Afternoon, welcome back to TD Cowen's 46th Annual Healthcare Conference. I'm Ellen Horste, TD Cowen Biotech Associate. On behalf of Phil Nadeau's team, I'm excited to introduce Timothy Lu, Co-founder and CEO of Senti Therapeutics. Timothy, your background is actually biomedical engineering and computer science, so I think it's not super surprising that maybe you're behind the first logic-gated off-the-shelf NK therapy. I know we're looking forward to hearing more about the Senti story, so I'll let you take it from here. Great. Thanks a lot. Fitting to be in the MIT room, given that I was at MIT for many years. Senti's building something we call logic-gated cell therapies. We're really excited about the opportunity to do so. Logic gates allow us to solve one of the key central problems in oncology, which is how do you selectively kill cancer cells without killing the rest of the patient? The way this works is we have developed the technology that allows us to recognize one or more targets on the cancer cells to trigger direct killing. We also have developed a way to recognize healthy cells and protect those healthy cells from being killed. That dual activity allows us to achieve a better therapeutic window and go after diseases like AML that don't have a clean single target. Our initial program, SENTI-202, contains this technology. It is an off-the-shelf allogeneic NK program. I'll walk through some of the data in a little bit. However, more broadly speaking, our logic-gating technology does work in both NK and T cells, and we're really excited about the opportunity to continue to innovate and develop these programs in AML, expand to MDS, but even go into solid tumors in other areas. SENTI-202 specifically is a program that we're very excited about. We did present some exciting data at ASH just a few months ago, where we showed in our 20 relapsed/refractory AML patients, really exciting outcomes in terms of at the RP2D confirmation, showing that we're able to get, you know, durable responses with a high response rate of 50%, 42% CR/CRh rates at the RP2D, and a 7.6-month estimated median duration of CRs. We also demonstrate a very high rate of MRD negative negativity, and that's something that we are very excited about. It does, to us, demonstrate this ability to generate and drive deep responses in the disease, and we know that MRD-negative status can correlate to better outcomes in patients with AML. This is all accompanied with an excellent safety profile and the potential for outpatient dosing. As I'll show you, I'll show you some data further confirming the MOA of our product. We did show selective killing of our AML blasts and leukemic stem cells as we designed, at the same time, the sparing of healthy bone marrow stem cells. That's the key cell population we're actually trying to protect. Based on this, we also got RMAT designation last year as well as ODD. Our plan for this year is to launch our pivotal study and to expand in relapsed/refractory AML and to expand into other indications, including newly diagnosed AML, pediatric AML, and MDS. AML is, on its own, a very exciting commercial opportunity. In the U.S., there's about 12,000 relapsed/refractory AML patients. One of the things that makes SENTI-202 stand out from many of the other AML treatments out there is that SENTI-202 is not genetically restricted. Patients do not have to have a particular genetic mutation to come on our study. Essentially, they just need to be positive for CD33 or FLT3, which, you know, over 95% of patients are. This represents a significant opportunity, and clinical need, in relapsed/refractory AML. There certainly is a larger population in newly diagnosed AML we think we can address given the profile of the product. Beyond this, solid tumors is what we're aiming for to come, there will be some inklings of what we can do in solid tumors towards the end of this presentation. Diving into it, you know, what are we developing at Senti is a suite of technologies to enhance cell and gene therapies. Logic-gating is one core component of this. It's on the upper left-hand corner here, and I'll walk through some of the more details of how this works. Logic-gating essentially allows us to address the key issue of antigen escape and specificity in the treatment of cancer. There are other technologies shown here that I won't get into in a lot of detail other than to say that we think many of these other tools will be very useful as we go into the solid tumor space. Why are logic gates important? If you think about existing cell therapies, existing ADCs or T cell engagers, they're all faced with the same challenge, which is that they have to find a target that's clean or one in which you can go into the body, kill every cell that expresses that target, and the patient's still okay. And it turns out there are some cancers that are amenable to that. You know, cancers, targets like CD19 or BCMA or HER2 have that sort of profile, which is why you see a tremendous amount of crowding of these modalities against