lines that you see. So the first line that you see in blue at the top and the corresponding thick red line staff that -- these represent the HOPE-2 study. Then in the dotted red lines, both on the top and on the bottom is the gap phase. And then in blue, at the bottom, you can see the open-label extension data, those patients that came back on to CAP-1002, which I've just described. And what you can see here is that if you were in the original treatment group, essentially, you have a light up, so to speak, in delaying the course of the disease. And the area between these 2 lines is actually the preservation of skeletal muscle function. That means that we are seeing here disease-modifying behavior. This is not just symptomatic, make you better for a short time and go away type of therapy. This is where you're seeing the patients that have the delay in the decline of the disease, even in the year that they're off and they're declining, they're going down, and you'll see in the next slide in a very similar fashion, they are going down, but they don't go down as far. So I'm going to ask you to put in your mind the idea that if these patients that have stayed on CAP-1002 for this entire time, in this 3 years of study, think about where that line would take them, and I'm going to show you that hypothesis-driven digestion in the next couple of slides. So on this slide, and it's a complicated graphic, so I'm going to take you through it relatively slowly. Because I think that this is another supporting statement in terms of the fact that CAP-1002 is changing the course of the progression of Duchenne muscular dystrophy in the patients that received it in the clinical trial open-label extension. The blue box shows the statistical significance of the data, and I'll talk to you about that in the next few minutes. And these was a prespecified or primary endpoint of this clinical trial. And you can see that the chance that this data was acquired by chance is extremely low. So I want to call your attention to on this particular slide are the slope of the line. Again, you see on the left for your reference, the data from the HOPE-2 clinical trial, always shown in the followed line in blue are the CAP-1002-treated patients and in red are the placebo-treated patients. And you can see again that this is similar to the natural history of decline. If you look at the slope of the line at the time off of CAP-1002, they pretty much near what you see in terms of the natural history of the placebo group. There is a steady and precipitous decline even if you receive CAP-1002 in the first year. So you are better off receiving CAP-1002, but ultimately, if you stay off of CAP-1002 you're going to be back where your co-trial participants who received placebo were, which is in a steady precipitous downward decline in this chronic progressive disease. However, when you look at the PUL open-label extension data shown in the far right in blue, and you compare that slope to the HOPE-2 data, you again see a very similar slope, a slowing of the rate of the decline of the disease. So this data is very powerful because you see a very steady decline when off therapy or receiving placebo and yet you see a significant and very marked and clinically significant, I might point out, not just statistically significant delay in the decline of the disease. So now let me talk to you about the clinical significance of the statistical data that I have just shown you. It's shown in this slide here. And the slide here is one that makes a very important point, shown in blue and red is the HOPE-2 clinical data. As we mentioned, we published it in The Lancet, we have a slowing of the disease by approximately 70%. That means for every year on treatment. You're preserving 8 months of function on the performance of the upper limb scale. Now I'd like you to imagine the benefits of preserving skeletal muscle function for these patients over a 3-year uninterrupted course of treatment, potentially preventing up to 2 years of functional decline. That would be analogous to, for instance, 9 points on the performance of the upper limb scale, which could be related to being able to, as I said, drink a cup of coffee or a bottle of water or push an elevator button or move your wheelchair or feed yourself or, as I said, it's the parent product for muscular dystrophy meeting, and I think really took the community quite by store, which was the concept of being able to hug a family member, use your arms to convey affection, a very important part of our human experience. So taken together, we're showing a very relevant and important impact of CAP-1002 on the disease progression, disease modifying activity of CAP-1002 and DMD. And this supports HOPE Duchenne, HOPE-2. And now we have open-label extension, which allows each patient to be compared back to themselves. We have [indiscernible] a muscle and -- point of phrase internally that time is muscle for DMD patients. And we will continue to move that forward as we continue the journey with CAP-1002 towards approval for all patients with DMD. Patients on therapy experienced a slower progression of their disease. I showed you that in the previous slide, there's an urgency, obviously, to initiate therapy. You saw that. Remember, the area between the curves and preserved muscle function. So treatment benefits are maintained and loss of PUL points are never recovered. And there's a potential sustained benefit because we see a durable benefit of treatment in 2 years, suggesting that even when you're off CAP-1002, you're still better off, but you need to get on it to keep that muscle function going. Remember that the safety profile of CAP-1002 has been reinforced over 90 infusions in the open-label extension and more to come, by the way, as we go through year 2 and year 3 of open-label extension, stay tuned for more data coming from us on this open-label extension program. I want to remind you of the cardiac benefit in HOPE-2. We'll be measuring that again in HOPE-3. Our pivotal Phase III clinical trial is open for enrollment. That's a 70-patient randomized double-blind placebo-controlled trial that will be conducted at 20 to 30 sites in the United States. And the primary efficacy endpoint of that clinical trial is the performance of the upper limb at 12 months which, as you've seen today and has been published was statistically significant and HOPE-2 is statistically significant in the open-label extension. And so we go into this Phase III clinical trial with very high hopes with CAP-1002 and DMD. We are positioning CAP-1002 as an opportunity for backbone therapy in Duchenne muscular dystrophy. We see whether your patients or whether patients are on Exon Skipping treatments potential gene therapy treatment, steroids, which all of our patients are required to be on series, so that's getting the best standard of care possible or any other therapeutics that are currently under investigation or coming up for approval. You can see this giant plus sign, which shows that we believe that CAP-1002 can be used with any one of these and will likely be additive in the armamentarium of treatment opportunities for Duchenne muscular dystrophy patients. I'd like to close out by thanking all of the patients and their families. Of course, we can't gather this data and move it forward without there -- without them giving us the opportunity to test CAP-1002 in them. And what I can say is those that are receiving CAP-1002 are continuing to be very bullish on the opportunity to do so, and that's why we've decided to continue the open-label extension for several more years. We have the parent product and muscular dystrophy to [indiscernible]. And then I have Dr. Craig McDonald, our National PI on the line. I was going to ask Dr. McDonald to make a few comments today just to close out this presentation. Dr. McDonald.

