Great. I think the slides are up. Hopefully, you can see them. Hey, good morning, good afternoon, everyone. Abizer Gaslightwala, I'm the CEO of Akari Therapeutics. Relatively new to the role, just came in a little bit over a month ago, but I came in with a lot of excitement because we're going to talk about what Akari is doing on antibody drug conjugates, advancing them from their current state with what we believe are novel immuno-oncology payloads that will make a big difference in the oncology space and in the ADCs. What do we mean by that? At a high level, these immuno-oncology payloads are very different than the ADCs, antibody drug conjugates that you hear about today, that you see about today in the news and in updates. ASCO is coming up. You'll see a lot of these ADCs in the news.
These novel immuno-oncology payloads are a different way to construct these ADCs, and we believe a really differentiated method. I'm going to show you some data and why we believe and why I joined Akari, frankly. Let's go to the next slide. Sort of forward-looking statements. How about the next slide? I just want to kind of spend a minute here. I talked about our vision a little bit. You saw up front the kind of subject line. Our vision is very similar in terms of we're focused on innovating antibody drug conjugates as immuno-oncology therapies for patients to be cancer-free. The reason we were very intentional around this is that currently, when you look at antibody drug conjugates, these ADCs, they tend to have what we call these Cytotoxic Chemotherapeutic Agents on them that kill cells, just like chemotherapy. They're fairly targeted chemotherapy.
What we believe we're doing is we're actually innovating that toxin or payload as an immuno-oncology therapeutic. The reason that's important is because, as you've seen in the cancer space recently, in particular because of big products like Keytruda, Opdivo, they're called checkpoint inhibitors, immuno-oncology, immunotherapy is really one of the most enduring ways to make cancer go away, to help patients be cancer-free. If we can do that with an ADC, just like checkpoint inhibitors, but do it for even more patients that would respond than they do to checkpoint inhibitors, which is only about 20% of all cancer patients, we have a chance to help patients be cancer-free. That is the ultimate goal. Let's talk more about why we believe and we're strong about why we have such strong confidence in this. As I mentioned, we have this novel payload. It's called PH1.
That's our internal name. What that means, its internal nomenclature, is that it targets something called the spliceosome, the spliceosome machinery in cells. This is an important thing because by attacking the spliceosome, which is responsible for making critical proteins for the cancer cell to survive, it causes the cell to die. More importantly, it actually causes the cell to look foreign to the immune system, which means that's when the immune system gets primed up and starts attacking it. Once it starts attacking that cancer cell, it attacks similar cancer cells. That's what makes our payload really unique, that it kills a cell, but it also revs up the immune system. We're really excited because we've been able to develop this payload.
Once all the engineering and the work and the testing has been done on the payload, now we can put it on a lot of different targets, what we call the missile for ADCs. Where does that guided GPS missile go? Our first asset, our lead asset, it's called AKTX-101. It targets something called TROP2, which you may have heard of. It's an antigen expressed on cancer cells or a marker that's on cancer cells. This TROP2 is conjugated to the PH1 payload. What we've seen in data to date is really robust activity in preclinical models, both as a single agent and, importantly, in combination with those agents I mentioned before, checkpoint inhibitors. The holy grail. How can we synergize with this $40 billion class of checkpoint inhibitors to go beyond what they can do today?
That is what we believe we have some really early promising data around. We have also been able to show we have favorable safety in what we call a non-human primate study. That is a monkey study. That is important because, as you know, the monkeys are very close to humans in terms of Physiology. You know, obviously, you do rat toxicity. This monkey toxicity is a good study that helps us determine that we think we have some good early safety data to ensure that this product can be safely dosed. More to do there, but that is a good early sign. What it also means is we can take this payload, this PH1. We started with TROP2, but we can move on to other things. We have a couple of other novel cancer targets we are developing that could target colon cancer, lung cancer, and prostate cancer.
