Excellent. Good afternoon, everyone, and welcome to the annual Citizens Life Science Conference. It's my pleasure to introduce Chen Schor, President and CEO of Adicet Bio. Really appreciate you being here. Good morning. Thank you for inviting me. Always a pleasure to talk to you. Excellent. I never know who exactly is in the audience or who might be listening to the webcast. I like to always kind of set the stage with an overview of the company. What is Adicet? What is Adicet about? Absolutely. Adicet is considered to be the leader in gamma delta CAR T cell therapies. Gamma delta CAR Ts have a couple of key advantages. One, we can dose them to patients completely off the shelf. They do not cause this graft versus host disease that requires modulation of the cells. Completely off the shelf. The second advantage is that they are well tolerated compared to other classes like alpha beta T cells or even bispecifics, because these tend to cause frequent CRS and sometimes high grade CRS. Gamma delta 1 T cells have a different profile and do not cause frequent or high grade CRS or ICANS. That is the second advantage. Off the shelf and generally safer. The third advantage is that gamma delta 1 T cells, once we dose them to patients, we see exposure that really looks like autologous cell therapies. When you look at the Cmax, it's the same Cmax as autologous cell therapies. When you look at the day 28 persistence, it's the same as autologous cell therapies. The fourth advantage is that the gamma delta 1 T cells distribute to tissues. Running your gamma delta 1 T cells during your skin, of course, very little of it is in your blood. Most of them are in your skin. They're in your kidneys. They're in your lungs. They're in your GI tract. That is really important because that lends itself to two potential advantages in two different therapeutic areas. One in autoimmune, where eventually the damage happens in the tissues. The second one in solid tumors, where most cell types haven't shown very significant advantages. In gamma delta 1 T cells, that's where they live in tissues. In solid tumors, there is one more advantage that is important. Gamma delta 1 T cells have innate anti-tumor activity, which means they can go after the tumor cells that express the target we're going after. If there is a cell next to it that does not express the target for the cell, they can also kill that tumor cell. That is how we're built as a company. We're focused on two key fields, one autoimmune and other solid tumors. We currently have two clinical programs, and there are two very, very exciting preclinical programs that we hope to update the street about in the near future. Terrific. Just for the audience and the webcast listeners to know, the cell therapy space is not like a sci-fi story. This is an established space. We have approved therapeutics, right? Currently, at least some of the leads generating over a billion dollars in revenues. This is all in oncology. We will get to the oncology part of your pipeline. I guess I'd like to start off with autoimmune and kind of the translatability of data that you got in oncology and how translatable that is to autoimmune, because it is a much bigger market. There are some profound results that we are seeing in autoimmune. Let's maybe just start off, if you can just remind the audience, what kind of data have you seen in disease indications like MCL, LBCL, and how translatable is it to autoimmune? Then we can unpack the autoimmune disease. Absolutely. We dosed about 40 patients with either the LBCL or MCL. In terms of the CR rate, we've seen the same CR rate as other autologous cell therapies. In terms of Cmax and day 28 exposure, we've seen levels that are consistent with Yescarta or even higher. In terms of durability, in DLBCL, our durability was not on par with the durability of the autologous cell therapies. Now, granted, about half of our patients progressed on Yescarta. When they progressed on Yescarta, some of them progressed on Yescarta very rapidly. Comparing a drug versus post CAR T to a drug pre CAR T might not be a very fair comparison. In MCL, our data actually, in terms of CR rate, and in terms of the median durability of complete response, was actually in line with approved autologous cell therapies. Safety profile was by far better. It's just that MCL is a relatively smaller market and didn't justify the investment in a pivotal study when we look at the data that we have seen and we understand what's required in autoimmune. I'm happy to talk about what data from the study in oncology is very important for autoimmune if you want to go there as well. Yeah. No, I'd like to. In autoimmune, the goal is a little different. Essentially, we're focusing on diseases that are primarily B cell mediated autoimmune diseases, which means there are B cells that secrete autoantibodies that go and attack different tissues. What we understand is required in oncology. We understand that from different studies from Germany, famous Schett from China, other ISDs, and now also from other small studies or small data sets reported by BMS or even Novartis. Essentially, what we need in autoimmune is to completely deplete the CD19 B cell. It's like we press reset. If you can, for a short time, completely deplete all the CD19 B cells, it looks like once the B cell compartment builds itself, it builds itself in a more naive way so the patients can experience