Adicet Bio, Inc. (ACET) August 2026 Conference Transcript

Hey, great. Good morning, everybody, and thank you very much for joining us at the 46th Annual Canicorge Unuity Growth Conference. I'm John Newman, one of the senior biotech analysts here at the firm. So we're very excited to have Adaset with us today and the CEO, Ren Shor. So, Ren, to start, could you give us an overview of Adaset and also your lead asset, excuse me, Proulacel? Thanks.

Absolutely. First of all, John, thank you very much for inviting us. Very timely. We expect to have very, very significant disclosures in the very near future. So excited to be here and talk about what we expect to, the data we expect to share. So ADISET 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 CRT 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 the, I believe, the largest data set ever reported by an allogeneic of 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 BMS. So 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 B-specifics. 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 Plovicto with two very important bolt-on technologies that are a result of about four years of research that makes this cell very potent and address some of the key challenges that we have seen with cell therapies in a 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 so there's going to be a lot coming from us in the next few

months and could you remind us of the advantages of targeting c20 in these autoimmune indications, you know, versus other targets that many people are familiar with like CD19?

Yeah, absolutely. So maybe I'll start by focusing on the targets and 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 the CD19. And when we look at our data with CD20, you couldn't actually tell the difference. So 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 and 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. And 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. So 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.

That's okay. Let's move on for now and come back to that. So you mentioned just a moment ago, that you have an important data read outcome in SLE and lupus nephritis. Just wondered if you could just give us kind of a general overview as to what to expect?

Sure, absolutely. So 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-shell therapy that doesn't require leukophoresis. So 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 the people to study we don't need more patients now so we were in that position we could have enrolled many more patients i want to be very 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 so out of the 22 patients and 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 six months follow-up.

Okay, great. Thank you. On durability for both lupus nephritis and SLE, you know, 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 absolutely so that's really why we focused on the 12 months because if patients can get a single therapy and then be essentially have a drug-free remission or drug-free complete renal response and at least a year that's a big step for these patients so 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 announced data in this quarter. So one year seems to be the benchmark that people are looking at and our goal is really to have a SIA rate that is similar to the SIA rate that we see with the autologous CAR-Ts at a 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 and Lubbis, 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. So let's, there's a lot to unfold here. So 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 B-specifics. If you think about it, B-specifics have been around for more than two years. There is yet a data set that shows some significant CR8 and any durability with B-specifics. Roche, as a very smart company with a very rich pipeline of B-specifics, terminated their B-specifics for lupus nephritis and SLE, and continues to focus on their autologous cell therapy. So all these people that we go to conferences with, they have participated in these studies. 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 is high cardiovascular events from again organ dysfunction from the disease so 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 and 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 read those them but that's okay you get a single drug and And then, you know, essentially it's almost like a cure for a while that is immunosuppressant and pretty much steroid-free or very low dose of steroids. So 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. So I see a patient, God forbid, you know, Mr. X or Mrs. X usually. has lupus or let's focus for a second on lupus nephritis as an example you know she tried one immunosuppressant she tried another immunosuppressant she keeps coming back and you look at her protein urea it's not good if you continue like this they might die from an infection or they might need to might might go to end stage renal disease that's the path that's what's going to happen so you say 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. So stop taking your drugs for a month. And you came because you're not feeling well. Stop taking your drug for a month. Then I'm going to call and I'm going to get you an appointment for the leukophoresis. I hope to get a chair there in a month from now. You'll go for the leukophoresis. We'll send it to manufacturing. At some point, I can't 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'll give me a date. Then you need to come five days before, and we'll start the conditioning, and then we'll get the therapy. And you should know there is a chance you'll get ICANNs, because certain patients get grade 3, 4, and ICANNs. I can't tell you if you'll get it, because your fitness might be great and then you're more likely to get it, the TCL fitness or not great and then it might not work as well and you're not going to get it. But you might get it. So we're going to put you under very close monitoring, hopefully you're not going to get an ICANN, but if you do we'll treat you very quickly, but you've got to be in the hospital or very close to the hospital and come every day so we check if you have ICANN. So that's a lot of hassle. That's 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 you saw their patients, they 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 don't feel well. They say, hey, you should really benefit from cell therapy. why don't you go to the nurse, we'll start the conditioning, it's Tuesday, you'll take it Tuesday, Wednesday, Thursday, and come Sunday, we'll give you the drug. That's it. And it's better tolerated, by the way, because this type of off-the-shell therapy with gamma-delta-1 don't secrete these high levels of IL-6. And in their studies, at least what's reported to date, I can say, we haven't seen any of those high-grade ICANs. Actually, in their oncology studies, there's those like 40 patients where there's 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 is with my mother, I can tell you what I would choose. And that's, 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. So we have met with the FDA quite recently, so we know more that, and we will announce that when we announce data, so there will be regulatory feedback. So I'll step back and I'll 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 a 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, or the patients that joined the study, many of them also have nephritis. So you kind of capture most of the market when you focus on patients with lupus and nephritis and 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 some changes in the design, changed the inclusion criteria and their order of the endpoints and included SLE patients. So our plan, because most of our data are in LN, is to start with LN, and we keep the option to expand to Wesley as well.

