Hello, and welcome to the Senti Biosciences Senti 202 Clinical Update Conference Call and Webcast. As a brief reminder, all participants are currently in a listen-only mode. If anyone requires operator assistance during the event, please press star zero on your telephone keypad. Following the presentation, there'll be a question-and-answer session. Note that this webcast is being recorded at the company's request, and a replay will be made available on the company's website following the end of the event. At this time, I'd like to remind our listeners that remarks made during the webcast may state management's intentions, beliefs, expectations, or future projections. These are forward-looking statements and involve risks and uncertainties. Forward-looking statements on this call are made pursuant to the safe harbor provisions of the federal securities laws and are based on Senti Biosciences' current expectations, and actual results could differ materially. As a result, you should not place undue reliance on any forward-looking statements. Some of the factors that could cause actual results to differ materially from those contemplated by such forward-looking statements are discussed in the periodic report Senti Bio files with the Securities and Exchange Commission. These documents are available in the investor section of the company's website and on the Securities and Exchange Commission's website. We encourage you to review these documents carefully. Additionally, certain information contained in this webcast relates to or is based on studies, publications, surveys, and other data obtained from third-party sources and the company's own estimates and research. While the company believes these third-party sources to be reliable as to the date of this presentation, it is not independently verified and makes no representation as to the adequacy, fairness, accuracy, or completeness of, or that any independent source has verified any information obtained from third-party sources. Joining us on today's call are Dr. Timothy Lu, Chief Executive Officer and Co-founder, and Dr. Kanya Rajangam, President, Head of R&D and Chief Medical Officer from the Senti Bio leadership team, and Dr. Nosha Farhadfar, Hematologist and Bone Marrow Transplant Physician, Sarah Cannon Transplant and Cellular Therapy Program at Methodist Hospital. I would now like to turn the call over to Dr. Lu. Doctor, please proceed. Good morning. Senti was founded on the idea of transforming the treatment of diseases with high imminent need through the use of gene circuits in powerful new cell and gene therapies. I'm excited to report today that we've realized that vision through updated, promising results from our ongoing phase 1 trial for Senti 202 in the treatment of relapsed refractory AML. Next slide. Today, we will be making some forward-looking statements. Next slide. So on the agenda today, Dr. Nosha Farhadfar will give us an overview of AML and the role that Senti 202 can play in AML treatment. Dr. Kanya Rajangam will give us a detailed presentation on the Senti 202 clinical trial results themselves. Next slide. I will start by giving an introduction on Senti, as well as our logic-gated pipeline of cell therapies, and a detailed description of how Senti 202 is designed and how it works. Next slide. Senti has developed an exciting pipeline of logic-gated cell therapies that have the potential to achieve superior performance in the treatment of cancers with high unmet needs. Our logic gates work in both NK cells and T cells, and ultimately, we believe in choosing the right cell type for the right indication. What the logic gates do is they solve a central challenge in the treatment of cancer: how to selectively kill cancer cells while preventing toxicity. Existing cell therapies and biologic drugs, including antibody drug conjugates and T cell engagers, have traditionally relied on identifying a single target that must be cleanly expressed on the cancer cells and not on the healthy cells in order to give them sufficient selectivity to achieve the efficacy desired. If such a target cannot be found, killing of both cancer cells and healthy cells will happen, thus limiting the ultimate therapeutic window and restricting the indications that can be expressed with these existing drugs. In contrast, Senti's logic-gated approach allows us to go after cancer indications where such clean targets don't exist, and therefore existing modalities are unable to address. Our logic gates essentially contain two elements. The first element recognizes one or more cancer targets through what we call an OR gate, and the engagement of either of those cancer targets will trigger potent killing of the cancer cells. The second element of our logic gate is implemented through something called a NOT gate, which essentially recognizes healthy cell targets and protects those healthy cells from being killed. This logic gate technology opens up major commercial opportunities in oncology therapies' indications that are not adequately treated today. Next slide. Today, we will focus on Senti 202 specifically. Senti 202 is a first-in-class off-the-shelf logic-gated CD33 or FLT3 NOT endomucin CAR-NK cell therapy. I'm excited to report that we have achieved further clinical proof of concept with this product in our ongoing phase 1 trial, now with 20 relapsed refractory AML patients. Earlier this year, we confirmed our recommended phase 2 dose, and we are continuing to see a high rate of deep and durable responses in heavily pretreated relapsed refractory AML patients, which differentiates Senti 202 from current drugs used in this population. This includes a 50% overall response rate and a 42% CR/CRh rate at the recommended phase 2 dose. These responses are durable, with estimated median duration of composite CR being 7.6 months. Importantly, Senti 202 achieves high MRD negative