Good morning, everyone, and thank you for joining us today. I'm Ian McDonald, Chief Executive Officer of Bright Minds Biosciences. Before we begin, I'll remind you that certain statements made today are forward-looking and subject to risks and uncertainties described in our SEC and CDOR filings. Our comments reflect current expectations as of November 2025, and we undertake no obligation to update these forward-looking statements. Today's presentation is for informational purposes only and does not constitute an offer to sell or solicitation of an offer to buy any securities. I'm joined today by an exceptional group of colleagues and collaborators who bring deep experience across science, medicine, and patient advocacy. From Bright Minds, Dr. Jan Pedersen, our Chief Scientific Officer, and Dr. Stephen Collins, our Chief Medical Officer, will provide scientific and clinical context. We're also honored to welcome three leaders in the Prader-Willi community: Dr. Jennifer Miller from the University of Florida, Dr. Theresa Strong from the Foundation for Prader-Willi Research, and Elizabeth Roof from Vanderbilt University, each of whom has devoted decades to improving care, understanding, and quality of life for individuals and families living with PWS. Here's a quick look at today's agenda. We'll begin with a brief update on our ongoing Phase 2 BREAKTHROUGH Study evaluating BMB-101 in Absence Epilepsy and Developmental and Epileptic Encephalopathies. That program continues to progress well and sets the stage for what we're building next. From there, we'll transition into our focus for today, Prader-Willi Syndrome. We'll start with an overview of the disorder and its major unmet needs, led by Dr. Jennifer Miller from the University of Florida. Next, we will hear directly from leaders in the Prader-Willi Syndrome community: Dr. Theresa Strong of the Foundation for Prader-Willi Research and Elizabeth Roof from Vanderbilt University, who will share perspectives from both families and clinicians on the impact of the disease. The gaps that remain in current care. We'll then move into the Bright Minds Development Strategy, where Dr. Jan Pedersen and Dr. Stephen Collins will review the scientific rationale, our clinical plans, and how our 5-HT2C agonist platform is uniquely positioned to address both the metabolic and behavioral components of Prader-Willi Syndrome. Finally, I'll wrap up with a short Q&A session. Our goal today is to provide a clear view of how we're advancing multiple programs across our serotonergic platform, starting with Epilepsy and now expanding into Prader-Willi Syndrome to bring differentiated treatments to families with urgent unmet needs. Turning to our Epilepsy program, the breakthrough study evaluating BMB-101 in Absence and Developmental Epileptic Encephalopathies continues to progress well. To date, BMB-101 has demonstrated an encouraging safety and tolerability profile. There have been no drug-related serious adverse events and no safety signals requiring any protocol modifications. Exposure levels achieved in patients remain consistent with that of what we modeled in Phase 1 pharmacokinetic studies, providing further confidence in our dose selection for the next stage of development. Participation in the Open-Label Extension is also progressing well, with nearly all eligible patients choosing to remain on therapy under investigator supervision. That level of engagement underscores the commitment of our investigators, the dedication of participating families, and the strong collaboration across our clinical sites. Collectively, these operational milestones reflect the quality of execution and strength of our partnerships with the Epilepsy Community. We're deeply grateful to everyone involved in advancing this important program. The Bright Minds team looks forward to sharing top-line data from the breakthrough study in early January. In parallel, we have been preparing for the next Phase: two global Phase 2/3 Trials, one in DE and another one in Absence Epilepsy. Designed to build on this foundation and move BMB-101 forward decisively into late-stage development. We'll share additional details on the upcoming studies along with our broader clinical roadmap in the new year. In addition to our Epilepsy portfolio, Bright Minds has now initiated clinical development of BMB-105, a next-generation highly selective 5-HT2C agonist designed specifically for patients living with Prader-Willi Syndrome. BMB-105 is protected by freshly filed composition of matter claims, providing robust intellectual property coverage around this novel chemical entity and extending the long-term value of the program. While BMB-105 advances through its first in-human study, we're taking a parallel and efficient approach by initiating a Phase 2a proof of Pharmacology Study in PWS with BMB-101. This strategy allows us to generate early clinical insights within the PWS population, including receptor engagement, metabolic and behavioral endpoints, as well as overall tolerability, well in advance of BMB-105's pivotal program. By leveraging BMB-101's established safety, PK profile, and central target engagement, we can effectively save a year of development time while also de-risking and informing the design of future BMB-105 studies. Once BMB-105 completes Phase 1, we'll be positioned to transition directly into late-stage development with confidence. Prader-Willi Syndrome is a complex neurodevelopmental and neurobehavioral disorder that presents a wide and often severe range of symptoms. As shown here, the condition affects both energy balance and neuropsychiatric function. On the metabolic side, patients struggle with hyperphagia, obesity, feeding difficulties, and growth hormone deficiency, each contributing to substantial health complications and long-term risk. On the neuropsychiatric side, the challenges are equally profound. Patients experience compulsive behaviors, cognitive impairment, sleep disturbances, self-injury, aggression, anxiety, epilepsy, and psychotic symptoms. Each of these manifestations is debilitating on its own, but together they create an overwhelming burden for both patients and their caregivers. While there has been recent progress, most notably with Soleno's recently approved drug, VYKAT, addressing hyperphagia in PWS patients, treatment options remain strikingly limited. Current approved therapies such as glutides for obesity, SSRIs for anxiety, or antipsychotics for serious neurobehavioral symptoms only target isolated aspects of this multifaceted disease. The reality is there is no single therapy that addresses the full complexity of PWS, meaning the majority of patients remain underserved. There is an urgent and unmet need for comprehensive drug solutions that can simultaneously target the spectrum of PWS symptoms rather than relying on a piecemeal approach. The goal must be to develop therapies capable of meaningfully improving both the metabolic and neuropsychiatric outcomes in PWS. Now, I'd like to turn it over to Dr. Jennifer Miller to give an overview of Prader-Willi Syndrome and touch on some of the unmet medical needs within the disorder beyond hyperphagia, also addressing the neurobehavioral issues associated with the disorder. Hi. Thank you for asking me to speak today. My name is Dr. Jennifer Miller, and I'm a Pediatric Endocrinologist at the University of Florida. I currently follow over 500 individuals with Prader-Willi Syndrome from around the world. Today, I'm going to speak to you on an overview of this condition as well as the unmet medical needs in Prader-Willi Syndrome. Prader-Willi Syndrome is caused by lack of a paternal contribution of part of chromosome 15 in the q11 through q13 region. It affects approximately 1 in 15,000 to 1 in 20,000 live births, and there are currently over 400,000 individuals living with Prader-Willi Syndrome around the world. Prader-Willi is often referred to as a complex neurobehavioral condition. The reason for that is while there are certainly physical manifestations of this condition, including low tone, low muscle mass, short stature, need for growth hormone therapy, and other hormone replacements, there are also a lot of very complicated behavioral pieces that go along with Prader-Willi Syndrome. Thus far, the most actively targeted by clinical research trials of these conditions is hyperphagia. Hyperphagia is often defined as the inability to feel full or always feeling hungry. It's a little bit of a simplification for what hyperphagia actually is, but in real