Good. All right. Thanks, everyone. I appreciate being here. I see a lot of familiar faces here. Sorry, I was literally running from another meeting, which probably people are here. My apologies for the lack of breath on this beautiful day outside, but not here and not at the market so much. Talk a little bit about Praxis and why we're so excited about the step forwards for the company and what we have in stock. We're going to be making some forward-looking statements. Please check our SEC disclosures in the EDGAR system. Why are we here so excited about what we have at the moment in the company? We have these four late-stage assets, tons of readouts in the next several months and years to come, two platforms enabling them.
Quite importantly, I think at these markets, at this point in time in our cycle in biotech, we can execute all of that with the cash we have in hand. We're being arguably, and I think we all agree, fairly disciplined about deployment of capital, driving clinical execution across the board, being very diligent on how we look into the science and execution in general. That is what enabled us to be in this very strong position here today. The principles by which the company was once created as an idea and then put together, and to the stage we are right now, are still pretty solid. We're looking through genetics to indicate whether or not a given pathway, biology in the brain, channel, neurotransmitter, you name it, is important. We try to understand how the genetics might be disturbed and use that as information for drug development in general.
You heard me saying this before. I'm certain we care a disproportional amount for the patients. The ones that are on the market are being served by different drugs right now, incomplete treatments in most of the case, or all the cases in the drugs we're developing. Particularly their inputs and how clinical development and potentially commercialization of this drug should be. It's not only writing the wall. It's something we care quite importantly and fundamentally in everything we do. Where does it lead us? Where are we right now in the company? I'm going to go very quickly through the platforms. We have two very active platforms in terms of clinical developments and discovery. Arguably, most of the programs to date have been on the top here on the small molecule Cerebrum platform. I'm going to go through a bunch of them in a minute.
The Solidus is maturing quite fast. They serve different purposes. There are different ways when you look into a target, when you look into a disease, on picking what might be most beneficial for patients. That is what we're looking for here. We mix and match to some extent what serves patients the best and try to address that very diligently and quite rapidly if we can. When we look into the catalyst, which is kind of important for all of us here in this room, in the webcast as well, there are a number of things coming up in the coming months, in the coming years that are really exciting. I'll focus most of the conversation today on the lead assets in epilepsy.
It's quite important, I think, number one, for better we became as a society, as drug developers, as companies on developing drugs, on commercializing drugs in epilepsy. It's still quite depressing the amount of patients that don't get resolution or even amelioration to begin with what's happening. The words medical unmet need or the term medical unmet need has thrown out there a lot. Fundamentally, epilepsy is still a massive market in that regard. We're going to explore a little bit each one of them. Probably the focus of most of you, and definitely the focus of most of my conversations here in the conference today, have been over Vormatrigine. Understandably so. This is a quite unique drug with a very exquisite profile. The next catalyst for the company is in relation to Vormatrigine as well.
As you can see there, we have three drug-related outcome studies where we have an active. It's POWER1 , POWER2 , and RADIANT. RADIANT is the most imminent readouts. We also have something quite important here since a lot of the questions I get throughout the interactions with all of you is the pace of enrollments, the fact that we continuously deliver quite, I would say, outside of the average, outside of the norm, delivering different disease stages for clinical research is on EMPOWER. EMPOWER was a very unique initiative that we decided to do not that long ago to understand better, number one, what patients with epilepsy need, and number two, if they would be willing to participate in one of the trials below. That is enabling and helping us quite a lot with the recruitments on those studies.
Next, we're going to review a little bit about Relutrigine. While there are a lot of options and a lot of understanding for focal onset seizures, for primary and secondary generalized seizures, for Relutrigine, there's really nothing that is quite as effective as we expect this to be for Relutrigine in this space on GE. Quite complementary to current approaches, but quite different from what we're expecting here moving forwards. We're going to touch very quickly on Ulixacaltamide. As we just had some news recently, I'm just going to address what the next steps are there. I think for all intention and purpose, there is a zero in our model. It should be a zero in everyone's model right now. Just to do a little quick update on where we are there, wrapping up those studies and close down with our ASO platform.
This is one of the reasons why from a value creation perspective, we should be incredibly excited about these markets. For Vormatrigine alone, when you look into the prevalence of focal onset seizures and generalized seizures in the U.S. in general, it is a multi-billion dollar opportunity. It is a little bit sad to be here four or five decades after the first kind of commercial mainstream drugs being launched, saying that there is still this size of a market for new drugs to enter. The actual very first description of a pharmacological treatment was done more than 100 years ago for epilepsy. We are really at the point that we understand the disease better, we understand the mechanism better, and we can get to these patients to a significantly more comfortable place in terms of seizure reduction and other.
