Our next speaker for this session is Dr. Tim Lu, Chief Executive Officer and Co-founder of Senti Biosciences.
Okay. Thanks a lot for the opportunity to be here. My name is Tim Lu. I'm the CEO and Co-founder here at Senti Bio. Really excited to spend some time sharing with you guys our lead program that uses something unique called a logic gate to solve one of the central problems in oncology, as well as some of the clinical data that's coming out for this. Senti Biosciences is trying to tackle one of the major challenges in the cancer space, which is how do we uniquely target cancer cells while sparing the rest of the body? Classically, the idea of a silver bullet has been to try to find a single target that is on the cancer cells but not on the healthy cells and focus all of your killing activity against that target.
However, there are many cancers for which that silver bullet single target doesn't exist, and this is an area where we believe our logic gated platform can solve that issue for many, many patients. We have a logic gate technology I'll walk you through that works in both NK cells and T cells, and this opens up opportunities for us to address both liquid and solid tumors. Our lead program, SENTI-202, is currently actively in a multicenter, multinational clinical study in the phase I dose expansion phase. This product is an off-the-shelf allogeneic CAR NK cell that goes after two well-validated AML targets. CD33 or FLT3 will engage the product and allow you to kill cancer cells.
However, to spare the healthy cells, including the healthy bone marrow stem cells, from being killed, we've built something called a NOT gate that recognizes this target called EMCN and protects those healthy cells from being killed. This product received orphan drug designation earlier this summer. We were selected for an oral presentation at AACR back in April, and we showed some exciting positive preliminary efficacy data, and we will have additional phase I data to be reported before the end of this year on this program. Why are we so excited about what logic gates can do? As I mentioned earlier, there's a ton of indication crowding today around similar targets, right? ADCs, T cell engagers, radiopharmaceuticals, CAR T cells, essentially are all going after the same targets.
There's only so many of those targets that are out there, and for many cancers, including AML, as well as many solid tumors, you can't find a single target that's not found on healthy cells but only found on cancer cells. The way our logic gates overcome that issue is saying, you know, instead of recognizing just a single target, let's recognize two or three or four and allow us to both protect the healthy cells but kill the cancer cells at the same time. Our SENTI-202 program aims to prove this concept out in AML, where we think there's a tremendous unmet need.
We have the ability to potentially move this program from where it is today into a pivotal study based on the totality of data that we're starting to accumulate, and I think we also view that this has a lot of opportunity to move into, you know, downstream applications in solid tumors, which we hopefully will unveil in the future. SENTI-202 targets a significant opportunity in AML. We are starting with the relapsed/refractory AML population, but we very much believe that there's opportunities to move this earlier in line. The AML disease burden in the U.S. is about 20,000 patients per year. 60% of those patients actually relapse or experience death within 12 months, so it's a very fast progressing disease. There have been some recent approvals in the relapsed/refractory AML space, including the menin inhibitors. These are small molecule drugs that require patients to have specific genetic mutations.
Up to maybe 30% of patients in the population have those. Those drugs were approved on a basis of about 100 patients, single-arm type studies with CR rates in the sort of teens, 15%- 20%, and what we call composite CR rates in the 20% range. We think there's still a tremendous opportunity here for patients that either don't qualify for those drugs, for patients that relapse after those drugs, or even in combination with those drugs as we start thinking about moving frontline. The challenge, however, in targeting AML with something that, with a biologic or a cell therapy, is that there's no single target that uniquely marks the AML cells, right? Number one, we want to be able to target heterogeneous clones in AML. That includes AML blasts.
It also includes AML leukemic stem cells, but there's no single target that's known to cover both of those. At the same time, many of the targets that people have tried to attack in the past are not just expressed on the AML cells, but they're expressed on the healthy cells, including the healthy hematopoietic stem cell or the endothelial cell populations. Our logic gates help address this problem. We have an off-the-shelf allogeneic CAR NK cell that's engineered with a single virus that carries with it three different genes. The first gene is on the upper left-hand corner. It's an activating CAR that recognizes CD33 or FLT3 or both. Both these targets are well known in the space. The reason why we chose the two is we believe they're complementary to each other. CD33 is well expressed on the AML blasts and has some expression on leukemic stem cells.