potentially a complete response. One additional important difference between autoimmune and oncology, in oncology, some of those cells persist for a long time. Those CAR Ts persist for a long time. In autoimmune, they do not. All the data that we have seen so far, the CAR T stays in the system about 30 days-90 days. When you look at our data in oncology, they are really comparable to what we need in autoimmune. Number one, in terms of the PK of the cells, it stays in the system in the dose levels that we are targeting about 30 days-90 days, exactly the same as autologous do in autoimmune. Number two, when we look at the blood and in tissues, it completely depletes CD19 positive B cells. In all of our lymph node biopsies, when we look at day 10 at CD19 positive B cells, we have not seen a single one. That is important. That is why cell therapy targeting CD19 works. Same PK, same CD19 positive B cell depletion, but they're off the shelf. They're relatively well tolerated, and they go to tissues. We know that that's a big advantage because in autoimmune, eventually depends on the autoimmune disease, the problem eventually presents in the different tissues. You guys are in autoimmune disease indications right now, lupus nephritis and SLE, I think it is. Yes. The kind of poster child data that everyone looks at is Georg Schett's data that came out of an academic site in Germany. I'm kind of curious, what's the latest kind of learnings that you have or you've learned from those data? Ultimately, what kind of data are you looking for from your current studies right now when we first see that data? Sure. Absolutely. First of all, we're going after multiple diseases. LN and SLE are enrolling now, but in the next quarter, we expect to start enrolling to systemic sclerosis, myositis, stiff person syndrome, and oncovascularitis. This study is a global study. We have centers in the U.S. and outside the U.S. Focusing for a second on efficacy, there is the data that was generated by academic studies. Generally, academic studies do not necessarily suggest the exact or the industry has not been able to repeat the efficacy of academic studies. That is true in oncology. That is true in autoimmune. I think the only therapeutic area where maybe there is much more correlation between academic studies and industry studies is actually infectious diseases, because if you clear a virus, you clear a virus. In autoimmune, it is very different. I think, first of all, the bar will be defined by the industry players, not necessarily by what we've seen in academic studies. Those might have enrolled younger patients. Those might have enrolled patients with short duration of disease where there is very little damage to the tissues. Industry studies will actually enroll the patient population that's in need for these therapies, and the need is very significant. When you think about these patients, lupus nephritis, they'll go to end stage renal disease. Systemic sclerosis, the prospect for patients is not very positive when you think about the 5 years-10 years horizon and so forth. When you look at SLE, the mortality in SLE is much, much faster compared to the mortality that we see in healthier adults. The unmet medical need is huge. If we can take patients and provide them a one-time therapy and then a significant percentage of them to be defined has a complete response or their disease stops and they do not need any additional immunosuppressants, that's a big deal for a patient because we stop the disease from continuously essentially killing their organs. The B cells need a reset. I kind of feel like investor expectations need a little bit of a reset. Like you said, I think industry is going to have to kind of show what the results of a commercially viable product is ultimately going to look at. When we focus in on Adicet's program, let's just say in LN, I think originally we were expecting some data in the first half of 2025. You reported your results yesterday. It seems like that's been pushed out to the second half. Can you talk a little bit about why the shift? On top of that, when we ultimately see that data, about how many patients' worth of data do you need to see to kind of push that go, to push the go decision versus the no-go decision? What kind of data are you honing? Absolutely. We communicate with investors frequently, and we actually ask them, what's important to you? The feedback from investors overall is we want to see at least six patients with three months of data. Why? Because within the first three months, you can see most of the effect, at least on the SLEDAI score, and you can start to see the effect on the kidney function as well. This is why. At least six patients with at least three months follow-up. We expect to have this data actually in the very near future, but it's not going to be in the first half of the year. That is why we updated it. It's going to be in the second half. The other part, there's always the opportunity to come back with a smaller data set. We felt like in today's environment, where everybody's focused on tariffs and pharmaceutical pricing, let this wash out a little bit in the very near future, and then we'll present our data, but people will be behind this turmoil in the industry. So it's more purposeful deployment of these results as opposed to, I don't know, there isn't enough patients that are out there or a slowdown in enrollment. No, no. Actually, we