These are three of the largest solid tumor cancers out there that affect patients today. We believe we have an opportunity to address those with this payload and the right antibody. Let's go to the next slide, please. I just want to introduce you to the team. I'm here today. I'll give a little background on myself, our team as well, our senior leadership team, Torsten Hombeck. He's our Chief Financial Officer. He's been with Akari. Recently joined again, was with Akari before as well. A lot of Senior Veteran and tenured experience there. Satyajit Mitra, he's our Head of Oncology. He developed many of the aspects of this PH1 and this lead antibody in our platform. He's been with Akari through the Peak acquisition that recently happened and has been one of the pioneers of this platform. Really excited to bring on Mark Kubicki.
Just announced a little short time ago. You may have seen some more PR around this. Mark is our Head of Business Development for Oncology. He was brought in based on a really successful track record in the ADC space, and particularly, he was at Seattle Genetics, which many of you probably know. In the early days, though, he did one of the first deals on their ADC with Takeda and has been in the space ever since. Really excited to have someone of this caliber join us to help think about partnerships with other companies as well. You know, why did I join? I mentioned I joined about a month ago, a little over a month ago. What excited me? Before I was at Akari, I was at Jazz Pharmaceuticals.
Prior to Jazz, I was at many large pharmas, including Johnson & Johnson, Pfizer, and Amgen. We had a variety of different roles, in particular, a number of roles in oncology. At Jazz, my role there is I led our oncology business across a pretty broad portfolio of products that were both in the hematological blood cancer space and solid tumor. We had about a six-product portfolio. We grew that from three to six. Before I left, we were about a billion dollars in the US and a little bit bigger than that ex-U.S.. Really tremendous growth and success we had at Jazz. Why would I leave Jazz to come to Akari? The reason is at Jazz, as we were launching into the solid tumor space with some of our assets, we got to really be familiar with antibody drug conjugates.
We got to, as we had to think about how to compete with them, we learned how strong and what a benefit impact they've had, in particular, some of the HER2 antibody drug conjugates out there in terms of the efficacy and the responses they had and the benefits for patients. What we also saw was some of the liabilities and the toxicities of these ADCs and the limitations. You start to think, wow, these work really well as a class, but there are obviously areas of improvement. Are there people working on ADCs that go beyond these that can address these limitations? I was approached by Akari about joining their board and then after that, joined as CEO. The reason I joined is because Akari has that special secret sauce.
Many of those things I just spoke about around limited efficacy, toxicity, safety effects from some of the current ADCs, Akari has ways to address that to go beyond. That is what excited me to join the board in December and then recently take over the CEO role. Let me speak to you about some of the reasons why I'm so excited around this platform. Go to the next slide, please. As I mentioned, I'll just cover real quick. Our lead asset is the TROP2 ADC. We think that could play in lung cancer as well as potentially in gastric cancer. We're working on advancing that to what we call IND-enabling studies that would enable us to start a phase one trial.
Behind that, we have two other undisclosed targets we're actively working on to develop our novel payload with these antibodies across targets we haven't disclosed that could play in colon cancer, pancreatic cancer, and potentially prostate. Large solid tumors, unmet need there as well. Again, what we say is the universality here, the real beauty of this payload is that now that we've developed a payload, we can find many different antibodies that can select antigen targets on cancer cells. We can create multiple therapeutics very quickly. This can be done with Akari alone, or we can do it with partners. We're open to both those options. Let's go to the next slide. Just to give you a background, you know, why are ADCs so exciting? As you can see here, they are doing very well in the market.
