Hello everyone, and thank you for joining us for the H.C. Wainwright 27th Annual Global Investment Conference, taking place from September 8th- 10th in New York. My name is Joseph Brusca, and I'm an Equity Research Associate at H.C. Wainwright, and I'm pleased to introduce Adi Mor, who is the Co-founder and CEO of Chemomab Therapeutics. Thank you, Joseph. It's our pleasure to be here today. As mentioned, I'm Adi Mor. I'm the CEO and Chief Scientific Officer at Chemomab Therapeutics, and we are very excited to be here today at the H.C. Wainwright Conference. Please note I will be making some forward-looking statements throughout my presentation, so please refer to our risk factor in our SEC filings. Chemomab is a clinical-stage company focused on the development of novel treatments for inflammatory and fibrotic diseases. Our lead asset in the bucket is a first-in-class monoclonal antibody targeting the unique protein CCL24, a protein that was found to play a very fundamental role in the biology of both inflammation and fibrosis. We are targeting rare diseases with large commercial opportunity and significant unmet medical need, and the lead indication is primary sclerosing cholangitis, or PSC, a disease that involves significant inflammation and fibrosis in the bile duct and has no approved drugs to date. Over the years, we have significantly de-risked nebokitug before entering into the phase II clinical study, so we have seen from very comprehensive types of early clinical data and preclinical data the activity of nebokitug in being able to attenuate inflammation and fibrosis. Recently, we successfully completed our phase II clinical study in primary sclerosing cholangitis, where we have reinforced everything that we've seen before in earlier clinical studies and showed for the first time proof of concept for this drug in primary sclerosing cholangitis. We also completed an end of phase II meeting with the FDA and have a very clear route forward for phase III and approval. Chemomab is supported by top-tier investors, including HBM Partners, OrbiMed, Sphera, PhillipCapital, and others, and there is also significant interest from potential strategic partners based on the strong results that we've shown in our phase II clinical study. CCL24, the target of nebokitug, is a soluble protein that belongs to a subfamily of cytokines. What makes this protein so unique is the fact that it's available and able to simultaneously and directly enhance the two main processes that lead to inflammation and fibrosis. On the one hand, CCL24 triggers a very specific immune response that is essential to support fibrosis, and at the same time, CCL24 also activates the cells that are responsible for the scarring in the tissue. After many years of validation of CCL24, where we've seen its activity in the liver, in the lung, and in the skin, we have generated nebokitug, a blocking antibody to CCL24 that was indeed able to show a very significant attenuation of both inflammation and fibrosis across multiple organs, including the liver and specifically in PSC in the bile duct itself. Primary sclerosing cholangitis is a rare liver fibrotic disease characterized by obstructive damage to the bile ducts that eventually leads to inflammation, fibrosis, and end-stage liver disease. This is a terrible disease that affects mainly men, relatively young men around their 40s, and as I've mentioned, there are simply no FDA-approved treatments to date, so a very significant unmet medical need. Unfortunately, the only treatment with curative potential, I would say, is liver transplant, and this is what patients are facing eventually. Even then, after a new liver is being transplanted, we see a relatively high percentage of recurrence of the disease. Obviously, the need to find a cure or a potential treatment for PSC is very significant. There are approximately 70,000 patients in the seven major markets, and the expectation is, like we're seeing in many other diseases, that more patients will be diagnosed once effective therapies are going to be available. In terms of the competitive landscape, I would say that we're facing a very unique environment here since nebokitug is the only drug in development that actually suggests disease modification that can stop the progression of the disease and prevent the patient from getting to the need of a liver transplant. This is as opposed to all of the other assets that are currently in development that are mainly focusing on bile acid metabolism and trying to hold some of the symptoms, mainly pruritus or itch that the patients are suffering from, but those changes are not impacting the trajectory of the disease at the end of the day. Nebokitug is positioned as a potential cornerstone in primary sclerosing cholangitis with very limited competition, targeted efficacy that actually interferes with the core mechanism of the disease, and a potential effect on disease progression. Nebokitug can become the first approved drug in primary sclerosing cholangitis. We are expecting that based on the significant unmet need, the first-in-class mechanism of action, the rare disease focus, and of course, strong comparable benchmark, a premium pricing will be approved that would result in an annual commercial opportunity that can exceed $1 billion per year under very conservative assumptions. Now let's move on to see some of the data, the exciting data that we have