Akari Therapeutics, Plc (AKTX) Earnings Call Transcript & Summary

Okay. We are ready to get started. Good afternoon, everyone, and thank you for joining us today for another virtual investor closing bell segment. My name is Jenene Thomas. I am CEO of JTC IR, and I will be the moderator for today's event. I am very pleased to be joined by Abizer Gaslightwala. He is President and Chief Executive Officer of Akari Therapeutics. Welcome, Abizer.

Thanks, Jenene. Thanks for having me here today.

We are so excited to showcase Akari on our platform today and share your story with our audience. And before we get started, I do want to remind our audience that Akari Therapeutics is publicly listed on NASDAQ and trades under the ticker AKTX. So we're not going to wait any longer, Abizer. We've been looking forward to having you on. So let's dive right in. I'm going to turn it over to you for an overview of Akari.

Great. Well, thank you, Jenene, and welcome to everyone who's joining live and those of you watching the recorded, thank you for taking the time to watch. So I would like to just maybe go through the disclosures, but let's get to the first page. We are Akari Therapeutics, and let me reemphasize our new vision and focus based on being an oncology company. We're focused on innovating antibody drug conjugates or ADCs, as you hear the term. And I'm going to focus on 2 terms as immuno-oncology therapies and for patients to be cancer free. And I want you to remember those 2 terms because we're going to reference those as we go through what the opportunities are and what our special approach is around addressing those with our unique platform and payload that we put on our ADCs. You'll learn more about that, but immuno-oncology and the opportunity for patients to be cancer free. So with that, let me just give a corporate overview. As I just mentioned, antibody drug conjugates, ADCs. We are developing ADCs with what we call novel immuno-oncology payloads. Just as a reference, when we say ADCs, there's an antibody and think about that as a super smart guided missile. It knows exactly it's GPS, it knows exactly where to go in a very targeted way. But what's the actual payload that's in that antibody or that missile, that's what's unique about what we're doing at Akari. We are developing very good missiles and those guidance systems, our own unique one. But more importantly, we're attaching what we think is the most innovative payload out there today. We think it has the potential to redefine ADCs in the way that these current ADCs on market are not, and we'll speak to that in a minute. But that's the idea. It's what we -- our payload is called a spliceosome modulator. We call it PH1 and it's designed to both kill cancer cells and activate the immune system, which is why we call it immuno-oncology. So then what does that mean? That sounds some fancy science and high level, what are we actually going to do with this guided missile with is really novel innovative platform, a payload called a spliceosome modulator. What we've already put it into specific programs. Our lead program, AKTX-101, it's directed against a cancer target called Trop2 that's expressed differentially or higher on cancer tumors. And we've attached the PH1 onto it. So it's a Trop2 target, PH1 payload ADC. And we'll go into more detail when we go through the Trop2 program, but this is some of the specifics of that we're focusing on a number of solid tumors and have a clear plan on how to potentially get to a filing to start clinical trials in the second half of 2026. More to come on that. And then we have a second program where we've been able to take the same payload, PH1, and we're developing a novel antibody or that guided missile that we think is unique and potentially best-in-class and first-in-class from what anyone else is doing out there. So we're going to create this really cool new guided missile, and we're going to put our PH1 spliceosome modulator payload. We don't want to disclose the target yet. It's still a little early, but we hope to -- we'll talk more about this a little later in the presentation as well. But you can see here we're focusing on a number of solid tumors, including colon, gastric and lung. So before I move over and now you have a sense of the corporate overview and where we're going to go with these 2 programs and our spliceosome payload, I want to take a step back and make this more personal because cancer is personal for all of us. When you see these terms on here, you see bladder cancer, lung cancer, colon cancer, gastric cancer. Many of you either know people in your family or friend circle that have had these tumors or if not these tumors, other types of cancers because there are many other solid tumors and blood cancers like lymphomas and leukemias. And that's exactly what we're trying to do. We're really trying to go after these tumors that have significant unmet needs. So despite the advances in therapy across these, think about those patients in your family, and your friend network or people you've heard about through colleagues who've been affected by these and think about the outcomes that they have and think about their treatment paradigm and the difficulty it is. And we want to change that. And we think we have a great platform here to go after some of these tumors, maybe even more with more molecules or these molecules, and that's our opportunity. So if you think about, again, as you go through this presentation and listen me present, think about that patient, that picture of that patient that you know through your network and think about what we're trying to do for that patient, and that's the opportunity and promise of what we're trying to do when we think our advanced ADC platform. That's something I think about every day. That's something our team thinks about at Akari and keeps us motivated around ultimately what our mission is to help patients be cancer free. So as I just give an overview, again, we're going to talk about 2 programs a little later. AKTX-101 is our lead. It's pretty advanced. It has significant work done behind it. We'll actually share some really compelling, what we call preclinical data before we get into clinical trials or humans. And we are doing what we call IND-enabling, which are studies that were at the big scale where you need to do things so you can make the product and it's safe -- very safe to support going into clinical trials. That's on target to get into the second half of '26 to enable us to start clinical trials potentially. And then the AKTX-102, which we'll talk about a little bit more, we're still advancing that. Again, really novel science there where we think we can couple the advanced antibody or missile with our payload as well, and we'll speak a little bit more to that later. So I just want to give some background on the ADC class in totality. So you may have heard about ADCs. Maybe you know some background. If you don't, here's the kind of net summary of it. ADCs are the fastest-growing and one of the most prevalent now cancer modalities of therapies that are being used to treat cancer patients. And you can see on this chart here, there are 7, what we call -- sorry, 6 products here that have achieved what we call in our industry blockbuster status, which is more than $1 billion in annual sales, which is no easy feat. So ADCs have been on a long journey, and now they've reached this prime time and you see these products across many different solid tumors and what we call liquid tumors or blood cancers, you see ADCs now penetrating these markets because of their compelling design in the way they're constructed around the smart missile with the payload. So yes, there's success. And this class is expected to grow over $30 billion by 2032. We think the potential could be even bigger given how many ADCs in development and what the opportunities are. We're just scratching the surface. However, if you look at ADCs, despite the success, which has been significant, what you see is that it's been in a pretty narrow way, and it's been limited because all the ADCs today and the ones in development, over 90% of them are using -- remember that payload I mentioned are using the same 2 types of payloads. Those 2 types of payloads, one is called the microtubule inhibitor, you see on the chart on the right, about 23%, almost 1/4. And you see this big red called Topoisomerase I inhibitors about over 