Good day, and thanks for. The company's lead molecule, INB-200, is currently in a phase I clinical study, being evaluated as a therapy for GBM. The second molecule, INB-100, which is also in a phase I study, is being evaluated as a therapy for leukemia. Beyond 200, the company has started an INB molecule in a multicenter study in phase I, again, to look at GBM. Beyond this, the company has also been developing off-the-shelf iPSC derived gamma delta T cells and also a non-signaling CAR T platform. So there's been lots of interesting developments happening within IN8bio, especially in the last 12 months. I'm sure there's going to be new interesting data coming up in the next 12-18 months. To discuss all that, I welcome Will to this fireside chat this afternoon. Great. Great. Thanks, RK. Thanks for having us. It's always glad to participate in these conferences with HC Wainwright. I will note that our INB-400 program, it's a national multicenter study, is now actually in a phase II study. We have enrolled patients and have actually treated our first patients in that study. Sorry for that. No worries. And then, so gamma delta T cells, right? This is an interesting set of T cells, which you have been working on for quite some time now. But at the same time, I think there's quite a bit of misunderstanding about the utility of the gamma delta T cells and how they can be really therapeutic. So if you can help us understand the utility, please give us an overview and how you think this is differentiated from other cell engagers. Great. Thanks, RK. Look, we are one of the world's best experts in the area of gamma delta T cells. The gamma delta T cell is an ancient primordial cell that has unique features. Not only can this cell kill by itself, hunt out, and seek out targets, but it also has the ability to communicate with all the different components of your immune system. This is not just another alpha beta T cell. It serves as a functional bridge between the innate and the adaptive or memory immune response of our body. And as such, these particular cells have features across both. When we first started with cell therapy in CAR T, people focused on the alpha beta T cell, mostly because we found that those cells were plentiful. They encompass about 70% of the total white blood cell population in our body. And we thought, there's a lot of them. They must be important. The alpha beta T cells are like the infantry of our immune system. More recently, people have focused on the natural killer cells or the NK cells. These are the early killers. They respond immediately to a threat. But the natural killer cells, once they kill, they die away, and they have very little persistence. The beauty of the gamma delta T cell is that they have properties across both. They have memory, just like an alpha beta T cell. So we can find these cells a year and beyond still in the blood. They're not MHC-restricted, meaning they don't require to be programmed or be primed to see a prior antigen before knowing what to kill. And they can kill directly, just like an NK cell. But unlike the NK cell, they don't extinguish themselves within days. As I said earlier, they last a long time. We believe these particular cells that can serve to distinguish between what's safe and what's not safe in our body can serve a primary role to accomplish our mission to eliminate cancer cells. Our mission is what we call cancer zero. And we've applied our gamma delta T cell in unique ways to play the role of cleanup, to enable to eradicate more cancer cells so that patients can be walking around longer without relapse and remaining in durable complete remissions. Very good. So let's start off with your pipeline and start off with INB-200. So INB-200 is being looked at as a therapy for GBM in a phase I clinical program. And you have been releasing data as it matures. But recently, you put out some data, which has been very interesting. So can you please highlight and review for us the complete data set that you have released so far so that we and then I also would like to understand how we should think about this data in the context of INB-400. Sure. So first of all, INB-200 was the phase I study. I'll note that our phase I studies were originally filed as an investigator-sponsored study, so investigator-sponsored IND. The INB-400 program is a corporate-sponsored IND, so we hold the IND. So we recently presented data at ASCO. That's the American Society of Clinical Oncology. That's the largest oncology meeting in the world, where about 40,000 people descend upon Chicago every June. At ASCO, we announced the initial data across all 3 of our cohorts. In this particular study, we dosed patients across 3 cohorts, those that received 1, 2, or sorry, 1, 3, or ultimately 6 sequential doses. The patients in our study are all newly diagnosed GBM patients or newly diagnosed glioblastoma. Their typical standard of care is surgical resection followed by 6 weeks of daily radiation and chemotherapy, followed by 6 monthly cycles of maintenance chemotherapy. The maintenance cycles are 5 days of chemotherapy followed by a 23-day break. So in our treatment and the maintenance phase of therapy, the patients either get 1 dose on day 1 of cycle 1, 3 doses on day 1 of cycles 1, 2, and 3, or 6 doses on days 1 of cycles 1 through 6. At ASCO, we announced that we had treated 13 patients. Of those 13 patients, we are seeing initial signs of a dose response between those who received 1, 3, and 6 doses. We have 5 patients who remain alive and relapse-free, with the longest patients now remaining relapse-free for over 36 months. What was exciting about that, although it's a small number, that one patient was an IDH mutant patient. In 2021, we reclassified IDH mutants as low-grade gliomas. That patient had received 1 or 3 doses and remained