life, what hyperphagia means is that individuals with Prader-Willi are very preoccupied with food. They are often thinking or talking about when their next meal or snack will be, who's going to prepare it for them, what it's going to be, where it's going to be, and things like that. They often are so focused on food that it impacts their education, their friendships, their social relationships, and even their family relationships. Because this is the most life-limiting aspect of this syndrome, it is the most often targeted by pharmaceutical companies in order to try to find therapy for this complex condition. However, Prader-Willi Syndrome causes a lot of behavioral abnormalities as well as hyperphagia. Some of these include such things as aggression. Individuals with Prader-Willi Syndrome can have explosive outbursts, physical violence toward their caregivers or peers. They can have impulsivity issues with poor decision-making and inability to delay gratification for too long. Agitation can be seen with chronic irritability, difficulty with routines or transitions. You can see here at the bottom of this slide a picture of me on the floor with one of my patients because she was upset with how the visit was going, and I had to sit on the floor with her in order to get her to comply with what I needed her to do during the visit. Cognitive issues in Prader-Willi Syndrome can include executive function defects, working memory problems, and inflexible thinking patterns. There's often also emotional dysregulation with mood swings, anxiety, depression, and obsessive-compulsive behaviors. These behavioral symptoms are often more disruptive to family life and to social life than hyperphagia alone. They provide significant barriers to education, employment, and independent living. Because the behavioral issues in Prader-Willi Syndrome are so multifactorial and complex and difficult, there is a very high rate of burnout and depression in families with a huge caregiver burden. There are limitations in residential and day program options for adults with Prader-Willi Syndrome given the behavioral problems that occur with this condition. One of the reasons that these behavioral things are thought to occur in Prader-Willi Syndrome is due directly to the genetic etiology of the syndrome. The area of chromosome 15 that is affected in Prader-Willi Syndrome, the q11 through q13 region, actually results in insufficient expression of a receptor called the 5-HT2C receptor. This receptor is expressed in areas of the brain that directly regulate food intake, compulsivity, and behaviors. It's thought that the 5-HT2C receptor, which directly modulates serotonin, a neurotransmitter, is one of the primary disease-causing mechanisms within this syndrome, causing a spectrum of the neurobehavioral conditions that are seen in this condition. Thus, targeting the 5-HT2C receptor would specifically target the etiology of a lot of the problems in this condition and not just focus on hyperphagia alone. Currently, the existing interventions are primarily symptomatic and behavioral. There is a lot of behavioral therapy done. Drugs are used off-label often to control a lot of the behavioral issues in this syndrome, things like selective serotonin reuptake inhibitors, atypical antipsychotics, and antianxiety medications are very commonly used off-label in people with Prader-Willi Syndrome in an attempt to control some of the neurobehavioral manifestations of this condition. There is growth hormone therapy, which is FDA-approved for Prader-Willi and does affect growth and physical manifestations of the syndrome by improving muscle tone, muscle mass, muscle strength, and height, but it does not affect the behavioral or hyperphagia mechanisms of this condition. There is a need for. A drug that would affect the full spectrum of behaviors in this syndrome. A selective 5-HT2C receptor agonist would be critically important to address all of the neurobehavioral aspects of Prader-Willi Syndrome, including appetite, but also weight, obsessive-compulsive behaviors, impulsivity, anxiety, and emotional lability. Individuals with Prader-Willi Syndrome want to have a normal life, and we want that for them. They have such plans for their futures as individuals. They all want to achieve. They all want to contribute to society. They all want to be like everyone else. We want to provide that for them. We want them to be able to live as normal a life as everyone else and as normal a life as possible. I firmly believe that targeting the 5-HT2C receptor may provide. An intervention that actually will allow for success of individuals with Prader-Willi Syndrome in this world and society and allow them to achieve their goals. Thank you for allowing me to give this talk. Hi. I'm Theresa Strong, one of the co-founders and the Director of Research Programs at the Foundation for Prader-Willi Research. Importantly, I'm also a mom to a young man living with PWS. Today, I'll speak a little bit about the unmet needs of the PWS community and also about some of the challenges that individuals with PWS and their families face in day-to-day living. As you've heard, PWS is a complex neurodevelopmental disorder caused by the loss of paternally expressed genes on chromosome 15. This disorder occurs in about 1 in 15,000 births, and it's usually spontaneous, meaning that there's no family history and that it usually just occurs once in a family. It affects both males and females equally and also all races and ethnicities. There is an accurate genetic test for PWS, so if the physician is familiar with PWS and knows to order the right test, a DNA methylation analysis, that will detect more than 99% of cases. In these days, most individuals with PWS are diagnosed with the disorder in the first six months, although if their failure to thrive or their feeding problems are not as severe, they may pass through that first initial time of diagnosis and may not get diagnosed for several months or even years later. You have heard a little bit from Dr. Miller about the major clinical features of PWS: endocrine problems, scoliosis, gastrointestinal problems, along with a slew of other clinical concerns. The hallmark symptom is that transition from infancy, where babies with PWS are poor at feeding and not very interested in food at all, but sometime during childhood develop hyperphagia, which is this unrelenting, overwhelming urge to eat. If the environment is not strictly restricted, individuals with PWS will always go on to become obese. In a food-restricted environment, they may not become obese, but they still do show that hyperphagic behaviors. They also have a challenging behavioral profile with a high risk of mental illness, and it is these behaviors, in addition to the hyperphagia, that presents the most challenges for the person with PWS and their entire family. This slide shows some pictures of my son from right when he came home from the hospital all the way through adulthood. He's had a pretty typical course of PWS, which is to say that we've faced a fair number of challenges over the years, beginning right after birth when he required a NICU stay. You can see even when he came home from the hospital, he still had a feeding tube and was on oxygen for several months. We were fortunate in that our medical team was quite astute, and they tested him for PWS, and we got the diagnosis before he left the hospital. That was pretty unusual. This was back 30 years ago. We were able to hook up with other families and with advocacy groups, learn about how to create as good an environment as we could to help him along. That's one of the things about PWS: the symptoms of PWS really change over the lifespan, so families really need to be very proactive and looking ahead to the next challenge. In infancy and early childhood, some of the biggest challenges include that poor feeding. There's really a fair lack of interest in food, and getting babies to get enough nutrition can be a challenge. They also have hypotonia, that is, they're kind of floppy, as is said, and decreased muscle mass. Even if the baby is a normal weight, there will be more fat and less muscle than a typical baby. There is some developmental delay. This tends to be mild, but it really is necessary to have some early intervention, physical therapy, occupational therapy, speech therapy. Families are having to do a lot of. Extra to help their child develop as close to a typical rate as possible. The weight in a child with PWS will begin to be put on even with sort