Hi everyone. Thanks for joining us at the H.C. Wainwright 27th Annual Global Investment Conference. My name is Emily Bodnar. I'm an equity research analyst here at H.C. Wainwright. I'm pleased to introduce our next presenter, Chen Schor, who's the President and Chief Executive Office r of Adicet Bio. Thank you, Wainwright team, for inviting us. I'm Chen Schor, President and CEO of Adicet, and I'm very glad to be with you today. Adicet is considered to be the leader in developing off-the-shelf gamma delta 1 CAR T cell therapies for autoimmune diseases and cancer. This is our forward-looking statement. I assume that you guys have seen one of those in the past. I'm going to skip to the next slide. Our platform has been clinically validated. We've demonstrated in our clinical studies in oncology, starting with the NHL, clear proof of concept with quite high CR rate and overall response rate. Our platform is completely off the shelf. There's no graft versus host disease. We've seen exposure that is robust, very consistent with autologous CAR Ts. In terms of safety profile, gamma delta 1 CAR T cells have a more favorable safety profile compared to alpha beta strategies like alpha beta T cells or even bispecifics in a sense that they have less CRS and ICANS and less severe CRS and ICANS. One of the unique things about gamma delta T cells, and we're focusing on gamma delta 1 T cells, is that these cells are tissue trafficking, i.e., they home to tissues, which tends to be quite important, as we know and as we'll see later in the presentation, in the field of autoimmune diseases. Our lead program is with ADI-001. We're developing ADI-001 for six different autoimmune indications. It's in phase II. We expect to report clinical data in the second half of this year. We're quite encouraged by the potential of this program given our clinical experience in oncology, where we've seen complete depletion of CD19 positive B cells both in the blood and, as we'll see, more importantly, in the lymph nodes, and we've seen a favorable safety profile. Our next program is in solid tumors. It's targeting PSMA. It has a gene editing that we added to this program as well as armoring. We'll be able to talk much more about this program in the near future, but what you'll see is enhanced potency and ability to deliver multiple mechanisms of anti-tumor activity to prostate cancer patients. This is a snapshot of our pipeline. We started enrolling about a year ago. We started enrolling with lupus nephritis. Then we started adding SLE patients, and we've recently started enrolling systemic sclerosis patients. The trial is open for enrollment for other indications like myositis, stiff person syndrome, as well as AAV or ANCA vasculitis. We're going to focus today a little bit more about LN because most of the patients that we enrolled when we started the study have been lupus nephritis and then some SLE. Since our clinical data are coming in the second half of this year, it probably makes sense to focus our attention on LN. I'm very fortunate to be surrounded by a great executive team. Each of us has more than a decade or sometimes decades of experience in their respective functions, and we work very, very well together. Perfect. This is a snapshot of some of the key learnings that we gained from our clinical study with ADI-001 so far in NHL patients. In terms of PK, we've seen quite robust PK exposure comparable to autologous alpha beta CAR T. As I mentioned earlier, complete depletion, although ADI-001 targets CD20. We've actually always measured CD19 in the blood and in the lymph nodes, and we've seen complete depletion of CD19 B cells both in the blood and in the lymph nodes. It's been also documented that the CD20 strategy like obinutuzumab completely depletes the B cell lineage in the peripheral blood, including plasmablasts. Off the shelf, no graft versus host disease, no need for leukapheresis, and very favorable safety profile compared to autologous cell therapy in similar settings. So really here, the potential given this safety profile is to go eventually to the community setting and provide this therapy on a larger scale to patients with autoimmune diseases. This is probably one of the two most important slides in this presentation. I'll go quickly. In panel one on the left side, we see really the difference between CAR T and antibody strategies. In the blood, by the way, CAR T and antibodies, whether you target CD19 or CD20, completely deplete CD19 or CD20 in the blood. The difference is in the tissues. As we know, antibody approaches haven't reported treatment-free remissions. What you can see in this case, it's rituximab, but it has been shown, I believe, with other antibody modalities, does not really deplete neither CD19 positive B cells nor CD20 positive B cells in the lymph nodes. CAR Ts do deplete CD19 positive B cells in the lymph nodes and are associated with quite robust activity. So really, what matters seems to be depletion of the B cell lineage in the lymph nodes. In the middle, you can see the advantage of gamma delta 1 T cells. So here we compare the exposure of the CAR T in the lymph node of Axi-cel. You can see about 20,000-60,000 cells per million in the lymph node. And you can see the exposure of ADI-001 in the lymph node in the range of 250,000 to almost 500,000 cells per million in the lymph node. So very robust trafficking of our CAR T cells into the lymph nodes. And in panel number three, you can see the actual depletion in the lymph node. So there is a screening biopsy where you're seeing green CD19 positive B cells. And on the right, you can see a biopsy from day 10, complete depletion of CD19 B cells in the lymph nodes. So we know that that is paramount to show clinical activity or even durable clinical activity with CAR Ts in patients with autoimmune diseases. The unmet medical need in autoimmune is huge. Patients are taking immunosuppressants and sometimes high-dose