Morning, everyone. Thank you so much for joining us. I'm Salveen Richter, biotechnology analyst at Goldman Sachs, and we're really pleased to have the Rapport team with us. Next to me is Abe Ceesay, Chief Executive Officer, and then Troy Ignelzi, Chief Financial Officer. To start, Abe, it's been about a year since Rapport went public. Can you provide us an update on your progress since then and an overview of the near-term catalyst path, recognizing clearly big data coming this year? Sure. Yeah. No, it's been a really productive year, as you said, Salveen. We went public just about a year ago, and we've been able to accomplish a lot over the course of that year. Our primary focus has been the clinical development of RAP-219, our lead program. We have been able to complete some really informative phase one studies, multiple ascending dose studies, as well as a human PET study that I think have really increased our confidence in the overall pharmacology, PK profile, specificity of this compound, as well as just the receptor overall in terms of the receptor-associated protein. The second element has really been the focus of our phase IIA proof of concept study, which is a phase IIA proof of concept study in refractory focal epilepsy patients. The difference is that these patients have an implantable neurostimulation device that we're really leveraging for the diagnostic purposes. We've been really heads down executing that study and looking forward to our data readout in September, which we kind of just narrowed the focus of that data readout or the guidance to September last week. Maybe framing that, starting with the epilepsy program here, walk us through the study design as well as frame what we should be looking for in the context of that data set. Sure. Maybe what I can do, just a couple of seconds on why we chose to do this study in the manner that we did. Our strategy as we thought about the 219 program in epilepsy was to produce compelling proof of concept results that we believed were highly translatable to a phase III registration setting and, two, be able to do that in a very efficient manner. When you look at the proof of concept models that exist in epilepsy, historically, they've been models such as photosensitive epilepsy as well as external EEG readings. Both of those models, while interesting and provide some pharmacodynamic insights, really are not translatable as you think about efficacy in your registrational patient population. They are not in refractory focal epilepsy patients. Through really collaboration with the community, but also us really looking at the literature, what we decided to do was to do a phase IIA proof of concept study in refractory focal epilepsy patients, leveraging a diagnostic biomarker, an EEG biomarker, that based on the literature is highly correlated with clinical seizures, which is ultimately your endpoint that you'll be assessing in phase III studies. Our study specifically enrolls refractory focal epilepsy patients, patients that have had this device implanted for a minimum of 15 months. These patients have a background seizure burden. They're on multiple antiepileptics, just as refractory focal epilepsy patients are in phase III settings. We're leveraging this EEG biomarker as well as collecting clinical seizure diary data for our endpoints. It's a really interesting design, one that I think we've gotten a lot of credit for in the community. We have an eight-week retrospective period where we look at these patients, given the fact that we have all of their historic electrographic data to really confirm kind of the consistency of their disease, but also ensure that no changes have been made to either their device or their background medications. Once they have and reach the inclusion criteria over those eight weeks of retrospective data, they go into a 28-day prospective period where nothing, again, can be changed. In that 28-day prospective period, they actually keep their clinical seizure diary, and then they go into an eight-week treatment period where they're introduced to RAP-219. Maybe just to kind of walk back on that point, what was the rationale for this study design? Why conduct a trial in this manner that's different from the other epilepsy trials that have been conducted? Yeah. So when you look at epilepsy trials, clinical seizure diaries are really the mainstay endpoint that you will ultimately use in phase III studies. What the literature has really started to communicate and the community has communicated is that clinical seizure diaries are really wrought with error. These clinical seizure diaries really, at the end of the day, are the seizures that a patient remembers, but they are not a reflection of the ongoing seizure burden that patients have and disease burden. What we looked at was, and clinical seizure studies as an endpoint for a proof of concept study take a long time. That would be almost two and a half years to data. By leveraging this biomarker, you really get the best of both worlds. You get a highly objective reading on electrographic activity that, at the end of the day, are seizures. We're able to do a study very efficiently. We're going to be able to have data in about a year from the initiation of this study to top-line results. We're going to be able to see that electrographic activity and then be able to match that up against clinical seizure data. When we really talk to the community and we've seen some reports on this, the majority of the community thinks that this is really a superior design to what's been done historically. You recently hosted an investor event with Dr. Jacqueline French, who's a thought leader here in the epilepsy space and a primary investigator in your phase II trial. Can you walk us through the key points that you took away from, or you were trying to basically provide to the investor community out of this event, but also the rationale for why long episodes as a biomarker are valid with regard to proving proof of concept? Sure. Do you want to, Troy, maybe add the things that we highlighted at the investor event, and then I'll talk a little bit about Jackie's insights? Sure. Because it is an open-label trial, we'll be going quiet at probably an earlier stage than companies might. The data coming in September, so you could see us going