of typical food at age two. There needs to be very early management of food intake to keep the child at a healthy weight. I think, as we've heard, growth hormone therapy is very helpful in PWS, and I think for parents today, particularly trying to get their child started on growth hormone therapy as soon as possible, can be really helpful. It's during that transition from early childhood towards adulthood that we start to see the onset of some of the most challenging behaviors in PWS. The onset of hyperphagia is variable. It usually starts in young childhood and oftentimes will start with just an obsession or an overfocus on food. For example, I knew a five-year-old little girl with PWS who knew every type of pasta that there was, all of the variations, and who also, no matter what house she went into, asked for the cookbook so that she could sit and look at the food. This was not a child who was overeating at the time, but just had an extreme focus on food. Sometime during childhood, that focus on food transitions to full-blown hyperphagia, where there is this intense drive to eat. I think it can be difficult to understand hyperphagia. We've all been hungry. We all know what it is to be delayed for a meal and want to eat. I think what's important here is that the brain of an individual with PWS is really signaling that the body is starving, even when it is clearly not starving. The signal is starvation. Therefore, the individual with PWS has this overwhelming drive to eat. That drive to eat can really allow them or set up a situation where they are taking risks to get at food. If they see a McDonald's across a busy highway, they are so focused on the food and the potential to get food, they may run across the highway without any regard to the cars, for example. Putting an individual in a situation where they are around a lot of food is going to trigger a lot of anxiety and potential outbursts. My son with PWS, I have not taken him to a grocery store since probably for 15 years. That amount of food, he would really want something that he should not be having, and it would set up a conflict. The thing is, when you have maybe a six or eight-year-old child who is having a tantrum because they can't get at food, people just think you're a bad parent. When you have a 20-year-old grown man who is screaming because he cannot have access to the Hershey bars, people get anxious, and there is the potential for someone to call the police. If the policeman is not going to let him have the Hershey bars, he's going to yell at the policeman. There is just this potential for conflict and intervention from law enforcement that we see fairly often, actually, in PWS. Families respond by trying to restrict the environment. They decrease the social interaction because almost any social interaction you have, any social event, is going to have food associated with it. They put locks on their pantries and locks on the refrigerator, and we've had that in our house since my son was in late childhood. In addition, the behavioral issues become much more prominent at this time as kids move towards adolescence. There are lots of different behavioral issues, in addition to the hyperphagia, that really impact the day-to-day living of the person with PWS and their family. Just looking at that a little bit more closely, temper outbursts occur in PWS, and they persist throughout the life of the individual with PWS. An adult may be having the temper outbursts that you would normally see in a small child, except they're an adult. It may lead to destructive behavior, sometimes to aggressive behavior. In addition, there is a cognitive rigidity, so moving from transitioning from one thing to another is very difficult for a person with PWS. There's also impulsivity, obsessive-compulsive behaviors, and a general anxiousness, sometimes about food, like, "When is the next meal going to be coming? When is my snack?" That anxiousness that they're not going to get food, but also about pretty much every other thing. A lot of anxiousness. There are some social cognitive deficits that often show in PWS, so that can also contribute to difficulties with relationships with others. The behavioral incidents that we see are many times related to food and not having access to food that they would like, but individuals with PWS will also have behavioral issues around things completely unrelated to food. In fact, we've recently completed a natural history study, a four-year natural history study, looking at what sends individuals with PWS to the emergency room or into the hospital or into an acute care setting. Most of the time, the top category is these behavioral incidents or mental health concerns for the individual with PWS. These are driving not only behavioral problems, sometimes medical problems if there's an altercation and the person with PWS or someone else gets hurt as well. It really is a big concern for families, as you might imagine. These behaviors, the social isolation of trying to keep the person with PWS from having too much access to food, and the restrictions around eating really lead to a very high caregiver burden for the primary caregiver caring for the person with PWS. We did a study where we looked at caregiver burden as measured by the Zarit Burden Interview, which is a measure of caregiver burden that's been used across many different disorders. We found that the caregiver burden for PWS was very high and even higher than has been reported for someone who's taking care of an individual who has had a stroke or Alzheimer's disease. It is highest for caregivers who are caring for adolescents and young adults with PWS. As we said, this is the time where we see most of those extreme behaviors. Not surprisingly, individuals who had the highest level of hyperphagia, so the strongest drive to get food, that was associated with a higher caregiver burden. These behaviors and associated symptoms of PWS had impacts on the caregiver's ability to sleep, their family relationships and social relationships, and their ability to work outside the home. This social isolation is really common in PWS. It is very difficult for people without PWS to understand the behavior of the person with PWS. Families do tend to retreat and stay away from a lot of social gatherings, which feeds into additional feelings of isolation. In addition, the medical care of the person with PWS is very complex, and many healthcare providers are not familiar with caring for a person with PWS, and that can also contribute to those feelings of isolation. If we think about, on the right, you can see, rather on this slide, some of the phrases that came out of a meta-analysis of looking at the burden of illness in PWS. You can see these themes of this having to secure food at all times, the impact on family dynamics of having a lot of controversy or conflict in the house. There is a lot of mental strain having to monitor and supervise the person with PWS 24/7. This does continue to develop as the person with PWS reaches adulthood and wants more independence. I mean, my 31-year-old son with PWS does not want me telling him what to eat, and I do not want to tell him what to eat, but we have to do that in order for his weight to stay at a reasonable level. It is really challenging. If we look at what the caregivers, or typically parents of people with PWS, want to see new treatments for, we do see hyperphagia leading the list. There are also some of these very important other behaviors, this anxiousness, the temper outbursts that we see in PWS. The parents really want new options for treatment of these aspects. I think it is also important, though, to ask. What does the person with PWS want themselves? This can be tricky to ask in a population that is sometimes not good at expressing themselves. Doctors Elizabeth Dykens and Elizabeth Roof, who you will hear from later, did a really nice paper interviewing individuals with PWS. Those individuals expressed things very similar to their parents. They struggled with their hunger, their food, and their eating. They did not want to be disobeying and getting into food, but the physiological drive to eat was so overwhelming, they felt they, in many cases, were not able to control it. They also struggled with anxiousness and stress. The outbursts that they have, quite frequently, are no fun for anyone. It is not fun for the person that is in the middle of the conflict. It is no fun for the person with PWS. They really do not like it. They feel bad about it. They do not want