Hello everyone, and thank you for joining H.C. Wainwright's 28th Annual Global Investment Conference. My name is Madeleine Rogers, and I am an analyst on the corporate access team. H.C. Wainwright is a full-service investment bank dedicated to providing corporate finance, strategic advisory, and related services to public and private companies around the world. We have 19 publishing senior analysts covering over 650 companies across all sectors. Please visit our website for more information. You can reference your online conference portal for the links to your meetings and all company sessions. With that, I am thrilled to introduce Adi Mor, the CEO and CSO of Chemomab. Thank you very much, Madeleine. Good morning, everyone. As mentioned, I am Adi Mor, the Co-Founder and CEO of Chemomab Therapeutics, and it is a pleasure to be here today at the H.C. Wainwright Conference. 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 biotechnology company developing novel therapies for inflammatory and fibrotic diseases. Our lead asset, nebokitug, is a first-in-class monoclonal antibody targeting CCL24, a key disease mediator involved in both inflammation and fibrosis. Over the past several years, we have built a substantial clinical data set with nebokitug across multiple studies establishing its biological activity, mechanism of action, safety and tolerability profile, and its therapeutic potential. Most recently, we completed a phase II study in patients with primary sclerosing cholangitis or PSC. That study provided important clinical validation of nebokitug, demonstrating favorable safety and broad anti-inflammatory and anti-fibrotic activity with particularly encouraging effects in patients with moderate to advanced disease after 15 weeks of treatment, which were further reinforced by data through 48 weeks of treatment. Building on this clinical foundation, Chemomab recently announced a merger with Scipher Medicine, a leader in immunology precision medicine. Supported by compelling new translational and precision medicine data, we are joining now forces with Scipher to advance nebokitug into rheumatoid arthritis. Rheumatoid arthritis, or RA, represents an approximately $24 billion global market, but despite the availability of multiple therapies, substantial unmet need remains as many patients do not adequately respond to the existing treatments. We believe that nebokitug actually offers a very differentiated opportunity in this setting because it is the first drug candidate that targets biology that involves both inflammation and fibrosis, which may be particularly relevant in RA patients who remain inadequately controlled by the current therapies. At the same time, it is important to emphasize that PSC, a potential lethal disease with no FDA-approved drugs, remains an important opportunity for nebokitug, potentially via partnering. Importantly, the positive PSC clinical results provide further human validation of the drug's mechanism of action and help de-risk its continued development as we expand into rheumatoid arthritis. A bit about the rheumatoid arthritis market. Obviously, a very large market and growing market with significant unmet need. Despite multiple approved therapies, treatment selection remains largely trial and error. Only about 1/3 of the moderate to severe patients achieve low disease activity, and many of the leading therapies carry significant safety warnings. In addition, most current treatments focus primarily on inflammation, leaving a large opportunity for differentiated approaches that address both inflammation and fibrosis. A bit about who Scipher is. Scipher actually brings a set of capabilities that are highly complementary to Chemomab, and particularly relevant to the development of nebokitug in rheumatoid arthritis. At the core is Scipher's RA data and analytics platform, built on a leading transcriptomics data set in rheumatoid arthritis. This platform has already been translated into a commercial product. PrismRA is actually the first and only CMS-approved molecule test designed to guide treatment selection in RA. About 1,700 rheumatologists who are PrismRA customers are already known to Scipher. Scipher also has the operational infrastructure to support this work, including its own commercial laboratory capabilities and an established network of more than 30 RA clinical sites from the company's PREDICT study. Together, these capabilities provide a strong foundation for a precision medicine approach to RA, combining biological insight, patient stratification, and clinical development infrastructure. Scipher developed Spectra, its well-validated AI-driven precision medicine platform designed to identify novel therapeutic targets in immune-mediated diseases and assess their potential for clinical success. Spectra combines network biology, proprietary disease-specific patient data, and AI analytics to identify and prioritize disease-relevant targets. Importantly, this platform can also support biomarker discovery and companion diagnostic development, and that actually creates an integrated approach that links target discovery with patient selection and therapeutic development. PrismRA that I have mentioned is a very good example of Scipher's ability to translate its Spectra platform and deep expertise in RA biology into clinically validated precision medicine product. The PrismRA is actually the first CMS-approved molecular treatment response test in immunology. It uses a combination of genomic markers and patient-specific feature to identify patients