quieter. What we wanted to do was get information out there so folks could continue to do work, come back to us with some questions. The first thing is we noted, as suggested here, the trial is fully enrolled. We'll have 30 patients to evaluate. We had originally targeted approximately 20, but because of the trial design and where patients were in the screening process, we wanted to allow them to stay in once the 20th patient was dosed. Secondly, we noted the specific timing, meaning September, is when we'll have the data. We also outlined the baseline characteristics of 14 of the ultimate 30 patients that we were almost half. Fourteen wasn't a magical number. That was just the number of patients that we could get fully QC'd baseline characteristics from at that point in time when we put out the investor and analyst materials on Monday of last week. We also set out the first treatment emergent adverse event full table. I think people were very happy to see that it is truly a differentiated profile, at least at that stage in development, meaning phase I, as Abe talked about, two meds and one PET results. The idea was to put the information out there. Jackie talked a lot, and Abe can go into that about the correlation there. I think people were happy to see that. It was nice to see that there is room in there for clinical seizures. We announced that there were 10 was the median. Also, 51 patients, excuse me, long episode events for the baseline characteristics, and importantly, a 92% concordance with electrographic seizures. Those were the key baseline characteristics that we put out. Yeah. Dr. French, I think, did a really nice job highlighting a few things. One is the ongoing unmet need with refractory focal epilepsy patients, the fact that really nothing has changed over her entire career in terms of the percent of patients that are refractory. This burden of disease has not changed, although there have been multiple medications that have been introduced to patients. Second, she really highlighted the value of this study design. The last aspect that I think she really was able to articulate very well was why this study design and this endpoint is a really objective analysis to really be able to understand the efficacy of a drug very efficiently and how translatable that is to really predicting the reduction of clinical seizures. There's one other thing I actually forgot to put out there. We did establish what we saw were the trial goals from a numerical perspective. I guess the reason I forgot is because they're not, we didn't try to set this goal. What we want to do is demonstrate that we have a drug from an efficacy perspective that's competitive. What we said was from a long episode, we wanted to see a 30% reduction in 40% of the participants. If you recall, the long episode correlation is 30% reduction in long episodes correlates to a 50% reduction in clinical episodes. That was our starting point when we were doing this analysis. It wasn't just us that's done it. There have been multiple other groups that have published on this correlation. A 50% reduction in clinical episode is kind of what you're seeing as the standard of the drugs that are out there today. We wanted to see a 50% reduction in clinical episodes in 40% of the participants there, again, realizing that the trial is really designed around the long episodes. Before we kind of walk into the bars that we want to see, you mentioned data in September. Have you disclosed the forum for which this data would be presented? It'll be some kind of a specific press release around the data, yes. Perfect. So help us understand the bars for success from both the primary and the secondary efficacy measures, which you laid out at the meeting and briefly touched upon here. How could the potential reasoning be if the bars achieve clinical seizures? Yeah. We see that as a low probability. When you look at kind of the correlation between electrographic activity and clinical seizures, it's pretty tight. We were, again, confident in terms of putting those efficacy expectations out there because, as we said, the literature is really supportive of those two things moving together. When you really think about the efficacy parameters, it starts where Troy said, is that what the publications and the literature has supported is that there is a threshold for long episode reduction that you need to achieve to see a 50% reduction in clinical seizures. That threshold is 30%. That's really how the study was powered. Also, really, we were focused to make sure that we see a healthy responder rate there, and that is that 40% responder rate. When you think about the 50% clinical seizure reduction, when you look at approved medications as well as medications that are in development, such as Xenon's agent, as well as a newly approved or most recently approved medication, such as Cenobamate, you see roughly 25%-55% of patients across both Xenon, Cenobamate, but other medications can achieve a 50% clinical seizure reduction. We set the bar at 40%. We believe if we see a 40% responder rate, again, achieving a 50% clinical seizure reduction, that's a compelling profile, especially if you think about the other differentiating factors of RAP-219, lack of sedation given the target and the biology, once-daily dosing, a highly potent drug. We think that should really afford itself to be a highly differentiated profile. Let's say these bars are met, and this is a positive trial. How do you think about the translatability of this data to success in a phase III or pivotal study? Yeah. Again, one of the reasons that we did this study design is because we believe that the data in a positive scenario will be highly translatable. We will be able to understand in a refractory focal epilepsy patient population that demographically looks very similar to those patients that are enrolled in a phase III study. We will be able to define highly objective electrographic activity as well as clinical seizure activity. Being able to take those results, we think we can really be thoughtful about effect size as well as the powering of a phase III study. Our strategy has been and continues to be that based on a positive result, we will step into an end of phase II meeting with the FDA and then right into trials that are designed to be