Good morning, everyone, and welcome to Adicet's specially scheduled conference call. This call is being recorded. At the end of the company's prepared remarks, we will open the call for questions, and we will provide specific instructions at that point. I would now like to turn the call over to Anne Bowdidge. Please go ahead. Thank you. On the call today from Adicet are Chen Schor, President and CEO, Dr. Francesco Galimi, Chief Medical Officer, Nick Harvey, Chief Financial Officer, and Dr. Blake Aftab, Chief Scientific Officer. In addition, we're pleased to have Dr. Sattva Neelapu, Professor in the Department of Lymphoma and Myeloma at the MD Anderson Cancer Center, joining us today. We'll start the presentation with some introductory remarks by Chen, and then Francesco will review the interim results in more detail. Dr. Neelapu will then provide his thoughts on the data and speak to the potential opportunities offered by gamma delta CAR T cell therapy. After that, we'll open up the call for Q&A. Before we begin, I'd like to remind you that various remarks that we make on this call contain forward-looking statements that are made under the safe harbor provisions of the securities laws, including statements regarding interim clinical data resulting from studies with ADI-001, including future plans or expectations, as well as the expected potential therapeutic effects, safety profile, expectations regarding the initiation, design, implementation, timing, and success of future clinical studies of ADI-001, our future opportunities and upcoming milestones, and our expectations regarding uses of capital. In addition to our prepared remarks, we may make forward-looking statements in response to questions including, for example, statements regarding potential future trials and our financial position and results. Any statements made in this call that are not statements of historical fact may be deemed to be forward-looking statements. Forward-looking statements involve risks and uncertainties that could cause Adicet's actual results to differ significantly from those projected, including without limitation, the risks and uncertainties detailed in Adicet's most recent annual report on Form 10-K and our periodic reports on Form 10-Q and Form 8-K filed with the SEC. This call is the property of Adicet, and any replay of this conference call cannot be made without Adicet's express written permission. With that, I'll turn the call over to Chen Schor, President and CEO of Adicet. Thanks, Anne, and thank you all for joining us today. Before we begin, I'd like to thank Dr. Sattva Neelapu for joining us for this call. His valuable insights into the clinical management of non-Hodgkin lymphoma patients has contributed greatly to the success of this study. I'd like to also extend my sincere thanks to the patients, physicians, investigators, and study sites, and to our dedicated employees, all of whom are instrumental in helping us achieve this important milestone in advancing this study. Before handing it off to Francesco and Sattva, let me provide some context for the data we announced today in our press release, beginning with a summary of what we believe are the key takeaways. ADI-001 has the important distinction that it is the first ever off-the-shelf gamma delta CAR T cell therapy to reach clinical studies and report clinical data. As you saw in our press release this morning, we reported interim data showing that ADI-001 is highly clinically active, demonstrating complete responses starting from our lowest dose level with favorable safety profile in patients treated to date. The other important takeaway is that gamma delta T cells may provide significant advantages both in terms of antitumor activity and safety when compared to other allogeneic cell platforms or bispecifics. Finally, in the gamma delta field, gamma delta 1 T cells may provide significant benefits as compared to gamma delta 2s. Our gamma delta CAR T cells are unique as they are designed to have three mechanisms for antitumor activity. First, innate antitumor activity, which targets multiple surface proteins selected by evolution to mark tumors for cell killing. Second, adaptive antitumor activity by an MHC unrestricted T cell receptor. Finally, CAR-mediated antitumor activity. The combination of these three antitumor activities in one cell therapy product may result in more limited ability for the tumor to escape the therapy. What is unique about our gamma delta 1 T cells is that they may provide adaptive antitumor activity like an alpha beta T cell without the need for gene editing, innate antitumor activity like an NK cell, and all these antitumor activities with potentially a broad therapeutic window. Not all gamma delta T cells are created equal. While I will not go into details on this slide, there are a number of reasons why we selected to focus on gamma delta 1 T cells, including tissue tropism and function in the tumor microenvironment. Enhance cytotoxicity and excellent cell expansion while maintaining a durable functional persistence in preclinical models. Let's talk about manufacturing. Historically, gamma delta 1 T cells were challenging to manufacture, mainly due to their tissue tropism and the lack of biologics that can selectively expand these cells. We made a significant investment manufacturing over more than 5 years to overcome these hurdles, and we believe it has paid off. The manufacturing process for ADI-001 is scalable and transferable to CMOs. Currently, our manufacturing process provides up to 1,000 off-the-shelf doses per batch, which gives it the potential to be truly off the shelf. In May this year, we dosed the first patient in our phase I study evaluating ADI-001 in patients with B-cell non-Hodgkin lymphoma or NHL. This is the first clinical study ever with off-the-shelf gamma delta CAR T cells. As pioneers in the field of gamma delta CAR T cells, we had a few key topics