Growth spending and sort of your balance sheet management. It looks like you have a lot of irons in the fire, both just from the core product as well as sort of the Parkinson's, ataxia, skincare, just so many there. Help us understand sort of how you want to balance the growth versus the cash flow and how can investors think about that? As I said, the ideation phase, we're extremely aggressive, and at the execution phase, we're extremely conservative. Our philosophy is we think of ourselves as almost like we're in a quantum superposition. At At the early stage, we can do everything all at once, and all ideas are good ideas. There are no bad ideas. We think that the NAD space is already quite big, but just at the absolute tip of the spear as people learn more and more how elevating NAD improves their health for specific indications, but also generally as well, and not just as they age, but as they recover, and cellular health in general is becoming more popular, and mitochondrial health is becoming more recognized and appreciated and respected, so we think that the opportunity is tremendous. It's our goal to make sure we are presently at the pole position, the leader in the space, and we always maintain that. So at the ideation phase, we feel we can do anything. But then once we get into the execution phase, we let the realities of the rate limiting factors like upside potential and resource allocation help us to prioritize. We all know what it's like to run businesses that are low on cash. We don't want to be in that place. We operate very conservatively. We have no debt. We have no warrants. We have plenty of cash. We're cash flow positive. We make money. We're not obsessed with short-term announcements. We're not obsessed with things that will move the stock. Look, our stock has been very volatile. It's not because of us. It's because of all of you guys out there that like to buy and sell and trade and buy the stock when it's hot and sell the stock when it's not. But we as a business operate in a very deliberate, slow, brick-by-brick conservative manner, but we think extremely big because we recognize the size of the opportunity that we're on. All right. Well, Rob, thank you. And thank you, everyone, for watching. If you have any questions or would like to schedule a meeting with ChromaDex, please send me an email at shamsian@lythampartners.com. That's shamsian@lythampartners.com. We have another presentation and fireside chat coming up next, so please stick around for more. And thank you, everyone, and have a good rest of the day. Thank you, Ben. It was great hearing more about ChromaDex. If you're just tuning in, don't worry. All our webcasts will be available to watch on demand after the summit. Up next, we have a corporate presentation with Reviva Pharmaceuticals. So stick around for more. Hello, everyone, and welcome back for another company webcast. We're featuring Reviva Pharmaceuticals, which trades under a ticker RVPH on the NASDAQ. For today's discussion, Dr. Lax Bhat, CEO of Reviva, will be taking us through their slide presentation, followed by a Q&A discussion. With that, let's get started. Lax, welcome. Hey, Ben, thanks for having me here. Good afternoon, everyone. I would like to welcome you all to our company presentation today. Before I begin my presentation, I would like you to take a look at our forward-looking statements displayed here. We are a clinical late-stage pharmaceutical company focused on developing novel therapeutics or next-generation therapeutics for diseases of narrow targets. That's our focus as well as a core strength. We have currently a lead candidate in phase III development. Last month, we announced the top-line data for long-term safety. We expect to start the second confirmatory studies soon. Our timeline, as highlighted here, NDA submission is sometime in early 2026. In the next 12-18 months, we expect to give multiple catalysts. This is our pipeline. We have two molecules currently in development. Both are discovered in-house. Brilaroxazine is the most advanced molecule currently in phase III development. Based on the available data generated to date in close to 900 patients, we believe the drug can be readily developed beyond schizophrenia to additional closely related neuropsychiatric diseases such as bipolar, major depressive disorder, and ADHD. The drug has differentiated from other antipsychotics currently used as standard of care. Primarily, a mechanism was to anti-inflammatory effect because most schizophrenia patients, as well as in general psychiatric patients, suffer from systemic inflammation. So anti-inflammatory effect is believed to be beneficial, not only enhancing the efficacy, but also to address some of the side effects seen in the current treatment options. So based on the available translational data, robust data in the translational model for inflammatory conditions highlighted here, pulmonary arterial hypertension, pulmonary fibrosis, as well as psoriasis. We believe the drug can be readily developed for these inflammatory conditions as well. Today's presentation, I would like to walk through a few slides highlighting clinical data for schizophrenia. That's our advanced program, as well as in the next 12-18 months, clinical milestones, what we are expecting to provide. Just before presenting the data, just quickly to connect you to some of the background information of schizophrenia. Schizophrenia is a very large indication. 