What has been underestimated, I would argue, until recent acquisitions in this space is the play or the size of the GE market. I think for the longest time, most of us were paying attention to these large indications and somewhat neglecting the needs for these patients with GE and just the fact that nothing really helps them. We had the likes of GW did a really good job in the first Zogenix and most recent Longboard kind of continue to elevate the profile, at least on our markets for that. I think right now we can quite confidently say there is a quite important opportunity, quite massive opportunity to be explored. Likewise, I don't have to tell all of you how important it is when you can deliver a disease-modifying antisense oligonucleotide to patients.
It's been quite challenging in CNS, but we have fascinating and quite positive early results for Elsunersen . I'm going to review in a second. This base here is what feeds the previous slides that I was telling all of you in terms of just how positive the developments on the next several months and years can be for the company if you solely focus on epilepsy. That does not account for any of the new molecules that we have preclinically to move to the clinic. That is only drugs that are on the clinic right now. Maybe spending a few minutes on Vormatrigine. When we first thought about the idea of Vormatrigine, it sounded a little bit out there. Can we modulate something that we know to be incredibly important for controlling seizures?
One of the ways I oftentimes talk about this is you cannot have a seizure if you actually block sodium channels. It's just technically impossible for that to happen. Why not just do that? The majority of the drugs in the market that attempt that mechanism today hit a wall from a reliability perspective. Yeah, it can be done, but it cannot be done to patient satisfaction, to the market satisfaction, and therefore to shareholder satisfactions like all of us. Vormatrigine has a very different profile where you can be quite effective, as we're going to discuss in a second, but also spare the toxicity that has been seen with other drugs that are similar in terms of the target, but not necessarily similar in terms of how they interact with the target.
We love looking into numbers and seizure reductions and talking about and measuring a drug's ability to deliver or not deliver on something by that number alone. It is quite important to listen to the markets as well and to physicians and patients who are suffering this and prescribing. The ability to give the drug to patients is incredibly important. The simpler, the better, number one. Two, the number one cause of discontinuation is not primary loss of effects. It is safety. When you are assessing a drug for a disease like we are talking here for focal onset seizures or many others in the epilepsy state, that triad has to be figured out. Once again, that is why we are so excited about Vormatrigine, because based on the data we have in our hands right now, it seems to do exactly that.
The one thing became very clear from a preclinical de-risking to an execution in the clinic for patients or drugs with focal onset seizures. I encourage all of you to go to our website. We have a resource page with the specific papers and posters giving details about what I'm presenting here. The most predictive model is the maximum electroshock seizure model. You can not only predict the effects. We can predict somewhat the magnitude when you correct that to the exposure in humans. It's very unique. We just don't see that in a lot of diseases and gives a window here in epilepsy that we don't really have anywhere else.
As you can see here on the left-hand side, 6-8, as it's labeled there, Vormatrigine as it's called now, that is you can run like a train, a freight train between that potency and response that is possible and everything else. I'm sure you can appreciate a lot of those other drugs that are there. It starts there. Potency is important not only because you want the most potency, because potency tends to be more precise modulation of the target you are after without any other undesirable modulation for other targets. It might reduce DDIs by the overall load of drug you give and so on and so forth. When you look into the ability to dose humans with exposures that translate to that efficacy that we are seeing in animals, that's what gets really exciting here with Vormatrigine. That's the right-hand side panel here.
I don't believe anyone here in the audience or elsewhere would disagree that Cenobamate is doing a phenomenal job on developing 1101 for focal onset seizures. Very good, strong results on their previous study. I personally expect to be the same on the next study. No one would disagree that Cenobamate is the best drug you can give to a focal onset seizure patient right now. One of the limitations of those approaches was they work really well for a subset of patients but you hit toxicity very quickly. You can predict that, as you can see here in the charts. At the time you get to the toxicity multiples on those drugs, the line, the green line there, that's where we start exposing patients with Vormatrigine. Our 20 mg dose has anywhere between C trough and C max around five- to tenfold.
You can just compare and contrast here in the chart. Everything we're doing with this drug as we progress then for the clinic is showing a differentiated profile. That's incredibly exciting. Where are we now? We did tons of pharmacology work, more than 100 healthy volunteers exposed to the drug, very good understanding of the PK profile, of the safety profile at this point. We had a very exquisite PK-PD relationship on the PPR study. Where are we right now? We are enrolling all those studies that I mentioned before, RADIANT coming up first half. That bar might have gone a little bit beyond that. Don't read into it. It was just a formatting thing. That's a first half readouts. The POWER1 study was a double-blind and one-to-one randomized is reading out by the end of the year.
