Good morning, and thank you all for joining us today for our virtual R&D event. I'm Chen Schor, President and CEO of Adicet Bio. We're excited to spend the next hour providing you a deep dive into our pipeline programs. Let's go ahead and get started. As a reminder, we'll be making forward-looking statements today as detailed on this slide. Please refer to the Risk Factors section of our most recent 10-K and subsequent SEC filing for more detail. This call is being recorded. On the call today, I'll provide a quick introduction before handing it over to Dr. Blake Aftab, our Chief Scientific Officer, who will be giving you the bulk of today's presentation. Also joining us today is Dr. Marco Davila, Vice Chair of Cellular Therapies and Senior Vice President and Associate Director of Translational Research from the Roswell Park Comprehensive Cancer Center in Buffalo, New York, who is also a member of our Scientific Advisory Board. Throughout his career, Marco's clinical and bench research programs have focused on developing gene-engineered cell therapies with the goal of identifying optimal therapies for patients. We're pleased to have him join us and provide his unique perspective. Finally, Dr. Francesco Galimi, Chief Medical Officer, and Nick Harvey, Chief Financial Officer, will join us at the end for Q&A. Adicet Bio was founded in 2016, and during the past seven years, with more than $500 million in funding, we focused exclusively on developing gamma delta T cell therapy. We developed a fundamental understanding of the biology of gamma delta T cells and built significant expertise, IP portfolio, know-how, and reproducible and scalable manufacturing capabilities of allogeneic off-the-shelf gamma delta 1 T cell therapies. The data from our ongoing clinical trial of ADI-001 offers the potential for best-in-class clinical profile and outpatient dosing, making ADI-001 potentially available to many patients across non-Hodgkin's lymphoma lines of therapy. Today, we'll be focusing on four new highly differentiated gamma delta T cell therapy for clinical programs, all building on years of expertise, IP, and know-how in gamma delta T cell biology. On slide 6, we turn our attention to Adicet Bio's gamma delta T cell platform. Gamma delta 1 T cell therapies may offer several advantages over alpha beta CAR T, CAR NK, or bispecific approaches. We've now reached a point where every check mark in blue on this slide is supported by either a publication or a poster presentation from a scientific or clinical conference. We believe our gamma delta 1 T cell programs offer the following differentiated profile. One, innate antitumor activity with mostly activating receptors. Two, adaptive antitumor activity. Three, CAR or CAD-mediated antitumor activity. Blake will walk you through our first-in-class CAD program shortly. Four, differentiated tissue tropism and active homing to tumors. Five, significant proliferative capacity. And last but not least, no GvHD and a benign safety profile with no significant incidents of CRS, ICANS, or Grade 3 infection reported to date. Building on these advantages, we developed a pipeline of programs. Why don't we move to slide 7? Let me share with you the high-level pipeline strategy that guided the selection of the 4 programs we will be presenting today. We focus on gamma delta T cells leveraging their innate and adaptive antitumor activity. These are two antitumor mechanism of action as compared to one in the case of alpha beta or NK cell. We engineer our gamma delta T cells to significantly increase their potency. We follow the gamma delta 1 T cell's known tissue residence and infiltration to solid tumors. This increases the exposure of the engineered gamma delta 1 T cells in the target malignant tissue. We armor the cells to enhance their resilient functionality in the solid tumor microenvironment. This is in the case of solid tumor programs. We focus on indication where we believe there is increased probability of success, such as hematological malignancies where ADI-001 established clinical proof of concept, or indications where donor lymphocyte infusion enriched with gamma delta T cells have already shown clinical benefit, or cancers where infiltrating gamma delta T cells correlate with increased overall survival. We believe these pillars may differentiate our programs from other cell types or bispecifics with the potential to address significant unmet medical needs. Turning to slide 8. Today, we'll be focusing on 4 new gamma delta 1 T cell programs that we have unveiled at SITC this week. Moving to slide 9. Let me tell you why I believe our next clinical candidate, ADI-925, has the potential to introduce a fundamental advance in the fields of cell therapy and innate immunity. Our team engineered our gamma delta one T cells to significantly enhance their intrinsic, innate, and adaptive antitumor activity by rewiring signaling pathways in the cell. This means that ADI-925 has the potential to provide significant antitumor activity in multiple hematologic malignancies and solid tumors without a CAR, simply by targeting multiple tumor-stressed antigens defined by evolution to mark malignant cells. As you'll see shortly, this is a potential major advancement in the field of gamma delta T cells, and one that we hope will translate to deep responses in cancer patients. Let's now move to the next slide so Blake can walk you through the data for our preclinical pipeline, starting with our next clinical candidate, ADI-925. Blake? Thanks, Chen, and thank you everyone for joining. Here, we will introduce our preclinical pipeline programs, each representing meaningful steps forward in our evolution as a company and in the development of our unique gamma delta 1 T cell therapy platform into relevant solid tumor indications. Next slide, please. Let's get started by introducing a brand-new class of engineered gamma delta T cells in our ADI-925 program on slide 12. ADI-925 represents the introduction of a novel type of gamma delta T cell engineering that we call chimeric adapter technology, or CAd for short. Gamma delta T cells have long been associated with well-reported tumor surveillance and survival benefits across many cancer types, and we are quite excited by what this