Hello everyone, and thank you for joining H.C. Wainwright's Virtual Liver Disease Conference. My name is Vivian, and I am an analyst on the Corporate Access team. HC W is a full-service investment bank dedicated to providing corporate finance, strategic advisory, and related services to public and private companies across multiple sectors and regions. We have a total of 19 publishing senior analysts and over 650 companies covered across all sectors. If you would like more information, please visit our website at hcwco.com. As a reminder, please reference your online conference portal that provides your individual links to your meetings and all company sessions. With that, I would like to introduce Joel Lewis, the Chief Executive Officer, and Khurram Jamil, the Chief Medical Officer of Galectin Therapeutics. Thank you, Vivian, and thank you to everyone joining us this morning and to H.C. Wainwright for inviting us to the conference. My name is Joel Lewis. I'm the President and CEO of Galectin Therapeutics. Due to the time constraints on our presentation, I'm going to turn the rest of the meeting over to our Chief Medical Officer, Dr. Khurram Jamil. Go ahead, Khurram. Thank you, Joel. Thank you to the organizers of H.C. Wainwright MASH Conference for the opportunity to present an overview of our lead compound, belapectin, currently in development for patients with MASH cirrhosis and portal hypertension. We'll cover our differentiated approach and how, leveraging a unique clinical endpoint, we have demonstrated promising data in advanced MASH cirrhosis while pursuing a novel therapeutic target. This presentation includes forward-looking statements. They reflect our current plans and expectations, but actual results may vary based on clinical, regulatory, or operational factors. We encourage you to review our SEC filing for a full discussion of the risks. MASH cirrhosis with portal hypertension represents one of the most serious and underserved conditions in hepatology. Galectin-3 is upregulated in multiple chronic inflammatory conditions and is known to be a key driver of fibrosis. Belapectin, our proprietary galectin-3 inhibitor, blocks this pathway directly, offering true antifibrotic activity. Importantly, belapectin at 2 mg has consistently shown to prevent the development of new varices, a clinically relevant endpoint aligned with current clinical practice. We believe this program has the potential to change the treatment landscape for a patient population that currently has no FDA-approved therapy. Belapectin is a complex carbohydrate. In multiple preclinical studies that included both liver injury and diet-based models, belapectin reduced galectin-3 expression, collagen deposition, portal pressure, and overall fibrosis. It was well tolerated even at high doses. These strong mechanistic and safety foundations supported our clinical development path. Based on a recent epidemiology study that was published earlier this year, roughly 1% of the U.S. population may have MASH cirrhosis and portal hypertension. There are no FDA-approved therapies to reverse portal hypertension once it develops in MASH cirrhosis. If left untreated or unresolved, liver transplant is the only curative option. Yet, it's only available to a fraction of at-risk patients. With no FDA-approved therapy and the high risk of complications once portal hypertension develops, there remains a critical unmet need for effective therapies. We have generated encouraging clinical data in patients with MASH cirrhosis and portal hypertension. Belapectin's direct antifibrotic action uniquely positions it to help patients where metabolic approaches may fall short, such as those with lean MASH or cryptogenic cirrhosis. This differentiation provides a clear strategic advantage over other mechanisms in development. Based on market research feedback from both treating physicians and payers, even while using conservative optics scenarios, we believe belapectin represents a significant market opportunity. The holy grail in MASH has been to reverse fibrosis and/or to prevent the progression of disease once cirrhosis develops. As this slide shows, mortality is relatively low in compensated patients without varices. Once varices develop and bleed, one-year mortality can reach 50%. The lesson is clear: intervention must occur before varices develop. Belapectin is designed precisely for this moment in disease scores where the trial patient not only had MASH cirrhosis but also portal hypertension. In our phase II-B GD26 study, we enrolled patients with MASH cirrhosis and portal hypertension, and some of the enrolled patients had even advanced disease, those with clinically significant portal hypertension. Among patients without varices at baseline, belapectin at 2 mg not only significantly reduced hepatic venous pressure gradient, the gold standard measure for portal hypertension assessment, but also completely prevented the development of new varices in this population at the one-year mark. The NAVIGATE trial, our current global trial, was designed using the latest clinical guidelines for portal hypertension assessment. Patients had to have portal hypertension confirmed by non-invasive markers. They also had to be cleared for not having any varices via upper endoscopy that were centrally adjudicated by blinded multiple reviewers, a process that is unique to our trial and also accepted by regulatory agencies. We enrolled 357 patients across placebo, 2 mg, which was the same dose as the GD26 trial, and a new experimental dose of 4 mg. Subjects received three drugs for 78 weeks. The trial enrolled compensated MASH cirrhosis patients with portal hypertension, which was assessed based on non-invasive markers including liver stiffness measure by FibroScan and platelet count. Our primary endpoint was the incidence of new varices assessed as a composite endpoint. Key secondary endpoints included liver decompensation, mortality, transplant, and biomarker progression. Analyses included the ITT population, that is all randomized subjects, and per protocol or completer group, which is all patients who completed 18 months of therapy and had an endoscopy at baseline and 18 months. The primary endpoint was a composite of incidence of new varices, intercurrent event, which itself had four subcategories as outlined here, or dropout patients without an EGD or intercurrent event. The patient population in Navigate reflects the patient with compensated MASH cirrhosis and portal hypertension. You can compare these baseline characteristics with some of the recent MASH trial readouts, and