FLT3 is well expressed on the leukemic stem cells and has some expression on the blasts. By combining the two together, you can cover a much wider range of the AML tumor burden. These two targets are expressed in over 95% of the AML patient population, so we think we can capture a pretty wide range of patients coming on the study. These targets are both really well known. Why haven't they been addressed in the past? It turns out that they are also expressed on healthy hematopoietic stem cells, and you're going to run the significant risk of bone marrow suppression if you simply try to target CD33 or FLT3 with a cytotoxic agent. To try to solve this problem, what we did was identify a target called EMCN or endomucin, which is highly expressed on the healthy HSCs but not expressed on the cancer cells.
It has the opposite polarity of typically what we're looking for. What endomucin is basically triggering inside our product is recognition by this purple receptor in the middle called an inhibitory CAR that basically shuts down the killing activity, and it blocks the anti-cellular effect. That's where this killing and protection type of mechanism can be built into a single product. We also have an IL-15 that's designed into the cell therapy that allows us to stimulate the activity of the NK cells even further. I mentioned earlier that AML is a very rapidly progressing disease, and it's important for us to have a product where we're not constrained by manufacturing timelines. This is where an allogeneic off-the-shelf CAR NK process has a lot of advantages.
We can isolate NK cells from select adult donors, expand the cells in the manufacturing facility, transduce them with the virus, expand them further, and cryopreserve them. This product is literally sitting on the shelf in frozen vials and is shipped out basically the next day once we have a patient on study. We have an ongoing phase I study where we reported data at the AACR back in April. This is primarily being conducted in the U.S. as well as Australia. The main enrollment criteria for us, these are patients that are adult, over 18, under 75. They basically have to be positive for either CD33 or FLT3.
You know, CD33 is part of the diagnostic criteria for AML, so a vast majority of patients are coming on with CD33 positivity, and they must have received one to three prior AML treatments, including targeted agents if applicable. We've been exploring dose escalation with two aspects. The first is by increasing the dose. On the left-hand side, we've tested two different dose levels, either 1 billion cells or 1.5 billion cells per dose. On the right-hand side, we're testing two different dose schedules. In both these dose schedules, you have an initial round of lymphodepletion. We're using fludarabine and ARSC, which is an AML-specific regimen. The two reasons for this are flucide, which is commonly used for CAR T, is actually a B-cell regimen, and we wanted to use something here that was more specific for AML.
Secondly, from a preclinical data perspective, we found that flu and ARSC had the potential to increase the expression of CD33 and FLT3 in our cancer cells, so there may be some opportunities for complementary or synergistic activity here. In the two different dose schedules, the main reason they differ is between dose numbers. The dose schedule one has doses being given at 0, 7, and 14 days. Schedule two has it being given at 0, 3, 7, 10, and 14. We assess for efficacy at 28 days, and then patients are eligible for up to four cycles of treatment, although all of our patients to date have received only one or two cycles because if we're going to see responses, we've been seeing them actually pretty quickly. Study enrolled a very high risk relapsed/refractory AML population.
In general, these patients were less than one year from AML diagnosis, so this is a very fast progressing disease. They've received several prior lines of therapy, including exposure to regimens with fludarabine or ARSC, venetoclax, bone marrow transplant. All of these have been prior therapies that, unfortunately, the patients relapse on. Many of these patients were primary refractory, meaning that they failed to achieve a three-month or longer response in their upfront therapy, and many of them were adverse risk by ELN 2022 criterion. In general, our safety for the product was very quite good. It was well tolerated. No SAEs or DLTs that were found attributable to SENTI-202. In general, we found that the main AEs on the study were related to lymphodepletion. After lymphodepletion, you have some drop in your healthy blood cell count.
I'll show you some data later that we see actually pretty quick recovery of that in our patients. Based on the totality of data, we selected our dose level two, schedule one, for our go-forward RP2D dose. At the same time, we also had concurrence from the FDA that we could potentially administer this drug in an outpatient setting, given the safety profile that we're seeing. This is data from back in April. We have more, obviously, now that we hope to present before the end of the year, but essentially what we found was that five out of seven of the patients that were evaluable at the time of the data cutoff achieved an ORR response that includes a full CR, a CR with partial hematologic recovery, or an MLFS response.
