Good day. Thank you for standing by. Welcome to the Longboard Pharmaceuticals conference call. At this time, all participants are in a listen only mode. After the speaker's presentation, there will be a question and answer session. To ask a question during the session, you need to press star one one in your telephone. You will hear an automated message advising your hand is raised. To withdraw your question, please press star one one again. Please stand by. Please be advised that today's conference is being recorded. I would now like to hand the conference over to speaker today, Brandi Roberts, Chief Financial Officer. Please go ahead. Thank you and good afternoon, everyone. Welcome to Longboard's conference call and webcast, where we will be discussing our 2022 financial results and providing a corporate review of the past year and an update on the year ahead. Before we begin today, I would like to remind everyone that this conference call and webcast will contain forward-looking statements about the company, including, without limitation, statements about the anticipated timing of commencement, enrollment, and completion of clinical trials for our product candidates, the anticipated timing of release of clinical trial data, the market opportunity for our product candidates, and the expected timeframe for funding operations with current cash equivalents, and short-term investments. These statements are subject to risks and uncertainties that could cause actual results to differ. Factors that could cause actual results or outcomes to differ materially from those expressed in or implied by such forward-looking statements are discussed in greater detail in our most recent reports filed with the SEC. Please note that these forward-looking statements reflect our opinions only as of the date of this call, and we undertake no obligation to revise or publicly release the results of any revisions to these forward-looking statements in light of new information or future events. With that, I'll hand the call over to Kevin Lind, Longboard's President and CEO. Kevin? Thanks, Brandi. Thank you very much to everyone joining us today on our first earnings call. We wanted to provide an update since it's been just about two years since our IPO and just over three years since we started this endeavor. I'm extremely proud of what our team has accomplished during this time, and I'm incredibly excited about the opportunity ahead of us in 2023 as we expect top-line data readouts for both LP352 and LP659. On today's call, I will provide a high-level business update for our potentially best-in-class pipeline. Our Chief Medical Officer, Dr. Randall Kaye, will give key updates on LP352, and then Brandi Roberts will provide an overview of our 2022 financial results before we open the line for Q&A. As many of you are aware, we spun out of Arena Pharmaceuticals and formed Longboard with the mission of advancing neurology assets with differentiated pharmacokinetics, pharmacodynamics, and targeted engagement. To do this, we focused on building a world-class neuroscience team with the ability to strategically select the best indications, design the right clinical trials, and move the assets through clinical development in a differentiated way. Ultimately, our goal is for our compounds to deliver differentiated clinical outcomes that meaningfully impact the lives of patients. What is so compelling to me today is that I'm seeing a lot of the same characteristics that we saw at Arena when I joined. What drives our team is that our assets have the attributes of great medications that have successfully helped patients. First, each one utilizes a more precise approach, targeting a well-understood mechanism of action. Second, each one has been developed for a target patient population to remove receptor interactions that negatively impact patient safety or are not known to contribute toward efficacy. Third, each one is going after a potential billion+ opportunity with multiple relevant multi-billion dollar M&A analogs for similar mechanisms of action. Importantly, each is going after a mechanism of action where the legacy Arena discovery scientists have had success. Let's start with LP352. LP352 is an oral, highly selective, centrally acting 5-HT2C superagonist. LP352 is the only 5-HT2C receptor agonist being dose optimized for Developmental and Epileptic Encephalopathies, or DEEs. Given its greater selectivity and specificity, we believe that LP352 could be a treatment for individuals with DEEs who either, 1, have not had access to newer therapies or, 2, are still searching for a safer, more efficacious, easy to add on treatment in the syndromes where current therapies are inadequate. We're advancing LP352 in our ongoing Phase 1b/2a PACIFIC study, which is a basket study accepting participants with a range of DEEs. We expect to have top-line data from PACIFIC in the second half of this year. I'll now turn it over to Randall to go deeper into DEEs, the reason to believe for 352, and why we are so excited about the PACIFIC study. Randall? Thanks, Kevin. Good afternoon, everyone. As Kevin mentioned, we have a really unique opportunity and responsibility to