program may represent in unlocking best-in-class potential for a naturally targeted gamma delta T cell product candidate. With the introduction of CAD molecules, ADI-925 has essentially boosted the targeting of tumor stress antigens like MICA, MICB, and ULBP 1, 2, 3, 4, 5, and 6, using naturally present innate and adaptive tumor surveillance mechanisms, albeit with significantly enhanced antitumor function in ADI-925. It is important to note that this technology has been developed completely in-house, and as such, we have broadly patented the underlying technology across many potential uses and combinations. Before we jump into the data, let's take a look at exactly what CADs are on Slide 13. To describe more clearly what we have done here, let's look at the CARs that most are familiar with, shown here in green. Like in ADI-001, these CARs are engineered with an extracellular binding domain that introduces new targeting and redirects the T cell to new antigens, like CD20, for example. You'll see that upon binding these antigens, the signal is transduced to activate two different engineered costimulatory domains that drive antitumor targeting. These CARs and the engineered domains function to increase cellular potency of the T cells against tumors. This antigen activation is also complemented by the additional targeting of the T cell receptors and innate receptors that are built into the gamma delta T cell. Before we move on to chimeric adapters, we must next look at these built-in innate receptors, like NKG2D, shown here in gray. These receptors recognize a long list of eight or more stress antigens that are naturally used for the purposes of tumor surveillance. Under normal conditions, recognition of these stress antigens and subsequent tumor targeting is conveyed to the gamma delta T cell via a signaling adapter called DAP10, shown here in purple. This drives the natural innate pathway, not only in gamma delta T cells, but also in other innate effector cells. What we have done here with our chimeric adaptor technology is to modify multiple functions within the DAP10 molecule to redirect that signal and amplify it down the same clinically validated engineered pathways that are found on our CARs. Essentially, without any additional extracellular targeting, these CADs are designed to boost the natural targeting of receptors already found on the gamma delta T cells and to significantly enhance the tumor killing achieved through the innate and adaptive activation pathways. With CADs, we have gotten under the hood of these cells and have supercharged their natural function against their familiar targets. Let's move to slide 14. Looking at the expression of these targets like MICA, MICB, and ULBP 1 through 6, they are core to common cancer transformation and tumor-forming events. As such, they are commonly found expressed across a wide variety of oncology indications. On the right, for example, we can see expression of MICA and MICB in solid tumors of interest like breast, lung, ovarian, and renal cell carcinoma, just to name a few, all of which are reported in association with natural presence, residence, and infiltration of gamma delta 1 T cells. Not shown here is standing for ULBP 1 through 6, which also has a broad expression pattern across indications. As clinical correlation studies have established relevance for gamma delta 1 T cells in these same indications, there are a lot of potential applications for a program like ADI-925, which aims to elevate the relevance of these correlations to a potential therapeutic. Turning to slide 15. Given the broad relevance of these targets in cancer, it is not surprising that we see here in blue the enhanced cellular antitumor potency of ADI-925 across a broad set of cancer cell lines. Reminiscent of what we have previously shown for ADI-001 targeting lymphoma cell lines, ADI-925 and the CAD technology significantly enhanced baseline potency for gamma delta 1 T cells, which is shown in red. Consistent with the designed mechanism for enhancement with CADs, blocking experiments here on the right support that this enhancement is specific to activation of innate receptors like NKG2D. On slide 16, transitioning to some examples in hepatocellular carcinoma, we can see on the left in blue that over time, the targeting of these cancer cells by ADI-925 is quite durable, and the overall cellular potency from natural targeting alone can now achieve activity comparable to that of targeted CARs, shown in green. It goes without saying that this cellular potency translates to potent efficacy in solid tumor models. For example, shown on the right in blue. What's more intriguing for both ADI-925 and our platform as a whole, is what we see occurring inside these tumor models as this efficacy develops. On slide 17, tracking these cells in vivo over time, we observed some interesting characteristics that we believe are hallmarks of ADI-925 and the larger gamma delta T cell platform. On the left, following a single injection, these cells bio-distribute and home to multiple tissues and can also be seen to a lower extent in whole blood over the first week or so. After this period of homing, we can appreciate three different behaviors. In blue, we see expansion at the site of action in the tumor. On the right, this expansion was coupled to specific proliferation of ADI-925. In other solid tissues with these data, we see our gamma delta T cells take up residence with more stable levels over time. While at the same time in blood, we have seen a more rapid distribution out of this compartment and a return to undetectable levels by day 14. We believe that this example serves as a potential window into the unique tropism of our gamma delta 1 T cell platform that is retained in ADI-925, while it exerts broad antitumor activity in these solid tumor models. Moving on to slide 18. Let's put ADI-925 in context here. Simply put, we believe that with a CAD on board, ADI-925 provides unparalleled potential for the natural targeting by gamma delta 1 T cells against multiple tumor-associated stress antigens that are relevant across multiple indications. When this is coupled with the requisite tissue homing, tumor infiltration, marked cell expansion, and other characteristics of