Four out of seven actually were in that composite CR category, and all of those patients achieved an MRD negative response. MRD is not something that's routinely achievable right now with current AML drugs, especially relapsed/refractory AML. We can assess for MRD status through next-gen sequencing as well as through flow cytometry with a high sensitivity of up to 10^-4 . With that, we believe this is a great outcome for the patients since MRD negative status is known to translate into better clinical outcomes. Across all the patients, looking at their bone marrow before and after treatment, we saw a pretty wide range of bone marrow blasts to start, but also significant reduction in bone marrow blast counts with the treatment in almost all patients.
At the time of this data set back in April, we had durability data in our patients from anywhere from four plus to eight plus months. The plus indicates that those responses were still ongoing. Obviously, we're in October now, so we've been continuing to follow patients, and we will have more patients to report on by the end of the year. Many of our patients, especially ones we saw responses in, were either primary refractory, adverse risk, and also refractory or exposed to fludarabine and ARSC in the past. We were excited to see that for our patients. We've also been doing some detailed CyTOF analysis with our collaborators at MD Anderson. The goal here is to try to test, are we actually achieving the MOA that we designed this product to achieve?
Using CyTOF, you can simultaneously look at a very large number of biomarkers on the cells, on the healthy and the cancer cells at the same time. Here, we're looking at leukemic stem cells. Here's two pieces of data here on the left-hand side. Across the patients, you can see that our LSCs in those patients are generally in the G0 state, so they're not actively cycling. This is well known in the space, in the field, in that LSCs are not easily killed by small molecules or chemotherapy drugs, and that's probably one of the reasons why this is a very refractory population of cancer cells that can repopulate and cause relapse to happen.
However, on the right-hand side, we are able to see that with our drug, we are able to achieve LSC killing in many of our patients, and actually in all the patients that achieved a CR or composite CR, we saw LSCs decreasing by over tenfold. At the same time, we want to make sure that we're sparing or allowing the recovery of the healthy cells, right? Patients with AML oftentimes are dependent on transfusions because of low platelet counts. They may be susceptible to infections because of a poor immune system, in part due to the significant tumor burden they're carrying in their bone marrow. What we can see here on the left-hand side is platelets as well as neutrophil counts. Within the first few days of lymphodepletion, you see a significant reduction in both of these cell counts, and that's consistent with lymphodepletion.
There's about a 14 to 21-day time window after which you see a significant recovery, actually, of many of these patients above the threshold for CR in some cases, which is that blue line on the left. In actually some patients, we saw complete normalization of platelets and neutrophils, which was very exciting to see. On the right-hand side is actually looking, using CyTOF, at the healthy hematopoietic stem and progenitor population. We see in the patients that were treated with the drug, we saw a maintenance or even increase in these healthy progenitor cells in the patient bone marrow. That's consistent with the mechanism of action we've designed this for. Finally, we've seen that the PKs, as expected with an allogeneic cell therapy, we're not expecting this product to be a one-and-done sort of approach. This is a multi-cycle, multi-dose type approach, which is enabled by our off-the-shelf manufacturing.
We can see across both cycles that we're generally detecting patient product. We're detecting product in the periphery of the patients for about a two-week time period, and we're able to give repeated dose safely and still detect product in those populations. In summary, we're very excited about SENTI-202 and what it's been able to achieve so far in this very difficult-to-treat relapsed/refractory AML population. We are actively in the dose expansion phase of the trial. We will have a significant data set to report by the end of the year and aim to be able to then move this, assuming the data continues to hold, move this into a next study downstream.
Given the precedence in the area of relapsed/refractory AML, being able to generate FDA breakthrough status, 100 patients, 150 patients to get it to approval with the menin inhibitors, we think there's a well-trodden path for us to move this program forward. In the last few minutes, I just wanted to highlight the potential for this logic gate technology, more broadly speaking. Beyond relapsed/refractory AML, we think there's opportunities to move this into the newly diagnosed AML and MDS opportunity space. We also think that the logic gates here can have broad applicability for solid tumors. In solid tumors, we have a lot of modalities chasing the same targets, but there are many solid tumors for which these targets are not clean enough for us to get a really good therapeutic window.