We are starting some information from RADIANT. To be honest, we don't want to compete with ourselves either on the enrollments. That's why we're executing POWER2 staggered too. There was no reason not to start it now, but we think it's more appropriate for the overall package. In the course of the next year and a half, we would be, as everything goes to plan, with a registrational package of a very differentiated drug in focal onset seizures and potentially on primary generalized as well. If we see levels of seizure control, full seizure control, not reduction, full seizure resolution that are similar to what we see on the models, on what you can borrow a little bit from our GE program, this would be by far the best drug anyone possibly developed for focal onset seizures.
Is that going to be the only drug used? Absolutely not. This patient's going to have different drugs they're using. Is that going to eliminate the market for other drugs? No. One of the interesting things about this market is, one, it's growing just from an overall relationship with population and age and so on. The second is, unfortunately, a lot of the patients, way more than 30% that is quoted, fail every year. Very nice market and, of course, very excited execution here. I'm going to jump quickly into Relutrigine because the story is a lot similar here with Relutrigine. We are developing Relutrigine, and some of you might know that as PRAX-562, that was the previous name. The original screening was, can we modulate this very specific current on Nav1.6, which is persistent current? We screened towards that.
We found molecules that were very potent, very good at modulating because we knew that was pro-excitatory. If something happens to that current, patients have a lot of seizures. I think what we did not expect at that point in time is that the mechanism could just be broadly used across the boards on many other developmental encephalopathies. We did a lot of work on this molecule preclinically, early clinic, and particularly something we're quite proud of was the first controlled study in this population ever. To put in context, SCN2A patients, for example, which are one of the two populations included in this study, have a 6-10-fold higher mortality by age 18 than Dravet patients. I'm not saying Dravet is not important. Don't get me wrong here. Dravet is incredibly important.
There was a lot of fixation throughout the years into that population and their early mortality and the seizures. The seizures, at baseline for the EMBOLD study, were three to four times higher than any LGS or Dravet study ever conducted. I'm just trying to frame how severe this population is and how hard it is to see any reduction. In our proof of concept study, as you can see here, we saw 46% reduction in countable motor seizures. That alone would be more than reasons for us to be incredibly happy with what we're seeing. What's quite incredible, actually, one could argue, is that a third of those patients became seizure-free. That's never been seen. There is not such a thing as those patients becoming seizure-free on anything.
The nice thing is that if you isolate one month, just one month on those patients, which you should see basically nothing, go back and compare with other drugs in GEs, with other drugs in focal, I really encourage you to do that. You should see nothing. We've seen already incredibly meaningful results. That was a single month. When we follow those patients, all of them through, the 46% goes to 77% seizure reduction. I'm not sure there's anyone crazy enough to say that 77% seizure reduction when you start at over 50 seizures per month at baseline is not important for these patients, for their families, for the communities, for the healthcare system. Very, very exciting. Another point that I believe is worth mentioning here is that it's not only that they have a lot of seizures, they have no break.
There are other GEs that you can see a very long period of time. They don't have a lot of seizures, then they have more. Once again, a condition is a condition. I'm not trying to make this better or worse. Having any of those GEs is bad. The average number of days without seizures at baseline for either patients who got randomized to placebo or drug here was very, very short. They are not only having the seizures, they are having them almost every day. The longest average was three days. We followed them for 16 weeks, and the average went up to 20 days. We followed them on the long-term extension, and the average went up to 46 days, which means that now more than half of these patients are not seizing for entire months.
It is very, very hard to argue against the drug effect that is happening here. That was all somewhat expected if we believe in the translatability of the models and the early work that was done. What was particularly impressive is something that some of the key opinion leaders, especially Dr. Devinsky at NYU, always tell us. These patients are there. They are locked into this cage that we put in, nature puts them in. When you start to get better activities, when you reduce their seizures, when they are more physiologically firing just like we are, you are going to see everything else getting better. Here it is both clinician-assessed and caregiver-assessed independently. The change on the global impression with subdomains, this is not only the overall global impression, tell me how you are doing, with all subdomains on things that are quite meaningful for this population.
You look across the boards, this is very unexpected. You're not expecting to add a drug on top of a cocktail of drugs and see disruptive behavior get better, communication get better. Severity and intensity, I'll give to all of you. Maybe we were expecting that to get better. Alertness, the opposite. What we've seen before, you add a drug, you decrease alertness. That's one of the biggest concerns from parents, from physicians in general. Very, very meaningful. What did you do with that? EMBOLD , which was the first study, addressable in the United States, about 5,000. We put a pick potential revenue there to the right. We continue testing this in other models.