You can see the multi-billion dollar sales being led by some of the lead ADCs. Some of these are actually acquired through acquisitions. This is a brief reminder. Trodelvy was a product that Gilead acquired from ImmunoGen or, sorry, Immunomedics, sorry, about two, three, four years ago for about a $20 billion acquisition price. Clearly, there was a lot of excitement then. Enhertu was out of the AstraZeneca-Daiichi Sankyo partnership. That was a multi-billion dollar investment by AZ into Daiichi about almost seven, eight years ago. That has resulted in that great product. You know, Padcev is a product that Seattle Genetics had initially commercialized. Obviously, you're familiar with Seattle Genetics being bought by Pfizer for over $40 billion. Elahere came from ImmunoGen, recently acquired by AbbVie about a year, year and a half ago for about $10 billion.
You clearly see large sums of cash and interest by big pharma in ADCs. There is clearly opportunity on exits and opportunity. Big pharma is very motivated, but not just big pharma, mid-sized pharma and other players. Everyone wants to play in the ADC space. The unique thing is that all the ADCs you see here and all the ones in development, with the exception of ours, pretty much use the same payload, same set of payloads. Those are what we call microtubule inhibitors or TOPO1 inhibitors. The microtubule inhibitors are the ones that often are found on some of the Seattle Genetics ADCs. The TOPO1 inhibitors are the ones that you see here for Trodelvy or Enhertu or the AstraZeneca or Gilead ADCs. That is what all the other ADCs in development are really using, those two classes.
What excites us is that we have something that's very different that acts very differently on that spliceosome, but also activates the immune system in a different way, in a novel way that these others do not. Let's go to the next slide. Just to highlight continued interest in ADCs, you know, those are some of the commercial ADCs. This shows just recently, even in the last year, actually in the last three to four months from late 2024 to 2025, there is continued early stage activity in the ADC space. You see the licensee, you see the licensee. I'm not going to go through all these.
You see a lot of these are still getting pretty sizable upfront payments, which are huge value inflection points for these licensees as they advance their early stage ADCs, which is exactly the space we're in as well with our novel payload. Again, the point to highlight here is that every one of these ADCs and platforms are all using those same two payloads that I just mentioned or potentially some different linker strategies with the same payloads. We are differentiated than all these other ones out there by our payload PH1. Let me tell you again some of the benefits and attributes of our product. Again, our ADC therapies with this PH1 payload, as I mentioned, you know, we do multiple things. We kill the cancer cells that are targeted with that antigen, like TROP2, for instance, while activating the immune system.
This is really important because we're basically causing these cancer cells to make misspliced or bad proteins that are considered foreign, which really rev up the immune system to kill them. That is really different than any other payload out there. What that means is that we can synergize or combine with those checkpoint inhibitors, those Keytrudas and Opdivos and Tecentriqs, which are multi-billion dollar products in themselves, but have not really found a good marriage partner. You know, big pharma has tried for years to find what else could combine well that synergizes with those, and they haven't found anything. However, we have data that shows we're synergistic, not just additive. This could crack the nut on one of the big opportunities of combination checkpoint inhibitor immunotherapy. We've also engineered this payload to overcome resistance mechanisms by the cancer cells.
That's often why you see some of these products, the current ADCs, lose effect. The cancer cells are smart. They know how to overcome those mechanisms. We've actually engineered this payload to be a little bit resistant to those resistance mechanisms that it won't get cleared out in the way some of these current payloads do. We've also found ways to reduce the off-target toxicity by some of the novel engineering work around the linker and the payload, et cetera. These are some of the attributes. What that means, what it translates. Let's go to the next slide. I'm just going to give you one high-level image of some of the data we have that excites us. On the left, what you can see here is this is a mouse that's been injected with a specific type of colon cancer.
You have four different arms or treatment arms. One is a placebo called the vehicle. The blue is called on the very left immuno-oncology. That is the PD-1, PD-L1 inhibitor that I mentioned as a control as well. The orange dotted is our product. That is a monotherapy single agent with the PH1 payload. The last line at the very top, the solid, is the IO drug plus our agent, the immunotherapy checkpoint inhibitor with our drug, the combination. You can see clearly our orange lines are better both as a single agent and as a combination. In particular, the combination agent, seven out of eight, almost 90% of these mice survive up to 150 days. 150 days. Now, remember, the mice do not live very long, even when they are healthy, much less when they are injected with cancer cells.