to upset others, but they just have difficulty in regulating these emotions. I think parents and caregivers and the people with PWS are all on the same page about what they would like to see new treatments for. I will bring up one more aspect, which is that PWS does not happen in a vacuum. In many cases, it is in the context of a larger family, and these families can be complex. My family at different ages is shown on this slide. It was a real challenge to raise my son. His siblings are close. He has a twin brother, who's obviously not an identical twin, but he has a twin brother and then two sisters who are close in age. His brother, in fact, was a little bit underweight most of his childhood because he was a typical boy. He was always running around, and he didn't care about food. This struggle of trying to make sure that one son got enough food to eat while keeping my son with PWS from eating too much food was a real challenge. The other thing is, growing up in a family where food is restricted and there's sort of these unusual emotional issues around food can be very difficult for the siblings. These kids, literally, are having to sit in their closets and eat a treat because they don't want their sibling with PWS to know that they have it. Not surprisingly, there are real impacts on the lives of siblings of those with PWS. There has been some really nice work in the last couple of years, in particular on this, including some done by Dr. Lauren Schwartz, who is a member of the FPWR team, who did some qualitative interviews. What we see is that many siblings of those with PWS grow up with unusual thinking about food, having lived in an environment where food is locked up all the time. It may take them a while after they get out of the house to have a normal relationship with food. The behavioral feature that they said was the most impactful were the temper outbursts. That conflict that they may have with their sibling or that they see their sibling having with their parents can be really distressing to them. Many individual siblings have some symptoms of PTSD having grown up with PWS. That's not to say it's all bad. Siblings of those with PWS, they have a lot more empathy, and they can recognize and deal with differences between individuals. Just to say that. Any treatment that would impact favorably hyperphagia and other behaviors associated with PWS would benefit everybody in the family. I'll end by saying that these are urgent needs for our communities. Our kids are wonderful. They're resilient. They're resourceful, but they are struggling mightily. They have these challenges in controlling their behavior. They have this overwhelming drive to eat, which pushes out so many other things that they could be focusing on. Our community is really in need of some effective therapies to treat hyperphagia, many of the behavioral aspects of PWS, and give our families options for. Being able to manage PWS and help our kids lead a full and independent life. Thank you. Hi, I'm Elizabeth Roof from Vanderbilt University. Prader-Willi Syndrome is a complex genetic neurodevelopmental disorder that has many psychiatric, physiological, and behavioral features, things like delayed milestones, motor, speech, and cognitive functioning, along with poor feeding the first year of life. These are lifelong, and even with related therapies, are delayed throughout life and continue to lead to impaired daily functioning. Other symptoms are poor temperature regulation, excessive daytime sleepiness, GI issues like constipation, aberrant pain sensation, issues with balance and coordination that make daily monitoring and accommodation necessary. Somewhere before the age of five, an increase in food interest starts. We're talking about food, focused on when and how food will be served, and becoming upset when details about food aren't communicated right away or food is delayed. It is often described by families like turning on a light switch. The change is dramatic, unexpected, and after months of struggling to get their child fed, their child won't stop eating. Around ages 5-8, this food interest develops into hyperphagia, an increased hunger drive that is unremitting and very intense, leading to meltdowns, tantrums, food stealing, and a fixation on food that becomes all-consuming. It can make it hard to focus on relationships, educational learning, and anything else. The drive to eat becomes very maladaptive, leading people to take risks, ignore no, and even assault people who keep food from them. Kitchens are locked, pantries and refrigerators are bolted, and parents often install cameras for safety and monitoring at the same time as keeping eyes on their child during all waking hours. It's incredibly stressful for families to manage. Traditional weight loss drugs like GLP-1 drugs are not effective in managing the hunger in this population. The intense hunger can increase to the point that an individual with PWS can eat so quickly or so much that they can rupture their stomach and die. Parents live with this knowledge and fear every day. As difficult as the food issues are to manage, there are considerable psychiatric problems that emerge in middle childhood and are often even more problematic. Tantrums, rigidity, inability to let things go, it leads to constant questioning, demandingness. Also compulsive behaviors. They can become easily upset over small issues, leading to meltdowns or screaming and aggression. It can last hours and sometimes can include police involvement if they are in a public place. There are also increased risks of psychosis, autism, seizures, and anxiousness, which are difficult to treat with current medications or behavioral therapies, as they seem to be driven by brain differences that are caused by the genetic phenotype. Parents note that intellectual delays result in impaired reasoning, poor academic performance, and inability for age-appropriate social functioning, which further isolate their child from peers and their siblings. Families feel an intense pressure to manage their child's behavior and their access to food at all times, and the need to exert a great deal of control to keep them safe, which is exhausting. One of the main issues that current therapies do not address is the complex PWS phenotype. They target one symptom, hyperphagia, and not always very successfully. Current therapies target hunger and may not tackle the additional issue of lack of satiety, which indeed is indifferent. Hunger is a physiological feeling of wanting to eat, but you can still feel unsatisfied. PWS causes people to feel unremitting hunger, but also to never feel full, which makes them constantly search and think about getting food. Current therapies do not address the pathophysiology of PWS. Therefore, they cannot treat all of the symptoms. In addition, current treatments may come with unwanted side effects like fluid retention, pulmonary and peripheral edema, and increased risk of diabetes. No family wants to treat one set of problems for another chronic health problem, but existing treatments fail to target core neurobehavioral pathophysiology. Families and patients are looking for real answers that address the complex needs of PWS without sacrificing future health. Families are looking for ways to satisfy their child's hunger and allow for more freedom from food noise, which can be deafening and which would give them more opportunities with less supervision and less monitoring. Being the food police changes the nature of family relationships in ways that most people cannot imagine, and it undermines the nurturing tendencies for parent and child. Bringing trials that target this complex disorder could provide families with relief from stress and worry that your child would eat so much that they could die. Though this is dramatic, it is true. I have lost several PWS patients with ruptured stomachs from eating too much. It is truly heartbreaking to witness the hyperphagia in PWS. In order for a clinical trial to be successful, it's critical to select appropriate and validated measures developed specifically for this unique phenotype. Our lab at Vanderbilt has spent many years doing exactly that. We decided that after trying to alter measures used in ASD or other ID populations and try to make them fit, though poorly, that we would develop our own. With extensive interviews with more than 450 PWS families, we found core symptoms that parents wanted drugs to target: hunger, distress associated with food-related behaviors, food security, and