Greetings and welcome to the INmune Bio first quarter 2025 earnings call. At this time, all participants are in a listen-only mode. Later, you will have the opportunity to ask questions during the question-and-answer session. You may register to ask a question at any time by pressing star one on your telephone keypad. You may withdraw yourself from the queue by pressing star two. As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this conference call. At this time, it is my pleasure to introduce Dr. excuse me, Mr. David Moss, CFO of INmune Bio. David. Thank you, Jesse, and good afternoon, everyone. We thank you for joining us for the call for INmune Bio's first quarter 2025 financial results. With me on the call today are Dr. RJ Tesi, CEO of INmune Bio, and Dr. Mark Lowdell, Chief Scientific Officer of INmune Bio, who will provide an update on our cord-surrounding immune programs. Also on the call is Dr. CJ Barnum, head of neuroscience, who will be here to answer questions. Before we begin, I remind everyone that except for statements of historical facts, the statements made by management and responses to questions on this conference call are forward-looking statements under the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. These statements involve risks and uncertainties that can cause actual results to differ materially from those such as forward-looking statements. Please see the forward-looking statements disclaimer on the company's earnings press release, as well as risk factors in the company's SEC filings, including our most recent quarterly filings with the SEC. There's no assurance of any specific outcome. Undue reliance should not be placed on forward-looking statements, which speak only as of the date they are made, as the facts and circumstances underlying these forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligation to update these forward-looking statements to reflect future information, events, or circumstances. With that behind us, now it's my pleasure to turn the call over to RJ Tesi. RJ. Thank you, David. For our first quarter 2025 call, I will review key takeaways and provide an update on our platform programs. Following my comments on recent developments, Dr. Mark Lowdell, INmune Bio CSO and inventor of both Cordstrom, will provide an update on those programs. David Moss, INmune Bio CFO, will then conclude with a review of first quarter financial results and update future catalysts. We will be happy to take your questions. I'm sure everyone on this call knows we will soon be reporting top-line results from MINDFuL. That is our phase 2 trial in patients with early Alzheimer's disease. The results are expected mid to late June. That is, in give or take 50 days, we will know the answer to the question, what happens in Alzheimer's disease when you properly target neuroinflammation. Our last investor update call was just a short six weeks ago, but there have been important and I believe positive changes in the Alzheimer's disease marketplace during that short period of time. We believe these changes will be beneficial to XPro's market opportunity in early Alzheimer's disease. Last month at AD/PD, which is the largest Alzheimer's disease meeting in Europe, INmune Bio reported the biomarker profile of patients enrolled in the MINDFuL study. The data confirmed that we have been underestimating the market opportunity for XPro in patients with early AD. Historically, we stated that up to half of the early Alzheimer's patients will qualify for XPro based on the biomarkers we use as our enrollment criteria. Based on the data, INmune Bio and other companies presented at AD/PD, we now believe more than two-thirds of early Alzheimer's disease patients will be eligible for XPro based on APOE4 status alone. I remind you that APOE4 positivity was one of the four enrichment or enrollment criteria we used in the MINDFuL study. The APOE4 status of patients in the MINDFuL is almost identical to what is reported in recent major trials in Alzheimer's. Patients with at least one APOE4 allele make up more than two-thirds of the patients in these trials. This means the market opportunity for XPro in early AD has increased to nearly 70% of early AD patients, not the 40% we have previously been talking about. On the call six weeks ago, I also mentioned the safety profile of XPro in the MINDFuL trial. Nothing has changed. There are no reports of ARIA. No patients have had unscheduled MRIs due to CNS symptoms or headache, et cetera, and there have been no deaths. So far, XPro is safe and well tolerated in this patient population that has an average age of 73 years old, and many of them have a long list of comorbidities. The excellent safety profile of XPro in these patients provides a unique APOE4-related market opportunity for XPro. Let me explain. Both the EU and the U.K. have approved lecanemab, the Eisai Biogen drug, for patients with early Alzheimer's disease who have none or one copy of the APOE4 gene. The market authorizations specifically exclude patients who carry two APOE4 alleles. In the early AD trials that report APOE4 status, APOE4 homozygotes, that's the patients that have two APOE4 alleles, are 15% of