The fact we had almost 90% of our mice survive to 150 days, you can see the results for the other arms that did not have such success. What's really interesting is those mice that survived 150 days, those seven, when we go actually, they're kind of cured. They don't have their cancer anymore. They've been cured at least by our combination regimen. When you go re-inject those mice on the very right, the first graph, you see the orange line flat because basically the tumor doesn't grow. Whereas when you do a control with mice that were not treated with our product in the past, you see the tumor grow. What that means is we're actually creating immunological memory, which means we've taught the immune system how to attack the cancer cell.
It remembers when it sees that cancer cell again, if it ever comes back, it's ready to prime and activate to kill it. That's pretty unique. That's pretty novel. That's something that current ADCs we believe don't do today that we think we can differentiate on to pay off that longer-lasting remission that patients want ultimately. Where do we go from here? Let me just go to the next slide. You know, this is the why now. This is clearly compelling data we have for Akari. We believe we have this unique payload, PH1. We've already advanced it in our lead ADC called the TROP2 PH1 ADC that has opportunities in the largest solid tumor space, lung cancer. We know that ADCs have a lot of deal interest even in early stages, as we talked about earlier.
We're also actively looking at how to take this payload, this PH1 immuno-oncology payload, into new antibodies. We're going to do that by ourselves. We're also going to do it with big pharma and other partners that want to work with us to do this as well, because we believe by advancing this platform, either independently or with partners, we're going to create multiple value inflection points moving forward. That's a little bit of my why. That's why I'm excited about Akari, why I joined, and what our mission and task is here. We would love for all of you to continue to be on the ride with us. We thank those of you that have been invested in our stock to continue.
We encourage others that are just learning about Akari to continue to get more interested and learn more and follow us as we evolve this journey. With that, let's take some questions. I think let me ask one question. You know, those of you, there's one why shift from inflammation to oncology ADCs. That was a question, you know, just to kind of highlight Akari is a company that was in existence since 2015. They had an inflammation portfolio. Unfortunately, that portfolio did not get advanced, maybe in the ways that the board and the leadership team at that time thought. There was an opportunistic way to merge and repivot the company to oncology. In particular, because Peak Bio had this really unique platform that we just talked about, the PH1 payload combining with ADCs.
I think the direction was Akari wants to pivot and shift out of inflammation and move to oncology. Hence, that's the story of oncology. Hence why I'm here, ultimately, because I'm an oncology person and I see a vision and great data and forging a path forward. I think, you know, a little bit of the past is the past. What's the forward look? The forward look is Akari is an oncology company. However, we will be outlicensing those inflammation assets. We do think they have value for other people outside the space who are in inflammation. We are actively looking to outlicense those to create non-dilutive financing capital for us to invest in the oncology business. You know, ultimately, there are a couple of other questions. What's the recent uptick in big pharma interest in early stage ADC platforms?
Can you comment on our current partnering and deal discussions? Sure. You know, I think because some of the current ADCs, as I showed, some of the multi-billion dollar sales have really taken off, it's really validated ADCs as one of the top modalities, if not in oncology, the hottest way. There are a lot of ways to attack cancer. You know, things have been in the past. ADCs are the hottest. Now you see this tremendous focus and efforts to create ADCs early, mid-stage to kind of go after the opportunity, just like people saw with antibodies, general antibodies about 20 years ago. What you see, that's the reason why people get in there. Now, because there's so much momentum, people are looking earlier and earlier because a lot of the mid to late stage products are gone. They've been acquired.
