Great. Welcome, everyone. My name's Jessica Fye. I'm a biotech analyst at J.P. Morgan, and we're continuing the 43rd Annual Healthcare Conference today with Stoke. First, you're going to hear a presentation from the company, and then we're going to go into Q&A. And if you guys in the room have questions for the management team, just raise your hand. Someone will bring you a microphone, or alternatively, you can submit them via the portal, and I'll read them up here from the iPad. So with that, let me turn it over to Stoke's CEO, Dr. Ed Kaye.
Thank you, Jess. So my name is Edward Kaye, and I'm CEO here at Stoke Therapeutics. During this presentation, I will be making some forward-looking statements, so I'd refer you to our SEC documents for full disclosure. One of our goals, really, at Stoke is how do we upregulate protein production? Our goal as an RNA company is we are focused on upregulating protein. And the question is, how do we do that? Well, we do it by using the body's natural occurrence in a normal copy of the gene, splicing out a retained element and increasing the amount of protein that we can deliver. It's really a very elegant method to upregulate protein. And if you think of most of the companies in the field, everyone's trying to downregulate a toxic gene function. We're upregulating a protein.
We have a unique space in these RNA company platforms. What we do is we're, again, really focusing on diseases that we can make a difference by upregulating the protein. If we think about the advantage of this approach, I really think of it as a gene therapy light. It's a target approach, genetic approach, that we're really harnessing the body's own mechanisms and enhancing it. We're enhancing splicing to increase full-length message. There's some real advantages of this approach compared to other therapies, like, so to say, gene therapy or CRISPR. What we're doing is we're upregulating the normal copy of the gene to get it back up to 100% from a 50%. We do this by splicing. We're agnostic to any mutation.
And we also have the ability to be very specific in that we can increase the protein based on the dosing that we're giving. So it acts like a drug, but it's a genetic target. We also know that, very specifically, we increase only in those cells that naturally have the message. So we don't have a lot of off-target toxicity because we're upregulating in the wrong region. So, again, a lot of advantages of this approach. So as we think about what do we do with this interesting platform technology, well, we're very focused on Dravet syndrome and using our drug, zorevunersen, to upregulate the NaV1.1 protein. In addition to what we're doing in Dravet syndrome, we have an interesting program in OPA1 upregulation. And if people remember, OPA1 is one of the critical mitochondrial proteins that is responsible for the structure and function of protein.
What we've demonstrated in cells, we can increase ATP by upregulating this protein expression. Again, a very interesting product that we're looking at, autosomal dominant optic atrophy, but it has broad implications into other ophthalmologic diseases and potentially neurology diseases. We've also made, in this last year, some significant progress in our partner programs with Acadia. We have announced Rett and SYNGAP1 as programs that are really very, very interesting and can be addressed using our TANGO technology. What we've discovered is that if we look at SYNGAP1, there's a natural follow-on to what we're doing in Dravet. Very similar mechanism, similar neurologic disease with developmental epileptic encephalopathy. Also, it turns out it's as frequent as Dravet syndrome. The idea of going after developmental disorders using TANGO to upregulate is a way to get at these diseases that previously were thought to be undruggable.
One of the things that sometimes is a little daunting, when we look at genes that have a TANGO signature, we have 6,500 genes that we can go after. Needless to say, that's more than we could possibly do. We're looking for potential partners to help us unlock this potential. One of the things is what we really, what can we say that we have done this year? I think we've gotten a lot of interest in Dravet syndrome and the people, the clinicians, and certainly the families, because we have been able to demonstrate really interesting clinical data, not only for seizures, and it's really a dramatic reduction in seizures, but also a durable effect, which has not been seen before in Dravet. We've also been building out our team in preparation for a phase 3.
And we've had really very good interactions with the FDA, and we've been given Breakthrough Therapy Designation, which means that there is the potential that this could really show a substantial improvement in the current therapies for Dravet. So all of this has focused us on getting ready for a phase 3 and really trying to be the first company to have a disease-modifying therapy for Dravet in the clinic in a phase 3. So one of the things that we're often asked, well, Dravet is a rare disease, right? How many patients can you do? Can you do a clinical trial based on the population? And I think we've done a lot of work to really look at the prevalence of Dravet.