60%. It's cousin or DNA damaging agent, the 10%. So if you sum all those up, you're talking over 90%, 95% of all ADCs use 2 classes of payloads, DNA damaging agents, which include the Topo-1s or microtubules. Well, if you go back to anything in life, if everyone is doing the same thing, would you expect a different outcome? Probably not. And so that's the kind of take home from this, that what Akari is trying to do is go outside that window, not follow what everyone else is doing. Because when you do that, you usually get incremental innovation. And I'm going to speak why incremental innovation is not what cancer patients need. They need what we call step function or revolutionary advancement. And if you're going to focus on the same payloads that are already out there today, these 6 products in the left use 1 of these 2 payload classes, all the ones we talked about over 90%, 95% use these 2 payloads, you're probably not going to get a different outcome or it's going to be incrementally better. So that's where we think we have a unique competitive advantage because we're approaching this with a different payload, a better payload and importantly, a payload that we think activates the immune system, which is the best way to potentially get patients to be cancer free. So as I mentioned on the slide before, I wanted to kind of give a sense of where that opportunity is. So despite the success of ADC therapies in those lung cancer -- well, not even lung cancer because ADCs are not penetrated lung as much, but in gastric or if you think about breast cancer or you think about other areas in bladder cancer today, you look at those 2 payload classes, the Topo-1 inhibitors I mentioned and the microtubule. And you see in general across some of these ADCs that are approved today, when they use a single agent, in general, you see a couple of interesting kind of generalizations that come about. Irrespective of the antibody, the tumor, the payload, you see a little less -- about 50% of all patients get a response. And a response is measured by something called in cancer objective response rates as the clinical trial term. So when you define response by that term, it's about 50%, a little less than 50% of patients actually get a response. And when they do, that response, again, as measured by defined endpoint, is about 6 months. So imagine irrespective of the antibodies out there today and the payloads they're using these 2 classes, about 50% of patients don't respond, if you see on the red. And even when they do respond, they only get about a 6-month benefit. Think about 6 months. Think about that in terms of a patient. That's 2 seasons. Maybe that's fall and winter or maybe that's summer and fall. Don't cancer patients want more than just 2 seasons, don't they want a year, don't they want 2 years, don't they want 5 years? Don't they want to see children graduate? Don't they want to see grandchildren born? Don't they want to see moment changing event -- life-changing things in their lives -- moment -- sorry, moment event in their lives. And so when you think about that patient need, it's not being met. So despite the success of ADCs today, we're not getting the level of responses and the durability we want. So we call that duration, durability and the deep responses we want. And that's where we think we have the opportunity with Akari with our novel payload, the spliceosome modulator to drive these more durable and deeper responses. So this is the opportunity that we can do better than the 50%, and we can do better than the 6 months. And let me show you some data why that gives us conviction about why we think our payload approach can do that. So again, as we think about our spliceosome modulator, this unique payload, PH1, as I mentioned, we kill cancer cells, but importantly, activate the immune system. And we think this is the most important part. Our mechanism of action, which is called a spliceosome modulator affects splicing. I mean you think about splicing, think about a film, that's the best analogy. No one watches an uncut unedited film. They actually just spice it together because if you don't, the sound doesn't match with the video, the video is out of frame, none of it's in sequence and no one wants to watch a movie that hasn't been edited. That's what we actually do. We actually prevent the splicing machine from doing its job. So our modulator actually interrupts that splicing machine from splicing and editing the RNA, which then helps kill the cell, but importantly, makes the cell foreign to the immune system in a really profound way, and that activates the immune system in a powerful way. And it's so powerful. We actually see it synergizes with other immunotherapies, the most important class being called checkpoint inhibitors. So you've never heard of a big product called KEYTRUDA or maybe it's cousin OPDIVO. KEYTRUDA is the most successful oncology product ever. It's premised, it's based on immunotherapy, and it's based on activating the immune system. It's a $25 billion product and the entire class that KEYTRUDA created is probably about a $50 billion product across 7 other similar products. So think about the opportunity, and they have not found a good partner to synergize with these checkpoint inhibitors. There's been a lot of work in our industry and biotech to figure out to make some bets, but none of those have played out. And what we've seen in our preclinical data is not only do we activate the immune system, but we do it in a complementary way in a synergistic way with checkpoint inhibitors. So synergy is 1 plus 1, it doesn't equal 2, it equals 4. And that's where I'm going to show you some data shortly that says this is why we believe in the power of our approach in that it kills cancer cells while activating the immune system and amplifying the immune system when we put it with the most successful oncology class that we've seen in the history of our cancer therapies. We've also engineered our payload to be next generation in terms of some of the payloads today. We want to make sure the cancer cell can figure out how to go after it and circumvent it. So we've engineered some resistance mechanisms. We've tried to reduce the off-target toxicity and improve the safety and tolerability profile. So I just want to give you that sense of this payload is designed with a lot of deliberate intentionality in terms of how do we maximize its efficacy while also improving its safety tolerability perspective. So now we have some background on our special secret sauce, the spliceosome modulator. Let's actually talk about Trop2, our lead program, AKTX-101. As we mentioned, it's -- a Trop2 is the guided missile that focuses on that target, which is expressed on cancer cells, a number of different cancer cells. And we've advanced this pretty far in terms of we have a really good molecule. We've characterized the molecule. We've seen really good efficacy and safety in initial preclinical studies. So that leads us to give confidence that we are going to try to start some additional activities later this year, moving into 2026 that would help us actually get to what we call a regulatory filing to start clinical trials. That is a big deal in cancer space because if you actually look at cancer R&D, many products never make it out of this phase. They don't even make it to the phase we're in with AKTX-101, which is what we call a final product candidate because most of them failed the safety or efficacy or combination. So the fact we've advanced this far and now we're ready to take some steps to kind of make it even more formal is a tribute to the work that's already been going before on this AKTX-101 and years of work that have helped us not only advance the payload, but this molecule. And where we're going to go with that? Well, if you go back to that slide I mentioned around the unmet need, we think bladder cancer is still a particular space with unmet need. And there is a product called PADCEV that's very successful there. It's a multibillion-dollar product, and it works well in the first line. But unfortunately, people get that -- they lose their response. As you said earlier, about almost 50% of people don't get a response when they take single-agent PADCEV. And when they do get a response, they may only last for 6 months, and we think that's a perfect opportunity based on the data I'm about to show you that gives us a lot of conviction that