those sort of indications. That means that there are cancers out there that do not have clean targets that are sort of left on the wayside because these existing modalities just don't have the therapeutic window to address them. That's where our logic gates can come in. In those diseases for which you cannot find a clean single target, what we can do is design our product to recognize and kill the cancer cells, but also recognize and protect the healthy cells. It's gotta have this multi-pronged activity. SENTI-202 embodies this technology. We are very excited with that data we presented a couple of months ago. We are planning to move this into a pivotal study later this year. We do also have additional solid tumor programs that leverage the same backbone here. As I mentioned earlier, this works across modalities. We have this working in NK cells and T cells and has the opportunity to expand into other delivery vehicles in the future. Diving into AML, you know, relapsed/refractory AML is still an area of high unmet medical need. This flowchart on the left-hand side here comes from the journal Blood, showing, you know, a typical flowchart of treatment once a patient's in this relapsed/refractory AML category. Oftentimes, clinicians are actually looking to see if patients are actually eligible for clinical trials as their first option because the other existing options are not great. Number two, if the patient's eligible for a transplant, they may go down one of two arms here. Either they can get a targeted therapy if they have a specific genetic mutation, if they don't, they can get a mutation-agnostic therapy such as salvage chemotherapy, followed by consolidation with a transplant. In the absence of getting a transplant, there's not a ton of great standard therapies that are out there, basically physicians just have to try to figure out what they can offer the patients. In general, patients with relapsed/refractory AML have a poor prognosis. CR rates are in that 12 to low 20% range, CR/CRh rates at the 20%-30% range. The most recently approved Menin inhibitors, for example, had CR/CRh rates in the 21%-23% space. Median overall survival still quite short in this disease area. Tremendous need for new products, especially ones that are not genetically targeted to come in and hopefully change the landscape of treatment. In AML, there is a couple of different diagnosis criteria in terms of response categories. They're essentially segmented by, number one, are you getting a direct cancer response? If you look at AML blasts, you have to have bone marrow blasts less than 5%, and a couple other criteria listed on this slide. In addition to that, it's also important to look at MRD status. Using techniques such as multiparametric flow, you can detect any residual disease, for example, down to a sensitivity of 10 to the - 4. On the right-hand side, there's also a second set of criteria that dictate basically response criteria categories. For a full CR, you need your neutrophil count or your platelets to be above a significant level. CRh or CRi, those are intermediate response categories where the healthy peripheral blood counts have not recovered fully. They're in that intermediate category. Something called MLFS is when you don't see significant count recovery. We know that in patients, with relapsed/refractory AML, if you can achieve a CR/CRh or MRD negative status, this does correlate, to better outcomes, but existing therapies are limited by that. What I'm gonna present, in a little bit is just summaries here. Some more details on the summaries shown here. We have a very novel MOA into this product. Our phase I shows evidence of efficacy and safety and durability consistent with this MOA. This product is not mutationally restricted and therefore has a broad reach, and we think there's opportunity to expand this, beyond relapsed/refractory AML. What is our product? SENTI-202 is an off-the-shelf allogeneic cell therapy. It's engineered to express three different proteins. The first protein is on the upper left-hand corner. It's an activating CAR that recognizes two different targets, CD33 or FLT3, or both. The reason why we chose these two targets is that both these targets are well known in AML. They're ones that have been identified for a very long time. And we know that, for example, CD33 is expressed on the AML blast population. FLT3 is expressed on leukemic stem cells. By putting them together, you can potentially target a much broader set of AML cells once you deliver this product to patients. We estimate that this combination of antigens covers about 95% of all AML patients. What's wrong with these targets? In the past, when people have looked at CD33 and FLT3 expression, you can find them on healthy cells. If you simply go in and try to ablate everything that has CD33 or ablate everything that has FLT3, you run the risk of, you know, bone marrow toxicity. To protect against that risk, we built in our second CAR receptor. This is called the inhibitory CAR or iCAR. What that does