steroids, but treatment-free remission is very, very rare. Flares are common, reflecting ongoing disease activity of the patients and essentially continued damage to their organs, which leads to early mortality. The average age of mortality for patients with lupus nephritis or SLE is about 55. They primarily die from renal disease if these are lupus nephritis patients, which is about 40% of the patients, or cardiovascular disease because of this continued damage to their cardiovascular system or infections. Depending on the publication you read, between 5% and 25% of mortality is because of infections because they've been taking immunosuppressants and steroids for, you know, sometimes two decades or even three decades, so very significant unmet medical need. In terms of the side effects of these chronic therapies, they are quite significant, whether it's infections, patients with bone fractures because of these steroids, they develop diabetes. It really impacts the quality of life. Many of these patients don't go to work. They experience fatigue, anxiety, pain, and many other qualities of life that, unfortunately, you know, they suffer from. So the unmet medical need is very high. If there was an opportunity for a one-time therapy with favorable safety profile that can deliver treatment-free remission, that would be pretty amazing for these patients. So what's the target product profile that we hope to see from 001? In terms of efficacy in lupus nephritis and SLE, we hope to see efficacy similar to that observed with company-sponsored autologous CD19 alpha beta CAR Ts. In terms of safety, hopefully better safety than alpha beta T cells. We have seen this in oncology. We hope that that will translate to also autoimmune diseases because then we can dose in outpatient settings and make this really available to many patients. Pretty simple to administer off the shelf, no leukapheresis, one time. In terms of immune reset, we hope to see immune reset similar to autologous CD19 CAR T. Bottom line, free those patients from these immunosuppressants and either eliminate or reduce the dose of steroids to below pharmacological level. That's a summary of the difference between alpha beta T cells to ADI-001 that we hope to see. I mentioned most of these, so I'll probably skip. I'll just mention that on safety, what has been observed with some of the autologous cell therapies is primarily grade three and above ICANS, which is really something you need to manage in the hospital. You never know who is the patient that might present with a high-grade ICANS, so if you don't dose in the hospital, you better be pretty close to the hospital. With gamma delta 1 T cells, we have seen better safety profile and hence the potential for outpatient. The design of our clinical study is quite standard. It has four arms. One arm is the LN and SLE. The second arm is the systemic sclerosis, and then you see the myositis, stiff person syndrome, and the ANCA-associated vasculitis arm. We start with standard conditioning consistent with some of the other autologous cell therapy companies in autoimmune, and then we observe a DLT window of 28 days and report efficacy over time. The primary endpoint is essentially efficacy. And then in terms of secondary and exploratory endpoints, on the left side, you can see the pharmacodynamic endpoints, which is the dynamic of B cell depletion, the reconstitution of the B cells, do we see an immune reset, and a few other pharmacodynamic, but these are, I believe, the most important one. And then the efficacy is depending on the disease. So in LN, it would be CR or PR. In SLE, it would be the SLEDAI. So here is what we hope to see in our study based on our understanding of the competitive landscape as well. So number one, that's probably, again, one of the most important slides in this deck. So number one, a favorable safety profile. Hopefully one without grade three and above CRS or ICANS, which means we can dose in outpatient settings and make it available. So that would be number one. Number two, we hope to achieve disease remission or halt disease progression as evidenced by sustained decline in the SLEDAI score. Number three, we hope to see preserved or improved kidney function in patients with LN. The threshold for efficacy has been defined recently by a couple of companies that reported data. Essentially, what the regulatory agencies want to see in LN is quite small. I'll describe the design shortly of a clinical study in patients with LN, single arm, and the endpoint is CR rate at six months. And if it's 40% or above, it would meet the threshold for regulatory authority. So hopefully we'll see CR rate of 40% and above. If we will, then that sounds like it suffices the need for regulatory agencies for a single arm, pretty small clinical study. We'll analyze the pharmacodynamics following a therapy and hope to see immune reset, which supports the one-time therapy that one could expect from ADI-001. We'll monitor the therapies that patients take after ADI-001. What we hope to see is discontinuation of chronic immunosuppressants and either discontinuation or reduction to below pharmacological levels of corticosteroids. And then the last one, obviously, off the shelf with no need for leukapheresis. But if we're able to see this, then it's something that we can dose in potentially outpatient settings, no leukapheresis, well tolerated, and with efficacy that meets the bar for a single arm, small clinical study. The endpoints for lupus nephritis, as defined by regulatory authorities, essentially is a CR in lupus nephritis. CR is essentially defined. It includes two key components. One is the UPCR below 0.5 or 0.5 and below, and normal or stable eGFR. The nice thing about the endpoint for lupus nephritis is it's highly objective. In systemic lupus, the endpoint, and these two endpoints that I'm describing are the endpoints that have been generally agreed by regulatory