from our phase II clinical study in primary sclerosing PSC. We enrolled 76 patients into this study divided between three groups: nebokitug 10 mg/kg, nebokitug 20 mg/kg, and placebo. Patients were treated for 15 weeks, and this is the double-blind part of the study that we have reported first. In addition, patients were offered to join the second part of the study, open-label, where all patients are receiving drug up to 48 weeks of treatment in total with nebokitug. The primary endpoint of this study was safety and tolerability. The secondary endpoint is composed from a variety of markers that represent disease progression, first and foremost, liver stiffness and ELF score, but we've also evaluated PRO-C3 and pruritus and other inflammatory and fibrotic biomarkers. Important to emphasize that we have predefined in our analysis plan two main populations as part of the analysis. The first one, all completers, all patients that completed the study were evaluated. The second one, those are patients that have moderate to advanced disease. The reason for this is that PSC is a slowly progressing disease, so we wanted to make sure that when we're looking at activity, we are looking at activity at patients that can really show a change in activity within 15 weeks or even 48 weeks, and that's why the focus on this population. Overall, I can say, and I'm glad to say that the study was very successful. We met both the primary safety, the primary endpoint being safety, and the secondary endpoints showing a very clear anti-inflammatory, anti-fibrotic, and anti-cholestatic activity of nebokitug. With this study, we've identified first the dose to move forward with, so 20 mg/kg is the dose that we're planning to continue with towards the phase III, and we've also identified the population that we're going to continue with through the phase III. Those are patients with moderate to advanced disease, patients that can benefit more from nebokitug in the timeframe of the phase II and the phase III that is anticipated. When we're looking at the activity markers, first of all, we're very excited to see that nebokitug was able to alter, to improve all of the markers that are associated with disease progression. One example in this slide is liver stiffness measured by ultrasound liver elastography. We're able to see here clear differentiation when we're looking at all of the patients between placebo and nebokitug, but even a more clear differentiation when we're specifically looking at the target population for activity, the moderate to advanced, where we're seeing a substantial change between placebo and nebokitug that even reached statistical significance. I should say here, the study was not powered to detect statistical significance, so these are very, very exciting data that show another evidence of the uniqueness and the strong activity of nebokitug being able to interfere with both inflammation and fibrosis. Beyond liver stiffness, we're looking also on the ELF score, quite a validated composite marker that represents risk for disease progression in PSC. In patients with moderate to advanced disease, we're able to see a very clear attenuation, per se, absolute reduction of ELF after 15 weeks of treatment with the 20 mg/kg dose group. This data is also supported by publications and showing that this is actually clinically relevant reduction in ELF that can project less clinical events over time. Other markers of inflammation and fibrosis were also evaluated: TIMP1, PIIINP, TGF-β, PRO-C3. All are showing that nebokitug, and more so in the 20 mg/kg group, is able to attenuate those biomarkers that are relevant to inflammation and fibrosis and further support the mechanism of action of nebokitug in PSC. Similarly, when we're looking specifically on markers of inflammation, markers that we know are relevant to primary sclerosing cholangitis like IL-6, IL-18, soluble CD14, et cetera, we see again a dose-dependent improvement in all of those inflammatory biomarkers. This is another evidence for the anti-inflammatory arm or activity that nebokitug proposes. Even beyond the main mechanism of action, blocking inflammation and fibrosis, when we're looking at features of cholestasis as a secondary effect, we're very excited to see changes in pruritus, changes in bilirubin, meaning the fact that we are attenuating or relieving the injury of the strictures from an inflammatory and fibrotic point of view also has an effect on the cholestatic nature of the disease, and you can see that in the results in this slide. The second part of the study was open-label extension. In this case, patients that completed the 15 weeks part of the study, the double-blind, were offered to join an open-label extension and get only the drug for up to 48 weeks. The aim of this part of the study was to evaluate long-term safety. This is the first time that nebokitug is being given for one year. We wanted also to evaluate the durability of the effects that we were seeing in 15 weeks versus 48 weeks, and we wanted to make sure that the population that we selected to continue through the phase III, meaning patients with moderate to advanced disease, still remained the target population, and it was for the dose, making sure that the 20 mg/kg remains the effective dose that we would like to move forward with. It was very encouraging to see that 93% of the eligible patients elected to continue through the