registrational. Those would be two parallel registrational trials. Stepping back into the success for this upcoming trial, you have presented full phase I SAD and MAD data and PET data. Discuss how your confidence lies in the context of the datasets that you have in hand, but also the differentiated half-life of the drug and the titration schedule that can be pulled here. Yeah. In our two multiple ascending dose studies, when we look back at the preclinical data, which is, again, highly translatable in epilepsy, one of the benefits of epilepsy drug development, we saw a range of efficacy in 50%-70% receptor occupancy, and really very limited benefit at 80% receptor occupancy. That has really always been our target. In the multiple ascending dose studies, we tested many different titration schemas and dosing schemas to basically achieve that 50%-70%. In our human PET study, what we were able to do is, one, confirm the localization of the target or reconfirm that, but then also to define that PK-RO relationship. What we saw there is actually the RO relationship tightened in our human PET study. From the animal data, it was about 3-7 nanograms per ml, 3 nanograms being 50% receptor occupancy, 7 being 70%. What we saw from our human PET study is that's narrowed to about 3-5.5. What that now allows us to do is have a lot of dosing flexibility as we move forward. The dose that we are currently using, which we assessed in our multiple ascending dose study that was generally well tolerated, we saw very limited treatment emergent adverse events, is a dose of 0.75 for the first five days, stepping up to 1.25. What that showed in our human PET study is that achieves a receptor occupancy of 85%. We are really confident in the dose that we are bringing forward. Now, given the data in a positive data scenario, plus the work that we've done in the MAD setting, we believe we're going to have a lot of flexibility as we think about bringing kind of really balancing that tolerability versus efficacy as we think about phase III. How are you managing right now in this trial with regard to baseline characteristics and the ability to deal with any noise from prior therapies or even just that washout period or wash-in period that you need? Yeah. So it's another real benefit of this study design is that you're able to ensure that these patients have a really robust set of baseline data. So we have eight weeks of retrospective data, four weeks of prospective data. Throughout all of those data periods, these patients can have no changes to their device settings. They can have no changes to their background medications. To a certain extent, these patients serve as their own control. There's 12 weeks of data. Then they enter in the eight-week treatment period where we're introducing RAP-219. We're looking at both electrographic outcomes as well as the clinical seizure diaries. And then, as you mentioned, Salveen, after the eight-week treatment period, there's an eight-week washout period. What's really interesting about that eight-week washout period, that eight-week washout period will not be a part of our top-line results. Once we have that data, we're really interested in that data because this drug has a really long half-life, 8-14 days, which is beneficial to epilepsy patients because most epilepsy drugs, anti-seizure medications, have short half-lives. The concern there is patients miss a dose. They can have a breakthrough seizure. I thought Jackie told a very powerful story about that at our investor and analyst day about how risky that can be. What we'll be able to see in that washout period, given the long half-life of our drug, given the fact that we're measuring electrographic activity, basically based on the washout of our drug, is when you see that electrographic activity start to come back. We think that that will be another compelling differentiating factor with the drug. Got it. Assuming a successful readout here, what would the pivotal developmental path look like? The pivotal developmental path will look very similar to previous drugs or drugs that are currently in development. We'll be looking at a clinical seizure outcome and enrolling and powering appropriately for what we know exists in terms of a placebo effect in clinical seizure diaries. That exists, and we'd be powering effectively for that. They would be very standard trials. Moving to the rest of the pipeline, you are developing RAP-219 in bipolar mania and neuropathic pain. Can you discuss the biologic rationale behind developing the drug in these indications and provide an update on where the program stands? Yeah. So when we looked at RAP-219, we always saw it as a pipeline and a product opportunity, both in terms of formulation that I can touch on as well as the indications. In terms of indications, anti-seizure medications have been shown to be effective in both bipolar as well as neuropathic pain. With bipolar, you're looking at both anti-mania agents but also mood stabilization agents. When you look at data, admittedly, the preclinical rationale as well as the preclinical translatability in bipolar is nowhere close to what it is in epilepsy. It's somewhat nonexistent. We do know that some of the effective anti-seizure medications are working through in some way, in some form, on glutamate pathways. We obviously are working there, and we believe we have a drug, again, that is focused in the regions of the brain where hyperexcitability exists in mania and also has a differentiated profile in the fact that it's non-sedating. For neuropathic pain, the biology is a bit stronger given the fact that AMPA receptors containing TARP gamma-8, the other place that they exist outside of the brain, is actually in the dorsal horn of the spinal cord. We've had some really encouraging preclinical data for neuropathic pain as well. We're looking to initiate the bipolar study here in the third quarter. For the neuropathic pain program, the FDA did put that program on clinical hold, requesting for some protocol changes. We're currently working through those, and we hope that we'll be in the position to re-guide on the initiation of a neuropathic pain program this year. Do you have an understanding of the next steps required with regard to coming off clinical hold? Yeah. It's really about some protocol changes as it