Good morning, and thank you for joining us. This is Ian McDonald, Chief Executive Officer of Bright Minds Biosciences. Today we're reporting the top-line data from the phase II breakthrough study of BMB-101 in adults with drug-resistant absence seizures, as well as developmental and epileptic encephalopathies. These are patients with highly refractory disease and substantial treatment history, and the results you'll see today should be interpreted in that context. Before we begin, please note that this presentation is current as of January 2026 and contains forward-looking statements within the meaning of applicable securities law, including statements about clinical development plans, timelines, regulatory pathways, and potential safety and efficacy of BMB-101. Actual results may differ materially due to risks and uncertainties described in our filings, including our annual report on Form 40-F and other SEC and SEDAR+ disclosures. This presentation is summary in nature, and we do not undertake to update or revise forward-looking statements except as required by law. Joining myself today from Bright Minds are Dr. Jan Pedersen, our Chief Scientific Officer, Dr. Stephen Collins, our Chief Medical Officer, and Alex Vasilkevich, our Chief Operating Officer. Before we turn to the data, we wanted to take a moment to recognize the people who made this study possible. We thank the principal investigators and their outstanding teams for the execution, and we thank our clinical partners who supported trial operations, a nd most importantly, we thank the patients and their families who participated. Their commitment is what enables progress, and we're grateful for the opportunity to share these results with you all today. We'll start with the top-line takeaways. Then Dr. Collins will walk you through the study design, the patient population, and the supporting efficacy and safety details behind the headline numbers. This slide is a quick overview of what BMB-101 is and why we think it has potential to be differentiated as a chronic therapy. First, BMB-101 is a highly selective biased serotonin 2C agonist. The rationale for a biased agonist is to maintain sustained signaling without driving receptor desensitization, which is a key mechanism behind tolerance development with chronic dosing. Second, BMB-101 has linear pharmacokinetics across the dosing range. In practical terms, that means dose adjustments are more straightforward and predictable without unexpected spikes in peak exposure that can drive Cmax-related adverse events. Third, administration is practical. It's currently dosed twice daily with potential for once-daily dosing, and it's stored at room temperatures, features that support adherence and scalability in global trials. Finally, across our phase I and phase II experience, BMB-101 has demonstrated that it is safe and well- tolerated, which is the foundation for phase II/III regulatory studies we've outlined. Here's the top line. BMB-101 demonstrated meaningful efficacy in both cohorts we studied. In drug-resistant DE, we observed a 63% median reduction in major motor seizures as measured by seizure calendar. In the Absence seizure cohort, using objective 24-hour EEG with independent blinded reads, we observed a 73% median reduction in seizure events for episodes longer than three seconds, along with a strong reduction in seizure burden as well. What matters most here is the context. These were highly refractory adult patients, heavily pretreated on substantial background polytherapy, and representative of the hardest end of the clinical spectrum. Seeing this magnitude of effect in that setting is a compelling efficacy signal that excites us about the possibilities of this compound to help these patients in need. With that, I'll turn it over to Dr. Stephen Collins, our Chief Medical Officer. This slide is the clinical bottom line, why the total package points to potentially best in class. First, BMB-101 is demonstrating a profile that works in both populations we studied: developmental and epileptic encephalopathies and absence seizures. That matters because it suggests this isn't a narrow one-subtype effect. Second, we achieved the key objectives in each cohort using pre-specified measures: major motor seizures in DE and objective 24-hour EEG metrics in absence. The combination of robust effect size and objective measurement in absence is particularly important for how clinicians will interpret the status. Third, when you put those outcomes together, clinically meaningful efficacy across two high-need epilepsy settings with a tolerability profile that supports continued dosing, you get the ingredients for a potentially best-in-class therapy: strong efficacy, broad applicability, and the ability to stay on drug for long enough to benefit. F inally, from an adoption standpoint, the dosing profile supports real-world use, which is ultimately what converts into clinical performance, into standard of care practice. Thank you, Ian. I am Stephen Collins, the Chief Medical Officer of Bright Minds Biosciences, and I'm very happy to share our top-line efficacy, safety, and tolerability data from our Phase 2 study in patients with absence seizures or developmental and epileptic encephalopathies. The study uses a classic design for measuring the effect of an anti-seizure medication, having a one-month baseline period, then weekly titration over four weeks using weight-based dosing to a maximum