the patients. That means because of labeling restrictions on lecanemab in the U.K. and EU, early AD Alzheimer's patients who are APOE4 homozygotes will not be eligible for therapy with the anti-amyloid drugs. This group now is an important unmet need, ideally suited for XPro therapy. In the U.S., recent surveys of practice patterns indicate that this patient population is not treated in many centers due to the risk of ARIA. Even in the U.S., where the labeling is different than you see in the U.K. and Europe, we believe that after approval, XPro will be the best and only treatment option available for this subgroup, important subgroup of early Alzheimer's patients. We should have an exclusive biologically based market. Finally, the biomarker landscape of Alzheimer's disease is really evolving quite quickly, and it's evolving in a way that really benefits our focus in these patients. Now, once the diagnosis of Alzheimer's is made, pTau217 in blood has become the biomarker of most important interest by clinical teams treating these early Alzheimer's patients. PTau217 levels define the severity of Alzheimer's. PTau217 levels in the blood have prognostic value and correlate with stage of disease. In the near future, we predict that changes in pTau217 blood levels will be used as a pharmacodynamic blood marker of therapeutic response in these patients. As a reminder, XPro significantly decreased pTau217 during the three-month phase one study, and this biomarker is included in the package of biomarkers that we are studying in the MINDFuL's phase two program. Having a great drug is a necessary element for a successful clinical program, but it is only part of the story. Since the last patient was enrolled in November, we have been highlighting the hard work needed to report the top-line data in June. These are the busiest of times. For example, after the last patient has their final safety visit, but before the database is locked, a complex series of critical data management and quality assurance tasks are undertaken to ensure the data are complete, accurate, and ready for analysis. The process begins with data cleaning, where we review patient port forms and entries into the electronic data capture system to resolve discrepancies, fill in missing data, and look for outliers. This is a patient-by-patient process. It is labor-intensive. Queries are issued to trial sites to clarify inconsistencies, and there is source data verification to confirm that the recorded data matches the source documents, for instance, the medical records. This phase also involves ensuring compliance with regulatory standards such as GCP by maintaining log trails and documenting all changes. After data cleaning are complete, the focus shifts to the final quality checks and preparation for database lock. A comprehensive review of the data is performed to confirm that all queries are resolved, deviations documented, and validation checks satisfied. The statistical plan cross-check to ensure that all data points are present and correctly formatted, and the data monitoring committees conduct final safety and efficacy reviews. We don't lock the database until we are sure the database is clean and accurate. I will also say that this is all done with blinded data. No one knows who got what during this process. We don't run the statistical programs until the database is locked, and it's only when that statistical package comes out that the real unblinding occurs. We remain on track for this process to be completed in mid to late June, and I can tell you we can hardly wait to see the fruits of our labors. This is the moment we've been anticipating for several years. We are confident we will report results that will change the care of patients with early Alzheimer's disease, and this confidence is highlighted by management's substantial share ownership. Like you, we are investors in INmune Bio. Our interests are aligned with yours. As important as MINDFuL, our Alzheimer's trial, is to the company and our investors, it's not our only program. Cordstrom for the treatment of children with recessive dystrophic epidermolysis bullosa, or RDEB, is expected to file a BLA in 2026. The program continues to move forward in men with metastatic castrate-resistant prostate cancer. The light is shining more brightly on Cordstrom these days. It is an orphan disease program, and after recent comments from the FDA, we are increasingly excited by its prospects. The FDA has stated their intention to move rare disease treatments through the approval process faster, with more input from patients and caregivers. In our group, Cordstrom provides a systemic therapy for a systemic genetic disease that has the support of patients and caregivers. Enough from me. I will turn the microphone over to Mark Lowdell, the CSO and inventor of both Cordstrom and INmune Bio to give you a more in-depth update on those programs. Mark. Thanks, RJ. Good afternoon, everyone, and thank you for joining us. With regard to the latest developments with Inmune, the CaRe PC trial in prostate cancer completed the phase one dose escalation cohorts in December, which allowed us to open the phase two extensions of both the high