If we truly believe that we do, that fundamentally you can stop seizures by just modulating sodium channels properly, meaning not being there all the time, having the proper dynamics of binding on and off, like modulating primarily the currents that are pathological, avoiding the ones that are physiological, you'd be able to treat a very large number of GEs. We decided to engage with the FDA to ask them a little bit of questions. I can tell you we completed that process right now. We are imminently started the EMERALD study. That's going to be enrolling patients with phenotypically defined GEs with high seizure counts. That opportunity, as I'm sure you are quite familiar with because of other companies in the space, is very large. I always prefer to focus on how meaningful that is to patients.
Of course, it's incredibly important for all of us that that translates into our ability to develop other drugs. That's where the revenue comes in on the right-hand side here. By pretty soon, and I would say no later than the first half of next year, we're going to have the second cohort, the registrational cohort for EMBOLD readouts, 80 patients on that cohort, as you can see on the right-hand side there. In the next several weeks, I would say by Q2, we'll have the initiation of EMERALD. If the indication of the investigators and the patient community is any important lever here in the forecast, we believe that the readouts of those trials are going to be actually quite close to each other next year. Fairly eventful, quite interesting, quite meaningful for all of those patients with GE. It doesn't stop there.
We have an ASO. We just recently talked about that as well. One of the key things with ASO's deliverance, particularly, may I say, unfortunately, because there are a number of people doing this in a not so appropriate way and end up always slowing down for the ones who are, like ourselves, like Stoke, like others in this space that are really trying to do this quite positively and helping the patients. It took a long time to get an agreement with the FDA, but we are finally there. You might have seen on our Form 10-K a few days ago that we're running now a study based on the preliminary data we have for the first cohort, which was incredibly meaningful in this population, which is probably the shortest, well, it is the shortest disease-modifying, like six months, 24 weeks.
It's definitely the lowest dose here, which shows just the potency. Once again, I encourage you to look into the preclinical data here for this drug. We're doing a one-to-one randomized about 40 patients. When you look into our disclosures, you're going to see there are cohorts going down to birth. There are cohorts going down to zero. They are not included on the controls. Together with the acknowledgments that we can run a registrational trial in a one-to-one manner on the 2 to 18 population, we also got the agreement from the agents to run two open-label cohorts that will bring the initial indication, of course, if all of this is positive, to that age group, which we consider to be a huge upside as well, since we would want to stop seizures and developmental delays as quickly as we can on this patient population.
That study is going to be up and running in Q2 as well. It's being in final preparations right now. We expect, based on the interest, once again, to be quite quickly the enrollments in general. Looking to epilepsy, what I just discussed in the last 20 minutes or so, Vormatrigine advancing quite nicely, like two really trial reading outs mid-year, study reading out by the end of the year, a second study reading out next year, which is the registrational package altogether right there. We're looking to SCN2A and 8A and EMBOLD reading outs no later than the first half of next year. Elsunersen about the same time. The big upside here for all of that is the EMERALD study, what it would bring this to about 200,000 patients in the U.S.. We say 100,000+ .
I think the actual calculation in turn is 198,000 that would benefit from this based on the extrapolation on Epi. Incredibly meaningful to move all of this on a disease area that, while there's always risk in drug development, there's a lot of paths that have been tried out before in terms of how to collect this data, how to manage these patients, and so on, which facilitates drug developments tremendously. On the two minutes I have left, I just wanted to very quickly give an update on our movement disorder franchise. You might all have seen you are very familiar with what ET patients need. We talked about this several times. There is still, to this date, only one Phase III program ever in ET. Essential 3 is our Phase III program that is still ongoing.
We did have most recently, and I'm sure you've seen this, a little bit of a setback that made us pause and rethink. Study one here did have an interim analysis that was not positive. What I would recommend, and I'm saying this pretty clearly out loud, is the value of ET on everyone's model should be zero. Having said that, we did decide to finish the study. The study is basically completed at this point in time for a number of reasons. One is study two. Study two wouldn't suffer from methodological, like statistical or otherwise issues as study one, since that is by definition an enriched study set, and it uses very different analytical methods to compare. That might be incredibly important. We might end up learning from study two that that's the only way to measure drug effects in a disease like that. We'll see.
Study one being virtually all enrolled and complete at this point in time. With the little hints that there might be some small modifications that might show a better distinction between drug and placebo, we thought it would be appropriate, considering that the cost of these studies already sunk at this point in time. That is largely completed, very minimal. There is always cost to close to finalize and get that understanding. Now, we consider this to be something that is not going to work. I also think we all in this community did not really have any proper disclosure and readout before the full packaging here. If that is something, then you are going to have a different discussion at that point in time. We finished with the same slide we had before.
A lot to be excited about, a fair bit of things happening on the next several months, and really looking forward to, number one, better days in the biotech market for all of us in general, and certainly to share results with each one of you and all of you on all the problems we have. Thank you.