dose followed by a maintenance phase. The study was performed in Australia at five very experienced epilepsy centers as an open-label trial with two separate cohorts of adult subjects: those with refractory absence seizures and those subjects with refractory developmental and epileptic encephalopathies. The baseline and titration periods were the same for both cohorts, while the maintenance phases were different. The absence subjects required a shorter two-week period due to the high number of seizures they experienced, while in the DEE group, a four-week period was used. The titration of the liquid formulation was from 0.67 milligrams per kilogram, taken twice a day, upwards by 0.33 milligrams per kilogram to a maximum dose of 2 milligrams per kilogram, subject to the subject, caregiver, and investigator deeming an appropriate stopping dose based on desired efficacy or tolerability had been obtained. As stated above, the maintenance period was two weeks for absence subjects and four weeks for developmental and epileptic encephalopathy subjects. Subjects or their caregivers maintained seizure calendars in both cohorts, as well as having 24-hour ambulatory EEGs during baseline and maintenance phases. Absence seizure subjects had two 24-hour ambulatory EEGs in baseline, as well as two 24-hour ambulatory EEGs at the end of maintenance phase. DEE subjects had one 24-hour ambulatory EEG in baseline and one 24-hour ambulatory EEG at the end of maintenance phase. Subjects could, with the agreement of the investigator, enter an open-label extension phase, which may continue until regulatory approval of BMB-101. Major entry criteria for DEE subjects required them to have four or more major motor seizures in the four-week baseline, and for the absence seizure subjects, an average of four or more absence seizures in each of the two 24-hour ambulatory EEGs. Key endpoints for both cohorts were changes in clinical or laboratory safety parameters, while the efficacy endpoints were change in seizure frequency based on the 28-day seizure diary for the DEE subjects and change in seizure frequency based on the 24-hour EEG recording for the absence subjects. As Ian had mentioned, the study was in highly refractory patients. 15 absence and nine DEE subjects were enrolled. The patients were highly refractory based on the numbers of failed therapies, the duration of epilepsy, and the seizure burdens. In the absence cohort, up to seven of the treatments had failed to control seizures, and in the DEE cohort, subjects had histories of even more failed medications and devices, including use of fenfluramine and vagus nerve stimulation. The absence cohort all had three per second typical absence seizures as their major or only seizure type. The DEE cohort was largely comprised of Lennox-Gastaut syndrome subjects: seven with LGS and two with DEE other category, one with Dravet syndrome and one with Rett syndrome. The study mirrored real-world treatment of refractory treatment patients. Since there was no limit on the number of anti-seizure medications or therapies, the patients were allowed to be taken on entry into the study. Study demographics are shown below. Major elements included adults with an average age of 30 who were well matched by sex in the absence cohort and with a slight increase in numbers of female subjects in the DEE cohort. Medication was quite high in both absence and DEE subjects. As you can see, absence subjects were taking an average of three anti-seizure medicines or therapies, having failed previously multiple treatments, up to 16 in one case. I n the DEE group, there was a mean of five anti-seizure therapies on entry and nine previously failed treatments. Many of the subjects had also failed vagal nerve stimulation in addition to the multiple failed anti-seizure medications. The study screen-to-enroll ratio was quite good: 17 screened with 15 enrolled in absence, 10 screened with nine enrolled in DEE. Absence cohort: we had three discontinuations in the absence cohort. One was related to drug product, with the subject unable to tolerate the taste. The original formulation was extremely sweet, so a reformulation with a much reduced amount of sweetening agent was produced. The new formulation had the same concentration of active agent as the prior formulation. No subsequent subjects had objections to the t aste. Two other subjects discontinued, due in the first case to flu-like symptoms of fatigue, rated as possibly related, and in another subject who complained of dizziness, rated as possibly related. 12 subjects completed the maintenance phase. The absence evaluable population consisted of 11 subjects, including one DEE subject who met absence entry criteria and excluding one who did not meet entry criteria and one with uninterpretable EEGs. In the DEE group, 10 subjects entered screening, nine were enrolled. Three subjects discontinued: one for re-emergence of fluctuations in behavior seen prior to the study, rated as possibly related to drug. One falling with shoulder fracture suffered from a seizure-related fall, rated as not related to drug, a nd one with lethargy deemed possibly related. Six subjects completed the maintenance phase and formed the DEE evaluable population. We are confident that BMB-101 was well tolerated by most subjects and that ensuing studies will similarly demons trate good tolerability and safety. Our study is the first using quantitative and robust EEG technology to