Good afternoon, everyone, and welcome to the Jefferies Global Healthcare Conference in New York. My name is Jonah Scherl. I am with the Jefferies Healthcare Investment Banking team, and it is our pleasure to introduce Gad Soffer, Chief Operating and Business Officer of LB Pharmaceuticals. All right. Thank you very much for the introduction, Jonah. Thank you to Jefferies for having us. Very excited to take you through the LB Pharma story. As you'll hear, our lead asset, LB-102, is biologically and clinically de-risked and moving forward in late-stage development across schizophrenia, bipolar depression, and MDD. I'll be making forward-looking statements as we go through the presentation. The vision of LB Pharma is very much to build a fully integrated neuropsychiatric company. How do we intend on doing this? Our lead asset, LB-102, is derived from one of the most successful antipsychotics and is standing on the shoulders of 40 years of clinical and real-world validation. We have late-stage trials ongoing in schizophrenia, bipolar depression, and soon to be adjunctive MDD. Earlier last year, we read out positive registrational data in schizophrenia that supports a very differentiated profile in what is a large branded antipsychotic market. We have a streamlined path to approval in schizophrenia and a mechanism that supports expansion broadly across psychosis and mood disorders. We have strong IP life and a balance sheet that supports multiple clinical readouts and runway into the second quarter of 2029. We believe LB-102, as a result of the data we've generated to date, has a differentiated profile across neuropsychiatric disorders. This includes competitive clinical activity with rapid onset of response, a class-leading safety profile, the opportunity for robust effects on residual symptoms that cut across all of these diseases, and this is a validated mechanism. It's a D2 antagonist with convenient once-daily dosing and starting therapeutic dose. LB-102 has the potential to be the first benzamide antipsychotic in the U.S., and as we develop a long-acting injectable formulation, the potential first global benzamide LAI. Our pipeline includes late-stage development with multiple clinical milestones expected and runway into the second quarter of 2029. This is headlined by our development efforts in schizophrenia, which includes a pivotal phase III study, as well as all of the other activities we would need to do to put ourselves in position to support approval. We have a bipolar depression trial that's ongoing, and early next year expect to start a trial in adjunctive MDD. Let's talk about the origin story of LB-102. LB-102 is a derivative of amisulpride. Amisulpride is a generic antipsychotic that was approved around the world but never made it to the U.S. It's approved outside the U.S. for schizophrenia, negative symptoms of schizophrenia, as well as dysthymia, which is a persistent form of depression. Even more than 40 years after its initial approval, it is still very widely used, with more than 2 million prescriptions per year in Europe. It has among the highest effect sizes of the approved antipsychotics and a favorable safety profile with a very low all-cause discontinuation rate. It does have a number of limitations, however. It has very poor blood-brain barrier permeability, which results in the need for high doses, as you see on the bottom, 400 mg- 800 mg. That leads to high systemic exposure, and it also requires BID dosing that hinders adherence. How did we improve on amisulpride? LB-102 was designed to retain the benefits of amisulpride and solve those limitations. As you can see in the figure, we added a methyl group to the structure. The methylation increased the lipophilicity of the molecule and enhanced the ability to transit the blood-brain barrier. It also improved the residence time in the CNS. This resulted in a drug with improved potency, lowered the required dose, and systemic exposure. We determined from dopamine receptor occupancy studies that 50 mg of LB-102 was approximately the equivalent of 400 mg of amisulpride. It also supported once-daily dosing and new chemical entity status that led to issued composition of matter. Very importantly, we also retained the binding profile of amisulpride. LB-102, like amisulpride, is highly selective and potent antagonist of D2, D3, and 5-HT7. D2 provides antipsychotic efficacy, and D3 and 5-HT7 are known to provide antidepressant and cognitive effects. One of the really interesting features of these molecules is that at low doses, they preferentially engage presynaptic autoreceptors implicated in mood, anhedonia, and cognition by increasing dopamine signaling. At high doses, they suppress dopamine signaling, and at low doses, they can enhance it. The development path that we're following for LB-102 is well-trodden. Most antipsychotics, when they have a mechanism like this, start in schizophrenia to anchor dose and pricing, and then expand from there to the much larger indications of bipolar depression and MDD. This is the path that Vraylar followed, leading to nearly $4 billion in sales in 2025. It's also the path that Intra-Cellular followed, leading to its acquisition for $14.6 billion. Let's jump into schizophrenia. We'll take you through our phase II data, as well as our ongoing phase III development efforts. Schizophrenia is a prevalent, debilitating disease with no cure and significant persistent treatment gaps, despite the availability of a wide number of therapies. We know that 74% of patients discontinue their medications due to lack of efficacy or side effects. We know that many patients suffer from residual symptoms. 