bladder cancer could be a big opportunity for AKTX-101. But it doesn't stop there. We think we have the bigger, bigger opportunities even in gastric, which is a horrible disease. If you think about a gastric cancer patient, if you know any, they often have their stomach resected. They lose the ability to eat food, which is a horrible situation for a patient that's trying to maintain the nutrition while fighting their cancer. So we think there's an opportunity to go in gastric. And then in cancer, lung cancer is still the largest solid tumor, the largest tumor of any in terms of its incidence and its mortality, and we think there's a tremendous opportunity in lung cancer. And by the way, that's where KEYTRUDA made its mark in lung cancer immunotherapy, that is still its biggest source of business. And we think we can complement that and add on to that. So why do we believe? Well, let me start with this bladder cancer preclinical data set. So this is an experiment on the left where we looked in bladder cancer cells, and we tested what we call a placebo vehicle. We tested an IO drug, which is a checkpoint inhibitor. And we tested our AKTX-101, which in this graph is labeled as Trop2 P. And then we did something else. We actually took our AKTX-101, which is Trop2 PH1 and we added it to the checkpoint inhibitor. You see the respective lines, you see on the left this axis is called tumor volume or how fast the tumor grows in the mouse when it's implanted. You can see in the black, unfortunately, you can expect that the tumor grows unchecked and usually, these mice cannot survive once they're 3,000, they usually die or are sacrificed. You can see that on placebo or vehicle, the mice progress pretty fast. You see some effect, whether they're treated with our AKTX-101 in the initial part up to 15 days or IO drug, the checkpoint inhibitor, but you see after while that effect stops and the tumor takes over and continues to grow. So we do have an effect that's important. We have an effect in 15 days. And by the way, these models are not 100% predictive of human bladder cancer, but they're meant to be a surrogate. So we see some effect. We see a flattening of the tumor growth curve, which is a good sign that we can actually impact the tumor growth. But unfortunately, it escapes these drugs and it continues to grow. What's really exciting is that you see the combo arm. You take our AKTX-101 and you drive it with a checkpoint inhibitor and you not only see the tumor flat line, but you actually see it regress. You actually see it get close to 0 within 3 weeks of initiation. Now often, these tumors grow unchecked after a certain period of time. But for 3 weeks, for us to maintain this tumor to 21 speaks to the synergistic effect we're having with the checkpoint inhibitor. It speaks to the mechanism that I just mentioned around killing cancer cells, activating the immune system. That's what's really exciting. And when you've got to go to the right and you play out, these are called survival curves. You take those same groups and you put them on survival and you look at the survival, you can see that the black, as I mentioned, they usually die out when the tumor gets that big. You see they have the shortest amount of survival in days. You see the single agent AKTX-101 and the IO are about comparable when you look at that. But you see a dramatic difference in the combination regimen in terms of overall survival. 60 for a cancer mouse is pretty long when you look at these models. So we're really excited about this data, which we think is super unique. But this is not the only data, you can say, well, okay, I've heard there's other Trop2s out there, and you're not the first to market to compare against those other Trop2s. Well, this is an experiment to answer that. So we actually took an approved -- the first Trop2 approved product called Trodelvy. It's a Trop2 ADC. It uses one of those payloads I mentioned earlier, the topoisomerase I inhibitor. It was approved in 2019, I believe. And you see -- this is not an indication where it's approved, this is a gastric cancer model. And you see when we -- when Trodelvy is given, the vehicle on the very left in this chart is, again, when you don't treat with anything, you see 0 out of 10, which are tumor responses, basically no response. That's what you expect. When you dose Trodelvy at its approved dose, you actually see only about 20% of the mice get a total remission in this gastric cancer model. But when you take our Trop2 AKTX-101 as a single agent, you see 50% of the mice actually get a total response. And we see that statistically significantly when you go to the table at the bottom, when there are 2 different kind of molecules we tested on our AKTX-101. I won't get into the nuances, but you see what we call PH1 DAR4, you can see even the DAR4, the DAR2, the 2 different versions, we are statistically superior to Trodelvy in this model, in this preclinical model. So this gives us more conviction that, yes, we may be not the first Trop2 ADC in the market, but we think we're much better and we're better than the first Trop2 that got approved if you believe this experiment. So this is due to the payload, not the antibody. Our antibody is a high-quality antibody. It's different than Trodelvy, but it does what an antibody does. It targets, it's a smart missile. It hones in on the actual cancer tumor. The reason we see this difference is the payload. Our payload, our spliceosome modulator works in such a fundamentally different way than the topoisomerase I inhibitor on Trodelvy, and this is where we think we're seeing the benefit in an experiment like this. I'll show you the last piece of data. This is actually done not with our Trop2, but with another proof-of-concept antibody drug conjugate we built called hHer2. This is not something we're taking forward, but this proves again the technology. This is probably one of the most exciting experiments because if you go back to what we said around it, stimulating the immune system, and the immune system is key to getting patients to be cancer-free and how you combine with checkpoint inhibitors, the most successful class in oncology today. However, checkpoint inhibitors only work in 20% of patients. So how can we improve their ability to work in a broader set? Well, this is an experiment that gives us reasons to believe around all those 3. So again, if you believe -- if you look at this mouse, it was injected with colon cancer cells. And you can see the black line, which is basically placebo, there was basically no responses. And even on the checkpoint inhibitor, the blue line, this is a pretty tough cancer model. None of the mice responded. When you look at our single agent, trastuzumab PH1, this antibody drug conjugate with our payload, you see almost 40% of the mice survived. And what's really impressive, when you combine the checkpoint inhibitor with our ADC with the payload, almost 90% of the mice survived up to 150 days. And this is after we stopped injecting them after 3 weeks because that was the way that this experiment was designed for this model. Imagine, we got a 90% survival cure remission rate after only 3 weeks of dosing out to 150 days. So that's the synergy I talked about with combined with checkpoint inhibitors. And even as a single agent, we see that almost 40% of these mice survive. What's really compelling is if you take these mice, these naive mice and you actually rechallenge them. And you're not redosing with our product, but you're just rechallenging them with cancer cells comparing to mice that were never treated in this first experiment. That's the black line, the mice that were never treated. But you see that this orange line is the ones that were rechallenged. You see none of them actually develop the cancer tumor. That's really profound because what that means is that these mice have what we call immunological memory. They have learned how to attack the cancer so that when they see it again, they can actually defeat it. And this is without us dosing any more drug. So this is a proof of concept that helps to validate our idea of stimulating and activating the immune system in a profound way and doing it in synergy with a checkpoint inhibitor that we trained the mouse's immune system to like essentially beat the cancer, not just once but on an ongoing enduring way. And if we can demonstrate that moving forward in humans, this is a unique value