other psychiatric and behavioral problems that are key characteristics of this syndrome. The first measure is the Hyperphagia Questionnaire for Clinical Trials. The HQCT, originally published in 2008 with 13 items, was reduced to 9 after careful feedback from the FDA related to observable behavior and more concrete responses to measure change. The HQCT has been used in more than 20 clinical trials in PWS since 2014 and has been shown to be sensitive to treatment. Parents answer this questionnaire in a semi-structured interview with a trained and experienced PWS clinician to record baseline symptoms and document change over time. The FDA has recognized the HQCT as a reliable way to measure change in hyperphagia and allowed it to be the primary outcome measure in many trials. The PWS Profile is a recent addition to trials and consists of a way to measure change in core psychiatric and behavioral features of PWS: depression, anxiety, compulsive behavior, aggression, negative distorted thinking, magical thinking, repetitive questions, repetitive speech, and critical items looking at infrequent behaviors that are concerning to families like safety risk and elopement. This measure has been validated on more than 900 patients with PWS and serves as a measure of behavior problems that are common and specific to PWS. This measure was recently used in the recent approval of the only FDA-approved drug for PWS, VYKAT XR. This measure showed that it was sensitive to change and that symptoms decreased when treated. The Food Safe Zone was also recently developed to see how many food safety precautions and measures that families use to manage hyperphagia. It consists of 21 items that help parents assess how these accommodations may change how hyperphagia presents in their unique environments. It also helps parents acknowledge the extreme ways that they must control food in their environments to keep their child safe, and this often leads to more honest answering of the HQCT, which is why it's given before that one. As accurate and appropriate assessment is crucial to clinical trial outcomes, we are ensuring that sites have deep experience with this population and that they have extensive training on the selected outcome measures by combining clinician, caregiver, and, when possible, self-reported measures of the target symptoms, as well as incorporating physiological and biochemical markers to be correlated with behavioral changes. As you will hear next from the Bright Minds team, the current clinical trial is laser-focused on selecting carefully chosen outcome measures that will give us the best potential for measuring clinically significant changes in symptoms like hyperphagia, aggressive impulsiveness, and daily functioning. Given the complex nature of PWS with both physiological and psychiatric symptoms, we hope to show meaningful reduction in life-limiting symptoms. Selecting the right outcome measures ensures that families of individuals with PWS will benefit from targeting the most important symptoms that impact family stress and relationships. Future directions are promising as there is a desperate need for treatments for PWS that are safe, effective, and without significant side effects. Paramount is the need for a treatment that targets the underlying pathophysiology and primary disease mechanism instead of individual symptoms. Families deserve a comprehensive treatment for a very complex disorder like PWS that shortens and really limits lives. Thank you. Thank you, Dr. Miller, Dr. Strong, and Ms. Roof, for those powerful insights into the challenges facing families and clinicians in Prader-Willi syndrome. Building on that perspective, I'll now hand it over to our Chief Scientific Officer, Dr. Jan Pederson, who will walk you through the biological rationale and mechanistic foundation behind our 5-HT2C program in Prader-Willi syndrome. Thank you, Ian, for the kind introduction. My name is Jan Torleif Pedersen. I'm the CSO of Bright Minds Biosciences. It's today my pleasure to take you through the clinical and preclinical rationale for initiating a clinical study with a 5-HT2C agonist in Prader-Willi Syndrome. PWS is a complex neurodevelopmental and neurobehavioral disorder with a well-characterized genetic origin. We consider the disorder to be a disease in which the serotonin system is dysfunctional. The serotonin system is one of the main neurotransmitter systems of the brain and regulates many important functions such as cognition, behavior, reward management, and food intake control. In short, the serotonin system is involved in all the symptom domains affected in Prader-Willi syndrome. The genetics of Prader-Willi syndrome is directly linked to the 5-HT2C receptor function. Prader-Willi occurs when the paternal genetic region 15q11-q13 is not expressed. In half to two-thirds of the cases, the disorder is caused by a deletion on the father's copy of chromosome 15. In a quarter to a third of the cases, the disorder is caused by duplication of the mother's chromosome 15. Missing a copy of the paternal chromosome 15. Finally, in a few cases, the disorder is caused by genetic imprinting. Resulting in a non-functional copy of the father's chromosome being inherited. The interesting common consequence of these genetic aberrations is that all variants are deficient of SNORD116 expression. SNORD116 is a regulatory RNA that's responsible for regulation of RNA splicing of a small number of genes and one of the most prominent genes that is the 5-HT2C receptor. The ultimate consequence is that PW S patients express lower levels of the 5-HT2C receptor. This means that boosting 5-HT2C on remaining functional 5-HT2C receptors with a receptor agonist directly targets the underlying pathophysiology of Prader-Willi Syndrome. The 5-HT2C receptors are an apex regulator of the neuroendocrine axis. 5-HT2C expressing neurons directly project to hypothalamic melanocortin neurons to suppress food intake and thereby directly regulate satiety and appetite. We know that 5-HT2C receptors are also involved in regulation of compulsive behavior. As said before, Prader-Willi patients express lower levels of mature functional 5-HT2C receptors, resulting in an unabated appetite and compulsive behavior. For that reason, a 5-HT2C agonist may compensate for the loss of 5-HT2C receptor and thereby treating both hyperphagia and new behavioral symptoms associated with PWS. We also have direct human evidence for the causality. Genetic analysis of populations of obese individuals has identified loss of function polymorphisms in the 5-HT2C receptor gene. Those individuals that carry these polymorphisms have a PWS-like phenotype with overeating and maladaptive behavior among the main phenotypic traits. We also have a large body of preclinical evidence from animal models, in particular from the 5-HT2C knockout mouse. In the 5-HT2C knockout mouse, we see overeating as demonstrated in the graph here on the left. It develops a prediabetic phenotype with poor glucose control as demonstrated in the middle. On the behavioral side, these mice exhibit hyperlocomotion, attenuated contextual fear response, and altogether, behaviors that translate to compulsive OCD-like behavior. At Bright Minds, we've also generated preclinical data that substantiates the utility of a 5-HT2C agonist in PWS. First, we've demonstrated that one of our G- protein-biased 5-HT2C agonists can dose-dependently reduce food intake and body weight in a rat model of binge eating. On the left-hand side, we've demonstrated that it dose-dependently can reduce the number of binge episodes, which on the right-hand side translates to reduced body weight upon chronic dosing. We've also demonstrated that a G- protein-biased agonist can reduce aggression. We've tested the effect of our lead agonist BMB-101 in a model of aggression attacks in the rat resident intruder model. In this model, we can dose-dependently reduce the number of attacks from a dominant intruder male when entered into the domain of a docile male. More recently, we've also demonstrated that 5-HT2C agonism can improve cognition in a mouse model of new generation. We've here looked at a tau transgenic mouse ability to find and remember the position of a hidden escape platform in the radial arm water maze. Dosing of BMB-101 dramatically improves both the learning and the memory of the mouse. In terms of the effect of 5-HT2C agonism on compulsive behavior, we've tested BMB-101 in several models of addiction. We've demonstrated that 5-HT2C agonism can dose-dependently