Great. Good morning, everyone, and welcome to day one of Oppenheimer's 35th Annual Healthcare Conference. I'm Jeff Jones, one of the senior analysts here on the biotech team, and I'm delighted to welcome Adi Mor, CEO of Chemomab Therapeutics. Adi, in the interest of time, I'll hand it off to you to take us through the Chemomab story. Thank you very much, Jeff. Our pleasure to be here. Please note I will be making forward-looking statements, so please refer to the risk factors in our SEC filings. Chemomab is a clinical stage company developing CM-101, now also officially known as Nebokitug, a first-in-class monoclonal antibody that neutralizes CCL24, a unique dual-acting target to the biology of fibrosis and inflammation. We're targeting rare diseases with large commercial potential and significant unmet medical need. Initially, primary sclerosing cholangitis, PSC, for which we have recently reported positive top-line results in a Phase II clinical study, as well as systemic sclerosis, for which we have a Phase II ready program. We substantially de-risked the clinical program over the years by extensive preclinical and early clinical data that we have assembled, and the latest positive results in PSC not only confirmed the excellent safety and activity that we've seen for the drug before, but also achieved, for the first time, clinical proof of concept, as well as validated the role of CCL24 in fibrosis. We are very pleased to have strong support from top-tier investors, including OrbiMed and HBM Partners, and substantial interest from potential pharma partners. Our current cash runway takes us through the beginning of 2026, assuring we have the resources on hand to reach our upcoming catalytic event. In this quarter, the first quarter of 2025, we are planning to report two substantial milestones. The first one, we're going to report the feedback from the FDA following our end of Phase II meeting. The feedback that we are planning to share will provide full clarity as to the regulatory route in PSC towards approval. In addition, the second milestone would include additional clinical data from the open-label part of our PSC study. Based on strong and very comprehensive preclinical and clinical data showing Nebokitug's strong interference in inflammation and fibrosis, whether it's in the liver, in the skin, or in the lung, we consider the drug to serve as a pipeline in a drug and to see the great potential in its disease-modifying activities across multiple indications. Our lead indication, PSC, is a rare liver fibrotic disease with no approved therapies. We recently conducted or completed an end of Phase II meeting with the FDA based on the positive clinical results from a Phase II clinical trial in patients with PSC, showing clinical proof of concept for the first time. Given the lack of regulatory clarity in PSC and the requirement that we've seen in the past for liver biopsies in pivotal studies, we believe that the guidance that the FDA has provided to us will be transformative for this field, and as mentioned, we're planning to report it in the very near future. As mentioned, the study also has an open-label extension part, and we are planning to report data from this part of the study in the first quarter of 2025 as well. The positive data that we've seen in PSC opens up multiple additional opportunities in other indications, and I should say first and foremost, maybe in systemic sclerosis, for which we already have a Phase II ready program and an open IND. Who is CCL24, this unique target? CCL24 is the target of our antibody. It's a soluble protein that belongs to a subfamily of cytokines. It was found to play a very significant role in promoting the two key processes that eventually lead to fibrosis. On the one hand, CCL24 recruits immune cells from the circulation and therefore enhances inflammation, and at the same time, CCL24 also directly activates the fibroblasts, which lead to extracellular matrix secretion and the scarring of the tissue. The ability of CCL24, a single target, to induce these two pathways simultaneously and directly is very unique for a target and implies its central role in promoting fibrotic diseases. Based on many years of validation of the target, we've generated a neutralizing antibody to CCL24, CM-101, now, as I've mentioned, also known as Nebokitug, and we have seen CM-101 to be able to significantly attenuate inflammation and fibrosis across multiple models. Our lead indication, as I've mentioned, is primary sclerosing cholangitis. A quick review on PSC. It's a rare chronic liver disease in the bile ducts inside and outside the liver. In this disease, those bile ducts become inflamed and scarred and eventually narrowed and even blocked. When this happens, bile acid builds up in the liver and causes further liver damage, and the damage will result in eventually end-stage liver disease, need for liver transplantation, as well as liver cancer. This is obviously a terrible disease, affects mainly men, and unfortunately lacks any FDA-approved drugs to date. The only treatment with curative potential is liver transplant, and even there, we can see relatively high recurrence of the disease with about 20% of the patients that went through a liver transplant. If we're looking at the market, serious unmet medical need, approximately 80,000 patients in the seven major markets, and a commercial opportunity that is estimated to exceed, I should say, $1 billion. As to the competitive landscape, the PSC field is definitely evolving. There are several ongoing clinical trials. I should mention, however, that CM-101's unique and dual mechanism of action is well differentiated from all other drugs that are currently in development, and the fact that CM-101 has shown clearly a strong