that we wanted to address. Safety. Will we see graft-versus-host disease, neurotoxicity or high-grade CRS? Expansion or proliferation. Will ADI-001 proliferate and be detected in the blood? PD biomarkers. Will we see any PD biomarkers consistent with ADI-001 activation? Last but not least, antitumor activity. Will we see any signs of antitumor activity? While the study is ongoing, we did get answers to these questions, and we're excited to share our early data, which to date has far exceeded our expectation starting from dose level one. Let me quickly summarize what we've seen so far in the study. We observed a favorable safety profile in patients treated to date. No graft-versus-host disease, neurotoxicity, or high-grade CRS have been reported. We observed clear evidence of ADI-001 in vivo expansion. We observed circulating PD biomarkers that are consistent with ADI-001 activation. Regarding antitumor activity, we observed complete responses in what investigators are calling a near complete response, starting at ADI-001 lowest dose level in heavily pre-treated NHL patients, including a complete response in a CAR T relapse patient. The overall response rate was 75% and the complete response rate was 50%. What's remarkable about this data is that we're seeing these complete responses starting at our lowest dose level of 30 million CAR-positive cells per patient. For perspective, this is approximately 5x lower than the approved dose for Yescarta and represents a dose level for which CD19 CAR-NK cell therapies have seen limited clinical activity. We believe these data are highly encouraging and we are committed to advancing our robust pipeline with the goal of helping many more patients living with cancer. This is our mission and this is our passion. With that, I'll now turn the call over to Dr. Francesco Galimi, our CMO, to review the data in more detail, and then to Dr. Neelapu, who will provide some additional thoughts on the data. Francesco. Thank you, Chen. Good morning, everyone, and thank you for joining us today to review initial clinical results from our phase I study evaluating ADI-001 in B-cell malignancies. We believe the initial results are rather impressive. Before we discuss the clinical data, let me provide a quick reminder on how our multifunctional cells operate. As shown in blue in the top left plot, ADI-001 targets non-Hodgkin lymphoma cells via a CD20-targeted CAR that confers high potency for tumor cell killing. The top right plot shows ADI-001 cytotoxicity against rituximab-resistant cells. The CD20 epitope targeted by ADI-001 does not compete with the rituximab binding site and is designed to retain this high level of potency even in the context of rituximab resistance, which is typically associated with CD20 downregulation. In all contexts, the innate and adaptive receptors found naturally on our gamma delta T cells provide complementary activity. The graphs showing red, the cytotoxicity of the gamma delta T cells without the CAR. Altogether, ADI-001 demonstrated high anticancer potency in vitro and durable antitumor activity in vivo in non-clinical models. This potent anticancer activity is coupled with release of polyfunctional cytokines that provide a signature for activation when ADI-001 cells encounter their target. This polyfunctional cytokine profile includes interleukin two and interleukin eight, which can be monitored in vivo. Notably, the profile does not include release of high levels of interleukin six, which we believe supports the expectations for limited CRS frequency and severity in association with ADI-001 activation and tumor cell killing in the clinic. Based on this preclinical rationale, we are conducting a first-in-human study in late-stage non-Hodgkin B-cell lymphoma. This is, to our knowledge, the first clinical trial with an allogeneic off-the-shelf gamma delta CAR T investigational therapy. We will now show you the first peek into the clinical data collected so far. We have completed the first dose level of the dose escalation at 30 million CAR positive cells, flat dose, and we are currently in the second dose level cohort at 100 million CAR positive cells. The first dose level of 30 million CAR positive cells is approximately fivefold lower than the approved dose of Yescarta, and is the first dose level in a recent CAR NK cell therapy study where there was 1 partial response observed out of 3 evaluable patients. While preliminary, we believe our data so far are very encouraging for the following reasons. First, we have clear evidence of ADI-001 cell expansion. Second, we have clear evidence of pharmacodynamic engagement. Third, the safety profile in patients treated to date is generally favorable. Finally, and most importantly, we have observed impressive clinical responses starting at the first flat dose level of 30 million CAR positive cells. A quick reminder on the first-in-human study design. The dose escalation portion of the study includes three dose levels, starting at a rather low dose of 30 million CAR positive cells and continuing on to 100 and 300 million cells. Higher doses can also be tested under this protocol, depending on data. Each enrolled patient receives a five-day lymphodepletion regimen required to deplete the endogenous T and NK compartments and to allow engraftment of the subsequent allogeneic cell infusion. As I will discuss in a minute, we are exploring two different lymphodepletion regimens, both based on fludarabine and cyclophosphamide. After lymphodepletion, each patient receives a single infusion of ADI-001 at the appropriate dose level and is then followed for a 28-day window called the dose limiting toxicity, or DLT window. Safety findings emerging during the DLT window are the main drivers of the dose escalation decisions. After the DLT window is over, each patient is followed up for safety and efficacy evaluations. The first efficacy assessment is scheduled on day 