Greetings and welcome to today's CytoDyn Investment Community Webcast. My name is Ignacio Guerrero-Ros, and I will serve as your moderator today. At this time, all participants are in a listen-only mode. As a reminder, this webcast is being recorded today, April 30, 2026. Following the conclusion of the webcast, a replay will be available for approximately 30 days on the Investor Relations section of the company's website. During today's presentation, you may submit questions at any time by using the questions chat panel located at the bottom of the webcast window. There will be two Q&A sessions on today's call. Following Kasi's presentation, he will address questions related to the CLOVER trial. After the company update, management will be available to respond to additional questions. Given the number of questions submitted in advance, as well as those that we expect to receive during the webcast, we may not be able to address every question today. If your question is not answered today, as always, feel free to email your questions to ir@cytodyn.com. I'd now like to turn the webcast over to Tyler Blok. You may begin. Good afternoon, everyone, and thank you for joining us today. This is Tyler Blok with CytoDyn. Before we begin today's company update, it is essential that we provide you with important cautionary language consistent with certain federal securities laws. Our remarks during today's webcast will include forward-looking statements. Forward-looking statements are not guarantees of future performance and involve known and unknown risks, uncertainties, and other factors that are difficult to predict. Actual results may be materially different from any future results expressed or implied by such forward-looking statements. These risks and uncertainties include and relate to, among other things, statements regarding leronlimab's early performance in clinical studies, statements regarding leronlimab's anticipated performance in clinical studies, statements regarding leronlimab's potential efficacy in certain indications, the company's ongoing ability to raise capital, the clinical trials may not commence or proceed as planned, the products may not receive regulatory approval or market acceptance, that our patents may be challenged and/or unenforceable, that competition may reduce the commercial potential of our products, and that the company may experience recalls, manufacturing issues, or other product liability. Although forward-looking statements help the company complete provide complete information about the company, such statements may be less reliable than historical information. The company undertakes no obligation to publicly update these forward-looking statements except as required by law. Please refer to our recent quarterly and annual reports filed with the Securities and Exchange Commission for more information about the risks and uncertainties that could cause actual results to materially differ as compared to current expectations. Once again, guys, thank you for joining us today. I will now turn the podcast over to Robert E. Hoffman. Thank you, Tyler. Thanks to all shareholders and interested parties who are listening to our call today. I'll provide a brief financial overview, then we'll turn the call over to our CEO, Dr. Jay Lalezari. We recently completed a financing for gross proceeds of $17.5 million. We were very pleased to complete this financing, allowing us to continue to support leronlimab development. Earlier this year in January, we announced that a compassionate benefactor committed funding to support the company's expanded access, or EAP, for patients with triple-negative breast cancer. We are thrilled to announce earlier this week that the first patient was dosed in the EAP. Last year, we announced a $30 million funding commitment from Yorkville Advisors Global. Under the terms of the agreement, CytoDyn has the right to sell and Yorkville has the obligation to purchase up to $30 million worth of CytoDyn's common stock over the next 36 months. CytoDyn, at its sole discretion, will control the timing and all sales of common stock to Yorkville, and there are no warrants, derivatives, or other share classes associated with the funding arrangement. CytoDyn is not obligated to utilize any of the $30 million available, and there are no minimum commitments and minimum use penalties, and arrangements does not impose any restrictions on the company's operating activities. With very favorable financial terms to the company, we view this facility as another tool in our toolbox. On the debt side, we negotiated a 3-year extension on the maturity dates of our debt facilities with Chicago Venture Partners. We also agreed to make a monthly payment covering both debt facilities in the amount of $1 million paid in shares of common stock. The annual interest rate for both debt facilities were reduced to a 5% rate as part of the extension. I am very pleased with our ongoing relationship with Chicago Ventures. As reported on our 10-Q recently filed, we reported cash and cash equivalents totaling $15.7 million at February 28, 2026. On the investor relations/business development side, we continue to be very active communicating the leronlimab story. We recently attended AACR in San Diego, which included an AACR partnering module. We accepted an invitation from the investment bank D. Boral. I will be presenting at their conference in New York on May 7. Unfortunately, there is no webcast option for that conference. I will be presenting at the 16th annual LD Micro Invitational taking place in L.A. from May 17th through May 19th. We will be at ASCO in Chicago from May 29th through June 2nd, 2026. We'll be in attendance at BIO 2026 in San Diego, June 22nd through June 25th, and we are actively setting up meetings with investors, potential partners, and other stakeholders. I will now turn the call over to Jay. Thank you, Robert, and thanks to everyone for taking the time to join the call today. I wanted to start by particularly acknowledging and thanking the long-term investors who have kept faith with us during this unique journey together. I know for sure that the great things that are happening for CytoDyn now don't happen without your steadfast support over these last several years. I'm a few days short of a 67th birthday and consider the opportunity to host this call the best birthday present of my life. During this call, we'll review and update some of the remarkable data that CytoDyn just presented at the AACR conference. I absolutely believe that this moment represents a crucial inflection point for CytoDyn as we transition from a company built on faith and belief and a whole lot of ifs to a company with solid perspective, unassailable, and by