study a novel anti-absence therapy. The study demonstrated that the 5-HT2C mechanism appears to effectively shut down the spike-wave discharge numbers and total burden. To further explain the importance of 5-HT2C regulation of generalized seizures, our Chief Scientific Officer, Dr. Jan Pedersen, will review the pathophysiology of absence seizures. Thank you, Steve. As you said, let's just pause for a minute and reflect upon the mechanism by which 5-HT2C mechanism controls absence seizures. Typical absence seizures is a well-defined form of generalized epilepsy. An absence seizure is a distinct 2-5 Hz spike-wave discharge, an abnormal and unique paroxysmal pattern of a high-velocity spike followed by a slower dome-shaped wave on the background of a normal EEG. The EEG signature of the absence seizure is pathognomonic and constitutes the actual seizure event and has been so defined for over the past 70 years. Spike-wave discharges, or generalized spike-wave discharge activity, is generated by oscillations in the well-understood corticothalamocortical network, or the CTC network. The CTC network is a key neuronal network involved in cognitive functioning. Activation of 5-HT2C receptors in the CTC network releases serotonin and effectively switches off calcium-dependent bursting in the CTC network by depolarizing and desynchronizing reticular neurons that carry calcium channels. For this reason, 5-HT2C mechanism constitutes an efficient and selective mechanism for switching off spike-wave discharges independent of calcium channel type. I'll now hand over the microphone to Steve Collins again to take you through the top-line results for the absence seizure patients in the breakthrough study. Clinicians and patients currently have very limited treatments for absence seizures. In the case of absence epilepsies, which have absence seizures as the only seizure type, ethosuximide is the first-line therapy most used. Unfortunately, especially as children age and as other absence epilepsies emerge in adolescence and adulthood, ethosuximide works less well, and in epilepsies with mixed seizure types, such as juvenile myoclonic epilepsy with generalized tonic-clonic seizures, ethosuximide does not provide any efficacy in these other seizure types. Next most often added therapy is valproic acid, Depakote, which, while efficacious for many patients, has considerable issues with safety and tolerability. Depakote has multiple black box warnings and multiple associated adverse effects, including teratogenicity, liver failure, weight gain, and hair loss. After ethosuximide and valproic acid come a series of drugs which clinicians use, but none are either very effective nor without safety issues. Therefore, patients with absence seizures, regardless of epilepsy type, need a new, effective, safe, and well-tolerated therapy. As stated, this study uses modern, quantitative, and robust EEG methodology to demonstrate the effect of a novel absence therapy, BMB-101. We show that we significantly reduce both the number of absence seizures and the total burden of absence seizures. That is, the total time subjects experience absence seizures or three or more seconds' duration over 24 hours. The median reduction in the number of seizures was 73.1%, while the median reduction of seizure burden was 74.4%. The reduction of seizures is statistically significant, with a p-value of 0.0117, as determined by the Wilcoxon signed-rank test. Seizures are counted based on two 24-hour ambulatory EEG recordings with the absence cohort done during the baseline and two 24-hour ambulatory EEGs performed at the end of maintenance. Additionally, in the one DEE subject with absence seizures, there was one 24-hour ambulatory EEG recording done at baseline and one 24-hour ambulatory EEG performed at the end of maintenance. EEG analysis and seizure counting was done by independent and blinded readers. We have defined seizure as those seizures with the classic 3 per second spike and wave pattern of absence seizures and with a duration greater than or equal to 3 seconds, since this is the commonly clinically used metric for defining an absence seizure. The very clinically significant reduction of 73% in the numbers of seizures mirrors nearly exactly the decrease of 74% seen in total seizure burden. To explore the reduction of absence seizures induced by BMB-101 even more, we have shown that reductions in seizures, whether by numbers or burden, occur independent of seizure duration. Thus, subject seizures and burden are reduced across a wide spectrum of seizure durations. Given the importance of sleep in general, and particularly in patients with epilepsies, since we had multiple 24-hour EEG recordings, we were able to explore sleep architecture in the absence seizure cohort. Quality of sleep is intrinsically related to the normal progression and duration of sleep stages. Here, we see a substantial and significant increase in REM sleep, nearly doubling from baseline. Why is REM sleep important? Because REM supports memory consolidation, emotional regulation, and cognitive function, and so improvements in sleep architecture with increased REM may be beneficial to patients with absence seizures. For perspective, the normal healthy adult REM sleep duration is between 90 and 120 minutes during a seven to eight-hour sleep cycle. Since a near 2-hour duration of REM sleep was attained while on BMB-101, the data generated indicates that we have acted