disease-modifying potential, proven the ability to interfere with inflammation, fibrosis, and even cholestasis, definitely paved the way forward towards a Phase III. Those are actually the key pathological pathways that are involved in PSC and that the antibody can target. We evaluated over the years multiple animal models, I should say, more than 12 different animal models, hundreds of patient samples, and we've seen a very extensive anti-inflammatory and antifibrotic effect. Just to give one example out of many using the TAA liver fibrosis model, this is a very aggressive model conducted in rats, and it is clearly seen, even only by looking at the picture here on this slide on the left, that a scarred fibrotic tissue is generated in the middle here after the induction of this model. In this model, we have administered the drug after fibrosis is already generated in the tissue in the liver, and you can see here in the bottom that after the administration of the drug, the liver looked quite similar to what we're seeing with the healthy tissue. Based on the very strong scientific and early clinical data supporting the anti-inflammatory and antifibrotic activity in the liver, and specifically in PSC, of course, Chemomab moved forward and conducted a Phase II study in primary sclerosing cholangitis. You can see in this slide the design of the Phase II SPRING study. We randomized approximately 70 patients to this study, divided between three arms, so we have two doses of the drug versus placebo. Patients are treated once every three weeks for a total duration of 15 weeks, and this is the double-blind part of the study. In addition, patients were offered the opportunity to join the open-label extension part, which provides all participants additional 33 weeks of treatment with the drug, and we will report, as mentioned, this part of the study later in this quarter. The inclusion criteria in this study included, of course, diagnosis of PSC, but also elevated levels of alkaline phosphatase. Primary endpoint of the study was safety and tolerability, and secondary endpoints are composed from a variety of measurements that represent disease progression, liver stiffness, ELF score, fibrosis biomarkers, pruritus, bilirubin, etc. The study actually aimed to evaluate the activity of CM-101 of the drug using two main populations. First, all double-blind completers were evaluated, meaning all patients that received the five doses of the drug during the 15 weeks. In addition to that, given that PSC is a slowly progressing disease, we also predefined another population. Those are patients that started the study with a moderate to severe disease, and we evaluated this based on liver stiffness. Again, if we want to see any change in those biomarkers, whether it's improvement or regression or deterioration of the disease, we need to look at the patients that have a more active disease. Those are the patients with a moderate to severe disease at baseline. Maybe to summarize the results of this study, I would say first and foremost that we have established proof of concept for the first time for CM-101 and validated the role of CCL24 as a target and a contributor, I should say, to the inflammatory and fibrotic cycle. The primary achieved the safety endpoint, the primary endpoint, so both doses demonstrated a very good safety and tolerability profile. In addition to that, the study also achieved the secondary and exploratory efficacy endpoint across anti-inflammatory, antifibrotic, and anti-cholestatic elements of PSC. Actually, again, the full pathways that lead to disease progression. Even though the study was not powered to detect statistical significance in the secondary endpoint, we were still very excited to see statistical significance in multiple of the parameters that we have evaluated. is also important to mention that the key takeaway message that will inform the Phase III as well includes first the dose. The 20 milligram per kilogram dose is the dose that we are planning to take forward towards the Phase III. This is the dose that shows a very broad and consistent effect across all of the markers that we have evaluated. In addition to that, we do see that patients with moderate to advanced disease are the patients that have more benefit from the drug in this relatively short duration of a trial, and we are planning to enrich for this population in the upcoming Phase III as well. As to safety, as I've mentioned, the study has met the primary endpoint, and the drug appears to be safe and well tolerated. We've seen three serious adverse events in this study. None of them was considered to be related to the drug, and most of the AEs were mild and distributed similarly between placebo and the drug-treated groups. If we're looking specifically, and again, we've looked at a variety of measurements, we will present some of these today, but we do see that the effects of Nebokitug was shown across many of the parameters and more pronouncedly, as expected, in patients with moderate to advanced disease. The first measurement, liver stiffness, is measured using elastography. We all know it also as a FibroScan, and it's probably the most known and frequently used tool to evaluate liver fibrosis in PSC. Studies demonstrated that both of the doses of the drug improved liver stiffness relative to placebo at week 15, with a statistical significant improvement achieved in patients that started the study with moderate to advanced disease. Those are patients that had a baseline level of 8.7 kilopascal. This is the first time that a drug has shown statistical significance in liver stiffness over 15 weeks of treatment in primary sclerosing cholangitis, and this is likely attributed to the dual mechanism of action of the drug being able to attenuate