All right. Okay, everyone. Welcome to the next session at the H.C. Wainwright 28th Annual Global Investment Conference. My name is Matt Keller. I am a VP in the equity research department, and it is now my pleasure to introduce our next presenting company, Galectin Therapeutics. Presenting for the company, we have Joel Lewis, CEO, and Khurram Jamil, CMO. Gentlemen, please go ahead. Thank you. Good morning, everybody. On behalf of Galectin Therapeutics, I am pleased to provide an update on our clinical development program and share an update on our path forward as we are preparing for our phase III registration trial. Our presentation contains forward-looking statements regarding our plan and activities. For a full description of these risks and plans, please refer to our SEC filing. Galectin Therapeutics is focused on developing therapies to address a high unmet need in patient population of MASH cirrhosis with portal hypertension and oncology. Our lead compound is belapectin, which has been in development for MASH cirrhosis, and portal hypertension. It is a complex carbohydrate, and it is a potent inhibitor of galectin-3. Galectin-3 has been implicated across multiple chronic fibrotic and inflammatory conditions. In terms of MASH cirrhosis, and portal hypertension, we have conducted two phase II-B studies and have generated data showing belapectin-led improvement in portal pressure, reduction in incidence of new varices, and favorable changes in multiple fibrotic biomarkers. We have also done a phase II-B study in metastatic cancer, and it also had a cancer showing favorable data in combination with belapectin and PD-1 inhibitor. In terms of patient landscape, it is based on the most recent epidemiology study. It is estimated that 3.3 million patients in the U.S. are afflicted with MASH cirrhosis, and portal hypertension. These patients are at increased risk of developing complications of chronic liver disease, such as hepatic encephalopathy, ascites, bleeding, and eventually death. If left untreated, the only definitive treatment is a liver transplant. Yet for these patients in the U.S. currently, our estimated annual liver transplant rate is around 12,000. You can imagine the desperate, high unmet need for the millions of patients where there is no FDA-approved therapy, and these are at imminent risk of developing liver complications. Based on the clinical data generated so far and the treatment landscape, we have conducted blinded market research where we interviewed both treating physicians and payers about belapectin's potential. Based on very conservative forecasting model, we estimate the opportunity to be a multibillion-dollar opportunity. Once approved, belapectin could be a major player in this patient treatment landscape. As I shared earlier, galectin-3 as a target for managing chronic inflammation and fibrosis has been studied across multiple organs, not just liver, but even kidney fibrosis, pulmonary fibrosis, by leading researchers all over the world. In liver specifically, galectin-3 levels are increased in MASH cirrhosis, and portal hypertension. Once these levels are increased, there is activation of what we call hepatic stellate cell. Hepatic stellate cells are the primary cell that drive buildup of collagen or scar tissue in this patient population. Across multiple preclinical studies, belapectin led to reduction in portal pressure, reduction in collagen buildup, and favorable changes in the biomarker results. Based on the strong preclinical data, we have designed our first phase II study. In this study we published in 2020, patients with MASH cirrhosis, and portal hypertension were given treatment with belapectin for up to 52 weeks. The primary endpoint was assessment of hepatic vein pressure gradient which is a gold standard to measure portal pressure. Portal pressure in cirrhotic patient is a key predictor of developing complications and outcome. In this trial, patients who did not have varices at baseline, which was roughly half the patient population, there was significant reduction in hepatic vein pressure gradient that was also accompanied by significant reduction in incidence of new varices. Remember, development of varices based on the natural history of MASH with portal hypertension is the first complication these patients tend to develop. Based on the finding of the GT-026 trial, we designed NAVIGATE trial. Here, we tested the same 2 mg dose from the last trial. We also studied now a 4 mg dose along with placebo. All patients were treated for 18 months of therapy, one-one and to one. One more unique thing about the study was we assessed the varices, sub-visual varices at baseline and at 18 months using a central blinded multiple reviewer setup. That is a process that also FDA approved and accepted, and we have since noticed other companies following track and using this central blinded adjudication of varices as an endpoint. In terms of patient population, we enrolled patients with MASH cirrhosis, and portal hypertension. Portal hypertension was assessed non-invasively using widely accepted biomarker and imaging data. Our primary endpoint was a composite of varices, and I will talk about that in the next slide. As secondary endpoint, we also looked at other complications of the liver disease, such as decompensating events, MELD increase or mortality. The two key populations that I will be talking about, one is the overall population or ITT, intent to treat. That is the 357 patient minus the two patient who had varices at baseline. And per-protocol population, which is all patients who completed 18 months of therapy as protocol required and had endoscopy at baseline, endoscopy at 18 months. It is a similar definition that you will see in the MASH trial where they have biopsy at baseline, biopsy at end of treatment. In terms of composite primary endpoint, while the key component was development of new varices at 18 months by blind central adjudication, we also had conservative assessment, meaning