patients, given the value that we believe our highly selective molecules have over existing medications in the space. Let's begin with LP352. Just as a reminder, DEEs refer to a group of severe heterogeneous epilepsies that are characterized by significant developmental delay, treatment refractory seizures, and abnormalities in brainwave function, as an example, EEGs. While there have been significant advances in the treatment of DEEs over the past decade, the unmet medical need of these patients and their families is striking. Most of you are familiar with a few of the DEEs, syndromes like Dravet and Lennox-Gastaut. Beyond these two, there are over 20 other DEE syndromes that are described. In total, only four of these DEEs actually have specifically approved therapies. These patients still have a significant unmet medical need and multiple seizures that interfere with their development. Physicians and caregivers are looking for a safe, efficacious, and easy-to-add-on therapy, and we know that safety is incredibly important to this community. Why do we believe that LP352 is a potential best-in-class 5-HT2C superagonist for the treatment of DEEs? Let's start with selectivity and precision. 352 is the only 5-HT agonist that has no detected activity at receptors that are associated with significant adverse side effects. In the case of 5-HT2B, with valvular heart disease and pulmonary arterial hypertension. In the case of 5-HT2A with psychiatric AEs such as insomnia, hallucinations, and euphoria. Second, preclinical validation. We have reported multiple preclinical models that demonstrate significant reduction in seizure activity and epileptiform events where we expect it to, and this is similar to other compounds that are in the class. Third, clinical validation. In our phase 1 SAD MAD studies, LP352 was demonstrated to have favorable safety and tolerability, and with adverse events that are generally consistent with the expected effects of serotonergic medications. Fourth, clinical CSF EEG data. We designed an interesting CNS phase 1 study to see if we could further characterize LP352 in plasma and CSF, as well as get a read on EEG or brainwave function. The results confirm that plasma and CSF PK concentrations increased in a dose-dependent and consistent manner, that LP352 demonstrated effects on QEEG activity within the first few doses with a sustained dose-dependent effects on this activity after continuous dosing. This is really important because this indicates that LP352 is getting into the brain as evidenced by receptor engagement. Well, let's turn to the PACIFIC study. I'd like to start by thanking the epilepsy community as we are extremely motivated internally by the engagement that we have had with parents, caregivers, physicians, our trial sites, as well as advocacy groups. In my 30 years involved in drug development, I have never seen a more engaged community. As a dedicated company, we take an extremely hands-on approach to the conduct of our clinical trial. We personally conduct in-person visits in every one of our participating sites. We feel this is incredibly valuable in order to ensure the speed of enrollment as well as the consistency across the seizure analysis. We also work very closely with the Epilepsy Study Consortium to help review every trial participant and train sites and caregivers on how to categorize and count every seizure for even greater consistency. In the PACIFIC study, we plan to enroll 50 participants, 40 on medication, 10 on placebo, across 30 sites in the U.S. and Australia. Our goal is to have a mixture of patients across multiple DEEs with approximately 10 patients with Dravet, 10 patients with Lennox-Gastaut, and then a combination of 30 patients diagnosed with other DEEs. Well, as we're out there and we're interacting with our sites, what do we hear from our study sites? Excitement, commitment, passion, and we're excited to be part of this journey. We continue to hear that there's tremendous remaining unmet medical need across both the DEEs with approved recent medications and the DEEs without any recent approvals. We are looking forward to the completion of the enrollment of the PACIFIC study in the first half of this year and presenting top-line data in the second half of this year. I'd like to now pass it back over to Kevin. Thanks, Randall. As you can tell, we're very enthusiastic about 352. This is also an important year for LP659. A significant reason why we started Longboard, because we saw the striking results generated by etrasimod and realized that there remained a tremendous opportunity for more selective next-generation S1P receptor modulators with optimized pharmacology, PK, and target engagement. In this case, LP659 was designed to be a centrally acting S1P receptor modulator focused on the modulation of the S1P1 and S1P5 receptors that are known to contribute toward efficacy while having no observable impact on the S1P2 and S1P3 receptors that have safety concerns and are involved in some of the potential off-target effects, including renal injury, hypertension, pulmonary issues, and macular edema. We believe LP659 could have potential in a number of inflammatory neurological