Okay, great. Some of the physicians that we spoke with also mentioned that the traditional lupus endpoints, such as sleet eye and door submission, don't always capture the full benefit of cell therapies, particularly in lupus nephritis. And 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. So 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. So 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. So the slidae is a very, it's not a very accurate measurement of efficacy because even if you see a reduce in slidae 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. So slidae is a little bit limited. Doris is actually better from that perspective, because for Doris, you need what's called clinical slid IO0. So all your clinical symptoms, it's okay if you have some biomarkers, but what matters for Doris is the clinical symptoms. So we don't want to see any of the clinical symptoms. Arthritis, no. If you have arthritis, there is no Doris. But you can, Doris includes, you can take steroids up to five milligrams, which is fine. That's, you know, essentially symptomatic relief. It's not associated with high rate of side effects, but you can continue to take immunosuppressants on Doris. So 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. So Doris is limited. The benefit that we have from a drug like ADI-001 or Prulacel is that we can actually measure, for example, CRRs, but also we can measure immunosuppressant-free and low steroids. So 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 cannot, 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. You know, 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. Like if they, 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. So it's a whole different ballgame in terms of what you can see in endpoints.

Just a follow-up on your last comment. You know, 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? Could you talk about sort of the kind of the dichotomy between maybe here's what the physicians are thinking, but then you have the patients over here who are on this chronic immunosuppressants?

Yes, absolutely. So I'll address it in two levels. First of all, the patients who are the physician will have a tough time even telling them to take something else. So in the U.S., as an example, there's about 250,000 patients with SLE, and 100,000 patients approximately have LN. Out of these 100,000 patients, I'm rounding the number, about 35,000 patients tried at least two immunosuppressant therapies, and it just doesn't work. And for these patients, the likelihood that a different immunosuppressant will work is very, very slim. So for these type of patients, really, what could be an option is a cell therapy that has been shown to really be efficacious. So I think for that part of the market segment, these 35,000 patients, they actually need it. Once it's available, I would expect pretty high uptake, and I think that's 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 you know every now and then they have an exacerbation in their disease and you know 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 and then you know after some time taper it down over a bunch of weeks and 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, so I would expect it's going to start from these 35,000 patients, which is the type of patients we expect to enroll in our studies. So that's not inconsistent if you look at the inclusion criteria of other autologous cell therapy, especially companies like Novartis and bms and then i would expect this will expand either by just market expansion because it's going to be advantageous even for the insurance companies at some point i'm going to pay all the time for these immunosuppressants and keep paying for hospitalizations versus this one-time therapy you know forget about it for a while so the insurance companies will probably want to want to have it or you can also run a study and show that it works in earlier lines okay great um i I believe you're also planning to share data in systemic sclerosis this year.

I'm just curious as to what we should expect from that update.

Sure, absolutely. So we didn't 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'll provide some more when we announce data. But it's a reasonable number of patients, and at this point we're following up on these patients and see how they perform, and we expect to have the data in the second half of the year.

Okay, great. I believe you're also evaluating cruella cell 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, and will those findings potentially influence the lymphodepletion strategy down the road for other indications?

Yes, absolutely. Great question. So we are running a study in RA. Essentially, it's a very small study, and really we're comparing one conditioning which includes psi and flu and one conditioning that includes psi only. We're aware that other companies that tried avoiding flu derby like Encarta and a few others figured that we probably need it. We've never tested it with the gamma delta 1 CAR-T, so that's why we're running the study. And if we learn that we don't need the flu therapy, this could affect how we think about other indications. But I want to step back. When we talk to some of the KOLs, they actually believe that the conditioning that you use in one indication might not be the magic conditioning that you need for all indications. So, for example, for a disease that's focused in the blood, maybe you need less stringent lymphodepletion. For a disease that's focused in specific organ and you need good organ penetration, maybe you need a more stringent lymphodepletion. So, so far, we haven't tested that question in our study in SLE and LN and other indications. In RA, we're 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 site flow consistent with small companies like Novartis and BMS.

Great. Well, it looks like we're out of time. Thank you very much, Henn, for joining us today. Thank you to Anaset. Very, 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.