is it recognizes the healthy cell, and it delivers a negative signal into the CAR NK. It basically shuts down the product, so it does not kill those healthy cells. It does this by recognizing a particular target called EMCN or endomucin. Endomucin is highly expressed on the healthy cell but has low expression on the AML cells. Finally, the third protein I expressed here is an IL-15, and that IL-15 serves to enhance the overall NK activity. This is an exciting product given that it's off the shelf, meaning that we can essentially manufacture the product from healthy adult donors. We genetically modify the cells with a single transduction step, further expand the cells, then we can cryopreserve the cells. Essentially, the cells are sitting frozen in vials and can be shipped out the next day once we've enrolled the patient onto the study. An allogeneic product we believe is important in the treatment of AML. These patients don't have a long time to live. Being able to have a product that does not have vein-to-vein manufacturing time that can be delivered the next day is very helpful. This definitely fits in that category. We've been evaluating SENTI-202 in a national multicenter study. This is being done in both the U.S. and Australia. Our key enrollment criteria is patients have to be positive for either CD33 or FLT3. We estimate, you know, vast majority of patients are actually eligible by that criteria. Our protocol actually allows us to assess patients with both relapsed/refractory AML and MDS, though we have focused on that relapsed/refractory AML category first. We were looking at both safety and efficacy with this study, as well as MRD assessment and PK/PD. In terms of our study treatment and dose escalation strategy, we actually looked at two different parameters to titrate. The first one is looking at two different dosing schedules. That's what's shown on the upper left-hand corner. In Schedule 1 and Schedule 2, they're both the same in terms of lymphodepletion. There's an initial lymphodepletion step using fludarabine and Ara-C, followed by either three doses of cells or five doses of cells in Schedule 1 or Schedule 2. In both cases, we assess at day 28 by taking a patient bone marrow, and then we can repeat this whole overall cycle up to 4x in the treatment of the patient. We also tested two different doses in the treatment, either 1 billion CAR-positive NK cells or 1.5 billion CAR-positive NK cells. In terms of our RP2D, we ended up going with Schedule 1, Dose Level 2. Dose Level 2 provides a higher dosing level. Schedule 1 is a convenient dosing schedule for these patients, coming in once a week for dosing. That we actually saw, you know, no inferior, in fact, numerically increases, in that dose level one schedule. In terms of the enrollment criteria for the patients, we enroll patients with multiple baseline adverse risk characteristics. If you look at a couple of key line items here, you know, majority of our patients were considered adverse risk by ELN 2022 at diagnosis, had pretty widely ranging levels of bone marrow blast, but pretty significant levels of bone marrow blast counts in these patients were observed. If you look at mutational status, we had several patients that were FLT3 mutated or IDH mutated, and those did receive those target inhibitors prior to coming on our trial. Many of our patients actually had low neutrophil counts or low platelet counts indicating that, you know, that's correlated with severity of or challenges with their disease. These patients were heavily pretreated in the past. All these patients received one to three prior lines of therapy, including chemotherapy, fludarabine, cytarabine-containing regimens, Venetoclax, hypomethylating agents. When eligible, patients that were eligible for targeted therapy should have received that before coming on the study, that includes FLT3 inhibitors and IDH inhibitors. Many of our patients did have a prior stem cell transplant or relapse afterwards. Many of our patients, especially in the RP2D, were actually refractory to their most recent regimen, meaning that they failed their most recent regimen before coming onto our study. In general, patients received a median of 1 cycle. Some patients received up to 2 cycles. No patients discontinued the treatment due to adverse events. In terms of AEs or SAEs, this is looking, regardless of relationship to SENTI-202, the majority of the grade 3+ treatment adverse events were essentially related to lymphodepletion. I'll show you some of the data in a little bit. Essentially, with lymphodepletion, you do expect a decrease in the immune cells in the hematopoietic system in the patients, and we do see some febrile neutropenia, low platelet counts, anemia, thrombocytopenia. AML doctor well suited to manage these sort of adverse events. As you'll see, patients that did respond on our treatment, oftentimes their healthy blood counts did recover in about two weeks after treatment. It's a very transient nature in terms of these AEs and well-managed. In terms of