conditions. We look forward to initiating our Phase 1 shortly. Why do we think 2023 will be an important year for LP659? Typically, Phase 1 data are not particularly telling. In this Phase 1, we think we will see some really interesting potential data which could highlight certain differentiating characteristics of 659. First, we obviously will be looking at safety and tolerability. Secondly, we expect to see rapid reduction in lymphocytes as well as rapid recovery of lymphocytes, which we have seen in preclinical models. Of note, this was a significant advantage that etrasimod has seen over some of the other S1P receptor modulators. We look forward to sharing the SAD data later this year and framing the opportunity and thoughts on initial indications as we get closer to advancing the compound beyond healthy volunteers and into patients. With that, I'll pass the call to Brandi to review our financial results. Brandi? Thanks, Kevin. We ended the year with $67.6 million in cash equivalents, and short-term investments. Our 2022 operating expenses were just under $45 million. R&D expenses were $34.6 million for 2022 compared to $19.8 million in 2021. Our 2022 R&D expenses increased over 2021 levels as we progressed both of our programs and added headcount to our team. G&A expenses were $10.2 million for 2022 compared to $8.1 million in 2021. Our 2022 G&A expenses increased over 2021 levels as we continued to build out support functions as appropriate for a public company of our size. Net loss was $43.9 million or $2.56 per share for the full year of 2022, compared to $27.8 million or $1.93 per share for the full year of 2021. We expect that our expenses will trend upwards during 2023 as we continue the development of LP352 and advance LP659 into the clinic. We are providing expected guidance for 2023 operating expenses to be in the range of $57 million-$63 million, excluding stock-based compensation. We are focused on spending responsibly as we progress our programs. We have built a very solid team with a lot of expertise, and they are able to do a tremendous amount of work. As we prepare for a phase 3 program with LP352 and down the road, a phase 2 for LP659, we are planning for the resources we will need both internally and externally, and we'll bring them on board at the appropriate time. We want to be able to move our programs through clinical development as quickly and efficiently as possible. I also wanted to take this opportunity to provide a little bit more color on our recent financing. In February, we completed a $23 million follow-on public offering of our common stock. This financing was a result of receiving several reverse inquiries from strong institutional funds that indicated interest in building a position in our stock. We are happy that we were able to bring some new funds into the Longboard family, as well as increase investments from some of our existing holders who have strongly supported us through our Series A financing in October of 2020, our IPO in 2021, and now our follow-on offering. We are focused on creating long-term value for those who believe in our technology and are supporting us through our journey. We believe that the proceeds from this financing, along with our cash equivalents, and short-term investments as of year-end 2022, will be sufficient to fund our current planned operations into mid-2024 and importantly through our PACIFIC data later this year. I'll now turn the call back to the operator to open the line for Q&A. Operator? Thank you. As a reminder, to ask a question, please press star one one on your telephone and wait for your name to be announced. To withdraw your question, please press star one one again. Please stand by. We'll compile the Q&A roster. One moment for our first question. Our first question comes line of Neena Bitritto-Garg from Citi. Your line is open. Hey, guys. Thanks for taking my question. I was just wondering if you could remind us of a few things on the PACIFIC study design. First, appreciate you giving updates on the number of patients with Dravet and LGS that you expect to have in the study. Can you remind us if you will have both active and placebo patients in each of those subgroups so that we can potentially see a difference there? Also thinking about, you know, what you would consider to be a success from the PACIFIC study. Can you lay out for us, you know, what sort of reduction in seizure frequency you would consider to be a success on the top line? Thanks. Thanks, Neena. Yeah, happy to take those questions. Randall, do you want to take both of them, in terms of study design, active and placebo? Sure. We put, as we noted, 10 patients with Dravet, approximately 10 with Lennox-Gastaut and a mixture of the other DEEs. We have not stratified in this design because of the size of the study. Statistically, we'd expect to see equal numbers of placebo and drug in each of the groups, you know, that would be the general hope. The in terms of efficacy expectations, remember primarily this is a safety and tolerability study as the most important of the endpoints. We are looking in the primary endpoint position at reductions in seizure frequency relative