We've been working to adapt our logic gate technology to go after new targets, including in the solid tumor space, as well as to get them to function into T cells because certainly for some applications, one may want the optionality to choose a T cell-based approach versus an NK approach. This is just one example of this in action. This is actually microscopy imaging where we are mixing red cells, which represent cancer cells here. The cancer cells express a target called CEA, which is a well-understood target that is overexpressed in colorectal cancer, some lung cancer, and even gastric cancers. The problem with CEA as a target is that it's also expressed on healthy epithelial cells, including in the lung and the colon.
In prior efforts, for example, NIH had a TCRT trial against CEA where they saw evidence of efficacy but also significant colitis that actually paused the trial. We went through a whole underlying design process again and actually identified a protective target called VSIG2, which is found on the healthy cell shown in green here, and we've built that into a CAR T cell to kill CEA-expressing cells but not VSIG2-expressing cells. You can see on the left-hand side here, if you basically have no treatment and you mix red and green cells together, both of them grow. In the middle here, if you simply go after CEA on its own, you kill both populations, but if you have our CEA not VSIG2 CAR T cells, you're able to selectively kill the red cells but spare the green cells.
This is the type of opportunity we see downstream beyond the hematology space with this technology platform. With that, I'd like to thank you very much for your time. In summary, we've built this logic gated technology that allows us to leverage the intelligence of cells to recognize cancer cells but spare those healthy cells from being killed. We are driving through our RP2D dose expansion now, hope to have data by the end of the year, and look forward to being able to advance this program into a pivotal study downstream. With that, thank you very much for your time.
We do have time for one or two quick questions. Maybe can you touch on what we can expect to see in your next data release for SENTI-202?
Sure.
It should be this year.
Yeah, I think at AACR, I think the data was exciting, but obviously it's a relatively small number. What we've been doing is dose expanding now. I think we'll have close to 20 patients' worth of data by the end of the year, and I think that'll give us much better statistics to confirm sort of the responses that we're seeing. Certainly, we're also looking at durability, right? Just with the increasing passage of time, assuming that patients continue to be in response, and we have new patients as well that we're following, you'll see significantly longer following of those patients as well. We're also going to have a significant amount of additional correlative data using CyTOF analyses.
Our next speaker for this.
Co-founder here at Senti Bio. Really excited to spend some time sharing with you guys our lead program that uses something unique called a logic gate to solve one of the central problems in oncology, as well as some of the clinical data that's coming out for this. Senti Biosciences is trying to tackle one of the major challenges in the cancer space, which is how do we uniquely target cancer cells while sparing the rest of the body? Classically, the idea of a silver bullet has been to try to find a single target that is on the cancer cells but not on the healthy cells and focus all of your killing activity against that target.
However, there are many cancers for which that silver bullet single target doesn't exist, and this is an area where we believe our logic gated platform can solve that issue for many, many patients. We have a logic gate technology I'll walk you through that works in both NK cells and T cells, and this opens up opportunities for us to address both liquid and solid tumors. Our lead program, SENTI-202, is currently actively in a multicenter, multinational clinical study in the phase I dose expansion phase. This product is an off-the-shelf allogeneic CAR NK cell that goes after two well-validated AML targets. CD33 or FLT3 will engage the product and allow you to kill cancer cells.
However, to spare the healthy cells, including the healthy bone marrow stem cells, from being killed, we've built something called a NOT gate that recognizes this target called EMCN and protects those healthy cells from being killed. This product received orphan drug designation earlier this summer. We were selected for an oral presentation at the AACR back in April, and we showed some exciting positive preliminary efficacy data, and we will have additional phase I data to be reported before the end of this year on this program. Why are we so excited about what logic gates can do? As I mentioned earlier, there's a ton of indication crowding today around similar targets, right? ADCs, T cell engagers, radiopharmaceuticals, CAR T cells essentially are all going after the same targets, but there's only so many of those targets that are out there.
For many cancers, including AML as well as many solid tumors, you can't find a single target that's not found on healthy cells but only found on cancer cells. The way our logic gates overcome that issue is saying, you know, instead of recognizing just a single target, let's recognize two or three or four and allow us to both protect the healthy cells but kill the cancer cells at the same time. Our SENTI-202 program aims to prove this concept out in AML, where we think there's a tremendous unmet need.