prop for our payload that has not been demonstrated elsewhere in other antibody drug conjugates. So this is, again, some of the reasons we have a lot of conviction and belief in the science of our payload the spliceosome modulator. So I'm going to move on because as every good antibody drug conjugate, any therapy, efficacy is important, but so is safety. So we have to make sure that this product is safe enough to take into clinical trials testing and establish further. And many products fail because they don't. So essentially, -- when we look at this, we've actually done some safety work in rats, but importantly, what we call nonhuman primates, which are large animal species similar to humans. And that is a standard that we do in our industry before we test in humans. And what we found is that we found that we have a dose that's tolerated at what we think is an effective dose to go into humans and that we feel confident then we can actually dose in the humans at a place that will be therapeutically effective. That's one of the most important things out of this study. The other thing is that we did see some side effects as with any therapy, but we found that many of them were mild, reversible or transient and that they can be managed. And oncologists are very good at managing toxicities of therapies given the armament that they have today. So this is important that we found that we can mitigate the side effects and then the transient and they reset after a while. We also found that our toxicity profile could be compatible with checkpoint inhibitors. Again, we mentioned we want to combine. It would be bad if you actually had cumulative toxicities that actually make it worse, that would be a bad thing because that would prohibit you from combining with a checkpoint inhibitor. We find that our toxicity profile is compatible and there's no evidence of similar toxicities that you see with checkpoint inhibitors, which is good. And I think finally, the last thing, what we think is really compelling is that this is a very differentiated safety profile than the other Trop2s, like I mentioned, Trodelvy or others that are approved. We see what we call myelo or bone marrow toxicities, things like neutropenia, which are white blood cells, diarrhea, Trodelvy actually has warnings in its label around these. Or what we see is lung disease or lung scarring with some other Trop2 ADCs that use the Topo-1 inhibitor. We don't see any of those because our payload is different. It works in a very different way, and it targets cancer cells in a different way. And so again, the theory and the design and the intent of our ADC is being played out even in our safety studies. So that's the Trop2. Hopefully, you walk away with more knowledge and excitement around it as much knowledge and excitement as we have and how we continue to advance the science. I do want to transition to AKTX-102 before I kind of wrap up. This is what we think potentially a best-in-class, first-in-class ADC with our payload. We don't want to disclose the target yet. We're developing some really novel proprietary ways to develop this antibody to guide missile that we want to kind of link up with our payload. Once we do that, we will disclose more, and we want to advance this rapidly into preclinical development to get to the same stage as AKTX-101. Importantly, what we think is really unique opportunities, colon cancer, we think, is a huge opportunity for this target that we haven't disclosed yet as well as gastric and again, going back to lung. And I want to call out colon because this is the -- probably the fourth largest, most common tumor type. It's actually increasing in incidence, unfortunately. It's one of the few that's actually growing today versus declining. Think about anyone that has been affected by colon cancer. It's -- outcomes are devastating for patients. And to be honest, there hasn't been as much advancement here. We think this is a big opportunity in addition to gastric cancer and then, of course, lung cancer, where we think there's continued unmet need given how large the market size is for AKTX-102. So very novel science, more to come on this later in the year, but I just want to kind of leave you with the market opportunity is significant given the unmet need and our ability to go in these spaces where some of the ADCs are not playing as well. So I want to kind of give a perspective of -- I want to talk about partnerships as well a little bit. So how are partnerships looking? That is a core part of our strategy. We want to bring in partners early. We want to continue to bring them along. And how is that? Well, this is like a reflection of the ADC space, and this is why we believe ADCs as a modality will continue to grow, continue to be successful, as I talked about earlier. And this is just the deal flow in the last 12 months of early stage, and the majority of all these are even preclinical discovery stage. And you can see the list of these from December of last year to this year. You see upfront payments. You see some of the terms that are publicly disclosed that they are. And I think this shows that there's still a robust set of deal activity happening, and there's opportunities to partner with players around these ADCs. And we believe we offer a unique opportunity because all these others are doing the same thing. As I mentioned, they're all using the same classes of payloads, and they're not really changing the approach. This is where we think we have a unique opportunity. We're actively talking to many of these companies, whether they're on here or the general pharma biotech sector around partnership opportunities. So I want to leave you with what some of the value drivers are and what to continue to -- as you follow Akari, what to be on the lookout for. We are continuing to advance the science on AKTX-101. We expect to hopefully have some new preclinical study data in lung and some other areas in the fourth quarter. And as I said, we're going to continue to advance the development of this to get to human trials. We're going to start what we call large-scale high-quality manufacturing, which is called good manufacturing practice, GMP. We're going to start some of that work and hope to have some of the initial work done in the first half of next year. And then that will lead to potentially us finalizing all the work needed to get to a potential clinical trial application in the second half of next year. So we're rapidly trying to advance AKTX-101 to the clinic, and we will be looking for partners along the way as they see that progress. These are the things that partners like to look for. Have you left the product nomination stage to actually manufacturing and what we call advanced safety testing. And these are the things we're going to do that make us more attractive for partners either at that stage or even beyond. And then AKTX-102, we're going to continue to disclose more about that by the end of the year. So stay tuned on that. And I also want to just highlight, just continue to stay abreast of our corporate overviews, our news updates, our website. We will have some data that we're going to present at upcoming scientific conferences later this year, really compelling data. I won't speak too much to it. I just want to set it up for your anticipation, get you excited about it, but there's a lot of stuff happening in terms of data generation and marching the science in new directions. So with that, if I would just close, if you look at our investment summary as we talked about, basically, on our antibody drug conjugate, we have a novel immuno-oncology payload. Immuno-oncology, we think, is a differentiated way to approach the cancer market and in particular for ADCs and our spliceosome modulators of heart. It's different than over 90% of the payloads being used today. Our lead asset, AKTX-101, is off to the races, has clear time line milestones as we've talked about. And 102, we think can be a best-in-class, first-in-class ADC, as we talked about, more to come on that. We continue to look at high market opportunities across both assets in lung, bladder, colon and gastric and then I want to reemphasize our continued strong focus and momentum on trying to capitalize on the deal flow for early-stage ADCs and how we can create near-term value for Akari and its shareholders. So with that, I want to turn it back over to Jenene, and thanks for the opportunity.