rates. For example, 100% of our complete remission patients were MRD negative. MRD stands for measurable residual disease, and a negative MRD outcome is associated with significant clinical benefits. Senti 202 has an excellent safety profile, supporting the potential for outpatient dosing. In detailed correlative analyses on these patients, we've confirmed that the logic gates in Senti 202 worked as designed. Specifically, the mechanism of action of selective killing of both AML blasts and leukemic stem cells, along with sparing or enrichment of healthy cells, was observed in our responding patients. In addition, we're excited to report that based on clinical data, Senti 202 has received the FDA's Regenerative Medicine Advanced Therapy designation, also known as RMAT. Earlier this year, Senti 202 also received Orphan Drug designation. These designations provide tangible benefits of working closely with the FDA to receive guidance on generating the data needed to support Senti 202 approval in an efficient manner. In summary, the data we are reporting today support the potential for rapidly advancing Senti 202 into a pivotal study for relapsed refractory AML, as well as potential expansion into other indications such as newly diagnosed AML, pediatric AML, and myelodysplastic syndrome. Senti 202 has a differentiated mechanism of action compared with the targeted therapies or chemotherapies currently used in AML, and is continuing to demonstrate deep, durable, and MRD negative responses. This data also continues to validate our logic gate technology more broadly, which can be expanded into other cell types, including T cells and in vivo CAR, for additional indications with high unmet needs, such as solid tumors. Next slide. So getting to the design of Senti 202, Senti 202 has three key elements. The first element is an activating CAR, which recognizes CD33 or FLT3. These are two well-validated targets in AML and are expressed in over 95% of AML patients. CD33 was chosen because it's predominantly expressed on AML blasts, whereas FLT3 has good expression on leukemic stem cells. And therefore, this activating CAR, which can engage either target and kill, allows us to cover a broader population of AML cells in patients. Now, the challenge with both these targets is that they can be expressed on healthy cells. And so, in order to protect those healthy cells from being killed, including the healthy hematopoietic stem cells, we basically designed an inhibitory CAR or ICAR that recognizes those healthy cells and shuts down the NK cell killing when it encounters those healthy cells. This implements what we call a NOT gate. The way we did this is by identifying a target called EMCN or Endomucin, which is highly expressed on the healthy cells but rarely expressed on the AML cells. Finally, our product expresses something called a calibrated release IL-15, which serves to enhance Senti 202 as well as the host immune system. We've implemented this gene circuit into healthy NK cells from selected adult donors. The selection of NK cells allows us to create this product in an allogeneic fashion and also leverage the fact that NK cells have inherent anti-AML activity on their own. Next slide. Our manufacturing process for Senti 202 is a scalable and off-the-shelf process. We isolate the NK cells from selected adult donors, genetically modify the cells with a single transduction step. We can then expand the cells further and cryopreserve them. When patients come on trial, we can immediately ship out the frozen product to the clinical site, whereby it can be thawed and infused into patients. The choice of this allogeneic off-the-shelf program allows us to deliver product quickly to patients with high unmet needs, especially for patients with relapsed refractory AML that have, unfortunately, a short median survival. This time to delivery is really important. Next slide. In the following presentation, we will be sharing detailed clinical data update on Senti 202 in the relapsed refractory population. Before we get there, I want to mention that we are currently focused on the relapsed refractory AML population, which is estimated to be about 28,000 patients in the U.S. and E.U. But we also believe that Senti 202 may have expansion opportunity into other indications, including the newly diagnosed AML population, which is over 40,000 patients in the U.S. and E.U. And therefore, we believe the potential addressable market for Senti 202 is broad and represents a multi-billion dollar commercial opportunity. Next slide. So now I'd like to introduce Dr. Farhadfar, who is a hematologist and bone marrow transplant physician at Methodist Hospital. Thank you, Tim. In the next few minutes, I'm going to review the current standard approach to managing relapsed refractory AML and the challenges we face in this area, and then highlight how Senti 202, a novel therapy, has the potential to address key unmet needs in this space. As shown in the flow chart here, the first step in management of relapsed refractory AML is to assess whether the patient is eligible for a clinical trial, which should be prioritized whenever possible. Then the key question is whether the patient is a candidate for allogeneic stem cell transplantation, since allotransplant represents the only potentially curative treatment for the majority of the patients. So if you have a few patients who are transplant eligible, treatments usually involve a mutation-agnostic salvage regimen, typically high-intensity chemotherapy such as FLAG-IDA or MEC, often combined with venetoclax. Alternatively, we can use targeted therapy when actionable mutations are present. And once the patient achieves a remission, the patient proceeds to allogeneic transplant as soon as possible. Now, what about patients who are not fit for transplant, which are the majority of the patients? So there is