A lot of those products I talked about were acquired by big pharma. Now everything's a lot earlier. We believe what's really unique about us is our payload and our approach is different than all the other things you're seeing, than any of those deals we just talked about. That's where we're going to stand out. Hence, that's the conversations we're having with a number of companies across the spectrum. Obviously, I can't name names around their interest in our payload and our interest in our approach and where we go from here. I think the last question, I know we're almost out of time. I'll just try to take one more. You know, I think what is the missplice? How do we actually work on the proteins? How do we cause these misspliced proteins? Essentially, ultimately, think about a film.
When you make a film, you have raw, bad footage. You have to cut it, you have to splice it, you make the perfect. That is the perfect film you watch and enjoy. What happens with protein production, in particular in cancer cells, they need a lot of proteins to survive. They're always making these proteins. What we do is we inhibit that splicing process. Imagine if you do not take the bad edits out of a film, you have a bad film to watch. That is kind of what we do. We create a bad film. That bad film is not fun. It is not entertaining. It is not interesting. That is what happens to the protein. What happens is that protein does not look like normal proteins. The immune system is very good at recognizing what we call foreign proteins, such as bacteria and viruses.
These proteins become more like that. That is what really revs up the immune system and gets it activated against those proteins and against the cancer cell right there as well as surrounding cancer cells. That is a bit of a nutshell of how we work. I just want to thank everyone for your attention. Really excited to tell the Akari story. Mike's excitement to come here, the vision, the passion we have as a team to kind of carry forward the new Akari. We love your support on this journey. Thank you for those that have been with us. We want to encourage those who are not, learn a little bit more, go to our website. We will continue to educate you. Really excited about some evolving data that we are going to be presenting later in the year as well, hopefully. Thank you.
Thanks so much for your time, Abizer. Again, please make sure to head to the Akari Therapeutics Corporate Connect page on the Webull app for updates. Now we will hear from the CEO of Senti Biosciences, Tim Liu. Senti Bio is a clinical stage biotechnology company developing a new generation of cell and gene therapies for patients living with incurable diseases. To achieve this, Senti Bio is leveraging a synthetic biology platform called Gene Circuits to create therapies with enhanced precision and control. Before I pass it off, again, please note that Webull was not involved in the preparation of any of the presentation materials, and this is not a research recommendation, solicitation, or endorsement of any kind. No investor should rely solely on the information provided in making a decision to invest. Now I'd like to introduce the CEO of Senti Biosciences, Tim Liu.
You can share your screen now.
All right. Thank you so much for the opportunity to be here. I'm really excited to tell you about what we're doing here at Senti, really trying to transform the landscape of cancer therapeutics. We're making some forward-looking statements here, so just a brief disclaimer. In terms of an overview of Senti, we are a clinical stage biotech company that's developing something called Logicate. As I'll show you, these Logicates allow us to target cancers that are previously untargettable by conventional modalities, including T-cell engagers, ADCs, CAR T-cells, et cetera. Our lead program, Senti-202, is currently in the clinic. It is designed to attack relapsed refractory AML and related cancers. We recently reported positive clinical data, both from an efficacy, safety, and durability perspective at the AACR 2025 meeting. We're quite excited to share that with you here today.
Our product enables scalable off-the-shelf manufacturing, which streamlines treatment for patients. The Gene Circuit platform allows us to specifically target cancer cells while sparing healthy cells, a very unique feature that other products are currently unable to achieve. Senti-202 is the company's lead clinical program that we're advancing into and through early stage clinical trials. This technology, called Logicate, does have applications beyond AML, though. We do believe that there's much use of this in areas outside of just the hematological cancers, for example, into solid tumors. We have programs that are actually in active development there as well. Today, I'm going to focus on this Logicate technology. It allows us to essentially separate disease cells from healthy cells and really concentrate therapeutic activity against the disease cells while sparing the healthy cells.
