Good morning, everyone. My name is Kanya Rajangam. I'm the President, Head of R&D, and Chief Medical Officer at Senti Biosciences. Thank you to Kuli for inviting us, and thank you all for your time. We at Senti Biosciences, can everyone hear me okay at the back? Yeah. We at Senti Biosciences are a logic-gated cell therapy company. What that means in a nutshell is if you think of the CD19 CAR-Ts or the BCMA CAR-Ts, what they do is when they see a target, they kill. What we do is we engineer our cells with what we call logic gates so that they can do more than one thing depending on the totality of inputs they are getting from the cell, from the host cell. Our lead program is SENTI-202. That is a first-in-class program that we are developing for acute myeloid leukemia, which is, of course, a devastating leukemia that affects predominantly folks who are 65 and older. We recently received an orphan drug designation for this product, and we have demonstrated positive preliminary efficacy data in our ongoing phase 1 clinical trial, which I will be going through today. We expect to have additional data end of this year. What is the logic gate? In fact, what is a gene circuit? A gene circuit is essentially you engineer in the cells to do different things based on the inputs it gets. In our pipeline, we use these four main types of gene circuits. One is the logic gate. Second is to multi-arm the cells, a regulated diet, and smart sensors. I will be focusing on the first two today because those are the two components in our lead program, SENTI-202. I have a little bit more about that coming up in the next slide. What is the logic gate? First, I want to look at the non-logic gate approaches below. These have been very commercially successful, but they work only in cancers which have, quote unquote, a clean target or a target which is found on normal cells, which even if you eliminate them, the physicians are able to handle the side effects. For instance, if you had a look at the commercially approved CAR-T cell therapies or the biologics, they recognize a single antigen, and any cell which expresses that antigen is killed, right? There's no differentiation between cancer and healthy. What we do with our logic gate is we also have in, we have what we call different gates, right? We have an OR gate which allows our Senti Biosciences to recognize more than one cancer antigen because some of our cancers, especially AML or acute myeloid leukemia, are notoriously polyclonal. Different cancer cells express different antigens. Secondly, even if those antigens are present on a healthy cell, we have engineered in the selectivity, so it will not kill a healthy cell even if it expresses those antigens. I'll get into the details of that. That is the key component of our logic gate. We also have the multi-arming, which I'll get to in a second. We are currently developing SENTI-202, of course, in acute myeloid leukemia and other related blood cancers. We are towards the end of our phase 1 trial, and I'm delighted with the data we've got, we've seen so far, and I'm happy to share that with you all today. We also have another program in our pipeline, which is early, towards the end of its discovery, which we are building to target solid tumors. First, a little bit about acute myeloid leukemia. Acute myeloid leukemia is a devastating disease, affects about 20,000, 21,000 Americans every year. Even at front line with the best available standard of care, more than half the patients do not respond to the first line of therapy. Once they don't respond, their median survival is even more dire, median survival of 5.3 months. The current standard of care responses for these patients, there are some targeted therapies approved for the subset of AML patients which have the specific mutation. For example, if they have a mutation known as IDH1, there's an IDH1 inhibitor. All of these are in subsets of patients. Even with those targeted therapies, the response rate of complete remission is about 20%. The most recent ones are the menin inhibitors. Some of you may have heard of those. Their CR rates were 14% and 13%. There's a big unmet need here. One of the things with AML, unlike with solid tumor, because it affects the bone marrow, not only do you need to eliminate the AML cells, you also need to give space for the normal healthy blood cells to come back. Otherwise, the patients are still susceptible to infections and bleeding and so on. The CRH refers to a partial hematologic recovery, which also has been shown to have clinical benefit because the counts come up enough to sustain the patients and not have them be susceptible to infections. One of the big, there are two big challenges to developing new anti-AML therapies. Both of these we address with our logic gates. One is AML is notoriously heterogeneous. Specifically, there are these niche therapy-resistant cells called leukemic stem cells or LSCs. They are this niche population of cells which are refractory to current