Cytodyn CC April 30 2026 -- transcript for anyone who can't access Brentie's Seeking Alpha link
Operator
Greetings, and welcome to today's CytoDyn Investment Community Webcast. My name is Ignacio Guerrero Ros, and I will serve as your moderator today. [Operator Instructions] 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. There will be 2 Q&A sessions on today's call. Following Dr. 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 e-mail your questions to ir@cytoyn.com. I'd now like to turn the webcast over to Tyler Blok. You may begin.
Tyler Blok
Chief Legal Officer & Corporate Secretary
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, and I will now turn the podcast over to Robert Hoffman.
Robert Hoffman
Chief Financial Officer
Thank you, Tyler. Thanks to all shareholders and interested parties who are listening to our call today. I'll provide a brief financial overview, and then we'll turn the call over to our CEO, Dr. Jacob 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, and 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 arrangement 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 Ventures Group. 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 World, and I will be presenting at their conference in New York on May 7. Unfortunately, there is no webcast option for the conference. I will be presenting at the 16th Annual Micro -- LD Micro Invitational taking place in Los Angeles from May 17 through May 19. We will be at ASCO in Chicago from May 29 through June 2, 2026. We'll be in attendance at Bio 2026 in San Diego, June 22 through June 25, and we are actively setting up meetings with investors, potential partners and other stakeholders. I will now turn the call over to Jay.
Jacob Lalezari
Chief Executive Officer
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. So 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. And 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 prospective, 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. But 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 going to stand on our ground, and we're not backing down. So 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 Pistell's data on the reduction of tumor metastasis in mice. We 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. And Dr. Kasi, who will be joining us shortly on this call, is going to show some data indicating what happens with leronlimab impact on the tumor microenvironment.
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. So 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 has been well tolerated in more than 1,600 patients across more than 20 clinical studies. And 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. And beyond that, of course, on the side, CytoDyn is running studies also in other indications such as Alzheimer's disease.
So 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. And the CRC study was launched in an effort to try and prospectively confirm that paradigm. But what we observed along the way is that leronlimab as a stand-alone agent as an anticancer therapy has remarkable abilities. And indeed, it's that stand-alone activity, which makes the prime and pair regimen even possible because of what leronlimab does on its own to prime the tumor. So that's background.
On the next slide, we're going to start moving into the CRC data that was just presented at the AACR meeting. And on the next slide, this is a Phase II study that the FDA gave us. open-label and randomized to 350 and 700 milligrams, they did require a dose comparison. And I would stress again that in the 350 or 525 or 700-milligram dosing choices, there is no safety data that distinguishes those 3. So the ultimate decision about the optimal dose will very much rest on any efficacy data we generate. But this Phase II study has already 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. And just not to put too fine a point on it, these are patients with very advanced disease and very fragile indeed.
And as I mentioned, Dr. Kasi, our wonderful lead investigator, will be joining the call shortly. We announced last week that target enrollment has been completed. There have been 2 data and safety monitoring board meetings. The first in December opened up the 700-milligram arm and the second took place after 20 patients completed 1 full cycle of treatment, each cycle being a month long. And in both of those meetings, safety was reviewed and there have been no safety concerns registered.
So the next slide is the beginning of some very important points about the CRC study that I want to 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 3 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. And 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. And it was obviously remarkable that 100% of patients qualified for the study and then generated the data that we have, but it also helped us rapidly recruit this study. And most importantly, it helped us eliminate the waiting period involved with completing the CCR5 testing. So on the second bullet point here, again, the safety observed in this study. Specifically, there are no grade 3 or 4 adverse events or serious adverse events attributed to leronlimab.
And even more important, I think, there are no leronlimab-related dose or treatment-limiting toxicities, meaning no patient has had to adjust or discontinue the leronlimab dosing due to any side effect or adverse event. So a remarkable safety profile to date, including in this fragile and highly advanced population. And then the remarkable data that Dr. Kasi presented in San Diego, showing CT circulating tumor DNA declines using the Signatera essay from Natera in 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.
And Ignacio, if you can show the next slide. So 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. So 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. And 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 13 of -- 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-milligram dose. And so this observation is both surprising and certainly surprising to me and very exciting. And we're naturally keen to determine if there's a dose response with the 700-milligram dose, at least measured by circulating tumor DNA. And 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. And these mutations are generally associated with the hardest-to-treat patients in oncology. And these preliminary results indicate that leronlimab's early biologic activity might also be agnostic to the KRAS mutation.
Six, I'm also pleased to share new information that we've recently confirmed that 4 patients in follow-up have had at least 1 undetectable circulating tumor DNA level during that follow-up period. And although this is very preliminary, it is also remarkable to note that 3 of those 4 patients who have gone undetectable are being treated with the 350-milligram dose.
And lastly, I just want to 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. And 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. And these, of course, are also the metrics that matter most to the FDA. All right, Ignacio, if you could advance the slide now.
I want to update bullet point 4 that we now have 22 patients with RECIST data available at week 8, of whom 15% or 68% are demonstrating shrinkage or classify as having stable disease on their scan. So 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 are being treated with the 350-milligram dose, which at least in the TNB setting -- TNBC setting was not as -- had a vigorous PD-L1 response. But 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.
And 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 an 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.