Yes. Thanks, Linda. And that was really a very exciting data, and I've had the privilege of treating about, I believe, it's 9 patients as part of the open-label extension. Some of these patients are flying to California from Seattle, from Texas, really from all over the Western United States in order to receive the CAP-1002 treatment. We have also, during the open-label extension, we have employed some other novel endpoints. The Duchenne video assessment has been done as a pilot measure. And we actually have been able to collect some pretty impressive videos really demonstrating preservation of function in these patients on some novel tasks in terms of a trunk positioning and trunk movement. One of the most important aspects of the quality of life of these patients is the ability to position themselves in bad. And so we actually have some videos that would that would demonstrate some improved debility to maintain truck positioning. And we will be incorporating the Duchenne video assessment as a secondary endpoint and some of the subscales will be exploratory endpoints in the HOPE-3 trial, I think there are several sites that are activated now. We have a long list of patients who are really lining up to be in this HOPE-3 trial, which we're really excited to participate. And I'm just really excited about this open-label extension data because it really gives us unforeseen opportunity just because of this gap phase, this prolonged period off treatment for patients to really demonstrate the ability of CAP-1002 to actually preserve function and slow the progression of the disease even in a fairly progressed more severely affected patients. And I think the data lines up really quite well with our HOPE-2 data which was published in The Lancet. So I'm really quite encouraged by these data. I'm excited to get started with the HOPE-3 trial. Because as Linda said, probably 60% of our entire DMD population is non-ambulatory and so this is an incredibly important therapeutic on top of standard of care for this population. But thanks, Linda.

Thank you, Craig, and thank you for those remarks. And mostly thank you for continuing to be such a great colleague throughout this process. All right. Any more questions?

[Operator Instructions] Our first question comes from the line of Joe Pantginis with H.C. Wainwright.

And a very exciting update, and thanks for sharing the details. A couple of questions, if you don't mind. So first, can you just remind us right now with regard to the blinding, is it just the patients that remain blinded?

No. The investigators remain blinded as well. So the only unblinding has been done by the statistical group and then, of course, the company.

Okay. So that helps my next question. So I guess, even maybe for Dr. McDonald. Any -- so it's nice you're using the video assessment and what have you, and you shared some anecdotes, any sort of more specific anecdotes you can share about the general population since you don't know their treatment status with regard to, say, tying it directly to what the point change in the PUL means, like any specific examples you can share?