to normalize REM sleep patterns in the study participants. Now, we will discuss top-line efficacy results in the DEE cohort. Treatment with BMB-101 led to a clearly significant and very clinically meaningful decrease in major motor seizures in both the Lennox-Gastaut syndrome patients and in the DEE other patients. In the Lennox-Gastaut group, there was a 60.3% median reduction in major motor seizures, and in the DEE other, a 76.1% median reduction in major motor seizures. On a per-patient review, we see one subject had a small worsening of seizures, while the remainder all had significant reductions ranging from 47.3% to 100%. Importantly, in the DEE other group, while small in number, we see a significant drop in seizures in the Dravet subject, who as an adult had failed multiple medications, including fenfluramine, and who achieved a 50.3% reduction on BMB-101. Also, the Rett subject, who had an average of 15 seizures a day at baseline, achieved a 100% reduction of seizures, which has lasted as of this update for 43 days. This seizure freedom included a period wherein the subject developed pneumonia, usually a trigger for increased seizures in this vulnerable population. The effects of BMB-101 in the previous slide clearly are significant, but even more so when viewed in light of the refractory nature of the patients in the study. These adult patients had years, even decades, of unrelieved seizures after having failed multiple anti-seizure therapies. The study did not artificially restrict subjects by numbers of concomitant therapies or numbers of previously failed drugs or devices to control their seizures. This study then accurately reflects current clinical practice for the highly refractory seizure patients who will be enrolled in future studies and who would be the treatment profile as seen in actual clinical practice. Individual illustrations of the refractory nature of this cohort include subjects requiring frequent rescue interventions with benzodiazepines to preclude serial seizures and trips to the emergency room who no longer needed those rescue therapies, a subject who failed fenfluramine yet found effect with BMB-101, and subjects gaining seizure-free periods never experienced. Why do we emphasize the treatment burden of our subjects? Well, for two reasons. As is seen in this first slide on burden, this study mirrored the real-world care of DEE patients with documented prior failed therapies ranging from 6-15. Refractory DEE patients in real clinical practice experience the same large range of prior failed treatments. In this next slide, we further our discussion on treatment burden. In real-world clinical practice, clinicians often use four or more anti-seizure treatments, not two or three. Why is this point important? It is because response rate to anti-seizure medications decreases with increasing numbers of concomitant treatments. This was shown at the most recent American Epilepsy Society meeting, as seen here on the left, data from the PACIFIC study of bexicaserin in DEE subjects. Responses decreased from a median of 75% with two or less concurrent therapies down to 51% with three or more concurrent treatments. Thus, subjects do substantially better on two or three therapies than they do on three or more. In our study, nearly all, eight of nine subjects, were on four or more therapies, with over 50% on five or more, truly a refractory population. Overall, BMB-101 demonstrated a safe and well-tolerated profile, which strongly supports advancement into registrational studies in both absence seizures and in developmental and epileptic encephalopathies. This study demonstrated that BMB-101 had quite good tolerability and safety. Important takeaways from the study include: one, there were no drug-related serious adverse events; and two, there were no significant adverse effects on vital signs, clinical, laboratory findings, or electrocardiograms. Adverse events occurring at greater than 10% either were not related to the drug, for example, respiratory infections, or were possibly related, including fatigue, constipation, headache, or drowsiness. The treatment emergent adverse events were mostly mild and not related to drug. The one severe adverse event related to drug was an instance of dry mouth, which resolved without alteration of drug dose. The two other severe events were due to a fracture of the humerus related to a seizure-induced fall and subsequent drowsiness following potent opiate administration, both of which were unrelated to study drug. Thus, in summary, BMB-101 was both safe and well-tolerated. N ow back to Ian McDonald. To close, I want to summarize what these top-line results mean in plain terms. First, on safety, BMB-101 was safe and well-tolerated across both cohorts, DEE and absence seizures, with no signal of systemic toxicity and a profile that supports moving forward with confidence. Second, on efficacy, in DEE, we're seeing approximately a 63% median seizure reduction in major motor seizures. The reason that matters is who these patients are: highly refractory adults who have failed more than eight prior anti-seizure therapies, including fenfluramine, and who are still taking roughly five concomitant anti-seizure therapies. In that context, this level of seizure reduction is exceptional and supports real best-in-class potential. Third, these data are not narrow. We're seeing significant activity in absence seizures as well, a seizure type that is