if a patient developed any other liver complication or had any discontinuation of trial due to adverse event or TIPS, which is a shunt procedure, or had GLP or beta blockers used, which were the prohibited medication for more than 12 months, all of them were adjudicated as having met the primary endpoint. In terms of patient population, it reflects typical patient with MASH. 2/3 of the patient had hypertension and/or diabetes, Type 2 diabetes. The key criteria is highlighted in light blue, and that is platelet count, liver stiffness, and your spleen length. These are used non-invasively to assess portal hypertension. As you can see specifically around platelet count, it is around 130,000. If you compare that to other recently published cirrhotic trials, this is the lowest platelet count of any trial, meaning our goal was to have enriched population for outcomes, and that is exactly how we intended to do. This is patient not just who have cirrhosis, but have portal hypertension on top of cirrhosis. These are breakdown of primary endpoint composite. Overall, as you can see, while numerically lower number of patient had the composite endpoint on belapectin, 37.8% compared to placebo 47.7%, that did not achieve statistical significance. I will draw your attention to the incidence of new varices, that is the inside box. You will see on the leftmost in the gray bar, placebo, 17.8% had new varices compared to belapectin, the dark blue shade, 2 mg, 10.1%. That is a 43.2% reduction in incidence of new varices. The other component of composite endpoint was numerically similar. Even though less number of patients dropped out without endoscopy or varices, that is 11% on placebo compared to 6.7% on belapectin 2 mg. Remember the number 21 versus 12 for the varices in the ITT population. If you look at the per-protocol population, 21 versus 11. There is only one patient who dropped out from the per-protocol population. That is a patient on 2 mg dose that developed varices shortly after randomization and did not complete the 18-month therapy as per protocol. Yet the result becomes statistically significant in terms of difference versus placebo. The central blinded adjudication also involved looking at size of varices, small versus large. Why? Because we know large varices are more likely to bleed and also more likely to develop other complications. Equally importantly, FDA accepts development of large varices as viable clinical outcome when we assess broad indication trials. You can see that the overall difference of 21 versus 11 was primarily driven by difference in the large varices, eight versus one, belapectin versus placebo. We also assessed secondary outcome composite in terms of other liver complication, numerically slightly lower, five versus three. Again, placebo versus 2 mg belapectin dose. The trial was not designed to show a statistical difference in the composite secondary outcome. Again, just to reiterate, it was an 18-month trial looking at only 350 patients. This was not powered to show a statistical difference. This just gives you the flavor of patient population. We have roughly 17 composite clinical outcomes in 18 months, which is much higher number than you will see in other compensated cirrhosis patient with even two-year trial. Safety profile is one of the strengths of belapectin program. There was not a single drug-related SAE reported in the entire trial. No drug-induced liver injury. The discontinuation rate due to adverse event was similar across the three cohorts. Also, the incidence of adverse event, ACS adverse event was similar, no differences. That is extremely important in our patient population, which is MASH cirrhosis and portal hypertension. Why? Because this is a fragile patient population which is at increased risk of other adverse events. For example, GLP-1, which is now widely studied and used in some of the patients for Type 2 indication obesity. We all know if you lose weight, you also lose some element of your muscle, up to 20%. Cirrhotic patients have what we call sarcopenia. Some of them have low muscle mass to begin with. What you cannot do is afford to lose even more muscle mass because that will lead to complication. Same thing is potential risk of some of the FGF21 therapies of bone resorption, and you can lead to further complications. Having a tolerable safety profile is important for any drug, but it is even more important in our patient population which is more fragile and sicker. I will briefly share some of the biomarker data we have generated to provide mechanistic and biological proof of the efficacy data we have shown so that the clinical outcome is not just by chance, but it is driven by the biological effect of belapectin in this patient population. First is improvement in liver stiffness measure, we see by VCTE or FibroScan. You can see placebo-adjusted rate of 10.1%. Placebo cohort actually increased in their FibroScan data. Again, something to contrast, you will see most of the trials run in compensated cirrhosis. Even placebo cohort has some improvement in biomarker. Here it actually worsened. That tells you if you do not treat these patients, they are at imminent risk of further progression of disease. We also looked what we call categorical worsening of biomarker, and the cutoff we use is 30% increase in LSM or 5 kPa increase. One of these cutoff I will be talking about today are all cutoff. These are widely used, studied, and described as clinically meaningful changes or increases in biomarker. One of the more thing that you should keep in mind is I am sharing all the biomarker, most of the data as progression of biomarker, because our endpoint is progression of disease. That is something also claim if you are used to looking at biopsy data in MASH F2, F3, where biopsy, you are looking at improvement in biopsy and hence you are looking at improvement in biomarker. Our endpoint is progression of disease, preventing that, and biomarker we are showing is preventing progression