you'll notice that patients in NAVIGATE had a lower platelet count, as well as some other biomarkers that are indicative of a more advanced stage of disease for patients with MASH cirrhosis and portal hypertension than some of these recent trials. In the ITT population, looking at each element of the composite endpoint, there was a numerical 43% lower incidence of varices in the 2 mg dose compared to placebo, 21 varices in placebo and 12 in the 2 mg group. While other categories of the composite endpoint, there was no numerical difference, and overall results were not statistically significant. In the per protocol or completer population, belapectin 2 mg dose significantly reduced the incidence of new varices at 18 months. Please note that there is only a difference of one varix between ITT and per protocol population, yet the results are statistically significant here. While the 2 mg dose showed consistent findings in both GD26 and the NAVIGATE trial, the higher experimental dose of 4 mg was less efficacious. Another favorable finding was that belapectin 2 mg also reduced the incidence of medium or large-sized varices. These are the types of varices that are more likely to bleed and lead to decompensation. Thus, this finding is of great interest to clinicians. While Navigate was a global trial, two-thirds of the patients were enrolled in the U.S. In the U.S. subgroup, results were even more remarkable than the completer population, with even a significant reduction in the incidence of varices in the belapectin 2 mg cohort compared to placebo. While there was no difference in the baseline characteristics of patients enrolled in the U.S. or ex-U.S., we observed that patients in the U.S. had a higher use of GLP-1 agonists and statins across all three cohorts. This highlights the potential for synergy between belapectin and metabolic agents, a combination strategy that could further expand its value. The incidence of liver-related events or major adverse cardiac events, or MACE, was similar between placebo and belapectin 2 mg dose, 4 and 3 respectively. Please note that the incidence of these complications is much higher at the 18-month time point compared to the complications reported at the 24-month time points in recent other cirrhosis trial readouts. Again, underlying the severity of disease in patients enrolled in the Navigate trial compared to some of the programs currently in development. Non-invasive markers further reinforce the clinical findings and provide pharmacodynamic evidence of the belapectin effects. Liver stiffness measured via VCTE technology or FibroScan showed that while the placebo subjects had overall worsening liver stiffness at 18 months, subjects in both those groups showed improvement in LSM in the ITT population. This difference was magnified in the per protocol or completer population, where we saw a double-digit difference in the change in LSM from placebo from baseline to 18 months in the 2 mg dose versus placebo. Again, you may compare these results with some of the recent trial readouts, where even placebo subjects showed improvement in LSM at the one-year and two-year mark. Using well-established cutoffs for worsening of LSM, fewer patients on belapectin experienced significant worsening in LSM compared to placebo. These findings validate the clinical finding of lower incidence of varices in belapectin 2 mg versus placebo. These results further support the finding of less progression of disease for subjects in the belapectin cohort in the NAVIGATE trial. Similarly, the ALF test, which predicts the risk of hepatic decompensation and mortality, fewer patients progressed to the high-risk category, that is, the ALF score of 13 and above in the belapectin 2 mg cohort compared to placebo at 18 months. Similarly, when using FDA-approved label cutoffs of ALF tests to stratify patients into three categories, belapectin 2 mg consistently demonstrated lower incidence of varices across all categories, with the biggest difference in varices received by placebo for the patients with the highest risk of developing liver complications. We also evaluated another well-established marker of fibrosis, PRO-C3. While baseline levels were comparable across all three dose groups, at 18 months, when assessing the absolute change from baseline in the completer population, the 2 mg showed a more than 50% greater reduction compared to placebo. These findings mirror the differences observed between the two groups in the incidence of new varices. belapectin exhibited a favorable safety profile. Discontinuation rates due to adverse events were low and balanced across treatment arms. Importantly, there was not a single drug-related serious adverse event reported in the entire trial, and no subject was adjudicated to have drug-induced liver injury. Apart from nausea, vomiting, and diarrhea, we have not observed any class effects in our trial to date. This is especially critical in this fragile patient population. We know of the class effect of GLP-1 agonists where weight loss is accompanied by some degree of muscle loss, which could be concerning in patients with advanced cirrhosis who have sarcopenia. Similarly, for FGF21 analogs, which may have a bone health signal, that's worth paying attention to in this population. To summarize, belapectin is the first therapy to demonstrate clinical effect or prevention of varices in patients with decompensated MASH cirrhosis and portal hypertension. Biomarker evidence, including results for key markers of fibrosis that are commonly used in MASH cirrhosis drug development, aligns with this clinical effect. The data of the 2 mg dose validate prior findings from the GD26 trial. belapectin's safety profile remains favorable and comparable to placebo. belapectin has shown promising data for development both as a monotherapy and/or in combination with GLP-1 agonists or other metabolic agent pathways. With a strong foundation of clinical and biomarker data, we are now focused on advancing discussions with regulatory agencies while identifying the right partner to move the program forward. This is a truly exciting time in drug development for MASH cirrhosis, and we are energized by the opportunity to bring meaningful advances to the patients who have long been waiting for an effective therapy. Thank you for your attention today. Great. Thank you, Joel and Khurram, for leading a productive and informative presentation on behalf of Galectin Therapeutics. We appreciate the time that went into putting this together and are grateful for the team's participation in our conference this year.