the gamma delta 1 T cell, we believe ADI-925 provides an innovative and compelling program to advance to the clinic, and we look forward to filing an IND for this program in the second half of 2023. Let's now turn back to the pipeline on the next slide. Moving on to our deepening CAR-T portfolio. Let's take a look at our newly created approach to targeting CD70 at Adicet, starting with slide 20. Approaches to targeting CD70 to date have seen limited response rates, due largely to narrow mechanisms of action that do not address tumor heterogeneity and which rely on potentially suboptimal antibody-based targeting. Additionally, these approaches generally lack tissue-specific tropism in targeted indications like renal cell carcinoma. For ADCs here, payload-associated toxicities exist. For this program, we believe we have formulated a compelling approach that addresses all of these opportunities in the current landscape. Let's turn to slide 21. We have focused on addressing these opportunities head on as we approach this target at Adicet. By first addressing the previous use of suboptimal FCs, here we are focused on harnessing the most sensitive means for CD70 targeted engagement. This is found in its natural biological ligand, CD27. We have specifically designed our CAR to use components of CD27 to bind to CD70 with an extraordinary level of specificity and sensitivity. Second, to address tumor heterogeneity and homing to sites of action, we have chosen this target and the related indications specifically to leverage the innate and adaptive mechanisms inherently present on gamma delta 1 T cells, and the natural homing of these cells that are associated with infiltration in these same tissues. For AML and in renal cell carcinoma, the same relevant indications for CD70 expression, the natural presence of gamma delta one T cells here is associated with survival benefits. Third, we are addressing presence of potentially immunosuppressive tumor microenvironments. Here, we have included an engineered dominant negative receptor to reinforce a more resilient mechanism for attacking the tumor in the face of immunosuppressive factors like TGF beta, which is also associated with advanced forms of disease. Together, we have formulated a highly active program and are in late stages of preclinical development. Before we look at the activity of this program on slide 22, let's first address one key hurdle in targeting this antigen. CD70 expression is largely restricted to cancer. However, it can also be found in some subsets of normal lymphocytes. When targeting CD70 with T cells, some consideration must be spent on whether this targeting is resulting in the cells turning on itself, a process we refer to as fratricide. Here on the left, we show preclinical manufacturing data supporting our ability to generate these CAR T cells with a high level of efficiency, and most importantly, with a phenotype that largely resembles our clinically active ADI-001 CAR T cells. On the right, we also see that our yields match that of other CARs that do not carry a similar consideration for potential fratricide. This is a key finding in that it demonstrates that our approach to targeting CD70 and arming our gamma delta 1 T cells in this way does not require highly cumbersome gene editing and antigen deletion steps that other platforms require when attacking this target. Now on slide 23. Moving on to how this works against cancer cells. One of the key benefits to using CD27 to target CD70 is that it is the natural ligand for CD70. Because of this, its binding to CD70 has benefited from honing by evolution and represents an exquisite level of affinity and specificity. This translates to a CAR that is capable of recognizing lower levels of CD70 expression on tumors. On the right, we see that this translated to highly effective killing in a panel of solid tumor cell lines, each expressing a different level of CD70. These are just a few of the reasons that we and others have reported and published on the superiority of this approach for targeting, particularly when compared to other standard CD70 CAR designs that are based on antibodies. Let's move to slide 24. On addressing potentially suppressive tumor microenvironments, we have also turned our attention to aspects of armoring. In this regard, we appreciate that immunosuppressive factors like TGF beta are commonly found at high levels in and around advanced tumors, including those associated with this program. Shown on the left in red and blue, these levels of TGF beta can alter the activation profile in T cells and may subsequently blunt therapeutic potential of cell and immunotherapies in general. Armoring aims to build into our cells a blockade against these alterations and subsequently reinforce resilience of our mechanisms for killing in the face of these factors. Let's move on. To accomplish this, we have introduced armoring with a dominant negative receptor against TGF beta. As seen on slide 26 on the right, we can appreciate that with the introduction of this armoring, our cells now withstand alterations introduced by exposure to TGF beta. On slide 27, the functional consequences of this armoring are presented here in blue, arriving at a product candidate whose tumor targeting is more functionally persistent and that demonstrates a more resilient serial killing capability, even in the presence of this immunosuppressive factor. In solid tumor models of renal cell carcinoma illustrated on slide 28, this translated to clear and durable antitumor activity on the left, and this efficacy can be linked directly to these cells homing to as well as infiltrating and proliferating within solid tumors. This is a core attribute to what we now have seen across much of our gamma delta 1 T cell pipeline. Moving on to slide 29. Based on the data reported here at SITC, we believe we are well on our way here with creating a differentiated cell therapy approach for this target and its indications. Introducing two new firsts here with both the design of our CAR and inclusion of this armoring for the first time in a gamma delta 1 T cell, a cell type whose inherent mechanisms of action and homing may be best suited to address these tumors. Given these data and the activity supporting