Dr. Pashtoon Kasi
Thank you so much for having me. And... If we could clip on what you have said so far, I wanted to narrate the story of our index first patient and 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 trying to bring novel therapies and immunotherapies and options for our patients to clinic is this whole field of liquid biopsies. As some of you might be aware, the term liquid biopsy is a misnomer since there's no biopsy being performed, these are noninvasive blood draws.
And 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. And 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, what is the mutational makeup. But as you might be aware now, these assays are also being used as response metrics.
So in general, trial, I do check ongoing circulating tumor DNA assays in these patients because these crude tumor markers, CEA, CA19-9, at least 1/4 of the patients don't even make the marker. And then in this first patient, for example, often the half-life of these glycosylated 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 from the SUNLIGHT study with this oral chemotherapy, the TAS-102 or the brand name LONSURF with bevacizumab as the anti-VEGF, it's one more option, but it's not necessarily a great option.
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. So -- and in this particular study, this -- as a clinician, not just as a PI on this trial. It helps me because the study was not restrictive. So it was not like cherry-picking patients who only had 1 or 2 chemotherapies. Some of these patients have exhausted all aggressive types of therapy. So this particular patient had the standard double FOLFOX chemotherapy with bevacizumab, then FOLFII 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 30x the amount of chemo to be given in the liver. So this person had that installed as well and completed all that therapy. But then after a few months of disease control lo and behold, there was reemergence of liver metastases as well as lung metastases and also was RAS mutant, which 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, this is the kind of patient that an average trial will probably refuse.
So the fact that when we started this patient on treatment as early as a 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. But then the CA actually has blipped up, which as a patient, you're used to looking at tumor marker, that's a sign of concern that maybe my cancer is getting worse. And that's where ctDNA can be helpful. So 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.
So if you multiply that by 5 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. And 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 2 months or 3 months, but then it gives you that early lens, early readout that can be not just important scientifically, but to a patient who sees these results, it's a very good sign because sometimes scans shrinkage of growth, these are criteria that are somewhat archaic made 30 years ago that can underestimate the amount of kill.
As you can see, this is not just decimal point ctDNA blipping up and down. So 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 1, as you can see, was 130,000 parts per million. So that going down to just a few thousand, that's a significant over 90%, 95% fall in ctDNA. And then more importantly, maintaining that in some of our patients, we've also seen oscillating levels and even clearance, 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 by RECIST at the first scan, tumor volume shrinkage of cumulatively about 21%. And that's just at the first 8-week look at week 16, this actually deepened as well up to 24%. And as you can see, the liver metastases, they not only have shrunk with these novel therapies and biologics, we also see the nature of the lesions change. So if you kind of look at the lesions closely, the lesions on the left are -- have this gray or white shoe around it as if somebody picked up a piece of chalk and started shading them.
That's really 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 death tissue inside. So the scans often, even though they are the primary endpoint, they underestimate the amount of kill as evident by this patient scan as well as the ctDNA fall. So you could argue that the shrinkage is about 24%, but the ctDNA fall is about 95%, 99%. Next slide, please.
So 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. So again, not to replace traditional measurements, but clinical improvement, pain going away, improvement in performance status so much so that some of these patients who initially were on disability or took time off are 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 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. 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, and 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. So it's just twice a month very practical resistant follow-up and not much in the ways of adverse events that increase the toxicity. So it's more so that the regimen is not necessarily something that's really efficacious.
We'll see what the larger readout of central RECIST is. But 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. But just to kind of reiterate, even the so-called "stable disease patient, ctDNA, some of these novel tests as well as CDCs are probably providing insights that these scans would miss. Next slide.
And again, a repeat biopsy that we've done now in several patients a few months into treatment, we are noticing 2 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. But then also it's the environment that potentially might be changing to the prime and payer comment or analogy that was made earlier. So 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 generate hypotheses about what to pair these drugs like leronlimab with -- from an immune standpoint. Next slide. I think with that, I'll stop.
I think we're excited to see what we've seen. I would say, while the readout and follow-up continues, it's not just the shrinkage. The clinical outcomes Jay was pointing out, you want to make sure is this going to be durable and which will equate to the PFS and the OS, so to speak. So while that follow-up continues, at least early on, 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 Lancet on its own 10 years ago and then Lancet with bev with the LEG 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.
Question-and-Answer Session
Operator
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?
Dr. Pashtoon Kasi
Yes. So 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. So 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, their diagnosis proceed 2, 3, 4 years before entering this kind of a trial. So 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, at least over half of those patients, about 10% have BRAF, 4% MSI high, which are excluded from this analysis. So all that mutational makeup is very well known already as part of their clinical test and it's being collected. And then we don't check PD-L1 routinely on patients with colorectal cancer, at least it has relevance in other tumor types. But some of the -- from a scientific research trial standpoint, yes, we are.
So as you can see some of the slides 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 Creative 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. So 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 macrophages like cells, the so-called Camel cells. So we'll have a lot of rich data to analyze in the upcoming months to come, as was pointed out earlier.
Operator
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 compared to other patients who receive only the backbone of LONSURF and Avastin?
Dr. Pashtoon Kasi
Yes. I think I kind of answered that in my later slides. But to reiterate, when people start talking about this backbone regimen, -- some patients actually never even try this regimen and then they're already so sick that they just pretty much are given the option of do you want to try this regimen as well? Or do you want to consider best supportive care or hospice.
