Okay, great. Good morning, everybody, and thank you very much for joining us at the 46th Annual Canaccord Genuity Growth Conference. I'm John Newman, one of the senior biotech analysts here at the firm. We're very excited to have Adicet with us today, and the CEO, Chen Schor. Chen, to start, could you give us an overview of Adicet and also your lead asset, prula-cel? Thanks. Absolutely. First of all, John, thank you very much for inviting us. Very timely. We expect to have very significant disclosures in the very near future. So excited to be here and talk about the data we expect to share. Adicet is a leading cell therapy focused on off-the-shelf cell therapies for autoimmune diseases and for oncology indications. We also have an in vivo CAR T pipeline that we expect to disclose in the very near future. Our lead asset, ADI-001, is an off-the-shelf gamma delta 1 cell therapy targeting CD20 for autoimmune diseases. Our next disclosure this quarter is expected to be in LN and SLE. This will be, I believe, the largest data set ever reported by an allogeneic off-the-shelf cell therapy in the field of LN and SLE, which probably shows the excitement that physicians and patients have in our study. The only other companies that have comparable number of patients reported in LN and SLE that are cell therapies are small companies like Novartis and Bristol Myers Squibb. We're glad to be in that company. No other company, as far as we know, also either allogeneic or actually autologous, has reported this type of data set, and certainly not bispecifics. We have another asset going into clinical studies, and that is for prostate cancer. It's an off-the-shelf gamma delta 1 cell therapy that targets a validated binding modality on the PSMA consistent with PLUVICTO, with two very important bolt-on technologies that are a result of about four years of research that makes the cell very potent and address some of the key challenges that we have seen with cell therapies in solid tumors. Happy to elaborate about that. We also expect a disclosure about our in vivo pipeline, which also has been in the work for a long time, in the very near future. There's going to be a lot coming from us in the next few months. Excellent. Could you remind us of the advantages of targeting CD20 in these autoimmune indications versus other targets that many people are familiar with, like CD19? Thanks. Yeah, absolutely. Maybe I'll start by focusing on the targets, then I'll kind of step back and focus on our therapy versus autologous. Regarding the targets, actually, most of the validation in this field has been primarily on CD19. When we look at our data with CD20, you couldn't actually tell the difference. What you want to see is complete depletion of B cells in the blood, and we actually look also at the CD19 B cell depletion in the blood, and we see absolute complete depletion of CD19 in the blood. That's number one. Actually, more important is complete depletion of CD19 B cells in the lymph nodes. It's the tissue penetration that matters. When we look at our biopsies from lymph nodes, we consistently see complete depletion of CD19 B cells in the lymph nodes. I don't think we've identified one CD19 positive B cell when we look at the lymph nodes that we have obtained so far. Then you want to see that once the immune system recovers, it recovers as a naive immune system, and that has been consistent with all of the patients that we have tested that at least announced so far. We see complete immune reset, whether it's CD19 or CD20. Happy to focus about the differentiation of our program versus others if you want, or we can discuss it later. Whatever you prefer. Sure. That's okay. Let's move on for now and come back to that. You mentioned just a moment ago, Chen, that you have an important data readout coming in SLE and lupus nephritis. Just wondered if you could just give us kind of a general overview as to what to expect there. Sure. Absolutely. We have enrolled in five countries. One of the key advantages that we have, we can actually enroll in centers that do not necessarily do cell therapy studies because this is such a well-tolerated and off-the-shelf therapy that doesn't require leukapheresis. Physicians can make this available to their patients. We actually had much more interest in the product. At some point, we said, "Hey, we have enough patients. Wait, because we want to start a pivotal study. We don't need more patients now." We were in that position. We could've enrolled many more patients. I want to be very clear. We stopped at some point. We expect to share data from 22 patients that have been enrolled. We really wanted to see at least 12 months data. Out of the 22 patients, 13 will have at least 12 months follow-up. These will be primarily LN patients because we started enrolling LN, but we will have some SLE patients, and all the 22 patients will have at least 6 months follow-up. Okay, great. Thank you. On durability for both lupus nephritis and SLE, some of the autologous CAR T therapies have shown that in some cases, their efficacy holds up beyond six months. Your upcoming data set will likely be the first allogeneic CAR T with long-term follow-up, as you just mentioned, for a meaningful number of patients. What can you say, just generally speaking, about how