28, post-infusion. This diagram also shows the current design for the dose expansion part of the study, which will start after the dose escalation is complete. We may end up changing the focus of the dose expansion based on the data emerging from the dose escalation. This is the overview of the patients enrolled so far. We dosed the first patients in early May. The first two patients in dose level one came off study before completing their DLT window, and per protocol they had to be replaced so that the characterization of the dose level one cohort could be completed. We ended up dosing a total of five patients at dose level one, 30 million CAR positive cells, three of which were DLT and efficacy evaluable. We are now dosing in dose level two at 100 million CAR positive cells, and we can show you preliminary data from the first patient on this second dose level. This slide shows the characteristics of all the patients dosed so far. The two patients at the bottom of the table, shown in gray, are the first two patients in dose level one who came off study early on due to progression. They were replaced per protocol and are not part of our efficacy subset. One was a primary refractory Burkitt lymphoma, a very rare aggressive non-Hodgkin lymphoma subtype that we will no longer consider for this trial for the time being, at least until we get to the maximum tolerated dose. The second replacement patient was a late-stage diffuse large B-cell lymphoma patient with high tumor burden, five prior lines of therapy, who also progressed before completing the DLT window. The efficacy subset that we're discussing today includes four patients shown on the table, three at dose level one. They were a diffuse large B-cell lymphoma transformed from CLL, a high-grade B-cell lymphoma transformed from follicular lymphoma, and a diffuse large B-cell lymphoma. In the fourth patient at dose level two, a patient with mantle cell lymphoma. All the patients had been heavily pretreated with a median of five prior lines of therapy. As you can see on the table, some patients received what we call standard lymphodepletion, while others received an enhanced lymphodepletion regimen. The details of the two regimens are shown on the slide. Our lymphodepleting regimens do not include additional agents on top of cyclophosphamide and fludarabine. As you can also see on the table, we have some patients whose prior lines included cell therapies and some who were cell therapy naïve. We expect to have more patients in each group as the trial progresses. This slide shows a summary of key treatment-emerging safety findings collected so far. The only grade three event was a pneumonia 2.5 months after ADI-001 infusion in a patient who developed COVID. This patient also developed a grade two CRS, probably due to the COVID infection. All the other CRS occurrences reported were grade one. We have not seen any event of ICANS or GvHD. Overall, in patients dosed to date, ADI-001 appears to be rather well-tolerated. This table shows the responses observed in the 4 efficacy-evaluable patients. While the first patient had progressive disease, the other three showed very impressive responses. One patient with transformed follicular lymphoma with 4 prior lines of therapy showed a very deep partial response at the first assessment on day 28 post-infusion. A response that we would characterize as near complete. Unfortunately, approximately 2.5 months after receiving the ADI-001 infusion, this patient developed a COVID pneumonia and later died of complications from it, unrelated to ADI-001. The second responder was a patient with diffuse large B-cell lymphoma with 5 prior lines of therapy, including 2 cycles of CD19 autologous alpha/beta T cell therapy, who showed a complete response on the Lugano criteria. The third response was in a mantle cell lymphoma patient in dose level 2 with 5 prior lines of therapy, who received 100 million CAR-positive cells and showed a complete response at day 28. In summary, from the 4 efficacy evaluable patients, we have seen 75% ORR, 3 out of 4, and 50% CR rate, 2 out of 4. Notably, the partial response was a very deep one, essentially a near complete response. Now let's look at the scans in detail. The first response we saw at dose level 1 was in a 66-year-old female with a follicular lymphoma transformed into high-grade B-cell lymphoma. This patient had received four prior lines of therapy. The baseline scans show a significant tumor burden, in particular, a large supraclavicular mass at the base of the neck and axillary lesions, as well as extensive tumor masses in the abdomen. The brain tissue and the bladder, shown by the blue arrows, are sites of normal FDG uptake. The areas shown by red arrows are the actual cancer lesions. A few days following dosing of ADI-001, the patient started reporting shrinking of the large mass at the base of the neck until it became no longer palpable. The scans at day 28 show a virtually complete disappearance of PET signal. We can see that the PET signal shown in yellow pseudocolor is gone from the areas previously occupied by tumor lesions. Let me remind you that this patient received a low dose of 30 million CAR-positive cells. The response was assessed as being a partial response, not a complete response, due to the persistence of very limited FDG uptake in the abdomen and in the neck, not visible in these images. However, it was clearly a near complete response. This is a sagittal section of the same patient, showing the extent of the disease at baseline in the side of projection and the disappearance of the PET signal at day 28. As I mentioned, two and a half months following ADI-001 dosing, this patient unfortunately developed COVID-19 pneumonia and later died from complications of it, but unrelated to ADI-001. She did not reach the 3-month efficacy assessment, which was scheduled for late November. The second response we saw in dose