So again, it's a regimen that's not necessarily something that's a rescue agent. So 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. But quantitatively, we'll have all the response data to analyze and we can -- and as Dave was pointing out, we are trying to see if there are data sets 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 2 doses, which is randomized. So even though we don't have a placebo arm, we do have 2 arms. So some hypothesis generating insights probably will come in the upcoming months.
Operator
Thanks. Last question for you, Dr. Kasi from the audience. Looking ahead, what excites you? And please tell us a little bit about the investigator-initiated project that you will be kicking off shortly.
Dr. Pashtoon Kasi
Yes. I tell my patients when I put them on any trial is, of course, I want to get the maximum mileage out of any treatment or trial. But then also with these novel drugs and treatments, it's also intriguing and something to keep in mind is that did the tumor change, hopefully for the better for future options. It's not just what we're doing for the patient today. So we're seeing both early hints of 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. So that itself is reassuring. But then 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 will be very exciting to see in the upcoming years to follow.
Now on the trial that we mentioned, so we serendipitously again, stumble 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 is being done by some of the colleagues regarding how it can help with the fatty liver, the so-called NASH, NASH, MAFLD or nonalcoholic steatohepatitis. It goes by different names. But 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 fluorosle pump that they go home with the oxalipatin, platinum-based chemotherapy, irinotecan chemotherapy. the so-called liver pump that this particular patient also had where we are able to inject something called FluoxyuridineFUDR chemotherapy at 300x 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 microcode, some sort of fibrosis. So 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 hep B, hep C, alcohol or other causes of steatosis and cirrhosis. So the idea with the observation that we were seeing with the CLOVER trial was we do a lot of these liver pumps.
If you look up liver pump on Google, you'll see now I think it's over 30, 40 places. The company, the Boston Scientific that bought Entera, the makers of the liver pump, they have a map that guides patients where can they get a liver pump. 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. But now there are experts and surgeons. So 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. So we did, for example, just 30 pumps in our clinic last year.
So our question was if we have a drug that has potential efficacy and maybe even mitigate the toxicity that we are doing with the chemotherapy, 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, what would have happened if we had done leronlimab a year ago when the patient was actually getting the liver pump. So that's in a nutshell, that trial. So we'll have about potentially 36 patients, all getting the recommended Phase II, the 700-milligram dose of the leronlimab in conjunction with their 4 months of the pump chemo.
And 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. But we'll also see does it help prevent the liver damage. So there will be a liver biopsy as well. So I think we're kind of moving this up the journey of a patient with cancer. And 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. So we may also have an opportunity to see what leronlimab alone does on that trial. So we're now kind of -- we have the approval at our so-called disease team or scientific level.
Now it's going to go through the hoops of the usual regulatory and contracting and FDA. So hopefully, sometime in the very near future, we can open this liver pump trial with leronlimab that we have abbreviated as an acronym called the CHAMP trial.
Operator
Well, once again, we thank Dr. Kasi for his time today and thoughtful insights. At this time, we will continue with the management update. So I would like to turn it back to Dr. Jacob Laresari.
Jacob Lalezari
Chief Executive Officer
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. Okay. 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 is only less than 1% of patients that had an overall response rate. But the combo in 246 patients published in the New England Journal showed a median progression-free and overall survival on the order of 6 and 11 months and 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. So that's the bar the FDA is looking at, 6% response rate.
But then a subsequent real-world data set published more recently showed similar progression-free and overall survival, but the overall response rate, meaning the percent of patients who responded in terms of their scans was under 3%. So 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. So 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 to 700 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. And 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 or 700, and we're now delaying introducing the checkpoint inhibitor until after a patient has a documented progression, and that amendment was just submitted to -- 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.
In addition, as Tarun 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. And as Dr. Kasi indicated, he's leveraging both the liver protection and the antitumor effects of leronlimab. And 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. So the possibility exists that we will enroll patients who are CCR5 negative on their tumor and to then still be able to determine if there's any antitumor activity in that subset of patients. And then 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.
And then finally, I would say that evaluating leronlimab in combination with a checkpoint inhibitor is definitely a priority for us at CytoDyn. And 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. So that's a decision pending in the next few weeks or months. Next slide, Ignacio.
So just quickly looking at the breast cancer data. I know we're running short on time. In the next slide, we've never actually discussed this on a call before, but these are a summary of the data. Again, we were -- CytoDyn was trying to figure out when patients may have deceased from the prior TNBC studies. We found out that 5 patients were still alive. We tracked down their medical records, and we were able to coordinate the 3 variables of who induced PD-L1 above the 400 threshold from Creative Microtech that's considered clinically relevant, who received a checkpoint inhibitor and who is still alive.
And all 5 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 5 patients who induced above 400 got a checkpoint inhibitor, either atezolizumab or pembro were still alive now 5-plus years later. And so that created the paradigm of the prime impair that led us to the CRC study and then in attempting to replicate and prospectively demonstrate the prime impair is when we've seen this extraordinary activity of leronlimab as a stand-alone agent.
On the next slide then is a summary of what we've presented on TNBC. Previously, Dr. Pastoon'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. And never -- I never quite knew what to make of that data. But 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-milligram dose, and then it was almost 90% of patients at the 525 or 700-milligram dose.