had a couple of screen fails. There's certainly some of the screen fails will go into the SLE arm. That's OK. They'll eventually end up in the study. I think in terms of interest in the study, we see significant interest, and we see patients in screening and enrolling. We expect to have this data in the near future. Are you learning anything in terms of patient selection? Like we mentioned with the Schett data, it could be younger patients and things along those lines. Are you focusing on any particular patients in general within the LN community? Again, going back to this endpoint, you mentioned, I think it was SLEDAI score, how important are other metrics like proteinuria or any other biomarkers? Absolutely. Obviously, the ideal patient is a young patient who quite recently discovered that they have LN, and we do not expect any significant existing damage to their tissues. That is not necessarily all the patients. There are some more metrics that we are looking into in order to select the patients. I think the entire industry is trying to do this together and in parallel, and nothing is yet completely validated except for young and very few years of duration of disease. What is nice about SLEDAI is that it compounds different metrics that suggest the overall disease of SLE. If you have a drug that works, we should see some significant effect on the SLEDAI. Regarding proteinuria, proteinuria is known to be something that is much more variable. I think if the patient has long duration of disease, you might be able to, you might have a limited opportunity to affect the kidney function because there is existing tissue damage. That is something that the industry overall is learning, and we are also trying to implement those learnings. Got it. This is a pretty competitive space. Last year, a lot of cell therapy companies, I want to say almost all of them, made a pivot from oncology to autoimmune disease, largely based on the promise of these Schett data. We have seen this happen in the industry before where academia kind of leads by producing some very tantalizing results. Then our commercial companies perfect this and get it out to the patients. What do you think about the data that has been generated to date from your competitors? Ultimately, how do you thread the needle, if you will, especially given the amount of competition that is in the space? Sure. Absolutely. First of all, how does this time in the autoimmune space remind me of two different periods in my career? One, I had a lot more hair. You and me both. That was when TNF alpha went into the market. People were initially hesitant, but boy, it works. It became, I think, tens of billions of dollars of industry. The second one was when PD-1 were developed. It became also a huge class. I do think this will become a very, very big class, and there is room for multiple players in the industry. Regarding the differentiation, we can go cell type by cell type. I'll just pick autologous alpha beta targeting CD19s just as an example. It's a very different therapy because, first of all, the physician needs to schedule leukapheresis. Those leukapheresis beds are, there's a lot of demand for them. Essentially, they need to take out one spot from an oncology patient to put a different patient with autoimmune for leukapheresis. It's tough. It's tough to enroll, and it's tough to deploy it this way. You wait for the product to be manufactured. The patients come back and get their personalized medicine. If the manufacturing went really well and those alpha beta CAR-T cells have great fitness, they'll go in and they'll kill all the CD19 positive B cells really quickly. They'll secrete a lot of IL-6. Guess what? The patient most likely will have serious ICANS. You can't really do it in a community setting for many, many patients because those cells don't tell you, hey, I have great fitness. I'm going to cause serious ICANS. For a different patient whose T cell fitness is not great, they're not going to proliferate great. They're going to have a very good safety profile, but not going to work as good. In our case, it's very different. It's completely off the shelf. It's the same release criteria for all of our products. You dose the patient off the shelf. It shouldn't cause any significant serious ICANS because they don't have the same profile as the alpha beta T cells, and they go into the tissues. That's a big advantage compared to alpha beta T cells. That's the same advantage for both autologous and allogeneic, except for allogeneic, you don't need to wait because these are off the shelf. At the same spot, I think an advantage versus bispecifics, which at least if you look at what happens in lymphoma, what happens to the bispecifics, we all spoke about the bispecifics, oh, they're going to come into the market, and let's see what will happen to cell therapies. Guess what? Check the cells of the bispecifics and the cells of the autologous alpha beta T cells in oncology. If any of the people in the audience had a relative and they had DLBCL and MCL, and you had choices for a bispecific or a CAR T, do your homework. Within 30 minutes, you'll get to a pretty clear conclusion what you want to give to your relative. I think there is significant differentiation versus alpha beta T cells in terms of safety, availability, and tissue tropism versus bispecifics that will likely require chronic dosing and might not