who are likely to respond to the TNF inhibitors that are approved in rheumatoid arthritis. As I have noted, approximately 1,700 rheumatologists have ordered about 50,000 PrismRA tests today, providing Scipher with substantial real-world experience in rheumatoid arthritis biology, in patient stratification, and in the prediction of treatment response. This same underlying platform and expertise were then applied to the therapeutic target discovery, which ultimately led to the identification of CCL24 as a key target in rheumatoid arthritis. As you can see in this slide, using the Spectra platform, Scipher identified CCL24, the target of nebokitug, as the highest-ranked target with potential in RA. Nebokitug ranked in the top 1% for predicted efficacy in RA, ahead of several of the established RA mechanism, including the TNF inhibitors, the IL-6 inhibitors, JAK inhibitors, and others. For us, this was a particularly compelling finding because it provided an independent data-driven rationale for expanding nebokitug into rheumatoid arthritis. The combination of Scipher and Chemomab brings together two highly complementary sets of assets. Scipher contributes its AI-powered precision medicine platform, deep RA data sets, biomarker capabilities, and RA-related clinical infrastructures. Chemomab brings nebokitug, a first-in-class dual-acting drug candidate with an established clinical safety and clear evidence of anti-inflammatory and anti-fibrotic activity. Together, this creates the opportunity to develop nebokitug as the potential first precision medicine therapy in RA, using Scipher's capability to identify the patients most likely to benefit from nebokitug, and thereby potentially improving the probability of clinical success. It also creates a broader opportunity beyond rheumatoid arthritis, giving the potential applicability of nebokitug across additional inflammatory and fibrotic disease. What additional evidence do we have to support the development of nebokitug in rheumatoid arthritis? The rationale for rheumatoid arthritis is actually supported by two separate aspects. One of them is the independent disease biology around CCL24 and rheumatoid arthritis, and the second one is actual clinical evidence demonstrating the biological effects of nebokitug of CCL24 inhibition. Studies have shown that CCL24 levels were significantly higher in the synovial fluid in patients with a form of arthritis that is similar to RA, who ultimately required advanced therapies compared with patient managed without advanced therapies. It is also important to notice that in those patients with disease who did not require the escalation to advanced therapies, CCL24 expression decreased over time. While in patients who progressed to advanced DMARD or other biological therapies, CCL24 was actually increased. Ultimately, higher CCL24 levels track with a more severe disease trajectory and the need for advanced treatment, providing additional support for CCL24 as a relevant therapeutic target in arthritis. Beyond the levels of CCL24, a very important aspect of the rheumatoid arthritis biology is the role of fibroblasts and the fibrotic signaling, particularly in patients that do not show benefit from the pure anti-inflammatory drugs. Recent work published in Nature Immunology showed that RA patients who failed to achieve remission and also had increased fibrogenic fibroblast activity and TGF-β signaling within the synovium. This actually suggests that this persistent disease may not be driven by inflammation alone. This is very relevant to CCL24 biology. CCL24 has established pro-fibrotic activity, including effect on fibroblast activation, collagen production, and is highly linked to pathways that involve TGF-β signaling, and we've shown that pre-clinically and clinically over the years in multiple studies, and models. By blocking CCL24 with nebokitug, we expect to address not only the inflammatory component of rheumatoid arthritis, but also the pro-fibrotic biology that appears to be very relevant in the treatment-resistant RA patients. The second important part of the rationale of why treating RA patients with nebokitug comes from what we've already demonstrated clinically and pre-clinically with nebokitug. This slide provide actually a very important bridge from the pre-clinical data, the phase II data, directly into the RA biology. What we've done here is evaluated a panel of biomarkers that are known to be elevated in rheumatoid arthritis, covering adaptive immunity, inflammation, chemokine pathways, and tissue remodeling biology, meaning fibrosis. On the right, you can see the expected pattern in RA patients compared with healthy control. While on the left, you can see that when we've asked what happened to those same markers in the PSC study following treatment with nebokitug, we have seen a very clear dose-dependent effect. Nebokitug reduced a broad set of the RA associate biomarkers, including markers that are relevant to the TNF signaling, to IL-6, adaptive immunity, and fibrosis. Even though those are patients with primary sclerosing cholangitis, the biological effect of nebokitug was highly relevant to RA. nebokitug was modulating multiple pathways that are known to be active in rheumatoid arthritis in a dose-dependent manner. Importantly, in the phase II PSC study, nebokitug also showed a dose-dependent reduction in the levels of TGF-β, and the largest reduction was seen with the higher dose, the 20 milligram per kg. As mentioned, this pathway is increasingly recognized as an important driver of