this program, we're excited by what we have here in a potential clinical candidate. Slide 30. Moving on down the pipeline, we have taken a similar approach with our next program targeting PSMA. Let's move to slide 31. PSMA, or prostate-specific membrane antigen, like its name implies, is a validated target for therapeutics in prostate cancer. In the immunotherapy landscape, although active, cell therapies and bispecifics have been significantly limited by toxicities, demonstrating very narrow therapeutic indices largely due to CRS, ICANS, and macrophage activation syndrome, which are closely linked to mechanisms of action that rely on alpha beta T cells. We believe that our platform is well positioned to go beyond here for reasons that we have already discussed, like aspects of natural homing and infiltration, and multiple mechanisms of action for the gamma delta 1 T cell that associate with survival. These are all also true here for prostate cancer. These considerations, together with data we are gleaning from our own current clinical experience, where we see a decoupling of these CRS-like profiles from clinical responses. We may be best positioned to significantly enhance antitumor activity against this target, and likely without eliciting serious CRS and ICANS that are found in current alpha beta and bispecific approaches. Next slide, please. To make this happen, we have turned our focus onto engineering a CAR that is best suited to engage this target, which has heterogeneous expression in this disease. Also, calling back to what we saw with our previous program, we have included here the dominant negative armoring approach against TGF beta, which has been clinically explored before on the back of CRS-associated alpha beta CAR T cells. Again, this is a specific area of safety where we believe we have a key advantage. Slide 33, please. Focusing on our novel CAR, we conducted a screening campaign of over 90 novel CAR binders to achieve specific criteria that we believe are critical to making further inroads on this target. We have arrived at a lead molecule that demonstrated efficient activation and function and tailored recognition against specific biologically relevant conformations of this target. Most importantly, using these criteria, we have developed a CAR that retained activity against heterogenic PSMA expression patterns. This compares favorably to a clinically experienced benchmark that we can use for bridging purposes on our data. With this, the 22Rv1 prostate cancer model serves as a surrogate for intermediate and heterogenic PSMA expression. For both cell killing and T cell proliferation illustrates this differentiation for our lead CAR. Slide 34, please. Coupling this CAR to armoring with the same dominant negative receptor for TGF beta that we previously presented, we can similarly arrive at a product candidate shown in blue, whose tumor targeting is more functionally persistent and that demonstrated more resilient serial killing capabilities in the presence of this immunosuppressive factor. On slide 35 on the left, in the solid tumor setting, specifically looking at this highly challenging model of 22RV1 prostate cancer, again challenging due to both issues of intermediate and heterogeneous PSMA target expression, a single dose of our armored lead had profound antitumor activity in this setting, shown in brown on the right. All in all, given the data presented at SITC and the underlying clinical experience supporting the potential safety of our platform, we look forward to advancing this program into prostate cancer, representing another solid tumor where gamma delta biology is highly relevant. Moving on to slide 36. The last pipeline program that we'll cover today is one of our earlier programs, here representing a potentially first-in-class CAR T program targeting B7H6. Slide 37, please. B7H6 is a member of the B7 family that is well-characterized for its role in innate immunosurveillance of tumors. It is also the subject of active early clinical development with a few modalities. Building on the same themes for our overarching pipeline strategy, B7H6 is highly expressed in colorectal and GI cancers, a tissue microenvironment that is defined by the presence of gamma delta 1 T cell subsets, and again, an area where this is closely coupled to favorable survival. Together, the novelty of this target, the specific characteristics of the gamma delta 1 T cell, and its tissue residence in these diseases form a unique, potentially differentiated approach to this target and its indications. Slide 38, please. For this program, we similarly are developing a set of lead CAR molecules that focus on obtaining critical characteristics that are important and potentially differentiating for targeting B7H6. In this case, antigen shedding is a key consideration in this design. We also anticipate armoring for the eventual clinical candidate, and we have demonstrated the function of TGF beta dominant negative receptor in the SITC data presented today as an example. Given the earlier status of this program and the potential for iteration here, we have the benefit of exploring additional degrees of freedom for armoring beyond this, whether that be with receptor modification or via use of stimulatory cytokines. Definitely more to come in this regard. On slide 39, like we have seen previously, when developing a CAR, we start from the ground up and focus heavily on the nuances of the molecule that we are targeting. Here on the left, circled in blue, we've arrived at a set of CARs that can convey active cytotoxicity across a physiologically relevant range of target expression. More critically, one of the many goals of our discovery campaign was to strategize our screen to enrich for binders that could retain activity against tumors in the presence of shed B7H6 antigen. On the right, circled in blue, we have achieved many examples of this and have a lead set whose cytotoxicity is more resilient to interference by shed antigen compared to a relevant benchmark, circled in red. On slide 40, we have honed in on leads that demonstrated improved polyfunctional killing capabilities, as illustrated on the left. We see encouraging activity in vivo with these early lead CARs that elicited complete