Yes. No, that's a great question. And I think certainly what's been -- we don't know who originally was in the placebo group or the treated group. I will say, though, that after this gap phase, what I'm noticing is patients are definitely appreciating the ease of movement in particular, what I'm impressed with is the number of patients that continue to be able to get their hand to their mouth for independent feeding and to be able to scratch their nose or -- and so I'm really quite impressed with that. That's actually one of the key milestones in Duchenne muscular dystrophy, disease progression is the loss of the ability to get the hand to the mouth that's something that we can easily assess in clinic. And it's an item that's actually been noted to be either the most important or the second most important item to quality of life in Duchenne patients as well as their caregivers. I'm also impressed with just the ability of patients to move their trunk forward and then move their trunk back and in general, I think the -- just the ease of movement and the quality of the movement, there's one of these video movements -- video assessments, that's called the Eat 10 Bites. And so we actually videotaped the patients sequentially taking 10 bites of food and just the ease at which they're able to do that without assistance by a caregiver is pretty noticeable to the clinician. I've seen some of these videos. So those are just a few examples, I think, clinically.

No, that's very helpful. And hopefully, that certainly correlates with the slope data that you were talking about. And I guess talking specifically to the slopes and I think it's pretty encouraging to see that the gap off phase really mimics the natural history. So I appreciate hearing those comments. So I guess Linda and Dr. McDonald, when you look at the cardiac data in HOPE-2 and I'm going to make an assumption here, and I know assumptions can be dangerous. Is it possible that during the gap off phase that the cardiac decline just passes a particular threshold that you wouldn't then be able to say rescue?

Yes, I think that's a good point. I think certainly, when you get down below 30% ejection fractions or 35% ejection fractions, there's a possibility that we may actually reach a point where it will be very difficult to rescue heart function and keep them from developing symptomatic heart failure in the future. But we -- the hope is that we would be able to actually collect some cardiac MRI data at the end of their 2-year open-label extension phase or at a time when they're sort of approaching around their 2-year end mark. And we have their cardiac data at the end of the HOPE-2 trial. And so I think we will be able to capture some additional cardiac slope data. That would be our hope.

Got it. Got it. And then just lastly, I mean, it's very encouraging to hear you say that the -- that there's a very -- how do you put, an increasing backlog of patients to be able to get into HOPE-3. So that's very good to hear. I'm hoping that's translating to additional centers as well. What would you and/or the company consider the rate limiting steps to get these patients in as soon as possible?

Well, I think from my point of view, a Linda can speak to this. I think just getting sites activation and site initiation is probably one challenge that we all have. There's a number of Duchenne muscular dystrophy clinical trials being conducted. I will say that this HOPE-2 and HOPE-3 trial designs are sort of being used as the model trial designs by the Duchenne scientific community for non-ambulatory clinical trials that are focused on upper limb and cardiac outcomes. So I think certainly, the sponsors that are focused on gene therapy trials are really, I think, borrowing from our successes in trial design thus far with HOPE-2 and they're paying attention to what's being done for HOPE-3. But Linda, can you comment on just what you feel or some of the greatest challenges or hurdles?

Yes. I think, Joe, that's the only 1 there as you know, getting sites up and running, and it's not even competitive trials at this point. It's just -- through the pandemic, a lot of people are working from home, a lot of turnover and staff has occurred at different centers. And we're using a lot of the same centers as HOPE-2, and the PIs couldn't be more enthusiastic as you can imagine. And of course, the families are lining up. It's going to be just a matter of the logistics of getting the site sort of -- it's like pulling the [indiscernible] chain on the lawn mower, getting that engine going. And once we get going, it should go very well. I just want to hark back for a moment to the ejection fraction question as well, Joe. And that is, I think within the field, and that's why we are positioning CAP-1002 as backbone therapy is the thought that if these other therapeutics start to work in terms of creation of dystrophin and preservation of skeletal muscle function, even in younger kids, it's going to be more important than ever to sustain ejection fraction or cardiac performance because they're going to need their hearts more. Right now, the loads on their hearts are pretty low once they're non-ambulant. And I think a lot of the cardiologists in the field are laser focusing on anything that will help stabilize cardiac function.