And as I said, 5 out of 5 patients who upregulated and received a checkpoint inhibitor are alive now 5-plus years later. 3 of those 5 currently have no evidence of disease. 2 of those 3 started leronlimab with lung metastasis and 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 5 years later. And then 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 kind of arbitrarily given by the oncologists who were just shooting for whatever they could, 100% of those individuals, unfortunately, are now deceased.
So on the next slide, how we're progressing in breast cancer is we've had very productive conversations with the pre-spine network, and they are going to take on Part 1 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 PSpine network, they are extending the patient population from TNBC to include all HER2-negative patients with breast cancer. And we're fortunate to have Dr. Paul Polman 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 start-up time can be measured in weeks to a few months.
At the same time, we are then going to 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. And that is still the case that in the EAP program, we will be measuring PD-L1 at baseline and then at month 1, 2 and 3, and we'll report on that later. And as previously indicated, we have funding in place for the first 20 patients on the program.
And then 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. And they 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. So a lot happening in colon and a lot happening in breast cancer. Next slide.
So in terms of upcoming milestones and what the year ahead has in store, on the next slide, priorities First, the stand-alone benefit of leronlimab in this case, with the backbone through the biomarker collection, primarily ctDNA, but other tumor markers as well. And then the disease control rate, the percent 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 stand-alone and developing leronlimab as a prime impair. And the prime impair definitely hinges on this PD-L1 induction. And so 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 PSPI and I-SPY studies in breast cancer.
We want to then demonstrate that the clinical benefit of adding a checkpoint inhibitor to leronlimab in PD-L1 induced patients, which will be the focus of Part 2 of our Phase II program in breast cancer. And then something I thought would be easier is we need to identify the optimal dosing of leronlimab in oncology. The pre side study will start at the dose of 525 and then dose escalate to 700 with an option to dose down to 350 depending on what the CRC study shows us in terms of a potential dose response. The 350 data on DNA is obviously remarkable. And the question is, will the 700-milligram dose provide either steeper or more rapid declines or more sustained declines in circulating tumor DNA -- and 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 Pulson 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. And my understanding from the pre-spine 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 and then a more robust presentation at ASCO GI in San Francisco in January, during which we should be able to provide final results.
And then 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 -- and the plan is to submit a fast track or breakthrough designation application later this summer or early fall. And of course, as these data become known and more widely disseminated, we will continue to evaluate potential opportunities for strategic partnerships. And Ignacio, I think from there, if we can go to some questions and extend our time by a few minutes, that would be great.
Operator
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?
Jacob Lalezari
Chief Executive Officer
Well, as I said earlier, I could not be more excited by what we're seeing. And I frame the results as being on the outer edge of what I even thought was possible. So the signals that we're seeing in colon cancer, obviously, saw in breast cancer and some of the data we've recently presented in glioblastoma 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. So yes, as a foundational backbone across multiple tumor types, -- and yes, we are pursuing monotherapy studies.
Operator
Thank you. Our next question, can you provide any updates or expected data time lines for the investigator-initiated trials, including the projects in glioblastoma, Alzheimer's and colorectal cancer, hepatic artery infusion project?
Jacob Lalezari
Chief Executive Officer
Yes. So CytoDyn is very busy. And the focus remains colon cancer and breast cancer. But 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. So that will 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 and the leronlimab-treated groups at necrosi seem to have far less and far fewer metachronous spread of the tumor, which was documented and statistically significant.
So 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 2 different cell lines with a survival endpoint. And 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. So we are moving forward on glioblastoma as well. And I would mention that I've had some preliminary conversations with several other major medical centers of investigators who want to propose their own investigator-initiated trials in 2 other separate solid tumors. And 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, Jonasz remains extremely active at Oregon Health Sciences University on a variety of HIV cure fronts with leronlimab. And then something we don't talk much about, but 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. So a lot of other activity besides the main emphasis, which is and will remain colon and breast cancer.
Operator
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? Specifically, when can we expect a more mature data set from the Phase II CLOVER NCRC study?
Jacob Lalezari
Chief Executive Officer
Yes, it's a great question. So Robert and Tyler and I are going to ASCO as primarily in networking. We are meeting with the pre-SPI and I-SPY folks and potentially a number of other pharma companies. But the main point of that question was finding out when the next update from CLOVER will be. And 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 and when appropriate, and that would be toward the end of the summer, early fall.
Operator
Thank you so much. Our final question. There seems to be a new FDA with shorter time lines for granting FDA approvals. Is Sightline exploring any of these expedited pathways with the FDA like the voucher program? NBC and MSS CRC both seem to be potential candidates for a voucher or some sort of expedited treatment.
Jacob Lalezari
Chief Executive Officer
Yes. I appreciate that. I think that my emphasis has been on generating rock solid prospective unassailable data that everyone can look at and agree and that there's a there. And that has been the great pleasure of being the CEO of CytoDyn lately as 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 be the trick. And so we're going to 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. And so it's not for us to decide exactly how the FDA is going to handle this. But 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.
Operator
Thank you so much, Dr. Lalezari. Now is the time for final closing remarks. The floor is yours.
Jacob Lalezari
Chief Executive Officer
Well, I don't know what else to say except that it's been an incredible journey in Odyssey. And 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. And indeed, I just want to mention that a number of folks who submitted questions had offered additional words of encouragement and super appreciated. Nothing about this has been easy. And 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. So 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.