level one was in a 75-year-old male with diffuse large B-cell lymphoma. This patient had received five prior lines of therapy, including two cycles of autologous anti-CD19 CAR Ts. In this case, the main tumor mass was in the right leg, encasing major nerves behind the knee, as shown by the red arrow. At the first assessment, the PET signal was completely gone. You can also appreciate the different position of the leg at day 28, since the tumor mass was preventing the patient from fully extending the leg at the time of the baseline scan. A few smaller tumor masses were present in the pelvic region, and they also disappeared at the first assessment. The radiologist scored this response as a complete response per Lugano 2014 criteria. Again, this patient received 30 million CAR-positive cells. He is currently on trial and continues to be followed up per protocol. The third response we saw was in the first patient dosed at the 100 million cell dose, a 62-year-old male with mantle cell lymphoma with five prior lines of therapy. This patient had two rather large inguinal tumor masses shown by the red arrows in the baseline scan. At the day 28 assessment, the PET signal had disappeared from both tumor masses. These scans on the right show a transverse view of the same lesions indicated at baseline by the red arrows and disappearing at day 28. The radiologist scored this patient as a complete response by Lugano 2014 criteria. Our trial design thoroughly measures PD biomarkers and PK assessment. So far, however, our sample size is too small and the observation timeframe too short to discuss the PK/PD data set in detail. We can mention, however, our preliminary observations, postponing a more detailed discussion on PK/PD when more data are available. We could document a consistent increase in circulating IL-15 following lymphodepletion, providing a suitable cytokine support for ADI-001 cell proliferation. We could detect ADI-001 cells in the peripheral blood by both flow cytometry and quantitative PCR. The timing indicated expansion of transplanted ADI-001 cells. It is too soon, however, to comment on the persistence of ADI-001. IL-2 and IL-8 production could be documented with the timing during the first 14 days, consistent with the activation profile of ADI-001. This pattern is also similar to the profile observed with the autologous alpha beta T cells. Importantly, IL-6 was not increased in any meaningful way, confirming the lack of serious cytokine-related findings observed in the clinic. Based on this profile, we currently do not expect high frequency or severity of cytokine release syndrome. Overall, preliminary data are very encouraging and provide evidence of ADI-001 cell proliferation. In vivo expansion, target engagement, and of course, potent antitumor activity. In conclusion, let me summarize the clinical data I just presented. ADI-001 administration was well-tolerated in the initial part of the dose escalation. In patients treated to date, the safety profile was favorable, with no GvHD, neurotoxicity, or high-grade CRS reported. Of the four efficacy evaluable patients, one achieved a near complete response and two achieved a complete response. Overall response rate 75%, complete response rate 50%. Complete and near complete responses were observed starting at ADI-001's lowest dose level, 30 million CAR-positive cells, including a complete response in a CAR-T relapsed patient. If confirmed, the safety efficacy profile of ADI-001 indicates a very broad therapeutic window with a virtual uncoupling of cytokine release syndrome and antitumor activity. Based on these data, we're planning expansion cohorts with potential pivotal intent in patients relapsing after autologous CD19 CAR-Ts and in non-Hodgkin lymphoma subtypes such as diffuse large B-cell lymphoma, mantle cell lymphoma, and follicular lymphoma. With that, I thank you all for your attention, and I'll now pass the call over to Dr. Sattva Neelapu from the MD Anderson Cancer Center. Thank you, Francesco, for the summary of the results to date with ADI-001 in this ongoing phase I trial. I think the high efficacy with an excellent safety profile observed at this low dose level is highly promising and to me suggests a potential for a broad therapeutic window and possibly even higher efficacy at higher dose levels. More importantly, I think allogeneic gamma delta CAR T-cell therapy offers several potential advantages over alpha beta CAR T-cells. Gamma delta T-cells mediate antitumor effects through their cell-intrinsic properties via the natural cytotoxicity receptors as well as gamma delta T-cell receptors through an MHC-independent manner. In addition, the CAR introduced in ADI-001 provides another potent mechanism for antitumor effects. Thus, therapy with ADI-001, I think, is equivalent to administering multiple immunotherapy products that impart both innate and adaptive immune responses besides CAR-mediated effects. Gamma delta T cells are also likely to have a superior safety profile. Since they do not require TCR gene editing to prevent graft-versus-host disease, the long-term risk of mutagenesis is less likely. Because they have a different cytokine profile, they likely have a lower risk of inducing CRS and ICANS, and this is supported by the data to date, where we have observed high efficacy without major toxicity. Lastly, because ADI-001 is an allogeneic product, the risk of long-term B-cell aplasia and hypogammaglobulinemia is unlikely as compared to autologous CAR T products. As an allogeneic CAR T product, ADI-001 may have additional advantages over autologous CAR T products. It could potentially improve efficacy as the T cell fitness is expected to be better. It provides consistent product quality and eliminates the variability observed with autologous CAR T while also eliminating the wait period. It could lower the cost of CAR T-cell therapy since up to 1,000 doses can be manufactured