Perfect. I really appreciate all the details and definitely a nice start to a great day in New York.

[Operator Instructions] Our next question comes from the line of Alan Leong with BioWatch News.

Congratulations on the data. One thing that's clear or seems clear from the OLE data that earlier treatment is better treatment. Now that you've seen this, how do you now think about someday expanding to other disease stages especially earlier disease stages in the future?

I'm sorry, say that again.

Well, okay. You have additional argument for earlier, earlier treatment is better treatment. And in light of that, how do you now think about someday expanding to earlier disease stages?

Yes. Well, of course, the earlier that we can get CAP-1002 to patients the greater the likelihood of sustaining their function. And we're going to be focused first on our non-ambulant patient population. That's going to be our first path to approval. And then we have every opportunity that we can to expand the indication we will take.

Yes, if I could just comment. In the HOPE-3 trial, we are including patients that reach a 10 seconds -- 10-meter walk time, which has been a milestone for being -- at least 2 years from loss of ambulation. So we're starting to expand into that transitional phase of late ambulation and those patients would have more preserved upper limb function but from -- I agree with you from my perspective, I think, ultimately, younger children could potentially be treated with this therapeutic. I think, first and foremost, we'll have to generate some additional safety and dosing data in those populations. But I think certainly as a clinician, I would want to try to treat patients earlier in the course of the disease. I think from a trial design perspective, there's a lot of competing therapeutics in that -- in those ambulatory populations that will have to be considered as we approach that from a trial design perspective.

Thank you Craig, that was helpful.

When we think of combination therapies, we often think of additive effects. Is there a way to think of combinations with CAP-1002 that really creates synergetic effects, for example, 1 plus 2 equals 3. I think, Linda, you used to talk about anti-inflammatory properties helping to boost the other drugs. For example, what could it -- is there a way that might increase the impact of the Exon-Skipping drugs?

Yes. So we've obviously been aware of this opportunity over the years of the development of CAP-1002. We have a unique mechanism of action, as I mentioned, immunomodulatory, anti-fibrotic and pro-regenerative. And by pro-regenerative, what we mean is it drives the endogenous skeletal muscle cells back into the cell cycle. We have data internally, which shows that the exosomes are taken up by the skeletal muscle stem cells and actually drive them to make new healthy muscle. We, of course, believe that there's going to be synergy. We have some preclinical data that we've collected over the years to suggest that and look forward to that opportunity as more and more therapeutics get approved for Duchenne to see that opportunity in patients.

Yes. I think a potential synergy from my mind, would be dystrophin expression. I think the microRNAs that are contained in CAP-1002 actually or some of the micro RNAs that have been associated with dystrophin expression that can be modulated by and of [indiscernible] modulation and so forth. So I wouldn't be surprised if ultimately we see enhanced dystrophin expression with [Technical Difficulty] low levels of dystrophin. Also, I think it potentially could enhance dystrophin stability and microdystrophin stability with gene therapy approaches. So I think there are definitely real opportunities here for synergies.

Congratulations again.

Thanks, Alan. We appreciate it.

[Operator Instructions] our next question comes from the line of Jason McCarthy with Maxim Group.

It's Chad [indiscernible] for Jason. I'm sorry if I may have missed this, but was there an update on enrollment and estate timeline for initiating the Phase III study?

Yes. We haven't talked about initiating enrollment yet, and we'll be looking for those opportunities very soon. So stay tuned. We expect HOPE-3 to get going very shortly, and we'll provide updates as they become available.

Ladies and gentlemen, this concludes our question-and-answer session. I'll turn the floor back to management for any final comments.

Thank you very much for joining our call today. We remain very optimistic about the future for CAP-1002 in DMD and look forward to providing you updates both on the continuing open-label extension than the HOPE-3 clinical trial and other updates from the company as they become available. I would like to thank Dr. Craig McDonald, our national PI for joining us today and for his very important comments and also for his sort of providing the context to the space, which is, of course, the most important. And Dr. Suzanne Hendrix for being available for statistical related questions, and look forward to seeing you around in New York as time goes on. Thank you.

Thank you. This concludes today's conference. You may disconnect your lines at this time. Thank you for your participation.