common and clinically important in Lennox-Gastaut syndrome and broader DEE populations. That breadth is a differentiator. Fourth, on convenience and real-world usability. The dosing profile is practical for chronic therapy with BID administration today and a clear path to evaluating QD dosing as we optimize development. In epilepsy, where adherence matters, that matters. F inally, on the tolerability relative to the class, we believe BMB-101 has the potential to be meaningfully better tolerated than other 2C agonists, including a somnolence profile that appears closer to placebo rates, which is exactly what you want for chronic use in a polytherapy population. On the absence side, the message is straightforward. This is a first-in-class 5-HT2C agonist demonstrating robust efficacy in absence seizures using objective endpoints with extensive use of 24-hour EEG. B eyond seizure counts, we're hearing consistent reports of meaningful improvements in sleep and day-to-day function. One patient described the drug as having life-changing benefit and was visibly emotional when they learned they could continue onto the open-label extension. So the combined picture is strong efficacy in a very difficult population, objective EEG-based efficacy in absence seizures, and a safety and tolerability profile that supports efficient advancement into global registrational trials. On the DEE side, the opportunity is broad and still underserved. DEE isn't one condition. It's a spectrum of 25 or so syndromes and etiologies where a large fraction of patients remain refractory despite heavy polytherapy. Even in settings where there are approved ASMs, many patients remain inadequately controlled, and there are substantial segments, particularly adults and broader DEE other populations, where there is no clear purpose-built, branded standard of care. That is the clinical and commercial gap we're focused on: patients with high seizure burden, multiple failed therapies, and limited practical options. The top-line efficacy we're showing in this kind of population is exactly what supports the thesis that BMB-101 can become differentiated, go-to therapy in refractory DEE. In a market like DEE, with a drug that is safe, well-tolerated, and highly efficacious, one could argue peak sales in the $2-$3 billion range are certainly possible. On the absence side, the opportunity is not smaller. It is comparable in scale to DEE. We are not treating one syndrome. We are targeting a seizure type: refractory absence seizures. A bsence seizures cut across multiple disorders, including juvenile myoclonic epilepsy, childhood absence epilepsy, juvenile absence epilepsy, Lennox-Gastaut syndrome, Dravet syndrome, and many other DEEs. When you aggregate these syndromes, you end up with a patient population that is on the order of the broader DEE population. What makes this strategically powerful is that absence is a space with a clear need and no dominant branded solution around objective quantitative endpoints. Physicians are left cycling generics and combinations, often with limited control and meaningful tolerability trade-offs, especially in refractory patients. So if BMB-101 is approved with a type of objective 24-hour EEG-based efficacy we're showing here, we're not solely relying on subjective reporting, and we're demonstrating large reductions in electrographic seizure events, then the product positioning becomes straightforward. In DEE, we have a strong case to become the go-to option across the spectrum. I n refractory absence seizures, we have the potential to be effectively the only dedicated branded seizure-first type play that works across underlying diagnoses, meaning 101 could effectively become the default therapy clinicians reach for when they have patients with refractory absence activity, regardless of whether the underlying diagnosis reads juvenile myoclonic epilepsy, CAE, JAE, or any other patient who experiences absence seizures. This slide puts our top-line results in context against key peers using published phase 3 or late-stage readouts where available. Starting with BMB-101, we're showing a 60% top-line median reduction in LGS and a 63% top-line median reduction across the broader DEE cohort. When you compare that to fenfluramine in LGS, the reported efficacy is materially lower: mid-20s at the higher dose and low teens at the lower dose with a modest placebo effect. We also know that real-world use outside of the core pediatric population can be constrained by practical dose limitations. For bexicaserin, the PACIFIC study showed about 51% in LGS with a placebo rate around 20% and about 60% across the entire study. That's a meaningful signal, but our top-line effect size in a highly refractory adult DEE setting compares favorably. For cannabidiol in Lennox-Gastaut syndrome, the pivotal program is in the mid-40% range with a placebo rate in the low 20s, and in absence, the reference trial missed its primary endpoint. Cannabidiol also carries well-known tolerability limitations in practice. Where we think BMB-101 clearly separates is in the combination of efficacy breadth and practical usa bility. We are seeing efficacy across multiple seizure types, including a robust signal in absence seizures using the objective EEG endpoint, which is approximately a 70% reduction, something the other agents here do not demonstrate, and mechanistically and operationally, BMB-101 is a selective G-protein-biased serotonin 2C