no single standard therapy. Again, clinical trial remains a preferred option with alternatives, including hypomethylating agents with venetoclax, of course, if not previously used. Targeted therapies are used when actionable mutations are present, which patients have actionable mutations in less than 20%-30% of them. When a patient is not a transplant candidate, treatment is typically continued indefinitely until the patient loses response or the patient no longer can tolerate therapy due to toxicities. Despite recent therapeutic advances, patients with relapsed refractory AML continue to have a poor prognosis with a median overall survival of five months. Current therapies yield complete remission rates of only 12%-25% and CR/CRh rates of 20%-35%, underscoring the limited efficacy of available options and the need for better therapies in this space. Next slide, please. So to understand how we measure progress with new treatment, let's briefly look at the ELN 2022 response criteria for relapsed AML. So based on 2022 ELN, a response is defined by bone marrow blasts less than 5%, absence of circulating blasts, or no evidence of extramedullary disease. Once these criteria are met, the response is further categorized based on blood counts, as shown in the table. So we categorize the response to complete remission, complete remission with partial hematologic recovery, complete remission with incomplete hematologic recovery, and MLFS, morphologic leukemia-free state, but no count recovery. We also need to keep in mind in AML, response assessment is not only about reducing blasts and normalizing the blood count, but also about achieving measurable residual disease or MRD negativity. So with today's highly sensitive techniques that we have, we can detect disease down to a level of as low as 10 to the - 4 or even lower, making MRD a critical marker for evaluating depth and durability of the response. So achieving any of these responses that are shown in the table correlates with meaningful clinical benefit, especially if we have the CR or CRh. Achieving the MRD negativity is also very important because it's a predictor of durable response and long-term outcomes. Unfortunately, the current treatments we have for AML not only yield low CR or CRh and low MRD negativity rate, but also lack sensitivity. So the current treatment can damage the normal stem cells, delaying count recovery and causing significant toxicities. So as a result, novel effective treatments with limited on-target off-tumor toxicities are urgently needed. Next slide, please. So how Senti 202 could fit into evolving AML treatment landscape? Well, Senti 202 has a novel mechanism of action. It targets not only leukemic blasts, but also the elusive leukemic stem cells while sparing normal stem cells. Eliminating leukemic stem cells helps achieve MRD negativity and durable remission, while sparing normal stem cells preserves the bone marrow function and decreases the toxicity we see in patients. In Senti 202, a study of 20 patients with relapsed refractory AML, the CR and CRh rates were 40% in a heavily pretreated population. And this is an impressive outcome. More importantly, all patients who had a CR were MRD negative. In the study, we also saw that patients who responded usually responded within one to two cycles of Senti 202. So we can basically make a decision on whether to continue or switch therapy fairly quickly, which helps reduce the need for prolonged treatment and minimize the toxicity. The responses we saw with Senti 202 were durable. The median duration of response was greater than seven months. Another key advantage of Senti 202 is that it is not restricted by mutation status, which means it can benefit a broad range of patients compared to the drugs that have that specifically targeted mutation. Senti 202 also has a favorable safety profile. In a phase 1 study, Senti 202-related adverse events were generally low-grade and manageable, with the most common being grade one to two pyrexia. Based on the preliminary efficacy results and manageable safety profile, Senti 202 has the potential to serve as a standalone therapy in patients not eligible for transplants. Also, the data we have in this study supports sequencing Senti 202 before and after targeted therapy. Since this drug is very well-tolerated with low toxicity, there is also a possibility of combining Senti 202 with standard of care in newly diagnosed AML, as well as maybe even expanding the indication into pediatric AML. To provide a deeper look at the study results and their implication, I'll now hand it over to Dr. Rajangam, who will review the Senti 202 data in more detail. Thank you. Thank you, Dr. Farhadfar. It's my great pleasure to review the results of our ongoing phase 1 trial in patients with AML today. Next slide, please. Senti 202-101 is a multicenter multinational open-label phase 1 trial in patients with relapsed refractory blood cancers. The key eligibility criteria for enrollment into the trial include adult patients between 18 and 75 years of age and an ECOG performance status of zero to one. Patients with relapsed refractory AML or MDS who are CD33 positive by local assessment are eligible for trial entry. Patients with AML must have received one to three prior therapies and must have received targeted agents if they have the addressable mutations. The study design is a standard 3 plus 3 study design with a dose-finding part followed by disease-specific expansion cohorts at the recommended phase 2 dose. We evaluated two dose levels and two dose schedules on the trial, and we anticipated the starting dose level and schedule to be biologically active. Key objectives of the trial include safety, determination of the RP2D for the recommended phase two dose, as well as efficacy for our expansion cohorts, which used the standard ELN 2022 criteria for AML that