authorities for a single arm, a pivotal clinical study, either in LN, complete response rate, at least 40%, or in SLE, which is DORIS remission. DORIS remission is comprised of four key components. One of them is the SLEDAI-2K, which is quite subjective. The other is physician global assessment, which is highly subjective, and as you can see, low dose steroids, five or below, and the stable dose of immunosuppressants. So when you look at data from other companies, we focus generally on company-sponsored data and not necessarily on ISTs or single-site INDs because these, especially for the DORIS and SLEDAI, these would be highly subjective. So let's look at data from a couple of highly credible companies. These were reported in recent conferences. On the left side, we can see BMS. You can see quite nice decrease in the SLEDAI. There's three patients where you see quite that the SLEDAI reduces to like eight or four. These patients had lupus nephritis and had proteinuria that was sustained. Generally, proteinuria takes much more time to resolve just because there's nephrons that are leaky in the kidney. And either you can resolve it or you cannot, but it takes more time to resolve it. Novartis has the most comprehensive data set with 21 patients. Most of them were LN. And you can see the very nice reduction in SLEDAI over time. Autolus also reported data in six patients. They've seen 50% CR rate in these patients. Autolus, after six patients, moved to a pivotal study, single arm in 30 patients with LN, and they need to beat 40% CR rate, and we hope that they'll be successful. BMS, based on this data, moved to also a pivotal study in 90 patients, both in SLE and in LN, and the endpoint is DORIS remission, I believe, at six months, and Novartis, based on this data, also moved to a clinical study in LN, I believe, and there's also the data for Cabaletta here. Novartis actually broke the data down to LN patients and SLE patients, and what you can see, the SLE patients are in blue, and you can see nice reduction in SLEDAI, and in green, you can see the LN patients, which have some more persistent proteinuria that slowly resolves over time. On the right side, you can see that they started with about 75% patients with proteinuria. After 6 months, it's about 50% proteinuria. After 12 months, it's about 37% proteinuria. You can see between 6-12 months, a reduction of 30%-50% reduction in proteinuria. That's why you have multiple points of data supporting this 40% CR rate in lupus nephritis to support pivotal studies in single arm studies. Stop working. Can you move the slide up? Okay. Perfect. Okay. This summarizes the data reported. Actually, Novartis and BMS did not disclose the specific complete response rate. Autolus reported 50%, and Cabaletta only had three patients, and it was one out of three. Bottom line, with regulatory agencies, 40% CR rate would suffice for single arm studies. One of the key issues with some of the autologous cell therapies is CRS and ICANS. You know, some of the companies experienced grade three and above ICANS, which really requires hospitalizations. Hopefully, we'll see more favorable safety profile, which would contribute to the potential to dose in outpatient settings. So if we are able to show better safety profile and no leukapheresis and off-the-shelf therapy and complete B cell depletion and immune reset leading to this 40%, at least 40% CR rate in patients with lupus nephritis, you can see that the potential that we're starting with is quite significant. 40% of SLE patients have lupus nephritis. We're starting there. We're now gathering data in SLE. We expect to have some SLE patients in our first data release. We started to dose systemic sclerosis. We expect to have potentially an update on systemic sclerosis next year, and slowly, we will dose other patient populations. So we're quite optimistic about the potential of this therapy for patients both in the US and the ex-US. This is a snapshot of our future milestones. We do expect to have a quite significant update about our program in LN and SLE in the very near future, this half of the year. And then there's going to be multiple updates for different indications, LN and SLE, systemic sclerosis, potentially others in 2026. We haven't focused today on our oncology program in prostate cancer, but we're very, very excited about this program. We expect to file an IND and start clinical development early next year. And we expect to have clinical data sometimes in the second half of next year for this program. So again, thank you for your interest, and we're happy to address any questions. Thank you, everyone. Thank you, Chen. Appreciate the time and enjoy the rest of the conference. Thank you for an excellent presentation. The bottleneck to go with CAR-Ts to solid tumors is so-called cold tumors. So lymphocytes, it doesn't matter which receptor you put on top of it. The best receptor possible, if it cannot penetrate a tumor, it would be of no avail. What do you plan to do to combine your magnificent CAR-T with a necessary door opener? Otherwise, you put a lot of policemen on the street, which cannot penetrate a skyscraper where terrorists are. Great analogy. This is a great question, I must say. And for four years, we focused on how to enhance the activity of gamma delta 1 T cells in solid tumors. And I mentioned that we actually had reasonable data with our program in RCC, 20% overall response rate, great penetration into the tumor, very good safety profile. But we decided to make our investment more focused on our next product, ADI-212. Why? There were a couple of reasons. One of those reasons is exactly what you mentioned. So once we'll share more data about the PSMA program, you'll see that the goal was one of the goals, one of the two key goals was to address exactly the concern that you mentioned. And we have done it through a certain bolt-on technology that we introduced into the.