Operator
Thank you very much. This concludes CytoDyn's investor update webcast.
Operator
Greetings, and welcome to today's CytoDyn Investment Community Webcast. My name is Ignacio Guerrero Ros, and I will serve as your moderator today. [Operator Instructions] 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. There will be 2 Q&A sessions on today's call. Following Dr. 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 e-mail your questions to ir@cytoyn.com. I'd now like to turn the webcast over to Tyler Blok. You may begin.
Tyler Blok
Chief Legal Officer & Corporate Secretary
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, and I will now turn the podcast over to Robert Hoffman.
Robert Hoffman
Chief Financial Officer
Thank you, Tyler. Thanks to all shareholders and interested parties who are listening to our call today. I'll provide a brief financial overview, and then we'll turn the call over to our CEO, Dr. Jacob 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, and 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 arrangement 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 Ventures Group. 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 World, and I will be presenting at their conference in New York on May 7. Unfortunately, there is no webcast option for the conference. I will be presenting at the 16th Annual Micro -- LD Micro Invitational taking place in Los Angeles from May 17 through May 19. We will be at ASCO in Chicago from May 29 through June 2, 2026. We'll be in attendance at Bio 2026 in San Diego, June 22 through June 25, and we are actively setting up meetings with investors, potential partners and other stakeholders. I will now turn the call over to Jay.
Jacob Lalezari
Chief Executive Officer
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. So 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. And 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 prospective, 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. But 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 going to stand on our ground, and we're not backing down. So 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 Pistell's data on the reduction of tumor metastasis in mice. We 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. And Dr. Kasi, who will be joining us shortly on this call, is going to show some data indicating what happens with leronlimab impact on the tumor microenvironment.
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. So 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 has been well tolerated in more than 1,600 patients across more than 20 clinical studies. And 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. And beyond that, of course, on the side, CytoDyn is running studies also in other indications such as Alzheimer's disease.
So 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. And the CRC study was launched in an effort to try and prospectively confirm that paradigm. But what we observed along the way is that leronlimab as a stand-alone agent as an anticancer therapy has remarkable abilities. And indeed, it's that stand-alone activity, which makes the prime and pair regimen even possible because of what leronlimab does on its own to prime the tumor. So that's background.
On the next slide, we're going to start moving into the CRC data that was just presented at the AACR meeting. And on the next slide, this is a Phase II study that the FDA gave us. open-label and randomized to 350 and 700 milligrams, they did require a dose comparison. And I would stress again that in the 350 or 525 or 700-milligram dosing choices, there is no safety data that distinguishes those 3. So the ultimate decision about the optimal dose will very much rest on any efficacy data we generate. But this Phase II study has already 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. And just not to put too fine a point on it, these are patients with very advanced disease and very fragile indeed.
And as I mentioned, Dr. Kasi, our wonderful lead investigator, will be joining the call shortly. We announced last week that target enrollment has been completed. There have been 2 data and safety monitoring board meetings. The first in December opened up the 700-milligram arm and the second took place after 20 patients completed 1 full cycle of treatment, each cycle being a month long. And in both of those meetings, safety was reviewed and there have been no safety concerns registered.
So the next slide is the beginning of some very important points about the CRC study that I want to 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 3 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. And 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. And it was obviously remarkable that 100% of patients qualified for the study and then generated the data that we have, but it also helped us rapidly recruit this study. And most importantly, it helped us eliminate the waiting period involved with completing the CCR5 testing. So on the second bullet point here, again, the safety observed in this study. Specifically, there are no grade 3 or 4 adverse events or serious adverse events attributed to leronlimab.
And even more important, I think, there are no leronlimab-related dose or treatment-limiting toxicities, meaning no patient has had to adjust or discontinue the leronlimab dosing due to any side effect or adverse event. So a remarkable safety profile to date, including in this fragile and highly advanced population. And then the remarkable data that Dr. Kasi presented in San Diego, showing CT circulating tumor DNA declines using the Signatera essay from Natera in 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.
And Ignacio, if you can show the next slide. So 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. So 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. And 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 13 of -- 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-milligram dose. And so this observation is both surprising and certainly surprising to me and very exciting. And we're naturally keen to determine if there's a dose response with the 700-milligram dose, at least measured by circulating tumor DNA. And 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. And these mutations are generally associated with the hardest-to-treat patients in oncology. And these preliminary results indicate that leronlimab's early biologic activity might also be agnostic to the KRAS mutation.
Six, I'm also pleased to share new information that we've recently confirmed that 4 patients in follow-up have had at least 1 undetectable circulating tumor DNA level during that follow-up period. And although this is very preliminary, it is also remarkable to note that 3 of those 4 patients who have gone undetectable are being treated with the 350-milligram dose.
And lastly, I just want to 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. And 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. And these, of course, are also the metrics that matter most to the FDA. All right, Ignacio, if you could advance the slide now.
I want to update bullet point 4 that we now have 22 patients with RECIST data available at week 8, of whom 15% or 68% are demonstrating shrinkage or classify as having stable disease on their scan. So 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 are being treated with the 350-milligram dose, which at least in the TNB setting -- TNBC setting was not as -- had a vigorous PD-L1 response. But 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.
And 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 an 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.