dose and intermediate dose cohorts in parallel, and we reported that in our last call. We saw no adverse events in any of the patients treated during phase one, which thus met the primary endpoint of the entire trial. Similarly, none of the patients treated in phase two to date has shown any adverse event, and Inmune remains extremely well tolerated in this challenging and elderly group of patients who've had lots of previous treatment and a lot of comorbidities. At the end of March, we reported that Inmune infusions had led to increased NK cell potency in the patients treated at the lowest dose, and the blood samples from patients at the intermediate and high dose cohorts of phase one and phase two are being received in the INmune Bio labs in London and are being prepared for testing. We'll share those results as soon as they're available. In parallel, we're receiving the independent reports of the PSMA PET screening of the phase one patients who've completed follow-up. This is a very precise assay of the sizes of individual tumor lesions in each patient before treatment and at three months after completion of Inmune treatment. This very complex data set is being reviewed by the lead clinician for CaRe PC, but we can already see from subjects in the lowest dose cohort that some lesions have resolved completely following Inmune treatment. We eagerly await the data from the intermediate and high dose patients, which we'll share as soon as they become available. The CaRePC trial continues to recruit phase two subjects and remains on track to complete enrollment this year. The INmune Bio team has manufactured all doses of Inmune for the completion of the trial, and we've successfully transitioned the US drug supply logistics from our previous contractor into a US company called Cryoport. We are set up for the successful conclusion of the trial. In line with our ambitions for INmune in prostate cancer and other solid tumors, we're transitioning our manufacturing into a U.K. government incubator facility where we can manufacture future drug batches for clinical trial and, if successful, commercial manufacture and global supply. While CaRePC is ongoing, in February, as RJ just said, we announced the development of our Cordstrom asset towards a BLA filing next year, 2026, for the treatment of the extremely debilitating disease recessive dystrophic epidermolysis bullosa, or RDEB. Epidermolysis bullosa, of which RDEB is the most severe form, is an inherited disease which manifests in the first two years of life. The outer layer of the skin, the epidermis, does not anchor properly to the underlying dermis, and children suffer horrific skin blisters over their whole body. Worse still is that EB is a systemic disease, as RJ said, so children suffer with lesions behind their eyes, down their esophagus, and throughout their gastrointestinal tract. There's no systemic treatment for RDEB. Cordstrom is an off-the-shelf allogeneic mesenchymal stromal cell drug from pooled donors, which INmune Bio has owned since 2019. It was developed by me and some colleagues with academic funding in the U.K. and is a platform that can be used to treat multiple clinical indications by specific selection of the individual donor products used to formulate the final pooled drug. We've been supplying one formulation of Cordstrom into the U.K. multi-center trial led by pediatricians from Great Ormond Street Children's Hospital in London to treat children with RDEB. This was a double-blind, placebo-controlled crossover trial which treated all of the eligible children in England with RDEB. The results, when they were unblinded, led to the clinicians and the U.K. National Institute of Health Research asking INmune Bio to develop Cordstrom as a licensed medicine for this disease, and we presented the trial data to the U.S. FDA in December, as RJ said. The FDA data review led to the award of rare pediatric disease and orphan drug status for the treatment of epidermolysis bullosa, and following a type C meeting with the FDA in February, we have a clear route to submission of a BLA in 2026 and parallel submissions to the U.K. MHRA and to the European Medicines Agency. On our last call, we said that clinical trials are the poster children of drug development, but moving from trials to market requires much more, not least a full development of the drug manufacturing pathway, which meets regulatory requirements, is cost-effective at scale, and meets likely global demand. We've taken this on board with respect to Cordstrom in the same way we have with Inmune, and in fact, have developed parallel processes for both drugs which can share the same manufacturing platforms at all stages of manufacture. This not only simplifies manufacturing facility setup and design, but it allows us to maximize the use of manufacturing space we rent by being able to switch between Inmune production and Cordstrom manufacture, thus controlling our production costs as we move towards commercial supply. Having used the income from selling Cordstrom into the U.K. trial in RDEB to subsidize the supply of CNDO-109 into CaRePC, the equipment we've been using to manufacture CNDO-109 is now subsidizing the