Good afternoon, ladies and gentlemen, and welcome to the Longboard Pharmaceuticals first quarter 2024 financial results and business update call. As a reminder, this conference call is being recorded. I would now like to turn the call over to Brandi Roberts, Longboard's Chief Financial Officer. You may begin. Thank you, and good afternoon, everyone. Welcome to Longboard's conference call and webcast, where we'll be providing a corporate update, including results from our LP659 single ascending dose study. 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 potential of our product candidates, the anticipated timing and design of clinical trials, top line data, commercial opportunities, and financial guidance. 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, and thank you very much to everyone joining us today during what is a very exciting time for Longboard. I'm extremely proud of what we have accomplished in 2024 across the entire organization and portfolio. I'm going to start off by providing an update on our lead asset, bexicaserin, a highly selective and specific 5-HT2C receptor agonist, and then hand it over to Dr. Kaye to provide an update on LP659. And then Brandi will give an update on our financials before we open the call for Q&A. We kicked off the year with positive top line data from our Phase Ib/IIa Pacific study evaluating bexicaserin in developmental and epileptic encephalopathies, or DEEs. We were incredibly pleased that bexicaserin achieved a median reduction of countable motor seizures of approximately 60% in highly refractory participants, and on top of 3-4 other anti-seizure medications in Dravet, Lennox-Gastaut, and a number of other DEE participants. Then in June, we had a very busy month. First, we shared an interim analysis of our open label extension study of Pacific, demonstrating a sustained response over an approximate 6-month period with continued favorable safety and tolerability, as well as successful titration of all of our placebo participants onto bexicaserin. Second, we completed our end of phase II meeting. And third, the FDA granted breakthrough therapy designation for seizures associated with DEEs down to the age of 2. We are the first and only company to receive this designation for DEEs. The Pacific data and breakthrough therapy designation have been the most rewarding achievements since the founding of Longboard. Both of these support our thesis and strengthen what we believe we have been working towards, which is to treat DEEs broadly and provide more equitable access to patients that are tremendously underserved. We have been overwhelmed by the outpouring of excitement and support from caregivers, advocates, and physicians. We're committed to making a difference for those living with DEEs. To that end, we are moving forward with our innovative design to study all DEEs in our global phase III program. We are so pleased to have the opportunity to collaborate with the FDA with the goal of addressing the tremendous unmet medical need for this population in an optimized manner. We are expeditiously preparing to start our phase III program, which will include two pivotal studies, one for Dravet syndrome and one DEE study that will include Lennox-Gastaut and all the other DEEs. We intend to initiate our phase III program in the second half of this year, and we'll provide additional details on the studies at an upcoming investor and analyst day on September 16th. With that, I'd like to switch over to our second clinical stage asset, LP659, a highly selective S1P1/5 receptor modulator. LP659 was created and optimized by Arena's world-class GPCR research team, the same team that discovered etrasimod. LP659 was designed to be a centrally acting S1P receptor modulator with some of the same differentiating characteristics built into etrasimod. S1P receptor modulators are considered well understood, and early data has been shown to be generally predictive of clinical effectiveness. We have been doing a lot of translational work here. That, coupled with additional learnings from the I&I space, has opened up several orphaned CNS indications that we think could be very interesting and have attractive commercial opportunities. LP659 works centrally to modulate S1P receptors, which play a crucial role in the immune and nervous systems. It exhibits a rapid onset and offset of action, making it potentially more effective and manageable in clinical settings. Its high selectivity to S1P1 and S1P5 receptors minimizes off-target effects, enhancing its therapeutic profile, and preclinical studies have shown no significant impact on S1P2 and S1P3, indicating a targeted approach. LP659 has high oral bioavailability, meaning it is effectively absorbed when taken orally, and it directly impacts CNS glial cell S1P receptors. It has shown promising results in preclinical models for various conditions. The market for S1P receptor modulators is substantial, with these treatments already generating significant revenue in CNS applications, primarily in multiple sclerosis. In multiple sclerosis mouse models, LP659 demonstrated lymphocyte modulation, suggesting its potential efficacy in similar human conditions. However, based on advancements in our understanding of S1Ps, we believe that LP659's unique properties provide it with the potential to be a best-in-class CNS-focused S1P addressing a range of orphan neurological disorders. With that, I'll turn it over to Randall. Good afternoon, and thanks, Kevin. Today, I'll be presenting on LP659, our promising S1P receptor modulator with broad applicability in treating various rare orphan neuro conditions. I'd like to delve into how