Great. Abizer thanks. I have to be honest, I did not want that story to end. Very compelling, certainly an exciting time for Akari. Congratulations on all your work so far. I can't wait to hear what's next. So we are going to move to the Q&A portion of this event. [Operator Instructions] Abizer while our audiences are thinking of their questions and typing them in, I have a few that I prepared in anticipation for this discussion. So our first one, so most ADCs today rely on the Topo-1 or microtubule inhibitors, which limit with limited innovation in payload. Sorry for that tongue twister. How do you see the PH1 spliceosome modulator breaking the cycle of group think and resetting the bar for ADC payload innovation?

Yes. No, great question. And it's a tongue twister as well I have to practice it myself, there's a lot of stuff to keep track of jargon. But no, what I would say is if you go back, and this is in our corporate deck, you look at that one slide that speaks to the unmet need and that 50% or less of patients actually get a response in terms of what's the response rate and then how durable is it? Only about 6 months on average maintain that response. And that's because not that the payloads are bad today, but those are the limitations of those payloads. So they're doing the work that they've been designed to do, but they're going to reach some ceiling or limit based on the biology of those payloads. So that's exactly the unmet need we're trying to tap into. And if we find a better payload, like what we believe the spliceosome modulator, we will have a different ceiling. We will have a different ability to change those numbers of 50% in 6 months. So those are the 2 numbers you should think about in terms of unmet need. We want to change that 50% of response rates and the 6 months of response duration, that's our opportunity, and we think the spliceosome modulator can address that over the current payloads that are being used today.