agonist. It appears well-tolerated and shows linear pharmacokinetics, and it has a convenient dosing profile, BID today with a potential path to once-daily dosing. Finally, we want to be disciplined about the limitations of the study. Our study was open-label, and the sample size is smaller than the phase 3 programs, but the effect sizes we're seeing across DEE and absence are compelling. They support a streamlined move into global registrational development. Here's what's next for the company and what taday's readout unlocks. First, we're moving forward to initiate global phase 2-3 regulatory studies in both developmental and epileptic encephalopathies as well as absence seizures. This work has started, and we are actively engaging with potential trial sites. Second, we will continue the full analysis of the breakthrough study, and we will report additional data throughout the year as that work is completed. Third, we are initiating the NOVA study in Prader-Willi syndrome. That trial will begin in Q1. Finally, stepping back, we're looking ahead to a very busy year with five clinical studies underway across the portfolio. Here we summarize the broader Bright Minds pipeline. BMB-101 is our lead program with top-line efficacy now reported in both DEE and absence. We're moving directly into registrational planning. Importantly, we intend to run two global registrational programs, one in DEE and one in absence seizures. So each indication has a clear purpose-built pathway to approval. In parallel, BMB-101 is advancing in Prader-Willi syndrome, where we are initiating the phase 2a proof of pharmacology NOVA study a nd BMB-101, our next-generation program for Prader-Willi syndrome, will be entering clinical development as well. Behind the lead programs, we have additional assets that broaden the portfolio: BMB-201, a serotonin 2A/2C program in preclinical development for depression, pain, and neurology; and BMB-202, a serotonin 2A agonist in preclinical development for fast-onset depression. The takeaway is that today's results strengthen the lead program and accelerate the near-term clinical roadmap, while the rest of the portfolio provides multiple additional shots on goal in high-value CNS indications. Importantly, the company is financed to execute these multiple value-inflecting clinical readouts. W ith that, our prepared remarks are concluded. We will move on to the Q&A portion of the call. Good morning, and thank you for joining us. Our first question comes from Pete Stavropoulos at Cantor. Could you comment on baseline seizure rates and baseline ASM? How do they compare to real-world patients? How do they compare to patients enrolled into clinical trials for other anti-seizure meds, a nd was there a difference in the magnitude of seizure reduction for patients as you go from patients with lower baseline ASM use to greater ASM use? Pete, thank you very much. This is Stephen Collins. A series of good questions, as usual. The baseline seizure rates and baseline ASMs, let's take that first. They absolutely compare to real-world patients. This is what clinicians are seeing daily in their clinics. I should note that the baseline seizure rate in our study was lower than bexicaserin. We'll get to this later. Generally speaking, the higher the seizure number, the more easily you see the effect of an anti-seizure medicine. The second question is, how do they compare to patients enrolled in clinical trials? They're very similar in terms of general characteristics of the seizures. However, our patients are generally older, have longer seizure burdens, have a greater number of anticonvulsant medications being taken, and, as I just spoke to, certainly compared to the bexicaserin trial, had a lower seizure total number. The last question is, was there a difference in magnitude? And I've spoke to it. I've alluded to it. We definitely see a trend towards better seizure reduction with the higher frequency of seizure at the baseline. Next question from Pete. For patients in the absence seizure cohort, you increased REM sleep duration. Was this observed across most patients? Can you help us understand, give us examples on how that could potentially impact patients? Do agents used for absence seizures impact REM sleep duration to the same magnitude observed in this study a nd can this be an attribute that could be possibly incorporated into a label? Thanks again, Pete. I'll take these one by one. So we did show increased REM sleep duration, and that was observed across the patients. Let me give you an example of how that could impact patients. For normal healthy subjects, and particularly for people who have epilepsy, having a greater than lesser portion of sleep, which is REM, improves multiple aspects of life. One is memory consolidation. The second is ability to regulate behaviors. And the third is general cognitive ability. There's a belief in the epilepsy community that improved sleep helps improve seizure control. And so this could be obviously both factors working together: better sleep, better seizures, and better REM, better quality of life. We don't have any reason to believe that other agents currently used for absence would increase REM sleep duration. Certainly, there's no reason to believe a calcium channel drug would increase REM. And there's no data in the past that valproic acid would increase REM density. The next question is, could this be possibly incorporated into a label? Yes, it could