development of Cordstrom, which is a nice, very circular situation. Having completed all manufacturing of CNDO-109 for CaRe PC, the U.K. team is dedicated to providing all of the data needed for the BLA submission next year for Cordstrom and transitioning into the new production space to allow Cordstrom as a commercial product and CNDO-109 as an investigational product for our next clinical trials. That ends my update on the CNDO-109 and Cordstrom platforms, just to say we're as excited about these as we are about the ADO2 trial, and I'd like to turn the call over to David Moss, our CFO, to discuss financials. David. Thank you, Mark. As usual, I'll provide a brief overview of our financial results and upcoming milestones before we head to our Q&A session. Net loss attributable to common stockholders for the quarter ended March 31st, 2025, was approximately $9.7 million compared with approximately $11 million for the comparable period in 2024. Research and development expenses totaled approximately $7.6 million for the quarter ended March 2025, compared with approximately $8.7 million for the comparable period in 2024. General and administrative expenses were approximately $2.3 million for the quarter ended March 31st, 2025, compared with approximately $2.3 million for the comparable period in 2024. At March 31st, 2025, the company had cash and cash equivalents of approximately $19.3 million. Based on our current operating plan, we believe our cash is sufficient to fund our operations through Q3 of 2025. As of May 8th, 2025, the company had approximately 23.2 million shares of common stock outstanding. Subsequent to the end of the quarter, the company raised gross proceeds of approximately $2.1 million from the sale of common stock on the ATM. Now I'd like to focus on some key upcoming milestones. As everybody's well aware, we expect to have top-line cognitive data from our phase two trial on Alzheimer's disease in the second half of June. As RJ stated, everyone at the company is looking forward to this event. We anticipate an end of phase two meeting with the FDA in the fourth quarter of 2026 to agree on the design of a phase three trial. We expect to complete enrollment in the phase two portion of the Inmune trial this year, as Mark mentioned earlier, with periodic updates on immunologic and therapeutic responses to Inmune as data becomes available. We anticipate filing a BLA for Cordstrom in RDEB in the first half of 2026. Finally, we will initiate a phase two trial of XPro in patients with treatment-resistant depression once NIH funding is made available. At this point, Jessie, I'd like to now pull for questions and open it up to Q&A. Jessie. Thank you. At this time, if you would like to ask a question, please press star one on your telephone keypad. You may remove yourself from the queue at any time by pressing star two. Once again, that is star one to ask a question. We'll go first to Gary Nachman with Raymond James. Hey, guys. This is Denis Reznik on for Gary Nachman. Thank you for taking our questions and congrats on all the progress. Just assuming a positive readout in June, can you just continue walking us through the exact next steps for the program? You mentioned you can meet with the FDA at the end of this year, but what's a realistic timeline as to when you can initiate the phase three? Could you provide maybe some metrics as to what's reasonable as to how many sites you can get online and how many patients could be enrolled each month? I've got a couple of follow-ups. Yeah, this is RJ. Thank you, Gary. I think expecting us to really design the trial before we have the results and before we talk to the FDA is, we would like to defer that opportunity. Our goal, as David mentioned in his milestones, is to, as quickly as possible, get to the FDA for an end of phase two meeting. It is classified as a type B meeting by the FDA process. There is a 70-day clock. Hopefully, as we said, it will be completed in the fourth quarter, and then we will move as quickly as possible to getting sites open and those first patients enrolled. We are lucky that we have got a lot of sites ready to go in Europe, and we know there is considerable enthusiasm for this program in the U.S. We anticipate being able to get the sites, but I don't want to put a date on it. We don't want to put a size on it. Because we can't put a size on it, we don't want to really predict what the capital needs will be at this point. Suffice it to say that we believe that it will look very much like the phase two trial, although we expect it will be larger, and there may be a fewer set of biomarkers, but we won't know until we talk to the FDA. I totally understand that, and that's helpful color. Just a couple of quick follow-ups. Just because there's been a lot of turnover and uncertainty at the FDA recently, can you comment on if the people who will be reviewing your program are all still there? Everyone who's previously signed off on the EMAC is all still there? With the poster presentation you guys had at AD/PD last month, maybe could you just talk a little bit more about the receptivity you've received at the conference and then overall the level of interest