Dr. Farhadfar just reviewed. Other key objectives include measurement of measurable residual disease or MRD for local protocols, pharmacokinetics or PK, and pharmacodynamics on serial bone marrow samples using CyTOF analyses in collaboration with MD Anderson. Next slide, please. This slide summarizes our phase one dose-finding portion of the trial. On the upper left is a schema depicting the study treatment. All patients received lymphodepletion for five days, comprising of fludarabine and cytarabine or Ara-C, followed by either three weekly doses of Senti 202 at schedule one or five weekly doses or five doses, forgive me, of Senti 202 at schedule two, all given over days 0 to 14. A bone marrow assessment was done on day 28, and a maximum of four cycles was allowed on trial in order to achieve optimal response. The schema on the bottom left shows the nine patients who were initially enrolled in the dose-finding cohort, six of whom received dose level one, three each in schedule one and schedule two, and three patients received dose level two, all three in schedule one, which was determined to be the recommended phase two dose or RP2D. The RP2D determination was based on the fact that no DLTs, Senti 202-related SAEs were observed in any patient at any dose level, and this was accompanied by a numeric increase in efficacy with patients who received dose level two compared to dose level one patients and schedule one compared to schedule two patients. The RP2D was further confirmed by enrolling three additional relapsed refractory AML patients with no DLTs and continued efficacy. Subsequently, the expansion cohort was opened to enroll additional relapsed refractory AML patients. Today, we present clinical data from a total of 20 relapsed refractory AML patients, including 14 at the recommended phase 2 dose and six at the initial dose level one. Next slide, please. This slide summarizes the baseline characteristics of patients who enrolled on trial. The study enrolled a patient population with multiple baseline adverse risk characteristics and poor prognosis. Across the trial, the median age for patients was 49 years. 50% were male and 80% were white. The majority of patients on trial had adverse risk genetics by ELN 2022 criteria. Further, the recommended phase two dose cohort enrolled patients with increased baseline blasts at 45% compared to 21.5% in dose level one and an increased proportion of patients with baseline thrombocytopenia and neutropenia compared to dose level one patients. Next slide, please. This slide summarizes the patient's prior treatment history prior to study entry. In general, patients were heavily pretreated and entered trial a median of one year from their diagnosis, having received a median of two prior lines of therapy. All patients were exposed to chemotherapy, including cytarabine or ARA-C, and 35% of patients had also received fludarabine. Most patients were additionally exposed to anthracycline, venetoclax, and hypomethylating agents. The recommended phase 2 dose cohort enrolled patients who were more heavily pretreated with a median of two prior lines of therapy compared to one for dose level one patients and an increased proportion of patients who entered trial after prior HCT, 43% versus 17%, and more patients refractory to the most recent treatment regimen before trial entry and receiving Senti 202, 79% being refractory to most recent regimen in the RP2D cohort compared to 17% in the dose level one patients. Next slide, please. Overall, on trial, patients received a median of one cycle on treatment, and importantly, no patient discontinued due to an adverse event. In general, the RP2D patients who received a higher dose of Senti 202 generally achieved response sooner and received a median of one cycle of Senti 202 compared to the lower dose level one patients who received a median of two cycles. Next slide, please. Moving on now to safety. This slide summarizes any grade three or higher treatment emergent adverse events or serious adverse events on study, regardless of relationship to Senti 202. The tables summarize all such events that occurred in 10% or greater number of patients on trial. As you can see in the table, the grade three or higher adverse events were predominantly hematologic events, and the SAEs were pneumonia or sepsis in the setting of neutropenia, both consistent with effects of fludarabine/ARA-C chemotherapy in patients with relapsed refractory AML. The hematologic events generally resolved rapidly in patients who achieved CR/CRh with Senti 202. I also want to note that all events listed in this table were assessed as unrelated to Senti 202 by the investigators, except for one patient with events of febrile neutropenia and thrombocytopenia. Next slide, please. Moving on now to adverse events of interest that were assessed as being related to Senti 202. These were predominantly grade one or two pyrexia events that were readily managed with standard of care. The table in the upper left summarizes all such events. They were noted in 35% or seven patients overall on trial. The table in the bottom left provides additional information about the events experienced by these seven patients. These events, as I mentioned, were grade one or two pyrexia in all patients, at times accompanied by either chills, hypertension, or hypoxia. They generally occurred. The onset day for these events was generally on the day of dosing, and they resolved rapidly, typically within 24 hours. They were all not serious, and they were, as I mentioned before, they did resolve rapidly with standard of care. These events are consistent with delayed infusion-related reactions that are typically reported with, that have been reported with NK cell therapies, typically within 24 hours, around eight hours or so after infusion. As shown in the graph on the upper right, cytokines, including IL-6 