However, I just briefly mentioned Senti does have other sets of technologies that are applicable to the cell and gene therapy space, including arming cells to make them more powerful when they attack cancers, enabling cell and gene therapies to be regulated. You may have seen recently some challenges in the gene therapy space when it comes to potential, you know, safety issues. Being able to control what these products are doing in the body is really important. We can do that with our technology platform. We also have the ability to design what we call smart sensors that trigger cell and gene therapies at the right time at the right place. Today, however, I'm going to focus on Logicate technology and really tell you why we're developing this key tool.
One of the major challenges in the treatment of cancer is how do you separate cancer cells from healthy cells so that you do not go in and kill the cancer cells, but unfortunately cause a ton of toxicity against the patient. Current non-Logicated approaches, you know, the drugs that are on the market today, including commercially approved CAR T-cells, ADCs, or T-cell engagers, generally rely on recognizing a single target. That target has to be found really cleanly on the cancer cells and not on the healthy cells for you to be able to have a therapeutic effect, but that is also safe. If, for example, you are not able to find that single clean target, you are going to have toxicity against both the cancer cells and the healthy cells. That is the case for many, many cancers that are currently not well treated with these technologies.
Our Logicate approach fundamentally aims to solve this problem. The way we do that is by recognizing targets on the cancer cells and killing those cancer cells when that happens, but also by recognizing targets on the healthy cells and protecting healthy cells or avoiding killing those healthy cells when that occurs. It is this accelerator and brake that we can build onto a single product that allows us to overcome, you know, this fundamental barrier to cancer therapeutics. Our lead indication is focused on treating acute myeloid leukemia. This is a disease that affects, you know, 20,000 plus newly diagnosed patients per year. 60% of these patients do relapse or unfortunately progress to death within 12 months. Patients that do relapse have a median survival of about five months.
Current standard of care achieves roughly, you know, 15%-at most 30% when it comes to complete response rates. The challenge with AML is that, number one, it's a very heterogeneous disease. To effectively treat it, we need to be able to target, you know, the many, many different types of AML cells that are in patients. Number two, though, is that there are no clean targets for AML that are known. In the past, when people have tried to attack AML relying on just a single target, you've at the same time seen very significant toxicities against those patients that have limited the efficacy of those products. Our approach here is to leverage our Logicates. The way we build our Logicates is through cell engineering.
We are using a type of cell called a natural killer cell that we get from healthy adult donors. These natural killer cells can be expanded and genetically modified to express three different proteins. The first protein is something we call the activating CAR or ACAR. This activating CAR recognizes two different AML targets, CD33 as well as FLT3. Both these targets are well validated in the AML space. They're well known to be expressed on cancer cells. The reason why we picked these two is that it allows us to target both AML blasts and AML leukemic stem cells. However, a fundamental challenge with these targets in the past has been that they're also expressed on healthy blood cells. If you do not protect those blood cells from being killed, you have significant toxicity that can happen with these types of therapies.
is what has been seen previously in the clinic. To solve this, we have our core technology, which is called a knot gate. This is the purple receptor shown here with the inhibitory CAR. What that does is it recognizes the healthy cell through a target called EMCN. When that happens, it basically provides a do not eat me or do not kill signal to the product. By doing so, we can protect those healthy cells from being killed. Finally, we have something called IL-15 that allows us to boost the overall activity of the cell therapy product. As I mentioned, we recently presented data at AACR, which I will briefly summarize later on in this presentation. In a nutshell, SENTI-202 is very well tolerated and has the potential for outpatient use.
This is, I think, a very important part in terms of thinking about the broad commercialization and enabling patient access to this technology. On the efficacy side, we were very excited to see in our first several patient cohorts that five of the patients we treated achieved an ORR response, and four of them actually achieved a complete response. In addition, we actually looked at something called MRD status in these patients, which is assessing whether there's any minimal residual disease left. All of those patients achieved a MRD negative response. These patients are durability is important here. Actually, our longest term patient is continuing to be in response at the time of AACR, that was eight plus months of durability, which is great for the patient to see. Our ongoing phase one clinical trial for this product is being performed in an adult patient.