SENTI-202-related events, primarily, these were grade 1, 2 pyrexia. We don't see high evidence of CRS as you do see with autologous CAR- T cells. These were generally happening on the day of dosing and well-managed with standard of care. These are very consistent with prior reports of delayed infusion reactions with other NK cell therapies, and we think this is likely the mechanism that's at play here. Interestingly, if you look at a panel of cytokines, this is just one excerpt of this in the upper right-hand corner. Looking at IL-6 levels, we see very low levels of IL-6 being produced with the product, certainly an order of magnitude or less compared to CAR- T cells, comparable CAR- T cells from treating B-ALL. In terms of responses, we saw, you know, 50% ORR in our patient population. At the RP2D, we saw a 40%+ CR/CRh rate, which we're quite excited to see. 100% of our CRs were actually MRD negative, and vast majority of our CR/CRhs or CRs plus MLFS were also MRD negative, indicating that we are able, in many of our patients, to drive deep responses in these patients. Even with the relatively short durational follow-up, due to the data cut timing of the ASH dataset, we estimated a median duration of those composite CRs for about 7.6 months. Again, this compares quite favorably with existing products that may have a range of durabilities from four to six months with some of the most recent LE-approved drugs as an example. Here's a swimmer's plot of our responses segmented by responders on the top and non-responders on the bottom. We did see responses across a pretty wide range of different patient backgrounds. Patients that were either primary refractory or refractory to Flu/Ara-C or refractory to their most recent therapies. We found responders in all those sort of categories. You know, two of our patients that are the longest on this particular slide have survived over a year and a half, so we're really excited for those patients to have that sort of outcome. Certainly, some of the earlier patients are continuing to respond, and we're continuing to follow those patients. In terms of MOA, I mentioned earlier, we did wanna really confirm that this logic gate works, right? This is a novel design, and we really wanna know, is this logic gate actually working as we designed it? That has a lot of implications, not just for this product, but also the design of future products. MD Anderson took all of our patient samples and ran what they call CyTOF analysis, which allows you to look at the patient bone marrow and do a simultaneous analysis of a variety of the different cells that are actually present. First, we want to look at both the AML blasts and the AML Leukemic Stem Cells in those patients. Firstly, on the data on the left at baseline, the vast majority of the Leukemic Stem Cells in patients are actually in the G0 state, meaning that they're in that quiescent state. This is consistent with literature. It's well known that LSCs are very difficult to kill because they're not actively cycling and they're not easily killable by, for example, conventional chemotherapy. In the middle here, we looked at AML blast reduction, both at baseline versus best response. Again, as I said earlier, we had a pretty wide range of baseline AML blasts in the bone marrow. but even at very high levels of baseline blast counts, we saw significant reductions in all of our responders and even in some of our non-responders, you saw some reduction actually happening in these patients. The thing that we're also very excited about is the data on the right-hand side here. If you look at those Leukemic Stem Cells that are very difficult to kill with existing products, we can compare baseline LSC levels to cycle 1 LSC levels and cycle 2 LSC levels. You see generally there's a pretty strong decrease in our responders. In general, our responders had over 10-fold reduction in LSC counts after SENTI-202 treatment, and in many cases even more than that. This to us represents a really differentiated MOA, where we can go in and really target those LSCs for killing. The problem with LSCs is they actually look very similar to Hematopoietic Stem Cells. Again, one of the key questions here is can we protect those Hematopoietic Stem Cells from being killed? We don't wanna kill both the HSCs and the LSCs at the same time. Again, using that CyTOF analysis, we looked at healthy hematopoietic stem and progenitor cells in these patients. What we found is on the right-hand side, in general, we're seeing a maintenance or even increase in proportion of HSPCs in the bone marrow. That to us indicates that this logic gate is functioning. We're killing the LSCs and the blasts without having toxicity against those HSPCs in our responders. The middle graph here is actually also very interesting. If you look at patients at baseline in terms of their hematopoietic stem cell counts, patients that ultimately re-achieved a CR/CRh had detectable levels of HSPCs. However, patients that had MLFS actually did not. Remember again, MLFS is that