I'm Stephen Harrison. I am a gastroenterologist and hepatologist based in San Antonio, Texas. I spent quite a number of years in the U.S. military. I retired from the Army back in 2016, and since then have spearheaded clinical trial development for NASH in the civilian community through my work at Pinnacle Clinical Research and Summit Clinical Research, which is a site network that includes about 60 sites around the country and leads the charge in NASH clinical trial enrollment. My interests, besides clinical trial enrollment, are in the development of non-invasive testing strategies for NASH, as well as epidemiology of this disease, with a focus on finding the rapid fibrosis progressor. Thank you for letting me be a part of this meeting today. Welcome, and thank you very much. I would like also to present Motti Farbstein, our CFO, who will be very happy to answer questions at the end of the presentations if there will be ones relating to the finance. Basically, Can-Fite is an advanced clinical-stage drug development company based in Israel. The management and the discovery labs are in Israel, whereas the preclinical and clinical development team is based in the U.S. We develop small molecule orally bioavailable drugs, which are in Phase II and Phase III clinical study. We have successfully concluded some corporate partnerships since our business strategy is to develop the drug, but not to market them. We have a highly experienced management on board. Last but not least, we are listed dually on the Tel Aviv and on the New York Stock Exchange. I would like to present you with our platform technology, which we think is quite unique. It's not a me-too technology. Actually, recently and during the last year, we were successful to show clinical proof of concept, and now we really believe that we are going on a solid ground regarding the technology. Basically, we are targeting a cell surface receptor, which belongs to the G protein-coupled cell surface receptor. The name is A3 adenosine receptor, and interestingly, it is very highly expressed on pathological cells in the body. It's a green structure that you see here. However, normal body cells have very low or no expression of the target. What does it mean? It means that when the drugs get into the body, they will bind only to the pathological cells, but not to the body normal cells. As a result, we have an excellent safety profile with both our drugs, piclidenoson and namodenoson. We have dosed till today more than 2,000 patients with a very good safety profile. As I mentioned, we have seen a clinical efficacy in both phase II and phase III clinical studies, and I will take you through it a bit down the road. What do we have in our pipeline? We have the first drug candidate, piclidenoson, currently positioned for the treatment of psoriasis. We have an ongoing phase III clinical study, and we have announced quite recently that an interim analysis basically led us to a very strong recommendation by a DMC, by a specific committee, which recommended to continue the study with the same number of patients. Also we were successful to select a dose. This was very good. We also had very positive data during our phase II and phase II/III study in psoriasis. We do hope to complete patient enrollment and to release data towards end of 2021. The very same drug, which has a robust anti-inflammatory effect and anti-cytokine release syndrome activity, has been already approved by the FDA for a clinical study phase II. We have been also approved by the local IRBs. We are going to initiate patient enrollment very shortly. We will focus today on the namodenoson drug, the second drug candidate, which is currently positioned for liver cancer. We have developed a phase III study going to initiate a pivotal phase III study in patients with advanced liver cancer very shortly. We have been approved for this protocol by both the FDA and the EMA. Today, we would like to focus on positive data that we have recently concluded from a phase IIa clinical study, and this is the reason that we asked Dr. Harrison to join us today, and the webinar will focus on this indication. As you most probably know, NASH is a liver disease. Maybe Dr. Harrison will further brief about it later on. The manifestations of the disease are fat accumulation, liver inflammation, and liver fibrosis. It starts from very early signs and symptoms. It may develop into an advanced liver disease and maybe even hepatocellular carcinoma at the very end stages of the disease. Namodenoson, our drug, markedly improved the function and pathology of NAFLD/NASH in preclinical studies, what prompted us to initiate a phase IIa with this study. I would like to mention that the market size is huge. It's $35 billion. M&A example can be Gilead-Nimbus deal, which was $400 million upfront money. namodenoson, our second drug candidate, is a very stable drug. Actually, it is a derivative. It has a definitive