Host: Corporate Connect service. Today we'll be hearing from three innovative companies within the healthcare sector. First, we'll hear from Marc Hertz, President, CEO, and Director of GRI Bio. Then we'll hear from Walter Klemp, Founder, President, CEO, and Chairman of Moleculin Biotech. And lastly, we'll hear from Thomas K. Equels, Chief Executive Officer, President, and Executive Vice Chairman of AIM ImmunoTech. Each company will present for 15 minutes, followed by a brief Q&A. Please submit your questions at any time through the Q&A portal located at the bottom of your screen. Before we begin, please note that Webull was not involved in the preparation of any materials, and this is not a research recommendation, solicitation, or endorsement of any kind. No investors should rely solely on the information provided in making a decision to invest. Okay, onto the presentation. To start, we'll hear from GRI Bio. GRI Bio is a clinical-stage biopharmaceutical company focused on fundamentally changing the way inflammatory, fibrotic, and autoimmune diseases are treated. Now I will turn it to Marc Hertz, President, Chief Executive Officer, and Director of GRI Bio. Marc, you can share your screen now. Great. Thank you so much. Some forward-looking statements. So I'm excited to be here. Thank you so much for this opportunity. Looking forward to introducing you to GRI Bio. We are advancing an innovative pipeline of immune modulators for the treatment of inflammatory, fibrotic, and autoimmune diseases. Our assets have unique mechanisms of action. We're developing an oral RAR beta gamma agonist as well as NKT-cell modulators to treat these chronic conditions, really targeting key immune cells earlier in the inflammatory cascade to interrupt disease progression. We've recently reported out positive phase 2A data in our IPF study that I'll walk through in this presentation. So GRI-0621, that is our lead program. As I mentioned, it's an RAR beta gamma agonist that targets multiple of the key drivers of fibrosis. I'll walk through that phase 2A data. In addition to that, we have a pretty deep pipeline. We have a library of about 500 proprietary compounds, the lead of which is called GRI-0803. These programs target a regulatory T-cell population called a dNKT cell and will be taking 0803, that lead molecule out of the library, through its IND-enabling studies and opening IND later this year. So a little bit more about the lead program. As I mentioned, we just came out with our phase 2A data. It's an IPF. IPF is an orphan indication. It's a really devastating disease that primarily hits people in their mid-60s. It is a chronic progressive pulmonary disease that leads to abnormal scarring and buildup of fibrosis in the lungs of these patients. Median survival is only about 3-5 years. There is no cure currently for this disease. The only curative procedure would be a lung transplantation. Unfortunately, that's difficult to get. There are a few approved drugs. There's 2 that are currently marketed and a third that was just recently approved. These drugs slow the decline in lung function, but they don't change the overall disease course. Unfortunately, they don't have a significant impact on survival. They have serious side effects and tolerability issues that lead to a majority of patients discontinuing treatment over their first year. Despite these challenges, these drugs still sell over $4 billion a year. We just completed this phase 2A study. We recruited 35 subjects, randomized 2 to 1 between active and control arms. If patients were taking background therapy, 1 of the 2 approved drugs at the time, nintedanib or pirfenidone, that was fine. They just needed to stay on their dose through the course of the study. About 80% of subjects in our study were taking either nintedanib or pirfenidone. The study was for 12 weeks. We did some interim analyses along the way and then top-line data after they completed those 12 weeks of treatment. Primary endpoints were safety and tolerability. Secondary endpoints were a series of biomarkers. That's where I really dig into a lot of that data. And then the exploratory endpoints were lung function that I'll walk through as well. And so we were happy to report we met our primary endpoints. GRI-0621 was shown to be safe and well-tolerated in this study, really consistent with what we expected from earlier studies of this molecule in over 1,700 patients treated for up to a year. Importantly, we saw no overlapping GI toxicities with subjects who were also taking standard of care, nintedanib or pirfenidone, which is some of the issues that those approved drugs have. This really sets this molecule up as a good candidate in combination therapies, both from a safety and tolerability point of view, but also from a mechanism of action point of view. The secondary endpoints, as I mentioned, were biomarker-based. We reported very positive, robust trends in changes of biomarkers of things like collagen turnover, immunomodulation, differential gene expression in the GRI-0621 treated arms compared to standard of care. These results were suggestive of not only resolution of