all accounts, remarkable data confirming leronlimab's early biologic activity in solid tumor oncology. It has been an incredible journey together, and it is truly astonishing for me that leronlimab appears to be performing at the outer limits of what I even thought was possible. Now, to be sure, there is a lot of work ahead. In particular, CytoDyn needs to demonstrate that these early biologic signals that we are seeing translates into sustained clinical benefit for patients. Instead of moving forward just on faith, I believe the solid data we're reviewing today gives us a clear line of sight on where we're heading and how to get there. I'm very excited about what comes next for CytoDyn, and as the song we played said, we're gonna stand our ground, and we're not backing down. Let's begin. For those who might not be aware, CytoDyn is a novel drug candidate, with data now supporting multiple mechanisms of action. Traditionally, we've talked about Richard Pestell's data on the reduction of tumor metastasis in mice. We've recently presented data from the Cleveland Clinic, showing a similar effect in a colorectal cancer model, but also a marked reduction in the vascular supply of tumors treated with leronlimab, another important MOA. Dr. Kasi, who will be joining us shortly on this call, is gonna show some data indicating what happens with leronlimab impact on the tumor microenvironment. As, as well, Richard presented some data about leronlimab's effect on immune exhaustion and direct induction of PD-L1 expression, as well as an effect on the secretome, which is the shield the tumor uses to protect itself from the host immune system. We have multiple MOAs with leronlimab, and I think what we're seeing playing out with our data from the clinic is an effect of the tumor of leronlimab's multiple ways of getting at the tumor. Equally important to any efficacy claims is the crucial safety profile of leronlimab, and I do not know of another therapy in all of oncology that has a safety database to match. This drug's been well-tolerated in more than 1,600 patients across more than 20 clinical studies. The data we'll review shortly from the colorectal cancer study aligns with this historical safety database. Of course, leronlimab is playing in with a huge market potential, not only in colorectal cancer and triple-negative breast cancer, but also potentially as a foundational drug for the treatment of other solid tumors. Beyond that, of course, on the side, CytoDyn is running studies also in other indications such as Alzheimer's disease. The journey in solid tumor oncology really began with the observation of sustained remission in a group of patients with triple-negative breast cancer, which seemed to propose a prime and pair regimen with a checkpoint inhibitor, creating a pathway to sustained remission. It, the CRC study was launched in an effort to try and prospectively confirm that paradigm. What we observed along the way is that leronlimab as a standalone agent, as an anticancer therapy, has remarkable abilities. Indeed, it's that standalone activity which makes the prime and pair regimen even possible because of what leronlimab does on its own to prime the tumor. That's background. On the next slide, we're gonna start moving into the CRC data that was just presented at the AACR meeting. On the next slide, this is a Phase II study that the FDA gave us, open label and randomized to 350 mg and 700 mg. They did require a dose comparison. I would stress again that in the 350 mg or 525 mg or 700 mg dosing choices, there is no safety data that distinguishes those three. The ultimate decision about the optimal dose will very much rest on any efficacy data we generate. This phase II study has already and now enrolled 60 patients, as we just announced, in patients receiving Lonsurf and Avastin as a backbone in patients with third-line microsatellite stable metastatic colorectal cancer. Just not to put too fine a point on it, these are patients with very advanced disease and very fragile indeed. As I mentioned, Dr. Kasi, our wonderful lead investigator, will be joining the call shortly. We announced last week that target enrollment's been completed. There have been two data and safety monitoring board meetings. The first in December opened up the 700 mg arm, and the second took place after 20 patients completed one full cycle of treatment, each cycle being a month long. In both of those meetings, safety was reviewed, and there have been no safety concerns registered. The next slide is the beginning of some very important points about the CRC study that I wanna go into in some detail. First was the remarkable observation that 100% of screened patients, which is now 91 out of 91, have tested CCR5 positive. It's important to note three things. One, that CCR5 positivity in this study was defined as 10% expression on the tumor cells themselves, or 1% expression on the immune cells in the tumor microenvironment. That was a liberalization of prior criteria CytoDyn used in their earlier oncology studies back in 2019 and 2020. We did that specifically to both expedite enrollment and to further understand what the boundaries were of what defines a patient who can benefit from leronlimab. It was obviously remarkable that 100% of patients qualified for the study and then generated the data that we have. It also helped us rapidly recruit this study, and most importantly, it helped us eliminate the waiting period involved with completing the CCR5 testing. On the second bullet point here, again, the safety observed in this study, specifically, there are no grade three or four adverse events or serious adverse events attributed to leronlimab. Even more important, I think, there are no leronlimab-related dose or treatment-limiting toxicities, meaning no patient has had to adjust or discontinue their leronlimab dosing due to any side effect or adverse event. A remarkable safety profile to date, including in this fragile and highly advanced population. The remarkable data that Dr. Kasi presented in San Diego showing a ctDNA, circulating tumor DNA declines using the Signatera assay from Natera. The first 19 patients enrolled at City of Hope, demonstrating that all 19 patients had a decline in ctDNA with a median decrease of 70% at week 2. Ignacio Guerrero-Ros, if you can show the next slide. This is a remarkable figure by any account, and there are a number of important points to make about these data. First of all, there's a growing consensus in oncology that even a small decrease in circulating tumor DNA generally associates with improved clinical outcomes. The observation that 100% of our patients are demonstrating a decrease in circulating tumor DNA certainly bodes well for what we are