reduce craving. In the data shown here, reduce episodes of fentanyl self-infusion. As shown here on the left. On the right, we've demonstrated that this is a 5-HT2C-specific effect by co-dosing of a 5-HT2C antagonist, and we see partial reversal of the behavior in the rat. In conclusion, we've demonstrated that Bright Minds 5-HT2C biased agonists can demonstrate preclinical efficacy across all key PWS symptom domains, that is, hyperphagia, aggression, cognition, agitation, and uncontrolled cravings and compulsive behavior. We also have historical clinical experience with fenfluramine. A small clinical trial was conducted in the late 1980s and published in 1990, where 15 patients were treated with fenfluramine for six weeks. This was the first clinical study to demonstrate that a potential treatment in PWS could address both physiology and behavior. In this trial, albeit small, a significant improvement in weight, food behavior, and aggressive behavior was observed. Taken together, this suggests that a G- protein-biased 5-HT2C agonist from our portfolio could potentially treat the PWS symptom complex. By directly targeting the underlying pathophysiology of the disease. We have circumstantial evidence from the use of lorcaserin and fenfluramine as diet drugs. We have direct clinical evidence from a small clinical study with fenfluramine. We have very good in-house preclinical evidence in animal models demonstrating that one of our G- protein-biased agonists could beneficially influence a long range of the behaviors observed in Prader-Willi Syndrome. We also have a case report from our ongoing clinical trial with BMB-101 in Epilepsy. In that study, we have one individual who weighs over 100 kg, who has to date lost about 10% body weight. This individual has also reported an improved relationship with food and an overall improved quality of life. In this individual, we've also conducted a 24-hour EEG monitoring and have detected a significant improvement in REM sleep behavior. If we take all of this together, we believe we have very good evidence that testing a G- protein-biased agonist in Prader-Willi Syndrome is warranted. With that, I'll now hand the stage to our Chief Medical Officer, Stephen Collins, to tell you more about the upcoming clinical trial. Thank you. Good day. We have heard from the experts about Prader-Willi syndrome, its pathophysiology, and the needs for a new, effective, and safe therapy. We've also heard from Dr. Pedersen about the biologic mechanisms pointing to the promise of a 5-HT2C-specific therapy with a biased agonist. I will briefly describe BMB-101 and then our Phase 2a exploratory study in Prader-Willi using BMB-101. Next slide. BMB-101 is a highly selective 5-HT2C agonist. It's biased to affect the GQ protein, which drives efficacy and avoids action at the beta-arrestin interstitial pathway. That pathway drives 5-HT receptor removal from the cell surface and therefore leads to tachyphylaxis or tolerance. We have performed a 64-person Phase 1 Study, which demonstrated that BMB-101 is highly druggable. First, it was very well tolerated with no serious adverse events at all, and the adverse events which did occur were generally mild and seen only at doses roughly 2x-3x the projected therapeutic dose. It also showed linear kinetics through the entire dose range. This is important since clinicians need to be able to understand how to increase dose and whether that will be predictable in terms of exposure. It also showed that the CNS target, that is, the serotonin receptors, were engaged at our predictive therapeutic doses as detected by two biomarkers. First, transient prolactin release, and secondly, the effects on the EEG via quantitative EEG. This study led to our first Phase 2 study in patients with severe types of Epilepsy. The study is currently ongoing, has 20 subjects, and like the Phase 1 study, has had no serious adverse events to date. Next slide. In our PWS study, we aim to demonstrate that our 5-HT2C specifically biased agonist will have effects on both hyperphagia and the neurobehavioral symptoms, which so clearly affect patients and their families. To study the hyperphagia, we will use the PWS HQCT questionnaire. As noted by Elizabeth Roof, this is the caregiver report questionnaire that examines nine eating behaviors and is the regulatorily accepted instrument for establishing treatment effect of an agent. To study PWS behavioral issues, we will use the PWS Profile, a multi-questionnaire instrument designed for PWS-specific emotional behavioral problems such as compulsive thinking, temper tantrums, and rigidity of thought. This instrument is the standard tool used by researchers. Designed for PWS-specific emotional behavioral problems such as compulsive thinking, temper tantrums, and rigidity of thought. This instrument is the standard tool used by researchers and is incorporated in all modern PWS therapy trials. Next slide. The study will be a randomized double-blind placebo-controlled multicenter study led by Professor Tanja Marković, an internationally recognized expert, highly experienced not only in research in PWS but also in giving care to patients and families with the syndrome. The study will use not only the HQCT and PWS Profile, but also use additional assessments of caregiver and clinician observation of treatment. For example. Potential changes in CGI and CGIS. We'll also look for potential changes in body weight and clinical and laboratory safety measures. The study will be randomized into one-to-one active or placebo arms with an N of 16. There is an Open-Label Extension Phase during which active arm subjects may continue on the dose they attained. If the placebo arm, they may be allowed to titrate up to active therapy. Next slide. As can be seen by the diagram, the study has a standard PWS design with a one-month baseline evaluation period, at the end of which those subjects who show an HQCT score of moderate to severe intensity will be randomized into either placebo or BMB-101 treatment arms. Weekly titration of BMB-101 or matching placebo will begin at 0.67 mg per kg and ascend by 0.33 mg per kg weekly to a target dose of 2 mg per kg. Subjects can reduce dose by 0.33 mg per kg or maintain an attained dose at or below 2 mg per kg and then continue into the maintenance phase by week four. The maintenance phase continues for eight weeks, followed by an O pen-Label Study where they will have visits every three months to assess safety, tolerability, and efficacy. Subjects who were in the placebo arm may elect to begin a weekly titration with BMB-101 in this Open Phase. The titration phase will mirror that of the double-blind phase. Subjects who elect to discontinue the study will undergo a weekly taper phase out. We're truly excited to begin this study in the hopes of providing people with PWS and their families a truly effective, safe, and well-tolerated therapy which addresses their multiple needs. Thank you. When you look at this slide, what I'd like to point out is the broad symptomatology that Bright Minds can potentially address in Prader-Willi Syndrome. This is in direct contrast to many of the other compounds on this slide that only target a narrow slice of the disorder. The biological rationale behind our approach is both strong and direct. The genetic root of Prader-Willi syndrome lies in the loss or dysfunction of the SNORD116 gene cluster, which regulates splicing of the 5-HT2C receptor in the majority of Prader-Willi syndrome patients. As a result, patients exhibit a deficiency in functional 5-HT2C signaling, disrupting key circuits that control satiety, reward processing, and behavioral regulation. This loss of serotonergic tone contributes to the hallmark symptoms of PWS, including hyperphagia, compulsive behavior, anxiety, aggression, and cognitive impairment. By selectively agonizing the 5-HT2C receptor, our compounds aim to restore balance in these neural pathways, directly addressing both the metabolic and neurobehavioral dimensions of this disorder. Preclinical studies with Bright Minds 5-HT2C agonists have shown robust dose-dependent efficacy across these domains, reducing binge eating, aggression, and compulsive behaviors, while also improving cognition and emotional control. This convergence of genetic, mechanistic, and translational evidence provides a powerful scientific foundation for our program and underpins our confidence that 5-HT2C agonism can deliver multidimensional benefit for PWS patients. When we look at Prader-Willi Syndrome as a