from a single run, and it can improve access to patients as it can be administered at non-transplant centers as an off-the-shelf product. As you saw in the presentation by Francesco, I think the early data from this phase I clinical trial is highly encouraging. The high overall response rate of 75% and a CR rate of 50% in the first 4 evaluable patients with 2 CRs and 1 near CR was observed in patients with bulky disease, including a patient who had prior autologous CAR T therapy, and in patients with 3 different types of lymphoma, diffuse large B-cell lymphoma, transformed follicular lymphoma, and mantle cell lymphoma, suggesting that this product could have broad applicability across multiple lymphoma subtypes. The safety profile so far has been very favorable, with no graft-versus-host disease, no ICANS, and no high-grade CRS, even in patients with bulky disease. Lastly, the multiple mechanisms through which ADI-001 could mediate antitumor effects, including the CAR, as well as the cell-intrinsic innate and adaptive properties of gamma delta T cells, make it possible that ADI-001 could improve durability of responses and minimize emergence of tumor resistance. In terms of clinical applicability, this product could fulfill unmet medical needs in patients with diffuse large B-cell lymphoma. In the third-line setting, we know that more than 60% of DLBCL patients treated with CD19 CAR T relapse, and a significant proportion of them relapse due to either CD19 loss or due to poorly functional CAR T cells. Since ADI-001 targets CD20 and is an allogeneic CAR T product derived from healthy donor T cells, it could potentially overcome both of these resistance mechanisms and thus provide a path for an accelerated approval process given the unmet medical need in these patients. In addition, ADI-001 could address another major limitation observed with autologous CAR T. It is estimated that only about 20% of eligible DLBCL patients are currently receiving autologous CAR T in the commercial setting. A product like ADI-001 that is highly effective with low toxicity and available off the shelf could improve access, and thus can readily be administered to CAR naïve patients at both transplant and non-transplant centers. If good safety and efficacy can be demonstrated in the third line setting and beyond, ADI-001 could be transitioned to earlier lines of therapy, either as a standalone therapy or as consolidation therapy, including in high-risk patients in the first line setting. Similarly, ADI-001 could possibly be evaluated through an accelerated approval process in mantle cell lymphoma patients relapsing after CD19 CAR T therapy given the unmet medical need in these patients. It could also be evaluated in CAR naïve patients in second line setting, and with evidence of good safety and efficacy, could be transitioned to first line setting in mantle cell lymphoma as well. With that, I will stop and pass it back to Chen Schor to wrap up. Chen? Thanks, Sattva. I would now like to summarize what we've seen today, provide a snapshot of our pipeline, and update you on some of our upcoming milestones before we go to Q&A. With today's data, we have solidified our leadership position in the field of gamma delta CAR T cell therapy. We're the first and only company developing off-the-shelf gamma delta CAR T cell therapy to report clinical data. We have seen complete and near complete responses starting at the lowest dose level, including a complete response in a CAR T relapsed patient. We've seen favorable safety profile with ADI-001, suggesting the potential for broad therapeutic window that may enable administration in the community setting. We've also seen evidence of in vivo expansion and circulating PD biomarkers that are consistent with ADI-001 activation. We remain well-funded with $192 million in cash equivalents, and marketable securities as of September 30, 2023 and are well capitalized into the second half of 2023 to achieve multiple near-term milestones. We're advancing a pipeline of additional gamma delta CAR T cell therapy product candidates with approximately one IND expected every 12-18 months. Our next program is targeting GPC3-expressing solid tumors such as hepatocellular carcinoma and squamous cell carcinoma of the lung. We have additional programs in preclinical development that we expect to announce in the near future. Gamma delta 1 T cells are tissue resident. They are resilient in the sense that they have been reported to function in tissues that are relatively deprived of oxygen and nutrients. These conditions are consistent with a solid tumor microenvironment. I'm excited to see the potential of our gamma delta 1 CAR T-cell therapy product candidates in solid tumors. We expect to provide you with a clinical update for ADI-001 in the first half of next year. As you can see on this slide, there are a number of upcoming milestones ahead which are listed here. We're excited about the data. This is a terrific outcome for Adicet and for patients, and we look forward to updating you on our progress. With that, I'll turn it over to the operator to open it up for Q&A. Operator? Thank you. To ask a question from the telephone, please press the star then the one key on your telephone keypad. To withdraw your question, press the pound key. Please allow a moment while questions queue. Our first question comes from Michael Schmidt with Guggenheim. Hey, guys. Good morning. Thanks for taking my questions and congrats on this you know impressive early data update. I just had a number of questions, perhaps just one at a time. The first one is, do you see any correlation with cell expansion and clinical efficacy in the study so far? Hey, Michael. Thanks for joining, and thanks for the question. Perhaps, Blake, our CSO, can help address this question. Yeah, absolutely. You know, I think it's quite early in the trial at this point with respect to translational endpoints. What