fibrosis but induction of a lung repair mechanism, so some early signals of potential disease-modifying activities. For the exploratory endpoint, the lung function data over the 12 weeks, we showed a 95% increase in subjects who saw preservation or an increase in FVC over those 12 weeks and a 60% decrease in subjects who saw a worrisome level of decline in FVC of 10% or greater over those 12 weeks in the GRI-0621 compared to standard of care arm. Looking at the adverse event profile, I will say what we saw in the GRI-0621 is kind of what we would have expected. So things like increases in dry lips, dry skin, muscle, and joint pains. Interestingly, we saw decreases in things like diarrhea and cough, so these GI issues, and cough that are two of the more two of the AEs that cause a lot of problems with standard of care. And so we're happy to see no exacerbation in those AEs in our study. Looking at clinical chemistry, we saw really no meaningful changes in the clinical chemistries that we looked at here. I'm just showing the liver aminotransferases, triglycerides, and cholesterol. I will say the slight improvement in ALT that we saw in this study is consistent with what's been shown in earlier studies with this molecule. And so really, the bulk of the efficacy data was around biomarkers. We did very extensive biomarker work in this trial, things like flow cytometry, serum biomarkers of collagen turnover, and RNA sequencing for differential gene expression. And the idea was, if we looked at a broad range of biomarkers and we saw signals across those panels of biomarkers, it gave us confidence in the results that we were seeing. And so first, I'll present some of the serum biomarkers of collagen turnover. In all of this, collagen is constantly being turned over. We're constantly synthesizing collagen and degrading existing collagen. And so what's important is the balance between synthesis and degradation of collagen. And what we often do in fibrotic indications is we look at the ratio of synthesis of new collagen to degradation of existing collagen. And that ratio is sometimes called the remodeling rate. And it gives us a sense over time if these subjects are worsening their fibrosis or resolving existing fibrosis. And so what we saw looking at type 6 collagen, looking at biomarkers of collagen synthesis, we saw a decrease in the synthesis of new type 6 collagen compared to the standard of care arm, an increase in the degradation of type 6 collagen. And we've changed that remodeling rate from when it goes positive. That means, like in the control arm and the blue arms, these subjects are continuing to worsen their fibrosis. But on the GRI-0621 treated patients, we saw a fibrolytic response or a resolution of fibrosis, at least type 6 collagen in this example, over the 12 weeks. We saw similar results looking at type 1 and type 3 collagen, including an epitope for cross-linked type 3 collagen that's really only found in fibrotic tissue. Looking at type 4 collagen, now that's a little bit different. Type 4 collagen is the major component of what's called the alveolar basement membrane. What happens in IPF is you have injury in the lung and you start destroying the basement membrane. And repair of the basement membrane is a first initial step in a lung repair mechanism. So here what we saw was an increase in the synthesis of type 4 collagen compared to control, a decrease in the degradation of type 4 collagen. Now we've switched that remodeling rate to building back up the basement membrane in these subjects compared to the control arm where they continue to break down their basement membrane. Looking at flow cytometry, we were able to show a shift in a profibrotic immune environment to an antifibrotic immune environment. Here I'm showing IL-4, a typical type 2 profibrotic cytokine that's reduced in the 0621 treated arms compared to control. Similar with looking across these biomarkers that we studied, we were able to show improvements in things like lung injury across the panel. So the serum biomarkers, the differential gene expression, and the flow cytometry readouts. Similar with extracellular matrix deposition, these signals of repair of the basement membrane and induction of a lung repair mechanism, and even repair of the epithelial cells, so AT2 epithelial cells transitioning to AT1 cells from the differential gene expression. We were also able to pick up signals of our mechanism of action. So RAR beta gamma agonist and inhibition of some of those key immune cells were also present in the biomarker data. Lastly, I'll walk through the forced vital capacity, the pulmonary function. These were the exploratory endpoints. As I mentioned earlier, we saw this increase of about 95% in subjects who saw preservation of FVC over the 12 weeks. So we went from 20% in the standard of care arm to 39% in the GRI-0621 arm. And then on the other side of it, we saw a 60% decrease in the subjects that saw a significant decline in FVC over the 12 weeks, so a decline of 10% or more. We reduced that from 20% in the placebo plus standard of care arm to about 8% in the 0621 arm. Lastly, I wanted