tumor growth inhibition in solid tumor models, illustrated on the right. Early days for this program, but we are already encouraged by the seeds that we are sowing here to yield a future clinical candidate, which we anticipate we will define following selection and preclinical validation of an additional armoring approach. Next slide. Let's summarize what we've done here. Slide 42, please. Today, we have delivered key details supporting four of our six wholly owned preclinical pipeline programs. What we have shaped here supports our multi-pronged approach to bring our platform deeper into the solid tumor landscape, a particular area where we believe significant potential exists for our therapies. This is in addition to ADI-001, where we believe we already have the potential for a best-in-class therapy. Overall, 2022 has been a fantastic year for our science at Adicet. On top of the clinical progress, publications for ADI-001 and ADI-002 were both independently awarded as Best of the Year by leading immunotherapy journals and societies, with those awards being received here at SITC and separately next month at ASI in Melbourne. These recognized results and the progress here are a testament to the quality of our team at Adicet. It is a true pleasure to be able to share that progress today. Chen, back to you with slide 43. Thanks, Blake. I'll now invite Dr. Marco Davila to join us for a discussion on the pipeline we've just presented. Marco, thank you for joining us today. Thanks, Chen. Happy to be here today. Let's jump right into our discussion, starting on slide 44. Marco, can you share your preliminary thoughts on the pipeline we presented today? What do these engineered gamma delta 1 T cell programs offer? The pipeline of programs presented today have the potential to bring the unique benefits of gamma delta 1 T cells to several solid tumor indications. We know from their biology that gamma delta 1 T cells have great potential for making inroads against solid tumors, and the pipeline here clearly emphasizes a focus on bringing these programs to bear across multiple solid tumor indications. The engineered gamma delta 1 T cell approach may address many of the limitations seen to date with alternative T and NK cell types, providing innate and adaptive anti-tumor activity that addresses tumor heterogeneity while limiting CRS and ICANS toxicities with reduced activation profiles for problematic cytokines and preferential distribution to solid tissues. Additionally, the engineering for all these programs is thoughtfully designed and executed against the targets of interest. All these factors open the possibility for achieving clinically meaningful activity where alpha-beta T cells, NK cells, and bispecifics have been limited. I'm quite excited about these programs and what they may hold for clinicians and the patients we treat. Thanks, Marco. Moving to slide 45 with our next question. Marco, can you share your thoughts on ADI-925 and the chimeric adaptor technology? I find the chimeric adapter in ADI-925 represents the most compelling and disruptive approach for gamma delta T cell therapies. The chimeric adapter is one of the first examples of rewiring the function of gamma delta T cells. The innate and the adaptive anti-tumor activity for ADI-925 is significantly enhanced and is broadly applicable across a variety of cancers. The field of early non-CAR gamma delta T cell infusion products is starting to introduce interesting clinical signs. We know that the potency for these unmodified early infusion products is limited compared to their engineered counterparts. Adicet has positioned this program to unlock and enhance the true potential for gamma delta T cell infusion therapy well beyond the emerging clinical signals. I would personally like to have a product like this for patients that offers an off-the-shelf solution, somewhat agnostic to their individual tumor type. ADI-925 has the potential to be that solution and to make significant advances beyond what is currently available in AML and solid tumors. Thank you, Marco. Perhaps we can move to our final question on slide 46. Marco, looking at the ARMOR CD70 and the PSMA program, can you provide your perspectives in the context of previous approaches to these targets? Sure. Both CD70 and PSMA are well-validated and are associated with either approved agents or clinical activity. Unfortunately, alpha beta T cells, bispecifics, and other biologics do not have tissue-specific tropism to tumor lesions, are highly limited in their dosing due to severe CRS and ICANS, and do not have multiple mechanisms for anti-tumor activity to address target heterogeneity. For Adicet’s programs, both are founded first on well-designed and executed novel targeting molecules. For CD70, the use of CD27 components offers greater sensitivity across the range of target expression, potentially further raising the bar for resistance. For PSMA, the CAR that has been selected demonstrates significantly increased potency and sensitivity to heterogeneous target expression. Simply said, these are better mousetraps. Across the programs, gamma delta T cells can potentially advance well beyond the limitation of other effector cell types. The clinical experience of these programs may redefine our expectation for treating solid tumors. Thank you, Marco, for joining us on the call today and providing your perspective. Let's move to the next slide. We're extremely excited about the pipeline we've developed and have some exciting milestones ahead. Let's move to slide 48. Let me now briefly talk about the next steps for the ADI-001 program. In particular, we'll be presenting additional clinical data from our ongoing phase I clinical study of ADI-001 in relapsed refractory aggressive B cell NHL at the upcoming ASH meeting. Adicet also plans to host a webcast featuring Dr. Sattva Neelapu, professor in the Department of Lymphoma and Myeloma at the University of Texas MD Anderson Cancer Center, on Sunday, December eleventh, at 8 A.M. Central Time or 9 A.M. Eastern, to discuss the updated data. This IR event will include clinical data from a data cut to be conducted during the next few weeks. We hope you can attend this virtual event. As we look to ASH, we thought it would be