mechanism of action, which has been published extensively by us and by others. As I mentioned, we develop it for advanced liver cancer and for NASH. We went through a couple of animal models, preclinical studies with namodenoson, and we got into the conclusion, and we also published it, that we are decreasing the ALT liver enzyme. We induce anti-inflammatory, anti-fibrotic, and anti-steatotic effects in the frame of the preclinical studies, and also liver protective effect. Altogether, this prompted us to initiate a phase IIa clinical study, which entailed three arms, placebo, namodenoson 12.5 mg, namodenoson 25 mg. The endpoints of this study, which entails 60 patients, included liver enzymes,% of liver fat, liver stiffness, serum adiponectin, serum lipids and patient's weight. Adiponectin is a positive cytokine. We will discuss it in a minute. I would like to share with you the data. You can see here the ALT liver enzyme, which was decreased in the two dosages upon treatment with our drug, namodenoson. Also you can see here statistically significant normalization of the ALT enzyme. The other enzyme, AST, also showed a significant decrease after treatment with namodenoson. As I mentioned, we looked also at the serum level of adiponectin, which is a very important cytokine or factor with robust anti-inflammatory effect, and also it affects fibrosis in patients with NAFLD/NASH. You can see here a very nice increase in the level of the adiponectin cytokine. We looked at the liver fat volume change from baseline at week 12, and this actually was a very important result. We looked at it via specific software while patients went through MRI prior to treatment and on week 12, and you can see here the significant improvement in the 25 milligram dose. Not only that, we also could show a decrease in non-invasive biomarkers like the CAP score, which represents steatosis staging, FIB-4, amount of scarring in the liver, fibrosis, and FIB-4 score, fibrosis based on the AST liver enzyme. Last but not least, we show, although non-significant, we show a decrease in the patient's body weight, and this was a very important result as well, and we expect that in a longer study that we are now designing, we will see even a further body decrease after a long period of treatment of the patient. The safety was just excellent. I will not go through all these points, but you can look at it and see the safety was very good, and this is very important for a patient population who suffer from NAFLD/NASH and who needs to be treated with a drug chronically to have a very good safety profile. Just to summarize the data, so we could show anti-inflammatory effect manifested by the decrease in ALT, AST, and the increase in the adiponectin cytokine level. We could show a reduced liver content, fat content, by the MRI-PDFF. We show the decrease in couple of biomarkers which are non-invasive and could show inhibition of fibrosis. The decrease in body weight. We selected the 25 mg as the dose for the next clinical study, and the safety, which was very good. We had an excellent safety profile. I would like just to conclude my part and mention that a company like us, which is engaged with the development, will not market these drugs later on. Our business strategy is to out-license our drugs, and typically, a deal structure will grant the company upfront money upon signing distribution deals, regulatory milestones, which will come later on when we will register the drugs with the agencies, the FDA and EMA, sales milestones down the road, and of course, two-digit royalties. We have already signed six different out-licensing deals to a Canadian company, to a European company, a Chinese company, and two Korean companies, which granted the company, us, Can-Fite, $18 million, which is non-dilutive money. I will conclude here, and I would like to ask Dr. Stephen Harrison to comment about our drug and its effect in NAFLD NASH. Please, Dr. Stephen Harrison. Yeah. I'll be happy to talk about where we are in the field and what this study shows and represents. As you guys may or may not know, fatty liver is a pandemic, and that's been illustrated by the COVID-19 pandemic that we're dealing with. Interestingly, what's come to light, at least through work done with the U.K. Biobank, for instance, is data that has come forth showing that patients with fatty liver and comorbidities linked to fatty liver actually are in a worse place often if they come down with COVID-19. It actually has built disease awareness, if you will, in a way that never was possible prior to COVID-19. In a way, it's allowed us to speak in terms that our patients can understand. They know that diabetes and obesity, hypertension, hyperlipidemia, and fatty liver all are things that put them at greater risk of having a worse outcome if they were infected. What shows up in our clinic are these people asking, do they have fatty liver? Is that a risk for them? Do