therapeutic area, it represents one of the largest and most underserved opportunities in rare neurobehavioral disease. There are an estimated 10,000 patients in the U.S. and roughly 400,000 globally. Based on current pricing benchmarks for VYKAT, that equates to an approximate $4.6 billion U.S. market opportunity. Despite the recent approval targeting hyperphagia, the therapies address only a narrow slice of the disease. The broader constellation of the symptoms, from obsessive and compulsive behaviors to cognitive impairment, sleep disturbances, and emotional dysregulation, remain largely unaddressed. For Bright Minds, this gap presents both a scientific and commercial opportunity to deliver a therapy that can have meaningful impact on the entire PWS symptom complex, not just one aspect of it. That wraps up our prepared remarks for today. I want to thank everyone for joining us, our investigators, collaborators, and supporters who share a commitment to advancing better treatments for patients. We're excited about the progress across our entire portfolio, from the Breakthrough Epilepsy Study to our new Prader-Willi program, with BMB-105 and BMB-101. With that, I'll open the floor to questions. Thank you, Ian, and thank you to the Bright Minds team and the KOLs for making this beautiful presentation. Now, we are going to the Q&A session and just reminding everyone that you can ask questions by question tab, which is in the bottom right corner. We'll try to answer as many questions as we could. Starting with the questions, the first one is coming from Yasmeen Rahimi from Piper. It comes to Dr. Miller. Dr. Miller, could you help us understand what lessons have we learned from the clinical development in Prader-Willi that could strengthen the path for BMB-105? The second question from Yasmeen would be, could you help us understand how the clinical product profile of a 5-HT2C agonist differs from the currently approved DCCR? I can answer the second one first, if that's okay. Can you hear me okay? Yes. Yes. Okay. It obviously differs from DCCR in that this particular compound will address a very specific. Defect that is part of Prader-Willi Syndrome and one of the sort of core problems in Prader-Willi Syndrome, and therefore has the potential to address, as mentioned, many of the core symptoms, such as aggression, behavior, compulsive behaviors, things like that. It is a very exciting additional possible therapy for individuals with Prader-Willi Syndrome, especially the thought that it could possibly address the cognitive piece as well. We know that while DCCR is a great drug in terms of treatment of hyperphagia, it does not work for everyone because no drug works for everyone. Some of the side effect profile of the drug makes it such that some people cannot use the DCCR because of safety issues, including edema and the risk of diabetes. This gives an option that seems to be a very safe drug. Possibility to address a lot of the symptoms that are core symptoms for Prader-Willi Syndrome. Thank you. The first question was about the understanding of what lessons we learned from the clinical development in PWS. Oh, lessons we learned. I feel like Theresa Strong should answer that one if she's on because she sees it from the parent advocacy side. I see it from the PI clinician side. I think lessons learned are that you need longer trials versus shorter trials, for sure, because the placebo effect in Prader-Willi Syndrome is strong and lasts, I think, longer than we ever anticipated it lasting. I think we've learned that through a variety of trials. I can see Elizabeth nodding that she agrees with that. I also think that the lessons that we've learned are that the tools that we have, while they are the best tools that we have and are regulatorily accepted. The addition in this trial of adding in the clinician assessment as well as parent assessments of just sort of global assessment of severity or improvement, I actually think is going to add a really strong aspect to this trial versus just relying on the questionnaires. I can just add, this is Theresa. I agree with what Jennifer said. I think that we struggle with the placebo effect, and I think taking steps to minimize that. Training people, as Elizabeth talked with, about administering the HQCT can mitigate some of those. We'd love to have a biomarker of hyperphagia, like a blood test, but we don't right now. I think having well-trained sites, sites that are familiar with PWS, and using these tools as effectively as possible is important, and I think that is aligned here. Thank you, Theresa. The second question comes from Peyton Bohnsack from TD Cowen. It is Jennifer, it is obviously to you as well. How many PWS patients are currently on SSRIs or other serotonergic drugs? Oh, actually, that is an Elizabeth question, probably more than me. I would say a fairly high proportion are on SSRIs. Over the age of 12, I would venture to say, Elizabeth. You might want to chime in and say, I was going to say maybe even 50%. Do you think that is a realistic number? That is about right, 50%. Again, not effective for a lot of the things that this drug will actually target. I think it's important to know that, yes, it helps irritability, yes, it helps anxiety, but it really doesn't fix them. And honestly, they're very suboptimal, to be very honest. Everything we've thrown at it just doesn't seem to work very well. Agreed. Thank you. Another question from Peyton. For the company, would you expect any DDIs with currently used drugs to deal with the symptomology of PWS? Steph, could you address the question? Yeah. The good news is that BMB-101 or BMB-105 do not have any significant interactions with liver metabolic systems, either by inhibition or induction. If you look at drugs, for example, the VYKAT drugs or some of the other drugs that are being used, growth hormone, we would not expect any drug-drug interactions. Thank you, Steph. Another question from Peyton Bohnsack. Coming to Elizabeth. How do you control the placebo effects on the symptoms or variability between patient and sites? What is the expected placebo rate using HQCT? Also, how do you validate the severity of patients in trial? That's actually a great question, and I think it's something that any drug company getting into this space needs to really talk about is the placebo effects. For people who don't have treatment for the core features of PWS, they like to see change even when they're on placebo, right? I think it's important for us as clinicians and also really talking to the parents about what is real versus what they want to see. Longer trials are definitely a thought. Also, maybe even daily kinds of diaries or texts or other ways to collect data throughout the trial period instead of waiting for that magic moment when they come into your office and they sit in front of you. As a clinician, it's so important to really talk to parents about what their experience is, what they're seeing, to also voice your own observations of what you see in the clinic instead of just letting parents think about usually the last most recent event, which may be traveling to the site or whatever else. We really have to do a better job of training sites. We have to make sure people are actually using the assessments correctly and really spending time getting to know their families. I think that's just the most important things. The HQCT has been used in multiple trials. It is not perfect. There are things that it does miss, and there are things that we haven't figured out a way for. I do think there are some really good ways, maybe placebo run-in and other things that would actually help us negate those placebo effects. People with PWS want drugs to work, and they often see effects even when there aren't any. We have to be really careful with people with intellectual disabilities and their families wanting to see magic when it's not actually happening yet, especially if you're on placebo. I will say, this is Theresa again. I'm sorry, I can't get my camera to work, but that's all true, and the placebo effect needs to be minimized. We do see, in drugs that are effective, you can see a difference between placebo and treated. It's an imperfect instrument, but it has shown that it is sensitive to change and is adequately sensitive to change to convince the regulatory and the clinicians of an effective treatment. I agree with Elizabeth also, though, that it is really important for investigators to sit down and actually have discussions with the families and with the