almost 3 years without relapsing. What's unique was last year in August in The New England Journal of Medicine, there was a paper reviewing a new trial for a drug in phase III that's an IDH inhibitor. In that particular trial, the control arm, the median progression-free survival was 11.1 months. The active arm was 27.7 months. In the control arm, every single patient relapsed by 25.5 months. Although it's a single N, our one patient is now out over 3 years remaining in remission and relapse-free and alive. As well, in the third cohort, we have MGMT unmethylated patients. Those are patients whose tumors do not respond to chemotherapy. They usually progress quickly, somewhere between 4 to 5 months. We now have 2 patients who are now out at 6 and 9 months remaining alive, in remission, and relapse-free. So we're quite excited. Again, small numbers, but in 1 case, we're doubling the progression-free survival of a patient who should not be responding to therapy. This is very good. So GBM, as you and I know, has not seen an approved therapy for a long time. And there's been a lot of different modalities, therapeutic modalities being tested both in the clinic and in the academic situations. And one such paper that was put up by Marcela Maus's group out of Mass General was actually using an EGFRvIII targeting CAR T. And they put out some positive data. So what's so novel about that data? And what does that tell us about the potential of CAR T at all in GBM? And how would you compare and contrast with what you are seeing against what they're seeing? Great. Thanks, RK. Look, you're right. We have not had a newly approved therapy in GBM since 2005, so almost 20 years. As you know, I spent a long time on Wall Street. One of the things that I learned, look, we use the euphemism in oncology, the war on cancer, since about 1972. The one thing about our immune system is you can think of our immune system as our shoulders. Most of the therapies that we've seen in development for glioblastoma, people have treated peripherally, whereas below the neck, assuming that whatever treatment they're going to deliver is going to cross the blood-brain barrier into the GBM or the glioblastoma, which is located in the cranium. Unfortunately, like in any war, if your soldiers are not on the battlefield, you can't win. One of the advantages for cell therapy was to go to GBM because we can deliver cells through a catheter directly into the tumor bed. In the frontline setting, about 95% of newly diagnosed GBM patients get a surgical resection. During that time, we can insert a catheter that allows us to deliver cells directly to the tumor at high concentrations. Now, Marcela is actually on my scientific advisory board. She's wonderful. When she first ran the studies using an EGFRvIII CAR, she dosed the patients intravenously in the arm, assuming things will cross the blood-brain barrier. Now, CAR-Ts could cross the blood-brain barrier, but not at high levels. In this particular study, she did something very similar to us, where patients are getting a surgical resection, they're inserting a catheter, and then delivering cells directly into the tumor bed or into the ventricle. This was a unique study. It's using what they call a CAR-T cells. It's a CAR that targets EGFRvIII, as well as secretes a protein to target the EGFR moiety as well. So in this case, they're targeting two. What she demonstrated was that the CARs we delivered directly could generate a rapid remission, a complete response, and shrink the tumor. In fact, they could eliminate the two targets, both EGFRvIII and EGFR. Unfortunately, like many solid tumors, the challenge of glioblastoma isn't just to shrink the tumor. It's tumor heterogeneity. And they showed they could eliminate the entirety of their two targets, and the rest of the tumors can grow back. And the patients, unfortunately, all relapsed. The responses were transient. The fastest patient actually relapsed within 30 days. And so that's the advantage we believe of the gamma delta T cells. With their unique receptor repertoire, they can target the heterogeneity of the disease. If we can get to deeper responses and eliminate more targets because of the ability of the gamma delta T cells to recognize numerous targets, more than six, in fact, then we think we can have a longer durability of remission. So I know that based on positive data that you have seen so far with the 200, you have taken an IST and made it into a multicenter study with INB-400. But again, INB-400 and 410, they're like two different molecules, and they're being tested a little bit differently as well. So can you just talk to us regarding the phase II study that you're doing with the 400 and how you're kind of testing the allogeneic and the autologous therapies? So let's start with the design first and then think about how to compare this against what we are seeing in 200. So great. The INB-400 trial is designed to have three arms. Again, there are numerous arms. The first arm is to recapitulate the INB-200 data in a multicenter national study across more patients and more centers. So arm A is very similar to the design of the INB-200 study. The gene modification is identical to the modification that we did in the INB-200 study. And these cells are autologous, meaning they come from the patient themselves. This particular study seeks to enroll 40 patients in the frontline glioblastoma setting, really trying to expand on the earlier phase I data and demonstrate that our original hypotheses were correct. Moving on, the allogeneic arms, this will require an additional IND that will require additional funding and likely to occur more towards next year because of newly composed FDA guidances for allogeneic cell therapies. This will have two arms. The first will be a phase IB run-in in approximately 