they need to address it? When we talk about fatty liver disease, we talk about the numbers being 100 million Americans with fatty liver, many more hundreds of millions of people around the world. When we target that group of people that is at greatest risk, it's the NASH patient with some degree of fibrosis. Remember, fibrosis portends a worse prognosis. That's the group we're focusing our drug development on. That's the group where the FDA and the EMA has given us very clear criteria for Subpart H or conditional approval of a drug. As you know, the two endpoints that are currently approved are NASH resolution without worsening of fibrosis and fibrosis improvement without worsening of NASH. You do not have to have both to get conditional approval. You do, however, have to go on and show that your drug changes outcomes in a positive way, preventing progression to cirrhosis, development of decompensation, liver transplant, or death. Having said that, there are really three different buckets of drugs where we focus our efforts on currently. One is metabolic, one is anti-inflammatory, and one is fibrosis. Now, within metabolic, you can actually cross through different types of buckets. You can be an anti-inflammatory and actually have positive metabolic effects and actually positive anti-fibrotic effects. For simplistic purposes, that's how we break them apart. Now, where I see this drug falling is in that middle bucket, the anti-inflammatory bucket. We see through its mechanism of action and we see through the pre-clinical models and reading into its proof of concept trial with 60 patients, positive impacts across a broad range of non-invasive tests that are linked to the inflammatory cascade that we see in NASH that ultimately translates into activation of stellate cells and the laying down of fibrosis. So positive impacts on ALT, AST, liver fat content, all point toward the possibility that this drug is having a big impact on fatty liver disease. Now remember, in a proof of concept trial, a short trial with non-invasive tests built in, really all we're looking for is a signal, a signal that we're moving the needle in the right direction. I think you see that here, as was pointed out. Not only are the aminotransferases and the liver fat content moving in a positive direction, but we have a test called FAST, which is FibroScan + AST, and that test is actually performing very well over the course of the trial. From baseline to end of treatment, there was a significant reduction in the FAST score. Now, ultimately, we don't have the final answer. That's liver biopsy, and that's where the study goes next in looking at patients with biopsy-defined NASH or patients that at least have phenotypic NASH at baseline, and then looking to see what happens with, as was pointed out, longer duration of treatment. So far, I think we have positive news, very positive news, in fact, with namodenoson, that it's able to move the needle on inflammation and even liver fat. Was mentioned also adiponectins. Maybe that deserves a little bit of discussion. In the setting of NASH, adiponectin levels are very low. Adiponectin is a cytokine that actually is involved with regulating insulin sensitivity at the adipocyte level. What we see in the setting of NASH is dysfunctional hepatocytes. They're not functioning well, and ultimately, they're not holding onto liver fat or holding onto adipocyte fat. That fat is released in the form of free fatty acids, gets into the portal vein, is taken up by the liver, which at the point that it gets to the liver is very lipotoxic, and the liver wants to try to do something with it. They either want to esterify it into triglycerides, they want to repackage it and ship it out in the form of VLDL, or it wants to burn it through beta oxidation. Suffice it to say that it's very toxic. Those lipids are very toxic. The liver begins to set up this inflammatory cascade. The cytokines that were mentioned through the Wnt pathway, through the NF-κB pathway, the PI3K pathway. This leads to activation of stellate cells, which begin to lay down the collagen that we call fibrosis, that, if left unabated, can lead to cirrhosis and end-stage liver disease. Targeting these inflammatory pathways that are upregulated because of free fatty acid flux into the liver is one novel way to approach this disease, and we've seen very early data suggesting that that is indeed effective. Now, the adiponectin piece to this is, where we're able to elevate adiponectin levels, what that means is that we're actually having an impact at the peripheral fat cell level to improve insulin signaling. Not only that, but there is some recent data to suggest that adiponectin may in fact be important for stellate cells. Where we're able to impact that's just a little extra benefit, I believe, that we'll see down the road when we begin to look at how this drug may modulate fibrosis through its effect on inflammation. As I