hopefully going to see in terms of clinical endpoints. Also, that 70% decrease at week 2 indicates a very potent early biologic response. To put these data into context, we're working with Natera, the company that makes the Signatera assay, to generate a comparator data set of similar patients treated with just the backbone alone. We think that that comparator data will be very important to provide the FDA during our forthcoming regulatory submission. We also are pursuing several strategies to obtain circulating tumor DNA from patients on leronlimab monotherapy to further confirm the activity of leronlimab on its own and absent the backbone in this study. Fourth, it is remarkable to note that, I'm sorry, Ignacio, if you go back to the waterfall plot, that 13 of the 19 patients included in this DNA chart were treated with 350 mg dose. This observation is both surprising and certainly surprising to me and very exciting. We're naturally keen to determine if there's a dose response with the 700 mg dose, at least measured by circulating tumor DNA. That's something we hope to report on to shareholders sometime later this summer. Equally important on this slide is that the majority of the CLOVER patients, or 62%, enrolled to date have KRAS mutations. These mutations are generally associated with the hardest to treat patients in oncology. These preliminary results indicate that leronlimab's early biologic activity might also be agnostic to the KRAS mutation. I'm also pleased to share new information that we've recently confirmed that four patients in follow-up have had at least one undetectable circulating tumor DNA level during that follow-up period. Although this is very preliminary, it is also remarkable to note that three of those four patients who have gone undetectable are being treated with the 350 mg dose. Lastly, I just wanna make this point very clear, that we have to remember that as exciting as these preliminary and early DNA decreases are, what matters to patients and what matters to their treating physicians are clinical outcomes. That generally means DNA levels going undetectable and remaining suppressed in association with improved outcomes in disease control rate, overall response rates, and improved progression-free and overall survival. These, of course, are also the metrics that matter most to the FDA. All right, Ignacio, if you could advance the slide now. I wanna update bullet point four that we now have 22 patients with RECIST data available at week eight, of whom 15 or 68% are demonstrating shrinkage or classified as having stable disease on their scans. The encouraging early results indicate that the scan results are correlating with the circulating tumor decreases we're observing. I'll also report that there are numeric increases in PD-L1 observed in the majority of patients. We need to remember that most of these patients were being treated with the 350 mg dose, which at least in the TNBC setting was not as had a vigorous PD-L1 response. There will be more on PD-L1 later. In the meantime, in addition to all the scans and the DNA data, we're hearing from the investigators that patients are responding clinically, in particular with less pain. With that, it is my pleasure to introduce Dr. Pashtoon Kasi. Dr. Kasi is the principal investigator for the CLOVER study and the CytoDyn family is extremely fortunate that Dr. Kasi has stepped into that role. Pashtoon is the Medical Director of GI Oncology at City of Hope Orange County. He's been a incredible collaborator, and he joins us today to share his perspectives on the data, provide some granular detail on the first patient he enrolled, and then update us on his investigator-initiated trial. Pashtoon, welcome to the call, and thank you for joining us. Thank you so much for having me and if we could upon what you have said so far. You know, I wanted to narrate the story of our index first patient, you know, and you know, why did this all ctDNA story come about is one of my other areas of research needs besides treating patients with colorectal and GI malignancies and, you know, trying to bring novel therapies and immunotherapies and options for our patients to clinic is this whole field of liquid biopsies, you know. As some of you might be aware, you know, the term liquid biopsy is a misnomer since there's no biopsy being performed. These are non-invasive blood draws, you know, for me, the journey for liquid biopsy was more so in the clinic first it added value, but then, now, in terms of our research, we're integrating it as well. Regardless of trials, I, at least in my clinic, pursue different types of liquid biopsies, some that are meant for genotyping, figuring out as Jay was saying, who has KRAS, who doesn't have MSI, you know, what is the mutational makeup. As you might be aware now, these assays are also being used as response metrics. In general, trial or no trial, I do check, you know, ongoing circulating tumor DNA assays in these patients because, you know, these crude tumor markers, CEA, CA 19-9, at least a quarter of the patients don't even make the marker. In this first patient, for example, you know, often the half-life of these glycosylated, you know, proteins that are these tumor markers is sometimes over days or weeks, and often things go up before it goes down. As was pointed out earlier, this regimen, the so-called, you know, from the SUNLIGHT study with this oral chemotherapy, the TAS-102 or the brand name Lonsurf with bevacizumab as the anti-VEGF. You know, it's one more option, but, you know, it's not necessarily a great option. You know, when patients and caregivers hear this being as the next step, it pretty much is a red flag and not necessarily good news because it kind of signals that we're running out of options. In this particular study, you know, this, you know, it's as a clinician, not just as a PI on this trial, it helps me because the study was not restrictive. It was not like cherry-picking patients who only had one or two chemotherapies. You know, some of these patients have exhausted all aggressive types of therapy. Like this particular patient had, you know, the standard double, you know, FOLFOX chemotherapy with bevacizumab, then the FOLFIRI chemotherapy with bevacizumab. At City of Hope, we are one of the centers of excellence that they can put something called a liver pump or medically pronounced as the HAI or the hepatic arterial infusion pump for liver-dominant disease. It allows 300 times the amount of chemo to be given in the liver. This person had that installed as well and completed all that therapy. After a few months of disease control, lo and behold, there was a reemergence of liver metastases as well as lung metastases, and also was a RAS mutant, which, you