patients. I love the idea of having sort of closer tracking by the parents recording stuff during the times in between visits, rather than just being in that moment. Because, as Elizabeth mentioned, travel for studies is very difficult for a lot of these families, and it often can color negatively some of their impressions of things that are going on, because sometimes drugs take a while to work. You would not want to miss that. I think some way of having the patients. Or the parents track things that are going on that they've seen, and then also really making sure the investigators know the families, know Prader-Willi, and are willing to take the time to sit down and have discussions with the families about what's going on. Thank yo u for that. Another question from Peyton Bohnsack from TD Cowen is again about the HQCT. What reduction on the HQCT from the baseline in the Phase 2a Trial would be seen as clinically meaningful and would support further development? I'm going to give that one to Elizabeth since she was elsewhere. Generally, the FDA thinks a point reduction of about seven points is considered clinically meaningful data. Somewhere right around there, I think for a Phase 2 Trial, I don't think that would be the gold standard. That's usually more for a Phase 3 Trial. I do think when we see movement, then we see that there's some improvement. I think this drug is really unique in the fact that it's going to target not just hyperphagia, but some of the other symptoms. I think it's going to be really interesting to see if there's an overall dampening of some of those effects of some of the really problem behaviors. I think, again, seven points is generally what they kind of expect to see in a phase three trial. Phase 2, as long as there's a signal and it's positive in the right direction, I think that just kind of leads to that Phase 3 T rial. Thank you. Thank you, Elizabeth and Jennifer, on these comments. Now we have some questions about the. Question from Tom Schrader from BTIG. How much does prior dosing work inform the correct level in PWS? Is dosing likely to be forgiven once you see activity, or is it too much stimulation? A potential problem? A similar question from Yasmeen that there is great genetic data plus strong preclinical results of 5-HT2C. Could you help us understand how predictable are preclinical models to clinical studies and how these preclinical results compare to DCCR? Jan, would you address this question, please? Maybe Steph should address the first half of that question. On the dosing question. Yeah, could you repeat that? I'm sorry. What was the first half? Yeah, the first one was about how much does prior dosing work inform the correct level in PWS? You mean prior dosing? Okay. So I think the question is, how much from our Phase 1 and from our Epilepsy studies inform? The answer is quite a lot. Again, go back to the biology. You're talking about not absent 5-HT2C receptors here, but injured, if you will, mutated ones. We have very good answers about what it would take for receptor occupancy and for driving serotonin, first from the Phase 1 in terms of pharmacokinetics. Secondly, we have very good biomarkers for effect on the serotonin system between the prolactin and the QEG endpoints. Now from our epilepsy studies, obviously, you can't translate effect in epilepsy, but what you can say is in the roughly 15-20 patients we've dosed, we have a very good handle on the tolerability. Because there are similarities in terms of trying to have an increased serotonin drive between epilepsy and Prader-Willi, that same dose range will very probably be effective, we believe, in the Prader-Willi subjects. Thanks, Steph. Okay, so let me take Yasmeen's question there. Which is, have we compared VYKAT with our lead compound or compounds. Side by side in the animal models that we have run? The answer to that is no. We know that the majority of the evidence for VYKAT was generated in mainly models of obesity, so genetic obesity, or in Prader-Willi genetic models. That is mainly a model called the MAGE-L2 model or in the SNORD116 model. We've not tested 101 or 105 in any of these genetic models of Prader-Willi Syndrome. Basically, because when we started this quite some time ago, we discovered that the translation validity of those models is not very good. SNORD116 has a different function in rodents than in humans. For that reason, we chose to really take naturalistic models or wild-type animals. Or wild-type animal models that recapitulate the core symptoms of what you see in Prader-Willi Syndrome, but also models that we know have demonstrated translation validity. That is, lorcaserin was originally developed using, amongst other models, the binge eating model. That does very well recapitulate the hyperphagia part and the effect on hyperphagia by modulating the 5-HT2C receptor. I hope that answers the question. Thank you, Jan. The question coming from Patrick Trucchio from Wainwright. How does the design of the NOVA Study compare with prior PWS trials in terms of the endpoints, patient population, and potential regulatory relevance? Probably the answers from all KOLs will be very helpful here. I'll give a chance. Elizabeth, Jennifer, Theresa. I mean, I can start. The HQCT is commonly used across PWS trials, so that's quite similar. I think the. Length of the study, since you're looking at changes in behavior, I mean, if you're looking for loss of weight, you would maybe want six months, but changes in behavior can be earlier than that. I think this is pretty comparable to what we've seen in PWS. I think the addition of the PWS Profile and some of the other assessments are probably getting at more of the behaviors than some of the previous studies, but it's fairly similar. I think having a blinded placebo period in a Phase 2 is nice for getting an idea of what the signal is like. I 100% second that piece for sure. All of it that Theresa just said, I agree with. Yes, it's very nice to have a Phase 2 with a placebo arm. I think it's really an important piece of it that not. All Phase 2s in Prader-Willi have. I think this will give us a good idea in terms of potential efficacy of this drug and the syndrome by having that. I also agree with the two of them that everything seems to be pretty much in line with other studies. Actually, what I'm most excited about is that Open-L abel Extension to kind of see what happens over time, what other kinds of effects that we see, maybe anecdotal. They may not always be on questionnaires, but just to see over time what actually kind of goes on with people. I'm really excited about the fact that that placebo double-blind part, really good questionnaires, good training, good experience in the sites, all those things really matter to have a really clean, good trial. Okay, thank you very much. And the last question probably that we will take today that we'll address to Ian. Again, it's coming from Patrick Trucchio from Wainwright. How does today's update reflect the company's evolution from a single-asset Epilepsy story to a more diversified serotonergic platform addressing multiple neurological and behavioral indications? Yeah, I think that's a testament to the hard work that the company did early on in medicinal chemistry, starting with my Co-Founder, Alan Kozikowski, and continuing with the development work that Jan and Steph have been doing. It's also a testament to what 5-HT2C can do. This isn't just an Epilepsy drug, but certainly has, or Epilepsy mechanism, certainly has the ability to affect different patient populations such as PWS. We see the entrance of a new molecule, really the start of building out our serotonergic platform, which also includes 5-HT2C assets. Steph or Jan, I don't know if you have anything to add on top of that. No, what you're looking at, just to reinforce that there are abnormalities of serotonergic transmission, which underlie a whole series of CNS diseases. With the high specificity we have with the bias agonist approach, we think that there would be a range of entities where we could really help patients and families with really catastrophic diseases. Yeah, maybe I can just echo that. I believe we have a treasure trove of 5-HT2C molecules, and what we are trying to do here is really to find the proper place for those. I think that we have a very good potential for many of these molecules. Thank you, Jan. With that, we will wrap up this session. Thanks, everyone, for joining. Thanks, Theresa, Jennifer, and Elizabeth, and thanks, Bright Minds team.