LP659 functions by selectively modulating S1PR1. So just as a reminder, S1Ps, and more specifically LP659, work by functionally antagonizing S1PR1. Binding of these agonists to the receptor induces receptor internalization and degradation. This disrupts the normal egress of lymphocyte subsets from the lymph nodes. So by reducing the migration of lymphocytes, LP659 decreases the release of inflammatory cytokines, thereby minimizing organ and tissue damage. And what's important is LP659 does this while maintaining immune surveillance, ensuring that the body's defense mechanisms still remain intact. In the CNS, S1P receptor 1 is expressed in astrocytes, and its activation has been shown to reduce astrogliosis and support microglial cell function. In oligodendrocytes, S1P5 may play a role in myelination. These effects on the glial cells are expected to reduce neuroinflammation and enhance neuronal survival. On the next slide, the selectivity profile of LP659 is directly coupled to its potential to decrease inflammation and enhance neuroprotection in the central nervous system. There are five S1P receptors that are known in humans, with the S1P receptors 1 and 5 mediating the anti-inflammatory and neuroprotective effects. S1P4 is generally considered to be non-active in the CNS. Importantly, S1P2, S1P3 have been associated with potential safety liabilities of the class, and that includes vasoconstriction, fibrosis, as well as decreased blood-brain barrier integrity. LP659 is a highly potent agonist of the S1P1 receptor while retaining some activity at S1P5. It does not bind or activate S1P2 or 3 and has little activity. So on the next slide, LP659 was designed to be a next-generation S1P1 receptor agonist to target the CNS-related diseases with greater precision. 659 is designed to be the most potent agonist at S1PR1 internalization, and this potency is crucial for its therapeutic effect. So when tested for its ability to promote total S1PR1 internalization mediated by both G proteins and beta-arrestin coupling, LP659 emerged as the most potent of all the approved CNS-focused S1P modulators. So we think of other examples such as ponesimod, ozanimod, siponimod, as well as fingolimod. So importantly, LP659 preferentially triggers beta-arrestin signaling over G protein signaling. Beta-arrestin signaling causes receptor internalization and functional antagonism. So therefore, this contributes to the anti-inflammatory effects of the class. The G protein signaling contributes to first-dose bradycardia. This is seen clinically with the less selective S1P receptor modulators. And then furthermore, LP659 demonstrated the greatest selectivity for S1P1 over S1P5. You're seeing this on the right-hand side of the screen when tested for activity at beta-arrestin signaling alone. So LP659's potency at S1P1 internalization positions it as a pioneering treatment with significant potential for managing CNS-related and autoimmune diseases. On the next slide, LP659 reduces circulating T and B cells without effect on natural killer cells and monocytes. So thus, this is what's maintaining the immunosurveillance. Those alternative cells are responsible for combating infection. This is data that I'm showing you from a preclinical model. This uses the EAE rats that are dosed with LP659 for two weeks, and this is compared to vehicle EAE rats. LP659 demonstrates potent in vivo activity. It effectively lowers, as seen on the left-hand side of the screen, T and B cell populations. Importantly, LP659 increases the proportion of the regulatory T cells, we'll call them T regs, over total CD4 cells. T regs are a class of T cells that have anti-inflammatory effects, and their function has been found to be beneficial in autoimmune and neurodegenerative disease. Now, it's notable that, described before, LP659 does not have a significant effect on natural killer cells or monocytes, and this indicates a selective modulation of immune cells. So therefore, in a preclinical model, LP659 promoted marked suppression of the CD3 positive T cells, a significant reduction of B cells, and an increase in T reg frequency. These effects are consistent with the mechanism of action of this drug class, and these preclinical data confirm that LP659 improved in vitro profile while increased selectivity is expected to maintain clinical efficacy. So next, what we're going to discuss is the phase I SAD trial, as well as its subsequent data. This slide represents the design and key study objectives of the 101 study. This is a first-in-human clinical trial. It's a phase I single ascending dose. We call these SAD studies in adult healthy volunteers. And just to call your attention to the cohorts, cohorts 1 and 2 and 4. On day 1, they're administered formulation one after an overnight fast, and this is followed by a discharge on day 1. And in cohort three, day 1, administration of formulation one after an overnight fasting. They stay in the clinic, and on day 8, they're administered for, and they have a washout. And they're administered formulation two of, I'm sorry, they're administered formulation two following a 1-week washout of formulation one, and then they're subsequently discharged on day 15. So the key study objectives are to assess the safety and tolerability of a single ascending dose of LP659, to determine the PK profile of LP659 and its metabolites in single ascending doses, and to determine the PD profile of LP659 in a single ascending dose. So next, I'm going to give an overview. We'll focus first on the safety aspects of the phase one study. LP659 was generally safe and well tolerated by the study participants. All adverse events were of mild