shown in the graph here, were generally not elevated on trial, including in patients experiencing any AEI, as shown in the blown-up version in the insert. Next slide, please. Moving on now to efficacy. Half of our patients, 50%, achieved response with Senti 202 treatment. This table summarizes available response data for 18 patients available at the time of data cutoff, with the remaining two patients early in cycle one and too early to evaluate response as of the data cutoff. As I mentioned, 50% of patients at the recommended phase 2 dose and overall achieved a response, with 42% at RP2D achieving a CR or a CRh. All CRs were MRD negative. Importantly, in terms of our other responses, the CRh and the MLFS patients, nearly 80% plus were MRD negative across all types of response noted on our trial. As mentioned by Dr. Farhadfar, achievement of MRD negativity is meaningful because it translates to better outcomes and more durable remissions. Responses were achieved rapidly, with a median time to response of about 1.2 months on trial. The median duration of follow-up for dose level one patients was eight months, and for dose level two or the RP2D patients being three months. With limited follow-up in RP2D cohort, our current estimate of median duration of composite CR across all patients is 7.6 months, with the upper limit not yet being estimatable. Next slide, please. This slide summarizes. This slide is a swimlane plot of all our response-available patients on trial. Senti 202 responses are durable, with longest durability of more than a year for the first two patients who achieved a response on our trial. The chart summarizes the time on study, including follow-up for the responding patients in the top half of the graph and the non-responding patients in the bottom half of the graph. I want to highlight a couple of points here. One, in general, as shown by the numeric annotation, patients with multiple poor prognosis indicators at baseline achieved a response, including those with adverse risk genetics by standard ELN criteria being primary refractory. That means they did not respond to frontline treatment for their AML, refractory to fludarabine and/or cytarabine or ARA-C containing regimen, and refractory to the most recent treatment. Patients in general received either one cycle or two cycles, as shown by C1 and C2, and then moved on to the follow-up phase with no further treatment given to them. Next slide, please. Moving on now to some of our pharmacodynamic data. We saw that both AML blasts and leukemic stem cell killing were observed consistent with Senti 202's CD33/FLT3 or logic gate mechanism of action. The graph on the left summarizes the baseline cell cycle status for LSCs or leukemic stem cells for all patients. In general, LSCs in these patients were mostly quiescent or in G0 phase at baseline and therefore not likely to be responsive to lymphodepleting chemotherapy. The middle graph summarizes AML blast reduction on study, and that was noted in all responders and in some non-responders. The graph on the right summarizes the LSC reduction by CyTOF analysis on study in responders, and we noted LSCs decreasing at least tenfold after Senti 202 treatment in all of our responders. Next slide, please. Moving on now to look at the protection of the healthy hematopoietic stem and progenitor cells, which are important to maintain and sustain normal blood count recovery. As shown in the cartoon on the left and as Tim summarized earlier, Senti 202 has a unique endomucin inhibitory circuit, which is designed to protect healthy cells even if they were expressing FLT3 or CD33. Endomucin is found predominantly on healthy hematopoietic stem or stem and progenitor cells and rarely on AML blasts. The graph in the middle summarizes the HSPC levels at baseline in all of our responders. Among all responders, patients with any detectable HSPC at baseline achieved a CR or CRh, while patients with no detectable HSPC at baseline achieved MLFS. In responders who achieved a CR or CRh, as shown in the graph on the right, the proportion of HSPCs in bone marrow was increased or maintained. Next slide, please. This slide summarizes the peripheral blood cell count recovery, again consistent with Senti 202's unique NOT gate mechanism of action, protecting the healthy hematopoietic stem and progenitor cells. The graph summarizes platelet count in black and absolute neutrophil count in gray for all of our patients who achieved a CR or CRh, with the thresholds for CRh and CR achievement denoted in the blue lines. In general, on study, we found that with the waning of the effects of lymphodepleting chemotherapy, the normal blood cell counts reached the threshold for CR or CRh, or indeed normalized very rapidly about 14 days into study treatment. Next slide, please. This slide summarizes Senti 202 peripheral blood exposure. This peripheral PK of Senti 202 is generally consistent across all those patients and consistent with allogeneic NK cell therapy profiles. Peripheral expansion was noted in the first 14 days, and with the waning of the effects of lymphodepleting chemotherapy and recovery of the host immune system, a natural clearance from the periphery after the first few weeks. Those patients who responded, as well as those patients who received a higher dose level, had preliminary trends to increase Senti 202 exposure, as shown in the graph in the top and in the bottom. Next slide, please. So in conclusion, Senti 202 has demonstrated promising results in the treatment of relapsed refractory acute myeloid leukemia. The trial enrolled heavily treated relapsed refractory AML patients with a poor prognosis. This finding is complete on trial with no DLTs, an MTD not reached, and RP2D confirmed. Dose expansion is ongoing at the RP2D. Senti 202 is extremely well tolerated with potential for outpatient dosing. The most frequent grade three plus AEs were predominantly hematologic and consistent with events observed in patients receiving LD. There were no Senti 202-related SAEs, no DLTs, or AEs resulting in discontinuation. The Senti 202-related AEs in general were grade one or two pyrexia, which resolved rapidly. Senti 202 demonstrates promising preliminary efficacy. 