Dr. Pashtoon Kasi
Thank you so much for having me. And... If we could clip on what you have said so far, I wanted to narrate the story of our index first patient and 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 trying to bring novel therapies and immunotherapies and options for our patients to clinic is this whole field of liquid biopsies. As some of you might be aware, the term liquid biopsy is a misnomer since there's no biopsy being performed, these are noninvasive blood draws.
And 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. And 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, what is the mutational makeup. But as you might be aware now, these assays are also being used as response metrics.
So in general, trial, I do check ongoing circulating tumor DNA assays in these patients because these crude tumor markers, CEA, CA19-9, at least 1/4 of the patients don't even make the marker. And then in this first patient, for example, often the half-life of these glycosylated 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 from the SUNLIGHT study with this oral chemotherapy, the TAS-102 or the brand name LONSURF with bevacizumab as the anti-VEGF, it's one more option, but it's not necessarily a great option.
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. So -- and in this particular study, this -- as a clinician, not just as a PI on this trial. It helps me because the study was not restrictive. So it was not like cherry-picking patients who only had 1 or 2 chemotherapies. Some of these patients have exhausted all aggressive types of therapy. So this particular patient had the standard double FOLFOX chemotherapy with bevacizumab, then FOLFII 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 30x the amount of chemo to be given in the liver. So this person had that installed as well and completed all that therapy. But then after a few months of disease control lo and behold, there was reemergence of liver metastases as well as lung metastases and also was RAS mutant, which 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, this is the kind of patient that an average trial will probably refuse.
So the fact that when we started this patient on treatment as early as a 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. But then the CA actually has blipped up, which as a patient, you're used to looking at tumor marker, that's a sign of concern that maybe my cancer is getting worse. And that's where ctDNA can be helpful. So 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.
So if you multiply that by 5 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. And 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 2 months or 3 months, but then it gives you that early lens, early readout that can be not just important scientifically, but to a patient who sees these results, it's a very good sign because sometimes scans shrinkage of growth, these are criteria that are somewhat archaic made 30 years ago that can underestimate the amount of kill.
As you can see, this is not just decimal point ctDNA blipping up and down. So 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 1, as you can see, was 130,000 parts per million. So that going down to just a few thousand, that's a significant over 90%, 95% fall in ctDNA. And then more importantly, maintaining that in some of our patients, we've also seen oscillating levels and even clearance, 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 by RECIST at the first scan, tumor volume shrinkage of cumulatively about 21%. And that's just at the first 8-week look at week 16, this actually deepened as well up to 24%. And as you can see, the liver metastases, they not only have shrunk with these novel therapies and biologics, we also see the nature of the lesions change. So if you kind of look at the lesions closely, the lesions on the left are -- have this gray or white shoe around it as if somebody picked up a piece of chalk and started shading them.
That's really 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 death tissue inside. So the scans often, even though they are the primary endpoint, they underestimate the amount of kill as evident by this patient scan as well as the ctDNA fall. So you could argue that the shrinkage is about 24%, but the ctDNA fall is about 95%, 99%. Next slide, please.
So 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. So again, not to replace traditional measurements, but clinical improvement, pain going away, improvement in performance status so much so that some of these patients who initially were on disability or took time off are 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 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. 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, and 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. So it's just twice a month very practical resistant follow-up and not much in the ways of adverse events that increase the toxicity. So it's more so that the regimen is not necessarily something that's really efficacious.
We'll see what the larger readout of central RECIST is. But 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. But just to kind of reiterate, even the so-called "stable disease patient, ctDNA, some of these novel tests as well as CDCs are probably providing insights that these scans would miss. Next slide.
And again, a repeat biopsy that we've done now in several patients a few months into treatment, we are noticing 2 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. But then also it's the environment that potentially might be changing to the prime and payer comment or analogy that was made earlier. So 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 generate hypotheses about what to pair these drugs like leronlimab with -- from an immune standpoint. Next slide. I think with that, I'll stop.
I think we're excited to see what we've seen. I would say, while the readout and follow-up continues, it's not just the shrinkage. The clinical outcomes Jay was pointing out, you want to make sure is this going to be durable and which will equate to the PFS and the OS, so to speak. So while that follow-up continues, at least early on, 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 Lancet on its own 10 years ago and then Lancet with bev with the LEG 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.
Question-and-Answer Session
Operator
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?
Dr. Pashtoon Kasi
Yes. So 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. So 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, their diagnosis proceed 2, 3, 4 years before entering this kind of a trial. So 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, at least over half of those patients, about 10% have BRAF, 4% MSI high, which are excluded from this analysis. So all that mutational makeup is very well known already as part of their clinical test and it's being collected. And then we don't check PD-L1 routinely on patients with colorectal cancer, at least it has relevance in other tumor types. But some of the -- from a scientific research trial standpoint, yes, we are.
So as you can see some of the slides 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 Creative 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. So 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 macrophages like cells, the so-called Camel cells. So we'll have a lot of rich data to analyze in the upcoming months to come, as was pointed out earlier.
Operator
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 compared to other patients who receive only the backbone of LONSURF and Avastin?
Dr. Pashtoon Kasi
Yes. I think I kind of answered that in my later slides. But to reiterate, when people start talking about this backbone regimen, -- some patients actually never even try this regimen and then they're already so sick that they just pretty much are given the option of do you want to try this regimen as well? Or do you want to consider best supportive care or hospice.