6 relapsed GBM patients with a genetically modified allogeneic or donor-derived cell. The advantage of the allogeneic cell is that you can take cells from a donor who is likely younger, healthier, and isn't immunosuppressed from a globally immunosuppressive tumor like glioblastoma. If we see safety in the first 6 patients, we would expand to arm B, which would encompass approximately a total of 40 patients in the relapse setting. This could potentially be a registrational path to the FDA. And then we would also enroll arm C, which would take this therapy with an allogeneic genetically modified program, again, into the frontline glioblastoma setting, being able to compare autologous to allogeneic genetically modified. Okay. So the only difference between the arm A and arm C is one is allogeneic and the other is auto. Is that all? Or is there? There are differences in the manufacturing because the allogeneic program has to arguably have higher purity and have fewer residual alpha beta T cells, which can cause graft-versus-host disease. But otherwise, very similar. Okay. And then at least as we see the 200 data maturing, and obviously, we just talked about not only the persistence of the data, I mean, persistence of the efficacy, but also the long ORR that we are seeing, the long survival we are seeing. Is that something we should expect from the INB-400? How should I think about INB-400 data? Currently, in INB-400, we've publicly announced that we've opened 8 sites. We've potentially up to about 15 sites nationally. We are enrolling patients. We have publicly announced that we have dosed the first patient in INB-400. I think we are not going to do what we did in the phase I programs, which is provide updates every 6 months. I think we're going to wait till we have a larger bolus of data to be able to present publicly. And in the meantime, we do expect to present updates in the INB-200 program, likely again later this fall. Look, at this point in the third cohort, we have patients who are out somewhere between 6 and 13 months who have remained in remission without relapsing and alive. By the time we get to this fall, there are certain medical meetings we may be able to present at, but we will have patients at that point somewhere between 12 and 18 months. If we can keep patients a year to a year and a half in remission and relapse-free, we're now getting to the point where we're surpassing just not median historical progression-free survival, but we'll actually be sorry, we'll actually be passing historical median overall survival for those patients. So we're really excited about the potential for the data that we expect to present later this year. Perfect. So the other molecule is the INB-100, where you have been testing it out in leukemia patients. So just to start off, what is the salient features of this clinical candidate? And very recently at EHA, you provided a clinical update that actually showed 100% of those patients remain in the morphologic have achieved morphologic CR for greater than 12 months. So please highlight the significance of that data as well. So these are cells that are allogeneic, meaning they come from a donor. They are unmodified, but they are expanded and primed to kill. We recently demonstrated data at the ISCT conference that our manufacturing process actually upregulates specific genes that lead to higher homing, higher killing, higher secretion of cytokines such as interferon gamma and TNF alpha. This particular program, the cells are haplo-matched. So this is important because when we initiated this trial more than three years ago, we followed the transplant biology and thought that for a donor-derived cell to reduce the risk, we wanted to match at least four out of the eight markers on these cells that signify self or your own cells. We hypothesized if we could match those cells, then we would have less of what's known as host-versus-graft, which is your immune system eliminating the graft that you've infused into these patients. What's important is recently a competitor, actually Caribou, ASCO, actually demonstrated data that unless you have at least 4 of the HLA alleles, the 4 of the 8 self signals matching, that the grafts are actually rapidly eliminated, and that's directly correlated to clinical response. And so we're pretty happy that after a number of years, our original hypothesis was proved to be correct. But what's salient about our particular approach, I think, is the in vivo expansion of our gamma-delta T cells and the persistence of those cells now demonstrated to be beyond 365 days and the long tails in our data. You're right. We went into the context of haplo-identical stem cell transplantation. There is a number of competing companies in this particular space with allotransplant, haplotransplant with reduced intensity conditioning. Most of the patients, about 50%, are expected to relapse by 1 year. 25% are expected to relapse at 100 days, according to Michael Bishop, who spoke on our behalf at our R&D day that I believe you attended last October. He's actually the director of stem cell transplantation at the University of Chicago. We are now seeing 100% of our patients cross the 1-year mark remaining in remission. We now have patients 3 and 4 years out remaining in remission. What's our advantage is the long durable tails and the length in follow-up that we have relative to some of our competitors. In addition, because of the unique properties of the gamma delta T cells, we have not seen any cytokine release syndrome. We have not seen any ICANS or neurotoxicity to date. We've seen a relatively low incidence of random infections. So based on these results that you're seeing, you've been achieving, there is a plan to start a registrational study soon. What's the design of the study? And then have you announced