This is a multi-center multinational study being conducted both in Australia and as well as primarily in the U.S. We have the majority of our sites here in the U.S. We're assessing two different arms of the protocol. One is at two different dose levels. Dose level one is 1 billion CAR positive NK cells per dose. Dose level two is 1.5 billion CAR NK positive cells per dose. We're also assessing multiple doses in these patients. This is an off-the-shelf allogeneic product, meaning that we can actually repeatedly dose this product into patients and do not have to just give the patients a single shot. We have two different dose schedules, one where we deliver three doses of cells at day zero, seven, and 14. The second schedule is where we do five doses at day zero, three, seven, ten, and 14.
We're able to assess for response at 28 days, and we can give patients multiple cycles of this treatment. In general, we've seen responses across all of the dose cohorts that we've presented at AACR, both at the dose level one and the dose level two, as well as both schedules. In general, we've decided to select a preliminary RP2D, or that essentially refers to a recommended phase two dose that's preliminary. That is potentially the dose we would move forward to into our downstream study. One of the ways in which you assess for activity in AML is by looking at bone marrow blasts. These are AML blasts, for example. In general, our patients at baseline start with, you know, a pretty wide range of bone marrow blasts. That is what you expect to see in heterogeneous AML population.
In patients that even started with very, very high bone marrow blast counts, almost all of the patients basically were able to achieve a very significant reduction in the bone marrow blast to achieve response. One of the ways in which we confirm the mechanism of action of our product is actually by doing something called Cytoph. Cytoph is a method where we can collect the patient bone marrow and do very detailed analysis of all the cells that are actually there. As I mentioned earlier, one of the key cell types that we're trying to attack in AML is something called the LSC or leukemic stem cell. This is a very difficult to treat AML population. It's a rare population of AML cells, but if you don't kill them, they basically regrow and repopulate the patient's disease.
On the left-hand side here, most of what we found is almost all of these LSCs actually are in the G-ZERO state. What that means is that they're kind of quiescent. They're sort of hiding out and not very active. Because of that, they're very difficult to kill with conventional chemotherapy. That's been well known in the field. On the right-hand side, though, we can see that post-treatment with our product, we see a significant reduction in many of the patients' leukemic stem cell populations. We believe that's correlated with the types of responses that we're seeing in these patients. You know, in patients that achieve our composite CR response, you know, LSCs decrease by, you know, over tenfold in these patients, which we're quite excited to see.
In addition to that, as I mentioned, one of the key mechanisms of this product is to enable patients to achieve maintenance of their healthy blood bone marrow. There are two ways of looking at this. One is on peripheral blood counts, for example, looking at patient platelets or neutrophil counts. What you can see from the graph here on the left is when patients initially come onto trial, they oftentimes start with a relatively low or abnormal platelet or neutrophil count. This does get decreased temporarily with the lymphodepletion, which is a brief period of chemical treatment prior to the therapy that all cell therapies essentially go through. That is why you see this low point on the graph on the left here between day zero and day 14.
For many of our patients, especially those that achieve our complete response rates, we see a significant recovery and actually recovery up to even normal levels of platelets and neutrophils, which is really important for these patients to be able to maintain a healthy functioning bone marrow in the future. On the right-hand side here, using that Cytoph analysis, we continue to also see that if you look at the hematopoietic stem cell population in the bone marrow, these are actually increased or maintained at a reasonable level in the patients. That is consistent with the protective mechanisms that we have built into this product. As I mentioned earlier, we have seen, you know, patient responses across all dose levels with durability up to eight months and ongoing for our patients. We are very excited for these patients to actually be able to achieve these responses.