to baseline. We haven't put out a number of what the expectations are. What we're looking to see is our hypothesis is that the reduction in seizure frequency is similar qualitatively across the DEE spectrum. I think that's something that we would be looking more closely at once we actually know what the mixture is per se of different DEEs. Remember. Okay. That's super helpful. Sorry, I was just gonna add, remember the placebo effect for across most of these DEE studies has been in a fairly acceptable band in the kind of 7%- 20% range along the way. We didn't feel that it was necessary to stratify. Got it. Okay, that's super helpful. Then can you just remind us as well of what we should expect and what you're kind of looking for on the AE side? I know you're not doing any cardiovascular monitoring in this study, but, you know, anything in particular that we should be looking out for there? Yeah. Hey, it's Randall again. You know, the AE profile that we've seen so far has been relatively benign. The most common adverse event has been headache, to some degree, some mild GI symptomatology. We'd expect to continue to see that to some degree. You know, again, we're focusing more on tolerability. Can we get patients, you know, on an initial starting dose and maintain them during the overall maintenance period? Thanks for bringing up the point about other adverse events. Since our compound LP352 does not interact with the 5-HT2B receptor, we do not anticipate the typical cardiovascular risks that are associated with other medications out there like such as FINTEPLA. In fact, in our study protocol, FDA did not require us to do echocardiograms, so we're just doing routine monitoring. Remember from a long-term perspective, we fundamentally believe safe and easy to add on to current standard of care is going to be incredibly important. At the same time, we're balancing out that this is the only 5-HT2C that's being dose optimized for these patients. What we're trying to do is really in this study, figure out where do we wanna push, how do we wanna push, how do we wanna get patients to that optimal dose where we're balancing both that safety profile that we hope to have, as well as that efficacy that comes from dose optimization. Got it. Appreciate all the color. Thanks. One moment for our next question. Our next question comes line of Josh Schimmer from Evercore ISI. Your line is open. Great. Thanks for taking the questions. First on LP352, would you consider a switch study from patients on FINTEPLA, and if so, any thoughts on what that might look like? For LP659, as you're considering potential indications, there are a number of indications that S1P modulators already address such as MS and ulcerative colitis. Would you be inclined to pursue those or find new territories and what might your thinking be to identify the best applications of this mechanism? Thanks. Sure. Thanks, Josh. We think that there's tremendous unmet need beyond MS and ulcerative colitis. Again, the unique characteristics of LP659 lend themselves towards these neurological conditions given the central action that occurs. We do have a license with Pfizer to make sure we don't compete with them in ulcerative colitis and Crohn's and some of the areas they're going after. That's not even possible. But we think there's tremendous unmet need in these orphan neurological conditions where lymphocyte reduction, T-cell trafficking, all these things that we've seen with these S1Ps over the last, you know, 10-15 years could be incredibly valuable to patients who have tremendous unmet needs. That's more what we're thinking about for LP659. Randall, do you wanna take a first cut at the switch study? Sure. A switch study from FINTEPLA over to LP352. I'm gonna answer this as a clinician. I'm not sure you need to do that. You have a medication that has one of the most restrictive REMS that are out there in the marketplace in a patient population that is fragile and challenging. Just what might sound simple as doing an echocardiogram prior to treatment and echoes throughout, I don't think you need to do a switch study. I think you will get natural movement over to our compound. It would be intrinsically obvious that LP352 would be safer and would be a right thing to switch without the study. It's a provoking question. I'll think about it a little bit ymore. It's something we've been thinking a lot, and it kind of gets down to, you know, how do we want to handle Dravet, given fenfluramine's usage there. You know, as of right now, we're not seeing a tremendous uptake with fenfluramine in even Dravet alone, let alone in Lennox-Gastaut, such that we think it's necessary, but it's something we've been kicking around for a while as a potential after we see PACIFIC data. Got it. And do you feel like you've got the resources, capitalized to potentially advance both the programs simultaneously, or do you feel like you at some point may have to choose which to prioritize? Look, we think we are going to be able to have the resources. As Brandi mentioned, this last financing was not about funding the phase 3 and for LP352 and the phase 2 for LP659. This was really a bunch of folks who could