We have the ability to potentially move this program from where it is today into a pivotal study based on the totality of data that we're starting to accumulate, and I think we also view that this has a lot of opportunity to move into downstream applications in solid tumors, which we hopefully will unveil in the future. SENTI-202 targets a significant opportunity in AML. We are starting with the relapsed/refractory AML population, but we very much believe that there's opportunities to move this earlier in line. The AML disease burden in the U.S. is about 20,000 patients per year. Sixty percent of those patients actually relapse or experience death within 12 months, so it's a very fast progressing disease. There have been some recent approvals in the relapsed/refractory AML space, including the menin inhibitors. These are small molecule drugs that require patients to have specific genetic mutations.
Up to maybe 30% of patients in the population have those. Those drugs were approved on a basis of about 100 patients, single-arm type studies with CR rates in the sort of teens, 15 to 20% percent, and what we call composite CR rates in the 20% range. We think there's still a tremendous opportunity here for patients that either don't qualify for those drugs, for patients that relapse after those drugs, or even in combination with those drugs as we start thinking about moving frontline. The challenge, however, in targeting AML with something that, with a biologic or a cell therapy, is that there's no single target that uniquely marks the AML cells, right? Number one, we want to be able to target heterogeneous clones in AML. That includes AML blasts.
It also includes AML leukemic stem cells, but there's no single target that's known to cover both of those. At the same time, many of the targets that people have tried to attack in the past are not just expressed on the AML cells, but they're expressed on the healthy cells, including the healthy hematopoietic stem cell or the endothelial cell populations. Our logic gates help address this problem. We have an off-the-shelf allogeneic CAR NK cell that's engineered with a single virus that carries with it three different genes. The first gene is on the upper left-hand corner. It's an activating CAR that recognizes CD33 or FLT3 or both. Both these targets are well known in the space. The reason why we chose the two is we believe they're complementary to each other. CD33 is well expressed on the AML blasts and has some expression on leukemic stem cells.
FLT3 is well expressed on the leukemic stem cells and has some expression on the blasts, so by combining the two together, you can cover a much wider range of the AML tumor burden. These two targets are expressed in over 95% of the AML patient population, so we think we can capture a pretty wide range of patients coming on the study. These targets are both really well known. Why haven't they been addressed in the past? It turns out that they are also expressed on healthy hematopoietic stem cells, and you're going to run the significant risk of bone marrow suppression if you simply try to target CD33 or FLT3 or the cytotoxic agent.
To try to solve this problem, what we did was identify a target called EMCN or endomucin, which is highly expressed on the healthy HSCs but not expressed on the cancer cells, so it has the opposite polarity of typically what we're looking for. What endomucin is basically triggering inside our product is recognition by this purple receptor in the middle called an inhibitory CAR that basically shuts down the killing activity, and it blocks the anti-cellular effect. That's where this killing and protection type of mechanism can be built into a single product. We also have an IL-15 that's designed into the cell therapy that allows us to stimulate the activity of the NK cells even further. I mentioned earlier that AML is a very rapidly progressing disease, and it's important for us to have a product where we're not constrained by manufacturing timelines.
This is where an allogeneic off-the-shelf CAR NK process has a lot of advantages. We can isolate NK cells from select adult donors, expand the cells in the manufacturing facility, transduce them with the virus, expand them further, and cryopreserve them. This product is literally sitting on the shelf in frozen vials and is shipped out basically the next day once we have a patient on study. We have an ongoing phase I study where we reported data at AACR back in April. This is primarily being conducted in the U.S. as well as Australia. The main enrollment criteria for us, these are patients that are adult, over 18, under 75. They basically have to be positive for either CD33 or FLT3.
You know, CD33 is part of the diagnostic criteria for AML, so a vast majority of patients are coming on with CD33 positivity, and they must have received one to three prior AML treatments, including targeted agents if applicable. We've been exploring dose escalation with two aspects. The first is by increasing the dose. On the left-hand side, we've tested two different dose levels, either 1 billion cells or 1.5 billion cells per dose. On the right-hand side, we're testing two different dose schedules. In both these dose schedules, you have an initial round of lymphodepletion. We're using fludarabine and ARSC, which is an AML-specific regimen. The two reasons for this is flucide, which is commonly used for CAR T, is actually a B-cell regimen, and we wanted to use something here that was more specific for AML.