So again, it's a regimen that's not necessarily something that's a rescue agent. So 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. But quantitatively, we'll have all the response data to analyze and we can -- and as Dave was pointing out, we are trying to see if there are data sets 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 2 doses, which is randomized. So even though we don't have a placebo arm, we do have 2 arms. So some hypothesis generating insights probably will come in the upcoming months.
Operator
Thanks. Last question for you, Dr. Kasi from the audience. Looking ahead, what excites you? And please tell us a little bit about the investigator-initiated project that you will be kicking off shortly.
Dr. Pashtoon Kasi
Yes. I tell my patients when I put them on any trial is, of course, I want to get the maximum mileage out of any treatment or trial. But then also with these novel drugs and treatments, it's also intriguing and something to keep in mind is that did the tumor change, hopefully for the better for future options. It's not just what we're doing for the patient today. So we're seeing both early hints of 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. So that itself is reassuring. But then 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 will be very exciting to see in the upcoming years to follow.
Now on the trial that we mentioned, so we serendipitously again, stumble 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 is being done by some of the colleagues regarding how it can help with the fatty liver, the so-called NASH, NASH, MAFLD or nonalcoholic steatohepatitis. It goes by different names. But 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 fluorosle pump that they go home with the oxalipatin, platinum-based chemotherapy, irinotecan chemotherapy. the so-called liver pump that this particular patient also had where we are able to inject something called FluoxyuridineFUDR chemotherapy at 300x 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 microcode, some sort of fibrosis. So 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 hep B, hep C, alcohol or other causes of steatosis and cirrhosis. So the idea with the observation that we were seeing with the CLOVER trial was we do a lot of these liver pumps.
If you look up liver pump on Google, you'll see now I think it's over 30, 40 places. The company, the Boston Scientific that bought Entera, the makers of the liver pump, they have a map that guides patients where can they get a liver pump. 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. But now there are experts and surgeons. So 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. So we did, for example, just 30 pumps in our clinic last year.
So our question was if we have a drug that has potential efficacy and maybe even mitigate the toxicity that we are doing with the chemotherapy, 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, what would have happened if we had done leronlimab a year ago when the patient was actually getting the liver pump. So that's in a nutshell, that trial. So we'll have about potentially 36 patients, all getting the recommended Phase II, the 700-milligram dose of the leronlimab in conjunction with their 4 months of the pump chemo.
And 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. But we'll also see does it help prevent the liver damage. So there will be a liver biopsy as well. So I think we're kind of moving this up the journey of a patient with cancer. And 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. So we may also have an opportunity to see what leronlimab alone does on that trial. So we're now kind of -- we have the approval at our so-called disease team or scientific level.
Now it's going to go through the hoops of the usual regulatory and contracting and FDA. So hopefully, sometime in the very near future, we can open this liver pump trial with leronlimab that we have abbreviated as an acronym called the CHAMP trial.
Operator
Well, once again, we thank Dr. Kasi for his time today and thoughtful insights. At this time, we will continue with the management update. So I would like to turn it back to Dr. Jacob Laresari.
Jacob Lalezari
Chief Executive Officer
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. Okay. 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 is only less than 1% of patients that had an overall response rate. But the combo in 246 patients published in the New England Journal showed a median progression-free and overall survival on the order of 6 and 11 months and 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. So that's the bar the FDA is looking at, 6% response rate.
But then a subsequent real-world data set published more recently showed similar progression-free and overall survival, but the overall response rate, meaning the percent of patients who responded in terms of their scans was under 3%. So 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. So 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 to 700 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. And 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 or 700, and we're now delaying introducing the checkpoint inhibitor until after a patient has a documented progression, and that amendment was just submitted to -- 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.
In addition, as Tarun 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. And as Dr. Kasi indicated, he's leveraging both the liver protection and the antitumor effects of leronlimab. And 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. So the possibility exists that we will enroll patients who are CCR5 negative on their tumor and to then still be able to determine if there's any antitumor activity in that subset of patients. And then 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.
And then finally, I would say that evaluating leronlimab in combination with a checkpoint inhibitor is definitely a priority for us at CytoDyn. And 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. So that's a decision pending in the next few weeks or months. Next slide, Ignacio.
So just quickly looking at the breast cancer data. I know we're running short on time. In the next slide, we've never actually discussed this on a call before, but these are a summary of the data. Again, we were -- CytoDyn was trying to figure out when patients may have deceased from the prior TNBC studies. We found out that 5 patients were still alive. We tracked down their medical records, and we were able to coordinate the 3 variables of who induced PD-L1 above the 400 threshold from Creative Microtech that's considered clinically relevant, who received a checkpoint inhibitor and who is still alive.
And all 5 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 5 patients who induced above 400 got a checkpoint inhibitor, either atezolizumab or pembro were still alive now 5-plus years later. And so that created the paradigm of the prime impair that led us to the CRC study and then in attempting to replicate and prospectively demonstrate the prime impair is when we've seen this extraordinary activity of leronlimab as a stand-alone agent.
On the next slide then is a summary of what we've presented on TNBC. Previously, Dr. Pastoon'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. And never -- I never quite knew what to make of that data. But 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-milligram dose, and then it was almost 90% of patients at the 525 or 700-milligram dose.