of biomarker. Here again, you can see corresponding roughly 50% or more increase in placebo cohort compared to belapectin for these biomarker data. We also looked at ELF score, which is enhanced liver fibrosis score, FDA-approved biomarker for prognostication and diagnosis of patients in MASH cirrhosis and portal hypertension. These three categories are based on ELF label. You can see at each increase in category, the incidence of varices increases, the highest rate in ELF 11.3, which indicates cirrhosis and portal hypertension. The biggest magnitude of change or difference is also in ELF 11.3. Again, very reassuring that the patient population you want to benefit the most, who is at risk the most, you see perhaps the most benefit. We also do what we call combination biomarker. Again, this is looking at ELF and LSM score and looking again widely accepted biomarker combination, say for example, ELF 30% or more increase, ELF 0.5 or more increase and LSM 30% or more increase, and you see similar concordant data. Roughly 50% or 60% more patient worsened on placebo compared to belapectin. Another way of looking at how sicker patients do is look at patients who have above median level at baseline. Again, compare LSM change per protocol on the left side, above median in the middle and below median on the right side. And just as a footnote, you can see the mean LSM for above median was 29 kPa compared to below median is 15 kPa. Again, you can see clearly the magnitude of change in LSM was bigger in those in above median patients. Similarly, categorical change, the worsening of LSM by the 30% of 5 kPa was greatest in the above median. You can see the belapectin response is much more consistent across all three population in terms of increase in LSM, but the placebo response in terms of worsening was greatest in the sicker patients. Hence, the magnitude of change gets even better in sicker patients. It is consistent result across three population, yet the greatest benefit in sicker patient population. We also looked at what we call Baveno risk category. You will see often in cirrhotic patient, any development program talk about Baveno risk categories. Baveno risk criteria are used for non-invasively assigning portal hypertension. Again, the definition that is used widely is at the bottom. The three categories, red is portal hypertension, blue is probable portal hypertension, clinical significant portal hypertension, and the gray is low likelihood of clinical significant portal hypertension or no portal hypertension. So if you look, compare the two gray bars in placebo, the percentage of patient who had no or low likelihood of clinical significant portal hypertension increased by 7%. 7% of patient went from danger zone to no or low. On belapectin, twice as much, roughly 15% of patients went from no portal hypertension to again at baseline to 18 months. So twice as many patient came out of danger zone. Again, all of these findings I have shared so far corroborate the finding I have shared earlier in the ITT and per protocol, are roughly 43%- 50% reduction in incidence of varices. YKL-40 is a marker of inflammation. Now the key concept is you cannot improve or resolve fibrosis if you also mitigate inflammation, whether that is inflammation drive by FAT or other components. YKL-40 is also a component of NIS4, which is another marker, prognostic combination marker used. Whether you look at 20% increase or 20% decrease of NIS4, again, you will see favorable changes in belapectin 2 mg compared to placebo. Similarly, Pro-C3, we all have probably heard about that. That is like a dynamic marker of collagen buildup or fibrosis, and you can see again, consistently belapectin has the same trend as other markers. Pro-C4 is another marker where it impacts basement membrane and type IV collagen implicated in multiple processes. You can see again, personally a patient who had 20% increase in Pro-C4, much higher in placebo compared to belapectin 2 mg dose. Again, I should have mentioned the 2 mg dose is the one we have seen consistent finding across two trials. As we have announced publicly, 2 mg is a single dose we are carrying forward in our planned registration trial. Last of the biomarker slides, we also looked at Pro-C3 and CTX-III ratio. Pro-C3 is used to have collagen buildup, fibrogenesis. CTX-III indicates fibrolysis of fibrosis resolution. The ratio indicates what is the overall equilibrium or balance. You would like to see the ratio going down because that means more fibrolysis, less fibrogenesis. You can see whether you look at patient with ELF 11.3 and above, or those with ELF increase, either way, belapectin 2 mg has favorable finding compared to placebo. To summarize, in our NAVIGATE trial in overall program, 2 mg dose led to significantly lower incidence of new varices in MASH versus in portal hypertension. The biomarker data across multiple biomarkers corroborate the findings we have seen and provide mechanistic and biological proof of belapectin mechanism of action. 2 mg dose findings validate the findings we observed in GT-026 trial. Our safety profile remains very favorable and lends itself well to both monotherapy and also current landscape where GLP-1 therapy are underlying standard of care, especially for Type 2 diabetes and obesity. Many of these patients come on that. In fact, we have synergistic data with GLP-1 therapy that we presented last year with senior corporate deck. We believe belapectin, due to its mechanism of action, due to its data we have generated so far, has the potential to really meaningfully address the critical unmet need in patient with MASH versus in portal hypertension. We have aligned with FDA on our phase III protocol key elements in Q2 this year. We publicly announced that we will be submitting our protocol by the end of Q3, which is end of this month, and we remain on target as we actively pursue partnership and collaborative opportunities. Thank you for your attention. Happy to answer any questions.