Secondly, from a preclinical data perspective, we found that flu and ARSC had the potential to increase the expression of CD33 and FLT3 in our cancer cells, so there may be some opportunities for complementary or synergistic activity here. In the two different dose schedules, the main reason they differ is between dose numbers. The dose schedule one has doses being given at 0, 7, and 14 days. Schedule two has it being given at 0, 3, 7, 10, and 14. We assess for efficacy at 28 days, and then patients are eligible for up to four cycles of treatment, although all of our patients to date have received only one or two cycles because if we're going to see responses, we've been seeing them actually pretty quickly. Study enrolled a very high-risk relapsed/refractory AML population.
In general, these patients were less than one year from AML diagnosis, so this is a very fast progressing disease. They've received several prior lines of therapy, including exposure to regimens with fludarabine or ARSC, venetoclax, bone marrow transplant. All of these have been prior therapies that, unfortunately, the patients relapse on. Many of these patients were primary refractory, meaning that they failed to achieve a three-month or longer response in their upfront therapy, and many of them were adverse risk by ELN 2022 criterion. In general, our safety for the product was very, quite good. It was well tolerated. No SAEs or DLTs that were found attributable to SENTI-202. In general, we found that the main AEs on the study were related to lymphodepletion, so after lymphodepletion, you have some drop in your healthy blood cell count.
I'll show you some data later that we see actually pretty quick recovery of that in our patients. Based on the totality of data, we selected our dose level two, schedule one, for our go-forward RP2D dose. At the same time, we also had concurrence from the FDA that we could potentially administer this drug in an outpatient setting, given the safety profile that we're seeing. This is data from back in April. We have more, obviously, now that we hope to present before the end of the year, but essentially what we found was that five out of seven of the patients that were evaluable at the time of the data cutoff achieved an ORR response that includes a full CR, a CR with partial hematologic recovery, or an MLFS response.
Four out of seven actually were in that composite CR category, and all of those patients achieved an MRD negative response. MRD is not something that's routinely achievable right now with current AML drugs, especially relapsed/refractory AML. We can assess for MRD status through next-gen sequencing as well as through flow cytometry with a high sensitivity of up to 10^-4. With that, we believe this is a great outcome for the patients since MRD negative status is known to translate into better clinical outcomes. Across all the patients, looking at their bone marrow before and after treatment, we saw a pretty wide range of bone marrow blasts to start, but also significant reduction in bone marrow blast counts with the treatment in almost all patients.
At the time of this data set back in April, we had durability data in our patients from anywhere from four plus to eight plus months. The plus indicates that those responses were still ongoing. Obviously, we're in October now, so we've been continuing to follow patients, and we will have more patients to report on by the end of the year. Many of our patients, especially ones we saw responses in, were either primary refractory, adverse risk, and also refractory or exposed to fludarabine and ARSC in the past, so we're excited to see that for our patients. We've also been doing some detailed CyTOF analysis with our collaborators at MD Anderson. The goal here is to try to test are we actually achieving the MOA that we designed this product to achieve.
Using CyTOF, you can simultaneously look at a very large number of biomarkers on the cells, on the healthy and the cancer cells at the same time. Here we're looking at leukemic stem cells. Here's two pieces of data here on the left-hand side. Across the patients, you can see that our LSCs in those patients are generally in the G0 state, so they're not actively cycling. This is well known in the space, in the field, in that LSCs are not easily killed by small molecules or chemotherapy drugs, and that's probably one of the reasons why this is a very refractory population of cancer cells that can repopulate and cause relapse to happen.
However, on the right-hand side, we are able to see that with our drug, we are able to achieve LSC killing in many of our patients, and actually in all the patients that achieved a CR or a composite CR, we saw LSCs decreasing by over tenfold. At the same time, we want to make sure that we're sparing or allowing the recovery of the healthy cells, right? Patients with AML oftentimes are dependent on transfusions because of low platelet counts. They may be susceptible to infections because of a poor immune system, in part due to the significant tumor burden they're carrying in their bone marrow. What we can see here on the left-hand side is platelets as well as neutrophil counts. Within the first few days of lymphodepletion, you see a significant reduction in both of these cell counts, and you know, that's consistent with lymphodepletion.