to talk just a little bit about GRI-0803. This is our lead program targeting this regulatory T-cell population. We're completing the IND-enabling studies and opening the IND later this year. We're initially focused on systemic lupus erythematosus. This is an autoimmune indication that primarily hits women of childbearing potential. Huge unmet need. There's been two drugs approved for SLE in the last 50 years and two additional drugs approved for kidney nephritis, one of the major complications of lupus. Briefly, in preclinical studies, we've been able to show after treatment with these dNKT or T-regulatory activators, decreases in inflammation, restoration of the normal glomerular anatomy in the kidneys, reduction in fibrosis. And then other key things you look at, so reduction in double-stranded anti-DNA antibodies, improved overall survival, and improvement in proteinuria and proteinuria-free survival. At that point, I'd like to take a pause and conclude and take any questions that may come up. Thank you, Marc. Definitely very exciting times for the company. I see that you received a few questions during the presentation that maybe you could answer. Please read aloud the question before answering. Sure. Great. Thank you. And just a reminder, if you'd like to ask a question, please use the Q&A button at the bottom of your screen and type it in. Marc, your first question: How should investors think about the biomarker changes translating into meaningful clinical outcomes? And what gives you confidence these early signals will carry over a longer phase 2b study? Yeah. So, I mean, it is an early phase 2a study. It's sometimes a biomarker study, sometimes called a signal-seeking study. And so I want to kind of caveat that. But what we're seeing is existing drugs slow the decline in lung function, but patients still their disease progresses even while taking those drugs. And so what we're trying to do in the field is to not only slow the decline in lung function but halt the disease at its current state or maybe even start to reverse disease. And the biomarker data that we are showing, we are seeing just that. We're not only slowing down the decline, we actually halt it and have good signals of potentially reversing disease. So true disease-modifying impacts. The other is the safety and tolerability. The current drugs are just they have enough tolerability issues that patients tend to stop taking them. So compliance is an issue in this patient population. Our safety profile looks fantastic and puts us in a really good position to be used in combination, which is, I think, where the field is going, to combining treatment options that have slightly different mechanisms of action that might be complementary to each other. I know I didn't show it today, but we've presented earlier preclinical data where looking at our molecule in combination with some of the approved molecules, we do see that kind of added benefit in combinations. Thank you, Marc. Next question, how does your approach compare to other anti-inflammatory and antifibrotic therapies in development or on the market? Yeah. I mean, I kind of touched on that already in the last question. I think the biggest differences are slowing down disease versus potentially reversing or having true disease-modifying potential. It's early data, and I do caveat that. But the signals that we're seeing line up with what we've seen in a dozen or so other models of fibrosis that we've looked at from a preclinical setting, including pulmonary fibrosis and in this phase 2A. So I think the big differentiation from current treatments is potentially an epithelial repair mechanism that we seem to be inducing and really, really strong overall safety and tolerability data. Great. Next question, given the unmet need in IPF and disease-modifying signals seen in the phase 2A, has the company had increased interest in potential strategic partnerships or collaborations? What would the ideal partner look like? Yeah. So we have conversations with potential partners. It is an interest of ours, the next stage of development, a phase 2B potentially pivotal study. It's an expensive trial, and we would love to do that in combination with a partner who has resources and expertise that complement what we bring to the table. I can't really comment on any ongoing conversations that we have specifically, but just to say that we do have those kind of conversations and we're amenable to partnering. Great. And last question. There were a few questions around it, so they were mostly around upcoming milestones and next steps. Yeah. So the next step for this program is to prepare for the phase 2B. There's some drug manufacturing that has to happen and some feasibility work that needs to continue, and we're working on that now. The other is bringing the 0803 program forward. We're doing that work. We will be finishing the IND-enabling scale-up work this year and getting that IND filed to run a phase 1, initially targeting systemic lupus erythematosus. All right. Great. That's all the time that we have for questions. Marc, thank you for your presentation and time today.