both inflammation and fibrosis. Next, we've also looked at ELF. ELF score is a well-established marker of liver disease severity and liver-related clinical outcomes in patients with advanced fibrosis. When we're looking at the ELF and its components, we can see that a clear and rapid improvement in the overall ELF score was seen as soon as six weeks post-treatment and until the end of the study using the 20 milligram per kilogram dose. In addition to that, as you can see on the right, when we're looking at the two components of ELF that actually represent active fibrogenesis, TIMP1 and P3NP, we see that those markers were reduced, even reached statistical significance following 15 weeks of treatment, once again reinforcing CM-101 antifibrotic activity. Looking at additional antifibrotic and anti-inflammatory measurements and the effect of Nebokitug on those markers, the result shows that markers like P3NP, IL-6, TGF-β, well-known markers of inflammation and fibrosis, were decreased in the group that was treated with the drug, more so in the 20 mg per kg, and even reached statistical significance in patients with moderate to advanced disease. Those were all evidence for the anti-inflammatory and antifibrotic activity of the drug, which is obviously the main mechanism of action of the drug. In addition, we also wanted to evaluate how the drug affects cholestasis, meaning the flow of the bile acid, and it was very exciting to see that we have seen impact on the cholestatic elements of the disease as well. First, we've seen effects on pruritus or itch, as you can see in the left hand of this slide, probably the most disturbing symptoms to patients with PSC. In addition, we are reinforcing that you can see on the right improvement in bilirubin in addition to the improvement in pruritus, and bilirubin is probably the most well-recognized marker that represents biliary disease progression. Again, seeing a very broad and consistent activity of the drug in targeting inflammation, fibrosis, and cholestasis. What comes next? The activity that we've seen for the drug obviously paved the way for an end-Phase II meeting with the FDA to align on the design of the Phase III, which we intend to report soon. We do believe that based on the FDA feedback, Nebokitug can potentially be the first therapy to gain full FDA approval for the treatment of PSC, and we will provide more details in the near future. I would also like to spend a few minutes on presenting the second indication for CM-101, systemic sclerosis. Much like PSC, systemic sclerosis is also a rare disease, only in this case an inflammatory rheumatic disease primarily affecting women. The disease involves inflammation and fibrosis in the skin, vasculature, and the lung, and actually the lung or lung fibrosis is probably the number one cause of death in these patients. We have seen over the years that CM-101, the drug, is able to interfere with those three mechanisms and have a significant disease-modifying potential for patients with systemic sclerosis. There are a few drugs approved for treating the lung disease associated with systemic sclerosis. However, there are no disease-modifying drugs in the market that include almost 180,000 patients in the seven major markets and have a commercial opportunity that may exceed $1.5 billion. We have evaluated the role of CCL24 in systemic sclerosis. We have seen CCL24 to be significantly overexpressed in the skin tissue of patients with systemic sclerosis, and we've also seen a lot of correlation or strong correlation, I should say, between the lung deterioration, as a reminder, the number one cause of death in these patients, and CCL24, and even we've seen that CCL24 predicts mortality specifically in patients with systemic sclerosis. We've also generated a lot of preclinical data demonstrating, for example, in the bleomycin model, the gold standard model for experimental systemic sclerosis. As you can see here on the right, both for lung fibrosis measurements and for skin fibrosis measurements, the drug was able to completely normalize the level of collagen in the tissue back to the level of the healthy animal. Our team, located both in the US and in Israel, has extensive biopharma experience spanning discovery, development, as well as commercialization. The team has a track record of success, and together we are driving the program forward towards the Phase III. Maybe to summarize, with its unique dual mechanism, Nebokitug represents a potential breakthrough with application to PSC as well as other fibrotic indications like systemic sclerosis. Those are diseases with a significant unmet medical need and no approved drugs to date. As mentioned, we have two upcoming milestones coming up in this quarter. First, based on the positive Phase II results, we had an end-of-Phase II meeting with the FDA where we discussed both the data and the potential registrational trial design. Second, we look forward to report the data from the open label extension portion of the Phase II trial in PSC, which we expect to provide additional insights on both safety and activity seen so far. Finally, maybe just to mention, the CM-101 has been for a long time an interest to potential partners, strategic partners. As expected, the positive data from the Phase II study, as well as the recent communication with the FDA, provides us opportunities to further advance those discussions and the optimal path forward for CM-101, potentially accelerating the timelines of development in PSC as well as in other indications. Very, very exciting time at Chemomab. We look forward to sharing more updates in the very near future. Thank you for your attention. Thank you very much, Adi. As a reminder, you guys can put questions into the chat function. A couple of follow-up