we do have today is clear evidence of expansion events occurring in the initial weeks following administration. Of course, you know, in an allogeneic setting, this is quite promising to see, especially when coupled with the cytokine emergence. Again, when taken together, looks very similar to what's seen with the autologous CAR T experience. As much as we would love to get into correlative science at this point, it's far too early with far too few data points. Of course, you know, in the totality of the CAR T world, it's not uncommon to see expansion events correlate with response, but we're just too early to see that at this point. Okay. Understood. Yeah. A question for the physician on the call. I think you mentioned that the two CRs are still ongoing. You know, there's been a lot of debate around duration of response in the CAR T and the CAR NK cell space. Just curious, you know, the physician's view on, I guess, what duration of response would be viewed as clinically meaningful in these sort of aggressive lymphoma patients. Sure. Hey, Michael. Again, great question. You know, since Dr. Neelapu is on the call, perhaps Dr. Neelapu can share his thoughts on durability with the gamma delta 1 T cells. Dr. Neelapu, is that okay? Would you be able to address? Yes, of course. Yes, I think what we learned from the CAR T literature and in aggressive lymphomas is that patients who achieve a complete response by the day 30 time point, about 70% of them remain in long-term durability. While we all would like to see the follow-up for these patients, none of them have reached the 3-month time point yet for the next assessment. Based on historical data, you know, and the way we think the gamma delta T cells mediate anti-tumor effects compared to alpha beta T cells, as you heard, there are three complementary mechanisms. The CAR, the gamma delta T cell receptor, as well as the natural cytotoxicity receptors, we think that there's a potential that the durability response is likely to be high. In terms of what is needed, what kind of durability is needed for a path to approval, historically, in autologous CAR T literature, in diffuse large B-cell lymphoma, there's about a 35%-40% durability observed at about six months time point. That's based on a modified intent-to-treat analysis in those patients, with some of the patients dropping off after leukapheresis and CAR T production, and they will receive the CAR T product. In contrast, for an allogeneic product like ADI-001, these patients will be analyzed based on the intent-to-treat analysis. I think if we see a durability of 30%-35% at six months, that would be, at least in my mind, equivalent to autologous CAR T therapy. Great. Thank you. Very helpful. Then Chen, I guess other companies are working on or have started to implement a multi-dosing or a consolidation dosing paradigm with allogeneic cell therapies. I know it's really early here, but is that something that you have been considering to potentially do as well in the future? Sure. Yeah, absolutely. Let me try to address. The data that we've seen so far with a single dose are very, very encouraging. At this point, we don't see the benefit for more than one dose. Our plan is to escalate to our third dose level and examine the efficacy at that point. If we see any benefits in adding additional doses under one lymphodepletion window, we could consider it. We can also consider consolidation dosing. At this point, when you look at the data at such low dose level, it's highly encouraging and it's premature to think about multiple doses. Makes sense. You know, lastly, I guess, you know, I think one of the main, you know, opportunities for gamma delta T cells is their potential in the solid tumor setting, you know, given the, you know, the natural affinity to, you know, to traffic to solid tumors. You know, how should we read through from this data to your solid tumor program? Absolutely. It's always a great question. I believe there is a quite significant read-through from the data that we're seeing today to the potentially solid tumors for the following reason. 1, when you look at the clinical data, we see that gamma delta 1s are powerful and show very strong and deep responses starting at a very low dose. 2, we see that that potent activity is quite potent when you compare it to alpha beta T cells or NK cells at comparable dose levels. The other key point is that gamma delta 1 T cells have 3 mechanisms of antitumor killing, adaptive, CAR, and innate. That's extremely important in solid tumors because in solid tumors, we expect heterogeneity, so we better have cells that can provide multiple cell killing mechanisms. We know that gamma delta 1 T cells, even without Adicet, go through the tissues and can survive in an environment that's relatively deprived of oxygen and nutrients. With the CAR, more of them will go to the solid tissue where the tumor is observed. We're quite encouraged, and we really look forward to progressing to solid tumors as well. In our pipeline, there's some hematologic tumors, some solid tumors, so it's a combination and, you know, more details to follow. Great. Thank you. I'll hop back to Nick here. Perfect. Our next question comes from Reni Benjamin with JMP Securities. Hey, Reni. Good morning, guys. Morning. Morning. Hey, good morning. Thanks for taking the questions and congratulations on this great data. Maybe just starting off for Dr. Neelapu. You know, you've had a lot of experience with a variety of other cell therapies, autologous and allogeneic, all the like. Can you maybe tell us how to be thinking about the grade 1-2 CRS that we're seeing here as compared to some of the other therapies? And in your experience, would you expect this to increase as the doses go higher, as we evaluate higher doses of ADI-001? Or do you think it's a function more on, you know, maybe patient tumor load? And I guess kind of sticking with that