not find volume in our stock wanting to get into the name and us using Financing in a formal setting as opposed to using the ATM. Our hope is that we can continue to finance as necessary, and we are going to try to be prudent in how much dilution we wanna take along the way, knowing that there has been this movement towards the haves versus the have-nots. We don't think we need to raise massive amounts of capital to really be still considered a have. Brandi, do you want anything? No, I just wanna say that I think we've really done a great job at building a lot of talent in the organization as well. You know, we've grown from just three employees back in 2020 to 33 at the end of 2022, and have brought in a lot of people with great epilepsy and neurology experience. I think we plan to capitalize on that and continue to move these programs forward ourselves. Thanks very much. Good luck with the updates this year. One moment for our next question. Our next question comes line of Charles Duncan from Cantor Fitzgerald. Your line is open. Yes. Good afternoon, Kevin and team. Thanks for the good cadence on the update and taking our question. I had a couple of questions on LP352. I'm just wondering if you could provide us a little bit more color on the types of patients that are really joining into this study. Can you tell us whether or not they skew to the younger ages? I note that exclusion criteria includes use of fenfluramine. Is that ever forever in a Dravet patient, completely naive, or could some of those people have been exposed to fenfluramine in the past? Yeah. Randall, do you wanna take that? Yeah. Hey, Charles. Randall. Thanks for those questions. We opened up the study originally starting as an adult population, 18- 18 and above, dropped the population as additional confirmatory preclinical safety data emerged. We felt comfortable moving into the adolescent population down to 12. We are seeing patients coming into the study within the adolescent population. We haven't put specific numbers out. It'd be hard to answer your question about skewing towards, but we're satisfied that we're getting a nice balance of patients. Your second question, let me clarify. We exclude patients who have failed fenfluramine. Failure would mean they had no discernible treatment response to fenfluramine, or they had an adverse event profile or side effect profile that would preclude its use. If a patient, let's say, had been on fenfluramine but insurance wasn't covering it or the parents didn't like the inconvenience of regular echoes, they, you know, that would be a subject that would potentially be included. Okay. That's helpful. In terms of the actual conduct of the study, are you allowing down titration during the maintenance phase or is that just not necessary? Are you not seeing any of that over the course of the study so far? Yes. It's an interesting question. The way the protocol is written, we use the uptitration portion to get them on a dose that they're tolerating. Start at six, g o up to nine, go up to 12. We're going up by tolerability. We're not forcing and pushing everyone up to 12. The expectation is when they get into the maintenance period, they're tolerating LP352 well, our expectation is that they will stay on that dose for the for that time period. You know, would we theoretically allow some flexibility? I guess we could potentially. Generally, the approach is that we'll have them on the right, the right dose so they can tolerate and stay on that during the maintenance period. Okay. Gotcha. Last question quickly is, if you considered success, I think the first analyst asked a question about seizure reduction frequency. Anything beyond just simple seizure reduction that you would be looking at from an efficacy standpoint that you'd be intrigued with being able to show, particularly given the safety profile of the drug and seeing, I guess compliance or dose density over time, what would intrigue you? I think it's important to frame this as a safety and tolerability study and also proof of concept that you can treat a heterogeneous group of patients across the DE spectrum. Success would be safe, well-tolerated, and some comparable seizure reduction. I'd love to start to talk about some of the other potential areas that you can start to look at in large, larger studies such as quality of life, clinical global improvement and so forth. That's just gonna have to wait until we move into pivotal studies next year. Okay. Good deal. Thanks for taking the questions. One moment for our next question. Our next question comes line of Laura Chico from Wedbush. Your line is open. Good afternoon. Thanks for taking the question. I've got two more strategic questions for you, I guess. The first one, assuming success with PACIFIC, I'm wondering how we should be thinking about the potential or the feasibility of using a basket registrational study, kind of, you know, expanding on the PACIFIC's design, if you would. Secondarily, Kevin, maybe from a strategic perspective, wondering if you could take a step back for us and comment on what gives you confidence in the market opportunity within the DEEs space, specifically. Thanks very