And as I said, 5 out of 5 patients who upregulated and received a checkpoint inhibitor are alive now 5-plus years later. 3 of those 5 currently have no evidence of disease. 2 of those 3 started leronlimab with lung metastasis and 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 5 years later. And then 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 kind of arbitrarily given by the oncologists who were just shooting for whatever they could, 100% of those individuals, unfortunately, are now deceased.
So on the next slide, how we're progressing in breast cancer is we've had very productive conversations with the pre-spine network, and they are going to take on Part 1 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 PSpine network, they are extending the patient population from TNBC to include all HER2-negative patients with breast cancer. And we're fortunate to have Dr. Paul Polman 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 start-up time can be measured in weeks to a few months.
At the same time, we are then going to 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. And that is still the case that in the EAP program, we will be measuring PD-L1 at baseline and then at month 1, 2 and 3, and we'll report on that later. And as previously indicated, we have funding in place for the first 20 patients on the program.
And then 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. And they 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. So a lot happening in colon and a lot happening in breast cancer. Next slide.
So in terms of upcoming milestones and what the year ahead has in store, on the next slide, priorities First, the stand-alone benefit of leronlimab in this case, with the backbone through the biomarker collection, primarily ctDNA, but other tumor markers as well. And then the disease control rate, the percent 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 stand-alone and developing leronlimab as a prime impair. And the prime impair definitely hinges on this PD-L1 induction. And so 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 PSPI and I-SPY studies in breast cancer.
We want to then demonstrate that the clinical benefit of adding a checkpoint inhibitor to leronlimab in PD-L1 induced patients, which will be the focus of Part 2 of our Phase II program in breast cancer. And then something I thought would be easier is we need to identify the optimal dosing of leronlimab in oncology. The pre side study will start at the dose of 525 and then dose escalate to 700 with an option to dose down to 350 depending on what the CRC study shows us in terms of a potential dose response. The 350 data on DNA is obviously remarkable. And the question is, will the 700-milligram dose provide either steeper or more rapid declines or more sustained declines in circulating tumor DNA -- and 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 Pulson 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. And my understanding from the pre-spine 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 and then a more robust presentation at ASCO GI in San Francisco in January, during which we should be able to provide final results.
And then 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 -- and the plan is to submit a fast track or breakthrough designation application later this summer or early fall. And of course, as these data become known and more widely disseminated, we will continue to evaluate potential opportunities for strategic partnerships. And Ignacio, I think from there, if we can go to some questions and extend our time by a few minutes, that would be great.
Operator
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?
Jacob Lalezari
Chief Executive Officer
Well, as I said earlier, I could not be more excited by what we're seeing. And I frame the results as being on the outer edge of what I even thought was possible. So the signals that we're seeing in colon cancer, obviously, saw in breast cancer and some of the data we've recently presented in glioblastoma 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. So yes, as a foundational backbone across multiple tumor types, -- and yes, we are pursuing monotherapy studies.
Operator
Thank you. Our next question, can you provide any updates or expected data time lines for the investigator-initiated trials, including the projects in glioblastoma, Alzheimer's and colorectal cancer, hepatic artery infusion project?
Jacob Lalezari
Chief Executive Officer
Yes. So CytoDyn is very busy. And the focus remains colon cancer and breast cancer. But 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. So that will 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 and the leronlimab-treated groups at necrosi seem to have far less and far fewer metachronous spread of the tumor, which was documented and statistically significant.
So 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 2 different cell lines with a survival endpoint. And 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. So we are moving forward on glioblastoma as well. And I would mention that I've had some preliminary conversations with several other major medical centers of investigators who want to propose their own investigator-initiated trials in 2 other separate solid tumors. And 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, Jonasz remains extremely active at Oregon Health Sciences University on a variety of HIV cure fronts with leronlimab. And then something we don't talk much about, but 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. So a lot of other activity besides the main emphasis, which is and will remain colon and breast cancer.
Operator
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? Specifically, when can we expect a more mature data set from the Phase II CLOVER NCRC study?
Jacob Lalezari
Chief Executive Officer
Yes, it's a great question. So Robert and Tyler and I are going to ASCO as primarily in networking. We are meeting with the pre-SPI and I-SPY folks and potentially a number of other pharma companies. But the main point of that question was finding out when the next update from CLOVER will be. And 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 and when appropriate, and that would be toward the end of the summer, early fall.
Operator
Thank you so much. Our final question. There seems to be a new FDA with shorter time lines for granting FDA approvals. Is Sightline exploring any of these expedited pathways with the FDA like the voucher program? NBC and MSS CRC both seem to be potential candidates for a voucher or some sort of expedited treatment.
Jacob Lalezari
Chief Executive Officer
Yes. I appreciate that. I think that my emphasis has been on generating rock solid prospective unassailable data that everyone can look at and agree and that there's a there. And that has been the great pleasure of being the CEO of CytoDyn lately as 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 be the trick. And so we're going to 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. And so it's not for us to decide exactly how the FDA is going to handle this. But 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.
Operator
Thank you so much, Dr. Lalezari. Now is the time for final closing remarks. The floor is yours.
Jacob Lalezari
Chief Executive Officer
Well, I don't know what else to say except that it's been an incredible journey in Odyssey. And 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. And indeed, I just want to mention that a number of folks who submitted questions had offered additional words of encouragement and super appreciated. Nothing about this has been easy. And 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. So 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.
Operator
Thank you very much. This concludes CytoDyn's investor update webcast.
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