24 million people suffer from schizophrenia globally. U.S. alone, close to 4 million people. Despite having few antipsychotics currently in the market, around 30% of patients do not respond to currently available treatment or partially respond. We call them as treatment refractory patients. This is a significant unmet need. And then the patient population, refractory patients, 1/3 is in a couple of millions. So if you look at the last two bullet points highlighted here, despite having multiple antipsychotics currently in the market, again, treatment has a lot of unmet need. And then ability to treat systemic neuroinflammation is one of the major unmet needs. But also, the negative symptom component in schizophrenia is suboptimally addressed with the currently available treatments. So the reason for that is highlighted on the right-hand side at the fundamental difference between the schizophrenia and other chronic severe conditions. So schizophrenia is not a single disease. Rather, it is a mix of multiple symptom domains. Major symptom domains are highlighted here: positive symptom, negative symptom, cognitive, and then mood. So negative symptom is the one this is kind of chronic in nature. So it is also connected to a great extent to cognitive impairment, mood symptoms as well. Addressing negative symptom, possibly the most important criteria to have long-term treatment effect. This is one of the biggest unmet needs. If you look at, to summarize here, possibly if you would like to compare multiple drugs currently, antipsychotics currently available. If you would like to see how good is our data compared to these approved antipsychotics, possibly considering a discontinuation rate can be a yardstick to measure individual antipsychotics because patients discontinue medication if the efficacy is not good. And then also if a drug has intolerable side effects. Combination of both suboptimal efficacy and then side effects or poor tolerability lead to discontinuation. To summarize here, brilaroxazine is our drug candidate. If you look at negative symptoms, the most difficult one to address, addressed very well based in the phase II as well as phase III, statistically significant outcome in addition to primary endpoint and overall outcome. And then the second is a good efficacy besides efficacy, better tolerability and side effect profile. That led to combination is a good compliance. If you look at the discontinuation rate highlighted here with our drug, less than placebo as well as less than historical data reported to any other standard of care. We believe the good compliance or less discontinuation rate derived from superior efficacy and safety data demonstrated by our drug, brilaroxazine. Now, quickly to coming to the clinical outcome, we have successfully completed two large randomized trials, phase II study in global study in 234 patients in three different doses. Two doses showed statistically significant outcome. In the phase III, 411 patients, top dose showed statistically significant outcome consistent with what we generated in the phase II. Low dose showed a directional improvement. And then if you look at the long-term safety data that we announced last month, so long-term safety data as well as an efficacy generated in this, again, further confirmed the data generated in the last two trials. Now we are expecting to start the second confirmatory study in Q1. This is a four-week treatment, similar to RECOVER-1 study successfully completed. We expect to complete the study sometime in early 2026. NDA submission is planned sometime in Q2 2026. Now to quickly highlight the phase III data. This is the phase III double-blind study data, as you can see here. The top dose showed robust efficacy in four weeks with a 10-point separation from placebo. Most important features associated with this data, treatment effect is that early onset of action with the separation, statistically significant separation in the first week itself, and then continue to improve throughout the treatment period, even at week four. The low dose took a week more to catch up because it is understandable a good dose response. If we continue to treat these patients in additional two weeks, we think the low dose also show statistically significant outcome. But the bottom line is the top dose consistently showed efficacy in the phase II as well as phase III with the separation of 10-point separation from placebo. 10-point separation from placebo is really a good magnitude of efficacy outcome in the historical data. If you look at widely used standard of care, antipsychotics showed in similar trial anywhere net of placebo or placebo-adjusted three to eight-point separation. Here, 10-point separation makes this drug really a well-differentiated product with the overall efficacy. This is about a primary endpoint for drug approval criteria. It meets. However, if you would like to evaluate this efficacy, what would be the long-term outcome? Possibly the secondary endpoints are most critical ones. I will walk through a few secondary endpoints just to show you how differentiated the clinical profile we have with our drug. Secondary endpoints: positive symptom is very closely related to the primary endpoint. Every single antipsychotic currently in the market showed statistically significant outcome on positive symptom because in the acute schizophrenia, primary goal is to stabilize patients by reducing the positive symptom. If a drug can't address positive symptom, you can't expect to have a primary endpoint to meet the statistical