mentioned earlier, there are different buckets at which we could target drug development for fatty liver disease, and I'll hit those again. There's metabolic, focusing on oxidative stress versus targeting the lipotoxic stress. They are a little bit synonymous and interchangeable, but in some ways, they're distinct also. You can go after those two metabolic buckets, or you can target inflammatory processes, or you can target fibrosis directly. Again, there are some drugs that actually hit multiple buckets, and I would say namodenoson potentially is one of those. It's a little early to tell yet exactly all the effects that are likely to happen in a NASH patient treated with namodenoson because we haven't done the larger trials treated for longer periods of time. Certainly, the proof of concept data suggests a very positive impact. Having said that, the liver is a very unique organ. In fact, the only other organ similar to that is the skin, for which a similar drug is being studied for psoriasis. What we know about the skin is if you cut the skin, that you form a scab. That scab allows skin cells to grow across the wound and heal, then the scab falls off. The liver regenerates in very much the same way. You injure the liver, a scab is formed. We don't call it a scab. We call it collagen deposition or fibrosis, that's affected through activation of stellate cells in the liver. Now, these cells normally don't do anything. They just kind of hide in the space of Disse in the liver, they just wait. They wait for injury to happen. Now, the cool thing about the liver is if you get out of the way and you take away the insult that causes the damage to the liver, the liver will heal itself. By laying down that scab, it allows for a framework of new hepatocytes to grow. When they have regenerated, that scab, that scar tissue, that collagen, gets reabsorbed by the liver. If we suppress the hepatitis B, we cure the hepatitis C, we quit drinking alcohol, we treat the autoimmune, we quit taking the offending drug that causes drug-induced liver injury, and sit back and watch, the liver very quickly will regenerate and heal, unless it's too far gone when that decision is made. In other words, they progress to cirrhosis and decompensation. We can't reverse it at that point, at least yet. Our whole idea behind this is either get the fat out of the liver or suppress new fat from coming into the liver, or we increase the burning of the fat that's in the liver, or we make the mitochondria work better to reduce inflammatory processes that activate the stellate cells. Remember, at the end of the day, this is a multifactorial disease with multiple different pathways that lead to that common denominator at the end of the day of inflammation ballooning and fibrosis. We firmly believe that the treatment at the end of the day for NASH will be similar to Hepatitis C or HIV. It'll be multimodality combination therapy. There's very unlikely to be one drug that fixes all of the problems in all of our NASH patients. We want to have different drugs that target different mechanisms with the idea that synergistically, they will come together to shut down this inflammatory process, shut down the stellate cell activation, and prevent fat from entering the liver. We have to study those individually, and then we study them collectively. Targeting the inflammatory processes that we see here is a very important pathway to show a positive impact on. Then down the road, we can begin to see how we can combine that with other modalities to affect an even greater percentage of NASH resolution and fibrosis improvement. Looking forward to where we'll be in a couple of years, I'm hoping that we will be pivoting away from a semi-quantitative assessment of NASH and collagen, which is our current approvable endpoint, as I alluded to at the beginning of the conversation. Interestingly, the FDA just put out a white paper, I believe it's out today, that you can read, referencing where they are today and where they're headed. My hope is that we are able to transition away from a pathologist read of a liver biopsy to a non-invasive endpoint, and potentially that can happen by the time this drug rolls around to phase III. In the meantime, if you were to put my finger on something and say, "What is this drug likely to impact?" I'm thinking probably NASH resolution. Remember, the longer you treat with a drug that resolves NASH, you still have ultimately a fibrosis benefit, or you should. If what we think about the natural history of this disease is accurate, if you take away the insult, eventually you suppress stellate cells, and fibrosis gets better. I believe both options actually are on the table. When I said it's a little too early, we just don't have that liver biopsy data yet to say which one is having a positive impact the earliest. Is it NASH resolution, or is it fibrosis improvement, or both? I think that will come out in due time