the company's been receiving recently as we approach the June readouts? Yeah, I'll let CJ answer the AD/PD call, but we've obviously, like any biotech, have been watching what's going on at the FDA quite closely. Our intelligence, which is pretty good, we believe, suggests that when it comes to drug development, the FDA has remained on track. The delays appear to not be developing that everyone feared. We can't predict the future, but everything we hear so far is okay. I remind you that the FDA has not yet completely signed off on EMAC. Our goal is, and CJ can add more color to this, our goal is to present them EMAC data side by side with the CDR data, and one of the major questions we'll be asking them at the end of phase two meeting is, can we use EMAC as the primary endpoint for the registration trial? Remember, and we've been saying this forever, that we believe that it's a far superior metric of cognitive function in these patients, but it's the FDA sandbox, and if they say no, we're not happy, but we will move ahead with CDR. In fact, the trial that we are currently doing will allow us to perfectly design the study to get the kind of result we need. CJ, you want to add any color to that and also comment on his AD/PD question? Yeah. Yeah, sure. Just to sort of clarify a little bit about what we've communicated with the FDA is we've given them the plans and what we intend to do with the EMAC, and what they've done is they've responded to that in a way that really outlines their guidelines on how you validate a measure, really think about it more like a checklist, which is what we've done in this trial. They are not going to comment on that until they see the data. That's just a standard response. We think we've done everything. We've hit all those bullets in those checklists, and I think we're in a good position. AD/PD was pretty interesting. I think there's two things that I think really came out of it as it relates to feedback we got from the poster. One is I think people are excited for an anti-amyloid or a therapy that's not targeting anti-amyloid. I would say even more so, we got a lot of traffic and interest in EMAC, and one of the comments that we, especially from neuropsychs that work with big companies or worked in the space and measuring cognition, are really excited that there is a company that's driving the appropriate measures moving forward. There is a lot of excitement and interest around the outcome there. Great. Thanks so much. We're looking forward to the readout. We'll move next to George Farmer with Scotiabank. Hi, good afternoon. Thanks for taking my questions. A couple from me on XPro. With the trial coming up and the data coming up, how do you think investors will react to a scenario whereby you hit on EMAC, but CDR is a bit equivocal? RJ, you were talking about the potential benefit of XPro in patients who would be ineligible for anti-amyloid therapy, including APOE4 homozygous. Do you have a feel for how many APOE4 homozygous are in your trial? Yeah. So CJ, why don't you address the specific question about hitting on EMAC and what CDR will look like because it will be more correlative than not? Yeah, I'm not sure where you're going with that, RJ, but let me just to answer the question about how investors feel, I actually would ask you that question. From a scientific standpoint, what I can tell you is that the EMAC is the tool that's actually capturing cognitive changes that occur in early AD. It's identifying those patients. It's the ability to measure cognitive decline. It's the right tool. The CDR is a more blunt instrument. I think what RJ is saying is one of the things that we're seeing is it correlates very well. We're seeing correlations between EMAC and CDR, which is a good sign, but the CDR is inherently more noisy because it's a blunt tool. I would say, I can't answer how the investors would think, and I'm hopeful that we've talked with enough of you so that you understand how we think in the scientific validity and rationale for using the EMAC. For us, the EMAC is really the primary driver, and we'll understand what if the EMAC, for example, is fuzzy. We'll have a clear understanding. The most likely scenario is just it's a power issue due to noise, but we won't know until we see the data. Yeah. And just to add a little bit more color, we believe that professionals in the field, i.e., the academics and potential biopharma partners, will be able to understand if they do not both are not both perfect. As CJ says, it is not going to be that CDR is going in a different direction. It is just going to be a power and a size of study issue, which is easily solved in the phase three trial. Yeah. Let's talk about the APOE4 homozygous. In both the lecanemab and the donanemab trial, they were 15% of the patients. In our trial, it is 9%. They are smaller trials. I do not see 15% and 9% that difference. I expect it will be in the 15% range. Interesting, aducanumab did not break out the homozygotes in number. At least I do not remember it. I think it's a pretty, and when you go into the literature and you look at clinical data, that's about where it stands. That's a pretty, in Europe, it's a big population. And