And if we look, we've seen over 38,000 patients that have been identified, spread equally between the U.S., the EU4, and the U.K., and also 7,000 patients that are expected to be in Japan. And again, the reason why there's such an interest in Dravet syndrome, there's such an unmet need that is not being addressed. And we believe that this approach that we're using can address a lot of the deficiencies of therapy in this disorder. So just to describe kind of the current landscape, if we think about trying to manage seizures for over 100 years, maybe 150 years ago when bromides were developed in the 1850s, we have done the same thing over and over again, repeated decade after decade. We give medicines that suppress electrical activity in the brain and control seizures.
The problem with that approach, it has a lot of side effects, a lot of changes in sedation and in cognition, so we're treating patients to control seizures, but we're creating another disease, and what is not available to date is there are no medicines that are designed to correct the underlying genetic cause of the disease. How do we treat the whole patient? How do we treat the syndrome and syndrome management? Not just one symptom, the entire patient, the entire syndrome, we think we can do this by using our TANGO approach, so one of the things that I learned, and I had the opportunity to actually treat patients with Dravet syndrome, and I will say, as a clinician, it's a very frustrating disease to treat, and why is that?
You have a normal child who unexpectedly develops a prolonged febrile seizure and goes into status epilepticus, goes to the hospital, and has to be treated with medication. You're not sure what the diagnosis is. You're put on an anti-seizure medication, and then it doesn't work, and then within a month or two, you get put on another anti-seizure medication that doesn't work, and then you go through a repetitive cycle of adding and subtracting drugs for years, and you never get the seizures under control. The problem also is that not only do we have a problem with the seizures. These children who were normal, and imagine you have a normal baby, and suddenly at nine months, it has this intractable seizure, and by two years, this child is not developing normally, and there's nothing that you can do to reverse this process.
So again, we have to do better in the treatment of Dravet syndrome. So we had showed back last month at the American Epilepsy Society some of the progress that were made in controlling the seizures. And what I'll say is that what we showed with a loading dose of 70 milligrams, either one, two, or three, given over a three-month period, we saw, again, a very dramatic reduction in seizures. And again, this is with single doses. We followed them for six months. I'll remind you that all of these patients are on multiple, multiple therapies. 75% were on three or more. 50% were on four or more medications. So despite putting more and more medications, they weren't getting better. When we add a single therapy, however, we do see a substantial reduction.
If we follow this same group of patients, and now we treat them not just simply with a loading dose, but we give them two doses of a 45 milligram maintenance dose, what we see is if we look at the two and three-dose patients, we see an 87% reduction in seizures at eight months. So again, this is really a substantial, but even more importantly, a sustained reduction. And remember what I said before, they would always have to be cycled in and out of other medicines. Now they're on a medicine that has maintained their seizure reduction for this period of time. So we have had the opportunity in an open-label extension to really follow these patients for a long time.
So on the top line, which is the orange line, we had patients that were on low doses of zorevunersen, 30 or 45 milligrams, and followed out for a couple of years. And the one thing we saw is that, again, it did not escape. There wasn't a tachyphylaxis or resistance to the seizure medication, the zorevunersen. If we look at the 70-milligram loading dose followed by two 45-milligram doses, again, we see a better reduction in seizures after that loading dose, but again, it's sustained, and it continues to show an effect. So we talked about the seizures, but the question is, what are we doing for the rest of the patient and the family? How are we making them better?
So one of the things that we've recently done is we had contacted 135 healthcare professionals, and we asked them, how do we make a better medicine for Dravet syndrome? What are the needs? And interesting, despite the fact that there's 20 or so different anti-seizure medications that are used, these healthcare providers said 75% of these patients, 75% said, we need to have a better seizure control. It's not good enough. 90% of the patients continue to have seizures despite being on multiple medications. The other important need that they identified is we do not have a treatment to really change the other aspects of the disease. There is no disease-modifying therapy. And they also concluded as a major problem, all of the existing therapies do not address the behavior or cognition problems.
Not surprisingly, 50% said a big problem that needs to be addressed is the side effects. It's the sedation and the lethargy that these drugs cause that is not helping the patients. So that's the problem that obviously we identified. So one question, how do we measure whether we're seeing an improvement in cognition and behavior? Well, fortunately, there are tests that are available. And we've previewed this in our behavior and our natural history study. We've used the Vineland-3. And what this is a very well-recognized test that is used to measure cognition and behavior, often in normal children. And it actually can be used from a newborn all the way to age 90. So it's a very sensitive test, but can be applied to a very broad age group.