severity. Importantly, no treatment-emergent adverse events led to a discontinuation of the study, nor did we observe any serious adverse events during the study period. The impact on heart rate was consistently low throughout the study duration. Notably, there were no instances of first-dose bradycardia, which is often a concern in similar treatments. Our ECG assessment showed no abnormalities, including no cases of atrioventricular block. Echocardiograms also were normal, indicating no functional adverse cardiac events. Pulmonary function tests, including spirometry, showed no abnormalities. Ophthalmologic assessments were normal with no adverse event findings reported. We observed no infections among the study populations, highlighting the treatment-favorable safety profile in this regard. Overall, LP659 demonstrated a very encouraging safety profile. Let's get to the good stuff. The graph that I'm about to show you is going to look at the mean percent change from baseline in absolute lymphocyte counts, and I'll code it as ALC. This is looked at over a 24-hour period. Just to remind you, this is just a single-dose study, not continuous dosing. The different lines that we're presenting here represent varying doses as well as formulations of LP659, as well as a pooled placebo group. It's important to note and to reiterate that lymphocyte reduction is an anticipated on-target effect of S1P modulators. It's indicative of the drug's mechanism of action is functioning as expected. I'll just overview for you the mean percent changes in the ALCs. We're just going to highlight right at hour six, post-dose. That's an important time point. Dose A, 3.5% reduction. B, 0.9%. Dose C, 18.8%. And here's where we're starting to see the effect that we're hoping to see is in dose C, formulation two, 58.9%, and dose D, formulation one, a decrease of 48% with a pooled placebo cohort of 4.1%. This data suggests that LP659 has a dose and formulation-dependent effect on reducing ALC, with higher doses showing greater reductions. This reduction in lymphocyte count is a crucial parameter as we evaluate our drug's potential effectiveness as well as safety profile. Further analyses and studies will continue to assess long-term effects and optimizing dosing strategies. So now we get to the point, what does this all mean? How do we start to bring this information together, and where do we go from here? What are the opportunities in immune and inflammatory conditions? There's been a lot of innovation in the I&I space since the approval of Fingolimod and the development of the other approved mods. The list of potential indications is continuing to grow. To that end, we have conducted preclinical studies of 659 in three broad areas of interest: autoimmune, neuroinflammation, and proteinopathies. This slide outlines the primary disease areas that 659 could potentially target. Each condition is characterized by its unique pathology and the role of T and/or B cells in disease progression. LP659 shows promise in targeting these indications due to its selective action on S1PR1 and its ability to modulate T and B cell behavior, thereby potentially reducing neuroinflammation and promoting better clinical outcomes. We continue to believe that the best path forward for LP659 will be in an indication where there's a high medical need, where there is a strong preclinical dataset and/or clinical support, and whereby clinical studies can be conducted that are practical and that are feasible. In order to finalize that decision, we want to see the results of our anticipated phase I MAD study, which we expect to initiate in the first quarter of 2025. And with that, I'll turn it over to Brandi to review our financials. Thanks, Randall. I'd like to take this opportunity to provide a bit more color on our Q2 results, our cash runway, scaling for our phase III program, and our strategy for bringing programs forward. We ended the second quarter with approximately $305 million in cash and investments, and this reflects a cash burn of about $19 million for the quarter. Our second quarter expenses were higher than our first quarter expenses due to increased R&D activities, primarily related to Bexacaserin, and a smaller amount for LP659. These expenses were in accordance with our internal expectations. For Bexacaserin, we had continued activities for our open label extension study, as well as significant activities to prepare for our phase III program. We expect that our expenses will continue to trend slightly upwards during 2024 as we continue to build out our world-class organization, focus on elucidating the potential best-in-class clinical and commercial characteristics of Bexacaserin, and continue to make progress on LP659. That means scaling our team and building out our infrastructure in order to make sure our global phase III program for Bexacaserin enrolls at a pace that's acceptable to our organization, exploring additional clinical and non-clinical studies to differentiate our portfolio, and taking advantage of the opportunity to interact with the DEE community and educate the broader community about the tremendous unmet need for DEE patients, their caregivers, loved ones, and healthcare specialists. We are very excited about the opportunity ahead of us for Bexacaserin and 659. We take our responsibility for managing resources very seriously. We want every dollar to matter. So when we consider plans for additional studies for either program, we are constantly evaluating the risk-reward and whether we believe that level of spend is the best course of action for the company and our shareholders. Our goal is to continue to build value, and