be. This would be the sort of secondary endpoint, which could be quite easily explored. And given the magnitude of effect we see here, it would be presumably quite a robust finding in a larger registrational study, as we plan to initiate quite soon. Our next question is from Charles Moore from WR Baird. Was the DEE patient in the absence seizure group included in both absence and DEE groups, or only absence? That's correct. That DEE patient was included in both absence as well as DEE, as they had displayed both major motor seizures as well as absence seizures. Another question from Charles. How many patients were able to titrate up to the maximal dose of two mg per kg? It was around 56% of the completers who got to two mg per kg. I'd point out that we had people who began seizure reductions at the very lowest dose. In point of fact, a couple of the patients, one, for example, who had 100% control, did not go to maximum dose. We allowed subjects and their caregivers and investigators to maintain a stable dose if they felt that there was a significant effect. And we certainly saw that some going seizure-free for quite considerable periods of time and others having a significant reduction of their seizures at doses lower than the two milligrams per kilogram. Thank you, Steve. Our next question comes from Joseph Thome from TD Cowen. Can you talk a little bit about the responder analysis from the absence population if possible? We are getting a couple of questions. Yeah. So let's talk about responder analysis. We certainly plan on releasing many more analyses later in the year. But clearly, with the median reduction, for example, in absence of about 73%. Thank you. Next question from Thomas Schrader, BTIG. The fatigue signal, is that real or about the level you see in most trials? Yeah. Good question, Thomas. So just for comparison, if you look at the last several Lennox-Gastaut studies at the placebo group and their adverse events, we're in the same range of people who expressed complaint of fatigue as the placebo arms of those studies. Thank you. The next question is from Yasmin Rahimi from Piper. Did you see a homogenous seizure reduction across the 11 absence seizure reductions? In other words, were there any non-responsive? The signal just got dropped. So I'll just repeat. In multiple recent Lennox-Gastaut studies, the placebo level of complaint of fatigue was in the same range as we see in this study. Thank you, Steve. The next question is from Yasmin Rahimi from Piper. Did you see a homogeneous seizure reduction across the 11 absence seizure reductions? In other words, were there any non-responders or super-responders in that cohort? I f you had run a placebo in this population, what do you predict the placebo responses would be? Thanks, Yasmin. Good questions, as always. We did see homogeneous reductions. We did not have any super-responders or non-responders. It was quite homogeneous. As you know, the EEG is not responsive to a placebo effect. S o there would be no effect on placebo in terms of the seizures as noted on the EEG. Additional questions from Yasmin. Outstanding data. What are your thoughts on timing and planning for the phase 3 in both DEE and absence epilepsy? Also, what is the regulatory path in absence epilepsy? Yes. We're planning on initiating both of those studies in this year. More on that later. I think we'd like to focus more on the data from today's study. But those studies will be beginning in 2026. Yeah. Just to respond to the regulatory path, I think what people need to remember is the vast majority of anti-seizure medications are approved for a seizure type. S o actually, a regulatory path for absence would be to gain an indication for the treatment of absence seizures. This would mean that the sales representative could go in and speak with the clinician about any patient who had absence seizures, regardless of epilepsy type. T hen a follow-up. Given the Prader-Willi syndrome opportunities development, did you observe any weight reductions across the two populations, especially in the obese individu als? Yeah. So we had a lot of relatively normal body weight individuals. That was the overwhelming majority of our study. We had two patients which we previously disclosed with obesity as well as binge eating disorder in one of the patients. Those two patients showed a notable improvement in the relationship with their food as well as showed some fairly substantial weight loss given the short duration of the study. So I think that certainly bodes well for our PWS study and makes sense when you think about the mechanism. Importantly, we didn't see a material reduction in weight of normal body weight individuals. It was more so specific to those cases. I'd just add that in neither of the cases did the subjects complain or have problems with nausea or GI. These were true weight reductions because of decrease of calories. Basically, ate less. Thank you. The next question is from Patrick Trucchio from H.C. Wainwright. You emphasized the context that these were highly refractory, heavily pretreated adult patients. How does that backdrop influence how we should interpret a 63% reduction in major motor seizures in DEE and a 73% reduction in absence seizures? Yeah. So this was an adults-only program. As Steve mentioned earlier, they're typically the hardest to treat and most refractory patients. This group was also, as we've mentioned many times in the presentation, you guys