you think about durability versus some of the autologous therapies? Yes. Yeah, absolutely. That's really why we focused on the 12 months, because if patients can get a single therapy and then they essentially have a drug-free remission or drug-free complete renal response in at least a year, that's a big step for these patients. That's why we wanted to get as many patients at 12 months, and we waited with this data cut, which I want to be clear, hasn't been even done. We expect to have this data cut in the very, very near future and announce data in this quarter. One year seems to be the benchmark that people are looking at, and our goal is really to have a CR rate that is similar to the CR rate that we see with the autologous CAR Ts at the 12-month period. Okay, great. We recently spoke with a key opinion leader, a physician who was very enthusiastic about the potential for CAR T in lupus, including your product. How are you thinking about the overall market opportunity here, and where do you see your product potentially fitting into the current treatment paradigm? Absolutely. There's a lot to unfold here. First of all, why is there a lot of interest in cell therapy? When you go to conferences in the field of lupus or lupus nephritis, almost all the chatter that you hear about is interest in cell therapies. Actually, less so in bispecifics. If you think about it, bispecifics have been around for more than two years. There is yet a data set that shows some significant CR rate and any durability with bispecifics. Roche, as a very smart company with a very rich pipeline of bispecifics, terminated their bispecifics for lupus nephritis and SLE and continues to focus on their autologous cell therapy. All these people that we go to conferences with, they have participated in these studies. They know it. Why is there interest in these cell therapies? Because what they see with these patients, they have to give them chronic immunosuppressants, chronic steroids. They continue to progress. They get high infection rates. Mortality of infections in their 50s is in the teens in terms of a percentage. Their kidney function deteriorates. There's high cardiovascular events from, again, organ dysfunction from the disease. They really want to find a way to stop with all these drugs and give something one time that gets them a remission or efficacy for as long as possible. When you ask them if they see at least 12 months, they want to continue with this type of therapy for their other patients. Maybe at some point they'll have to redose them, but that's okay. You get a single drug, and then essentially it's almost like a cure for a while that is immunosuppressant and pretty much steroid-free or very low-dose steroids. A lot of interest in autologous cell therapies. But the reason I think we've seen interest in our product is because, let me just play it out, how it works for the physician and for the center. I see a patient, God forbid, Mr. X or Mrs. X usually, has lupus, or let's focus for a second on lupus nephritis as an example. She tried one immunosuppressant. She tried another immunosuppressant. She keeps coming back, and you look at her proteinuria, it's not good. If you continue like this, they might die from an infection, or they might go to end-stage renal disease. That's the path. That's what's going to happen. You say, "All right. Let's try cell therapy. I know you're doing bad, but I need to take you off your immunosuppressants for a while. Not sure how long. Probably like a month. Stop taking your drugs for a month. You came because you are not feeling well. Stop taking your drug for a month. I am going to call, and I am going to get you an appointment for the leukapheresis. I hope to get a chair there in a month from now. You will go for the leukapheresis. We will send it to manufacturing. At some point, I cannot tell you when, because the manufacturing site might be in a different state or sometimes in a different country, but I will get a call from the company, and they will give me a date. You need to come five days before, and we will start the conditioning, and then you will get the therapy. You should know there is a chance you will get ICANS because certain patients get Grade three, four in ICANS. I cannot tell you if you will get it because your fitness might be great, and then you are more likely to get it, the T-cell fitness, or not great, and then it might not work as well, and you are not going to get it. But you might get it. We are going to put you under very close monitoring to hopefully you are not going to get an ICANS. But if you do, we will treat you very quickly, but you got to be in the hospital or very close to the hospital and come every day, so we check if you have ICANS." That is a lot of hassle. That is why some of our patients are referred from centers nearby that are actually doing CAR T studies for the autologous companies that I mentioned earlier. They actually sometimes refer their patients to us. We have seen patients that initially when we saw their patient, we were like, "Why are we getting patients from this side? Must be wrong." But it comes, it keeps coming. Versus in our case, the patient comes, they do not feel well. They say, "Hey, you should really benefit from cell therapy. Why don't you go to the