much. Yeah. Thanks, Laura. Great question. Look, I think from a company perspective, from a philosophical perspective, we would like to get to a broad DE approval because we think it's the right thing for patients and the community and the caregivers. We think that it's tremendously unfair. Rare Disease Day was earlier this week. We think it's tremendously unfair that some of these DEEs, and these families and these patients with DEEs don't have access to some of these newer medications. We think that the current development pathway leaves certain people behind unnecessarily. From a philosophical perspective, we really would like to do that, and we think that there's a tremendous market opportunity there, well beyond Dravet and Lennox-Gastaut, well beyond what has been seen with EPIDIOLEX or fenfluramine or some of these other cenobamate, that are more niche. We would like to get there. From a practical perspective, we wanna make sure we do the right thing for this molecule, and we wanna do the right thing for our shareholders because the last thing we wanna do is create a development path forward that doesn't work with regulators. That doesn't help anyone. We are going to continue to work on this messaging and this strategy over time. I think the most important thing we're going to see that will impact whether we go down the individual indication route versus the broader basket route is the data from PACIFIC. That's why we're so excited about that this year, because right now we can have great conversations with KOLs and patient advocacy groups and walk through why we think this will be so transformative. Until we see that data set, we can't make that call, and frankly, it's all theoretical. What gives me confidence today is we haven't seen these molecules work in one indication and fail in another. Remember, Lennox-Gastaut is really a catch-all basket. If these molecules were just working in SCN1A patients, then that's a very, very different thing. We already are starting to see that with some of the molecules in TSC that are more focused on the tumor side versus the epilepsy side. For us, we think this molecule has this tremendous opportunity, but what we have to do is make sure it gets to patients. Whether we can get it to the broadest group of patients is our hope and our dream, but we need to see this PACIFIC data. Does that answer your question? Yes, it does. Thanks, Kevin. Thank you. One moment for our next question. Our next question comes from the line of Yatin Suneja from Guggenheim Partners. Your line is open. Yeah. Kevin, could you expand a little bit more on the dose optimization point that you make? I think it is our understanding that FINTEPLA was never dose optimized. I'm just curious to understand from you what you are seeing on a PK/PD perspective in terms of CNS exposure that gives you confidence that the molecule is better optimized than, let's say, FINTEPLA. That's first question. The second one is what work you might be doing on the formulation to bring it, you know, currently it's TID, so maybe do a QD or a BID. If you can comment on these two questions. Thanks. Sure. Look, remember, fenfluramine was the weight loss dose arbitrarily cut by some folks in Belgium. Great outcome for the molecule, but we really don't know what's the optimal safety to efficacy balance with that molecule along the way. We saw some dose responses between the low dose and the high dose in a number of their studies, but we didn't ever really see where the top is. Lorcaserin, whether that drug ever makes it to market or not, we don't know. But again, that's the weight loss dose just carried over. For 352, what we're excited about is the opportunity to really figure out how much receptor engagement do we really wanna have, and it's why we got so excited about the 102 data. Randall, do you wanna walk through the 102 data for a second? Sure. In our 102 data, we learned that there was good solid dose proportionality between the oral dose given, what appeared in the plasma, and probably most importantly, what ended up in CSF. We compared the CSF dose concentrations that we observed relative to the Ki or the dissociation constant. What we found is that we were getting at or in most cases well above the Ki at our top dose at 12 mg tig. We also found that even at 6 mg which is the start of the titration, we're getting great receptor engagement, somewhere around 70% or so of the Ki. What that tells us is that means you can dose optimize, you can modify, you can adjust as we go into further clinical studies next year, that we can go up and down based on the data that we're seeing. That is the opposite of what you can do with FINTEPLA currently. At a point in time, as these patients go from young children to adolescents and older, as they gain weight, you will cap out, so you cannot continue to increase the level of fenfluramine in order to match the increasing weight. You just can't dose optimize the drug that has a restrictive range. On the second question, the BID formulation. Again, we are focused on making sure we have that BID for the phase 3. There's some intellectual property involved in that we're not ready to disclose at this point and