significance. We met both primary endpoint and then secondary endpoint positive symptom. However, the remaining secondary endpoints, what I'm going to show, not all antipsychotics showed similar data. So that's where the unmet need comes with the treatment. One of the secondary endpoints highlighted here is agitation. Agitation is one of the common symptom domains in schizophrenia. So as you can see here, in four-week study, we have seen statistically significant outcome. Again, not all antipsychotics showed statistically significant outcome. This further supports that broad spectrum efficacy. So negative symptom efficacy, there are two scales we use. One is a general negative symptom scale. This is a very traditional scale being used in the last 25 years. To some extent, this also comprises of other overlapping symptom domains such as mood and cognitive function. So this has shown statistically significant outcome. But if you look at the Marder factor, that is more related to core negative symptom. So this one, to some extent, it separates from cognitive dysfunction and mood symptoms. We consider in the recent literature, if you look at clinical understanding of negative symptom, so core negative symptom is considered as a kind of a more persistent or a predominant negative symptom. And then when if you consider the cognitive overlapping cognitive symptom, mood symptoms, they are to some extent influenced by secondary negative symptoms. So on both the scales, the drug has shown good efficacy, robust efficacy, especially if you look at the core negative symptom. In the first week itself, it separated from placebo. That's very hard to see in this space and then continue to improve. So this is really a reflective of a good remission as well as a recovery, possibly relapsing symptoms in this patient population. Now, the social cognition and then functional outcome, PSP. So these two are very closely related to negative symptom. Unless a drug has robust efficacy for negative symptom, you don't expect to see these two. These two outcome on secondary measurements or secondary endpoints further supports the strong data what we generated with the negative symptom. Now, CGI is further again, further supports the overall outcome. Most important thing is around 78% patients show statistically significant improvement on CGI. And then 81% patients showed improvement or compliance as well. This is really, again, further supporting overall broad spectrum efficacy and then good compliance. Now, this is about the efficacy. Now, quickly at the beginning, I mentioned about the neuroinflammation. Neuroinflammation is a part of the symptom domains in this patient population. So the longer this patient suffers, schizophrenia is a lifelong disease in most patients. Longer this patient suffers, they are likely to have more chronic neuroinflammation. IL-8 is the pro-inflammatory marker. Cytokine is highly expressed in schizophrenia patients. If you look at our data here, dose-dependent statistically significant improvement in this patient population, and then also another biomarker, chemokine, so if you look at the bottom highlighted here, besides these two biomarkers, there are multiple biomarkers related to inflammation also reduced. They are not statistically significant because you don't expect to have every single biomarker to show statistically significant improvement because there is quite a heterogeneity you expect in this patient population with different markers, so bottom line is there is a good trend in overall improvement in the decrease in pro-inflammatory markers. The most important one, highly expressed IL-8, showed statistically significant improvement, so based on this, we believe this has a strong anti-inflammatory effect as demonstrated in a number of translational models, so this is very well reflected in both efficacy and then side effects. To summarize here, as you can see in the middle column, this is the primary endpoint and then key secondary endpoints. Every single pre-specified secondary endpoints met with robust efficacy, and then also because of the broad spectrum efficacy, drug has shown good compliance, 16% discontinuation versus placebo, 22% historical data for other antipsychotics over 30%. So this is around 50% better than historical data reported with other antipsychotics, so overall, broad spectrum efficacy and then good compliance, treatment adherence reported. Left-hand side showed here are key biomarkers. Again, IL-8 showed statistically significant improvement. Similarly, with the hormones, prolactin is known to increase in schizophrenia patients as well as with the number of drugs currently in the market also known to increase. Increase in prolactin further causes mood symptoms. Patients will have difficulty to overcome mood symptoms and other conditions. So, decrease in prolactin is further supporting that a good efficacy. Lastly, the BDNF is another marker related to neuroinflammation showed statistically significant improvement that further supports good efficacy and treatment effect. Lastly, digital biomarker highlighted here. This is specific to negative symptom. If you look at here, enriched patients with a digital biomarker, out of 411 patients, 220 patients have high degree of negative symptoms. In this patient population, if you look at the treatment effect, almost double than the overall patient population. That further confirms the strong, robust efficacy for one of the most difficult symptom domains to