as you know, in Europe and the U.K., they don't do off-label prescribing. That group is ready and waiting for XPro, in my opinion. All right. Great. And then one more from me. The impact of XPro on p-tau-217 looks pretty compelling. Went back and looked at your presentation. How do you think that magnitude compares to other Alzheimer's disease treatment approaches that have been published? CJ, I'm going to leave that one to you. I think that's tough to answer. I think the only thing that I can say is you don't rarely, I can't think of another study where you saw changes in the CSF that early quite robustly. I think this is one of those things that holds a lot of promise, but we'll see what it looks like when we have the full data set. Yeah. We're the only company with data in a drug that treats neuroinflammation. The anti-amyloid drugs do decrease tau. I mean, I think when neurons stop dying, you see you get some decrease in tau. But we like p-tau-217. The clinical teams like p-tau-217, and I suspect most of the regulatory agencies are going to be very receptive to that biomarker as part of our data package. Okay. Thanks very much. Thank you. We'll go next to Tom Shrader with BTIG. Good afternoon. Thanks for taking the questions. You said something that I had not really thought of, and I am wondering if it is correct if I am hearing, what, are APOE4 patients inherently inflammatory? The other question, I kind of want to re-ask George's question with a little bit of a how much does CDR have to decline? How big does the reduction in decline of CDR have to be to hit in a trial of 300 patients that is only run for six months? Is it reasonable, or is it a pipe dream? Do you have a sense of what the reduction in decline would have to be for a trial of this size to hit? Thanks. Thank you. Yeah, I can take the first one. CJ? Or the second one. Tom, what's interesting is when we powered the study, which was powered on CDR, by the way, the assumptions that we had in terms of our expectation for decline over six months and the effect size of that decline was somewhat conservative based on the aducanumab group that was used to power the study. What's interesting is a few years later when lecanemab and donanemab came out, what we saw was the assumptions that we used were exactly what happened. Within a six-month period, both aducanumab or lecanemab and donanemab were statistically significant at six months, and their decline was about the exact same number that we used to decline for six months. I think that's important. The effect size of that decline was almost exactly what we used to calculate our power. I think that gives us a lot of confidence that our assumptions were right on. I think the other thing that I want to point out is this is for a cohort of patients that were not enriched for inflammation, and of course, we expect that we are going to get a little bit faster decline with inflammation. I think that gives us even a little more confidence. Yeah. Something that ApoE4 would be considered is an inflammation gene. It is considered that with your ApoE4, you are hot, so to speak. As CJ just said, if you look at ApoE4, either heterozygotes or homozygotes, they actually get their age of onset earlier, with the heteros being later than the homozygotes. Their progression of the disease, i.e., going from MCI to early mild AD, is faster. Actually, when you look at the ApoE4 homozygotes, they have a higher mortality rate. They have about a five- to seven-year worse survival compared to the other group. ApoE4 is a bad gene to have. Any of you that have done 23andMe and they ask that question, "Do you want to know what your Alzheimer's risk is?" the main thing they're going to tell you was whether or not you were ApoE4 positive. I do not know how many said yes, but I never wanted to know, quite frankly. If I can follow up with CJ, how much of the other two trials hitting, they are bigger trials, right? They are something like, I do not know, there are a few fold more patients. Is that the reason they separated in six months, or do you still think you are powered correctly to see it if you have a similar type effect? I think so. I mean, there's some variables we don't know. I think we're close. I don't think we're going to be off too much. It's hard to answer that question, but I would say that the data that we see, despite the fact that they've got more patients, we're looking at standard deviation. The standard deviation was around one for those trials, which is very similar to what we used in our projections. The decline was quite similar. I think we're going to be okay. I think we're going to be close. Tom, remember, we have bragged about the quality control that we've had in this trial, the precision of the type of patient we enrolled. I think that is really an unheralded advantage. When you're enrolling 1,600 patients, and I think it was like in 42 countries or something as those big trials, the quality control, you just get a messier patient population. It's not because people aren't trying. It's just it's a big animal to tame. I can tell you, we've spent a huge amount of time and resources on our quality control, and our trial was much smaller. It was, what, 208 patients in eight or nine countries. The quality will be reflected in the output, I believe. All right. Great. Thanks for all the color. Our final question will come from James Molloy with Alliance Global Partners. Hello. This is Laura Suriel on for James Molloy. Thank you for taking the questions. For Cordstrom, are you still on track to initiate the 12-month open-label trial mid this year? I also see that U.S. patients are expected to be enrolled later on. What is the enrollment aim here, and how many sites do you expect to have open in the U.S.? Mark? Yeah. Great. Thanks very much for that question. What we're doing at the moment is following the guidance from the FDA about how to make the U.K.