theme, I'm kind of curious if toci was used prophylactically at all in this trial. You know, no matter where the CRS goes, you know, since we have tocilizumab, does it really, you know, matter as much going forward as we evaluate this therapy? Sure. Hey, Reni. Thanks for asking. Since you asked Dr. Neelapu, thank you, Dr. Neelapu for answering. Thank you for the question. First, there's no prophylactic tocilizumab, you know, used in these patients. Now, there are grade 1, 2 CRS events observed, but it's actually really only grade 1. The grade 2 CRS, the single grade 2 CRS event that was observed was in the setting of a COVID infection, so it was unclear how much of that was actually related to COVID versus CAR T. We actually think it was more due to COVID rather than CAR T. It was only grade 1 CRS that's been observed to date. As you heard from Dr. Francesco Galimi's presentation, the cytokine profile for gamma delta T cells is slightly different compared to alpha beta T cells that produce IL-2, IL-8. What we are observing in the serum of these patients is we are not seeing any spike in IL-6 levels or IL-1, which classically activate the macrophage myeloid cell subset, which in turn produce multiple other inflammatory cytokines and lead to high-grade CRS or even ICANS. It's possible that with gamma delta T cells, the toxicity, the safety profile and toxicity profile could be different. Although we had to wait until we get to the higher dose levels, but so far, based on the biology as well as the early data that we are seeing, we think that the safety profile is likely to be better. Now, is the toxicity going to increase with higher dose levels? Probably. That's what's been observed. Again, the biology of gamma delta T cells. The difference is a new platform. We are in uncharted territory. So far the safety looks very promising. The patients who have been treated so far, as you saw in the images, they did have bulky disease. Even in those patients, so far, no high grade toxicity has been observed. Got it. Maybe just to explore a little bit, the standard versus enhanced lymphodepletion. You know, I'm you know, typically when we're playing around with the lymphodepletion, especially going higher, right? Safety is one of the key concerns, areas of concern. I'm kind of curious, you know, how you are if you're set on this enhanced lymphodepletion. I believe you mentioned in your prepared remarks you are, but is there any further modifications that could happen as the trial progresses? Sure, Reni. Thanks for asking the question. Perhaps, Francesco, our CMO, can help address. Francesco. Sure. That's an important point. First of all, our lymphodepletion regimens only rely on cyclophosphamide and fludarabine. We don't add any additional agent, nor do we have plans to do so. Moving forward, the plan is to use the enhanced lymphodepletion regimen whenever possible, unless on a case-by-case basis, individual patients in the trial might actually require more conservative approach. In which case, we would revert back to the standard lymphodepletion regimen. That is the current plan moving forward. Got it. I guess just the final question from me is, I'm curious as to the non-responders. In the three patients that didn't you know, outside of the aggressiveness of the disease, I think, and as you've mentioned, the primary refractory Burkitt is a very aggressive disease. Outside of that, were there any other observations that were made that might help with inclusion, exclusion criteria as you enroll more patients? Sure. Francesco, why don't you address it? Keep in mind one of them was transformed from CLL, which are known to have a very low CD20 expression. Francesco, why don't you address? Yes. So the sample size is too small to really have some real correlation considerations. The only thought that one can elaborate on is what Chen just alluded to, which is that the patient who had a progressive disease within the efficacy evaluable patient, the patient who progressed, actually had a CLL transformed into a grade B-cell lymphoma. CLL and transformed CLL is known to have relatively lower level of CD20. So that might be playing a part in this lack of responsiveness. We don't want to jump to conclusions, though. We don't have enough data to really formalize a correlation between CD20 level and response. That is, since you are asking about possible hypotheses, that is one that we are looking into. Terrific. Thanks for taking the questions and congratulations. Thank you. Thank you. Our next question comes from John Newman with Canaccord Genuity. Hi, guys. Thanks for taking the question, and congrats on really exciting initial data here for off-the-shelf gamma delta T cells. I think it's a really nice surprise and really impressive. Just had two questions. The first one is whether you could give us any color on just qualitatively what type of data we might see in the first half. Then the second question, given that you saw a complete response in a patient that had previously failed an autologous CD19 CAR T, question for Chen, is that a path that you think might be worth pursuing for initial FDA approval? Or will you simply consider that as one of a number of different options? Thanks. Absolutely. Hey, John. Thank you for joining, and great questions. I'll start with the first one. As you know, we're currently enrolling to our dose level 2. The data we expect next year is additional enrollment and data from additional studies in the next future dose levels, as well as starting to generate durability for the patients that are currently in the study ongoing. The patients that are ongoing, as of now, we haven't heard any evidence of a progression in these patients. Stay tuned, and there's more patients and durability data coming in the first half of next year, and we're quite optimistic. Regarding the activity in patients that have progressed on autologous CD19, yeah, there is