therapies, chemotherapy, what have you. They are the ones which drive relapse. You really need to be able to eliminate them to have durable responses. Second, the selectivity of killing. AML blasts and LSCs, there is no clean target. They share a lot of their targets with healthy hematopoietic stem cells called HSCs. It is very important to have therapies which can kill one, but not the other. That is where our logic gate comes in. The SENTI-202, there is a lot on this slide. Let me orient you through this. SENTI-202 is essentially a completely off-the-shelf cell therapy product. I am going from left to right. What are the key features in this product? I want to spend a minute talking about the mechanistic rationale and why we made the design choices we did for this product. Everything we chose to put in this product was done so very deliberately. First, the cellular backbone. The cellular backbone we selected for this particular application is what is known as an NK cell. NK stands for a natural killer cell. That is the normal lymphocyte that is found in all of us. 10% to 30% of our lymphocytes is an NK cell. It is a cousin of the T cell, if you will, part of the innate immune system. It has some big advantages, one of which is why we selected this for AML. The one big advantage is you can take an NK cell from one person and give it to another person without being worried about what is known as a graft versus host disease. The other big advantage is NK cells are specifically active against AML. In fact, non-engineered NK cells have had a response of about 20% comparable to current standard of care when academics have used that since about 2005. The issue with those responses is that it has not been durable. We know, in fact, data shows us that it's not durable because the LSCs that I mentioned specifically downregulate the ligands that NK cells recognize. Our gene circuit kind of overcomes the main challenge with NK cells. The other reason is it's well established that autologous T cells in patients from AML are dysfunctional. There's a lot of CAR-T studies that have been tried mainly by academics, but not a lot of success because of this reason. What's the gene circuit we put in there? Our first kill signal is our OR logic gate. It's a bivalent CAR. CAR stands for chimeric antigen receptor, and it recognizes and kills cells which express CD33. CD33 is a validated AML target. There is currently a commercially approved drug which targets CD33 and FLT3. FLT3 is important because that is predominantly found on the surface of the LSCs that I've been talking about. We want to go at the root of the disease. A CAR is pretty familiar to most of you, I would think, with the CD19 and the BCMA approval. That's very similar. That's what the CAR is, the A-CAR or the OR logic gate. The NOT logic gate is very unique to SENTI-202. That is our protect function, and that is what allows our cells to not kill healthy cells, even if they express CD33 or FLT3. How do we do that? What we did was we first identified a protein called endomucin, EMCN. Endomucin is found only on the surface of HSCs, and it's very rarely or not found on the surface of LSCs and CD33. Once we identified that, and we do this in a completely unbiased single-cell RNA sequencing method, what we did was we engineered our I-CAR such that when SENTI-202, the I-CAR binds to endomucin, it overrides the kill signal of the Kill-CAR, even if the Kill-CAR is present on, the signals are present on HSC. Before we came into the clinic, we spent years, three, four years, I believe, where we really perfected this interaction. If time permits, I have some videos which I can show you at the very end of how we do this, where essentially we go through hundreds of constructs, and that is not an exaggeration, to perfect these cells, selectively killing the leukemia cells without spillover killing of healthy, and on the other hand, not having tonic inhibition from the I-CAR. We really take a lot of time before we get in the clinic. The last protein is the multi-arming calibrated release IL-15 or interleukin-15. IL-15 is an important cytokine for NK cell function. That's five minutes, and I'm still on the MOA slide. That's because it's such a cool science, but I will get to the clinical data in a minute. That's necessary for protecting and, you know, enhancing not only NK, SENTI-202, but also host immune cell activity and persistence. Our manufacturing, very quickly, it's completely off the shelf. What's happening on the left is independent from what's happening on the right. There is no vein-to-vein time. We ship cells out the day we approve patients to enter our trial. Five minutes to go through the clinical data. This is our phase 1 clinical trial that we presented at AACR. One of the big advantages of NK cells, it's very safe. We were able to start at a high dose, 1 billion CAR NK cells per dose. It's a standard phase 1, but we put a lot of emphasis into efficacy because we knew we were starting with what we believe was an