know, by all means, when you look at a patient with metastatic colorectal cancer, presence of mutations, presence of liver metastases, number of lines of therapy, you know, this is the kind of patient that an average trial will probably refuse. The fact that, you know, when we started this patient on treatment as early as 1 week into treatment and also to the last bullet point that was made on the last slide, improvement in pain as early as 1 week was something that was very reassuring to me for not just this, but for many other patients. The CA actually had blipped up, which, you know, as a patient, you're used to looking at a tumor marker that's a sign of concern that maybe my cancer is getting worse, and that's where ctDNA can be helpful. As you can see, pretty much the first ctDNA was drawn a week into treatment for this exact same purpose that in my experience of using ctDNA that only has a few hours of a half-life. If you multiply that by five, within a day or so, whatever you did to the patient, whether it's surgery, chemotherapy, this trial, you should see improvement literally within days. I think we underestimate how quickly you can see that readout. That's where some of the novel trials are integrating liquid biopsies as early readouts, not to replace the scans. You can still do your scans at whatever, two months or three months, but it gives you that early lens, early readout that can be not just important scientifically, but to a patient, you know, who sees these results, it's a very good sign because sometimes scans shrinkage of growth, you know, these are criteria that are somewhat archaic, made 30 years ago, you know, that can underestimate the amount of kill. As you can see, this is not just decimal point, ctDNA blipping up and down. You could argue somebody with a ctDNA of 1.0 went down to 0.5. Is that truly a meaningful 50% decline? This person's ctDNA at week one, as you can see, was 130,000 parts per million. That going down to, you know, just a few thousand, that's a significant, you know, over 90%-95% fall in ctDNA, and then more importantly, maintaining that. In some of our patients, we're also seeing oscillating levels and even clearances, as Jay pointed out. That's a very clinically relevant time point. That's where we integrate that as part of routine evaluation, not just at my site, but also at other places. If you go to the next slide. This person also had a by RECIST at the first scan, a tumor volume shrinkage of cumulatively about 21%, and that's just at the first eight-week look. At week 16, this actually deepened as well to up to 24%. As you can see, the liver metastases, they not only have shrunk, you know, with these novel therapies and biologics, we also see the nature of the lesions change. If you kind of look at the lesions closely, the lesions on the left have this grayish or whitish hue around it as if somebody picked up a piece of chalk and started shading them. That's usually a sign of more viable tumor, whereas the tumors on the left are darker, as you can see, and more homogenous. That's a sign of more necrosis and dead tissue inside. The scans often, even though they're the primary endpoint, they underestimate the amount of kill, as evident by this patient's scan as well as the ctDNA fall. You could argue that the shrinkage is about 24%, but the ctDNA fall is about 95%, 99%. Next slide, please. If we go to the next slide, again, this is the indexed lung lesions. Again, you can see not just the size changing, but also the nature of the lesions changing as well. Again, not to replace traditional measurements, but you know, clinical improvement, pain going away, improvement of performance status, so much so that some of these patients who initially were on disability or took time off are, you know, going back to work and half the time our scheduling clinic is figuring out how to work around their work schedule. That's a good problem, you know, that a lot of our patients have actually gone back to work because they feel good on the study and to the point about AEs or SAEs, all the side effects that we're managing. You know, the concern about this particular backbone is not necessarily the side effects. Overall, it is a relatively well-tolerated backbone. The main side effects are low white count with the chemotherapy part of things, that too is overcome proactively by taking a white cell booster shot at home, the leronlimab injection as well. Starting second month, patients self-inject at home. It's just twice a month, very practical visits and follow-up, not much in the ways of adverse events that increase the toxicity. It's more so that the regimen is not necessarily something that's really efficacious. You know, we'll see what the larger readout of central RECIST is. If you look at the SUNLIGHT trial that led to the approval and also the real-world data on this backbone, it's a meager single-digit percentage proportion of patients who get shrinkage beyond 30% that counts as partial response based on the RECIST criteria. This to reiterate and narrate, even the so-called quote-unquote "stable disease" patient, ctDNA, some of these novel tests as well as CTCs are probably providing insights that these scans would miss. Next slide. Again, a repeat biopsy that we've done now in several patients a few months into treatment, we are noticing two things. One is, again, going to the point earlier I made that the scans underestimate the amount of kill. The repeat biopsy do show that the amount of cellularity in terms of proportion of cancer cells has gone down, indicating response. Also, it's the environment that potentially might be changing to the prime and pair comment or analogy that was made earlier. The CPS PD-L1, even though it's a pretty dirty test for what it's worth in oncology, it is going up, which might, you know, generate hypotheses about what to pair these drugs like leronlimab with from an immune standpoint. Next slide. I think those- Yeah That I'll stop. I think, you know, we were excited to see what we've seen. I would say, you know, while the readout and follow-up continues, it's not just the shrinkage, the clinical outcomes Jay was pointing out. You wanna make sure, is it gonna be durable, and which will equate to the PFS and the OS, so to speak. While that follow-up continues, at least early on, you know, not just me, myself as the PI on this trial, if you look at the data from a GI oncologist lens or any lens that's between what's published out there regarding the actual trial that led to the approval of the drug Lonsurf on its own 10 years ago, and then Lonsurf with bev, with the SUNLIGHT trial and also some real world data, at least early on, it's definitely more promising than what that