If we look at the Vineland-3, what we can see is there are some core domains that are very, very important, things like communication, daily living skills, socialization, and optional domains that also are important for this, for Dravet, motor skills like gross and fine motor and maladaptive behavior. The nice thing about this test is it is recognized in many different languages. It's been validated, and it has been supported by the regulatory agencies and also by payers. It's a test that everyone recognizes that if you can show an improvement, it should predict these patients should be better. If we look at our testing using the Vineland-3, we were very, very pleased to see that not only did we see this 87% reduction in seizures, for the first time in this disease, what we identified were improvements in cognition and behavior.
If we look on the left side of the slide, within nine months, we were starting to see, again, improvements in expressive and receptive communication. We saw fine and gross motor improvements, again, nine months after starting therapy. When these patients rolled over with other patients who were in the open-label extension, many of which were treated with the lower doses, what we saw is that if you look at the top bar, the first year we saw, again, very significant improvements in many, really all of the domains that we had studied. But if you follow them for an additional 24 months, not only do they maintain that improvement, they continue to get better. So again, this is the first time that any therapy has addressed the challenges in cognition and behavior.
This is what I think the community has been looking for, and we're very hopeful that this will address those problems and get back to treating the entire patient. This is an example, and obviously this is not representative of our entire population that was treated, but what does a change in the Vineland score mean? How is it improving patients? Just to demonstrate, this is a 12-year-old girl who then was started in November of 2022. As you can see, her handwriting is really illegible, is misspelled, very, very difficult. But we can see nine months later, after starting on zorevunersen, we saw a much better improvement in the organization, in the ability to spell and to correctly write these words. The written communication in this child was dramatically improved within nine months.
These are the kind of examples that we're looking for, and we've seen in other patients. If we look at the safety exposure, we have had to date over 600 doses of zorevunersen administered. Overall, it's been generally well tolerated. What we saw in the phase 1/2A is about 30% of the patients experienced a study-related treatment emergent adverse effect. What we saw is a treatment emergent serious adverse event. We saw 22% of the patients. However, in only one patient was it related to study drug, and that was a patient who had experienced seizures. All of the other treatment emergent serious adverse events were related to the procedure, which was a lumbar puncture. Now, one consistent finding that we've seen in the open-label extension, we did see an increase in the CSF protein defined as greater than 50 mg%.
The question is, well, what does this mean? Why does it happen? We think it happens because there is a slight disruption of the blood-brain barrier with the intrathecal therapy that it causes some of the serum proteins to get in. There is no inflammation. There's no gamma globulins that are increased. There's no cells. And most importantly, it doesn't seem to appear any clinical symptoms. There's no clinical manifestations related to this. It does appear to be a laboratory finding. Only one patient was discontinued because of the increase in the CSF protein. We had recently announced, last week, in fact, an alignment for our regulatory study between three geographies, between the FDA in the U.S., the EMA in Europe, and the PMDA in Japan.
I would say, in my experience, and I've been doing this more years than I can count, I've never been able to get all three agencies combined in one trial. Now, the reason why this is important is it allows us to do a single trial, not two phase three trials, but a single trial, multiple geographies, and with the same endpoints, so that gives us a huge advantage to try to accelerate the development of this program, not having to do more than several studies in a single disease, so this was a, we consider this a big win, and obviously, we're very interested in getting the study up and running as quickly as possible, so to briefly give you a picture of what this phase three study looked like, there's one thing that's very, very different in this study.
This will be the longest study that has been done so far in Dravet syndrome, and the reason for the duration is we have to get in the label improvements in cognition and behavior. We have to be able to identify us and this drug as a disease-modifying therapy. Improvements in cognition and behavior will demonstrate that. This is not your grandfather's anti-seizure medication. This is something different. This is a genetic therapy, and what we're trying to do is not only dramatically improve the seizures, we're trying to make the cognition and behavior better, so in order to do that, it does take longer, and we will have an eight-week lead-up where we'll measure the amount of seizures that the patients naturally have, and then we'll look at seizure reduction after a 52-week treatment period.