very significant unmet medical need in these patients. Essentially, they don't have any good alternatives. That opens opportunity for potential accelerated approval. The way we see the future development of ADI-001 is starting a couple of expansion cohorts. One of them is potentially in patients that progressed on autologous CD19 as an accelerated path for approval. In parallel to this, a couple more expansion cohorts that may be pivotal in DLBCL, MCL, and/or follicular lymphoma. We expect multiple expansion cohorts that hopefully will transition to pivotal studies. Okay, great. Thank you. Our next question comes. Yeah, please. Yeah. Yeah, thank you for asking. Our next question comes from Soumit Roy with Jones Trading. Hi. Congratulations on the robust data. I got a question maybe for Dr. Galimi or Dr. Neelapu. From your experience and given this robustness of the data, do you envision possibly fewer earlier line patients to get enrolled or maybe patients with less bulky disease to get enrolled? What has been your experience? Yeah. Why don't we start with Dr. Galimi and then Dr. Neelapu can add more color. Sure. The ongoing trial is enrolling patients who have received at least two prior lines of therapy. With the current protocol language, we only limit the focus to that type of population, essentially a third line and beyond. Within each line of therapy, of course, there are patients with different clinical presentations, and now that we have some form of comfort that this approach can be effective, then we expect an improvement on the, let's say, within a certain line of therapy, earlier patients are expected to join the trial. Future amendments to the trial and future parallel trials will of course try to move to other populations of patients in earlier lines. Maybe, Sattva, you can offer your view on how this approach might move around in the non-Hodgkin lymphoma indication. Mm. Yes. Thank you, Francesco. Yes, I agree. I think as we see evidence of efficacy, and we've seen now with low dose levels, it instills enthusiasm to move to earlier lines, as well. In the current first 4 patients you saw, they've had 4-5 prior lines of therapy. Given this efficacy that we've seen so far, and we've continued similar results in the other dose levels, there will be a trend. I foresee that patients who are CAR-naive and probably relapsing right after second line might be enrolled as opposed to waiting for 3, 4, 5 lines of therapy. Great. that also leads to newer patients generally who have lower bulk as well. Wonderful. Great. Sure. Just qualitatively, if you can tell us, like, what kind of fold expansion you are seeing in vivo. Are we looking at the range of, like, 30, 50x expansion or more like 200, 300-fold expansion? Sure. Thanks for asking. Perhaps Blake, our CSO can help address. Happy to address what we can there. You know, as previously described, you know, it's quite early, so we're only looking at a handful of data points in the majority of the 30 million dose cohort. Although we'd love to calculate a fold expansion, the reality is there's no real denominator at this point from the initial infusion. All we can say is that the emergence that we are seeing in the second week and really beyond is promising, right? We're going from undetectable to quite highly detectable levels in those initial weeks, based on the few data points that we have today. As much as I'd love to report a fold expansion, all I can say is that it's quite high and again, looks remarkably similar to what is seen in the autologous alpha beta CAR T space with respect to timing, cytokines and where we're seeing these peaks occurring time after administration. Hopefully that's as clear as we can be. Thank you and congratulations again. Absolutely. Thanks for asking. Our last question comes from Justin Zelin with BTIG. Hi, team. Congrats on this impressive data, and it's great to see such successful translation for the program from bench to bedside here. You know, first, given the encouraging safety profile you've seen so far, I was wondering if you can speak to your plans to dose this therapy in an outpatient setting moving forward. Sure. I'm happy to address. I think as we progress and gain confidence with the therapy, it wouldn't be surprising it will start some of the studies and enable dosing in the community setting. We haven't started doing this, but I think that's something that I would not be surprised if it's gonna come in the near future. Great. That's helpful. Maybe a question for Dr. Neelapu. If you could give us some thoughts on how you see ADI-001 fitting into the treatment landscape in non-Hodgkin lymphoma, just given some of the other cell therapies out there, autologous, allogeneic, and NK cells, just how you see the gamma delta approach fitting into the landscape, probably. Sure, absolutely. Dr. Neelapu, why don't you help address? Yeah. I think a couple of points to you know highlight here. The one, ADI-001 targets CD20, which is quite different from most other CAR T products, both autologous and allogeneic, that are currently being evaluated. Majority of them target CD19. And at least in diffuse large B-cell lymphoma as well as mantle cell lymphoma, there's a significant proportion of patients who do relapse with CD19 loss. This addresses a major unmet need for those patients. As you've heard earlier, one path is to use ADI-001 post CD19 CAR T relapse. Quite honestly, if the efficacy is strong and comparable or even higher than CD19 CAR T, it could, you know, be used even prior to CD19 CAR. We had to wait and see what the data looks like. Ultimately I think, you know, CD19 and CD20 CARs are likely to be complementary and improve overall outcomes for these patients. Great. That's really helpful. Congrats again and thanks for taking the questions. Absolutely. Thanks for joining today. Thank you everyone for joining. That concludes today's call. You may now log off.