fibrosis activation and treatment resistance in rheumatoid arthritis. Obviously, this further supports the rationale for evaluating nebokitug in RA, particularly in patients who remain inadequately controlled with current therapies. Beyond the preclinical evidence, the role of CCL24 in arthritis is also supported by direct preclinical studies. In an adjuvant-induced arthritis model, blocking CCL24 reduced arthritis severity, synovial inflammation, and joint damage. You can see in this slide that the imaging and histology shown are consistent with these findings, demonstrating less inflammatory tissue damage and structural joint injury following CCL24 inhibition versus, of course, controls. Overall, nebokitug is a highly differentiated drug candidate in rheumatoid arthritis, mainly due to its dual mechanism of action and potential ability to address both inflammation and fibrosis. Current approved drugs in RA, as you can see in this slide, are primarily focused on controlling inflammation, and we do see some effect on fibrosis, but it's mainly secondary or indirectly. Therefore, blocking CCL24, where we can achieve a direct modulation of both of these components, is highly valuable. Moving to the clinical development plan, we have designed a randomized blinded phase II study in moderate to severe RA patients using standard regulatory endpoints and incorporating Scipher's precision medicine capabilities. In this phase II study, patients are anticipated to be screened using the PrismRA platform to enrich for those patients that are predicted to be non-responsive to TNF inhibitors, and that, of course, represents the population with the most substantial unmet need. We're planning to include about 140 patients in this study randomized to placebo or nebokitug at 10 or 20 milligram per kg. The drug will be administered IV every three weeks for overall 12 weeks. The primary endpoint, which is also the registrational endpoint for RA, is going to be ACR20. We're also going to look at multiple secondary endpoints, including ACR50, 70, disease activity, remission, and functional outcomes, and also safety and immunogenicity. Importantly, this design combines the more conventional RA efficacy study with the biomarker-driven patient selection. That would allow us to test nebokitug in the population where its differentiated mechanism may be most relevant. Looking at the future of some of the most important value-driving catalysts, and we have several of those in the next 18 months. In the second half of this year of 2026, we expect to complete pre-IND activities and submit the IND to the FDA. In the first half of 2027, key milestones would include IND clearance, initiation of the phase II study, and first patient in. We then expect to complete enrollment in the second half of 2027, leading to the most important near-term clinical catalyst, the 12-week phase II readout targeted for the first half of 2028. In parallel to that, the program is expected to advance the development of next generation companion diagnostic for nebokitug, supporting the broader precision medicine opportunity for nebokitug in rheumatoid arthritis. Overall, the combined company, Scipher and Chemomab together post-merger, is designed around multiple opportunities to create value with nebokitug as the lead program. The first and most important near-term objective is to advance nebokitug through the phase II RA study with a 12 weeks readout expected in the first half of 2028. At the same time, the combined company intends to grow the PrismRA diagnostic business and leverage its proprietary immunology data, the molecular treatment response, and companion diagnostic capability in order to create additional value through this precision medicine approach and through multiple partnering opportunities. Before concluding, I would like to spend just a moment on the key terms of the merger. I think it's very important to understand the structure of the combined company and the value proposition for our shareholders. The transaction is structured as an all-stock merger with Scipher's shareholders expected to own approximately 68% of the combined company, and Chemomab shareholders approximately 32% at closing. In addition, Chemomab shareholders are expected to receive contingent value rights, CVRs, providing the opportunity to participate in additional value tied to further development milestones. When the merger is consummated, the combined company is expected to operate as Scipher Medicine Corporation and trade on Nasdaq under the ticker SCIP. Dr. Reg Tsitoh, Scipher's current CEO, will serve as the CEO of the combined company, and I'm glad to join the board of directors. Importantly, the transaction is also accompanied by $30 million PIPE financing from a group of high-quality healthcare investors at $150 million pre-PIPE valuation. This financing is expected to provide the combined company with runway through the anticipated phase II RA top readout in the first half of 2028. Overall, this transaction is designed to provide the capital, the capabilities, and corporate structure needed to advance nebokitug while allowing Chemomab shareholders to retain meaningful participation in the future value of the combined company. I'd like to thank you all for your time and attention today. Thank you, Adi, for such an insightful presentation on behalf of Chemomab Therapeutics. We appreciate your time, and I'm very grateful for your team's participation in our conference this year. Thank you very much. It was a pleasure, and thank you for inviting us.