We have two doses of a loading dose of 70 milligrams, two months apart, and then it's followed every four months with an additional two doses of 45 milligrams, which is the maintenance phase of the study. And if we look, the primary endpoint, not unexpectedly, is going to be a reduction in seizures. And again, what we're looking for, and this will be compared to a sham group, and we're going to be then looking also at key secondary endpoints. And these key secondary endpoints are going to be improvements in cognition and behavior in the Vineland-3. And again, I think one of the things that we were very pleased with is we had a lot of discussions, obviously, with the regulatory agencies. And the regulatory agencies were very encouraged that they wanted to demonstrate the improvements in cognition and behavior and have it in the label.
They saw the importance of this to be able to really talk about these improvements and to be able to get the medicine to patients with Dravet who will need it. So it was very productive discussions. We had no disagreement that the Vineland-3 would be acceptable in all jurisdictions. We also did, at the same time, a lot of payer research, both in the U.S. and in Europe and other regions. The payers were also in agreement that the Vineland-3 could be used to reimburse this as a disease-modifying therapy. So again, a big win for us to have agreement, not only in geographic areas for regulatory clearance, but to have payers say that this would be an important endpoint. So it's a one-to-one randomized sham control study. And as I said, it's two loading doses of 70 milligrams followed by two doses of 45.
And it would be a population from two to just under 18 years of age. To be qualified, you have to have a mutation in the SCN1A gene. So obviously, most of the patients have mutations that cause a loss of function in the SCN1A gene, and that will qualify you for the study. And then it is 150 patients randomized. It will be in the U.S., U.K., EU, and Japan. And again, a 52-week duration. So why do we think this is going to be a successful therapy? And why are we positioned and why are we so excited about what we're planning to do with zorevunersen? I think the ability to really change the natural history of this disease is exciting. And we believe it does represent a blockbuster potential. Why do we think that? First of all, the need is there.
We know that there are multiple anti-seizure medications, and even with the best available therapy, we still can't adequately control the seizures, and I think what we've also shown, our clinical data really is very, very supportive, not only in seizures, but improvements in cognition and behavior, so that makes us very optimistic about this study. The other thing that I think is very important is that we have had tremendous stakeholder support. When we talk with physicians, whether it's in Europe or the U.S. or Japan, everyone wants to be part of the study. People want to participate because they appreciate that this is a different way to treat epilepsy, and the patients are really excited to participate in this. Again, they want to have something that's better than what's currently available, so I think we're very excited about starting this phase 3.
We think this is going to be a significant advancement for Dravet syndrome, and that's why we're working so hard to get this phase 3 study up and running, so just to summarize, I think we are really focused certainly on Dravet syndrome, and it's something that we're utilizing all of our resources to get the study up and running and focusing on this, but we can't forget that we have the potential for a lot of other upregulating proteins and disease targets that we think we could help with that current therapy is not able to address, so we will be also looking at not only our OPA1 program. We're excited about our SYNGAP1 and Rett syndrome, and most importantly, we're looking in cardiac and renal and other indications where we have TANGO signatures on genes that we think that we could modify. Thank you very much.
Great. Thanks for the presentation. And as a reminder, any questions in the room, just raise your hand or submit them electronically. I'm curious, you reiterated that it's important to get the cognitive and behavior data in the label. Your primary endpoint is seizures. And I noticed the other drugs for Dravet are indicated for the treatment of seizures associated with Dravet. Is it possible that you could get a treatment of Dravet syndrome indication statement on your label?
Yeah, funny you should ask that. So in fact, when we got breakthrough therapy from the FDA, that's exactly what they said. So we currently are expected to be the only company that would have the treatment of Dravet syndrome rather than the treatment of seizures in Dravet. So that is our goal. And we think so far, the regulatory authorities, based on the breakthrough designation, are supportive of that.
You also flashed up some epi data, I think, talking about 38,000 patients. What proportion of those patients are represented in the age group you're going to be studying in this first pivotal trial?
Yeah, so it would be about 50% of that population would be in that age group. We have a commitment for a PIP, a pediatric investigational plan from PDCO and the EMA, to study patients under two. So those discussions are underway, and what that study would look like would be slightly different. But we would expect to have an experience in that younger population. And we're also having a lot of discussions about looking at adults. And one of the things that we've heard from the patient community is, please don't forget the adults. These patients are also desperately seeking improvements. And one of, I think, really interesting aspects about our phase one, phase two data, we saw very similar reductions in seizures, a little better in the younger group, but even in late teenagers, we saw very, very, very significant and sustained reductions in seizures.