any timing in terms of when you want to start this? So this particular study, we provided some guidance. We are still in discussions with the agency. We were looking at potentially AML and MDS patients and randomizing the arms into experimental those who receive gamma delta T cells and those who do not receive gamma delta T cells and potentially a FLT3 inhibitor for those who may have FLT3 mutations. Our guidance has been that we will provide additional details this summer as to the exact design of this particular study. There have been a number of studies in the past where patients have analyzed populations that have included AML, MDS, ALL, and different transplant modalities and different, I guess, maintenance therapies. We're trying to narrow things a little bit, reduce the variability a bit so that we have a tighter trial that's well-powered. And so we will provide an additional update. Ultimately, to initiate this trial, we will be required to file a new IND. Again, the original INB-100 trial was filed as an investigator-sponsored study. We will have to file an IND to outline our clinical portion, our CMC, and the Pharm/Tox. Again, we've done this before. Last time with the INB-400 program, we cleared it on first review in 30 days. I have high confidence in our team, and that's potentially later this year. Later this year, what sort of additional data would you be releasing from this study so that would actually give us that would also give us some confidence regarding the next study, which is supposedly registrational? I think when we look at this study, granted, we've treated 10 patients, but these were 10 patients that were the sickest of the sick. Remember, this was the first in human trial for allogeneic gamma delta T cells. When it's the first in human, the very first patients that you enroll have to be those who have few options and are very sick and are at high risk of relapse. Our patients included those who had trisomy 8, deletion of chromosome 7. We had concurrent FLT3 and IDH inhibitors. We had patients who were on 7 prior lines of therapy, patients who were older, a median age of 68, and 2 of them who had TP53 mutations who were all bad prognostic factors. Some of these patients would have been expected to relapse at an 80%-90% rate instead of the 50%. And yet we saw all of them remaining in remission and alive. In fact, we have not had any patients to date, knock on wood, who have died with progression. Later this year, we expect to provide additional updates, potentially at ASH, looking at the tails, seeing how many patients remain in remission, how long they remain in remission. And as we've said before, we're continuing to enroll up to additional 10 patients, mostly on publication because we feel pretty comfortable about this data. But we'll see a number of those patients in particular. I think the early data will be looking at the 100-day remission rates. Yeah. I know we are running out of time, but I want to kind of go over the non-signaling gamma delta CAR-T because I think it's a very interesting program because you're targeting two major well-validated targets, CD33 and CD123. Yeah. So our non-signaling CAR was to create a chimeric antigen receptor or CAR-T specifically for the biology of gamma delta T cells. We didn't do what a lot of people did, which was take the traditional alpha beta T cell CAR and put it onto a gamma delta T cell. But we thought about the biology and how do we create one for gamma delta T cells. And so we've created CARs at AACR, the American Association for Cancer Research. We created a CAR targeting both CD33 and CD123. These are difficult targets, mostly because they're not only expressed on the leukemic blasts, but also on the healthy CD34 expressing bone marrow cells. We've seen other people do other things such as try to knock out CD33 on the surface of the bone marrow, transplanting the patient so that they can use the CAR. We've seen people use an activating switch that unfortunately last summer resulted in 2 patient deaths. We believe by using the biology of the gamma delta T cell, we can create a CAR that will naturally distinguish between healthy and tumor cells. At AACR, we showed that our CARs will increase killing anywhere from 20%-80% over the untransduced control. And none of the CAR expressing cells killed leukemic or healthy cells anything above a naked untransduced cell, which we know because of our INB-100 program does not ablate the bone marrow. So for the first time, we're widening the therapeutic index, widening that window so that we think our CAR constructs can help target some of these undruggable targets that will become more prevalent in both leukemias and especially as we target solid tumors because we don't believe there is a single target that's expressed on the tumor cells, all of the tumor cells, and none of the healthy tissue. So Will, unfortunately, I only have about 15, 20 seconds left. In that time, can you just highlight some of the catalysts that we should be looking out for over the next, say, 6 to 12 months? Yeah. So as we said, we're excited. We'll be providing additional guidance on the potential phase II registrational trial for INB-100 and the path there. We look to provide updates across both of our phase I trials this fall, likely at medical meetings. So updates on both the glioblastoma program as well as the leukemia program. I'm excited especially about the glioblastoma program. There we'll be looking for, again, durability of those responses as patients remain in remission beyond where they should have already passed. And then we have potential new INDs that we'll be filing, the registrational trial for the AML program, a path to commercialization, as well as IND for the allogeneic program and so on. Thank you. And then more data, more data, more data.