60% of patients suffer from predominantly negative symptoms, and 80% of patients suffer from cognitive impairment that hinders function. Our phase II trial that we read out early last year, the schema is highlighted here. This was a very large, four-arm phase II study where we tested three doses of LB-102, 50, 75 and 100 mg. The primary endpoint of this study was PANSS change from baseline at day 28. Secondary endpoints included the PANSS positive and negative subscales, and we measured cognition as an exploratory endpoint. This trial was designed to be pivotal with a large sample size, robust statistical analyses, conservative means of imputing for missing data. At our end of phase II interaction, when we asked FDA if this trial could support approval, they highlighted that it appeared to have the characteristics of an adequate and well-controlled study. This is what gives us the confidence that we can file for approval in schizophrenia with just a single positive additional phase III trial. The results of the phase II trial at the primary endpoint are highlighted here. As you can see, all three doses were highly statistically significant versus placebo. The baseline PANSS in this trial was 94, the magnitude of the reduction here was clinically meaningful. It took these patients out of acute schizophrenia so they could leave the hospital. We were also very pleased with the placebo rate. As you can see on the bottom right, 9.3. We implemented a number of very deliberate measures in order to control the placebo rate, including use of vendors to identify and exclude professional patients, the use of central raters to act as quality control. We were judicious in the number of scales that we used because we know that patient and rater fatigue can impact placebo rates, and very close oversight of sites and the CRO. As you'll see, we'll be using all of these same measures in our phase III. We were also very pleased with the treatment effect in this trial. Whether you look at it on a completers basis or with a very conservative MMRM-based method, the results were near the top of approved antipsychotics, were in line with amisulpride, these results demonstrate how statistically robust the phase II trial was and give us a high degree of confidence heading into phase III. Let's talk about cognition. I mentioned we evaluated that as an exploratory endpoint. Cognitive impairment is one of the core domains of schizophrenia and a critical unmet need. We observed a robust dose-dependent, statistically significant improvement in cognition at each dose of this study, reaching an effect size of 0.66 at the 100 mg dose. This is among the highest that's been observed in an acute schizophrenia study. Beyond the magnitude of the fact, we were also really encouraged by the fact that these results were in a broad patient population without the need to enrich for patients who had severe cognitive impairment at baseline. Moving forward, we're going to be evaluating cognition in all of our studies, the phase III schizophrenia, as well as our studies in bipolar depression and adjunctive MDD. The adverse event profile, the treatment-emergent adverse event profile is highlighted here. Overall, adverse events were mild to moderate in severity and similar to placebo. The rates of adverse events leading to discontinuation were low, and the discontinuation rate overall in the study was fairly low among schizophrenia trials. We were also really excited about the very low rate of EPS. This is one of the keys to our belief that LB-102 has a potentially class-leading safety profile. Of course, efficacy is important in schizophrenia, but it's critical that we enable patients to stay on the drug long-term. Extrapyramidal symptoms are a class of movement disorders that are typically associated with antipsychotics and can be one of the primary causes of discontinuation. As you can see here at our 50 mg dose, we had just a single case of akathisia, a rate of EPS of less than 1%, compared with 3.7% placebo. Even at the 100 mg dose, where we had approximately 80% D2 receptor occupancy, we had an EPS rate of only 5.6%. This is in line with other approved therapeutics that are known to have very low EPS. As a D2 antagonist, there are a number of other adverse events of interest you can see here. Prolactin-related adverse events were low, all of them just 1% to 5.6%. All were mild to moderate, and none resulted in discontinuation. We didn't expect to see sedation. This is a common side effect associated with many antipsychotics. We don't have a mechanism for it, but we were very pleased to see that we had just a single case of sedation among the 251 patients exposed to the drug. QTc prolongation was also minimal, and no patients reached the pre-specified stopping criteria. Let's jump into the ongoing phase III trial. Our phase III trial is very similar in size, in scale, in scope, and in conduct to our phase II trial. The trial is 460 patients conducted at 25 sites around the U.S., and we're studying two doses of the drug, 50 mg and 100 mg. Primary endpoint is PANSS change from baseline at day 42, now six weeks instead of four. Secondary endpoints are the same. I mentioned that we're using the same mechanisms to control the placebo rate here as we did in phase II. That includes the use of vendors to identify professional patients. In fact, in the phase II, we used a single vendor. Here, we're using two vendors, close oversight of the CROs, use of central raters, and the additional scales. There's a high degree of overlap in sites between the phase II and the phase III. From a timing standpoint, we initiated this trial earlier this year, and we're expecting to read out in the second half of 2027. Alongside the phase III, we're conducting a large, approximately 900-patient open label study. This is designed to accrue the safety data set needed to support approval. We're also going to be looking at subsets in that open-label extension to evaluate both cognition as well as negative symptoms in a stabilized patient population. Summing up on schizophrenia, what I want to leave you with here is that LB-102 is a drug with compelling clinical activity, a potentially class-leading safety profile, and really unique opportunities to address residual symptoms that are a core unmet need of schizophrenia. Based on the results we've generated to date, we believe LB-102 has the potential to be a