But sometimes we saw even better improvements in cognition and behavior in the older population. So biologically, there's no real reason why we think that older patients and adults shouldn't respond to the therapy. So a lot of our work and working with Jason Hoitt, our new Head of Commercial, we're really getting in a disease awareness in the older population, doing more genetic testing, and really demonstrating. And we plan to have studies in the adult population.
And in addition to, we'll have 30 patients that will roll over in our open-label extension that will be adults. They started out as teenagers, but we'll have information as adults. So we think it's really, it's an obligation that we make sure we have information that patients who are older than 18 can have access to the drug. And that's obviously a sizable population that we want to make sure we don't forget.
Great. Can we spend a little time on the key powering assumptions for the MONARCH trial, both for the primary and key secondaries? In particular, I'm curious how you arrived at your assumptions for how the control arm will perform.
Yeah, I'll let Barry Ticho, our Chief Medical Officer, answer that.
Thank you. Yeah, so as you mentioned, there are two key endpoints that we're looking at. One is the seizure frequency, and the other is the Vineland. For the seizure frequency, we looked at what a range would be for potential placebo effect based on other phase 3 studies that have been done for Dravet syndrome. And that range is somewhere between 5% and 25% reduction. So we chose the upper end of that to be conservative and powered for potential for a 25% reduction, and then used the data that we've already shown in a similar population from our phase 1/2 studies to power what the expected effect would be. And so we arrived at the assumption there.
Also, because this is a single study, we are looking for a p-value of 0.01 to make extra sure that we would be able to achieve statistical significance and demonstrate the effect in just a single study. For the secondary endpoint, the Vineland, we used, first of all, the data that we have from the natural history study, which we ran with a very similar population looking over two years in those patients. And what we showed in that study was that on the Vineland scores, the patients really have very little, if any, change in their scores. Some of them even have a reduction in their scores over time. So we basically know that over that two-year period, and certainly within the one-year period that we're looking at for the study, we're not expecting to see much change there. Then we did allow for potential for a placebo effect.
So we added one to two points per subdomain there as a potential for placebo effect. And then we took the data that we already have. So in the same study population in our phase 1/2 and open-label extension study, we looked at what the changes were that we observed in the Vineland in those actual patients and used that as the effect there. Then we looked at the one subdomain that had the least change over that. We used that as our measure, and we powered against that. And so we came up with the 150 patients based on that. So we have adequate power, more than adequate power for both the primary and the secondary endpoints.
Yeah, so just maybe just simply to state it, what we've tried to do is to power the biggest problem is, of course, powering for the cognition and behavior. That's a more difficult objective to reach. But what we've done is we've powered it so that any way you look at the data, whether it's a combination, whether it's a key secondary or hierarchical, we've tried to make sure that we will get statistical significance based on the study design. And we feel so strongly about that, that we've probably over-enrolled to get there, but it's so critical we need to make sure we achieve that.
Do you need to achieve statistical significance, though? If you come close on these endpoints and you've got a substantial seizure benefit on top of best available therapies, is there flexibility with the regulators?
In the discussions we've had, to be clear, with the regulatory agencies, the focus has been trying to achieve basically statistical stat-sig. That has been our focus. In my experience, the phrase that the FDA uses, it's a review discussion, right? Sometimes there is more flexibility. I think what we're planning, our primary focus is we're going to reach stat-sig, and that's what we think. Is there some flexibility? I think there is. I think that's not our plan.
Okay. You have the breakthrough designation. Obviously, we've just had this conversation about the pivotal study you're going to run. Is there any possibility of filing in the U.S. prior to the full completion of the MONARCH trial?
The short answer would be yes, we could do that. The problem is, what is the problem if we did that? And I think what I've talked about repeatedly in the last discussion, if we did that, we would get approval just for seizures alone. And I think then we would have a price, as an example, that we'd be set as an anticonvulsant. Then we would have to go back and say, now we're going to add other endpoints of cognition and behavior, disease modification.
And I think there's no precedent in the U.S. that that's ever been done that you can suddenly change the price of that. And I think it's a short-term gain. And I think, what's the long-term play in here? And the long-term play is we need a drug that addresses the patient. The best way to do it is to have a thorough study that's long enough that we can include all the endpoints.
Okay. How should we think about the hierarchy of the various Vineland-3 subdomains that you're going to use to capture the non-seizure benefits in phase three?
I'll refer to Barry on that.