backbone alone would have done for our patients. Thank you, Dr. Kasi, for your time today and thoughtful insights. Our first question from the audience, "For the CLOVER trial, are we tracking specific genetic markers like KRAS mutations or PD-L1 levels beyond just microsatellite stable status? In particular, what early markers and other readouts have you find intriguing as a treating physician? Yeah. You know, at this point in time, at least in the year 2026, every single patient with colorectal cancer should know their mutational status. As Jay pointed out earlier, these are highly refractory patients who've had multiple lines of therapy, including chemotherapy, anti-VEGF, anti-EGFR, if they are so-called KRAS/BRAF wild type. Any patients entering this or any other trial in this late setting, already for the most part has this mutational status known, so you don't need to test or retest because these are things that they have been tested multiple times along their journey. Many of these patients, you know, their diagnosis proceed, you know, two, three, four years before entering this kind of a trial. All that is very well known, at least for the poster as Jay pointed out, 62% were RAS mutant, and that's pretty much what we know about an average patient with colorectal cancer. If you look at the RAS, KRAS, NRAS, HRAS, and all the RAS aberration, it's at least over half of those patients, about 10% have BRAF, you know, 4% MSI-H, which are excluded from this analysis. All that mutational makeup is very well known already as part of their clinical test, and it's being collected. We don't check, you know, PD-L1 routinely, or on patients with colorectal cancer, at least with its has relevance in other tumor types. Some of the, from a scientific research trial standpoint, yes, we are. As you can see some of the slides that I showed on the tissue, we are studying the microenvironment to see if it's changing. In parallel, real time, there's a CTC assay from the Creatv MicroTech from New Jersey that is being done at predefined time points along the way, similar to how it was done in the earlier breast cancer study. We'll have that data to analyze along the way to see not just the changes in circulating tumor cells, but also the cancer-associated macrophage-like cells, the so-called CAML cells. We'll have a lot of rich data to analyze in the upcoming months to come, as was pointed out earlier. Thank you, Dr. Kasi. Our second question, "The standard of care combination of Lonsurf and Avastin presumably has well-documented history. In your experience as a treating physician, do you have any comments on how patients in the CLOVER trial receiving leronlimab compare to other patients who receive only the backbone of Lonsurf and Avastin? Yeah, I think I kind of answered that in my latter slides. To reiterate, you know, when people start talking about this backbone regimen, you know, some patients actually never even try this regimen, and then they're already so sick that they just, you know, pretty much are given the option of, "Do you wanna try this regimen as well, or do you wanna consider best supportive care or hospice?" Again, you know, it's a regimen that's not necessarily something that's a rescue agent, you know. The fact that we're seeing clinical and biomarker improvement for what it's worth, I would say based on at least insights early on, I would say it's better than expected. Quantitatively, you know, we'll have all the response data to analyze, and we can. As Jay was pointing out, we are trying to see if there are datasets out there where we can even look at ctDNA to see how that compares to get a sense of contribution of components. Having said that, at least on this trial, we'll have two doses, which is randomized. Even though we don't have a placebo arm, we do have two arms. You know, some hypothesis-generating insights probably will come in the upcoming months. Thanks. Last question for you, Dr. Kasi, from the audience. "Looking ahead, what excites you? Please tell us a little bit about the investigator-initiated project that you will be kicking off shortly. You know, I tell my patients when I put them on any trial is, of course, I wanna get the maximum mileage out of any treatment or trial. Also, with these novel drugs and treatments, it's also intriguing and something to keep in mind is that, you know, did the tumor change, hopefully for the better, for future options? It's not just what we're doing for the patient today. We're seeing, you know, both early hints of, you know, better than expected treatment responses, at least early on based on ctDNA and clinical improvement and what we're seeing in terms of tumor shrinkage. That itself is reassuring. You know, will it help my patient in the future for other checkpoint-based therapies? Will the tumor be more conducive to a checkpoint blockade post-leronlimab exposure? I think that would be very exciting to see in the upcoming years to follow. Now on the trial that we mentioned, you know, so we serendipitously again stumbled upon the observation that as I was talking to a patient about this particular trial in the pipeline for what leronlimab is being used for, I saw the work that was being done by some of the colleagues regarding, you know, how it can help with the fatty liver, the so-called NASH, MASH, MAFLD, or non-alcoholic steatohepatitis. It goes by different names, the bottom line is, our patients' liver get damaged quite a lot over the years of therapy. Not just by the cancer itself, but every single chemotherapy that you've heard people get along their journey, whether it's the 5-FU fluorouracil pump that they go home with, the oxaliplatin platinum-based chemotherapy, irinotecan chemotherapy, the so-called liver pump that this particular patient also had, where we're able to inject something called floxuridine, FUDR chemotherapy at a 300 times the dose to try to eliminate the cancer in the liver or at least kill most of it. All that is causing some sort of fatty liver damage, some sort of microclots, some sort of fibrosis. We have so many patients that over the years, there's a term that's called pseudocirrhosis. They start behaving like as if they have cirrhosis from, you know, hep B, hep C, alcohol, or other causes of steatosis and cirrhosis. The idea with the observation that we were seeing with the CLOVER trial was, you know, we do a lot of these liver pumps. If you look up liver pump on Google, you'll see now, you know, I think it's over 30, 40 places. The company, Boston Scientific that bought Intera Oncology, the makers of the liver pump, they have a map that guides patients where can they get a liver pump. You know, back in the day, it was only a couple of places like Sloan Kettering in New