-manufactured cords usable in the U.S. We're starting a manufacturing program later this week, actually, of a new batch of products using U.S.-approved cord donors. That allows us, once we have those data, to draft the IND. We're expecting to submit an IND later this year. We've been delayed by various factors, including the funding situation. We're still on track to, or we're still planning an IND in the U.S. for Cordstrom. The BLA is not dependent upon the U.S. IND or indeed the open label in the U.K. We're going to submit for the BLA with the data we already have from the double-blind placebo-controlled crossover trial. We will run a follow-on trial in the U.S. opening next year in parallel with trials in the U.K., in which we will further explore the dosing of the drug and the periodicity of dosing. Does that answer your question? Yes, it does. Thank you. Just as a follow-up, with the BLA filing coming up, how would you describe the overall regulatory space for RDEB treatments? Like Abeona, for instance, just got approval for their gene therapy for RDEB. Do you consider this a positive for where you're at with Cordstrom? There are two things about that. It is a very good question. The synthetic skin gene-modified product, which has just been licensed, is a great product. The challenge is that it is applicable to open wounds on the skin, and that is its only indication. It requires a surgical intervention to apply it. One of the known side effects is itch. Obviously, one of our principal clinical outcomes from the first trial has been reduction in itch. Even in the presence of the gene-modified product, we have a window to treat the same patients with Cordstrom. More importantly, Cordstrom is a systemic therapy. As I said in the presentation just a few minutes ago, RDEB, and indeed all EB, is actually a systemic disease. These kids, and indeed when they get through to adulthood, suffer the condition throughout their esophageal tract, and it is more widespread than just the dermis. We see a role for Cordstrom in treating those patients with systemic disease as well as skin lesions. Indeed, a trial of a similar MSC product that is not going through to license in South Korea showed improvement in skin scores after treatment as well when the children were followed up long enough. We do see a really good opportunity for Cordstrom, even in the presence of the current licensed alternatives. Understood. Thank you for taking the questions. That will conclude the Q&A portion. I will turn the program back over to Dr. Tesi for any additional or closing remarks. Yes. Thank you all for attending today's call. I just make a moment of closing comments because we are excited. We are approaching the most significant milestone in the company's history. When we started INmune Bio and got XPro in 2017 and became a company focused on Alzheimer's disease, no one viewed it as an immunologic disease, or few did. At that time, the focus was exclusively on amyloid and tau. Since then, with two anti-amyloid drugs on the market, we have seen a sea change in the way Alzheimer's disease is viewed. Alzheimer's is considered by many a CNS disease driven by immune dysfunction. Neuroinflammation is no longer viewed as a side effect of Alzheimer's disease pathology, but a significant driver of that pathology. INmune Bio has positioned itself as a leader in targeting the immune dysfunction that drives destructive neuroinflammation. We are very careful and precise with our terminology here. Stopping neuroinflammation by immunosuppression, glial suppression, is very different than stopping destructive neuroinflammation by repolarizing glial cells to support the CNS cellular unit and improving remodeling and repair. The goal of effective therapy for the Alzheimer's disease is to reestablish normal glial homeostasis. The idea that the brains of the elderly with dementia can undergo remodeling and repair is novel. We believe data from the MINDFuL trial will change the direction of scientific research and discovery in the neurology and CNS drug development arena. I've said before that this is the dawn of the golden age of CNS development. We believe it is, and we look forward to leading the charge. With that, I thank you, and we will be talking to you all soon when the data are released. Thank you very much. Thank you. Ladies and gentlemen, this does conclude today's program. Thank you for your participation. You may disconnect at any time.