Excellent. Okay. So in your presentation, the preclinical data suggests your PH1 payload kills cancer cells while also activating the immune system. So how do you expect this dual mechanism to translate into better patient outcomes compared with the current single mechanism payloads?

Sure. Yes. And I think it's a great way to kind of connect the presentation with some of the data. And so let me kind of thread it in different ways. Think about that 6-month response rate, that durability. So getting patients to have better durability really means are you going to treat them with more toxic things because at some point, people have to stop taking therapies because they're too toxic and too many side effects or the cancer develops resistance and/or both as it happens. So we want to extend durability, the best way is actually the immune system. The immune system is the most powerful way to treat cancer. Unfortunately, it gets tricked by cancer initially into getting suppressed. So the idea behind the KEYTRUDA and the OPDIVA was that, and this was a lot of great science innovation creating those great products is that can you reawaken immune system to do a better job killing the cancer, because it's been proven checkpoint inhibitors, although they only work in 20% of the patients that they're treated when they work, they really work because if you get a response, the immune system starts to kick in and have what we call durability response, 1-year remissions, 2-year remissions, potentially complete remissions forever some patients if they're lucky. And so we want to build on that. And the best way to do that is that experiment I mentioned where we talked about creating immunological memory. So we see that we're creating that long-term duration of effect by combining with a checkpoint inhibitor. That gives us confidence that we can change the outcome to help patients be cancer-free and get back to that aspiration I mentioned earlier. So that's our opportunity to take the immune system, really wrap it up in a controllable way, combine it with a checkpoint inhibitor and really get that longer last duration effect. So do better than 6 months, do a year, do 2 years, do hopefully forever. And that's the power of the immune system. And that's why we believe in the spliceosome modulation, that's the most powerful aspect of this payload.

Excellent. So we're seeing a real spotlight on the ADC space, definitely a hot area. And with that, we've seen really strong deal flow in this space, even at a very early preclinical stage. I mean, I know you showed that chart in your presentation. So with AKTX-101 and the payload -- the PH1 payload being so differentiated, what is your partnering strategy? You touched on it a bit, but love to hear and have our audience here what your actual strategy is there.

Sure. No, I think it's a really good question, and I think a key area of interest because we do think that's an area of value creation for our current shareholders. So in the near term and even midterm, long term. So I think when we think about partnerships, if you look at that slide, again, it's in the corporate deck, you'll see that all those partnerships, there are similarities, but there are differences. And I think that speaks to partnership. We are open to the flexible nature of partnerships. There's going to be some that -- some people might be like, "Hey, we love your technology. We want to collaborate with you. Can we do a partnership where we do joint research". And if a company comes to us and says, "Hey, we have a great antibody, we want to pair with your payload, -- let's do a partnership, let's do that". That's a more in-depth partnership. There could be another partnership where someone says, "Hey, we like your molecule. We don't want to bring it in-house, but we're going to co-fund and develop it with you. So we'll make an investment and you'll get to certain milestones and then we'll revisit along the way if we want to license it or not". We'll be open to that, again, depending on deal terms and constructs. And I think the third option or bucket I would think about, again, these are general buckets and the flavors in between, is that someone might come and say, we love your molecule, can we license it? And okay, well, if the terms are right, we'll license the whole thing for you and you can take it from us, but then we won't have control or ownership but also responsibility. And we want to be thoughtful around who we do that with and whether they will take care of what we call our baby and our payload. But I just give you that example of that's probably one example on one side where we totally out-license the full asset and we let someone take it over. On the opposite side, it's, hey, there's going to be maybe a partnership of we're going to co-develop and create new molecules, new ADCs that aren't even on the map that we saw. Maybe a pharma partner has a target or an antibody that's different than the ones we are, and they want to combine it with our payload because our payload is so good, and that's the optionality of our payload, and they want to do a research agreement. Well, that's a different type of agreement. And then there's stuff in between. So we're open and flexible to all 3 of those. And we don't want to hinder ourselves because as a novel payload, we actually offer all that optionality. And so we want to be open to all those.

Excellent. Okay. And I do have one more question because I just think of you and listen to you and your enthusiasm for the Akari story and the opportunity that exists. And you are fairly new to the seat as CEO of Akari. You come from Jazz Pharmaceuticals, a well-established, very successful company. I think it's got to be anywhere around $7 billion to $8 billion market cap. What -- tell us, please, what made Akari so attractive for you to leave Jazz?

Yes. I think it's a great question. And if I had more time, I would have touched it earlier in the presentation, so I'm glad you're asking for it, but I'll ask you this now. Ultimately, yes, it was really the science and the opportunity. This spliceosome modulator really caught my eye because at Jazz, we -- as proud of the team what we did there when I joined, we -- in about 4.5, 5 years, we grew a $350 million business, 3 products to 6 products, about $1 billion before I left. So why would I leave such a growth momentum? It was because really the ADC market has done so well. But I knew I didn't want to just join any ADC company to lead. I wanted to join one that had a novel competitive edge because I see that's what makes the difference in cancer patients and the cancer market. So when I first came across Akari, I quickly saw this pivot to oncology, but it was premised on the spliceosome modulator. And the idea of novel payloads, that's where the innovation is going to happen. That's where the value creation is going to happen if you have the right set of people and the team and the plan to execute. So I believe coming here, I can bring the right set of leveraging the current team, but also bringing in other additional team members, but the focus and the plan and the strategy to execute. So we want to take the great scientists there, and I believe we have the opportunity to execute and make a high value for everyone for both patients, providers and importantly, for our shareholders as well. So that was the conviction that I had when I came and I still believe it even more so today.

All right. And thanks for that background. I appreciate that. I think it is important for our audience to understand that. I think it's a huge component of why the story is so compelling because it's not only attractive potentially to investors, potential partners, but you see the value there. So I appreciate you going through that.