branded antipsychotic of choice in schizophrenia. Let's turn to mood disorders, specifically bipolar depression and adjunctive MDD. We're very excited about the profile that we've generated in schizophrenia, and of course, schizophrenia is a very important part of the revenue streams for all antipsychotics. When you look at those antipsychotics that have achieved blockbuster status, as you can see in the pie chart on the left, it's clear that you need to expand to the much larger patient populations of bipolar depression and MDD. As we consider the profile of LB-102, we believe it aligns really well with the unmet needs in these diseases. In both bipolar depression and MDD, residual symptoms are common and not well addressed by existing therapeutics. That includes both anhedonia, which is closely related to negative symptoms, as well as cognitive deficits. Safety is even more important in these patient populations than it is in schizophrenia. Bipolar depression and adjunctive MDD patients have much higher baseline levels of function than schizophrenia patients. As a result, they can be especially sensitive to the adverse events associated with antipsychotics, like extrapyramidal symptoms or heavy sedation. As we look to the role LB-102 can play in this disease, just as we see in schizophrenia, we see line of sight to a drug with rapid onset, competitive efficacy, a much better safety profile, especially as it relates to side effects that can impact function, and really unique opportunities to address residual symptoms. As we embark on phase II trials in both bipolar depression and adjunctive MDD, we believe we have a very high probability of success. That comes from a strong mechanistic rationale, validating clinical and real-world experience with amisulpride, supportive results from our phase II trial, and of course, trial designs that we think set us up very well for success. Let's talk about the mechanism of LB-102. As I noted earlier on, LB-102 and amisulpride have this unique property that at low doses, they preferentially engage presynaptic autoreceptors that actually serves to enhance dopamine signaling, which is underactive in depression. We also hit D3 and 5-HT7 that are known to be implicated in both cognition and depression. When you look at the amisulpride clinical and real-world experience, you see the effects of that mechanism coming through very clearly. Amisulpride has approvals outside the United States for dysthymia, that persistent form of depression, as well as negative symptoms of schizophrenia, which is characterized by profound anhedonia and depressive-like symptoms. Amisulpride was studied head-to-head versus Paxil and Zoloft in depression, two of the most successful antidepressants, and shown to be as good or better. It was also studied head-to-head versus placebo in depression and showed a very nice MADRS delta of 4.8 points. In the setting of negative symptoms, amisulpride is one of the few drugs to be successfully evaluated in predominantly negative symptoms in three separate placebo-controlled trials that demonstrated highly statistically significant results. All of these data were generated at far lower doses, consistent with that mechanism. In schizophrenia, amisulpride is used at 400 mg-800 mg. In these studies, amisulpride, as you would expect, is used much lower, 50 mg in depression, 50 mg-300 mg, with 100 mg being the most common in negative symptoms of schizophrenia. When you look at the real-world data, among those 2 million scripts that I mentioned in Europe in 2023, 20% of those are for mood disorders. As you heard, our phase II data demonstrated competitive clinical activity and a very favorable tolerability profile with low rates of EPS, minimal sedation, and GI side effects. Even at these doses in schizophrenia, as you'll see as we get into the trial designs, we're now moving to even lower doses in the mood disorders. Before we jump into the specific trial designs, I want to just say a few words in concept about these studies. Both the bipolar depression and adjunctive MDD trial are using what's called a fixed flexible dose design. This enables us to study two doses of the drug in a two-arm trial. We know that every time you add an arm to a depression trial, you risk increasing placebo rate, and so this gives us an opportunity to identify efficacy at two doses while minimizing the placebo rate. As we did with schizophrenia, both trials are designed to be registrational. For bipolar depression, we initiated this study earlier this year and expect to read out top-line data in the first quarter of 2028. The trial will enroll 320 patients across approximately 30 sites in the United States. All patients will start at 25 mg, and if they haven't had a response by the end of week three, they'll undergo a protocol-guided blinded escalation to 50 mg. The primary endpoint of the study is MADRS 10. This is the regulatory preferred endpoint, and we've included prospectively dedicated scales to capture both anhedonia as well as cognition, those core residual symptoms on which we believe we can differentiate. The adjunctive MDD trial is highlighted here. We expect to initiate this trial in early 2027, with top-line data expected in the first half of 2029. This study is using the same fixed flexible dose design, but with a couple of notable differences. First, this is an add-on study. Whereas the bipolar depression trial was monotherapy, here, all patients will have had one to two prior trials of antidepressants, and then they'll get randomized to either standard antidepressant therapy plus LB-102 or antidepressant therapy plus placebo. The doses here are also slightly lower. All patients will start at 15 mg of LB-102, and if they haven't had a response by the end of week three, the protocol-guided blinded escalation will be to 25 mg. This is in order to ensure we maintain the right dopamine receptor occupancy level for this patient population and optimize for safety. We're also going to be conducting this trial both in the U.S. and Europe.