the approximately $305 million in cash and investments that we have as of June 30th, 2024, gives us the ability to execute on our vision into 2027. This concludes the prepared remarks from this afternoon's call, and I'll now turn the call back to the operator to open the line for Q&A, where I'll be rejoined by Kevin and Randall. Operator? At this time, I would like to remind everyone in order to ask a question, press star then the number one on your telephone keypad. We will pause for just a moment to compile the Q&A roster. For our first question, Laura Chico with Wedbush, please go ahead. Good afternoon, and thanks very much for taking the question. Congratulations on the progress, guys. I have one question just with respect to the Bexacaserin phase III efforts, and then just one on 659. With respect to the Bexacaserin pivotal programs, I'm wondering if you could just expand a little bit on the sizing of the respective studies, and just wondering if there are any kind of minimal numbers of certain types of DEEs that need to be represented on a patient number basis. With respect to 659, thank you, Randall, for all that commentary. Just wondering if you could kind of walk through the decision matrix a little bit in terms of indication selection for next steps. Thanks very much, guys. Yeah, hey, thanks, Laura. Appreciate the questions. On the phase III program for Bexacaserin, we want to make sure we roll it all out at the right time, not piecemeal. So look forward to a fulsome disclosure of what we're planning to do around the R&D day that we're scheduling for September 16th. With regards to your second question on the decision matrix, I'm happy to take it. It's a combination of 3 things. We've been talking about this for a while. It's commercial opportunity. Is this something we can do? Is this something that is attractive? Do we like the risk-reward on the commercial side? The competitive landscape on clinical feasibility. Can we find patients? Can we enroll the studies? Can we do this in a time-efficient manner and a cost-efficient manner? And then the last piece is translational science. Can we look at preclinical models as well as data generated from the other mods to help us elucidate other indications to go after? The interesting thing is that over time, that translational area, the data we can glean from other mods has really expanded the potential indications we could go after because of all the learnings in I&I. So I think when we started talking to folks, when we did the IPO, we were kind of triangulating around a couple of indications. As we have progressed in learning more about 659, as we have run it through additional preclinical models, as we have done additional literature searches, that lens has really opened wider. Where we are today is we have a good sense of what we want to see in the MAD to help us make that final decision. But I think it's a little premature to pick that indication until we see how the drug performs at steady state. And so while we were hoping to roll out the indication a little bit earlier, and frankly, if you had asked me when we did the IPO, when would we have selected that indication, I would have said it would be done by now. But the really interesting thing is we're continuing to learn a lot about this and expanding our potential indications. So my sense is we'll probably roll it out closer to the end of MAD or after MAD and as we move closer to the phase two or our expected phase two. Does that answer your question? Yes, it does. Thanks very much. Our next question comes from Joel Beatty with Baird. Please go ahead. Great. Congrats on the progress, and thanks for taking the questions. The first one's on Bexacaserin. I think the most common question I've been getting from investors since the Breakthrough Therapy designation is how large is the DEE opportunity? Are you able to share anything about your market research on that? Yeah. So we'll talk a little bit more about that in September. I think where we are today, there's a lot still left to learn. We're trying to make sure we're not double-counting by including patients who have a diagnosis for Lennox-Gastaut plus a genetic diagnosis or one of the other DEEs. We're trying to look at patients who will have their indication potentially migrate over the course of their life. But what we will say, what we do feel comfortable with saying is we think the market is very big. We're excited about that opportunity to really be able to address a number of DEEs and a number of patients who don't have access to the latest clinical trials and don't have access to the latest standard of care. And to us, that is tremendously exciting. So more to come on exact numbers, but we think that there's a real opportunity here to do something with that designation and that indication. Great. That's helpful. And then a question on 659. On the slides presented today, it looked like there were two formulations tested with quite a large difference in those two formulations. Are you able to share anything about what that formulation is, or at least how much you'll be testing different formulations in the MAD study? Yeah. Hey, great question. I think in the MAD study, we have triangulated on some variation of formulation two. Formulations will potentially adjust slightly on the margin, but we think formulation two gets into the plasma much better and has less variability. Obviously, you can see the impact on lymphocytes. And so formulation two is the path forward for the MAD. And I'm going to pass it over to Randall to add something. Yeah. Just an important point to add is both the formulations and doses have got us to where