nurse? We will start the conditioning. It is Tuesday. You will take it Tuesday, Wednesday, Thursday, and come Sunday, we will give you the drug." That is it. It is better tolerated, by the way, because this type of the cell therapy with gamma delta 1 do not secrete these high levels of IL6. In their studies, at least what is reported to date, I can say we haven't seen any of those high-grade ICANS. Actually, in their oncology studies, and there is those 40 patients where there is high grade of ICANS, they haven't seen any of those high-grade ICANS. This is just a better-tolerated drug. If it has overall similar efficacy, if this was my mother, I can tell you what I would choose, and that is, I think, what we see. Excellent. You previously indicated that a registrational study here could focus on either both SLE and lupus or perhaps lupus nephritis alone. Can you sort of walk us through the decision-making process there in terms of variability on different types of study design and maybe what you see as sort of the advantages and trade-offs? Sure, absolutely. We have met with FDA quite recently, so we know more. We will announce that when we announce data. There will be regulatory feedback. I'll step back and say what's known in the field. What's known in the field is whether you go to LN or SLE or SLE and LN, the registrational study can be single arm study. When you look at the number of patients, they're in the range of 35 patients, that's the smallest data set, which includes patients that failed more types of therapies, up to about 90 patients, which is patients that failed, I believe, two therapies. That's kind of the range. In our case, if you look at our recent press release carefully, we mentioned that we expect to update about the registrational study in LN. The reason is most of the patients that we have enrolled so far are LN. When you look generally at the studies, even if it's an SLE study, who are the patients that join the study, many of them also have nephritis. You kind of capture most of the market when you focus on patients with lupus nephritis. We keep the opportunity to expand to LN and SLE. That's exactly what actually Novartis did. They started with LN, they started enrolling, then they made slight changes in the design, changed the inclusion criteria and the order of the endpoints, and included SLE patients. Our plan, because most of our data are in LN, is to start with LN, and we keep the option to expand to SLE as well. Okay, great. Some of the physicians that we spoke with also mentioned that the traditional lupus endpoints, such as SLEDAI and DORIS remission, don't always capture the full benefit of cell therapies, particularly in lupus nephritis. I wonder, how do you think ahead in terms of the pivotal study design? Are there additional efficacy endpoints beyond the traditional endpoints that you're considering that could help to capture the true benefit of these therapies? Absolutely, we do. First of all, let me give some more background about your first statement. SLE essentially measures certain symptoms and gives a score to every symptom. If one patient here has arthritis, and they can't get out of bed, and it's really, really, really painful, and another patient here has arthritis, but it kind of bothers them on Tuesday, they both get four points. The SLEDAI, it's not a very accurate measurement of efficacy because even if you see a reduce in SLEDAI by four or eight points, there is another which is called Physician Global Assessment, the patient may do actually worse because some of the other symptoms are more pronounced. SLEDAI is a little bit limited. DORIS is actually better from that perspective because for DORIS, you need what's called clinical SLEDAI of zero. All your clinical symptoms, it's okay if you have some biomarkers, but what matters for DORIS is the clinical symptoms. We don't want to see any of the clinical symptoms. Arthritis, no. If you have arthritis, there is no DORIS. But DORIS includes, you can take steroids up to 5 mg, which is fine. That's essentially symptomatic relief. It's not associated with high rate of side effects. But you can continue to take immunosuppressants on DORIS. When you have DORIS for non-cell therapy studies, patients essentially take these immunosuppressive therapies for a very long time, and these are associated with high infection rates and mortality. DORIS is limited. The benefit that we have from a drug like ADI-001 or prula-cel is that we can actually measure, for example, CRS, but also we can measure immunosuppressant-free and low steroids. We can have some kind of totality of the data that says, "Hey, that's actually pretty much a drug-free complete response," while all the others All the other classes of therapies cannot show it because by definition, it's chronic immunosuppression. The other endpoints that we expect to have could be physician global assessment, patient quality of life. Everything improves so much when you get to a very significant response and they stop taking the other therapies that have very significant side effects. Even the steroids are associated with fractures, with diabetes. We have patients that joined our study that they already have fractures from their steroid use. It's a whole different ballgame in terms of what you can