open-label extension, so very high compliance here wanting to continue towards the remaining part of the study. Overall, what we have seen after 48 weeks of treatment is continued reduction in biomarkers that are associated with disease progression. We've seen continued reduction in ELF, in ELF-related components, in PRO-C3, and specifically again in patients with moderate to advanced disease that received the higher dose of 20 mg/kg. We're also able to show that nebokitug remains safe and well tolerated for up to 48 weeks of treatment. Some examples from the data that we were very excited to see: when we're looking at the ELF score, and just as a reminder, ELF is a composite marker that represents the risk for disease progression. We see that when we're looking at all patients that completed the study, the 20 mg/kg dose showed a sustained risk, meaning no change after one year, which is very good news because if there was a placebo group here, we would have seen that the risk of disease progression after one year would have been increased. Interestingly, when we're looking at patients with moderate to advanced disease, we are not only seeing stabilization, we're actually seeing reduction in ELF over time, meaning the risk for disease progression in patients that are more prone to show disease progression is actually reduced over time following treatment with nebokitug. Same when we're looking at the multiple fibrosis-related biomarkers: PIIINP, TIMP1, PRO-C3. All are showing the same effect, meaning patients with moderate to advanced disease are showing continued reduction in those markers of fibrogenesis up to 48 weeks of treatment with the drug. When we're looking specifically at liver stiffness, we can see here on the right hand that we had the opportunity to also use historical data from peer-reviewed publications. As you can see, patients that were treated with nebokitug 20 mg/kg for up to one year showed a much more mild increase in liver stiffness as compared to matching patients from historical data. We're actually seeing an 80% improvement in patients that were treated with nebokitug versus historical data showing much more elevated liver stiffness over time. When we're looking specifically at all of those biomarkers, and given the fact that the phase III is going to be relied on clinical endpoints, it's very important for us to understand what is the value of the changes that we are seeing in those biomarkers. What we have seen both for ELF and for liver stiffness is that the reductions that we are seeing after 48 weeks of treatment with the drug are relevant or reflective for less clinical events over time. This gives a lot of confidence and de-risking once we are entering the phase III clinical study because we already know that after a relatively long period of treatment, 48 weeks of treatment, we can see reductions in biomarkers that predict less clinical events. Even when we're looking specifically at clinical events in our study, in our phase II clinical study, we were able to witness an 80% less events in our study in patients that were treated with nebokitug for up to one year compared to matching patients from an historical control. Even though this part of the analysis, of course, is not powered in the phase II clinical study, it is very reassuring to see that after one year we already see very promising results in terms of reducing clinical events. We are very eager to start the phase III, evaluate nebokitug for a longer period of time versus placebo, and identify lower clinical events that could lead eventually to the approval of the drug. Chemomab also had a discussion, an end of phase II meeting with the FDA earlier this year, and we are very happy to report that we were able to get a very clear alignment from the FDA for the first time in the field, I should say, as to what would it take to get a full approval in PSC. The FDA and Chemomab agreed on a single pivotal study for full approval for nebokitug in primary sclerosing cholangitis. This study is going to be based on evaluating multiple clinical events, events that are happening much more frequently than just liver transplant and death, and that is part of the flexibility of the FDA here and part of the reason how we could identify eventually a design that could be effective and be completed in a timely manner. We are planning to initiate this phase III clinical study. We are working on preparations for this phase III clinical study, and given the strong partnership discussions that we are having, the goal here is to engage with a partner and be able to initiate this phase III as soon as possible and potentially get nebokitug into the market as the first approved drug in primary sclerosing cholangitis. Just to summarize here, I would say that with its unique dual anti-inflammatory and anti-fibrotic mechanism of action, nebokitug represents a potential breakthrough in PSC, first and foremost, but also in other fibrotic diseases where we have strong data for systemic sclerosis, IPF, and others. The positive phase II readout in PSC is a transformative event for Chemomab and for the entire field in primary sclerosing cholangitis. As I've mentioned, we are advancing discussions with partners at the moment, and we're very excited to continue the development of nebokitug and get it to the finish line as the first marketed drug in this rare and unmet need disease. Thank you.