treat. Our drug has shown good efficacy. So this is the safety profile and a very clean profile. So it's kind of comparable to placebo, 35% in treatment effect versus placebo. There is no dose-dependent in general overall side effect seen. And then, if you look at over 5% side effects reported are somnolence and then headache, when the remaining are pretty much clean profile. Now, if you look at the long-term safety study, one-year study, it further confirmed the efficacy generated in four-week study, again, comparable to four-weeks randomized trial. Most importantly, efficacy, sustained efficacy over one year, that is very important. All three doses showed good efficacy, sustained improvement. Most importantly, patients who rolled over from acute treatment to one-year treatment, over 86% patients showed over 30-point decrease in PANSS score. And then over 60% patients showed over 40-point decrease in PANSS score. These are really very good numbers, robust numbers compared to other standard of care. Most importantly, sustained long-term efficacy with a very good safety, favorable safety profile. This combination of this, we believe, our drug met the most unmet needs in this treatment regimen for schizophrenia. So this is a very differentiated profile. This should immensely benefit patients if it approached the market. Now, this is the comparison of phase II versus phase III data. I would not go into detail, but as I summarized in the previous slides, total PANSS scores are comparable, primary endpoint as well as a key secondary endpoints, including the discontinuation rate. So this is the compare, if you would like to compare the data with other marketed drug, widely used blockbuster drug, if you look at the blue bars are for marketed drug, and then purple bar is for our drug. On the primary endpoint, if you look at on the left-hand side, certainly our drug showed robust efficacy differentiated than other treatment options. If you look at the right-hand side, the total PANSS is a primary endpoint, or if you would like to compare three major secondary endpoints or symptom domains, positive symptom, negative symptom, and then functional outcome, again, our drug differentiated with one of the widely used antipsychotics, both in the acute as well as the long-term treatment, aripiprazole, so this is about the data, so we expect to, as I mentioned at the beginning, we expect to start the second study soon, and then as we announced last month in the top line data for long-term safety data, we expect to announce the full analysis data for long-term safety sometime in March, so with that, and then most of the non-clinical studies completed required for NDA, so we are very optimistic about the future prospects of this drug. In the next six to 18 months, we expect to give multiple catalysts as we make progress toward NDA, and then we expect to file NDA sometime in Q2 2026, so this is about the clinical outcome, so thank you all for your attention. Happy to answer any questions you may have. All right. Thank you, Dr. Bhat. Just a couple of questions while we have some time, so the big differentiation for brilaroxazine is that it's generally well tolerated, low rates of adverse events and discontinuation. Can you share some of the key reasons for that? Yes. The key reasons what we believe in the basic pharmacology of that one is it's designed to have not only target-focused efficacy, but also often we don't see, we don't hear from other drugs that the off-targets are optimizing. The off-targets are also equally important because off-targets cause a lot of side effects. We have addressed in our drug. So selectivity as well as selectivity for the targets associated with our drug, and then minimal or no activity for the off-targets, that makes difference, and then also ability of our drug to address systemic inflammation, we believe that significantly contributed. Secondly, the way the drug metabolizes in the body, that also contributes in the long-term treatment, a lot of side effects. We call it drug-drug interaction. Our drug, based on the clinical study completed, is unlikely to cause drug-drug interaction in the trial because variability is much less compared to other approved antipsychotics, so based on the combination of good safety profile and then efficacy, treatment adherence improved because this is a lifelong treatment. Patients' treatment adherence is extremely important. Combination of this translated very well into a good profile. We believe this would benefit significantly to patient population. Okay. And then finally, with regards to the open label extension of RECOVER and sort of expected in the first quarter here, what should we expect from the full set data here? Full set data in the top line, we announced only the key primary and then secondary endpoints and overall safety profile. We would provide further detail into multiple secondary endpoints as well as primary endpoints in the close to around 150 patients completed one-year treatment as well as around 300 patients completed six months. That is a much larger patient population data. And then also we will provide some of the biomarkers, especially the vocal biomarker for negative symptom data also we expect to provide. So the complete package of fully analyzed data, we believe the further confirm the strong data what we generated in the double-blind trial. Okay. Well, it looks like we are out of time. Thank you, Dr. Bhat. And thank you, everyone, for watching. If you have any questions.