see in endpoints. Just a follow-up on your last comment. I think there's still a lot of investors out there that sometimes look at the physicians that are currently treating lupus today, and they think about cell therapies and how new and different they are, and I'd say some are still a little skeptical as to what commercial uptake could look like. However, could you talk about what it means to a patient when you tell them, or when they suspect they could either drastically reduce their immunosuppressants or stop them? Because you talk about the dichotomy between maybe here's what the physicians are thinking, but then you have the patients over here who are on these chronic immunosuppressants. Yes, absolutely. I will address it in two levels. First of all, the patients where the physician will have tough time even telling them, "Take something else." In the U.S., as an example, there is about 250,000 patients with SLE, and then 100,000 patients, approximately, have LN. Out of these 100,000 patients, I am rounding the number, about 35,000 patients tried at least two immunosuppressant therapies, and it just does not work. For these patients, the likelihood a different immunosuppressant will work is very slim. For these type of patients, really what could be an option is a cell therapy that has been shown to really be efficacious. I think for that part of the market segment, these 35,000 patients, they actually need it. Once it is available, I would expect pretty high uptake, and I think that is what we see in our studies when you look at the enrollment. The rest of the patients are those 65,000 patients that have responded. Every now and then, they have an exacerbation in their disease. At some point, the physician will have a discussion with them, "Hey, this kind of works, but every time you come back here, we need to give you a load of steroids." Then, after some time, taper it down over a bunch of weeks. You gain weight, you lose weight. You gain weight, you lose weight. At some point, that patient will say, "Hey, is there anything else that we can try?" Or the physician will say. I would expect it is going to start from these 35,000 patients, which is the type of patients we expect to enroll in our studies. That is not inconsistent if you look at the inclusion criteria of other autologous cell therapy, especially companies like Novartis and BMS. I would expect this will expand either by just market expansion, because it is going to be advantageous even for the insurance companies at some point. I am going to pay all the time for these immunosuppressants and keep paying for hospitalizations versus this one-time therapy, and I will forget about it for a while. The insurance companies will probably want to have it. Or you can also run a study and show that it works in earlier lines. Okay, great. I believe you are also planning to share data in systemic sclerosis this year. Just curious as to what we should expect from that update. Sure, absolutely. We did not provide a lot of guidance, but all I would say is that we also saw interest in our systemic sclerosis study. We enrolled a number of patients. We will provide some more when we announce data. It is a reasonable number of patients, and at this point, we are following up on these patients and see how they perform. We expect to have the data in the second half of the year. Okay, great. I believe you are also evaluating ADI-001 in rheumatoid arthritis, which I believe includes two different lymphodepletion regimens. What are you hoping to learn from that comparison for those two different regimens? Will those findings potentially influence lymphodepletion strategy down the road for other indications? Yes, absolutely. Great question. We are running a study in RA. Essentially, it is a very small study, and really we are comparing one conditioning, which includes Cy and flu, and one conditioning that includes Cy only. We are aware that other companies that tried avoiding fludarabine, like Kyverna and a few others, figure that we probably need it. We have never tested it with gamma delta CAR T, so that is why we are running the study. If we learn that we do not need the fludarabine, this could affect how we think about other indications. I want to step back. When we talk to some of the KOLs, they actually believe that the conditioning that is used in one indication might not be the magic conditioning that you need for all indications. For example, for a disease that is in the blood, maybe you need less stringent lymphodepletion. For a disease that is focused in specific organ and you need good organ penetration, maybe you need a more stringent lymphodepletion. So far, we have not tested that question in our study in SLE and LN in the other indications. In RA, we are going to figure it out. If we see that maybe we need less, we can explore it in other studies. The current plan is to start the pivotal study with standard Cy/flu, consistent with small companies like Novartis and Bristol Myers Squibb. Great. Well, it looks like we're out of time. Thank you very much, Chen Schor, for joining us today. Thank you to Adicet. Very exciting and meaningful data that are coming. And thanks to everyone present here in the room in Boston and everyone watching online. Thank you for inviting us. Thank you.