Sure, sure.

All right. So we do have some questions. [Operator Instructions] And if you Okay. So our first question comes in when you're thinking about the Phase I, how do you envision the trial design and target indication? And have you had any interactions with FDA?

Yes. No, great question. I'd say we're early on that side. It's a little premature. I think we shared our initial thinking, we think the post-Enfortumab PADCEV market in bladder cancer is an attractive space. We think there's still continued high unmet need after people fail first-line ADCs or whatever therapy they're on. We think that's a unique opportunity. Our data, as we talked to that preclinical data is pretty compelling to give us confidence we could work in that area. We have not thought about trial designs yet. I think as we continue to progress the asset towards a first-in-human clinical trial, we will -- I mean listen, there's not probably a lot of permutations are fairly standard designs when you look at single-agent studies in refractory populations, you're probably going to do something that's been done or a flavor of that's been done in the past. I wouldn't say it's starting from scratch. We're going to leverage what's been done in the past and what other -- some Trop2s have done, in particular, Trodelvy, how they got approved and kind of a similar path. So I wouldn't say it's going to be that groundbreaking, but I would say we haven't finalized that work. We want to do some other things to kind of get us going, and then we'll kind of engage in that probably next -- later this year, next year.

All right. Our next question from a strategic standpoint, is your goal to take AKTX-101 through pivotal studies independently? Or do you see a partnership or acquisition as the most likely end game?

Well, without forecasting with certainty, I would say likely the latter. But again, we have to be open to all options. And one of the things that's interesting is the longer a company keeps an asset and develops it, the more value creation you have. Now that's premised on you have to keep on derisking the asset and you have to continue to invest in the asset to do that. If you look at late-stage companies or companies that are approved, the value that they get ascribed on their acquisition or licensing is significantly higher, and that starts to decline as you go earlier in the cycle. But again, that's because they derisk and they spent more money. So I think we want to be open to creating value as quickly as possible for our investors and what we're trying to and validate the platform. Because then if we validate the platform, that will enable us to do more opportunities and build more ADCs and do more partnerships. So I would say, although we're open to all options, our bias is going to be we would like to partner this when we have enough data and it's appropriate earlier versus later. That enables us to return value back to our shareholders quicker versus later. It enables us to reinvest the capital and building a broader pipeline. However, we just can't be close to all -- we have to be open to all, but I think if we had a choice, we would probably want to partner earlier versus later. But again, we have to be open to all options.

All right. Our next question is, these are great presentation. I found it to be very compelling. There's a huge disconnect between the current stock price valuation and where this opportunity sits. So what is your plan for the stock price and turning this around?

Sure. Great question. And I do want to make a comment, particularly in the last week or 2 and even over the late summer. Listen, we don't want to comment on day-to-day fluctuations in the stock price. However, we're as frustrated as many of our U.S. shareholders as well. And I think we have to remember that with small cap biotech market cap biotechs, there's often other factors, technical trading and broader sector dynamics that affect our stock as well. So I think that's part of it. But again, we can't get caught in the day-to-day. And so I'll just say we're frustrated as well where we sit because we don't think it reflects the science and the value and the strategy that we -- that I just articulated. So that being said, let me say what we're doing about it. What we're doing is we're going to continue to develop and execute on this plan. As you just heard this, we feel really confident and compelled on the data that we have to date. our plan moving forward. We want to continue to advance AKTX-101 and the broader pipeline, as I outlined earlier, and keep that going. We want to continue to generate high-quality science and data that's a big part of any oncology company or any successful pharma biotech. And I spoke to some of those things to look for in terms of data presentations later this year and updates on our pipeline. And we want to continue to execute. We have to be focused on our execution in a laser-like way. This is one of the toughest biotech markets in 20, 20 years plus. That means the operators and companies that are super razor-focused on the right things versus the peripheral things that the right things will stay -- will be successful, and that's what we believe. And so what I would say is on the stock price, hopefully, you walked away with as much excitement around spliceosome modulation that I have, that our team has, that we continue to do. And we feel we really have an opportunity to drive significant differentiation and address unmet need in the cancer market. And if we do that and we continue to execute and deliver on what we just said with a good strategic plan, as I just outlined, that will reflect in the share price. Sometimes there's a lag on that, but we do think it will reflect in the share price. And I'm just committed, I'm committing and our team is committing to all the shareholders, we're working extra hard every day, not because the price of the stock is not what we want because we truly believe that this is the plan of success, and we're committed to it. And so you have our commitment that we're working as hard as we can every day, every month, every year ongoing to execute on what you just saw, and we're going to stay laser-focused on execution, and that will then play out into the stock price.

Appreciate that, Abizer. Those questions are always tough, right? But I think that I go back to one of your first slides and your mission of making patients cancer free. That has to drive you. That has to be a part of it. And it's unfortunate because I think everything that you shared with us, all of the data that you've gone through your plans, your execution, the space that you're in that and all of the enthusiasm, it has to be frustrating for you. It has to be frustrating for shareholders. I look at it, I see the disconnect. So it's just -- it's down to execution and data, right?

Yes. And Jenene, can I discretely add. I mean, it is frustrating when you see that stock price because it's not reflective of what the team and I have been doing. I can tell you what I see that all of you don't see an insider everything I see these things, I continue to see data that makes me super compelling, like not just from the first time we run on this platform, but the experiments we're doing now, the future experiments we're going to do, I'm excited. Like I keep on seeing every time -- I won't say every time, but many times we're doing these experiments, we're seeing great results. Science is hard to predict, not every experiment works, but it just continues to add the body of confidence I see. And then we're going to bring some of that data to you in the near future. So you see it as well, and that's the stuff we're talking to partners about so they see it as well. So that's what again, gets me motivated that we are doing -- we have a really novel platform, and we're doing the right work to help it shine to make it attractive and thus advance it.