category where you basically don't see significant count recovery, healthy count recovery. We believe that, you know, essentially if patients are coming in with low HSPCs to start, even if our logic gate is working really well, you can't protect something that's not there. What this implies to us is if this trend continues, that as we move this product potentially further frontline, hopefully we can see even better outcomes for these patients because you would expect them to have better bone marrow reserve at those times. In terms of looking at the effect on the healthy cells, we actually looked at this over time, both in terms of platelets and the neutrophil count. As I mentioned earlier, we do see a transient reduction in these cell levels with lymphodepletion. That's something you expect with all lymphodepletion. That's what happens between day -7 and day 0 here. You see a drop in platelets and those neutrophils, and we think that correlates with those adverse events I mentioned earlier that are LD related. In the middle here from day 0 to day 14 is when we dose our cells. That's kind of the window of opportunity we see with lymphodepletion where the cells can go in and have their activity. You can see in our responders, really excitingly, after 14 days, you start seeing a really significant recovery of these platelets and the neutrophils. In many cases, we see a recovery above the CRh threshold, which is this low blue line here. Certainly in some cases above the CR threshold, which is really exciting. Some of these patients actually have normalization of neutrophil and platelet counts back up to even normal levels. That's a great outcome for these sort of patients going forward. In terms of PK, we looked at, you know, PK across the 2 cycles. Did not see anything statistically significant to report here, we've shown the data. Essentially what we're seeing is consistent with other allogeneic cell therapies. You kinda have this 14-21 day window where the cells can go in and have their activity. That's something we're seeing with our product as well. We very much view this as, you know, open some space, go in, hit hard with the NK cells, hopefully achieve an optimal response for the patients and then the patients can, you know, get multiple cycles and once they've achieved their optimal response, they can move on with their life. SENTI-202 has achieved really exciting outcomes. We've enrolled patients that are heavily pretreated with poor prognosis and demonstrated that SENTI-202 is generally well-tolerated. It does have outpatient dosing potential, with, you know, very reasonable AEs, certainly no significant CRS or other toxicities that you would see with CAR- T. The efficacy profile we're seeing is very promising, I think compared to existing drugs that are out there. Based on this, we plan to meet with the FDA and align on our... Kick off our pivotal study later this year. I think the RMAT and the ODD designation that we've achieved will help in that endeavor. That's part of our strategy for 2026. You know, we are well on our way in terms of upscaling our CMC process to have it pivotal and commercial ready and interacting with the FDA soon based on our RMAT designation to drive this plan forward. Last few things I'll mention is that, you know, logic gates don't stop at AML. We think there's a lot of opportunities here to go beyond AML into areas where existing ADCs and T cell engagers are not playing. Just to show you know, we have adapted the logic gates to work for solid tumor targets. For example, CEA is a target that's expressed in lung cancer, colorectal cancer, but has a history of off-target toxicities in the past. We repeated our whole engineering design process, which uses a lot of high throughput design, computational design to create these logic gates. We identified a protective target called VSIG2 that can serve to protect healthy cells that also express CEA. We put these into our NK cells. This is a microscope image where we mix cancer cells in red and healthy cells in green. The cancer cells have the CEA target but don't have VSIG2, whereas the healthy cells have both targets. You can see, with no NK cells, both populations grow and they both take over. If you simply target CEA by itself, both populations die. That's not good either 'cause you're killing off a lot of the healthy cells. With the NOT gate, you're able to spare the healthy cells in green and kill the cancer cells in red. That's a really exciting POC that we've been able to demonstrate. This also works in T cells, so we're not limited to just the NK chassis. This can work in T cells. We think there's opportunity to go even with in vivo CAR here. With the T cell work, we show the same thing, right? With no T cells, both populations grow. With CEA-only CAR- T cells, you see a pretty strong killing of. I know the image didn't fully work there, but trust me, this does kill all the way. There is enrichment of the green cells, essentially when we have our NOT gate at play here. Yeah, we're really excited. We