we wanted to be in terms of the preliminary findings. The target was to show a reduction in absolute lymphocyte count. We were in that 50%-60% range. That's great from an early clinical development standpoint in SAD. So an important thing to keep in mind is in a multiple ascending dose study with multiple doses, one would anticipate that that decrease in absolute lymphocyte counts will continue to decrease to get the best benefit of the product. But these are terrific early findings in both formulations. Great. Thank you. Our next question comes from Gavin Clark-Gartner with Evercore. Please go ahead. Hey, guys. Congrats on all the progress, and thanks for taking the questions. I'll follow the form of doing one Bexy and one S1P question. First, just on Bexy, could you just comment on the status of discussions with global regulators on the potential for the broad DEE path, since it sounds like you're clearly aligned with the FDA already? Sure. Randall, do you want to take this one? Sure. Well, we're planning a global phase three program. We're going to talk about all the details about that in September. We have initiated our discussions with global regulatory authorities. One would anticipate that our Breakthrough Therapy designation will set precedent in other areas. And as part of our discussions, believe it or not, regulatory authorities do talk with each other across the globe, and they are aware of the Breakthrough Therapy designation and the reasoning and the thinking behind it. We do share that information across. So we would expect that our discussions with other regulatory authorities will go in a similar positive fashion. Awesome. That makes sense. And on the S1P, I'm just wondering what the half-life of 659 in humans is. And at the one dose where you saw the largest ALC impact, what was the heart rate or the QTc impact there? Thanks, guys. Yeah. Let me pass it to Randall. Yeah. So the question on heart rate changes and ALC numbers, we did not see a clinically significant decrease in heart rate in any of the formulations tested. I also made a note that there were no abnormal EKG findings, so I can't comment on the QTc numbers because they were all normal. We did not see, I think you're implying did we see any QTc prolongation, and we did not. Half-life. Half-life, way better to have that discussion with the multiple ascending dose study. The half-life that you do see is only the half-life after a single dose. They sometimes, depending on the product, can be misleading. I'm not implying that there's a positive or negative here. I just think generally you want to wait until you have a multiple ascending dose until you talk about the typical PK parameters such as half-life, Cmax, Tmax, AUCs, and so forth. Thanks. Congrats on the progress again. Our next question comes from Kalpit Patel with B. Riley Securities. Please go ahead. Yeah. Hey, good afternoon, and congrats on the regulatory alignment. You mentioned that you'll have another DEE component included into the LGS study. I guess if you can comment before the event next month, how many different DEEs are you aiming to address in that other DEE component? Yeah. Hey, great question. I think it's almost actually the reverse. The 301 study is going to be a DEE study that includes Lennox-Gastaut. And great question, though, but we want to be very clear on that. It truly is a DEE study that includes Lennox-Gastaut patients. We haven't disclosed yet how many potential DEEs will be in there. The number of DEEs continues to go up as more genetic data has been generated. So we have a number in mind, but we'll probably roll that number out around the R&D day. We did see a number of DEEs in the Pacific study, and that gives us comfort that we can study the entire DEE population in this 301 study as we move forward. Randall, do you want to add something? So we haven't disclosed the individual DEEs from the Pacific study, but we know there were 19 patients in that study. And when asked before, I said it was a bunch of onesies and twosies. So if you want to do the math, you could imagine that there's a significant amount of heterogeneity in different DEEs that we observed in the Pacific study. We'd expect that to move forward in a much larger study conducted in the DEE population. And stay tuned for September, and we'll go through some more exciting details then. Okay. And then for the open-label extension late breaker data next month, what sort of analysis are we expecting? Is there more follow-up data, or is it the same cutoff date as what we have seen? Yeah. So a lot of the data that will be presented there, much of which we have presented, and that is data for the 6-month cutoff. So that will provide the percent reduction in countable motor seizures at that time point, as well as the full safety dataset for the cohort that has reached that point. We were pleased to see that it was accepted as an open-label extension study and it'll allow us to have a more in-depth discussion with our potential investigators. The beauty of this is it's in Europe. It gives us a great opportunity to start to engage with our potential European investigators. Okay. And then one last one for 659. I guess, where do you guys stand on the partial clinical hold there, and what do you need to resolve it if it's already not resolved? Right. So with regards to the partial clinical hold, it is still in place, and our plan is to move forward with a complete response to the partial clinical hold that will be coupled with the proposal for the multiple ascending dose study. And so we would anticipate resolving that soon. Okay. Wonderful. Thanks for taking the question. David Hoang