We certainly wish them well. Our goal is to continue to enroll this clinical trial through the phase one and to then use that to guide the transition to a potential pivotal study downstream. Now, towards the end here, I just want to briefly mention that our Logicate technology does have broad applicability. As I mentioned earlier, many targets today that are being addressed by ADCs, T-cell engagers, or current cell therapies are all essentially crowded around the same indications. That is because only, you know, so many clean targets are known. Everyone is essentially attacking the same thing. In contrast, though, there is a huge opportunity outside of those conventional sort of target areas where using our Logicate technology, we can go after cancers that basically are more heterogeneous or where you may have to address two or three different targets at the same time.
We're really excited to share this opportunity with the community here. You know, as a company, we really are focused on delivering best-in-class and this first-in-class Logicate technology to patients. We've assembled an awesome team here to execute on this. We're based in South San Francisco. Myself, I was previously at MIT as a professor where this technology originally came from and really been passionate about translating this forward. Dr. Kani Rajan is our President, Head of R&D and Chief Medical Officer, a very deep experience in the cell therapy and oncology development space with multiple approved drugs under her belt. I'll briefly mention here Faraz Siddiqui, who's our SVP of Technical Operations CMC, a lot of experience in cell therapy manufacturing, especially at the commercial and scale with his experience previously at Kaikilia. Overall, really excited to continue to advance this program.
In summary, I'll just say that SENTI-202 is our lead program. We're continuing to push this program forward. It's our main focus area, at least in the near term. We do anticipate additional clinical data as this phase one enrollment is progressing quite well. We look forward to sharing that with the broader community. We're also very excited about the applicability of gene circuits more broadly into the solid tumor space. We think there's ample opportunity there for us to enhance our pipeline or to partner with other companies to advance those programs forward. With that, I'd like to thank everyone and happy to take any questions.
Great. Thanks, Tim. I think there's a couple of questions in the Q&A. If you, we have a couple of minutes to answer those.
Yeah.
So, you know, we are focused, you know, the first question I see here is, you know, we do have a focus on synthetic biology and programmable cell therapy. What investor signals matter most now? For us, it's really about now that we've shown human clinical proof of concept with our initial patients, we want to continue to expand and increase patient numbers. That's really our key focus now. As I said, clinicians are very excited about this program and even more excited after the AACR presentation. We've gotten a lot of interest, actually even expanding additional patient cohorts. Our goal right now in terms of this program is clinical execution and continue to showcase what Logicates can do for patients. The next critical milestones for us really is, you know, more data coming out.
You know, relapse refractory AML continues to be a challenging area for patients and for other drug developers. I think that being said, you know, there are some other companies or other drugs, including the MET inhibitors, that we can look at to try to understand where the patient, you know, efficacy and the bar is and where the FDA is looking at these sort of products. We do believe that SENTI-202 has the opportunity to be quite differentiated. Just as a little bit of context, in AML currently, most of the sort of drugs in development now are targeted against genetic mutations. This particular product is agnostic of genetic mutations. It really brings complementary mechanisms to treating this disease. We are really, you know, looking to showcase that with our additional clinical data.
I think there's some additional questions about other cancers as well as sort of how we compare this to CAR-T. Senti here has always been focused on choosing the right cell type for the right indication. At the heart of it, we are a Logicate company, not an NK purist or T-cell purist company. For AML, we really believe that NK cells make a lot of sense because these patients don't have a long time to wait. Also, patients with AML oftentimes have dysfunctional T-cells. So NK can really serve as a safe, you know, off-the-shelf product for these sort of patients. For solid tumors, though, there is emerging clinical data continuing to showcase the opportunity and the activity of T-cells in those areas. We have done work to showcase that our Logicates do work in CAR-T.
We do think that there's opportunities there to, you know, drive solid tumor programs into the clinic.
All right. Thanks, Tim. Appreciate your time. Again, make sure to visit Senti Biosciences Corporate Connect page on the Webull app for updates. That will conclude the Webull Corporate Connect Biotechs webinar. Thank you for everyone's time and be on the lookout for upcoming Corporate Connect investment webinars highlighting different sectors in the near future. Thanks so much, everyone. Thank you.