have our CFO here in the room and our Chief Medical Officer and President Kanya here. Happy to answer any questions. In summary, we're really excited here at Senti. We think we have a very direct path forward to a significant unmet medical need with SENTI-202. We're gonna be going after relapsed refractory AML in the near term, expanding to newly diagnosed AML, pediatric AML and MDS, and then we can expand the logic gates into other solid tumors. Thank you very much for the time. Appreciate it. Thank you for that presentation. We have a few minutes for questions. I'll maybe kick it off. The durability is really impressive, much above what you see for approved agents in relapsed refractory AML. Is this enough? Is this what regulators need to see for approval? Is this what physicians wanna see for broad adoption in this indication? When do you think you might give an update on maybe some more mature durability? Sure. Yeah, I can start there. Certainly, Kanya, you can weigh in since she's CC and our clinical expert. I think if you look at recent approvals, including the MEK inhibitors, you know, many of those products, like I said, were CR/ CRh rates of 21%-23%, maybe 4.5 to 5-ish months of durability. We think this is well within the range of approvability. Obviously, the better, the longer, the better. We continue to follow these patients. I would say our clinicians are very excited about what they're seeing. I mean, post our presentation at ASH, we had, I think, like 20 sites try to come up to us and really try to and be part of this pivotal study. We're seeing a lot of excitement there, not just because of the data itself, but also the MOA here is really unique and distinct compared to the lot of the small molecule target inhibitors or chemotherapy drugs that are out there. Thinking about, you know, opportunities for patients that may not be responding to those or even combos or moving front line in the future, I think that's where this product really is quite unique in that sense. Yeah. In... Yes, being an all-comer therapy is definitely differentiated. Kind of to that point, as you move into the front line, how do you think about, in the current treatment paradigm, there are these buckets of unfit patients for intensive chemotherapy versus fit. How is that relevant, if at all, to Senti? Are these patients, or like would you expect efficacy to be differentiated across those two patient groups, or does it not matter? Do you wanna answer that or should I take it? Go ahead. Yeah. We are thinking of initially going up. One of the key things with SENTI-202 or any cell therapy is whatever you combine with also has to be something that can support expansion of the cell. Going to a younger fit patient population where chemotherapy is used would be the natural add on. That's our initial ideas for going up front. We also know that quite a few patients get Venetoclax. We are looking at ways in which we could combine the Venetoclax as well. This would be combinable with like a 7+3 regimen? Potentially, yeah. Yeah. 7+ 3, something like that, has the anti-AML effect, but could also potentially make the space for the cell therapy to go in and expand and be able to get rid of the AML, right? Yeah, that's a great point. That's a great point. What would a pivotal trial design look like here? I'm kind of surprised that most of the patients only went through one cycle of therapy. How many cycles would you potentially be looking at kind of your pivotal study? I mean, patients are eligible to get up to four. I think generally we were seeing patients segment pretty quickly. If they're gonna respond, you start seeing a response in the first cycle. We do oftentimes have patients that do wanna get a consolidation and something we also recommend. That's why some went to two. You know, up to four is possible. I think what we believe is meaningful as a pivotal study, if you look at other relapsed refractory AML studies, it's been single arm, you know, less than 100 patients. We think this is well within the range of something like that. Yeah. Maybe one follow-up. Sorry. Yeah. Like how are you thinking about COGS and. Yeah. I think one of the key things here is given that it's an allogeneic cell therapy, we spent a lot of time making sure this could scale. We initially for the phase I started off in smaller scale bioreactors. We have transitioned to bags, which gives us the ability to, you know, scale almost an order of magnitude in terms of production. So whereas we haven't put out concrete COGS numbers publicly, I would say that compared to autologous, this is much more scalable. And I think well within a range of an order of magnitude of improvements. Yeah. Yeah. I used the follow-up question about the front line AML. Given the results of the randomized phase II PARADIGM study at ASH, where VEN+AZA and younger fit patients was actually better than 7+3. Granted it's not a randomized phase III, but I would be highly surprised if AbbVie does not try to file that and get that approved. Also, you know, other