from Citigroup. Please go ahead. Hi there. Thanks for taking my question. So first, I just wanted to ask about, again, the indication selection. I think you had the slide up, and you showed quite a number of indications across a few different therapeutic areas. Should we really be thinking about it as, I guess, selecting just a single indication, or could you think about maybe going after more than one indication and, let's say, even having the potential to potentially partner and try to access larger indications? And then I had one follow-up. Yeah. Great question. I think we are waiting to decide how many potential indications we could take into phase II. And so we're going to continue to look at that along the way. The one challenge, to be honest with everyone, is that the patent life on LP659 is a little bit limited. We have composition of matter to 2031 plus patent term extensions. So it's helping us continue to think about orphan indications as we build out the entire intellectual property portfolio. That doesn't mean we can't go after broader, bigger indications, but we want to make sure we think about it in the right way. Great. Really helpful. And then I just wanted to ask quickly on the overall safety profile of the 659 molecule. You talked a lot about cardiac and not seeing anything there. But if you think about other physiological systems, ocular and such, how would you say 659 compares to other S1P molecules in the class? Thanks, Randall. Thanks for asking that. I went through that early on. It's the boring part of what I go through, the safety profile of a drug. In the mods, you do have to actually look more closely, not just at the cardiovascular system, but ocular and macular edema is a not uncommon finding. Impact on pulmonary function is a not uncommon finding. So this is a single ascending dose study. It's our initial dataset, but we did not see abnormalities in the other organ systems that are typically seen. But it's a big caveat. This is just a single ascending dose study. We'll continue, obviously, to monitor pulmonary, cardiovascular, and ocular findings. Plus, what I had mentioned at the very, very end is infections. There's an interesting aspect of the mods. You do want to have lymphocyte reduction, but you want to be kind of selective. You don't want to totally shut down the immune system and immune surveillance. So it's important to follow the potential for infections and opportunistic infections. We saw no infections in this dataset, and we'll continue to monitor that for that adverse event as well. Appreciate you asking that question. Thanks a lot. Yatin Suneja from Guggenheim Securities. Please go ahead. Hey, guys. Thank you for taking my question. Maybe two for me. In terms of the endpoint, if you go for the broader DEE indication, could you talk about how would you harmonize those endpoints across different subsets of DEEs? So that's one. And then the second one on the S1P molecule, I might have missed it. Is there a food effect that you are observing? So that's sort of one. And then maybe if you can specify what you want to see in the MAD specifically, that would be helpful. Thank you so much. Sure. Do you want to take the first ones? I can do the last one on that. You can. Yeah. So endpoint, again, we'll go through this in a lot more detail in our research call. But the primary endpoint that we utilized in the Pacific study was countable motor seizures. I would anticipate that is the likely endpoint that would be utilized in our subsequent studies. We anticipate that that can be harmonized across the global study because this is an endpoint that has been commonly used with other medications that have been approved in this space. I wouldn't anticipate this being a surprise or something unanticipated. Plus, as you can imagine, we have been having ongoing discussions with regulatory authorities outside the U.S. Then on 659, food effect? We don't analyze food effect in a single ascending dose study. Those are best done as separate studies. And I can't comment today because I don't remember if that would be a component of the multiple ascending dose study. And then what would we like to see in the MAD? Obviously, I think we would like to see continued safety. That's the first and foremost. Obviously, on the cardiovascular side, the other mods have used a combination of dose titration as well as monitoring to avoid cardiovascular risks. etrasimod didn't have to do either. Whether or not we'll have that final answer based on the MAD, unknown. Obviously, we will have to keep an eye on that all the way through the development of 659. We're going to want to see lymphocyte reduction over time, and we're going to want to look at that from a sustained perspective. That tends to be the dataset that folks look at. We're obviously incredibly pleased that we were able to see significant lymphocyte reduction in the single ascending dose. Tends to get a little bit better with the MAD. But we didn't see broad immune suppression, which obviously is important for the S1P space. So those were kind of the things we would be looking for from the MAD to make the decision to move the molecule forward. Does that answer your question, Yatin? Yes. Thank you so much. Thank you for the questions. That concludes our Q&A session. I will now turn the conference back over to Mr. Kevin Lind for closing remarks. I want to thank everyone for joining the call today and for sharing in our enthusiasm in the Longboard story. We'll continue to execute, deliver, and think differentially about clinical development and how we can best serve patients, the community, and our stakeholders. Have a great day.