So the data that we have already in our phase 1/2 and open-label extension study shows that in the Vineland that has multiple different subdomains, we're showing improvement across many of those subdomains, and especially focused on the ones that are looking at expressive and receptive communication. We know that communication is an important aspect. In fact, when we surveyed families and when they've spoken to the FDA, they've said that second to seizures, the most important thing they want to be able to do is talk to their child and have their child understand them.
And so when we looked at the Vineland scores from the treatment with zorevunersen, we saw that among the highest increases in scores was in that communication group. As we mentioned before, though, we've powered the study to be able to look at all those different subdomains and achieve statistical significance regardless of, as I'd said, regardless if we do it as a composite or as a hierarchy. So we have confidence that we will be able to demonstrate an effect based on the number of patients we've enrolled in the study.
Okay. Given that this is the first potentially disease-modifying therapy for Dravet, what's a reasonable expectation for market penetration?
I can start, and I can ask Tommy to comment on this too. What we have heard from our investigators and also from the patients is they expected this to eventually be first-line therapy. Again, it's because it would be the best in class for seizure control. More importantly, it would be the only drug that's approaching and improving on the cognition and behavior. I think there's a very high likelihood that we'd have very good penetration. Obviously, we won't know until we see. One of the things that does suggest to give us some information, and we've heard from the patients that they will not go on other studies with experimental medicines and Dravet. They're waiting to go on our medicine. That does suggest that there's a lot of interest, and we think that a lot of—I think—the penetration would be quite high.
Yeah, and the only thing I would add to that, Jess, is, again, it's the first disease-modifying treatment for this product. As we hear from investors, from caregivers, from ACPs, the bottom line is if this drug is approved, it's hard to understand why people wouldn't put their child, their children on this drug. And so we feel very confident that market penetration should be very high, and we should have a relatively aggressive ramp in terms of our sales.
Got it. So you talked about kind of interest in the product. How should we think about enrollment timelines for your trial?
Yeah, I can start, and Barry can certainly comment. Obviously, the challenge we've had, we just had the protocol. We've had feedback from the regulatory authority. So it was at the end of the month. So we're doing a lot of work to try to predict timelines. What we can't shorten is that 60-week trial. That obviously is part of the clinical design, and that's what we have to deal with. So it's a longer study than typical for Dravet syndrome.
We're working very hard to really reduce the timelines, typically in a four- to six-month lead time. We think we can do better than that, but that was the guidance that we have given. And our estimate now is really a one-year enrollment. We're working very hard based on all the recent information we've had from patients and caregivers. We may be able to do better. So it is a lengthy timeline overall, just because of the size of the study and the duration. We're doing everything we can to try to get this out to patients as quickly as possible.
About a year for enrollment?
For about a year, yes.
How does your ASO technology differ from the technology for ETX101?
Yeah, and maybe I'll let Barry talk about that.
Yeah, as I'd mentioned early on in the introduction, the zorevunersen mechanism of action will raise the protein levels of the sodium channel in the cells that are intending to make that protein and in the nerve cells where the sodium channel and that 1.1 is supposed to be. And we've tailored the amount of drug that we administer to achieve that doubling that's necessary to get back up to normal. The Encoded product is another factor that can increase the protein levels. It is not as selective, we think, in terms of cells that expresses it and does not necessarily distribute to the whole brain.
We know that, given studies that we've done, that zorevunersen can get to all parts of the brain. Dravet syndrome is a disease that affects all parts of the brain. It's important to make sure that we can get that medicine to the different parts in order to really treat the entire syndrome. That's why we think we have a disease-modifying therapy, because we're able to address the disease throughout the entire part of the syndrome.
You guys have talked about the possibility that you'll need more money to take the pivotal trial through to completion. But there's more than one way to bring money into the company. So what are the different options you're thinking about?
Yeah. Yeah, so look, I think there are multiple levers any company can pull in terms of being able to raise the capital or produce the resources that you need to get through something like a phase 3. I think we're very fortunate to have a highly differentiated product with a large unmet need, a large market potential where there's a significant amount of strategic interest around our asset. And so we're going to continue to explore potential relationships where we look at ex-US, potential BD here. There's other ways to monetize our platform. But in terms of the capital we raise, we feel confident that we could end up doing a potential deal if the economics are right that could actually fund the trial for the most part.
Great. Okay, so we're about out of time, so we'll stop there. Thank you.
All right. Thank you.
Thanks, Jess.