York or City of Hope here and a few other places like Duke doing it. Now there are experts and surgeons. It's a small liver pump that's installed in the belly, under the skin, kind of like a size of a hockey puck that delivers chemotherapy. We did, for example, just 30 pumps in our clinic last year. Our question was, you know, if we have a drug that has potential efficacy and maybe even mitigate the toxicity that we're doing with the chemotherapy, you know, instead of doing leronlimab in a patient who is a candidate for CLOVER, which is later on in their journey of a patient with cancer. Like this same patient, you know, what would have happened if we had done leronlimab a year ago when the patient was actually getting the liver pump? That's in a nutshell that trial. We'll have our, you know, potentially 36 patients, all getting the recommended phase II, the 700 mg dose of the leronlimab in conjunction with their four months of the pump chemo. The idea would be, again, we'll study ctDNA real time as we are doing this already. We'll study, of course, the microenvironment, the CCR5 expression. We'll also see did it help prevent the liver damage, so there'll be a liver biopsy as well. I think we're kind of moving this up the journey of a patient with cancer. Some of these patients would also have a chance to get leronlimab on its own as they prepare for the chemo washout to go for the liver surgery. We may also have an opportunity to see what leronlimab alone does on that trial. We're now kind of, you know, we have the approval at our so-called disease team or scientific level. It's gonna go through the hoops of the usual regulatory and contracting and FDA. Hopefully sometime in the very near future, we can open this liver pump trial with liraglutide that we have abbreviated as an acronym called the CHAMP trial. Well, once again, we thank Dr. Kasi for his time today and thoughtful insights. At this time, we will continue with the management update. I would like to turn it back to Dr. Jacob Lalezari. Thank you, Ignacio, and indeed, thank you, Pashtoon. It will always be true that the CytoDyn family is forever in your debt for the active and incredible collaboration on the CLOVER study. Next slide, Ignacio. As Dr. Kasi just mentioned, the bar that the CLOVER trial is attempting to jump over is actually pretty low, that the phase III SUNLIGHT trial, which looked at Lonsurf and Avastin, actually improved Lonsurf alone, which was only less than 1% of patients that had an overall response rate. The combo in 246 patients published in The New England Journal of Medicine showed a median progression-free and overall survival on the order of six and 11 months. Only 6% of patients even had a partial response, meaning a 30% decrease in tumor volume, and there were no complete responders on that study. That's the bar the FDA is looking at, 6% response rate. A subsequent real-world data set, published more recently showed similar progression-free and overall survivals, but the overall response rate, meaning the% of patients who responded, in terms of their scans, was under 3%. Given the again, the early biologic data we're seeing with the ctDNA and the early correspondence with scan shrinking, I'm very hopeful that we'll be able to surpass the current standard of care. Next slide. The plan in CRC is we are obviously finishing the CLOVER study. Initially the study was set up and I thought we would be dose escalating patients from 350 mg to 700 mg as quickly as possible based on the breast cancer data. I also thought that we'd be introducing a checkpoint inhibitor as soon as we saw a PD-L1 increase. Obviously those plans changed, and we pivoted as soon as we saw the remarkable DNA data that we talked about earlier. As such, we've kept patients on their original dose assignment, 350 mg or 700 mg, and we're now delaying introducing the checkpoint inhibitor until after a patient has a documented progression. That amendment was just submitted for publication to go to the FDA. It would be a mistake to introduce another variable like a checkpoint inhibitor or a dose escalation into the current CLOVER study and confound the endpoints until we get a clear look at leronlimab on its own and at both of these dose levels. As Pashtoon said, his investigator-initiated trial at City of Hope is going through regulatory approval. This is introducing leronlimab in an earlier line of treatment. It's a joint effort between City of Hope and CytoDyn. As Dr. Kasi indicated, he's leveraging both the liver protection and the anti-tumor effects of leronlimab. Because of that, we're actually not using CCR5 testing as a gating criteria on this study, because the primary endpoint is to protect patients' livers. The possibility exists that we will enroll patients who are CCR5 negative on their tumor, and then still be able to determine if there's any anti-tumor activity in that subset of patients. Importantly, one of the keys is to try and get DNA data on patients on leronlimab monotherapy, both to get a clear look at the activity of the drug on its own, and that's one of the goals of Dr. Kasi's study. Finally, I would say that evaluating leronlimab in combination with a checkpoint inhibitor is definitely a priority for us at CytoDyn. It remains a question of whether we're going to do it as an amendment with the existing CLOVER infrastructure and patient population third line subjects. I'll also mention that we're having conversations with an academic network involved with colorectal cancer, who's expressed interest in looking at that combination in an earlier line of therapy. That's a decision pending in the next few weeks or month. Next slide, Ignacio. Quickly, looking at the breast cancer data, I know we're running short on time. The next slide, we've never actually discussed this on a call before, but these are a summary of the data. Again, CytoDyn was trying to figure out when patients may have deceased from the prior TNBC studies. We found out that five patients were still alive. We tracked down their medical records, we were able to coordinate the three variables of who induced PD-L1 above the 400 threshold from Creatv MicroTech that's considered clinically relevant, who received a checkpoint inhibitor, and who was still alive. All five of the women who induced PD-L1 on the circulating tumor cells, and as Dr. Kasi said, mostly those are the cancer-associated macrophage-like cells. All five patients who induced above 400 mg got a checkpoint inhibitor, either atezolizumab or pembro, were still alive now five plus years later. That created the paradigm of the prime and pair that led us to the CRC study. In attempting to replicate and prospectively demonstrate the prime and pair is when we've seen this