There's about a 14 to 21-day time window after which you see a significant recovery, actually, of many of these patients above the threshold for CR in some cases, which is that blue line on the left. In actually some patients, we saw complete normalization of platelets and neutrophils, which was very exciting to see. On the right-hand side is actually looking, using CyTOF, at the healthy hematopoietic stem and progenitor population, and we see in the patients that were treated with the drug, we saw a maintenance or even increase in these healthy progenitor cells in the patient bone marrow. That's consistent with the mechanism of action we've designed this for. Finally, we've seen that the PKs, as expected with an allogeneic cell therapy, we're not expecting this product to be a one-and-done sort of approach.
This is a multi-cycle, multi-dose type approach, which is enabled by our off-the-shelf manufacturing. We can see across both cycles we're generally detecting patient product. We're detecting product in the periphery of the patients for about a two-week time period, and we're able to give repeated dose safely and still detect product in those populations. In summary, we're very excited about SENTI-202 and what it's been able to achieve so far in this very difficult-to-treat relapsed/refractory AML population. We are actively in the dose expansion phase of the trial. We will have a significant data set to report by the end of the year and aim to be able to then move this, assuming the data continues to hold, move this into a next study downstream.
Given the precedence in the area of relapsed/refractory AML, being able to generate FDA breakthrough status, 100 patients, 150 patients to get it to approval with the menin inhibitors, we think there's a well-trodden path for us to move this program forward. Last few minutes, I just wanted to highlight the potential for this logic gate technology, more broadly speaking. Beyond relapsed/refractory AML, we think there's opportunities to move this into the newly diagnosed AML and MDS opportunity space. We also think that the logic gates here can have broad applicability for solid tumors. In solid tumors, we have a lot of modalities chasing the same targets, but there are many solid tumors for which these targets are not clean enough for us to get a really good therapeutic window.
We've been working to adapt our logic gate technology to go after new targets, including in the solid tumor space, as well as to get them to function into T cells because certainly for some applications, one may want the optionality to choose a T cell-based approach versus an NK approach. This is just one example of this in action. This is actually microscopy imaging where we are mixing red cells, which represent cancer cells here. The cancer cells express a target called CEA, which is a well-understood target that's overexpressed in colorectal cancer, some lung cancer, and even gastric cancers. The problem with CEA as a target is that it's also expressed on healthy epithelial cells, including in the lung and the colon.
In prior efforts, for example, NIH had a TCRT trial against CEA where they saw evidence of efficacy but also significant colitis that actually paused the trial. We went through a whole underlying design process again and actually identified a protective target called VSIG2, which is found on the healthy cells shown in green here, and we've built that into a CAR T cell to kill CEA-expressing cells but not VSIG2-expressing cells. You can see on the left-hand side here, if you basically have no treatment and you mix red and green cells together, both of them grow. In the middle here, if you simply go after CEA on its own, you kill both populations, but if you have our CEA not VSIG2 CAR T cells, you're able to selectively kill the red cells but spare the green cells.
This is the type of opportunity we see downstream beyond the hematology space with this technology platform. With that, I'd like to thank you very much for your time. In summary, you know, we've built this logic gated technology that allows us to leverage the intelligence of cells to recognize cancer cells but spare those healthy cells from being killed. We are driving through our RP2D dose expansion now, hope to have data by the end of the year, and look forward to being able to advance this program into a pivotal study downstream. With that, thank you very much for your time.
We do have time for one or two quick questions. Maybe can you touch on what we can expect to see in your next data release for SENTI-202?
Sure.
It should be this year.
Yeah, I think at AACR, look, I think the data was exciting, but obviously it's a relatively small number. What we've been doing is dose expanding now. I think we'll have close to 20 patients' worth of data by the end of the year, and I think that'll give us much better statistics to confirm sort of the responses that we're seeing. Certainly, we're also looking at durability, right? Just with the increasing passage of time, assuming that patients continue to be in response, and we have new patients as well that we're following, you'll see significantly longer following of those patients as well. We're also going to have a significant amount of additional correlative data using CyTOF to confirm the mechanism of action. Those are all going to be coming soon and give us continued confidence on this program moving forward.
Great. If there are no questions, I think we've reached the end of the session. Thank you very much.