useful to provide a summary of the CR rates achieved by advanced therapies for aggressive NHL. Let's move to slide 49. The question many people may ask is, how do we know if a therapy may offer advantages over existing approaches? Let's start with third-line DLBCL. Several autologous CD19 alpha beta CAR T cell therapies have been approved by the FDA. The CR rate on month one is approximately 60%, going down to approximately 43% CR rate on month three, and then to approximately 30% CR rate. The six-month CR rate tends to be a pretty flat curve in the case of autologous CAR T. Unfortunately, approximately 70% of patients that receive autologous CD19 CAR T will progress during the first six months, and there is no approved therapy for these patients who have a median survival of about six months. One class of investigational products that have demonstrated a clinical benefit in this patient population is the CD20, CD3 bispecifics. On slide SITC, you'll see that the bispecifics have demonstrated a CR rate of approximately 34% in patients progressing on autologous CD19 CAR T. This CR rate is estimated to go down to approximately 20% following six months, which is likely best case, assuming comparable durability curve of the bispecifics to autologous CAR T. In terms of safety data, the autologous CAR T product has a relatively high rate of grade 3 CRS and ICANS, and the bispecifics have a medium rate. generally, when we look at new investigational therapies that strive to become potentially best in class, assuming comparable safety and ignoring access issues, we want a new therapy to show a CR rate comparable or to the right of the red graph in the case of third line DLBCL, or comparable or to the right of the orange graph in the case of post-CAR T patients. We're excited about the potential of ADI-001 and look forward to sharing another look at the data in December. As you can see on slide SITC-1, we've got a number of exciting upcoming milestones related to ADI-001 in our new pipeline programs. With $282 million in cash and cash equivalents as of September 30, 2022, we're well-financed into the first half of 2025 and look forward to achieving many milestones along the way. In the interest of time, I'll close by saying that we're very excited about the programs we discussed and ADI-001 and look forward to taking your questions. Operator? At this time, I would like to remind everyone to ask a question, press one then star on your telephone keypad. Our first question comes from Asthika Goonewardene with Truist. Hey, Asthika. How are you? Uh- Operator, can you open up Asthika's line, please? Asthika's line is open. Okay. Hey, Asthika. Good morning. How are you? She's not responding at the moment. We can move on to the next question. Brian Cheng with JP Morgan. Okay. Hey, guys. Hey, Brian. Hey, Chen, how are you? Thanks for taking my question. Thanks for doing this R&D day. We have a couple, first on 925. Can you provide a little bit more color on the variability of the targeted stress ligands? 'Cause it seems that on slide 14, you have kind of laid out the groundwork that these ligands are pretty much expressed in a couple of indications. Follow on that is, how do you think about prioritizing which cancer types to target next? Which one do you think has the highest conviction based on the data from today? Yeah. Perfect. Hey, great question. Blake, why don't you address the first part of the question and regarding the clinical applications that Francesco can help address. Blake, why don't you start? Yeah. Let's start with the targeting and what we see pre-clinically. Of course, you know, the zinc finger receptors with, you know, eight or more antigen specificities, how that manifests pre-clinically, we see a lot of activity across broad cell lines representing actually a quite wide array of indications. That activity is retained regardless of which of those antigens in particular are expressed. With low MICA and MICB, high ULBP 6, 1 through 6, we have, you know, quite robust activity. On counter to that, high MICA, MICB, low ULBP 1 through 6, we also have activity. I would just say broad range across the, expression patterns for all eight or more antigens. Francesco, you wanna cover on the indications? Sure. For the selection of the indications, the first-in-human plan will include essentially two parts, one in hematology and one in solid tumor oncology. For hematology, our main focus is going to be AML. It's an indication that we consider will be our proof of concept, if you will, in hematology. There is a relatively robust rationale to support the expectation the gamma delta ones with this particular configuration will deliver antitumor efficacy in that population. For the solid tumor part of the plan, we are prioritizing indications based on the expression of the stress molecules in tumor tissue, and based on the presence of gamma delta infiltrates in those tumor samples and the fact that the gamma delta infiltrate carries prognostic value. With this criteria in mind, we're currently we haven't defined and finalized the list yet, but we are looking with interest at particular four indications, hepatocellular carcinoma, triple-negative breast cancer, cervical cancer, and Merkel cell carcinoma. Mm-hmm. Brian, just to add a little bit of color, what Blake and Francesco outlined is really consistent with our strategy. Essentially, we follow the gamma delta-one tissue tropism to where they go. We try to focus on these type of indications, and we prioritize those indications where we believe that gamma delta-one should provide benefits based on either published literature regarding the connection between gamma delta-one and overall survival or indications in hematology, where there is established proof of concept either with ADI-001 or with the donor lymphocyte infusions that were enriched with gamma delta T cells that have already showed some benefit. We're trying to improve the probability of success and the benefits to patients using this strategy. Got it. Maybe just to follow up on 925 as well. You know, it seems that there are some of the cells also homing in liver, lung, and bone marrow, just looking at slide 17. Can you give us a sense of the potential safety implication? Can you