relates to patient monitoring. Remember that we see RAP-219 as a pipeline and a product. And those three indications that we just outlined, epilepsy, bipolar, and neuropathic pain, are three different divisions of the FDA. So they're all going to have different considerations based on the population that you're actually looking to assess. What we can say is the same package that enabled our epilepsy study is the same package that went to the pain division. The pain division had some questions on how patients should be effectively monitored in an outpatient neuropathic pain setting. So we're just working through those. What we want to make sure is with any study we do with RAP-219, we want to make sure it's a study, one, that is feasible to run, and two, puts the drug in the best position for success. You provided phase I MAD data and talked about the, and you've talked about the potential for an acute dosing regimen here in bipolar mania. Can you just speak to how that might kind of inform that approach? Sure. In bipolar, these trials are very short. They are three to five weeks. In an acutely manic setting, you need to show efficacy, and you need to show efficacy relatively rapidly within five to seven days in that patient setting. It is an inpatient setting for most of these trials. What we wanted to do in our MAD trials is really explore that to see how could we achieve a target receptor occupancy within five days that we felt would deliver efficacy in that setting. We did confirm that in our MAD studies and then tied that with the PET data. We are confident that we have a dosing regimen that we will bring forward in the bipolar study that will get to a target receptor occupancy within five days. You're developing a long-acting injectable formulation here. When do you plan to provide an update with regard to how that's working? If successful, would this be the optimal mode of administration in all disclosed indications? Yeah. So we, given the unique characteristics for 219, highly potent drug, which means low drug levels on board, no DDIs, somewhat of a built-in titration with a half-life of the compound, it really makes it amenable to a long-acting injectable. It would be the first long-acting injectable for epilepsy. If anyone listened to our investor and analyst day, I thought Jackie did a really nice job talking about this. This would be transformational for patients, truly. Long-acting injectable has not been developed with an anti-seizure medication, not based on the lack of need. It's based on the limitations of current therapies. If you have high drug levels on board, you have drug-drug interactions, you really can't have a long-acting injectable with current anti-seizure medications. We think RAP-219 affords the ability to do that. So we've done some feasibility work on formulation. We believe that we are in a really good position with formulation. On the backs of positive data, we'll be in a position to talk through kind of the development plan of a long-acting injectable and when it will be introduced. When you look at the utilization of a long-acting injectable, historically, LAIs have been used. Patients are on the oral formulation. They can tolerate the oral formulation. It's effective. Then a long-acting injectable is introduced. We think it will probably follow that kind of traditional approach, but it could be a real game changer for patients, really ensure patients aren't missing doses, which has very high risk of injury in certain cases, mortality, and also would be a really nice IP strategy for the compound as well. I guess overall, as we look to this data read in September in epilepsy, what is your confidence that that proof of concept data will emerge here? Where do you see the risks? Yeah. We can be as confident as one is in drug development. When I think about epilepsy drug development, it's an area that I think we really benefit from high translation between preclinical and clinical. That's where we start. We have a very robust preclinical package supporting 219. The second aspect is what Troy walked through. Key for us was to ensure that these patients had a baseline characteristic, a set of baseline characteristics that would put us in a position to detect a clinically meaningful change. We've seen a high level of disease burden electrographically. We've seen a concordance of 92% between long episodes and electrographic seizures. That means when we are reducing long episodes, we are reducing seizures. Patients have a baseline seizure count of 10. To put that in context, clinical seizure count of 10. Put that in context, if you look at the Xenon phase II trial, they had, I think, a roughly 13. You look at the pooled analysis of the phase III from Cenobamate, they had 6-8 baseline clinical seizures. 10 puts us in a really good position. I think we have everything going our way in this study. Obviously, we have a dose that we believe in that is getting to 85% receptor occupancy. We have to continue to keep the trial on track, which it is. I think we feel as good as one can. Troy, maybe a last question here. Where do you stand from a cash position? How does that, I guess, where does that equate to in the context of covering these programs to proof of concept dynamics? Yeah. So we ended the quarter, reported $285 million, which does get us through at least the end of 2026. Certainly well through the readout that we expect here in September. Assuming positive data, it would allow us to fully fund all of the activities to get the phase III up and running as quickly as possible. Keeping in mind, I did have someone ask me last week, would you be able to get the phase III going before the end of the year? Probably not. We're going to read out the top-line efficacy data, which is the first eight weeks or the eight weeks of treatment in September. As Abe mentioned, there's also an eight-week follow-up that's part of the trial. That information would be very helpful as we think about finalizing the phase III design or into phase II meeting with the FDA and move forward from there. We're in a position to be able to move all of that forward and continue to execute on the bipolar trial, which we'll initiate also in the third quarter. We'll go with that. Thank you so much. Thanks, Salveen. Thank you. Take care. Thanks, everyone.