extraordinary activity of leronlimab as a standalone agent. On the next slide, then, is a summary of what we've presented on TNBC. Previously, Dr. Pestell's data on the 98% reduction in metastasis in mice. We've previously shown the reduction of circulating tumor cells in the majority of patients after a single dose of leronlimab. Never, I never quite knew what to make of that data. Now that we're seeing these reductions in the circulating tumor DNA, obviously, this is an analogous result, with tumor cells that we're seeing with the DNA itself. In terms of PD-L1 induction, again, there was a lower rate of induction in patients who received the lower 350 mg dose. Then it was almost 90% of patients at the 525 mg o r 700 mg dose. As I said, five out of five patients who upregulated and received a checkpoint inhibitor are alive now five plus years later. Three of those five currently have no evidence of disease. Two of those three started leronlimab with lung metastasis. One of those patients who was recently highlighted in an investigative report was a patient who started with both lung and brain mets, and she is alive and well without evidence of disease five years later. The corollary, unfortunately, is also true, that 100% of the patients who either didn't upregulate because they got the lower dose or they didn't receive a checkpoint inhibitor, which was, you know, kind of arbitrarily given by the oncologists who were just shooting for whatever they could, 100% of those individuals, unfortunately, are now deceased. On the next slide, how we're progressing in breast cancer is we've had very productive conversations with the I-SPY network, and they're gonna take on part one of our phase II study, which as the FDA requested, is a dose escalation, confirming safety PK, the DNA and the PD-L1. Per the I-SPY network, they are extending the patient population from TNBC to include all HER2-negative patients with breast cancer. We're fortunate to have Dr. Pohlmann, Paula Pohlmann from MD Anderson, who will serve as the principal investigator for that project. Those contracts and budgets have been negotiated, and they have suggested that their startup time can be measured in weeks to a few months. At the same time, we are then gonna be following up with a contribution of components study, which will adaptively demonstrate the additive benefit of including a checkpoint inhibitor with leronlimab as part of a phase II/III study. In addition, we just announced the opening of the expanded access protocol for patients with TNBC running out of treatment options. First patient was dosed last week. This was initially imagined as a way to sort of quickly and prospectively confirm the PD-L1 induction we were seeing with leronlimab that some potential industry partners had asked to see. That is still the case, that the, in the EAP program, we will be measuring PD-L1 at baseline and then at month one, two and three, and we'll report on that later. As previously indicated, we have funding in place for the first 20 patients on the program. I would add that we've had very productive conversations with the I-SPY network, and they too are keen to start a study in leronlimab again in HER2- negative patients with breast cancer, but they're looking at the neoadjuvant setting, so newly diagnosed patients before they go to surgery. They're also have indicated a desire to look at the benefits of leronlimab as a monotherapy agent in that setting for up to a month before patients go to surgery. A lot happening in colon and a lot happening in breast cancer. Next slide. In terms of upcoming milestones and what the year ahead has in store, on the next slide, priorities, first, the standalone benefit of leronlimab in this case with the backbone through the biomarker collection, primarily ctDNA, but other tumor markers as well. The disease control rate, the percentage of patients with stable or partial responses. The overall response rate, which is the primary endpoint of our current CRC study, and then progression-free and overall survival. The second priority, again, there are two tracks of development. We're both developing leronlimab as a standalone and developing leronlimab as a prime and pair. The prime and pair definitely hinges on this PD-L1 induction, it's key to prospectively demonstrate that, and that's something we're doing in the CRC study, in Dr. Kasi's investigator-initiated trial, and in the PRE-SPY and I-SPY studies in breast cancer. We wanna demonstrate that the clinical benefit of adding a checkpoint inhibitor to leronlimab in PD-L1-induced patients, which will be the focus of part two of our phase II program in breast cancer. Something I thought would be easier is we need to identify the optimal dosing of leronlimab in oncology. The PRE-SPY study will start at the dose of 525 mg and then dose escalate to 700 mg, with an option to dose down to 350 mg, depending on what the CRC study shows us in terms of a potential dose response. The 350 mg data on DNA is obviously remarkable, the question is, will the 700 mg dose provide either steeper or more rapid declines or more sustained declines in circulating tumor DNA? As mentioned before, that is something we're keenly looking forward to understanding soon, and we'll report back to you this summer. On the next slide, a number of milestones recently crossed. We got funding for the Expanded Access Program. We closed $17.5 million through a Paulson raise. The initial DNA readouts were presented at AACR. The expanded access program has enrolled the first patient. We submitted the protocol amendment to FDA for inclusion of a checkpoint inhibitor in the CLOVER study in patients with documented progression. As Dr. Kasi indicated, the initiation of his investigator-initiated trial is imminent. My understanding from the I-SPY network is they too are moving very quickly toward initiation of their study in TNBC. Importantly, we are targeting the presentation at the ESMO meeting in Madrid, Spain in October to provide an update from the CLOVER study, then a more robust presentation at ASCO GI in San Francisco in January, during which we should be able to provide final results. Lastly, looking forward in 2026, we confirm these early exciting safety and efficacy readouts to generate an optimal data package, including updated biomarker and clinical data. The plan is to submit a Fast Track or Breakthrough Designation application later this summer or early fall. Of course, as these data become known and more widely disseminated, we will continue to evaluate potential opportunities for strategic partnerships. Ignacio, I think from there, if we can go to some questions and extend our time by a few minutes, that'd be great. Thank you, Dr. Lalezari. The