work as well. There is no immunosuppressant-free remission. Bispecifics are a new class of immunosuppressants. NK cells, I think the jury is still out because these are very different cell types, different PK, and there are some companies working with these as well. In the last kind of four minutes we have, I do not want to ignore the other half of your pipeline. Take us through, you stayed away or decided let's not invest more investment dollars. You were prudent with your portfolio management with MCL and LBCL. You did decide to go after RCC, which is a whole new target, right? Cell therapies in general have not made headways into solid tumors. Why did you guys do that? Why do you think you might be the first? Sure. Absolutely. Cell therapies, these would be alpha beta T cells or NK cells, gamma delta 1 are different cells. When we look at our data in oncology, and for example, for CD70, we see tropism to the tissues. That is important. We have a single chain of V, or other companies use a binder for the CD70. We use the natural receptor for CD70, so it binds better and requires less density of the CD70 on the tumor. That is the second advantage. The third advantage, and we published this, we see that once our cells go into the tumor, they also kill the tumor cells that do not express CD70, so potentially addressing the heterogeneity in the tumor. The fourth, we know that tumors have immunosuppressive environment. At least one of them is TGF-beta, and we have a bolt-on technology, dominant negative TGF-beta, that should address this. We are in the clinic with dosing patients with RCC or escalating well with the doses. There is another option to escalate to even a higher dose level. These cells have been very, very safe. I would not be surprised if you will even escalate to higher doses. The study is progressing very, very well. We have two other preclinical programs that we will update on later this year, hopefully, one in autoimmune and one in another oncology. The oncology program is in PSMA. We are very excited about the PSMA program. Just back to RCC, kind of the same question that we asked for AID. A, when should we expect data? B, about how many patients worth the data? C, the very, very important question, what is your go, no-go hurdle there in RCC? Absolutely. First of all, when we expect data, second half, at least six months with the three-month follow-up, potentially more. That is on when. What is the bar? I think the best is to look at what is available for patients that progressed essentially on PD-1 and VEGF inhibitors. What is available to them provides about 20% overall response rate and five months PFS. We need to see data that suggests that at a specific dose level, we think we can do better for these patients. That is the bar. Whether there is another competitor that defines a different bar during the time period, of course, we will take that into account. So far, there is some data from another allogeneic alpha beta T cell with some overall response rate, not a lot of data on durability. What we know, 20% overall response rate, five months PFS, we can get with what's approved in the market. It's a gangbuster sort of second half. A lot of data coming out, AID, oncology, some of the preclinical advancements. How much cash do you have? How long does that take you in terms of development? Especially in this kind of environment where you might not be able to rely on the capital markets, what's your kind of thoughts on BD and how our discussion's going? Sure. Absolutely. We have about $150 million in cash that will take us well into the second half of next year. Indeed, BD might be an option that we would consider. We do expect to have multiple catalysts coming up. Both sets of data will come up and hopefully will serve as a significant catalyst. Overall, I think we feel that we're well funded with multiple shots on goals and hope to report data that will excite people. One final question, even though I'm over. Everyone's concerned about the regulatory environment right now. It's just the topic du jour. Kind of very quickly in 15 seconds-20 seconds, how have your interactions been with the agency? Do you foresee any sort of issues moving forward? Our interaction with the agency has been nothing short of phenomenal. Very collaborative, very productive. I feel fortunate to have these types of interactions. I have not seen these types of interactions in some of my prior companies. In fact, it's one of the first times I see these types of interactions. What I think will happen is when you have a shortage of resources, you've got to focus on what matters the most. What matters the most are innovative therapies that provide significant advantage to patients and can save patients. If a company believes they have that and their data sets support that that's what they have, they're probably going to get the attention. If a company has something that has marginal efficacy compared to the next drug that's approved, then maybe it's going to be a little tougher to get that type of attention because that team will focus on somewhere else. At least for us, for RCC, we think that all the therapies that we develop should command this type of an approach with the FDA. They will continue to focus on us just like they have focused on us and continue to work with us to progress our programs. Sounds like a great place to end it. Ken, thank you very much. Thank you.