50% of patients at RP2D and overall achieved an ORR, and 42% and 39% at RP2D and overall achieved a CR or a CRh. The estimated median duration was 7.6 months. 100% of CR and around 80+% of all responses are MRD negative, with a sensitivity of 10 to the minus four or lower in general. The Senti 202 peripheral PK is consistent with allogeneic CAR NK cell therapy profiles, with preliminary trends to dose-dependent increased exposure, as well as increased exposure in responding patients. Senti 202 has received both RMAT and Orphan Drug designation by the U.S. FDA, and expansion cohort continues to enroll. The protocol is designed to permit a seamless phase one to pivotal study transition. Next slide, please. So in terms of next steps, as we wrap up 2025, we are excited to have demonstrated the preliminary clinical proof of concept with Senti 202, with its excellent efficacy and well-tolerated safety profile. In 2026, we intend, we are planning for interactions with the FDA to discuss our pivotal study plans, followed by initiation of the pivotal study, as well as cohorts with additional indications later in 2026. In parallel, in terms of CMC, our pivotal process for Senti 202 process development is continuing very well, with intentions to be ready to manufacture Senti 202 using the pivotal process to support our trials planned in 2026. With this, I turn this back now to Dr. Lu. Thank you very much, Kanya. So as you've heard today, Senti 202's updated dataset continues to validate the potential for Senti 202 to transform the treatment of relapsed refractory AML. In summary, I'm excited that this year we've achieved multiple major milestones in the development of this program. To recap, we've confirmed the recommended phase 2 dose for Senti 202 and continue to demonstrate that Senti 202 is able to achieve durable and high ORR and CR/CRh rates in patients of high unmet need in relapsed refractory AML. In addition to that, MRD negative rates are high, and this is coming along with an excellent safety profile that supports the potential for outpatient dosing. As you saw earlier, our mechanism of action, correlative analyses continue to confirm that this product is working the way we designed it to. In addition to that, Senti 202 has received both RMAT and orphan drug designation. Next steps for this program include launching our pivotal study in relapsed refractory AML and expanding into other indications, which could include newly diagnosed AML, pediatric AML, and others. Next slide. Before we end, I wanted to just highlight that the logic gates that are in Senti 202 are just one element of Senti's broader gene circuits platform. This platform includes four different types of genetic circuits. Our logic gate gene circuits enable selective killing of cancer cells and sparing of healthy ones. Our multi-arming gene circuits enable multiple payloads to be expressed from therapeutic cells, thus enhancing their durability and stimulating the endogenous immune system. Our regulatable gene circuits enable the control of cell and gene therapies after they've been delivered into the body using FDA-approved small molecule drugs, and our smart sensors enable programming of cell and gene therapies to achieve tissue or disease-specific activity. Next slide. These gene circuits can be used in multiple different therapeutic cell and gene therapy modalities. This includes the NK cells, T cells, iPSCs, and even in vivo CAR. We're very excited today to continue to demonstrate the clinical activity of our logic gated gene circuits in Senti 202 for relapsed refractory AML and firmly believe that this allows us to think forward to other applications of gene circuits in the future, including for solid tumors that also lack clean single targets and thus still have high unmet clinical needs. With that, I'd like to thank you very much for listening, and we're happy to take any questions. Thank you. Now I'll be conducting a question and answer session. If you'd like to be placed in the question queue, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. If you'd like to move yourself from the queue, please press star two on your telephone keypad. One moment, please, while we pull up our questions. Our first question today is coming from Emily Bodner from H.C. Wainwright. Your line is now live. Hi, good morning. This is Joey on for Emily. Congratulations on the data. So just to add a question, it looks like you're seeing some pretty encouraging efficacy in patients who are FLT3 mutants. Do you think these patients are more likely to respond to Senti 202 given its targeting of FLT3 with the bivalent CAR, or do you believe this is potentially a population you can enrich for in your pivotal trial? Thank you, Joey. This is Kanya. Can you hear me okay? Yes. Okay, terrific. So thank you for that question. So all FLT3 binders bind to the extracellular portion of FLT3, so it doesn't matter if it's mutated or wild type. We are not expecting to see a difference in activity based on that, and that's what our in vitro and preclinical evaluation showed as well. So what we are showing you here, of course, is we've seen responses in both FLT3 wild type and mutated, so it's our intention to continue, of course, we'll continue to monitor the data, but continue to develop in both of those populations. That makes sense. Thank you. And follow-up questions. Do you view the transition to transplant after treatment as important for long-term durability, given that a majority of patients who have had long survival and duration