work through, but we remain on track for BID for the phase 3. Thank you. Thank you. Thank you. One moment for our next question. Our last question comes from the line of Patrick Trucchio from H.C. Wainwright. Your line is open. Thanks. Good afternoon. I'm wondering first if you can tell us if there's any evidence that the 5-HT2 mechanism could be complementary or synergistic with that of cannabidiol. Would you expect a portion of patients enrolled in PACIFIC to be on cannabidiol background treatment? If so, what portion of those patients? Hey, Patrick, it's Randall. Great questions. Thanks for those. I probably should have discussed them earlier. We do allow patients to have background of cannabidiol, of EPIDIOLEX as long as they've been on a stable dose. I don't have specific numbers for you, but we actually. It's hard to say whether they'll be synergistic. I'd like to describe it somewhat differently. When you think about these complicated patients with these Developmental and Epileptic Encephalopathies, multiple modality treatment with the right medication is going to make sense. I can see a time, you know, I'll kind of refer to this as precision and targeted treatment of patients, where the clinician is going to the shelf and saying, "I wanna have the best, safest, efficacious cannabidiol." I think they're also gonna be reaching up to that shelf in the DEE space for the most efficacious and safest 5-HT2C. I can't say whether they'd be synergistic, but they certainly one would expect them to be to be complementary. Yep, that's helpful. How big of a concern is the FINTEPLA black box on adoption among clinicians and patients? What would need to be demonstrated in the LP352 program to avoid having a similar black box warning on the label? I wouldn't expect to have a black box warning. We've had the discussion with the agency. Our compound does not interact with the 5-HT2B receptor, a priori, there's no expectation to do the kind of work that was required with FINTEPLA. We asked the FDA specifically about conducting echocardiograms. They're not required by this program, and we wouldn't anticipate that that would be part of it. To answer your question more clinically, what I'm hearing from other clinicians, These are really complicated patients, and they're very, very fragile. Adding on the component of an echocardiogram, getting it scheduled, it's not like it's right down the hall in these clinics. It could be in another building. These are not the most mobile of patients. It's very, very inconvenient and they have to continue getting echocardiograms for the duration of their therapy and then one more if they do choose to discontinue it. We've heard numerous instances across the country where echocardiograms are available, but they're not readily available. There'll be a waiting list in order to obtain one. I think it's a significant challenge for patients. We feel really confident in the approach of interacting with 5-HT2C, but you gotta do it in a way where it's, where it's gonna be safe and convenient for patients. We think that's what LP352 has the promise of. Yeah. Again, you know, congrats to everyone involved in the fenfluramine approval and launch. I don't wanna speak negatively about them, but UCB just mentioned that they expect peak sales of that molecule to be about EUR 800 million. If you kind of back into what that translates to from a patient perspective, patient number perspective based on their current pricing, it doesn't appear that UCB expects to even get a large percentage of the Dravet market, let alone if you add the Dravet market on top of the Lennox-Gastaut market. We're not hearing a lot of feedback from the community, "I don't have any patients for you because all of my patients are on fenfluramine." We're not hearing a lot of feedback that, "Oh my gosh, I don't know how you're going to beat fenfluramine in the marketplace." That gives us great, tremendous and tremendous, you know, hope for our molecule and hope for these patients to make these parents, these caregivers' lives easier. We think a safer molecule does that. You know, it's back to that conversation that we were having based on Josh's question, which is, you know, do we even need a switch study? I think that's gonna be an interesting one along the way. The good news is we can see the specific data and see the continued launch trajectory of fenfluramine and then make that decision down the road. You know, fenfluramine's now been on the market for years and the sales are what they are. I think we're, you know, not overly concerned about our ability to differentiate ourselves and hopefully have a preferred molecule on the market down the road. That's great. Thank you very much. Thank you. This concludes our Q&A session. I would now like to turn the conference back to Kevin for closing remarks. Thanks, operator. I wanna thank everyone for joining the call today and for sharing in our enthusiasm in the Longboard story as we approach data readouts across our pipeline in the second half of this year. Have a great day. Thanks. This concludes today's conference call. Thank you for participating. You may now disconnect. Everyone, have a great day.