active dose. We looked at 1 billion cells or 1.5 billion cells, and we looked at two schedules of dosing, day 0, 7, and 14, or five doses 0, 3, 7, 10, 14. After lymphodepletion, you need to lymphodeplete patients to condition them for these cells to be able to work. Do a bone marrow on day 28, and they can get more cycles up to a maximum of four based on efficacy and safety. A lot of data here. Let's just focus on the highlighted column, which is our RP2D cohort. That's the recommended phase 2 dose, which is the main objective of your phase 1. We declared RP2D because of the totality of the data I'm presenting to you today. Our patients, very high-risk relapse refractory AML population, multiple baseline adverse characteristics. I want to highlight just two data points here. That is this one and this one, right? Our patients enter trial less than a year from diagnosis, and in that year, they had received two prior lines of therapy. These are really patients whose standard of care had failed them. Within a year of diagnosis, they came on a phase 1 clinical trial. Safety, very clean. All of these adverse events that I'm presenting here, these are hematologic events, febrile neutropenia, neutrophils are down, you have some fever, maybe some infection, decreased platelet count, anemia. These are very consistent with what happens to AML patients when you lymphodeplete them. It's very consistent with our conditioning therapy. When we drill down to SENTI-202-related AEs, no grade 3, no SAEs. We did have some grade 1 pyrexia, delayed infusion-related reactions, which sometimes PIs call CRS, very easily managed within a day of it coming on. Exciting on efficacy, what we see is we saw responses in every single cohort. Again, to focus on our RP2D, we saw two out of three patients had a complete remission. Not only was it a complete remission, they were also absent MRD. MRD stands for measurable residual disease. Our MRD is measured with a sensitivity of 10 to the minus four. That means one clone in 10 to the power of four cells. If it's detected, it's MRD positive, but ours were all negative. All of these responses are ongoing as of the data cutoff. Overall on our trial, we saw 57% CR, 100% MRD. We saw blast reduction in all patients. This is our time on study. As of April, you can see here the right is a standard swim lane, the recommended phase 2 dose cohort on top, other patients below, ongoing for all of our patients. On the left, anything with the red is a poor prognostic indicator. As you can see here, in the interest of time, I won't go through every one of them, but multiple poor prognostic indicators and our patients responded. Finally, on the correlative side, one piece of data here, what we do is we look at, we work with MD Anderson Cancer Center, who is a well-known oncology group. We do what's called a site off, where we are able to measure 49 different proteins in serial bone marrow samples. We're able to go beyond the response. The two pieces of data I'm showing you here on the pie chart are our leukemic stem cells in all of our patients at baseline. G0 is the resting cell phase. All of these patients with their LSCs, they're just sitting around in G0. They're neither synthesizing nor actively dividing, which means they're not chemotherapy, venetoclax, all of those agents require cells to be actively dividing for them to be able to act. That's why these are therapy resistant. Our data kind of corroborates that. The only way you can address these sort of cells, which are in G0, is by looking, by targeting something on the cell surface, which is what we do. Therefore, what you're seeing on the right is the LSCs go down, right, with treatment. The flip side of AML is to have normal blood count recovery. Platelet cells in black, neutrophils in gray, within the, you see the dip with lymphodepletion comes right back on the left. On the right, I'm showing you preservation of HSCs in our bone marrow as well, consistent with our logic gate MOA. Finally, PK, this profile is exactly what we hope to see. It's very consistent with allogeneic NK cell therapy. Modest expansion in 14 days does its job and then leaves. You're not worried about long-term side effects like with autologous T cells. Taking all of this data together, no DLTs, good exposure, great efficacy, corroboration of our MOA, we declared our RP2D. Next steps are to confirm that, put more patients on, and then present around 20 patients or so, hopefully with more than 15 minutes time by the end of the year. That's what we are planning on doing. I think we are done. I may not have time to address these things, but maybe have them in the background. This is how we select our logic gates. We can have them running in a loop. We do these cell-cell assays, and you can see how when you have our logic gate, green is good cells, red is the cancer cells. You have the specific killing when you have the logic gate built in. Thank you for your time. Happy to take any questions at this time. No time? Okay.