AML physicians I've talked to have said, you know, "If it's positive, I am switching and I'm starting to treat my younger fitter patients with VEN+AZA." With that, right, 7+3 may finally after, what, Cytoxin was approved in, what, 1970, like 55 years, be going extinct. I guess does that affect kind of how you're thinking about- Yeah ... the approach? The last piece is, you know, there's preclinical data suggesting that actually Venetoclax can enhance NK cell activity. Yeah. Again, you wanna talk about the combos that we're looking at? Yeah. Yeah. Yeah. The PARADIGM study, which was the president of the plenary session at ASH, we actually met with our investigators just after that study. Yeah. With that results fresh in all of our minds. That was certainly an intriguing result. There have been other VEN+AZA versus chemotherapy which have had. It's just been mixed results. This is not the only randomized controlled trial of 7+3 versus VEN+AZA. Certainly heading in that direction of what can you do which perhaps can help with mitigating toxicity while giving rise to more prolonged durability of response, right? That's the ultimate underlying goal. At least the investigators All the ones we've been speaking to, quite optimistic that there is still a role, especially if it can be used in a situation like ours, where it's essentially giving rise to the lymphodepletion type aspect. Mm-hmm. -giving the cell space to go in and get the MRD negative CR. I wanna highlight that even in our relapsed/refractory AML population, 100% of our CR patients were MRD negative. We expect that to only be enhanced upfront, and that could be like a really durable, almost curative type of outcome for patients, right? The way we are looking at it is we are initially thinking of adding on to chemotherapy because that will certainly help support cells. We are certainly, absolutely also thinking of combining with Venetoclax so we can be well-positioned depending on as the standard of care evolves. Yeah. I guess one thing, have you seen any differences in certain high-risk genetic features in terms of outcomes, right? For patients who have high TP53 allele burden or, you know, have, you know, a bazillion cytogenetic abnormalities or Yeah. We have seen... I'm not sure if on our swim lane slide we have these numbers annotating... Mm-hmm. -for the patients and, we have seen responses in patients with adverse genetics complex karyotype as well. I think overall on trial we maybe had one or two TP53s... Mm-hmm. who did not respond. Not surprisingly, small, patient numbers. We are getting them at the very end of a bunch of different things- Yeah. that's been tried for them. We have seen responses with adverse genetics as well. Yeah. I guess finally, a question about the making space concept, right? In your relapsed/refractory population, I guess, you know, what is a bit, I guess, maybe confusing to me is you guys are using higher doses of chemotherapy, right? You're giving Flu plus cytarabine, which is not typical for most NK. Granted, different disease state, but most other NK cell companies are using like Flu/Cy, right? So you're going to a patient population where they have very few cells, right? They don't have a lot of circulating lymphocytes to begin with. They're fully functional, and yet you're coming in with sort of higher lymphodepletion. So I guess trying to sort of put that together mechanistically in terms of, you know, is, you know, your LD doing something else besides sort of just making space? Theoretically there should be plenty of space in an AML patient relative to, you know, like a lymphoma patient. Yeah. LD in and of itself, if you think of the CAR- T, the flu cyclophosphamide, that has some activity against B cell malignancies as well, right? Historically, what the LD has done is also debulk as well as make space. Yeah. Which is a similar approach we are taking as well with Flu/Ara-C. Unfortunately for us, there aren't a whole lot of other NK companies doing AML still out there now, but we have validated targets... Yeah. Approaching that. In AML, there's a couple reasons we use Flu/Ara-C. One is also to debulk some of the AML. Secondly, what we found is preclinically when we expose AML cell lines to Ara-C, there's upregulation of CD33 and FLT3 giving rise to enhanced cytotoxicity. The idea of a product like ours or a cell therapy like ours is to go and get rid of the last AML cells, so to speak. We are very much focused on achieving MRD negativity and also the Leukemic Stem Cells, that niche population... Sure. Yeah. you know, which is gonna bring the leukemia back. That's really how we are approaching it. Some debulking and definitely, you know, it's multiple folks have shown right from the 90s that you need some sort of chemotherapy to get your cells to go in there and expand and do what it needs to do. That's really how we're approaching that anyway. That's great. Thank you so much for an engaging discussion. Great. Yeah, we'll see everyone at another session. Thanks a lot. Appreciate it.