of complete remission were transitioned to transplant? And for the patients who did not transition to transplant, did they receive any other therapies after Senti 202? To answer your second question first, none of our patients continued Senti 202 or anything like maintenance after exiting from trial, except for those who got consolidated by transplant, which I think is one of the benefits of Senti 202. You achieve a response pretty quickly if you're a responding patient, and then you're essentially treatment-free. The question about the importance of transplant, I think, as Dr. Farhadfar mentioned as well, current standard of care is to consolidate with alloHCT for those who achieve a good remission, especially if it's MRD negative CR. That's the only, at this point, that's the one potential for a cure for a patient. Obviously, our protocol does not include transplant as part of it, and we are looking at what the benefit is both in those patients who can get transplant and those who cannot. But once they go into follow-up, per standard of care, if they're consolidated with transplant, of course, that's the best outcome for the patients. So I hope that answered your question. Makes sense. Thank you, and congratulations again on the data. Thank you. Thank you. Next question is coming from Yale Jen from Laidlaw & Company. Your line is now live. Good morning, and thanks for taking the questions, and congrats on a very outstanding outcome at this part comparing to other targeted therapies in the AML space. I got two here. The first one is that do you guys start to be able to dissect the patient's pathophysiology differences between those responders versus the non-responders? Was that the HSPC level could be a gating factor? Maybe that could help design the next study? Then I have a follow-up. Thank you, Yale. Thank you. We are pleased with these results as well. To answer your question, I want to differentiate one thing as well with respect to HSPCs. So what we saw is among our responders, those who had some level of HSPCs, even if it was 0.1%, they went into CR. And as Dr. Farhadfar mentioned, achieving CR essentially means so the disease reduction criteria are the same, but your counts come back. And so what we saw was at baseline, when they came on our trial with any level of HSPC, our NOT gate potentially kicked in and enriched for the HSPCs, and we had nice count recovery as well. The two patients who did have a response, MLFS, they came on with zero HSPCs. So what this, and especially considering the late line and the multiple prior treatment that our patients received before coming on trial, what this tells us is potentially as we go to earlier line and maybe when patients can come on without having been exposed to prior myelotoxic drugs, potentially the responses could further skew towards CR. We already have a very high CR rate, but even the couple MLFS we saw, we thought that was an interesting observation that potentially as we go into earlier lines, perhaps more and more CRs because we are able to get and preserve the HSPCs before they're potentially completely knocked down by other therapies they received before coming on trial. Okay, great. That's very helpful. One more question here is that given you have the NOT gate, which preserves some of the help to fast recovery and some of the healthy cells, and so do you anticipate that provides some level of benefit on the disease-free survival side? Also, I just want to confirm that do you feel the patient probably will more go to the higher percentage of patients going to the transplant versus maybe another modality of treatment? Yes, we do believe that having the NOT gate in is going to improve the benefit-risk and hence the outcome and survival and so on for patients. One of the main reasons for morbidity and even mortality in patients with AML is secondary infections. The fact that we have the Endomucin NOT gate is a very unique and attractive feature of Senti 202 because we know that in AML, it is really difficult to find clean targets, so to speak, wherein the targets are enriched on AML blasts and LSCs, as we are also targeting, but not on the healthy hematopoietic stem cells. The logic gate that we have put in essentially engineers in that cleanliness, so to speak, wherein we are able to selectively kill the AML blasts and LSCs and selectively protect the HSPCs, which then should support hematopoietic recovery, which is what we are seeing, which leads to better outcomes for patients. Okay, great. That is very helpful. Maybe just squeezing one more question. In terms of the pivotal study you're planning or speaking with the FDA going forward, we noticed that in other targeted therapy, the size were ranging from somewhere between 65 patients to up to almost 200 patients. And given the scope your therapy may be able to treat, do you have thoughts in terms of what those numbers might be and any other colors in terms of the potential phase 3 study you can talk about? And thanks. Yeah, so what I will say, first of all, I'd start off by saying we received the RMAT designation, which certainly gives us the benefit of being able to discuss and collaborate with the FDA more often, more opportunities, and also more we are able to discuss with the FDA much more often and more frequently and sooner, perhaps, in our program than we would have been able to otherwise. So with that being said, we are very actively in the midst of designing our pivotal study. It is going to be in that range is what I anticipate, but I don't know that we are talking about details publicly, and we certainly don't want to get in front of any future FDA interactions that we are planning on having next year. Okay, great. And again, congrats on the outcomes, and I think that it beats most of the other therapies and so far approved in this space in quite good margins. And