questions for you. In terms of the open label extension data, can you remind us what dose was carried forward on these patients? Also, the open label extension doesn't include a placebo arm, if I recall correctly. How does that impact the data you're going to see coming out of these patients in the near term? Right. Essentially, the patients that were on the 20 mg per kg or the 10 mg per kg dose in the first 15 weeks will continue with the 10 and the 20 mg per kg towards the end of the study. The patients that were on placebo for the 10 mg per kg group will now receive 10 mg per kg. The patients that were on the placebo for the 20 mg per kg will now receive the 20 mg per kg dose moving forward. Yes, you are absolutely right. We are the open label extension. I mean, the main aim of the open label extension was actually to evaluate long-term safety. This is something that is essential for the development of CM-101 towards chronic treatment. So we will have data on long-term safety, and the activity data that we will have on the parameters that we've also evaluated in the 15 weeks will be compared to historical data. That's the best we can do given the fact that there is no placebo. Again, safety was the primary goal, and that's going to be very carefully evaluated, and the activity is going to be compared to what is known in the literature. Okay. Great. The Phase III trial, that is planned to be US, Europe, Israel, and other. Is that correct? Yes, correct. It's going to be a global study. We're going to include territories like US, Europe, Israel, and maybe even additional territories. Okay. In regards to ELF score as one of the sort of well-validated markers here, could you give a little more color about how ELF score is linked to outcomes in PSC patients, sort of the degree and nature of the validation? Yeah. Although it's not used routinely in the clinic, there is quite a lot of data generated on ELF over the years by the academy, by clinical trials, etc. There are clear references to the value of ELF as a predictive, I would say, marker. At the end of the day, when we're looking at prediction, we're looking at clinical events at the long term. For example, the Simtuzumab study, this is a study that was conducted by Gilead in the past that enrolled 238 patients, a relatively large study, has shown that there is a threshold of 0.19 of the ELF, that if the drug or a potential asset is able to reduce or not to exceed the 0.19 threshold within 12 weeks, this is very predictive for a reduction of long-term clinical events. If you see that over 12 weeks, you can see an elevation beyond this 0.19 threshold, then there is a large likelihood that those patients will also have more pronounced clinical events in the future. We can also see that there is a cutoff, a 9.8 cutoff that is described by this exact study, again, showing the predictive role of ELF here. Patients that started the study with an ELF that is greater than 9.0 are more likely to develop clinical events, while patients that are below the threshold are more likely to progress more slowly. Okay. You mentioned that your study is likely to enrich for patients with moderate to advanced disease, and I know we saw sort of more significant response in those patients from the data you've shared so far in your Phase II. How does that impact sort of patient availability as you look to your pivotal study? What portion of patients are seen or available for trials with moderate to advanced disease versus less severe disease? There are approximately 50-60% of patients that have moderate to severe disease. I think that's based on the strong relationship that we have generated over the last couple of years with the investigators, and we have been able to complete the recruitment in the Phase II six months ahead of time. We have a good opportunity to enhance recruitment as much as possible. I should also mention there is nothing for these patients to date. We know clearly from those sites and those investigators that patients are waiting for a drug and for a potential Phase III. We believe that recruitment, we can leverage again our expertise in recruitment, and we believe that we can definitely enroll those patients in the Phase III. Okay. We know UDCA is used to some extent in these patients, even though it's not approved. Have you looked at the impact or the potential for combination therapy with UDCA, and is that something that may be included as part of your Phase III? We have included it in the Phase II as well. We allowed patients to enter if they are on stable treatment with UDCA, and we're planning to do the same in the Phase III. Obviously, we'll need to stratify based on that. I can share that based on what we've seen in the Phase II study, we didn't see any impact on patients that were without UDCA or with UDCA to the effect of the drug. Okay. The last question would be just in terms of cash, cash runway, where do you stand today? I'm anticipating, obviously, that you need to raise additional funds to run the Phase III when you're able to share that design. Yeah. First of all, with regards to the cash runway, we have reported at the end of the third quarter having $19.5 million, and we will be issuing, of course, the financials in the near future for the entire 2024 timeframe. This cash should take us through the beginning of 2026, and we are evaluating currently multiple opportunities, including the strategic opportunities that I've mentioned in order to fully fund the Phase III clinical study. Great. Thank you very much, Adi. I think that is it in terms of questions. Thank you very much for your time today, Adi, and have a great day in terms of all the one-on-one meetings. I wish you the best of luck. Thank you so much. Operator, you can take us clear.