remind us how this compares to the ADI-001 just on the homing ability? Thanks. Sure. Absolutely. Blake, why don't you take that one? Yeah. You know, why don't we focus on the homing in general across the platform, maybe starting from the last part. You know, across these programs for ADI-001, ADI-925, we saw some data for even the CD70 program. That homing is seen across the entire platform, and we attribute that to the fundamental benefits of gamma delta 1 T cell platform. Specific on ADI-925, you know, look, we're really first out with a modification like this, so we have to look at two different areas to read through the potential safety considerations or toxicities. One would be the gamma delta T cell infusion dataset, clinical evidence for that, as well as our own clinical experience with ADI-001. I think we've shown and others have seen a quite benign profile with respect to safety considerations for the gamma delta in the allogeneic setting. You know, I think that reads through quite well. Outside of the world of gamma delta, I think the closest programs that I could say relates to this based on the NKG2D mechanism would be the NKG2D CAR T programs. Those had, you know, fairly significant safety considerations as those translated from preclinical to clinical. Many of those just haven't manifested in the early phase 1 programs that have been reported to date. I think the safety of the NKG2D CARs and fundamentally the safety that we're seeing in our own CAR modified gamma deltas and the wider allogeneic infusion product landscape reads through well to this program. Great. Thanks so much. Operator, next question. Oh, thanks. Perfect. Yeah. Operator, next question. Our next question comes from Michael Schmidt with Guggenheim Securities. Wonderful. Hey, Michael. Good morning. Hey. Hey, this is Kelsey on for Michael. Good morning, and thanks for taking our question. Sure. Hey, Kelsey. Hey, congrats on the exciting pipeline. We just had a couple. Maybe for 925 and then CD70, B7H6 programs, I guess kind of building on that last question, but based on the natural homing that you see and that you've shown, I guess how do you guys kind of think about potential efficacy in heme versus solid tumors? And then kind of bigger picture, how do you think about the dose, the dosing schedule, and lymphodepletion regimens for solid tumors? Do you think that it would be similar or different from what you've used, for example, in the 001 program? Thanks so much. Yeah. Let me start addressing, and then I'll open it to Blake and Francesco if they wanna add additional background here. In terms of the indications, when you think about nine-two-five or CD70, indeed both of them have indications in hematology, which we like because we believe they are significantly de-risked by the data with ADI-001 and donor lymphocyte infusions. That's in terms of hematology. In terms of solid tumors, each of them essentially we follow the gamma delta-1 tissue tropism. Then the way to increase the potency once we get to the tumor is different between nine-two-five and CD70. In the case of nine-two-five, we essentially let the cytotoxicity, the innate and adaptive cytotoxicity of the gamma delta T cells play a much more significant role using the CAR technology. In the case of CD70, we use this via the CAR. In terms of doses for solid tumors and the lymphodepletion regimens, we haven't guided yet. It's a little premature. We do expect to start clinical study for ADI-925 in the second half of next year. As Francesco mentioned, it should include a hemo arm as well as a solid tumor arm. You know, at the right point in time, we'll update more specifics once the protocol is finalized. I'm looking at Blake and Francesco, if you have anything to add here. You know, maybe just incrementally, I think slide 13 really looks at the way that we approach targeting as a whole, right? We have CARs, fundamentally, they add new targeting to the platform. I think we're already experiencing, you know, what can be done there with ADI-001 by adding CD20 antigen targeting to our already active platform. Next, we have these CADs, and again that's more to enhance the endogenous targeting and elevate the potency of that targeting to that that can be achieved similar to a CAR using the same exact activation programs in 4-1BB and CD3 zeta. You know, with 925 and CD70, just to kind of going back to your question, I think you've highlighted the, you know, both the differentiation and the unification of those approaches. Does that help? Yeah. Yeah. Regarding the clinical plan, if I may add one comment. In the heme and solid tumor part of the first in human plan, it's possible we haven't finalized the details yet, but it's possible that we might end up with slightly different regimens in the two parts of the plan for 925, for example. We don't know yet. What I can report is that we're getting a lot of traction, a lot of collaboration and interest from clinical sites across both U.S. and Europe. Yeah, when you think about it, just to add one comment on 925, because we are very excited about 925. When you think about solid tumors, we have all these therapies, you know, targeted therapies, which, you know, in some cases they do a great job debulking the tumor. You know, unfortunately these tumors are smart. Many of them express stress antigens and guess what? They grow back. For the first time, we have a cell therapy that goes to the right tissue, goes after stress antigen, and, you know, provides potentially excellent cytotoxicity at the site of action. We're very excited about the ADI-925 program. Great. Thank you so much. Awesome. Our next question comes from Ren Benjamin with JMP Securities. Sure. Hey, Reni, how are you? Hey. Hey, good morning, Chen Schor and team. Hey, Ren. Thanks very much for taking the questions. Can you hear me okay? Yeah, yeah. Go ahead. Oh, good. Okay. A couple of questions. Maybe just starting off, you had mentioned bispecifics in your talk. Now at this society and we know from other companies in our coverage, there is now those that are targeting or making bispecific gamma delta T cells bispecific antibodies and going after similar targets, for example, PSMA. I'm kind of curious is that as you evaluate the landscape and as