first question from the audience for you, based on the data generated today, how do you see leronlimab ultimately being positioned, primarily as a monotherapy in select settings or as a foundational combination backbone across multiple tumor types? Well, as I said earlier, I could not be more excited by what we're seeing. I frame the results as being on the outer edge of what I even thought was possible. The signals that we're seeing in colon cancer, obviously saw in breast cancer, and some of the data we recently presented in glioblastoma, it leads me to believe we're talking about a drug that will be foundational across multiple solid tumor types. In addition, we are pursuing studies as monotherapy, because when you talk about a drug that has so few or limited safety issues, then obviously you want to consider it in an earlier line of therapy, and it's certainly potentially possible to consider it as a monotherapy, particularly in the neoadjuvant setting. Yes, as a foundational backbone across multiple tumor types, and yes, we're pursuing monotherapy studies. Thank you. Our next question, can you provide any updates or expected data timelines for the investigator-initiated trials, including the projects in glioblastoma, Alzheimer, and colorectal cancer, hepatic artery infusion project? CytoDyn is very busy, and the focus remains colon cancer and breast cancer. In the meantime, as everyone is aware, there are a host of other potential indications. As Dr. Kasi indicated, his IIT at City of Hope, looking at hepatic artery infused chemotherapy, has received IRB review, institutional review, and they're submitting to the FDA. That'll start shortly. The glioblastoma data that Richard presented at an earlier AACR meeting is extremely provocative, and it's just not something we can ignore. Those mice received a stereotactic injection of an aggressive cell line, and they all developed a disseminated, diffuse, infiltrative disease, and then were randomized into their treatment groups. The leronlimab-treated groups at necropsy seemed to have far less and far fewer metachronous spread of the tumor, which was documented and statistically significant. I'm pleased to update the investors and say that yesterday we had a detailed call with a major academic center who's agreed to both repeat the preclinical studies looking at two different cell lines with a survival endpoint. At the same time, we are drafting, and I already have a rough draft of a pilot study for an investigator-initiated trial in patients with recurrent glioblastoma. We are moving forward on glioblastoma as well. I would mention that I've had some preliminary conversations with several other major medical centers of investigators who have proposed their own investigator-initiated trials in 2 other separate solid tumors. I look forward to updating shareholders later this summer, pending the maturity of those conversations. In the meantime, there are indications outside of solid tumor oncology that continue. I think many people are aware of the fact that the folks at Cornell are now up and running. Their PET scan was replaced, and the study in Alzheimer's disease is now actively screening patients. We hope to announce the first patient enrolled shortly. As well, Jonah Sacha remains extremely active at Oregon Health & Science University on a variety of HIV cure fronts with leronlimab. Something we don't talk much about, there is an ongoing preclinical study at the University of Hawaii looking at the role of leronlimab in recovery from stroke in a mouse model of stroke. A lot of other activity besides the main emphasis, which is and will remain colon and breast cancer. Thank you. Our next question, following the biomarker and ctDNA results presented at AACR, will the company have a presence at the upcoming ASCO 2026 meeting? When can we expect a more mature data set from the phase II CLOVER-NCRC study? Yeah, that's a great question. Robert and Tyler and I are going to ASCO as primarily a networking. We are meeting with the PRE-SPY and I-SPY folks and potentially a number of other pharma companies. The main point of that question was finding out when the next update from CLOVER will be. The interim results will be presented at the ESMO meeting in Spain in October, the final results at the ASCO meeting, ASCO GI meeting in San Francisco in January. In the meantime, it is our intention to either issue another shareholder letter or schedule another shareholder call when appropriate, and that would be toward the end of the summer or early fall. Thank you so much. Our final question, there seems to be a new FDA with shorter timelines for granting FDA approvals. Is CytoDyn exploring any of these expedited pathways with the FDA, like the voucher program? mTNBC and MSS CRC both seem to be potential candidates for a voucher. Yeah Some sort of expedited treatment. Yeah. I appreciate that. I think that my emphasis has been on generating, you know, rock solid, prospective, unassailable data that everyone can look at and agree and that there's a there there. That has been the great pleasure of being the CEO of CytoDyn lately, is I no longer have to spend my time trying to convince people of anything. I just need to show them our data and that seems to do the trick. We're gonna follow that data, and that data will be presented to the FDA this summer, and it will be presented in the context of either Accelerated Approval or Breakthrough Designation. It's not for us to decide exactly how the FDA is going to handle this, whether it's a voucher or whether a designation for Breakthrough Designation will be up to the agency. Our focus remains generating the data that will give them every reason and no choice really but to be responsive to what we're finding. Thank you so much, Dr. Lalezari. Now is the time for final closing remarks. The floor is yours. Well, I don't know what else to say except that it's been an incredible journey, an odyssey. As I said in the beginning, it wouldn't have been possible without the patience and the support of our long-term investors who have hung in there. Indeed, I just want to mention that the number of folks who submitted questions had also offered additional words of encouragement, and super appreciated. Nothing about this has been easy, I could not be more excited about the fact that we are at this crucial juncture where, as I say, we're transitioning from a company built on faith to a company built on solid data. It's an exciting time. I couldn't look forward more to what just lies ahead, and just grateful for everyone who hung in there with us. Thank you, Ignacio. Thank you very much. This concludes CytoDyn's Investor Update Webcast. Thank you all for your participation. You may now disconnect.