thanks. Thank you. Thank you. As a reminder, that star one to be placed in the question queue. Our next question is coming from Geulah Livshits from Chardan. Your line is now live. Thanks. Good morning, and I wanted to add my congrats on the data, and thanks for taking the questions. So maybe can you elaborate on any trends you're seeing with respect to any of the patient characteristics or features of the AML or features that you're seeing in the CyTOF data sets that might be starting to correlate with response or in those patients who respond and then progress with progression there? And also, if you're seeing any correlation between the responses and donor material with respect to the manufacturing of the cells, and then I have a follow-up. Thanks. Thanks, Geulah. So yes, we are currently in an open-label trial, obviously, so we are continuing to see what we are learning from our data as it comes in. What I will say at a high level is we have, having looked at all the different features, we are not seeing anything that's actionable in terms of modifying our trial eligibility criteria. As you can see on our swim lane, I know it's a busy slide, but we've annotated with the numbers. So we are seeing responses kind of across different patient populations. Those are prior refractory to adverse risk genetics, favorable risk genetics, so the whole spectrum. So nothing has come up for now that's making us think we want to either narrow or change our patient population. When we look at our correlated data by CyTOF, what we did see, and we presented that in our poster as well, is again, there might be some trends with the lower CD33 perhaps not responding. What was interesting is that was by CyTOF, and we didn't present this data, but by site CD33, even that trend goes away because there is a difference, obviously, in CD33 levels when it's measured by local flow versus a central CyTOF. Nothing really in any of our targets as well. I think your final question was on donors. On that portion, what we can say is that based on our emerging clinical data, we have refined our donor selection criteria to select for donors. We were able to find an attribute which correlated with response, something that's well known in the NK field, and found in about half the adult population. That donor selection has been updated, but beyond that, nothing on the trial or the patients or any of the characteristics that we've found that's caused us to modify our trial or think of modifying our trial. If I may just add, and thanks for the question. I think any donor selection methods that we're using for making the product doesn't restrict in any material way our ability to find donors and generate good product. The characteristics that Kanya mentioned or expressed are present in over 50% of donors that we regularly encounter, so there's no limitation on our manufacturing capabilities. Great. And I don't know if Dr. Farhadfar is still available for questions, but she is, I wanted to get a sense of her perspective on how she thinks about incorporating it into clinical practice and what percent of AML patients that you see would be suited for treatment with CD33. Yeah. Unfortunately, Nosha had to leave for another meeting, but if you're interested, we can try and follow up to find some time with you and her. Perfect. Thank you, or if there's anything I can answer as well. I guess from your perspective as well, in terms of the percentage of patients that you think would be suitable for this type of treatment, obviously, in the context of available therapies against the different targeted mutations, as well as we've seen some additional data from some of your peers at ASH as well, and to how you're thinking about that competitive landscape? Yeah, but thank you for that question. So based on our target CD33 and FLT3, that's nearly 90%-95% of AML patients should be eligible. And as we already discussed, we are not seeing any other further correlations that make us want to redo our eligibility criteria. So our intention as we go forward is to continue to have similar, if not identical, eligibility for our phase one. One of the things we've done with our phase 1 trial is we've envisioned that as being potentially a phase 1 to a seamless phase 1 to pivotal. What I mean by that is we put thought into our eligibility criteria and some of the way we do some of the assessments on trial such that we could easily amend and move it into a pivotal cohort. So that plan continues. The data that's coming in is not making us want to rechange or rethink what we are doing there. So we think it can be very broadly applicable. Our current trial design is at least one prior, no more than three. Those who have a targeted mutation, post our current standard of care, they must have seen it either in front line and then they come on to our trial as second line, or after two prior lines, then they come on our trial. We don't expect that to change. Just purely based on the target selection, that's about 90%-95% of AML. Perfect. Thank you. Thank you. We reached the end of our question and answer session. I'd like to turn the floor back over for any further closing comments. I want to thank everyone very much today for dialing in and listening to our updated data on Senti 202. We are very excited about the progress that this program has made over this past year, and we certainly look forward, given where we're at now in terms of advancing Senti 202, both in the relapsed/refractory AML space as well as other potential indications, and also to now consider the application of logic gates beyond AML into areas of high unmet need. So very much thank you for that, and hope everyone has a great morning. Thank you. That does conclude today's teleconference and webcast. We will now disconnect your line at this time and have a wonderful day. We thank you for your participation today.