are probably tired of hearing it, a heavily pretreated group on a lot of complementing medications. So given that, as well as the patient mix, this is an LGS-weighted trial with four out of the six or 67% of the patients in the DEE group being Lennox-Gastaut, which is typically the hardest to treat, doing well. So I think in that context, the difficulty of the trial, the results compare very favorably to other trials that have been run in this space. Maybe I can just add to that, Ian, that if we look at, and I think this is being said in the presentation, if we look at the remaining seizure burden, particularly in the absence seizure patients, is there anything left to treat there? We actually see in this patient population that they have up to hundreds of absence seizures in 24 hours, clearly demonstrating that there is a very high unmet need. If I can just add one more bit. This tells us, as we go into these registrational studies, that the population that we're going to be incorporating into the study and later in real-world use of BMB-101 is going to benefit and in this general range. That's quite a strong signal. Thank you, Steve. Another question from Patrick. How does the product profile emerging for BMB-101 in DEE compare to other compounds in the class, such as fenfluramine and Bexicaserin? Yes. Let's start with fenfluramine. Fenfluramine obviously has tremendous efficacy in Dravet syndrome, less so in Lennox-Gastaut syndrome. That's likely due to a dose limitation in heavier patients in that syndrome. Obviously, they have a REMS program associated with the cardiovascular liability of 5-HT2B, something that neither us nor bexicaserin have. With regard to bexicaserin, I think our compound compares favorably with regard to the pharmacokinetic profile, the BID dosing versus TID, the room temperature storage of our compound. And from a, obviously, this is still early data with both compounds, but our tolerability appears to be quite strong. The compound is also dose linear through the dose range, which makes it a lot easier for a physician to adjust dose without running into dose-limiting adverse ev ents. Thank you. And the final question from Patrick. Durability is central to the best-in-class argument. What early signals, if any, are you seeing from patients who have continued into the open label extension? Yeah. So obviously, this is an ongoing situation. We have anecdotes from the clinicians, first of all, that patients are retaining their seizure benefits. And also, and importantly, that some of the investigators have been able to successfully reduce concomitant medications, which is always a goal for therapy. You'd like to get people down to as few therapies as possible because, as we've said, that increases tolerability and durability, as you've asked. Thank you, Steve. And a follow-up from Cantor. For absence seizures, you had two 24-hour EEG readings at baseline and two for the primary endpoint. How consistent were the two readings at each time point? Was there similar frequency and duration for seizures for the two baseline readings and the two during the maintenance phase a nd how does it inform the phase three design for absence seizures? Jan, you want to take this one? Yeah. Let me just comment on that. That's a very good question. And it was kind of one of the unknowns when we began this study. And that was really the reason that we designed this study the way we've done with two 24-hour EEGs at baseline and two at maintenance dose and using the difference between the averages as the main endpoint. So the inclusion criteria for the absence seizure patients was an average of four generalized spike wave episodes of a longer duration than three seconds in either of the 24-hour periods. There is a variability in this population, which is typical to absence seizure patients. And we are continuing the analysis and will report more data later on this. But it is important to note that seizure reduction was robust based on an objective endpoint using blinded and independent EEG reads. Benefit was seen in nearly all patients independent of seizure frequency. So in our preliminary analysis, we found the baseline reads to be stable with a variability on the order of 25% between the two reads. And this is actually much less than we'd expected. That means if a patient has tens of seizures in a 24-hour day on day one, the patient also has tens of seizures on day two. If a patient has hundreds of seizures in a 24-hour day, they also have hundreds of seizures in their second day read. That gives you some idea of what the spread was in the baseline reads and the difference between the two reads. Yeah. Let me just add maybe a couple of points. It's really important to reemphasize that the EEG is not susceptible to a placebo effect. Having such a robust endpoint and method to get to that endpoint is going to be extremely important for the upcoming phase three study as well as discussions with regulators. Basically, what we'll be able to do is mirror this design for the absence and for DEE such that it will have a baseline period of a month, a titration, and then maintenance phase in order to capture these seizures. And we're quite confident that we're able to use these technologies to capture an appropriate number and variability of absence seizures on the EEGs. Thank you, Steve, and with that, I think we are all done for questions. Thank you so much for attending, and have a great day.