you're seeing these other platforms evolve and try to take advantage of what you guys have been generating, how you're viewing that and where it ultimately could fit. Yeah. Just as an extension to that, I know it didn't seem like we talked about it in some of the slides here, but how are you thinking about for any of these new programs, especially in solid tumors, the potential for combining with other therapies? Yeah, absolutely. Great question. Let me start addressing and again, Blake and Francesco might add. Let's start with the bispecifics and gamma delta. Not all gamma deltas are created equal. At Adicet we developed biologics that can expand any type of gamma delta, gamma delta one, gamma delta two. If you want gamma delta one and two, just please delineate, you know, what's the ratios that you need. We could have gone to bispecifics. We compared gamma delta one versus gamma delta two. We found a couple of key advantages with the gamma delta one. Better cytotoxicity, much more significant proliferative capacity with less exhaustion and homing to tissue. If you understand that, then the question is, if gamma delta one is the superior cell type, what is the best way to provide benefits to patients? Keep in mind that in the circulation, because gamma delta ones are, you know, about 1%-3% of the CD3 expressing cells, most of them, as we know, are in the tissues. If you go with a bispecific approach, you're starting from a small number and, you know, it might not be as beneficial as one would wish, versus if you go with, essentially our approach with allogeneic, you take gamma delta ones in the right numbers that have great fitness, and you provide it to a patient who, whose immune system to begin with was probably suboptimal. So, you know, there's room for everybody, but we believe that the approach that we've taken with the cell therapies and the and gamma delta ones specifically might play out favorably, when you compare to the bispecific family. Regarding a combination, you know, starting with ADI-001, when you look at the clinical activity, I'm not sure if at this point combination is a part of our strategy. When we think about the solid tumors, I think it's premature to think about the combination. We're gonna start obviously with monotherapy. If there is a potential benefit in, you know, combination, we could always consider it either by combining or by engineering ourselves to eliminate the need for a combination. That's how we think about it, but it's probably a little premature to think about the combination. I'm gonna look at Blake and Francesco, if you have anything. Okay, sounds good. Perfect. Let me just follow up with one question on manufacturing, because you have. Mm-hmm. You know, quite a few, you know, I don't wanna call it edits, but clearly enhancements. Can you- Mm-hmm. Can you kind of just take us through or remind us here about the manufacturing, especially with these new products that are, you know, coming online, how much more complicated it is? You know, what kind of what's involved? Are you still doing this manufacturing, you know, in-house or will it ultimately, you know, be brought in-house? Sure. I'll address it, and then I think we'll let Kelly ask a question or two. Absolutely. In terms of the manufacturing, we have the ability to manufacture in-house for early clinical development, and we have two CDMOs that we can potentially work with for manufacturing for late stage clinical studies as well as for early stage clinical studies. Before we declare a clinical candidate, we have very strict criteria for the manufacturability of our programs. For ADI-001, as an example, you know, we have great manufacturing capacity, and we're preparing for the pivotal studies. This is the case for ADI-925, and I'm sure this will be the case for the rest of the program. I would say we have quite good manufacturing capability, and I'm reasonably optimistic about the potential here. Anything you wanna add here? Yeah. I'll just add, you know, on the notion of additional manufacturing, you know, complexities associated with individual pipeline. Fundamentally, these are all meant to leverage the same established processes that we have for ADI-001 manufacture. No program that we presented today represents any deviation from the established process using the same vector platforms and general manufacturing that we've already established. Kelly, why don't you go next? Thanks for taking the question. Absolutely. Thank you. Our last question comes from Kelly Shi with Jefferies. Same vector platforms and general manufacturing that we've already established. Kelly, why don't you go next? Thanks for taking the question. Absolutely. I'm not sure that we hear what's happening, but operator, can you? I think that is clearly not Kelly, but I think that maybe with that, we should just go ahead and close down the call. Thank you all so much for joining today. If you have any questions, please reach out to the company. Hello? Hello. Hello. Hi. Who's this? Hi. This is Dave from Kelly Shi. I'm sorry. I realized that. No, no problem. You're right under the wire. Go ahead and ask your question. Shoot. A couple from me. One is, can you discuss any toxicity that you anticipate from the new CAd design? Building on the previous question on manufacturing, do you see any significant difference in terms of expansion when we compare the manufacturing with ADI-001? Yeah. Blake, why don't you address it? We kind of addressed it in a prior question. Yeah. Just to recap, right? Do you see any significant difference in terms of expansion when we compare the? Hey, Jeffrey, sorry. I think you have to mute your line. If you can mute your line. I think the webcast is just coming through a little later. We kind of addressed it in a prior question. Yeah. We'll address his question, and then I think we'll. If there's any other questions, please approach the company, and we're absolutely happy to address them by separate phone or Zoom. Blake, why don't you address this one? Just to recap on the first question we received. For ADI-925, based on the mechanism. If there's any- I think with that, thanks everybody for joining us today. If you have any questions, please reach out to the company. Thanks, everybody.