Excellent. All right. It looks like we have another question here. So Abizer, you showed a table of ADC deals due to the majority of those programs in those transactions using microtubule inhibitors. I don't know what it is with respect to the tongue twister for me, I apologize. Have you reached out to those companies about your technology?

Yes. I would -- yes, we have, and we continue to reach out to a broader spectrum than even on that sheet. We actively talk to a number of the major players that you can imagine, both in large, mid, even small cap biotech pharma around opportunities around partnership. And I think one of the things is we have to show people our data to show them why it's compelling. So although we're exciting and new, remember, there's also an adoption curve of anything new. And people go with what they know and pharma and biotech kind of rides in momentums and waves and herd. So the herd is around the Topo-1 and microtubule inhibitors since they're so prevalent, it's easy for people to follow what they know. So does that make it harder for us to have people see why we're doing something different. It doesn't -- it's not hard that people want to say, hey, I want to hear something different because I'm tired of the same story. It's just that they want to see more data to believe it. And so that's just being -- I mean, you can -- the honor of being leading edge and innovative is great because you have the first-mover advantage. But sometimes you have to prove people a little bit more than others because they want to see more data before they do something. So I think we are actively engaging a lot of these partners to show them the wide body of data that we have, why they should believe, how we continue to derisk this and get them excited. And we are getting traction. I mean I can't speak to specifics, but we are having the conversations with the right people and the right companies. And when we have enough of them, it's like collision, eventually, they're all going to -- one of them is going to successfully result in something.

Excellent. All right. So those are the questions that have come in from our audience. And before I close, I was just thinking about the question that came in related to valuation and stock price. I have a little bit of a different question. You shared -- again, you shared a compelling exciting story. We see your enthusiasm and the opportunity, I think you outlined very well for our audience and for potential investors. So if you think about Akari and you think about someone that is taking a look, maybe heard a presentation for the first time today or has been kind of following but really hasn't done more than just follow the story. What would you say to our audience, to those paying attention, why investors should do the work, make a decision and potentially become an investor in Akari Therapeutics right now?

Sure. So I would always go back to if you want to invest in biotech and life sciences, you got to do your homework and make sure you feel good. You also have to be ready to stomach a lot of ups and downs. And like that comes with biotech investing because it's unpredictable because it's biology and it's science, which is unpredictable by itself. But I think you have to get convicted around two things. One, do you believe in the science, you really fundamentally believe in what's being told you and you have a lot of faith and it's differentiated and you see that it has a compelling vision and value differentiation. But two, do you believe in what I would say, the team and the plan because ultimately, science is only as good as science and it sits on the shelf, but it's the team and the plan that, that team is going to develop and execute that's going to drive that science forward. And I think as you look at any company, knowing you got to have a little bit of a stronger stuff in the biotech space, particularly now, if you can answer those 2 questions, you feel good about an investment that you should go in. And I'm not saying you need to bet a lot, but bet a little. As an investor, I was buying and I see dips and I still have a conviction I buy more, nothing changes because you think it's a good investment. And so I think it's more about your overall risk profile and then your belief. And I'll tell you my personal belief, I'll just share an anecdote. -- when I first looked at a company called Seagen probably in 2007 as a personal investor, and I worked in the biotech space back then as well, this antibody drug conjugating sounds pretty interesting because people take systemic chemo and it kills you and no one likes systemic chemo because it's poison. Well, this seems like a cool way to developed to combine an antibody, which is high tech that Genentech put out there in oncology that has shown so much effect as a single antibody and combine it with these chemos. And maybe these people in Seattle have something interesting, and it's taken a long time. They've been around for a long time, but they seem like they do something interesting. And next thing you know, Seagen continues to get approvals and deals. And I came in late to the story. I think there were people that were wiser and smarter than me that even knew this 5 or 8 years before that. But I can tell you, I came in and I never looked back. to the point where Pfizer bought them for $43 billion, and I did personally decent on that transaction. So I think you -- but what happened is despite the dips, there were a lot of dips on Seagen. And I stayed and I doubled down many times because I believe in the science, and I believe in the team on the execution and what they were doing. And I think if you believe in those 2 things, you should buy an investment. And if you don't, you shouldn't invest or you should sell your position. So I tell you that is objective advice.

Excellent. Well, Abizer, I have to say I thoroughly enjoyed this conversation. Your presentation was compelling. I think you did a great job outlining the opportunity for our audience and really appreciate you taking the time and doing that. So with that, everyone, this does conclude the virtual investor closing bell featuring Akari Therapeutics. And I would like to thank Abizer for joining us today. I'd also like to thank our audience for your participation and as always, great questions. And as a reminder, Akari Therapeutics trades on NASDAQ under the ticker AKTX. If you like what you saw today, I encourage you to visit akaritx.com for more information on the company and to sign up to follow the company to receive their alerts as well as follow their social channels on X and LinkedIn to stay current on the latest information. And you can also visit virtualinvestorco.com for a replay of today's segment as well as our latest events calendar. Abizer, thanks again. I can't wait to have you back. Congratulations on your progress, and we really look forward to seeing what's to come for Akari.

Well, thank you, Jenene. Thanks for having me, and thanks to the audience for your attention. Appreciate it.

Absolutely. Thanks, everyone, and wishing you a great rest of your day.